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Principles
of
Critical Care
third Edition
Principles
of
Critical Care
Farokh Erach Udwadia

md frcpe frcp (London) Master fccp fams facp Hon DSc
Consultant Physician and Director—Intensive Care Unit

Breach Candy Hospital
Emeritus Professor in Medicine
Grant Medical College and the JJ Group of Hospitals
Consultant Physician
BD Petit Parsee General Hospital
Mumbai, Maharashtra, India
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Principles of Critical Care
First Edition: 1999
Second Edition: 2005
Third Edition: 2014
ISBN 978-93-5152-235-5
Printed at
Dedicated to
Vera and my children, for the love and happiness we share; my parents,
for showing me the way; my house-staff and nursing staff,
for their unstinted support; my patients for teaching me all I know.
Preface to the Third Edition
It is gratifying that this book titled Principles of Critical Care continues to be the standard text for critical care in
India, and that it is now also read in countries outside India. The third edition of this book has been overdue. The
task has been onerous, difficult and very demanding, but is at last completed. I felt it would be unwise to attempt at
being encyclopedic in both reach and content (as observed in many Western texts) and have therefore elaborated
particularly on problems often and commonly observed in intensive care units in our country. It is indeed difficult
to strike a balance on what to include, what to elaborate upon and emphasize, what to exclude and yet give a
reasonably coherent account of the subject. I do hope this balance has been achieved.
Almost all the chapters have been revised and many of them have been extensively rewritten. These include
the section on Cardiopulmonary Resuscitation and Cerebral Preservation in Adults, Clinical shock syndromes,
Critical Care of the Transplant Patient, Nosocomial Infections, Neurological problems, Organ System Dysfunction
Requiring Critical Care, in particular, Acute Pancreatitis and Critical Care in Acute Hepatic Failure. Besides, a new
chapter titled End of Life Care in the Intensive Care Unit has also been included in this book.
The present edition has an excellent format, far better than the earlier two editions. The quality of paper, the
quality of illustrations, line drawings, algorithms, tables, boxes and, above all, the quality of numerous images that
illustrate the text leave nothing to be desired.
I am very confident that this book will continue to be beneficial to intensivists, anesthesiologists, physicians,
surgeons, colleagues practising other specialties, as also to trainees in critical care, to residents, students and
nursing staff.
I very sincerely acknowledge my thanks to my distinguished contributors who have once again collaborated in
an honorary capacity to this edition, thereby enhancing its prestige. I would like to express my deep gratitude to
Dr Khyati Shah, my research assistant, without whose help this work would not have been possible and to Mr Neeraj
Chavan for his dedication, unstinted help and support. I thank Dr Aruna Poojari for her suggestions and help with
the chapter on Nosocomial Infections and dr Shilpa Bhojraj for her assistance with the chapter on Control of Pain
and Anxiety and the Use of Muscle Relaxants in the Critically Ill Patient. I am grateful to AV Graphic Designs Pvt
Ltd (Mumbai) for creating excellent illustrations and tables and also to Jaypee Brothers Medical Publishers (P) Ltd
for reproducing them. Their cooperation and punctuality during the course of this work has been outstanding.
I thank the publishers and authors who have granted me permission to publish some figures from their books/
journals. Although every effort has been made to trace copyright holders of material printed in the book, in some
cases the copyright holders are yet to respond. The publishers will be glad to hear from them.
My gratitude above all to my wife, Mrs Vera Udwadia, for correcting page proofs and for her forbearance and
care during the many days and nights spent on this work.
Finally, my sincere thanks to Mr Jitendar P Vij (Group Chairman), Mr Ankit Vij (Managing Director) and
Mr Tarun Duneja (Director-Publishing) of M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India and
Mumbai Branch for their support in publishing this book.

Preface to the First Edition
Critical care in India and other developing countries is nascent and needs to strike deeper roots if it is to flourish and
prosper. The history of critical care in this country started in the late sixties and early seventies with the establishment of
coronary care units in Mumbai and in a few other big cities of India. These units, though centralized, were designed and
equipped chiefly to offer intensive care to patients with acute myocardial infarction. They had a poor concept of overall
critical care, or of intensive respiratory care. Mechanical ventilator support was primitive, its use being mostly
restricted to a token gesture of grace offered to a patient about to depart from this world. In the mid and late sixties,
my medical unit at the Breach Candy Hospital, Mumbai, started offering overall critical care, intensive respiratory
care and successful ventilator support in critical illnesses due to a wide spectrum of disease. Intensive care in
my unit, to start with, lacked good monitoring facilities and was initially offered in a few separate rooms within a
general ward of the hospital. These were perhaps the first stirrings of critical care as we know it today in the city
of Mumbai, and perhaps in this country. However, the real impetus to organized, centralized, overall critical care
arose when, in early 1970, a 34-year-old, 6-month pregnant lady was hospitalized in my unit at the Breach Candy
Hospital for increasing breathlessness. She was dubbed as functional by the duty officer, when, in fact, she had
acute poliomyelitis presenting with intercostal muscle weakness. She evolved over 24 hours because of bulbar
and spinal involvement into an acutely ill, totally paralytic state which needed intensive care of multiple organ
systems, together with prolonged ventilator support. We used a pressure-cycled Bird’s ventilator, and with the
able assistance of an anesthetist colleague, Dr Bhatia, struggled and succeeded against great odds in keeping her
alive. Successful ventilator support was continued for many months, and she was delivered by caesarean section
of a healthy baby at full term, whilst on ventilator support. About 6 weeks after initiating ventilator support, we
fortuitously acquired a Radiometer through the patient’s brother who was a pediatric cardiac surgeon in Los Angeles,
enabling us thereby for the first time to monitor arterial pH and blood gases by the Astrup technique. This was
indeed the first blood gas analysis machine used for intensive patient care in this country. Unwittingly, the illness of
this dear lady (who is still well) became an important landmark in the history of critical care both in this city and
in this country. Starting in 1971, from a two-bedded, centralized, reasonably well-equipped, multidisciplinary all-
purpose intensive care unit, we graduated to a newly constructed eight-bedded well-designed and fully equipped
unit which admitted critical problems in all branches of medicine and surgery. This unit over many years continues
to have a medical audit as good as any unit in the West. It has also served to train numerous house physicians and
registrars who have carried the message of critical care to other hospitals of this city and to many hospitals in other
parts of the country. The concept of critical care has now been increasingly accepted and followed in most large
hospitals of the big cities of this country.
Some of my colleagues, particularly those engaged in community medicine, preventive and social medicine,
are of the opinion that in a poor large country like India, the encouragement of critical care is a misdirected effort.
It is indeed true that increasing the number of critical care units in the country will not inflict even a small dent
in the overwhelming health problems this country has to cope with. Should then the speciality of critical care be
fostered and encouraged? The answer on principle is unquestionably yes. It is the physician’s duty to care for the
ill, and the more critically ill a patient, the more intensive the care a patient needs for survival. We however need to
do this in all poor countries with a logical perspective. It would be unrealistic, futile and morally wrong to dot this
huge country with numerous critical care units when even basic primary health care is lacking, and when ordinary
hospital facilities in most parts of the country are hopelessly inadequate. Reason demands that well-equipped
critical care units should in the foreseeable future be confined to medium and large hospitals which have the
infrastructure to support such units. It would also be wiser and profitable to organize general all-purpose intensive
x Principles of Critical Care
care units rather than copy the West and establish critical care units in different specialities and subspecialities. A
multidisciplinary intensive care unit permits concentration of meager resources with regard to staffing, equipment
and technical expertise. Above all, it encourages a more holistic approach, so that problems in the critically ill are
considered in an overall perspective rather than in terms of disease afflicting isolated organ systems. There is also
a crying need to formulate laws and regulations (non-existent at the present time) that govern the establishment
and functioning of critical care units in the developing countries. Financial lucre will otherwise continue to allow the
mushrooming of so-called intensive care units which are veritable death traps for unwary, unsuspecting patients.
Efficiently functioning critical care units in the foreseeable future will be largely confined to the big cities of
this country. Should we not promote a modicum of better care for critical illnesses in the huge population of over
650,000,000 that resides outside these cities? This can for the present only be achieved by providing a better staffed
and better equipped high-dependency ward in every district hospital of this subcontinent. These wards would not
qualify by Western standards as critical care units, but in our experience, could offer better care, with improved
results, at a smaller cost.
This book is largely based on my numerous jottings and notes embodying my experience of problems in the diagnosis
and management of critically ill patients over the last 30 years. A book of this magnitude, authored in the main by a
single individual helped by just a few distinguished contributors, may seem audacious, but has the intrinsic advantage
of presenting the uniform view of one who for many years has had to grapple with a wide spectrum of critical illnesses.
It in no way detracts from the fact that for a successful outcome, critical care often needs team effort involving many
specialities in medicine, surgery and their allied branches. The emphasis in this book is on fundamentals that form
the basis of care and on important problems that find their way to a busy unit. The book also includes in most
chapters an insight into the nature of derangement of altered functions in a critical illness. Good management can
then be better understood and need not be ritualized or didactic.
Critical care in developing countries encompasses both diseases prevalent in the West, as also special problems
chiefly encountered in poor countries such as India. These problems particularly in relation to important fulminant
tropical infections have been given due emphasis in this book. We also have to necessarily contend with the lack of
sophisticated gadgetry and equipment in many of our units. The successful management of many life-threatening
problems under these circumstances and restraints is difficult but still possible, and has been discussed in relevant
chapters.
It is essential to stress that the principles of good critical care are the principles of good medicine and surgery.
Improvement in critical care can, therefore, only flow from improved standards in general medicine and surgery.
A careful history, a good physical examination, and the evaluation of relevant laboratory and imaging data will
always form the bedrock for correct diagnosis and management of life-threatening problems. Improved technology
and invasive gadgetry can be of help, but they can never be a substitute for sound clinical acumen and experience
gathered over years of trials and tribulations. The use of machines and, in particular, of invasive technique, should
never be an end in itself, but always a means to the solution of difficult problems. To feed a machine in a critical
care unit just because it is there, is to court medical nemesis.
The speciality of critical care by its very nature often incites the caring physician to prompt or hurried action.
Admittedly, there are a few emergencies which do demand immediate measures if life is to be salvaged. But in
most critical situations, there will be time to stand and wait, to think and deliberate—
“And time for all the works and days of hands

That lift and drop a question on your plate.”
The physician must take time to muster the clinical discipline that allows a focused view on an emergent
threatening problem, yet not lose an overall perspective of the patient. The initiate in critical care medicine should
first and foremost be reminded ever so often of the Hippocratic dictum, Primum Non Nocere—first of all, do no
harm. He should, therefore, be encouraged to think (without falling asleep) over a problem before jumping into
action, else he may well become the prime iatrogenic hazard in the unit.
Preface to the First Edition xi
In the final analysis, critical care is the care that aids and improves patient survival. It is doctors and nurses who
care for the patients and not machines. We should take comfort in the fact that there is no substitute for human
ingenuity, endeavor and resources. Motivation and dedication toward providing better patient care can indeed
compensate significantly in our part of the world for the lack of sophisticated technology and technical expertise.
I very sincerely acknowledge my thanks to all my extremely distinguished contributors who are all well-known
specialists in their own fields, and who have so kindly and willingly contributed in an honorary capacity to this
book. They have immeasurably enhanced the prestige of this book by their valuable contributors. I would like to
acknowledge my immense gratitude most of all to Dr Ruby Jal Kharas, my research assistant, who has made this
book her special baby. She has been of immense help in every single aspect of this book, and this book would have
had to wait for many more months to see the light of the day, if it had not been for her dedication and perseverance.
I also owe an immense debt of gratitude to Mr Oatta, Chairman of Hindustan Lever Ltd, India, who on behalf of his
company has been kind enough to give a very generous subsidy toward the publication of this magnum opus. The
price of this work has thereby been substantially reduced so that the book is now within the reach of all students and
all my medical colleagues. Dr Ramnik Parikh and Dr Rajgopal were instrumental in arranging for this munificent
subsidy, and to them I express my sincere gratitude. I would also like to thank the publishers and authors who have
granted me permission to reproduce some figures and tables from their books/journals. Although every effort has
been made to trace copyright holders of material printed in this book, in some cases, this has not proved possible.
In a few cases, the copyright holders are yet to respond. The publishers will be glad to hear from them.
I would also like to thank dr Shilpa Bhojraj for her assistance with the chapter on Control of Pain and Anxiety
and the Use of Muscle Relaxants in the Critically Ill. My special thanks are due to Mrs Lavanya Ray and Ms Rivka
Israel for their excellent editorial advice and assistance. I am grateful to Mr Abe Aboody and Mr Balagangadharan
of Alliance Phototypesetters for their kind cooperation and excellent work. I am also grateful to Mr V Pradhan
and Mr Prabhu for the good art work and X-ray plates. I also offer my thanks to Ms Katy Irani who has helped with
the typing of this manuscript and with the Index. My gratitude to my wife, Vera, for having helped to correct the
page proofs and for her extra forbearance and care during the many days and nights spent on this work. Finally,
my sincere thanks to the Oxford University Press in Mumbai and Delhi for their unstinted help and cooperation
in publishing this work.

Contents
section 1 An Introduction to Critical Care section 6 Clinical Shock Syndromes
1. Overview 3 13. Overview of Shock Syndromes 153
2. Principles, Philosophy and 14. Hypovolemic and Hemorrhagic Shock 160
Ethics of Critical Care 5 15. Cardiogenic Shock 169
3. Critical Care Scoring 10 16. Sepsis and Septic Shock 185
17. Cardiac Compressive Shock 203
section 2 Cardiopulmonary Resuscitation 18. Anaphylactic Shock 208
and Cerebral Preservation in Adults
4. Cardiopulmonary Resuscitation and section 7 Cardiovascular Problems

Cerebral Preservation in Adults 19 Requiring Critical Care
section 3 Basic Cardiorespiratory 19. Acute Coronary Syndromes 213

Physiology in the Intensive Care Unit 20. Unstable Angina 216
21. Acute Myocardial Infarction 224
5. Basic Cardiorespiratory Physiology 22. Acute Left Ventricular Failure
in the Intensive Care Unit 35 with Pulmonary Edema 239
23. Tachyarrhythmias in the
section 4 Procedures and Monitoring in Intensive Care Unit 247
the Intensive Care Unit 24. Bradyrhythms and Heart Block in the ICU 260
25. Antiarrhythmic Drugs Used in the ICU 263
6. Procedures in the Intensive Care Unit 49 26. Hypertensive Emergencies and Aortic
JD Sunavala
Dissection in the ICU 272
7. Cardiac Monitoring in Adults 61 27. Pulmonary Embolism 283
JD Sunavala
8. Respiratory Monitoring in Adults 82
section 8 Respiratory Problems
section 5 Imaging in the Critical Care Unit Requiring Critical Care
9. Introduction 93 28. Acute Respiratory Failure in Adults 299

Anirudh Kohli 29. Oxygen Therapy 314
10. Imaging Techniques in the Chest 94 30. Airway Management 323
Anirudh Kohli 31. Acute Exacerbation of Chronic
11. Imaging Techniques in the Abdomen 103 Obstructive Pulmonary Disease 335
Anirudh Kohli 32. Acute Lung Injury and Acute Respiratory
12. Neuroimaging Techniques 113 Distress Syndrome 347
Anirudh Kohli Zarir F Udwadia, FE Udwadia
xiv Principles of Critical Care
33. Acute Severe Asthma 363 section 14 Surgical Infections

Zarir F Udwadia
in the Intensive Care Unit
34. Community-Acquired Pneumonias
Requiring Critical Care 371 48. Postoperative Wound Infections 571
Zarir F Udwadia, FE Udwadia
49. Necrotizing Soft Tissue Infections 574
35. Massive Hemoptysis 378
50. Intra-abdominal Sepsis 578
36. Diseases of the Pleura in the Critically Ill 386
37. Negative Pressure Pulmonary Edema 391 51. Abdominal Compartment Syndrome 589
section 9 Mechanical Ventilation in section 15 Organ System Dysfunction

the Critically Ill Requiring Critical Care
38. Mechanical Ventilation in the Critically Ill 395 52. Multiple Organ Dysfunction Syndrome 593
39. Weaning from Ventilator Support 416 53. Acute Kidney Injury 607
54. Critical Care in Acute Hepatic Failure 623
section 10 Fluid and Electrolyte 55. Acute Pancreatitis 641
Disturbances in the Critically Ill 56. Acute Gastrointestinal Bleeding 652
57. Hemorrhagic Disorders 665
40. Fluid and Electrolyte Disturbances in 58. Transfusion (Blood Product) Therapy 677
the Critically Ill 425 59. Endocrine Dysfunction 683
60. Diabetes Mellitus 694
section 11 Acid-Base Disturbances 61. Neurological Problems 703
in the Critically Ill A. Raised Intracranial Pressure
Jimmy Lalkaka, BS Singhal
B. Traumatic Brain Injury
41. Acid-Base Disturbances in the Jimmy Lalkaka, BS Singhal
Critically Ill 443 C. Stroke
section 12 Nutritional Support in D. Central Nervous System Infections
the Critically Ill Adult E. Status Epilepticus
42. Nutritional Support in the F. Rapidly Progressive Neuromuscular Disorders with
Respiratory Failure
Critically Ill Adult 459 Jimmy Lalkaka, BS Singhal
G. Perioperative Neurological Care
section 13 Fever and Acute Infections Late Sohrab K Bhabha
in a Critical Care Setting

section 16 Critical Care after
43. General Considerations and Open Heart Surgery
Noninfective Causes of Fever in the ICU 477
44. Nosocomial Infections 481 62. Critical Care after Open Heart Surgery 753
45. Community-Acquired Fulminant
Infections Requiring Critical Care 515 section 17 The Immunocompromised
46. Antibiotic Therapy in the Intensive Patient
Care Unit 546
47. Invasive Fungal Infections in the ICU 562 63. The Immunocompromised Patient 767
Contents xv
section 18 Physical Injuries Requiring section 23 The Critically Ill Child

Critical Care
77. Cardiopulmonary Resuscitation
64. Intensive Care Management of Polytrauma 785 in Infants and Children 905
NS Laud, FE Udwadia YK Amdekar
65. Management of Critically Ill Burns Patients 794 78. Respiratory and Hemodynamic
SM Keswani, FE Udwadia Monitoring in Children 907
Mahesh V Balsekar
66. Critical Care in Poisonings 805
67. Envenomation 822 79. Approach to Shock in the Pediatric
Intensive Care Unit 914
68. Drowning 830 YK Amdekar
69. Heat Stroke 834
80. Hypertensive Emergencies in Pediatrics 918
70. Hypothermia 837 YK Amdekar
81. Heart Failure in Neonates and Children 920
section 19 Critical Care of the YK Amdekar
Cancer Patient 82. Acute Respiratory Failure in Children
and Hyaline Membrane Disease 922
71. Critical Care of the Cancer Patient 843 YK Amdekar
83. Fluid and Electrolyte Disturbance in
section 20 Control of Pain and the Critically Ill Child 928
Anxiety and the Use of Muscle Relaxants YK Amdekar
in the Critically Ill Patient 84. Nutritional Support in the Pediatric

Intensive Care Unit 930
YK Amdekar
72. Control of Pain and Anxiety and the
Use of Muscle Relaxants in the 85. Pediatric Life-threatening Infections
Critically Ill Patient 853 Requiring Critical Care 932
YK Amdekar
section 21 Critical Care of the 86. Acute Kidney Injury in Infants

and Children 936
Transplant Patient BV Gandhi, Ankit Mody
73. Critical Care of the Transplant Patient 867

section 24 End of Life Care in the
section 22 Critical Care in Pregnancy Intensive Care Unit
87. End of Life Care in the Intensive Care Unit 945

74. Introduction 889
75. Critical Illness Not Specific to Pregnancy 891 Appendix 949
76. Critical Illness Specific to Pregnancy 894 Index 957
SECTION
An Introduction to Critical Care
Overview
Principles, Philosophy and Ethics of Critical Care
Critical Care Scoring
CHAPTER 1
Overview
Critical care is the care of seriously ill patients with life- It was obvious from the 1960s onward that critically ill
threatening illnesses or trauma, as also of patients who have patients are best and ideally cared for in special units which
the potential to develop life-threatening complications from centralize equipment, staff and facilities, so necessary for
their disease. Critical care should, correctly speaking, be the care of life-threatening problems. Intensive or critical
reserved for patients with severe but potentially reversible care has blossomed into a specialty with special training
problems. Patients with chronic terminal illnesses, with the and certification in the West, and also in many developed or
end close at hand should be given every care at home or in quickly developing Southeast Asian countries.
the ward of a hospital, but not in critical care units. In India the seed of critical care planted in the mid and late
The origin of the present day intensive care unit started sixties has now grown into a strong tree trunk with spreading
with the use of the postoperative recovery room for immediate branches and deepening roots. The Indian Society of Critical
special postoperative care. This concept was given a further Care Medicine holds an examination that accredits trained
impetus during the poliomyelitis epidemic in the early 1950s doctors qualified to practice this specialty. These accredited
when the use of mechanical ventilation salvaged many intensivists will in future train junior colleagues, so that the
future of this specialty is assured. However, in large cities of the
paralyzed patients. Present day intensive care is however far
country there are still many privately owned so-called critical
more meaningful than mere postoperative care and ventilatory
care units, which are poorly equipped and poorly staffed.
support. It incorporates the knowledge and experience of
These are death traps for unwary patients. It would be ideal if all
numerous specialties that have blossomed over nearly four
units claiming to be intensive (critical) care units have a
decades from 1960 onward. Pulmonary medicine with the
certificate of accreditation from a responsible professional
concept of respiratory care, cardiology with the concept of the body.
coronary care unit and advances in anesthesiology have all Many practitioners of critical care medicine are specialists
contributed greatly to the evolution of the modern day critical in cardiology, pulmonary medicine, anesthesiology or in
care unit. While specialties in medicine or surgery are sharply critical care itself. However, the principles of critical care are
focused on a single organ system within the body, a general the principles of general medicine and general surgery, rather
medical or surgical critical care unit is devoted to the patient than the principles applicable to any particular specialty. An
as a whole, recognizing the overwhelming fact that there is a individual with a wide experience of medicine or surgery
tremendous interdependence and interrelationship between coupled with suitable training and exposure to acute medical
various organ systems, so that a serious involvement of one or surgical problems has perhaps the best aptitude and
strongly jeopardizes the function of others. The approach to philosophy for organizing and directing a critical care unit.
critical care medicine is thus simultaneously holistic, viewing It is important, particularly in a poor country like ours,
the patient in an overall perspective, and yet focused on one that the few good critical care units we have, admit patients
or more problems that constitute an immediate threat to life. who truly need appropriate care. It is sad to see critical care
4 Section 1 An Introduction to Critical Care
units cluttered with patients who are unquestionably better almost certain to cause death within a matter of months.
looked after in the wards or at home. A critical care unit has An example of this is a patient with cancer at a stage when
1 its advantages and disadvantages. The chief advantage is
that it provides better and more organized care. The main
his life expectancy is 3–6 months. An acute complicating
pneumonia in such a patient is a life-threatening emer
disadvantage is of a hostile environment contributing to gency, which is treatable, curable and may well necessitate
anxiety, emotional stress, loneliness, fear and above all a critical care.
greater risk of developing nosocomial infections. A critical care unit as already mentioned should not be
The following conditions require intensive or critical care— used for terminal cases where the end is close at hand. The
1. Acute life-threatening illnesses which are potentially tendency to use a critical care unit as the last halt or stopping
reversible. station before an expected departure from this world should
2. Acute illnesses with potential and likely to occur life-
be strongly deprecated.
threatening complications.
3. Monitoring of vital parameters of patients with symptoms This section first deals with the principles and philosophy
and/or signs that suggest the possibility of an evolving of critical care. This is followed by a short discussion on ethical
life-threatening illness. principles governing critical care, on ethical issues in terminal
4. Acute or immediate life-threatening crisis or complic illness, and on euthanasia. The section ends with a description
ations in a chronic illness, even when the latter by itself is of current critical care scoring systems.
CHAPTER 2
Principles, Philosophy and
Ethics of Critical Care
INTRODUCTION physician or surgeon who can know everything, there is to

know about the multiple facets of medicine and surgery. Yet,
The principles of critical care are in quintessence the same as team effort must be conducted and carefully orchestrated
those underlying good medicine and surgery. They include by a single individual, if it is to prove successful. Too many
the following— specialists and superspecialists individually looking after a
critically ill patient more often than not hasten his departure
Early Diagnosis and Identification of the Problem from this world. Their overenthusiastic and often overfocused
The doctor in the critical care unit often deals with life- attention on the organ system of their choice needs to be
threatening illnesses with serious dysfunction involving one tempered and viewed with reference to the patient as a whole.
or more organ systems. The early diagnosis and identification The many problems in such patients should be considered
of the problem is imperative for correct management. This in their overall perspective, priority being assigned to those
is a basic dictum for all fields of medicine and surgery but is needing immediate attention. Yet it must always be asked as
indeed a matter of urgency in critical care medicine. to how best one can engage an emergent problem without
seriously jeopardizing the function of other organ systems. A
management decision in a not so critically ill patient is often
Anticipation of Possible Events and Complications
easy and straightforward; a similar decision in a critically ill
I consider this the very essence of good critical care. The individual is beset with complex difficulties. The hazards
treating doctor must have a firm grip on what is happening involved in implementing a therapeutic procedure should
to a patient and must acutely anticipate possible events and always be balanced against the possible benefits. There are
complications in the immediate future. This he can only do, no clear-cut guidelines in many decisions that need to be
if he has the knowledge, wisdom and experience of judging made in the care of critically ill individuals. It is a question of
the possible evolution of a life-threatening illness in a given experience, wisdom, and at times an intuitive feel of what is
patient. To be one step ahead in one’s mind with reference to probably right or wrong in a given situation.
an acutely evolving disease is an important tactical advantage
that often leads to victory for the patient and his doctor. Considered Use of Technology
The patient is to be cared for by the doctor and the nurses
Holistic Approach to a Critical Illness and not by machines. Machines and sophisticated gadgets
The holistic approach has already been mentioned earlier. It are an adjunct to the doctor’s skill and care; they cannot
cannot be overstressed that the patient must be viewed in an replace them. Merely because machines have been provided
overall perspective with interrelated functions of interrelated is no reason to use them. Invasive procedures and invasive
organ systems. This is not to decry team effort involving gadgetry have an inherent risk even in the best of hands;
various specialists in the management of a critical illness. they pose grave hazards in inexperienced or poorly trained
Team effort is indeed crucial for success, as there is no single hands. Invasive diagnostic procedures may help to fine-tune
management in individual patients, but their overall influence management with regard to a particular problem in critical
on reducing morbidity and improving mortality in critically ill care. Yet, it must be remembered that the evidence provided,
1 patients is debatable. It is remarkable that how with increasing
experience, the use of invasive monitoring is significantly
though valuable, is based on a statistical study of large
population groups. The results of a statistical study of large
reduced. Again this is not to decry the use of sophisticated population groups, however scientific, need not necessarily
technology in the intensive care unit (ICU). It is merely to apply to the individual patient in one’s care. On the other
restress that in the final analysis, good care rests with doctors hand, observational studies are considered the weakest form
and nurses, and not with machines. of evidence in critical care medicine. Yet, some of the greatest
discoveries in medicine have been made by our illustrious
Primum Non Nocere ancestors through the sheer excellence of observation—
First of all, do no harm. This is an ancient Hippocratic tenet. discoveries far greater than some of the best double blind
Do not subject the patient to procedures and investigations randomized controlled studies of the present era. Witness
which add to pain and suffering, when one is certain or almost the discovery of small pox vaccination by Jenner, antirabies
certain that these can lead to no extra benefit. The risk-benefit vaccination by Pasteur, the observations of Lister that led to
ratio should always be kept in mind in all management advances in surgery and the observation of the importance
decisions in the ICU. of handwashing by Thomas Ignas Semmelweis.
The intensivist should also remember that evidence
can be imperfect, can change and is not sacrosanct. If it
Recognition of the Limits of Critical Care
were, medicine would be static, whereas history teaches us
Physicians involved with critical care must recognize the limits that it is ever-changing, dynamic. It is also possible that the
of such care. Critical illnesses are necessarily associated with conclusions drawn from evidence-based medicine in the
a high morbidity and mortality, and quite often this morbidity Western world will not always apply to the rest.
and mortality cannot be improved despite all the care available Therefore, evidence-based medicine should be viewed
in present times. The discerning physician learns to recognize in its proper perspective—good but not infallible, important
the limits of care, knows when to draw the line, and recognizes but not all-inclusive; applicable in many, but not in all.
the futility, and often the cruelty of aggressive management in Medicine has several other aspects —social, cultural, economic,
patients who are well past the point of no return. Learning the psychological, philosophical, religious, genetic, and other
limits of care is not easy; it is fraught with doubts, difficulties nebulous aspects that characterize a trusting caring doctor-
and danger. A working guideline is to struggle unto life or patient relationship. It is important to take all into consideration
death in a young individual with a potentially reversible life- when caring for acutely ill patients.
threatening illness, and to remember not to play God in the
ICU. Yet in the old and feeble, in patients who are clearly dying,
and in those with serious background illnesses, one must learn
CLINICAL JUDGMENT
through wisdom and experience to temper care with reason. A physician must be a judge. Judgment is difficult, for
indeed medicine has been defined as the art of coming to
CRITICAL APPRECIATION OF EVIDENCE- a conclusion on insufficient evidence. It is no surprise that
errors in judgment frequently abound. Clinical judgment does
BASED MEDICINE
not come within the purview of art or science. It is a special
Evidence-based medicine is the rallying cry of all modern quality, a faculty—often inborn and occasionally cultivated. It
medicine, a shining banner held aloft by the profession cannot be equated to intellectual ability for it may be lacking
for all to view, a promised trail for better health care and in brilliant minds and be present to a marked degree in those
for appropriate management of critically ill patients. It is who are in other respects for less clever or knowledgeable.
unquestionably important to judge the clinical effectiveness Perhaps a knowledge of and an interest in the humanities—
or otherwise of treatment options through scientifically literature, poetry, music, history, philosophy, religion—can
accumulated evidence. It is even more important to gather improve clinical judgment by providing a more holistic
evidence to ensure that a treatment option is not injurious perspective of man and medicine and of health and disease.
to patients. However, in critical care medicine, it may be To cope with the diagnosis and management of a life-
impossibly difficult and even unethical (in some situations) threatening emergency requires more than mere factual
to furnish evidence or proof as to the optimal approach to knowledge, reason, logic, experience and skill. It requires
acutely emergent problems occurring in very ill patients good clinical judgment—the hallmark of a good physician.
with many variables. In spite of all protocols and guidelines Clinical judgment is a rich blend of all the above requisites
based on evidence, the practice of critical care medicine and adds to these a further intangible, indefinable quality; a
today remains largely empirical. The student of critical care quality that encompasses faith, charity, hope and compassion;
medicine should be aware of a few more aspects of evidence- a quality that has a deep understanding of human nature. It
based medicine. Double blind randomized controlled trials is also the quality that gives the doctor in crisis the wisdom to
are the gold standard, which provide evidence for patient know what to say and do, and what not to say and do; when to
Chapter 2 Principles, Philosophy and Ethics of Critical Care 7
wait and watch, and when to treat vigorously without delay; and countries, but the absolute values of good and evil, right
when to fight death and when to give in to it; when to press and wrong, and the sanctity of human life are remarkably
for a cure and when to console with words, or to rest content
with palliative relief. Sound clinical judgment includes an
similar in all civilized societies.
There are three basic ethical principles derived from 1
extra-special perceptive ability that enables a doctor to sense a these absolute values, which govern the art and science of all
clue which his less fortunate colleagues will miss; the ability to medicine, and in particular of critical care medicine. The first
process this clue and judge its correct diagnostic, therapeutic is beneficence and its companion-in-arms, nonmaleficence.
and prognostic implications. A physician who combines the Beneficence is an all-important ethical principle and duty
sharpness of his perceptive faculties with a wisdom born of the physician, which has been emphasized in ancient
of reading and experience, with a compassion for and an Ayurvedic texts, as also by Hippocrates. Beneficence directs
understanding of human suffering and who also possesses the physician to do good by relieving suffering and restoring
the faculty of good clinical judgment in truly blessed by the good health. Beneficence does not merely involve technical
gods. He has an attribute which no medicine can duplicate expertise and medical skill; it equally involves human
and no science can invent. He enjoys a ringside seat in the qualities, particularly in the care of critical illnesses. It is these
theater of life and has the most intimate insight into many human qualities, which tend to be unfortunately forgotten
who seek his help.1 or pushed into the background by the frontiers of advancing
technology in medicine. The chief of these human qualities
ART OF MEDICINE expressed in a single word is humanity. Humanity can be
defined as the sensibility, which enables a physician to feel for
Today, science rules medicine. However, the practice of its the distress and suffering of a patient, prompting him to relieve
science without an equal measure of its art dehumanizes them. True humanity in a physician is the fount of sympathy
medicine, robs it of its essence. This is unfortunately the and care for a critically ill patient. A critically ill but conscious
trend today, which must be reversed. The art of medicine patient in my opinion has special antennae (very like what
lies in the artful, appropriate application of its science to the child has for the mother), which enable him to promptly
the overall holistic care of an individual patient. The art of recognize, reach out and clasp to his heart a physician who
medicine remains all pervasive even when its science fails truly cares. This often makes the difference between life and
or has reached its utmost limits. “For when all the marvels of death in a critical illness. In a similar manner, a critically ill
science are of no avail to unfortunately ward off the fatal end, it individual often recognizes the pseudosympathy exhibited
is no small portion of a physician’s art to rid his patient’s path by some physicians; however, brilliant and technologically
of thorns if he cannot make it bloom with roses.”1 well-equipped they may be. Knowledge and experience
The art of critical care medicine lies in hearing an unspoken when linked to humanity make a great physician and indeed
subtle nuance in a patient’s history and in the ability to spot a great man.
and appreciate the significance of one or more subtle physical Nonmaleficence is the companion-in-arms of beneficence.
signs that no gadget or machine could possibly recognize. It It reminds the physician that above all, he should do no harm.
lies in his ability to sift the evidence before him and give the Beneficence and nonmaleficence may at times in a critical
right answer (of several possible answers) to the appropriate care setting be in apparent conflict. Thus, the use of a narcotic
question. It lies in the intuitive feel for a solution either in to relieve pain is beneficence in a dying patient, yet this may
diagnosis or management. Above all, it consists of looking at hasten death by depressing respiration, thus violating the
a very ill patient holistically rather than compartmentalizing tenet of nonmaleficence. This conflict, as explained later, is
the patient into different organ systems. The art of medicine apparent and not real.
is the art of healing, not just treating, not even just curing. Yet The second basic ethical principle governing decision-
it is only when art and science join hands that healing is best making and management in critical care medicine is patient
accomplished. It is only then that a physician can engage the autonomy. This is the patient’s right to self-determination—
unique individuality of a particular human being so that a the right after being properly informed, to accept or refuse
critically ill patient becomes much more than a disease that medical treatment offered to him including life support
needs to be treated.1 measures like mechanical ventilation. It is indeed the proper
I came across the ancient description of a good physician interpretation of the balance between the principles of
and I feel that it has a timeless relevance—“it was his path to beneficence and the principles of patient autonomy, which
learn the practice of medicine and the practice of healing, and governs decision-making and management in critical care
careless of fame, to exercise the quiet art”. medicine. This balance is indeed difficult and not easy to strike
in a critical care setting. This is because seriously ill patients
ETHICAL PRINCIPLES GOVERNING may be unable to make proper decisions about their own
care. In fact, they may often make the wrong decisions under
CRITICAL CARE the physical and emotional stress of their illness. In these
The principles of ethics are rooted in religious, philosophical circumstances, the physician must lean toward the principle
and sociocultural traditions. These vary in different cultures of beneficence, and take management decisions, which he
genuinely believes, are in the best interests of the patient. quality of life. In this case, the patient is not involved in the
It is important to illustrate this point with true-to-life decision.
1 examples. A patient was brought in nearly dead after a sedative
poisoning, with a note informing the physician that it was her
Advocates of euthanasia remarkably enough invoke
the ethical principles of beneficence, stating that the act
express wish not to be resuscitated and treated. The directive is morally justified because it is doing good to the patient
was ignored; the patient was resuscitated and discharged in and is in his or her best interest. In my opinion, this act is
good health. She was forever grateful for being restored to life. wrong, unjustifiable, and violates the sanctity of life, as it is
A patient with quickly progressive respiratory muscle perpetrated with known intent to kill. Yet, it must be clearly
weakness, in his extreme fright, agitation, anxiety and distress, understood that withholding or withdrawing treatment, when
refused intubation and mechanical ventilator support. The it is certain that such treatment will be of no benefit and when
request was ignored, appropriate management decisions death is inevitable, does not constitute euthanasia (even
taken, and the patient was again ever grateful to the doctor though some prefer to call this passive euthanasia) because
for having ignored his directive. the intent is not to kill but to prevent prolongation of the act
There are many factors which distort, prejudice or inter of dying.
fere with autonomous decisions of patients in critical care I gather from discussions with my colleagues in the West,
medicine. These include fear, anxiety, depression, panic, that a significant number of acutely ill patients who are about
lack of information and abhorrence of invasive modalities to die, as also patients with chronic but terminal disease,
of treatment, which prompt them to decide (often wrongly) express a desire to be killed or to be medically assisted in
to die with dignity. The working ethical principle is that in suicide. It is amazing that in my long association of over 45
acute medicine, when confronted with a potentially reversible years with so many critically ill patients in their terminal state,
life-threatening illness, beneficence prevails over patient there has not been a single individual who has persistently
autonomy. wished for euthanasia. There have been a few who have
The third and final ethical principle is justice—to dis expressed a fleeting wish, but talking to them and gently
tinguish in patient care, the right from the wrong. If at times explaining measures to relieve their symptoms have led to
this is difficult or impossible to determine in absolute terms, a resigned and comparatively unanguished acceptance of
one should determine what is more right or less wrong. In their destiny. Why is there this difference between the East
developing countries where resources are limited, justice and the West? I think it is basically related to sociocultural
dictates that treatment is administered to patients who are and religious differences. A patient’s, and for that matter
more likely to benefit from them. This often produces an a physician’s attitude to suffering, pain, impending death,
ethical quandary. Witness for example a situation where there and death itself, is conditioned by these sociocultural and
are three ventilators in an eight-bedded tetanus ward and religious factors. Most people in our part of the world and
all eight patients have severe tetanus requiring mechanical in the Far East believe that life cannot be divorced from pain
ventilation. Physicians should unquestionably be involved and suffering, that we live in the midst of pain and suffering,
in the ethics of resource distribution that provide equitable and that each one in this world is apportioned one’s share of
medical care to the society in which they live and work. Yet, pain and suffering. This is the law of Karma—a belief that one
ethical arguments limiting care because of limited resources reaps in the present life what one has sown in previous lives,
should not in my opinion be applicable to an individual and that one will reap in future existences what one sows in
patient already under intensive care. Wisdom however the present.
dictates that in all situations requiring protracted intensive In our experience, suffering in a terminal illness (whether
care, the burden-benefit relationship should be carefully this is a sequel to an acute or chronic problem), almost always
considered, and care be tempered with reason, when judged can be relieved by appropriate medication and compassion.
to be an exercise in futility. This brings us to the question of whether it is imperative to
tell the patient the exact truth that his terminal illness will
inevitably end fatally. Here again, East and West may differ.
EUTHANASIA The relatives have a right to know the whole truth, and it is
No discussion of ethics in relation to modern day medicine, the moral obligation of the physician to apprise them of this
including critical care medicine, can be complete without a truth. Many terminally ill patients either in critical care units
short discussion on euthanasia. Euthanasia includes— or outside, know and feel that their illness is terminal, but
Voluntary euthanasia or intentional killing of patients who barring rare exceptions, they do not wish to discuss death or
express a competent, freely made wish to die, because of the dying with the physician. In fact, they will if possible, in no
pain or suffering they experience. uncertain terms stop the physician from broaching the issue.
Medically assisted suicide, at the patient’s insistence and I would agree that the ethical principle of patient autonomy
wish. includes the patient’s right to know and understand the nature
Homicide following a surrogate decision on a crippled or of his illness, so that an informed consent or dissent regarding
handicapped patient, or in a patient with a poor or hopeless management decisions is possible. Yet, a patient also has a
Chapter 2 Principles, Philosophy and Ethics of Critical Care 9
right to choose exactly how much he wants to know. If the would want to end his suffering as a matter of a cult, or even
physician is to exert beneficence, he must respect that right. as a matter of duty that needs to be performed in time to
Perhaps the patient’s disinclination to discuss the end is due
to a faint glimmer of hope that life will extend longer than
come? Is it ever possible to quantify suffering? Is not suffering
often a state of the mind? And cannot a state of the mind be 1
what the physician feels or what medical science expects. I subject to changing social pressures and social mores? Can
am of the opinion that under these circumstances, a physician most doctors claim to have the knowledge, experience, the
has no right to systematically destroy that glimmer of hope, Ostlerian wisdom and perspective to be truly able to enlist
which keeps the patient more happy and peaceful toward the themselves to the cause of euthanasia in a patient who states,
end of his life. I cannot bear the suffering I am going through? These are
To die with dignity and to legalize euthanasia are slogans pertinent questions which are difficult to answer. Finally,
often linked together, as if one needs the latter to achieve when one legalizes a solution to a problem like euthanasia,
the former. Legalizing euthanasia in our country, even in the would the good that accrues clearly outbalance the evil or
most diluted form, could well open the floodgates to murder. harm that could possibly result from this legal sanction. This
Euthanasia however, under strict clauses and safeguards, has again is a question that physicians all over the world should
already been legalized in Holland. Perhaps in time to come, seriously consider.
it may be similarly legalized in other Western countries as
well. I am in no position to comment on the Western world, Reference
but for all the safeguards and guarantees against misuse that 1. Udwadia FE. The Forgotten Art of Healing and Other Essays.
the Dutch for example have, is it not possible that a patient Oxford University Press. 2009.
CHAPTER 3
Critical Care Scoring
Optimized distribution of medical and financial resources is of Table 1: Glasgow Coma Scale
crucial importance in the delivery of health care, particularly
Eye opening Motor response Verbal response
in the poor developing countries of the world. To this end,
4 = Spontaneous 6 = Obedient 5 = Oriented
the critical care physician often has to make decisions about 3 = To voice 5 = Purposeful 4 = Confused
which patients are likely to derive the maximum benefit from 2 = To pain 4 = Withdrawal 3 = Inappropriate
admission to a critical care unit. 1 = None 3 = Flexion 2 = Incomprehensible
Illness scoring systems have been introduced in the 2 = Extension 1 = None
past three decades to formulate some degree of priority for 1 = None
intensive care unit (ICU) admissions in patients with acute
illness or trauma. These scoring systems are useful for medical TRAUMA SCORE AND REVISED
audit purposes and for comparison of therapy and results
in groups of patients who roughly have the same degree of
TRAUMA SCORE
physiological derangements produced by critical illnesses. These are useful for patients with trauma. The trauma score
However, scoring systems have strong limitations, and critical is based on the state of the cardiovascular and respiratory
care of individual patients should not be influenced by scoring systems and on the GCS (Table 2). Values are given to each
protocols. parameter and these are added to give the total trauma score,
The commonly used trauma and critical care scores are which ranges from 1 to 16. The lower the score the greater the
briefly discussed below. risk for mortality.
The trauma score was found to underestimate the pro-
GLASGOW COMA SCORE gnostic significance of head injuries. This led to the
development of the revised trauma score (RTS), which is
The Glasgow Coma Score (GCS) judges the extent of coma in now widely used to assess the severity of trauma. The RTS
patients with head injury. It is useful for pre-hospital trauma is based on the GCS, the systolic blood pressure (SBP) and
triage as also for patient assessment after hospitalization. The the respiratory rate. Coded values are given for the above
scale is based on eye opening, motor response and verbal parameters and summed up (Table 3). Higher values have a
response (Table 1), and can be tested and scored by the better prognosis and lower values a poor prognosis.
physician within a couple of minutes. The total score is the
sum of each response and varies from a minimum of 3 to a
maximum of 15. The lower the score the greater the severity
CRAMS SCALE
of head injury in relation to central nervous system (CNS) The circulation, respiration, abdomen, motor, speech
function. (CRAMS) scale is another trauma triage scale frequently
Chapter 3 Critical Care Scoring 11
Table 2: Trauma score
1
A. Systolic blood pressure B. Respiratory rate C. Respiratory effort D. Capillary refill
>90 4 10–24 4 Normal 1 Normal 2
70–90 3 25–35 3 Shallow or Delay 1
50–69 2 >35 2 retractions 0 None 0
<50 1 <10 1
0 0 0 0
E. Glasgow Coma Scale
1. Eye opening 2. Motor response 3. Verbal response (1 + 2 + 3)
4 = Spontaneous 6 = Obedient 5 = Oriented 14–15 5
3 = To voice 5 = Purposeful 4 = Confused 11–13 4
2 = To pain 4 = Withdrawal 3 = Inappropriate 8–10 3
1 = None 3 = Flexion 2 = Incomprehensible 5–7 2
2 = Extension 1 = None 3–4 1
1 = None
Trauma score (A + B + C + D + E) = __________
Table 3: Revised trauma score (RTS)* Box 1: CRAMS scale*

Glasgow Coma Systolic blood Respiratory Coded
Scale (GCS) pressure rate value Circulation—
(SBP) (mm Hg) (RR) (breaths/ xx Normal capillary refill and blood pressure (BP)
min) >100 mm Hg 2
13–15 >89 10–29 4 xx Delayed capillary refill or 85 < BP < 100 mm Hg 1
xx No capillary refill or BP <85 mm Hg 0
9–12 76–89 >29 3
6–8 50–75 6–9 2 Respiration—
xx Normal 2
4–5 1–49 1–5 1 xx Abnormal (labored or shallow) 1
3 0 0 0 xx Absent 0
*RTS = 0.9368 GCSc + 0.7326 SBPc + 0.2908 RRc, where the c refers to coded Abdomen—
value. xx Abdomen and thorax nontender 2
xx Abdomen and thorax tender 1
xx Abdomen rigid or flail chest 0
used to decide which patients require urgent admission to a
trauma unit (Box 1). Patients with a low CRAMS score need Motor—
urgent critical care. xx Normal 2
xx Response to pain (other than decerebrate) 1
xx No response (or decerebrate) 0
INJURY SEVERITY SCORE
Speech—
This system assigns numerical scores to different body xx Normal 2
regions that may be injured. A manual of codes provides xx Confused 1
information on the scoring of each injury. The worst injury xx No intelligible words 0
in each region is given a numerical value. This is squared and
added to numerical values from each of the other anatomical *Score <8 indicates major trauma; score >9 indicates minor trauma.
regions. The total score ranges from 1 to 75 and correlates with
the mortality risk. The injury severity score (ISS) has some
important limitations. It considers only the highest score from
each body region, and considers injuries with equal scores ACUTE PHYSIOLOGY, AGE, CHRONIC
to be of equal importance irrespective of the anatomical HEALTH EVALUATION
region injured. The ISS is frequently used as a measure of
overall trauma, and forms a rough guide to mortality risk in The acute physiology, age, chronic health evaluation II
the injured patient. (APACHE II) score is one of the most frequently used critical
scales in critical illnesses. It is used in order to stratify prognosis 7. Serum sodium (mmol/L).
and outcome in groups of patients, and to determine success 8. Serum potassium (mmol/L).
1 of different forms of treatment.1-6 The APACHE II score uses
twelve easily measured variables [acute physiology score
9.
10.
Serum creatinine (mg/dL).
Hematocrit (%).
(APS)] and takes into consideration background disease 11. Leukocyte count (cells/mm3).
or premorbid health (Table 4). The worst scores in the first 12. Glasgow Coma Score.
24 hours following ICU admissions are used. The twelve Depending on the degree of derangement, a weighted
parameters considered are— score is given to each parameter. Sedated, ventilated patients
1. Temperature (°C). are given a GCS of 15 when neurological problems seem
2. Mean arterial pressure (MAP) (mm Hg). unlikely.
3. Heart rate (beats/min). Scores are also assigned for increasing age, emergency
4. Respiratory rate (breaths/min). postoperative or nonoperative admission, and for the presence
5. Alveolar-arterial oxygen gradient (A-aDO2) if fractional of background diseases resulting in pre-existing organ
inspired oxygen (FiO2) is 0.5 or greater, or PaO2 if FiO2 dysfunction. Double weighting is assigned to derangements
less than 0.5. of serum creatinine in the setting of acute renal failure, due
6. Arterial pH. to marked increase in mortality in critically ill patients with
Table 4: APACHE II points (A + B + C below)

A. Acute Physiology score (APS)
Physiological High abnormal Normal Low abnormal
variables +4 +3 +2 +1 0 +1 +2 +3 +4
Temperature ≥41 39–40.9 38.5–38.9 36–38.4 34–35.9 32–33.9 30–31.9 ≤29.9
rectal (°C)
MAP ≥160 130–159 110–12 70–109 50–69 ≤49
(mm Hg)
Heart rate ≥180 140–179 110–139 70–109 55–69 40–54 ≤39
(beats/min)
Respiratory rate ≥50 35–49 25–34 12–24 10–11 6–9 ≤5
(breaths/min)
(A-aDO2) mm Hg ≥500 350–499 200–349 <200
if FiO2 ≥0.5
PaO2 mm Hg >70 61–70 55–60 <55
if FiO2 <0.5
Arterial pH ≥7.7 7.6–7.69 7.5–7.59 7.33–7.49 7.25–7.32 7.15–7.24 <7.15
Sodium ≥180 160–179 155–159 150–154 130–149 120–129 111–119 ≤110
(mmol/L)
Potassium ≥7 6–6.9 5.5–5.9 3.5–5.4 3–3.4 2.5–2.9 <2.5
(mmol/L)
*Creatinine ≥3.5 2–3.4 1.5–1.9 0.6–1.4 <0.6
(mg/dL)
Hematocrit (%) ≥60 50–59.9 46–49.9 30–45.9 20–29.9 <20
Leukocytes ≥40 20–39.9 15–19.9 3–14.9 1–2.9 <1
(cell/mm3)
Neurological points = (15-Glasgow Coma Score)
B. Age points Age ≤44 45–54 55–64 65–74 ≥75
0 point 2 points 3 points 5 points 6 points
C. Chronic health 2 points for elective postoperative admission
points 5 points if emergency operation or nonoperative admission, if patient has significant chronic liver, cardiovascular,
respiratory or renal disease or is immunocompromised
*Points are doubled in acute renal failure.

Abbreviations: MAP, mean arterial pressure; A-aDO2, alveolar-arterial oxygen gradient; FiO2, fractional inspired oxygen.
acute renal failure. The maximum possible APACHE II score consideration two obvious facts: (1) organ dysfunction is a
is 71. Increasing scores correlate with increasing mortality at continuum, varying from very mild at one end of the spectrum
each 5-point increment across a wide range of diseases.
The APACHE II scoring system is a useful scale in critical
to hopelessly severe at the other end; (2) organ dysfunction
is a dynamic process and the degree of dysfunction or failure 1
care medicine. Nevertheless, it is wrong to allow APACHE could vary with time.
II scores to influence management in individual patients.
A high initial APACHE II score in postoperative coronary Sequential Organ Function Assessment Score
artery bypass surgery is not necessarily associated with a high The SOFA score is made up of scores from six organ sys
mortality.6 It is also shown later in this book (see chapter tems graded from 0 to 4, depending upon the degree of
Multiple Organ Dysfunction Syndrome) that tropical problems dysfunction.15 A SOFA score greater than 15 is associated with
may be associated with severe multiple organ dysfunction a mortality greater than 80%.16 We use this scoring system in
(and high APACHE II scores), and yet do not have the grim our unit and find it valuable. However, as explained in the
prognosis forecast by the APACHE II score. A critique of chapter Multiple Organ Dysfunction Syndrome, we have
these scoring systems is given in the chapter Multiple Organ noted that in fulminant tropical infections (e.g. falciparum
Dysfunction Syndrome. malaria), high SOFA scores do not necessarily predict death.
Several variants of the APACHE II scoring systems have The recovery rate in these infections is significantly higher
been devised. These include Bion’s sickness score,7,8 mortality than that predicted by the SOFA score (see chapter Multiple
prediction models9-11 and the therapeutic intervention scoring Organ Dysfunction Syndrome). Table 5 gives the details of
system.12,13 organ function assessment through the SOFA system.
None of these scoring systems have any significant advan
tage over the more frequently used APACHE II score, and none
Multiple Organ Dysfunction Score
of these should significantly influence decision-making in
individual patients. There is also little or no difference in the The multiple organ dysfunction score was devised because
predictive ability of each of these systems over a wide range of the direct relationship between the number of organs that
of scores.11 fail to mortality in ICU patients.17 The score for each patient is
The APACHE II scoring system (and its modifications) was assessed daily, allowing a better prediction of morbidity and
not designed to judge individual patient outcomes. A new mortality (Table 6).
scoring system (the APACHE III score) has been introduced
to objectively assess patient risk for death and other important Simplified Acute Physiology Score
outcomes related to patient stratification. This new system The SAPS I score was developed from a small database
aims to provide (1) an APACHE III score; (2) a series of pre of about 700 patients in France, as a simplification of the
dictive equations that help to predict individual patient APACHE scoring system. 18 The SAPS I score had a range
mortality at different times during the patient’s stay in the ICU. from 0 to 56 and was based on physiological parameters, age
The APACHE III system is based on seventeen physiolo and invasive or noninvasive ventilation. Predictive results
gical variables or parameters, and includes within its ambit using the SAPS I were found to be comparable to those
a coma scale, age and pre-existing comorbid conditions.14 using the APACHE I score. The main drawback of the SAPS
The APACHE III score is calculated by adding the coded I as an outcome prediction tool was that it did not take into
variables for each category. A 5-point increase in the APACHE consideration the specific diagnosis and background diseases
III score (range 0–299) is associated with increased risk of or chronic health status of the individual.
death. Further use and evaluation of this scoring system is About a decade later, the updated SAPS II score was
necessary before it can be used routinely for triage decisions developed from a large database of more than 13,000 patients
in critical care. from ICUs across Europe and North America.19 The SAPS II
score is calculated using seventeen variables—twelve phy
OTHER IMPORTANT SCORING SYSTEMS IN siological parameters, age, type of admission (emergency/
elective), presence of acquired immunodeficiency syndrome
CRITICAL CARE
(AIDS), metastatic cancer or hematologic malignancy. The
In the 1990s three other important scoring systems were main outcome measure predicted by the SAPS II is vital status
devised to predict the outcome in critically ill patients. These at hospital discharge. It has been found to perform better
were: (1) the sequential organ function assessment (SOFA) than SAPS I and its performance is comparable to that of the
score, (2) the multiple organ dysfunction score and (3) the APACHE II. Modifications of the SAPS II have been used to
simplified acute physiological score I (SAPS I); this was further make it more applicable at local ICU levels and also for clinical
modified to SAPS II. Unlike the APACHE II scoring system, trials in specific diseases and conditions such as sepsis.
which is used only on admission of the patient to the ICU, The SAPS III is developed by the European Society of
the SOFA score, multiple organ function score and SAPS II Inte nsive Care Medicine. The database for this score is
score are determined daily in a critically ill patient till either expected to be very large, collected from ICUs all over the
recovery or death occurs. These scoring systems take into world. The SAPS III will consist of four modules: (1) a basic
Table 5: sequential organ failure assessment (SOFA) score
1
0 1 2 3 4
Respiration— >400 ≤400 ≤300 ≤200 with ≤100 with
• PaO2/FiO2 ventilatory ventilatory
support support
Coagulation— >150 ≤150 ≤100 ≤50 ≤20
• Platelets (× 103/mm3)
Liver— <1.2 1.2–1.9 2.0–5.9 6.0–11.9 >12.0
• Bilirubin (mg/dL)
Cardiovascular— No MAP Dopamine ≤5 Dopamine >5 Dopamine >15
• Hypotension hypotension <70 or dobutamine or epi ≤0.1 or epi >0.1
mm Hg (any dose)* or norepi ≤0.1* or norepi >0.1*
Central nervous system— 15 13–14 10–12 6–9 <6
• Glasgow Coma Score
Renal—
• Creatinine (mg/dL) <1.2 1.2–1.9 2.0–3.4 3.5–4.9 or >5 or
• Urine output <500 mL/day <200 mL/day
*Adrenergic agents administered for at least 1 hour (doses given are in µg/kg/min).
Abbreviations: FiO2, fractional inspired oxygen; MAP, mean arterial pressure; epi, epinephrine; norepi, norepinephrine.
Table 6: multiple organ dysfunction score

Points
0 1 2 3 4
PaO2/FiO2 >300 226–300 151–225 76–150 ≤75
Serum creatinine (μmol/L) ≤100 101–200 201–350 351–500 ≥500
Serum bilirubin (μmol/L) ≤20 21–60 61–120 121–240 >240
Pulse-adjusted heart rate* ≤10 10.1–15 15.1–20 20.1–30 >30
Platelet count (× 103/dL) >120 81–120 51–80 21–50 ≤20
Glasgow Coma Score† 15 13–14 10–12 7–9 ≤6
*PAR = HR × (RAP/MAP); HR, heart rate; RAP, right atrial pressure; MAP, mean arterial pressure.
†The best estimate in the absence of sedation.
Scoring method: The most abnormal value for each parameter over a 24-hour period is selected for scoring purposes. The addition of scores of all six
parameters gives the final score. It has been observed that scores between 13 and 16 carry a 50% mortality, scores between 17 and 20 carry a 75% mortality
and scores >20 carry a 100% mortality.
evaluation module, (2) an extended outcomes module, parts of the world is influenced by cultural, social and eco
(3) an infection module and (4) a resources module. Along nomic factors. For these reasons, it is difficult to quantify
with predictive models for patient outcomes, the score is also critical care with measurable values and compare these
expected to provide a reliable tool for evaluation of individual values with different institutions in different countries of the
ICUs with a special emphasis infection rates and cost-benefit world.
ratios of investigations and therapies. Present scoring systems are a valuable guide to patient
outcome and indirectly on how management can affect
CRITICAL CARE SCORING IN THE FUTURE outcome. Yet, it is our opinion that scores should not influence
management decisions in individual patients. Clinical
The evolution and practice of better future scoring systems
judgment should never be replaced by any scoring system
need to take into account: (1) factors which predict patient
or scale.
outcome, (2) effectiveness of therapy or management and
(3) efficiency of delivered care.
Critical care is however a complex process. Patients REFERENCES
receiving critical care constitute many variables related to 1. Knaus WA, Zimmerman JE, Wagner DP, et al. APACHE-acute
different disease processes. The problem is further com physiology and chronic health evaluation: a physiologically based
pounded by the fact that delivery of critical care in different classification system. Crit Care Med. 1981;9:591-7.
2. Scheffler RM, Knaus WA, Wagner DP, et al. Severity of illness and 12. Keene AR, Cullen DJ. Therapeutic intervention scoring system:
the relationship between intensive care and survival. Am J Public update 1983. Crit Care Med. 1983;11:1-3.
Health. 1982;72:449-54.
3. Knaus WA, Draper EA, Wagner DP, et al. Evaluating outcome from
intensive care: a preliminary multihospital comparison. Crit Care
13. Cullen DJ, Civetta JM, Briggs BA, et al. Therapeutic intervention
scoring system: a method for quantitative comparison of patient 1
care. Crit Care Med. 1974;2:57-60.
Med. 1982;10:491-6. 14. Knaus WA, Wagner DP, Draper EA, et al. The APACHE III
4. Knaus WA, Le Gall JR, Wagner DP, et al. A comparison of intensive prognostic system. Risk prediction of hospital mortality for critically
care in the USA and France. Lancet. 1982;2:642-6. ill hospitalized adults. Chest. 1991;100:1619-36.
5. Wagner DP, Knaus WA, Draper EA. Physiologic abnormalities and 15. Vincent JL, Moreno R, Takala J, et al. The SOFA (sepsis-related
outcome from acute disease. Evidence for a predictable relationship. organ failure assessment) score to describe organ dysfunction/
Arch Intern Med. 1986;146:1389-96. failure. On behalf of the Working Group on Sepsis-Related
6. Knaus WA, Draper EA, Wagner DP, et al. APACHE II: a severity Problems of the European Society of Intensive Care Medicine.
of disease classification system. Crit Care Med. 1985;13:818-29.
Intensive Care Med. 1996;22:707-10.
7. Bion JF, Edlin SA, Ramsay G, et al. Validation of a prognostic score
16. Vincent JL, de Mendonca A, Moreno R, et al. Use of the SOFA score
in critically ill patients undergoing transport. Br Med J (Clin Res
to assess the incidence of organ dysfunction/failure in intensive care
Ed). 1985;291:432-4.
units: results of a multicenter, prospective study. Working group on
8. Bion JF, Aitchison TC, Edlin SA, et al. Sickness scoring and
sepsis-related problems of the European Society of Intensive Care
response to treatment as predictors of outcome from critical illness.
Intensive Care Med. 1988;14:167-72. Medicine. Crit Care Med. 1998;26:1793-800.
9. Lemeshow S, Teres D, Pastides H, et al. A method for predicting 17. Marshall JC, Cook DJ, Christou NV, et al. Multiple organ dys
survival and mortality of ICU patients using objectively derived function score: a reliable descriptor of a complex clinical outcome.
weights. Crit Care Med. 1985;13:519-25. Crit Care Med. 1995;23:1638-52.
10. Lemeshow S, Teres D, Avrunin JS, et al. Refining intensive care unit 18. Le Gall JR, Loirat P, Alperovitch A, et al. A simplified acute
outcome prediction by using changing probabilities of mortality. physiology score for ICU patients. Crit Care Med. 1984;12:
Crit Care Med. 1988;16:470-7. 975-7.
11. Lemeshow S, Teres D, Avrunin JS, et al. A comparison of methods 19. Le Gall JR, Lemeshow S, Saulnier F. A new simplified acute
to predict mortality of intensive care unit patients. Crit Care Med. physiology score (SAPS II) based on a European/North American
1987;15:715-22. multicenter study. JAMA. 1993;270:2957-63.
SECTION
Cardiopulmonary Resuscitation and

Cerebral Preservation in Adults
Cardiopulmonary Resuscitation and Cerebral Preservation in Adults

CHAPTER 4
Cardiopulmonary Resuscitation and
Cerebral Preservation in Adults
GENERAL CONSIDERATIONS of symptoms.2 Cardiac arrest is a dreaded complication during

surgery and anesthesia; it can also complicate investigational
A sudden unexpected cessation of effective cardiac pump procedures—pleural, peritoneal or pericardial paracentesis,
function or beating of the heart is termed as cardiac arrest. intravenous (IV) pyelography, cardiac catheterization and
This may be reversible if promptly managed, but otherwise coronary or cerebral angiography. It can occur as a con
invariably leads to death. Cardiac arrest quickly results in a sequence of electrolyte and metabolic abnormalities, or may
respiratory arrest and resuscitation therefore involves establ be caused by drugs—particularly antiarrhythmic drugs like
ishing an effective stable circulation as well as maintaining quinidine, procainamide and digitalis. It is an important cause
effective ventilation. Similarly, respiratory arrest if unattended of death following trauma, blood loss, asphyxia (due to
leads within a few moments to cardiac arrest, illustrating drowning, carbon monoxide poisoning, and inhalation of
the inseparable link between the heart and the lungs. food or vomit), sudden large airways obstruction by a foreign
The approach to cardiopulmonary resuscitation (CPR) is body, and electrocution either by electric shock or lightning.
therefore always an integrated one directed both to the heart Closed chest compression in the management of cardiac
and the lungs. One should in the same breath also consider arrest was introduced in 1960. Between 1960 and 2000 there
cerebral preservation, because cessation of effective cardiac was no change in the long-term survival after cardiac arrest.
pump function results in severe hypoxia due to stoppage or Evidence accumulated over the last decade has stressed on
markedly inadequate blood supply to all important organs of special aspects of emergency management responsible for
the body, most importantly to the brain and the heart muscle successful resuscitation. Also, the importance of specific
itself. Hypoxic brain damage and death therefore always and meticulous intensive care after successful resuscitation
result if resuscitation is delayed, is not implemented or is is being increasingly recognized as being crucial to the
unsuccessful. In fact, for several reasons brain damage can prevention of brain damage and preservation of cerebral
result even after successful resuscitation. The preservation of function.
brain function (cerebral preservation) during and after CPR is An integrated approach to appropriate emergency re
therefore crucial to allow a meaningful quality of life. suscitation and postresuscitation intensive care has resulted
It is not the purpose of this chapter to enumerate the in improved final outcomes and increased meaningful
numerous causes of sudden cardiac arrest or cardiac death. survivals.
Ischemic heart disease (IHD) remains the commonest cause This chapter briefly mentions the epidemiology and the
in Western countries as also in India. In the sixties, 12% basic mechanisms underlying cardiac arrest. It next describes
of all natural deaths in the United States of America were the various aspects of emergency management of CPR as
sudden, and 88% of all sudden natural deaths were due to currently advised. It then deals with post-arrest care directed
cardiac causes.1 A prospective study in the same country specifically towards preventing or minimizing brain injury.
demonstrated that 50% of all coronary heart disease deaths are It ends with a brief discussion of neurological sequelae that
sudden and unexpected and occur within 1 hour of the onset can unfortunately occur even after successful resuscitation
20 Section 2 Cardiopulmonary Resuscitation and Cerebral Preservation in Adults
and the prognosis of neurological recovery (after restoration hospital, particularly in an intensive care unit (ICU)
of the circulation) based on clinical examination. setting, this graduates seamlessly almost pari passu to
Advanced Cardiac Life Support.
EPIDEMIOLOGY TT There is a window of approximately 4 minutes from the
cessation of effective cardiac function (with absence of
It would be appropriate to state that for several reasons, very major pulses) and of respiration, after which hypoxic
little is known about the epidemiology of cardiac arrest in our injury to the brain progresses rapidly, leading to irreversible
country. An out-of-hospital arrest in large cities of India is death. Resuscitation attempts after 10–15 minutes of arrest
invariably fatal. For one there are very few lay people trained have rarely been found to be successful, and most doctors
2
in basic life support and for another it may take hours (because hesitate to resuscitate when more than 10 minutes have
of horrendous traffic) for an out-of-hospital arrest to reach a elapsed after an unattended cardiac arrest. Permanent
hospital. brain damage and a vegetative state are the sequelae even
In Western countries, the incidence of out-of-hospital if the CPR is successful.
arrests is estimated at 52.1 per 100,000 people per year with a TT Cardiopulmonary resuscitation in terminal malignancy
reported median survival rate of 8.4%.3 The incidence of in- or in terminal hepatic, renal, or pulmonary diseases offers
patient hospital arrests is estimated at about 0.17 events per a cruel extension of life for a short span, and should be
hospital bed per year,4 survival to hospital discharge being just avoided. The ethical issues involved are fairly clear, but
17%. It is of note that 17% of episodes of respiratory arrest or should be decided in consultation with the patient’s
compromise may progress to cardiac arrest.5 relatives, and one’s own colleagues.
Only 44% of patients who suffer an arrest in the hospital
have return of circulation and 60% of those resuscitated from Management of the Individual Patient
cardiac arrest in hospital die prior to discharge from hospital.4
Post-ischemic brain injury and multiorgan failure are the The following steps are detailed for the management of the
causes of these deaths. Failure to awaken contributes to individual patient (Flowchart 1). In an in-hospital setting, and
withdrawal of care in Western countries in as many as 24–68% more so in an ICU setting, one step dovetails into the next,
of patients after initial successful resuscitation. and more often than not, many steps are in simultaneous
operation. It is important that in an ICU setting each doctor,
nurse or paramedical person knows exactly what is expected
BASIC MECHANISMS of him or her, and that there is one individual to supervise
The mechanisms underlying cessation of effective cardiac and direct operations.
pump function, which if uncorrected lead to rapid loss of
consciousness and death are— Recognition of Cardiac Arrest
TT Ventricular fibrillation (VF). A health-care provider (doctor, nurse, paramedical person)
TT Ventricular tachycardia (VT) resulting in pulselessness should assume that a person is in cardiac arrest if he or she
and an unconscious state. is unresponsive and has abnormal breathing. Since prompt
TT Cardiac standstill or asystole; a markedly severe brady and continuous chest compression is of utmost importance,
arrhythmia has well-nigh the same effect as an asystole searching for the pulse should never be a lengthy process.
or standstill. Health-care providers, and this includes trained intensivists
TT Pulseless electrical activity (PEA) In this condition, though
should spend a maximum of 10 seconds searching for the
carotid or femoral pulse. If a definite pulse is not detected,
the electrocardiogram (ECG) or cardiac monitor show a
chest compression should start immediately.6,7
normal or satisfactory electrical activity, the mechanical
Lay people are instructed not to attempt to feel the pulse.
pumping action of the heart is either feeble or absent.
They should assume cardiac arrest if the patient is unrespon
sive and has abnormal breathing and start chest compressions
OBJECTIVES AND PRINCIPLES OF promptly.
MANAGEMENT Once a cardiac arrest is diagnosed in hospital and in the
TT The chief objective is to restore and maintain stable,
wards, the rescuer should promptly shout for help. There
effective cardiopulmonary function resulting in effective should also be a provision for an alarm that summons prompt
transport of oxygen to the tissues of the body. help. This of course is unnecessary when an arrest occurs in
TT To prevent or minimize brain damage not only during
the ICU where prompt help from two or more doctors together
CPR but also after successful restoration of the circulation. with nurses and paramedical personnel is always available.
TT Since irreversible brain injury or death can occur within
4–6 minutes of the onset of arrest, immediate treatment Restoring Circulation
is mandatory. Time is of essence and every single second Restoring circulation is of crucial importance in CPR. This is
counts. specifically achieved by prompt uninterrupted well performed
TT A preplanned, well-organized management protocol chest compressions. Chest compressions augment both the
is essential. Initially, it aims at Basic Life Support. In a coronary and the cerebral circulation. Interruption in chest
Chapter 4 Cardiopulmonary Resuscitation and Cerebral Preservation in Adults 21
Flowchart 1: Steps in adult cardiopulmonary resuscitation order. The current 2010 guideline is circulation, airway,
breathing (CAB) in this new order. The stress first and foremost
is now rightly placed on the prompt restoration of circulation
by immediately starting chest compressions. Delay in starting
of chest compressions is thereby minimized. Care-givers who
hesitate or are fearful of performing rescue breathing can start
resuscitation more promptly and continue uninterruptedly
if they are required to perform chest compressions as their
first and immediate task. Another equally important aid
in the restoration of circulation is the use of cardioversion
and defibrillation in appropriate conditions. The current 2
guidelines also advise on the use of drugs such as epinephrine,
vasopressors, dopamine, atropine, antiarrhythmic, and other
drugs. They do not however lay great emphasis on these
medications, perhaps because they have not been shown to
influence outcomes. On the other hand, prompt recognition
of VF and prompt defibrillation is life-saving so that defibrill
ation in a number of patients is second in importance only to
chest compressions. Unfortunately, in the large metropolitan
cities of India, an out-of-hospital arrest can only be managed
by cardiac compressions either by a layperson or by a
doctor who happens to be present. The paucity of cardiac
ambulances, the time taken by the ambulance to reach the
victim, make timely availability of a defibrillator extremely
unlikely. Invariably by the time an out-of-hospital arrest
reaches hospital, meaningful recovery is extremely unlikely.
An in-hospital arrest, in the wards or in a department or
during transfer of a patient from the ward to a department
poses special problems. Chances of recovery are increased if
there is an organizational system and a protocol that allows
rescuers within the hospital to reach the victim as quickly as
possible. This aspect is discussed later in the chapter. However,
in an ICU, features of basic life support and advanced life
support are seamlessly dovetailed. This is because emergency
equipment is waiting and ready for use, and there are two or
more rescuers attending to the crisis. One continues with chest
compressions, the other handles the airway and ventilation,
Source: Adapted with permission from Adult Basic Life Support: 2010 American a third is ready if needs be to use the defibrillator and a nurse
Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency helps to gain access to one or more large peripheral veins in
Cardiovascular Care. Circulation 122. preparation for infusion of drugs.
This chapter will now discuss details of resuscitation
compressions or incorrectly performed chest compressions of the circulation through closed chest compression and
strongly jeopardizes recovery, leading to a less favorable the appropriate use of defibrillation. It next discusses the
neurological outcome. In patients who suffer an arrest due care given to the airway and breathing and then deals with
primarily to a cardiac cause, chest compressions take preced drugs that may help to restore circulation. Finally, there is a
ence over ventilation. In patients who have experienced discussion on the post-arrest care (i.e. care after successful
a primary pulmonary arrest rescue breathing should be CPR). Specialized intensive post-arrest care is necessary
started as soon as possible after commencement of cardiac chiefly to prevent or minimize brain damage and also to
compressions. prevent damage to other organ systems.
In 2010, the American Heart Association (AHA) drasti
cally revised its guidelines for emergency CPR and emergency Basic Life Support consists of—
cardiovascular care.8 This revision was based on research TT Continuous correctly delivered closed chest compress
contributing to improved morbidity and mortality associated ions at 80–100/minute.
with cardiac arrest. Prior to 2010, the basic life support TT Defibrillation of the heart in patients with pulseless VT
advocated was airway, breathing, circulation (ABC) in that or VF.
TT Ensuring patency of the airway (head-tilt, chin-lift man recoil (the upstroke) before starting the next compression.
euver). The time for compression and recoil should roughly be
TT Ventilation (mouth-to-mouth or bag-mask ventilation) the equal, the chest being seen to re-expand fully before the next
ratio of chest compression to ventilator breaths being 30:2. compression. The hands should be slightly removed (lifted)
from the chest wall during the upstroke to ensure full and
Advanced Life Support consists of— adequate recoil. Interruption of the recoil or inadequate
TT A combination of closed chest compressions and defibri recoil leads to increased intrathoracic pressures and a poor
llatory shocks for pulseless VT or VF. hemodynamic profile characterized by decreased coronary
TT Securing IV access. perfusion pressure, poor myocardial blood flow, decreased
2 TT Advanced Airway Management and Ventilatory Support.

TT Pharmacological therapy—epinephrine, inotropes, vaso
cardiac index and reduced cerebral blood flow.11,12
The recommended rate of delivery of chest compressions
pressors, antiarrhythmic drugs, atropine, and other drugs. is at least 100/minute. The number of delivered compressions
per minute is a predictor of return of spontaneous circul
ation (ROSC) and neurologically intact survival.13,14 The
Closed Chest Compressions
best outcomes have been observed with at least 80 chest
Adequate perfusion of the heart (through the coronary compressions per minute in in-hospital arrests and 68–89
circulation) and of the brain (through the cerebral circulation) compression per minute in out-of-hospital arrests.13 It was
is vital for meaningful survival. Chest compressions achieve believed earlier that external chest compression maintained
this by building and maintaining coronary and cerebral per circulation as a result of a squeeze or pressure on the
fusion pressures. 7,9 The coronary perfusion pressure is heart between the sternum and the thoracic spine. This
quantified by the pressure gradient between the aorta squeeze pushed blood out into the systemic and pulmonary
and the ventricular cavities (usually approximated by the circulations, followed by a filling of the heart when the
central venous pressure or the pressure in the right atrium). pressure was released. The current concept is that external
Measurements of coronary perfusion pressure are not pos pressure on the chest leads to an increased intrathoracic and
sible unless the patient has invasive monitoring devices intrapleural pressure, and this positive pressure is responsible
(such as a central venous catheter) before the cardiovascular for propelling the blood forward. Release of external pressure
collapse. With mechanical compression of the chest, leads to a fall in the intrathoracic and intrapleural pressures,
cerebral blood flow occurs during this phase of actual chest allowing blood to fill the heart. This thoracic pump theory
compression. However, the perfusion of the myocardium claims that the entire thorax acts as a pump to propel blood
through the coronaries occurs during the relaxation phase. forward, possibly by reducing the afterload of the left ventricle.
Coronary perfusion pressure (which is maximum at the end Afterload can be defined as the peak systolic transmural
of the relaxation phase) is strongly correlated with myocardial pressure, and increased intrathoracic pressure would reduce
perf usion and hence with the likelihood of successful this transmural pressure, thus reducing the afterload, and
resuscitation.10 It has been estimated that in humans the promoting emptying of the ventricles.
coronary perfusion pressure should exceed 15–20 mm Hg The general guideline for compression to ventilation
for successful resuscitation. It is likely that a lesser degree of ratio is 30 chest compressions to two ventilations if there
coronary perfusion pressure is unable to supply adequate is a single rescuer. If there are two, then one rescuer can
nutrients and energy to the myocardium to allow recovery administer uninterrupted chest compressions while the
following cardiac arrest. other delivers ventilation (see later discussion) keeping the
chest compression to ventilation ratio at 30:2. It is crucial
Position of the Patient and the Rescuer not to waste time by inserting an artificial airway at the
Proper positioning of the care-giver and the patient is start of resuscitation as this significantly interrupts chest
fundamental. In an out-of-hospital scenario, the care-giver compression. An advanced airway should be inserted at least
kneels perpendicularly to the patient’s torso. For the in- 3 minutes after uninterrupted chest compression and after
hospital cardiac arrest, the doctor or the rescuer should attempted defibrillation, if this is found to be necessary.
stand at the bedside at the level of the torso of the patient. A
soft mattress defeats the very purpose of mechanical cardiac Problems Preventing Effective Chest Compression
compressions as the mattress absorbs a great deal of the Chest compressions should start promptly and be delivered
force exerted during compression. If the patient is on an air continuously with the right technique so as to maintain
mattress, it should be promptly deflated. effective coronary and cerebral perfusion pressure. Even
a short pause results in a sharp fall in the coronary and
Compression Technique cerebral circulation pressures. 15 It has been noted that
Place the heel of one hand on the lower half of the sternum interruption in chest compressions are common, consuming
and then place the heel of the other hand over the top of the 24–57% of the total resuscitation time.16,17 It has also been
first. In adults, depress the sternum with a downward force noted that chest compressions must be continuous if they
(the down stroke), for at least 2 inches and allow of proper are to reach a threshold for successful defibrillation and
resuscitation18 and counter the brain’s extreme vulnerability More often than not a rescuer fails to recognize or admit
to ischemic injury. fatigue. Ideally, care-givers (i.e. rescuers) giving chest
compressions should rotate every 2 minutes. This switch
The following factors encroach upon and can significantly
should be seamless the second rescuer being ready and in
interrupt compression time—
position on the other side of the patient when the first rescuer
TT Advanced Cardiac Life Support interventions (ACLS)
is relieved.
These can result in numerous pauses in chest compression.
The insertion of artificial airways is observed to be res
Hands-only Cardiopulmonary Resuscitation
ponsible for 25% of all interruptions with a median
If there is a single rescuer there is necessarily an interruption
2
duration of 2 minutes. Endotracheal intubation should
not be attempted at the very start of resuscitation. It should in chest compressions since he or she needs to deliver two
preferably await restoration of the circulation or if deemed rescue breaths after every 30 chest compressions. The per
imperative should be attempted only after 3–5 minutes of formance of a hands-only CPR allows a single rescuer to focus
continuous chest compression. solely on continuous uninterrupted chest compressions. It
is believed that ventilation is not necessary in the first few
TT Frequent Pulse Checks form another Source of Interruption
minutes of resuscitation because blood oxygen levels remain
Pulse check should not exceed 10 seconds; frequent
adequate for some minutes after a cardiac arrest from a
pulse checks are not necessary and should be avoided
non-respiratory cause.8 The safe and acceptable duration of
unless there is other evidence of return of spontaneous oxygen levels in such circumstances is not known. However,
circulation (ROSC), such as an increase in the patient’s chest wall recoil may provide some degree of ventilation and
oxygen saturation as measured by an oximeter or an oxygenation during hands-only CPR.
increase in the end tidal CO 2 (EtCO 2) measurement. It should however be noted that the hands-only CPR
Studies have shown that the patients with ROSC had a concept contradicts the early work demonstrating that airways
mean increase of 10 mm in the EtCO2 as compared with collapse in most comatose patients, so that compressions
patients with cardiac arrest who failed to survive. EtCO2 alone cannot provide adequate ventilation.20 Recent studies
measurement can therefore monitor ROSC, obviating the suggest that chest compressions generate tidal volumes less
need to interrupt chest compressions. than the physiological dead space.21
TT Defibrillation It is another often necessary procedure
which interrupts chest compression. This interruption Alternative Cardiopulmonary Resuscitation
even while preparing for defibrillation leads to a sharp Techniques
drop in the coronary perfusion pressure. Till recently
Alternative techniques of CPR have been tried and described
the traditional method for defibrillation was to stop
with uncertain success.
compression, analyze the ECG rhythm, charge the defi
TT High frequency chest compressions are delivered at a rate
brillator and deliver the shock to the patient. This amounts of greater than 120/minute. Two clinical trials showed
to be an interruption of about 15 seconds. The correct improved hemodynamic profile but no improvement in
method is to charge the defibrillator in anticipation outcome.22
of shocking the patient, chest compressions being TT Open cardiac chest CPR Direct cardiac massage is resorted
continued throughout and being interrupted only during to in patients suffering cardiac arrest during thoracic
rhythm analysis and delivery of the shock. The average or cardiac surgery as also in patients undergoing other
interruption time for chest compressions is thereby close to surgery where closed chest compressions have been
just 4 seconds. If rhythm analysis show that defibrillation is ineffective. Open chest CPR with direct cardiac massage is
not warranted chest compressions are promptly restarted, also used after cardiac arrest from a traumatic chest injury.
thereby further saving on interruption time. Recent studies
Open cardiac massage (which was the only method to
have shown that it is completely safe for a care-giver treat cardiac arrest before 1960) has now been supplanted
wearing standard examination gloves to continue chest by closed chest compressions. At present, its main use is
compressions during the use of a biphasic defibrillator with when the chest is already opened at surgery or when cardiac
self adhesive pads.19 There is no danger of an electric shock arrest occurs soon after thoracotomy or occasionally after a
to the rescuer with biphasic defibrillators in contrast to the laparotomy (if prompt resuscitation through closed cardiac
legitimate fear with the use of monophasic defibrillators. compression is unsuccessful). It should be noted that direct
TT Rescuer fatigue can result in imperfect technique of chest cardiac compression via a thoracotomy procedure produces
compression. The depth and even the frequency of chest roughly a threefold increase in coronary perfusion pressure
compression may be compromised. A shallow depth fails compared to external chest compressions. Also VF and
to generate an adequate coronary and cerebral perfusion mechanical activity of the heart are directly visible so that
pressure. It is also associated with an impaired recoil direct defibrillation of the heart or direct ventricular pacing
which results in a reduced coronary artery blood flow and can be promptly used if necessary. Finally, cardiac tamponade
an increased intrathoracic pressure. causing arrest can be promptly relieved by pericardiotomy.
TT Interposed intra-abdominal compression (IAC) is another promoting coronary artery perfusion and the supply of oxygen
procedure reported to help increase coronary and cer and other metabolic substrates to the myocardium.16
ebral perfusion. It requires three rescuers (health care
workers). The first provides chest compression; the second Method of Defibrillation
compresses the abdomen (with the same hand position As soon as a defibrillator is available it is attached to the
and to the same depth) between the xiphoid process and patient and if pulseless VT or VF is present, defibrillation is
the umbilicus during chest wall recoil. The third provides carried out with a shock of 200 joules. The shock is delivered
ventilation preferably with an advanced airway device. through paddles (coated with a jelly), one paddle being held
IAC results in improved coronary perfusion. An in-hospital firmly in contact with the sternum and the other placed over
2 trial demonstrated improved survival compared to CPR.23
A further study is needed to validate this result.
the left side of the chest in the midaxillary line. The following
points are of importance as they add to the likelihood of
TT A precordial thump A precordial thump is a forceful blow successful CPR—
to the anterior chest wall. It can occasionally stun the
TT Most available defibrillators now deliver biphasic wave
myocardium and convert VF or a pulseless VT into a more
forms as these produce more effective depolarization and
stable rhythm. The precordial thump is not advocated for
achieve defibrillation with less energy than monophasic
unwitnessed cardiac arrest. It may occasionally be useful
wave forms.
in witnessed, monitored cardiac arrest showing VF and
TT The paddles must exert a firm pressure (0.5–0.8 kg) over
pulseless VT if a defibrillator is not immediately available.
the sites of application on the chest wall; this decreases
It should not delay prompt chest compressions.
chest wall impedance, increasing delivery of the current
to the myocardium.
DEFIBRILLATION
TT It is crucial that the transition from the chest compressions
The prompt delivery of transthoracic electric shocks is (which the patient is receiving) to the delivery of the
critical to survival in patients with cardiac arrest due to VF shock is seamless. Therefore, chest compressions should
or pulseless VT. The earlier these rescue shocks are given the be continued while the defibrillator is charged and
more likely are they to be effective. In fact, rescue shocks are compressions stopped only when the shock is just about
highly effective when VF is of brief duration (1–2 minutes). to be delivered. Reducing the delay between the last
The chance of successful defibrillation diminishes rapidly compression and the delivery of a single shock has been
over time. 24 The probability of successful defibrillation associated with more successful resuscitation.28 Following
declines by about 2–10% per minute starting with an estimated the delivery of the shock, chest compressions should
probability of 70–80% at time zero.25 Thus, if a patient with VF promptly recommence, the transition from shock back to
is not shocked (defibrillated) within 10 minutes of the onset of chest compressions again being seamless.
collapse or arrest the probability of survival approaches zero. Prior to 2010, it was recommended that defibrillator shocks
Interestingly, resuscitation is more difficult and less likely were delivered in stacks (2–3 at a time). The current recom
if rescue shocks covert VF into asystole instead of converting mendation is to deliver a single shock followed by immediate
VF into a stable organized rhythm. It is also to be noted that resumption of chest compressions. This recommendation
pulseless VT or VF may be resistant to cardioversion in the leads to a minimum interruption of chest compressions, so
presence of severe hypoxia, acidosis or electrolyte imbalance. crucial to successful resuscitation.
Transthoracic electric shocks act by depolarizing the Rescue shocks may need to be repeated with multiphasic
heart, thereby abolishing the VF wave fronts, and allowing the wave forms but they should be delivered singly in patients with
restitution of a stable cardiac rhythm. In all probability, a critical recurrent VF or pulseless VT, with as short an interruption of
mass of the myocardium must be depolarized to produce this chest compressions as possible.
depolarizing effect. VF may however recur perhaps related TT Hands-on defibrillation Uninterrupted chest compressions
to persistent foci within the myocardium which are not are crucial for recovery of spontaneous circulation. In
depolarized or perhaps because of heterogeneous areas of most units (including ours), chest compressions are
refractoriness within the heart muscle.26 necessarily interrupted, though briefly (hands off) during
the delivery of the rescue shock. This was due to the fear
CPR before Defibrillation of electrocuting the rescuer. Recent studies have however
The rate of survival is noted to be higher among patients who shown that it is perfectly safe to continue compressions
have experienced an unwitnessed sudden cardiac arrest, if during the delivery of a defibrillatory shock when a
these patients have received CPR for 1.5–3 minutes followed biphasic defibrillator is used with self-adhesive electrodes,
by defibrillation. 27 In a witnessed sudden cardiac arrest, and the rescuer wears standard examination gloves.19 The
immediate defibrillation is crucial, the patient receiving AHA has not adopted this practice in the 2010 guidelines,
chest compressions while the defibrillator is being prepared. but it is likely that in the future, interruption of chest
Chest compressions prior to defibrillation perhaps improve compressions may be recommended only and solely for
the myocardial readiness for a successful cardioversion by the purpose of rhythm analysis.
TT Current research has shown that quantitative analysis of is left unattended. This prevents oxygenation, causing or
VF wave forms can distinguish early VF from late VF.29 Large perpetuating cardiorespiratory arrest.
amplitude wave forms suggest early VF and is associated Obstruction of the airway can occur in any patient who
with greater success in defibrillation. Recording conditions is comatose, including a patient who suffers cardiac arrest
and body build may however affect the amplitude of from a primary cardiac cause. The airway can be opened by
wave forms. Future generations of defibrillators almost the simple maneuver of extension of the neck (head tilt) and
certainly will incorporate devices that provide a real- forward displacement of the mandible (chin lift). Following
time semiquantitative analysis as to the probability of a this, positive pressure ventilation can be provided by mouth-
successful cardioversion after delivery of a rescue shock. to-mouth or bag-mask ventilation. A positive pressure breath of
The intensivist would then use the information to shock
VF if the probability of success is high or continue with
400 ml delivered in 2–3 seconds is enough to cause a sufficient
expansion of the chest. Hyperventilation and hyperexpansion 2
chest compressions when the probability of success is low. of the chest can do more harm than good as this can impair
venous return and decrease circulation during resuscitation.
Pulse Check after Defibrillation30 The optimal rate and timing of pressure breaths must be
Chest compressions should be resumed immediately after balanced against the fact that interrupting chest compressions
defibrillation. The pulse should not be checked after defi frequently leads to a lesser survival rate. As mentioned earlier
brillation. This is because even if the patient is successfully the ratio of 30 chest compressions to 2 breaths for ventilation
cardioverted, the myocardium is generally stunned and has been recommended in the current guidelines.
unable to generate adequate perfusion pressure. The pulse The view that chest compressions alone without any
rate and rhythms can be checked at the next 2 minute interval, artificial ventilation may be sufficient to accomplish resuscit
either at the time when the rescuer is changed, or when ation has been mentioned earlier. This view is debatable and
the next defibrillatory shock is ready to be delivered. The is not acceptable to most intensivists.
importance of uninterrupted cardiac compressions lies at the
heart of the above recommendation. Relevant AHA recommendations with regard to airway
If the patient lapses into repeated VF, many defibrillating and ventilation are briefly mentioned below.
shocks may need to be given, notwithstanding the fact that TT The use of 100% oxygen is recommended during initial
repeated shocks may directly damage the myocardium. We resuscitation as there is no evidence that it causes harm
have had patients lapsing into repeated VF necessitating during short-term resuscitation.
numerous defibrillatory shocks. In some of these patients TT Chest compressions cause air to be expelled during
the underlying cause turned out to be a blocked left anterior compression and drawn into the lungs passively during
descending artery (LAD). Coronary angiography with ang the recoil. Therefore if the airway is patent, the passive
ioplastic stenting of the LAD led to survival. inhalation of oxygen via a face mask suffices for several
minutes after sudden cardiac arrest.
BASIC AIRWAY MANAGEMENT AND TT Bag-mask ventilation can maintain adequate ventilation.
VENTILATION It needs to be performed correctly and preferably needs
two trained care-givers. One holds the mask firmly in place
The current AHA basic life support and the ACLS guidelines from the bridge of the nose on top to well below the mouth
place circulation before airway and breathing in patients who at the lower end, so that there is no leak of air or oxygen
experience sudden cardiac arrest from a cardiac cause. This that is delivered. The other care-giver presses the bag pro
is because in the early stages, patients with sudden cardiac viding a tidal volume of 600 ml over 1 second at the rate
arrest suffer from severe hypoxia to the heart and brain due
of 8–10 breaths per minutes.
to decreased or absent perfusion and not due to decreased
ventilation. In the above situation oxygen reserves remain An important complication of bag-mask ventilation is
adequate for the first few minutes so that giving precedence to insufflation of the stomach. Normally the esophageal tone
ventilation over circulation as was done prior to 2010, reduces prevents air entering the stomach unless the upper airway
the chance of survival. However, in patients who have suffered pressure is close to 20 cm H2O. However, in cardiac arrest, the
cardiac arrest from a primary pulmonary cause (drowning, esophageal muscle tone is decreased allowing insufflation of
severe respiratory failure, sudden obstruction to the upper the stomach with air at an upper airways pressure of 5–8 cm
airways) a patent airway and ventilation should be restored H2O. Overvigorous squeezing of the bag during the bag-mask
as quickly as possible. If there are two rescuers at work, this is ventilation can therefore prove dangerous. Gastric dilatation
easily possible as one attends to chest compressions and the can cause vomiting, aspiration of gastric contents; it can also
other to the airway and ventilation. If there is just one rescuer, impair venous return and decrease lung compliance.
the task may prove difficult.
Though attention to circulation precedes that given to the Advanced Airway Management and Ventilation
airway and ventilation, it needs to be stressed that CPR cannot TT Insertion or placement of an advanced airway (such as
succeed if the airway is left obstructed and if ventilation an endotracheal tube) should be avoided in the initial
phase of resuscitation as the procedure interrupts chest prolonged circulatory arrest). Other important causes of PEA
compressions. The procedure should be delayed until are massive pulmonary embolism, tension pneumothorax and
the patient fails to respond to initial CPR or defibr cardiac tamponade.
illation attempts, or inserted if necessary after there is a Perfusion may not be absent but yet be very poor in
successful ROSC. In patients whose circulation has been pulseless VT, supraventricular tachycardia (SVT) and atrial
restored, the presence of coma or respiratory failure is fibrillation with a very rapid ventricular response. These
an indication for endotracheal intubation. Endotracheal rhythm disturbances though organized need prompt cor
intubation unquestionably secures a definite airway, but rection through rescue shock to improve the circulatory state.
it often involves fairly long interruption in chest compre In patients with a PEA, the rate of complexes in the ECG
2 ssions even when performed by an expert. Alternative

supraglottic airways such as the double-lumen tracheal-
may be used to monitor resuscitation efforts. With increasing
myocardial ischemia due to a fall in coronary perfusion, the
esophgeal tubes or laryngeal mask airways can therefore rate of PEA will slow. If resuscitation is leading to improved
be used to temporarily control the airway during resus coronary perfusion and improved supply of nutrients to the
citation. These devices can be inserted blindly in seconds heart, the rate of PEA will steadily increase. Often narrow ECG
without laryngoscopy and without interrupting the chest complexes exceeding 80/minute herald return of pulses and
compressions. Intensivists therefore often use supraglottic successful resuscitation. Falling rates of ECG complexes in
airways as the first advanced airway during resuscitation. PEA signal failure to resuscitate.
After endotracheal intubation, the patient is given The ECG monitor can also demonstrate the presence of
ventilator support. asystole or VF. Reperfusion of the heart in asystole (through
TT Continuous wave form capnography together with clinical chest compressions and ventilation) may restore VF. Also an
assessment is the best way to assess correct placement increase in the amplitude of fibrillating waves in VF points
of an endotracheal tube. Capnography also helps to to improved coronary reperfusion. On the other hand, a
judge ROSC. A rise in the EtCO2 by more than 10 mm Hg deterioration of VF to asystole is observed when resuscitation
often heralds recovery of circulation and gives hope for a attempts are unsuccessful.
successful resuscitation. Pulses The presence of a palpable pulse denotes mechanical
TT If the patient is ultimately on ventilator support, he or activity of the heart and when combined with an organized
she should be provided 8–10 breaths per seconds. stable rhythm as seen on the ECG monitor denotes successful
Higher ventilation rates and large tidal volumes (as has resuscitation. The importance of not interrupting chest
been mentioned earlier) increase intrathoracic pressure compressions to feel the pulse has already been stressed.
resulting in diminished venous return and a reduced It should be noted that a satisfactory arterial pressure or
cardiac output. a palpable peripheral pulse during chest compressions does
not necessarily reflect coronary perfusion pressure because
MONITORING CARDIOPULMONARY ventricular pressures are elevated simultaneously as well.
RESUSCITATION Therefore, palpable pulses during chest compressions (through
a necessary accompaniment to chest compressions) may be
The two most important parameters that need to be monitored misleading. The clinician should look for other evidence of
are the continuous ECG recordings (through electrodes placed improved coronary perfusion—as for example a return of the
on the three limb leads and connected to an ECG monitor) ECG to an organized stable rhythm, a palpable pulse during a
and the presence of pulses. break in the chest compressions and a rise in the EtCO2.
ECG Callaway CW31 gives an excellent practical division of Oximetry Monitoring O2 saturation through oximetry is useful
ECG rhythms into organized and non-organized. Organized to determine the presence or absence of hypoxemia during
rhythms include supraventricular rhythms and VT. Non- resuscitation.
organized rhythms include VF and asystole. Non-organized
rhythms cannot support the pumping of the heart and Capnography It allows the intensivist to monitor the EtCO2.
therefore cannot support circulation. Callaway rightly points A rise in EtCO2 by 10 mm Hg often heralds a possible ROSC.
out that restoring cardiac electrical activity to an organized Arterial pH and, PaO2 and PaCO2 need to be monitored
and stable rhythm is essential for successful resuscitation. so as to allow if necessary any correction of metabolic or
Organized rhythms can support circulation unless the rate respiratory acidosis.
is too slow less than 30/minute or too fast greater than 180/ Serum electrolytes This again may well be important as
minute. An organized rhythm in the absence of pulses is hypokalemia, hyperkalemia; hypomagnesemia may well be
termed pulseless electrical activity (PEA), formerly termed responsible for arrhythmias or even arrest and need to be
electromechanical dissociation. The absence of perfusion corrected for successful resuscitation.
and of pulses in the presence of an organized rhythm is due to Any other investigation which is necessary to determine
severe damage to the heart muscle [as in massive myocardial the possible cause of cardiorespiratory collapse needs to
infarction (MI)] or following cardiac rupture or following be done as it is important to remove or counter the cause if
uncoupling of electrical and mechanical activity (as in successful resuscitation is to be achieved.
PHARMACOLOGICAL THERAPY It must be stated that though clinical data and experience
support an increased probability of restoring spontaneous
Drugs chiefly used in cardiac arrest are vasopressors, inot circulation following the use of vasopressors during CPR, there
ropes, and antiarrhythmic drugs. Sodium bicarbonate may is no clear evidence that their use, improves overall survival.
need to be administered to patients who develop well marked
metabolic acidosis. Electrolyte disturbances may need Antiarrhythmic Drugs
appropriate correction, particularly with regard to potassium, A vagally induced bradyarrhythmia may be corrected by IV
magnesium and calcium. atropine. However, the nervous system does not influence
the heart rate once circulatory arrest has been present for
Vasopressors
There is evidence to show that vasopressors improve
2–3 minutes. Once VF is established the only drug of use
is amiodarone (5 mg/kg given as bolus). The drug works 2
circulation during CPR. They act by raising systemic arterial even better on pulseless VT. If a stable organized rhythm is
pressure, increase coronary perfusion pressure so that restored after its use in VF or pulseless VT, the drug should
restoration of pulses is more likely. Though current data in be given prophylactically in an IV infusion (750–1000 mg)
patients with out-of-hospital cardiac arrest concludes that over 24 hours. Unquestionably the therapy of choice for VF
no drug therapy influences long-term survival, vasopressors or pulseless VT is a rescue shock. If, however, VF or pulseless
must nevertheless always be used. The two vasopressors in VT persists after three rescue shocks, amiodarone should be
common use are epinephrine and vasopressin. Epinephrine given a try.
increases coronary perfusion pressure and systemic In earlier years, lidocaine, procainamide, and bretylium
arterial pressure through stimulation of α-adrenergic have been used for VF. These drugs have no effect once VF has
receptors. Epinephrine is administered intravenously in 1 occurred, though they may suppress the arrhythmia before its
mg increments (0.015 mg/kg). The duration of the action occurrence. Even as prophylaxis, amiodarone has replaced
of epinephrine in cardiac arrest is brief lasting just a few each one of these drugs. Occasionally, we have successfully
minutes, so the dose needs to be repeated. Also the dose of used both amiodarone and lidocaine in separate infusions as
1 mg is perhaps too small to produce a significant effect on prophylaxis for recurrent VT not controlled by either one or
the circulation. The dose should therefore be stepped up and the other of these drugs.
in most patients needs to be used at frequent 3–5 minute All pharmacotherapy is given intravenously. It is however
intervals.8 A 15 mg dose compared to 1 mg in patients with important to bear in mind that if the endotracheal tube is in
out-of-hospital arrests showed a significantly higher rate of place but if for some reason an IV line has not been secured,
restoration of the pulses and admission to hospital in those a few emergency drugs can be effectively administered via
the tube. Medications given by this route should be given in
receiving the larger dose.32 Yet, the overall survival rate was
a dose 2.5 times that recommended for IV use, and should
the same in both groups. A dose of 7 mg when compared to 1
first be diluted in 10 ml normal saline or distilled water. The
mg showed no difference either in restoration of pulses or in
emergency drugs which are thus absorbed and are effective
survival, both in patients with in-hospital and out-of-hospital
after administration through the endotracheal tube are
arrests.33 Though no definite dosage can be recommended,
epinephrine, lidocaine and atropine.
the drug is best used in progressive increments at 3–5 minute
intervals in the hope of restoring circulation and palpable
Treatment of Metabolic Disturbances
pulses.
Vasopressin acts on the vasopressin receptors raising Intravenous Bicarbonate is used to improve metabolic
the blood pressure and coronary perfusion pressure helping acidosis (pH <7.2). Cardiac function is believed to improve
thereby to restore the pulses. It is administered IV as 40 unit once metabolic acidosis has been corrected. Though the use
boluses (0.5 mg/kg). Its action is longer lasting (10 minutes) of bicarbonate in the presence of acidosis has shown higher
than epinephrine, so it may be repeated if necessary at 10 rates of successful resuscitation, there is as yet no evidence to
minutes intervals. Both epinephrine and vasopressin are show an improved outcome.
titrated with reference to the ECG wave forms, presence of Hypokalemia and hyperkalemia are important trigger
factors for VT, VF. Hyperkalemia can cause a sudden
pulses and changes in EtCO2. There is no evidence to show
bradyarrhythmia, wide ventricular complexes with absent
that any one of these vasopressor is superior to the other.
P waves. Marked ST changes may also be present. Pulseless
Nor does combination of these vasopressors confer added
electrical activity may supervene. This precipitating factor
benefit.34
should always be kept in mind, particularly in patients with
chronic renal failure who are on angiotensin-converting-
Inotropes enzyme (ACE) inhibitors. Correction of hyperkalemia in
The inotrope most commonly used is dopamine, particularly addition to the usual CPR procedures often leads to survival
in patients with a past history of IHD or in patients whose with good ultimate outcomes.
cardiac arrest is directly related to an acute myocardial infarc Similarly marked abnormalities in calcium, magnesium
tion (AMI). need correction as they may contribute to cardiac arrest.
Stopping Efforts to Resuscitate days after resuscitation. In other words, it is a reperfusion

Mere survival in a vegetative state can be an unfortunate injury.
sequel of CPR. The risk of organ dysfunction or failure in Several cellular and molecular mechanisms contribute
particular brain damage is related directly to the duration to brain injury. 36 During brain ischemia and soon after
of ischemic insult. The ischemic time following an arrest reperfusion there is an increased release of stimulatory
includes the time from the onset of arrest to the start of CPR amino acids, free radicals that harm both neuronal integrity
(arrest time) plus the duration of CPR efforts. In the study by and function. There are focal disturbances in blood flow and
the Brain Resuscitation Clinical Trial I Study group, Abramson an inhibition of protein synthesis.37 The activation of several
et al. found that if the arrest time is less than 6 minutes and extracellular and intracellular signaling pathways leads to
2 the CPR time does not exceed 30 minutes, half of the survivors
had a good neurological recovery. If, however, the arrest
specific changes in gene transcription.38 Most importantly
after 24–72 hours of reperfusion there is an activation of
time exceeds 6 minutes, a CPR lasting more than 15 minutes specific proteases which lead to neuronal death. Brain injury
always resulted in a significant neurological impairment in with neuronal death probably results as a culmination of
the survivors. Though it is perhaps impossible to be dogmatic, all these metabolic changes observed after reperfusion is
this observation suggests that CPR should be continued for established. There is no drug as yet that has been shown to
at least 30 minutes if the arrest time is less than 6 minutes. If prevent or counter brain injury. Calcium channel blockers,
the arrest time is longer than 6 minutes, the CPR should be magnesium, diazepam, thiopental have been tried in
terminated after 15 minutes.35 randomized trials but without benefit. This is because there
are multiple mechanisms contributing to neuronal injury
and death, and a single drug is not likely to act on all of these
POST-CARDIAC ARREST MANAGEMENT mechanisms. Perhaps different classes of drugs, each acting
Good post-cardiac arrest intensive care after successful on different mechanisms causing brain damage may in the
resuscitation is crucial for a good ultimate outcome future be discovered. Today, the focus on post-cardiac arrest
(Flowchart 2). The single most important objective to bear in intensive care rests on—
mind at this stage is the prevention of brain injury. Though TT Achieving therapeutic hypothermia (32–34°C) for 12–24
brain ischemia and injury can occur during prolonged hours after resuscitation.
CPR, most of it develops as an active process over hours to TT Maintenance of a cardiocerebral perfusion pressure.
TT Early cardiac catheterization with a view to opening up
and stenting critically blocked coronary vessels if these
Flowchart 2: Adult immediate post-cardiac arrest care be present.
Management of Post-resuscitation Arrhythmias

After resuscitation, patients may develop arrhythmias. Atrial
tachycardia is often met with. Flowchart 3 given below outlines
briefly their management.
The management of postresuscitation bradyarrhythmias
is given in Flowchart 4.
Also, refer to treatment of cardiac arrhythmias in the
section Cardiovascular Problems Requiring Critical Care.
Induced Hypothermia
Induction of mild hypothermia (32–34°C) for 12–24 hours
after resuscitation produces a 24–30% relative risk reduction
for death or poor neurological outcome. 39 Survival and
neurological outcomes were favorable when hypothermia
was used in patients resuscitated from VF or cardiac arrest. It
is advocated that hypothermia should be used in all patients
who remain comatose after resuscitation from a cardiac arrest
whatever the initial rhythm. To be maximally effective cooling
should be achieved within 6 hours after resuscitation and
should be continued from 12 to 24 hours; rewarming should
Source: Adapted with permission from Adult basic life support: 2010 American then be performed slowly (< 0.25°C/hour).
Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Hypothermia can be induced by either surface cooling or
Cardiovascular Care. Circulation 122.
through endovascular devices. Surface cooling is achieved
Abbreviations: ECG, electrocardiography; IO, intraosseous; IV, intravenous; STEMI,
ST segment elevation myocardial infarction; AMI, acute myocardial infarction by ice packs and cooling blankets. Neuromuscular blockade
Flowchart 3: Management of atrial tachycardia Flowchart 4: Management of post-resuscitation bradycardia

in adults
Source: Adapted with permission from Adult basic life support: 2010 American Source: Adapted with permission from Adult basic life support: 2010 American
Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. Circulation 122. Cardiovascular Care. Circulation 122.
and sedation may help if shivering or other compensatory Maintenance of Cardiovascular Perfusion Pressure
responses interfere with surface cooling. After resuscitation from cardiac arrest, myocardial function
Endovascular cooling through endovascular catheters is impaired. Hence, a degree of both vasopressor and
perhaps allows more stable control over time. An efficient inotropic support becomes necessary in patients where the
quick method of cooling is the bolus infusion of cold (4°C) resuscitation time has been 3–4 minutes or more. Dependence
IV crystalloid solution 30 ml/kg (unless contraindicated). on support usually diminishes over 24–72 hours.
Hypothermia can then be maintained by either surface Following successful resuscitation, there is evidence to
cooling or endovascular cooling. Use of sedation and at show that within the first 24 hours there is increased cerebral
times neuromuscular blockade enhance the cooling effect. vascular resistance and impaired cerebral autoregulation.40
There is a high incidence of seizures after cardiac arrest, Available data suggests that relative hypertension, with a mean
hence neurophysiological monitoring should be in place if arterial pressure of 80–100 mm Hg should be maintained,
neuroparalytic agents have been used. provided the heart can tolerate the increase in afterload. It
Hypothermia can lead to an increased incidence of has been noted that hypotension soon after resuscitation is
infections if prolonged over 24 hours. Mild hypothermia associated with increased neurological damage in patients
can inhibit platelet function and coagulation but bleeding admitted to the hospital after cardiac arrest. Dopamine 5–20
complications are rare. Elevation of pancreatic enzymes and mg/kg per minute and norepinephrine (0.01 mg/kg per minute)
a fall in creatinine clearance may be observed during cooling. are often used to increase blood pressure and maintain an
All these disorders are corrected following rewarming. effective coronary cerebral perfusion.
Two important points in neurological care of the post-
cardiac arrest patients is (1) to prevent any fever over the Early Cardiac Catheterization
first 24–48 hours of brain injury; (2) monitor for seizures if an Every patient resuscitated from cardiac arrest is a candidate
electroencephalogram (EEG) is available. for cardiac catheterization with a view to opening and stenting
Box 1: Main focus in post-cardiac arrest care Table 1: Important features in the care of organ systems in post-
cardiac arrest
CVS • Counter arrhythmias
xx Hypothermia (32–34°C) for 12–24 hours—
• Amiodarone prophylaxis
–– Slow rewarming
• Mean arterial BP 80–100 for the first 24–48 hours
–– Counter seizures; avoid and counter fever particularly in
• Primary angioplasty in inpatients with MI or IHD
first 48 hours
xx Maintain coronary cerebral perfusion— RS • Avoid hypoxia
–– Mean arterial pressure 80–100 mm Hg through use of • Avoid hyperventilation
dopamine, norepinephrine • Prevent and treat nosocomial infections
2 xx Consider early cardiac catheterization in patients with IHD GI • Consider early refeeding after hypothermia to
prevent translocation of bacteria
Abbreviation: IHD, ischemic heart disease.
CNS • Hypothermia, CT to exclude an intracranial bleed
one or more blocked coronary arteries. Most cardiac arrests or detect a massive recent infarct
are due to underlying IHD; hence most patients would require • Monitor (EEG) and counter seizures
the above approach. Primary angioplasty can be conducted in • Sedation + muscle relaxant if needed for
hypothermia
patients undergoing hypothermia treatment. The presence of
• Periodic CNS examination
continuing coma is no contraindication to primary angioplasty. • MRI, EEG to help with prognosis
Glucose Control Infection • Prevention and treatment of nosocomial

infections
Elevated blood sugar levels are associated with poor outcome
after cardiac arrest.41 Available data suggests that the blood Metabolism • Correction of fluid and electrolytes imbalance
• Correction of acidosis with sodium bicarbonate
sugar should be maintained within 140–180 mg/dl. Stringent
blood sugar control (72–108 mg/dl) is controversial and may Abbreviations: CVS, cardiovascular system; MI, myocardial infarction; IHD,
do more harm than good. ischemic heart disease; RS, respiratory system; GI, gastrointestinal; CNS, central
nervous system; CT, computed tomography; MRI, magnetic resonance imaging;
Use of Anticoagulants EEG, electroencephalogram.
Cardiac arrest is characterized by an activated coagulation
profile and diminished fibrinolysis. The profile resembles a The local spinal reflexes may be preserved in a brain-
mild form of disseminated intravascular coagulopathy, which dead individual. Deep tendon reflexes may thus continue
may contribute to multiorgan dysfunction. The use of low to be elicitable. The heart and circulation can function
molecular weight heparin has been advised by some workers effectively for as long as 2 weeks or even longer if ventilatory
to counter the above hematological change. support is continued. Before the act of Parliament, which
Finally meticulous intensive care needs to be given to legalized brain death as amounting to death (even if the heart
all other organ systems, to correction of fluid, electrolyte continues to beat), there used to be tremendous pressure
disturbances and to prevention and treatment of possible from concerned and at times angry relatives to continue with
nosocomial infections. life support even though the futility and anguish of this was
Salient features of intensive care following post-cardiac adequately explained. Prior to the legislation of brain death
arrest resuscitation are briefly tabled below (Box 1 and Table 1). as death, the longest survival we have recorded after brain
death has been close to 3 weeks. Gradually, multiple organ
Neurological Sequelae failure sets in. An interesting feature is the occurrence of
In spite of expert management even in good centers, neuro diabetes insipidus perhaps due to involvement or injury to
logical sequelae are all too common— the hypothalamus and pituitary. Another noteworthy feature
TT Brain death This is the most catastrophic sequel. Brain is the frequent occurrence of hyperglycemia in these patients.
death has been accepted by an Act of Parliament, as the Failure of gastrointestinal (GI) function is characterized by
criterion for death, even in the presence of continuing absent peristalsis, yet without any associated distension.
heart action or beat. Perhaps there is a decrease and virtual cessation of secretion
Brain death is characterized by an unarousable state of digestive and other fluids within the GI tract. Invariably
of coma, a flat EEG, and absent brainstem reflexes. These there is a final and merciful fall in the blood pressure, or the
include absent doll’s eye movements, no eye movements on development of a malignant arrhythmia, which pulls the
stimulation of the labyrinth by cold water syringed into the curtain on the tragic scene.
auditory canal, and absent corneal, pupillary, gag and cough TT Alteration in the state of consciousness It is a frequent
reflexes. There is also absence of spontaneous breathing. The sequel of CPR. This alteration may take the form of coma,
apnea test is considered positive if there is no evidence of a vegetative state, a locked-in state, or stupor. Coma is an
spontaneous ventilatory efforts for at least 3 minutes, and the unconscious state with absence of verbal communication,
PaCO2 is greater than 60 mm Hg at the end of the test. inability to respond to or to localize noxious stimuli,
and an absence of spontaneous opening of the eyes. A TT Brainstem reflexes (doll’s eye movements, response to cold
vegetative state is similar to coma except that the patient water irrigation of the external auditory canal, pupillary
opens his eyes spontaneously, and may appear to look and corneal reflexes) are often absent immediately after
around. A locked-in state is due to a brainstem lesion successful resuscitation. Their return within 1–2 hours is
in which though there is no movement of the limbs, the a good prognostic sign for possible recovery. The absence
patient is aware of his surroundings; he cannot speak but of pupillary or corneal reflexes at 6–24 hours after arrest
can communicate with his eyes. Stupor is a comparatively carries a grim prognosis. Levy et al.44 noted that not a
benign sequel in which the patient is arousable by a single patient with absent pupillary or corneal reflexes 24
noxious stimulus; significant and at times complete hours following CPR, was restored to a good quality of life.
recovery can ensue from this stage. Mental obtundation
and amnesia for present as well as past events are often
The data given above is useful not only in predicting
prognosis, but in identifying patients in whom critical care is 2
observed for 24–48 hours after successful resuscitation; likely to prove futile. In the West, care after restoring circulation
here recovery is the rule. is invariably stopped if clinical findings (as mentioned above)
TT Cortical blindness It is sometimes seen after recovery. This supplemented at times by EEG and imaging studies point to
type of blindness is associated with an intact optic nerve a hopeless quality of life. In our part of the world, it is often
and a normal retina. The condition usually improves over impossible to do so, as very often close relatives insist on
a period of time though full recovery may not occur. The continuing care at whatever cost and whatever the anticipated
longer it persists, the greater the likelihood of permanent sequel unless one can give proof of the presence of brain death.
impairment of vision.
TT Seizures These are an important sequel in the first
24 hours. In the worst form, they present as a status REFERENCES
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SECTION
Basic Cardiorespiratory Physiology in the

Intensive Care Unit
Basic Cardiorespiratory Physiology in the Intensive Care Unit

CHAPTER 5
Basic Cardiorespiratory Physiology
in the Intensive Care Unit
INTRODUCTION FACTORS REGULATING CARDIAC OUTPUT

All important organs and organ systems in the human body The regulation of the cardiac output (Q T ) is complex,
are interrelated and interdependent. This interrelation and particularly in critically ill individuals, and is dependent on
interdependence is most marked and evident between the tissue factors, neurohormonal factors, and on intrinsic cardiac
heart and circulation on the one hand, and the lungs on the mechanisms.
other. The heart (circulatory system) and the lungs (respiratory
system) form a single inseparable unit whose purpose is to
Tissue Factors
supply oxygen to the tissues, and to remove carbon dioxide
produced during tissue metabolism. The cardiac output is basically governed by the tissue
In any and every critical illness, adequate oxygen delivery needs for oxygen and nutrients. Each organ has a built-in
or oxygen transport to tissues is crucial for proper function autoregulation of blood flow through arteriolar dilatation
of different organ systems, and for survival. Oxygen delivery and vasoconstriction. The mechanism of this autoregulation
is controlled by, and is dependent on the cardiorespiratory is incompletely understood. It is related to local release
system as a whole. Poor function or failure of this system is a of vasodilator substances and other locally operating
common theme in numerous critical illnesses in the intensive vasoregulatory mechanisms.
care unit (ICU). Cardiorespiratory failure invariably heralds
a decline in the clinical state of a critically ill individual. Neurohormonal Influences
Cardiac failure has repercussions on pulmonary function
and gas exchange. Respiratory failure sooner or later wor Neurohormonal factors also play a crucial role in regulating
sens cardiac function. A vicious spiral of deteriorating cardiac output. Increased sympathetic activity is very imp
cardiorespiratory function spells death in any critical illness. ortant for increased cardiac output in stressed states. Neural
It is therefore important for the intensivist to be aware of basic and hormonal influences mediate compensatory mechanisms
cardiopulmonary functions and the factors, which affect these in a patient in acute circulatory failure. These neurohormonal
functions, particularly in relation to critical care medicine. compensatory mechanisms are life-saving as they override
This chapter briefly describes factors regulating cardiac local autoregulatory tissue mechanisms, reduce flow to the
function. It then very briefly outlines basic concepts of gas skin, muscles and the splanchnic circulation, and maintain
exchange within the lungs, which relate to the assessment an adequate flow to the brain, heart and other vital organs
and care of critically ill patients. It then goes on to stress the during shock.
importance of oxygen content of blood, oxygen transport,
and the interrelationship, as illustrated by the Fick principle, INTRINSIC CARDIAC MECHANISMS
between oxygen consumption, oxygen transport, and tissue The heart has a significant reserve, which enables it to increase
needs for oxygen. its cardiac output whenever necessary. This reserve may be
36 Section 3 Basic Cardiorespiratory Physiology in the Intensive Care Unit
impaired or totally absent in patients with cardiac disease.

Increase in cardiac output can be brought about by an increase
in the heart rate and in the stroke volume. The stroke volume
is governed by the following factors—
TT Preload or the end-diastolic fiber length, or the end-
diastolic ventricular volume (Frank-Starling’s law).
TT Contractility or the force of myocardial contraction, as
determined by inherent contractile properties of the
myocardium, and by neurohormonal influences.
TT Afterload which is the degree of wall tension developed
during ventricular ejection.
Preload
This is the degree of stretch of myocardial fibers at end-
diastole, just prior to myocardial contraction. The Frank-
Starling law states, the energy of contraction however
3 measured, is a function of the length of the muscle fibers.1,2

The greater the stretch of muscle fibers within physiological
Fig. 1: Effects of mean systemic pressure and right atrial pressure on
venous return to the right heart. The greater the difference between the
limits, the stronger the force of contraction. The resting length mean systemic pressure and the right atrial pressure, the greater the
of myocardial fibers is related to end-diastolic ventricular venous return. Increase in right atrial pressure without a corresponding
volume. Thus increased venous return increases the stretch of increase in the mean systemic pressure causes a sharp fall in venous
muscle fibers, increases the diastolic volume, and is translated return
Source: Adapted from Guyton AC, Jones CE, Coleman TG. Circulatory Physiology,
into an increased cardiac output. The heart can therefore
Cardiac Output, and its Regulation. In: Clemmer TP (Ed). PA: W B Saunders; 1973.
vary stroke volume and QT in response to changes in venous Cardiopulmonary Critical Care Management. Elsevier Inc.;1988.
return and tissue needs. The Frank-Starling mechanism is an
intrinsic property of muscle, and is independent of neural and largely dependent on volume of blood within the veins, and
hormonal factors. The normal heart can handle an increase in on venous tone.
venous return to 2–3 times normal, even if denervated.3 When
a further increase in QT becomes necessary, neurohormonal
Measurement of Preload and its Significance in Critical
factors must come into play.
Venous return by its influence on the preload, is one of
Care Medicine
the most important factors governing cardiac output. Venous It is difficult to measure end-diastolic volume in critically
return is governed by several factors. An important factor ill patients in the ICU. The next best option is to measure
is the difference between the mean systemic pressure and end-diastolic pressure or the filling pressure of the ventricle,
the right atrial pressure. The mean systemic pressure is the as an indirect measure of the preload. The higher the filling
volume weighted average pressure in the entire circulation— pressure within physiological limits, the greater the preload
arteries, capillaries and veins, and is chiefly determined by and the greater the force of ventricular contraction. The upper
the total blood volume and the tone of the vessels. It averages normal limit of the left ventricular end-diastolic pressure is
about 7 mm Hg. The greater the difference between the mean 15–17 mm Hg. Cardiac output can be augmented in critically
systemic pressure and the right atrial pressure, the greater the ill patients by increasing the left ventricular filling pressure
venous return. The relationship between the mean systemic to an optimum of 15–17 mm Hg, and in some instances to
pressure and the right atrial pressure is illustrated in graphic even 20 mm Hg. A further increase in the filling pressure
form by Guyton (Fig. 1).4 An increase in right atrial pressure will not increase cardiac output, but will lead to an increase
without a corresponding increase in the mean systemic in backward pressure and pulmonary edema. In a critically
pressure sharply reduces venous return. Venous return stops ill patient, a high left ventricular filling pressure (measured
when right atrial pressure equals mean systemic pressure. clinically as the pulmonary capillary wedge pressure) is
This is exactly the circulatory disturbance underlying cardiac usually related either to myocardial dysfunction, or to fluid
tamponade. overload.
The veins are far more distensible than the arteries, so Can one equate left ventricular end-diastolic pressure
that a small increase in venous tone results in a large volume (LVEDP) to left ventricular end-diastolic volume (LVEDV)?
of blood being returned to the heart. Similarly, a decrease The relation between LVEDP and LVEDV is dependent on
in venous tone leads to pooling of blood in the peripheries, the following—
with a decrease in the volume of blood returned to the heart. TT The venous return and volume of blood distending the left
Thus, venous pressure constitutes a very large portion of the ventricle at end-diastole.
mean systemic pressure, and is the most important factor TT The compliance or degree of stiffness or distensibility of
in determining venous return. Venous pressure in turn is the ventricle.
Chapter 5 Basic Cardiorespiratory Physiology in the Intensive Care Unit 37
A B C
Figs 3A to C: Influence of transmural pressure on pressure-volume
relationships in the ventricle. In B, as compared to A, the intrapleural
pressure (p) has risen from -2 to +4 mm Hg, and the intraventricular
pressure (P) has increased to the same extent (from 10 to 16 mm Hg).
The transmural pressure gradient remains the same, and therefore the
intraventricular volume (V) is unchanged. If however, as in C, the rise in
intrapleural pressure (pressure surrounding the heart) is not associated
with a corresponding rise in intraventricular pressure, the transmural
pressure gradient is reduced, and the intraventricular volume falls
Source: Modified from Clemmer TP (1988), as in Fig. 1
3
Fig. 2: Ventricular function curve showing effect of ventricular
compliance on stroke volume and end-diastolic filling pressures. It
should be noted that a reduction in ventricular compliance causes a fall
in the stroke volume (A→B), without any change in the filling pressure. systolic function (i.e. contractility) of the ventricle. In clinical
Similarly, an increase in ventricular compliance results in an increased medicine, it is important that a fall in stroke volume due to
stroke volume (A→C) for the same filling pressure decreased compliance (poor distensibility) is not wrongly
attributed to a reduction in contractility.
In a similar fashion, a decrease in ventricular compliance
TT The transmural pressure, i.e. the pressure surrounding would lead to an increase in end-diastolic volume, and to
the ventricle. an increased stroke volume for the same filling pressure
TT The volume of the right ventricle, which shares a common (Fig. 2).
wall (the septum) with the left ventricle, and a common Ventricular compliance does alter in critical illnesses.
limiting pericardial sac. Compliance is reduced for example, in ischemia to the
Venous pressure and its relation to venous return has ventricle, in hemorrhagic and septic shock, and following
already been briefly discussed earlier. It is a major factor the use of inotropic drugs like dopamine, epinephrine, and
influencing both ventricular end-diastolic filling pressure and isoproterenol.5 Compliance on the other hand is increased
end-diastolic volume. after relief of ischemia, in cardiac dilatation, and after drugs
Compliance of the Ventricle Altered compliance or dis such as nitroglycerin and nitroprusside.6-8
tensibility is also important in determining fiber length. Transmural Pressure Transmural pressure also influences
Compliance can be regarded as the change in end-diastolic the pressure-volume relationships in the ventricle. This
volume (ΔEDV) in relation to change in end-diastolic pressure is illustrated in Figures 3A to C. The intrapleural pressure
(ΔEDP). has risen from –2 to +4 mm Hg; the intraventricular
Compliance = ΔEDV/ΔEDP pressure (P) has increased to the same extent (from 10 to
A fall in compliance (i.e. a decrease in diastolic dis 16 mm Hg). The transmural pressure gradient remains
tensibility), will lead to a rise in end-diastolic pressure for the same, and therefore the intraventricular volume (v) is
any given diastolic volume. If a ventricular function curve of unchanged. If however; the rise in intrapleural pressure
stroke volume against end-diastolic filling pressure is plotted, (pressure surrounding the heart) is not associated
the stroke volume will fall for the same filling pressure, if with a corresponding rise in intraventricular pressure,
the compliance is reduced. When ventricular compliance is the transmural pressure gradient is reduced, and the
markedly reduced (stiff, very poor distensibility), two effects intraventricular pressure falls. The measured stroke volume
follow: (1) the stroke volume is sharply reduced because the is thus the same with a higher LVEDP. This could be wrongly
ventricular end-diastolic volume is reduced; (2) the high left interpreted as a fall in contractility, or to a decreased
ventricular end-diastolic pressure needed to distend the stiff compliance, when in point of fact it is related to an increase
ventricle leads to pulmonary congestion and edema. The in the intrapericardial or intrapleural pressure. The former
decrease in stroke output that accompanies a decrease in can result from pericardial effusion, and the latter may
ventricular compliance is termed diastolic dysfunction or occur in patients on ventilatory support, particularly when
diastolic heart failure, as it is independent of any change in the positive end-expiratory pressure (PEEP) is being used.
Volume of the Right Ventricle Acute dilatation of the right Influence of Pleural Pressure on Afterload
ventricle can shift the interventricular septum towards the Negative intrapleural pressures increase transmural pressure
left ventricular cavity, reducing left ventricular end-diastolic and increase ventricular afterload. Negative pressure surrou
volume without any apparent change in left ventricular end- nding the heart acts by impeding the inward movement of
diastolic pressure. This has been observed to occur following the ventricular wall during systole.9 This is responsible for a
a sharp increase in pulmonary vascular resistance due to reduced cardiac output and reduced systolic blood pressure
pulmonary embolism, in acute respiratory failure, and with during the inspiratory phase of spontaneous breathing.
use of high levels of PEEP. Acute right ventricular dilatation When the fall in inspiratory-related pressure during systole is
may thus reduce left ventricular filling and cardiac output. greater than 15 mm Hg, it is termed pulsus paradoxus. There
In summary, the left ventricular filling pressure (the is nothing paradoxical about this observation, as it is merely
pulmonary capillary wedge pressure as measured through a an exaggeration of a normal response.
Swan-Ganz catheter) is a good index of the preload. However, Positive intrapleural pressure can reduce the afterload,
when interpreting pressure readings, or when manipulating by promoting the inward movement of the ventricular wall
filling pressures through volume infusions, the influence of during systole, thereby facilitating ventricular emptying. It is
the compliance of the ventricle, as also of the intrapleural and likely that the beneficial effects of closed chest compressions
intrapericardial pressures should be given due consideration. performed during cardiac resuscitation are related to sharp
3
Septal shifts due to acute right ventricular dilatation may swings in positive pleural pressure, which exert a massage-
also compromise left ventricular end-diastolic volume, and like action and propel blood outwards from the heart into the
interfere with left ventricular filling, for reasons stated above. systemic circulation.
It is to be however noted that the reduction in afterload
Contractility effect produced by a positive intrapleural pressure during the
Stroke volume can be increased not only by augmenting inspiratory phase of positive pressure ventilation is negated
preload, but also by increasing contractility. This is accom– by the obstruction to venous return caused by the inspiratory
plished by the use of inotropes that increase both isometric rise in intrapleural pressure. In fact the sum effect is a decrease
force, and the velocity of isotonic muscle shortening at inspiratory cardiac output because of decreased venous
all loads. Neurohormonal mechanisms within the body, return (see chapter Mechanical Ventilation in the Critically
by stimulating beta-1 agonist receptors in the ventricles, Ill Patients).
also increase contractility with improved emptying of the
ventricles, for any given diastolic length. Cardiac Rate and Rhythm
The rate is also important in determining cardiac output. A
Afterload rate greater than 100/minute adversely affects cardiac output,
This is an important factor governing stroke volume. Afterload and a marked bradyrhythm acts likewise. Loss of atrial kick
is the ventricular wall tension generated during systolic may sharply reduce cardiac output in patients with a poor
ejection of blood from the ventricles. The aortic pressure is an cardiac reserve. Rhythm disturbances even in a normal heart
important determinant of left ventricular afterload. Increasing can reduce output; they can be catastrophic in diseased
the afterload moderately in a normal heart, causes a slight hearts.
fall in the ejection fraction. This results in a compensatory
increase in fiber length and diastolic volume, with stronger HEART FAILURE
contraction and an improved ejection fraction. On the other
This has been dealt with at length in subsequent chapters
hand, an increased afterload in a diseased heart, which has
of the book. A few basic concepts need to be stressed at this
poor contractility, can be disastrous. It results in a profound
juncture.
fall in the ejection fraction, and in the forward flow from the
Cardiac failure, in brief, is a failure of the pumping action
heart.
of the heart. Left ventricular failure leads to two recognizable
The relationship of a changing afterload to a failing heart
features—
is more clearly illustrated by the application of Laplace’s law,
1. Pulmonary edema, with or without systemic venous
Pr
T= congestion. Pulmonary edema is associated with an
2h increase in end-diastolic left ventricular pressure to greater
where T is the wall tension (afterload). T is not only directly than 15 mm Hg, and often as high as 30 mm Hg.
related to the intracavitary pressure (P), but also directly 2. Poor forward flow resulting in poor tissue perfusion.
related to the radius of the chamber (r), and inversely to (h), Cardiac failure may produce pulmonary edema, or poor
the thickness of the ventricular wall. Thus, T (wall tension forward flow, or both. It is important to consider these
or afterload) increases with the increased radius of a dilated two aspects of cardiac failure as separate facets, even
heart. It is reduced with hypertrophy or increased thickness when both are present at the same time. Death from acute
of the ventricular wall. cardiac failure can be due to a severe fall in cardiac output,
3
Fig. 4: Left and right ventricular function curves in an overinfused Fig. 5: Relationship of stroke volume to left ventricular end-diastolic
hypervolemic patient. Note that very high left and right ventricular pressure (LVEDP) in subjects with normal myocardial function (a), and
filling pressures that cause pulmonary edema and systemic venous in patients with moderate (b) and severe (c) left ventricular dysfunction.
congestion can occur in the presence of good pump function with high Note that in patients with myocardial dysfunction, a rising LVEDP
stroke volumes and cardiac output produces a smaller degree of rise in the stroke volume, as compared
to normal subjects
forward flow and tissue perfusion, without pulmonary

edema. This can only be appreciated if the interrelation
between left and right ventricular function curves is clearly
understood,10 and if both ventricles are considered as an
interlocked single functioning unit.
An explanation of the two above-stated facets of acute
cardiac failure has been given in the chapter Cardiogenic
Shock.
A final thought provoking statement that needs to be
made, is that the presence of increased filling pressures
with pulmonary edema and systemic venous congestion,
does not necessarily mean failure of the heart as a pump.
This situation (increased filling pressures with pulmonary
edema and systemic venous congestion), can also arise in
an over-transfused or over-infused hypervolemic patient.
Measurements of cardiac output in such a patient shows high
stroke volume and cardiac output readings (in accordance
with Frank-Starling’s principle), pointing to good pump
function. This is illustrated in Figure 4.
Left ventricular function curves in moderate and severe Fig. 6: Relationship of stroke volume to afterload in subjects with normal
left ventricular failure are illustrated below by plotting stroke myocardial function (a), and in patients with moderate (b) and severe
volume against LVEDP, and stroke volume against increasing (C) myocardial dysfunction. In subjects with normal myocardial function,
afterload (Figs 5 and 6). increase in afterload results in hypertension without much change in the
stroke volume (SV) or cardiac output (CO). In contrast, in patients with
The description of the applied physiology of the circulatory moderate or severe myocardial dysfunction, an increase in afterload
system given above has been chiefly related to the heart and produces a sharp fall in the SV and CO, the SV being inversely proportional
its function. There are other components to the circulatory to the afterload or outflow resistance. It is important to note that the
system that need to be considered.11 These components blood pressure may remain constant at points A and B on curve b, and
include the following— points C and D on curve c, even though the SV is sharply reduced
TT Intravascular volume which regulates mean circulatory

pressure and venous return.
TT The arteriolar bed, the tone of which chiefly determines
afterload, arterial blood pressure and distribution of
systemic blood flow. A marked fall in arteriolar tone causes
severe hypotension. A marked rise impedes left ventricular
ejection and tissue perfusion.
TT The capillary network where fluid and nutrient exchange
between the intravascular and extravascular compartment
occurs. Damage to capillary endothelium results in
increased capillary permeability with loss of intravascular
volume and tissue edema.
TT The venules which are responsible for 10–15% of the
vascular resistance. Fig. 7: Concept of alveolar ventilation
TT Arteriovenous connections. Opening of these connections
allows blood to bypass the capillaries and produces tissue mismatch is an important cause of hypoxia or poor art
3
hypoxia. erial oxygenation. A ventilation-perfusion mismatch
TT Venous capacitance which contains 80% of the intra is characterized clinically and physiologically by two
vascular volume. Decrease in venous tone or increase in features: (1) An increase in dead space—ventilation of
venous capacitance reduces mean circulating pressures, unperfused or poorly perfused alveoli which are hyper
filling pressures within the heart, and effective circulating ventilated in relation to the blood perfusing them; (2) an
volume. Increase in venous tone or decrease in venous increase in venous admixture, i.e. perfusion of atelectatic
capacitance has exactly the contrary effects—an increase alveoli causing a true right to left shunt. Alveoli which are
in the venous pressure and an increase in the filling hypoventilated in relation to blood perfusing them, also
pressures of the heart. contribute to a shunt effect.
TT Viscosity of blood Blood viscosity is chiefly due to TT Diffusion of oxygen across the alveolar wall into the
circulating erythrocytes (hematocrit). Increase in the capillaries perfusing the alveoli, and of carbon dioxide
hematocrit means increased viscosity, entailing greater from the capillaries out into the alveolar space. A severe
work for the heart to move blood through the circulatory diffusion defect may contribute to a low PaO2 but is hardly
system. This increase in work load may have significant ever its sole cause. Most pathologies producing a diffusion
clinical implications in patients with ischemic heart defect also lead to an uneven compliance within the lungs
disease or in patients with poor myocardial reserve. and thereby to a ventilation-perfusion mismatch.
Viscosity of blood increases following a loss of plasma or
fluid from the vascular system. Blood viscosity also increases Alveolar Ventilation
following repeated packed cell transfusions, a fall in body The pressure of CO2 in arterial blood (PaCO2) is the best
temperature, and a decrease in the flow rate of blood. This rise indicator of alveolar ventilation. This basic fact in respiratory
in viscosity can further reduce flow through the circulation physiology is explained below. Consider for purposes of
and thereby promote ischemic injury. Prevention of an illustration an alveolus of volume V· A (Fig. 7). It contains a
·
undue rise in viscosity is therefore of particular importance volume of CO2 (VCO 2). The fractional concentration of CO2
in critically ill patients. The degree of viscosity is best gauged (FACO2) in this alveolus is given by the volume of CO2 divided
by monitoring hematocrit values which should not exceed by the volume of the alveolus.
40–45% as the upper limit. 
VCO 2
Finally, the right heart, which pumps into the low re FACO2 =
V
sistance, low pressure pulmonary circuit, is intrinsically and A
inevitably locked to the left heart which pumps into the high The CO2 released into the alveolus from the blood perfusing it,
resistance, high pressure systemic circuit. It is a closed system, will be cleared from the alveolus by ventilation; the greater the
and by sheer necessity the stroke volume pumped by the two ventilation the lower the concentration of CO2 in the alveolus.
sides of the heart must be equal. The alveolar concentration will be a balance between the
alveolar ventilation and the rate at which the CO2 is evolved
·
BASIC CONCEPTS OF GAS EXCHANGE (VCO 2).

VCO 2
Efficient gas exchange in the lungs requires— FACO2 =
V
TT An adequate alveolar ventilation evenly distributed to A
both lungs. The fractional concentration of CO2, FACO 2 (0.05–0.06),
TT Even ventilation-perfusion ratios of 0.8 to 1. Uneven exerts a pressure equal to the same fraction of the barometric
ventilation-perfusion ratios or ventilation-perfusion pressure (PB).
PA CO2 
VCO 2
=
PB VA

VCO 2
PACO2 = × 0.863
VA
0.863 is the correction factor that takes into account the

·
barometric
. pressure and the different units in which VCO 2
and VA are expressed. This is the alveolar ventilation equation.
It shows that the PACO2 is directly proportional to the CO2
produced, . and inversely proportional to alveolar ventilation
(V· A). If VCO2 is constant, then PACO2 is inversely proportional
to V· A.
1
PACO2 ∝
V A
There is good evidence to show that PaCO2 (pressure of CO2

in arterial blood) is very close to the average alveolar PCO2 Fig. 8: Concept of anatomical and alveolar dead space and venous 3
i.e. PACO2. Thus admixture (right to left shunt within the lungs)
Source: From Udwadia FE. Diagnosis and Management of Acute Respiratory

VCO 2 Failure. Mumbai: OUP; 1979.
PACO2 = PaCO2 = × 0.863
V
A
The PaCO2 is thus inversely related toV· A. A high PaCO2 (>48

mm Hg) denotes hypoventilation; a low PaCO2 (<35 mm Hg) VD PaCO2 − PE CO2
=
denotes hyperventilation; a normal PaCO2 (35–45 mm Hg) VT PaCO2
denotes normal alveolar ventilation. It should be evident from
the above equation that if the normal PaCO2 of 40 mm Hg is where PECO2 is the pressure of CO2 in expired gas.
doubled to 80 mm Hg, it means that the alveolar ventilation
is just half of what is normally necessary to deal with the CO2 Alveolar Oxygen
produced by the body. It is to be also noted that the PaCO2 Fresh oxygen from inspired gas enters alveoli during
·
may rise if the VCO 2 rises and if the patient for some reason ventilation; the oxygen diffuses through the alveolar wall into
cannot increase his alveolar ventilation to get rid of the extra the blood perfusing the alveoli. For any given concentration
CO2. of oxygen in inspired gas (FiO2), the alveolar concentration of
oxygen (FAO2) will be a balance between alveolar ventilation
· ·
Concept of Dead Space ( VA) and the oxygen taken up ( VO2) by the blood perfusing
ventilated alveoli.
The anatomical dead space is that constituted by the 
VO
trachea and the bronchi right up to, but not including, the FiO2 – FAO2 = 2
gas exchange unit of the lung. It is the volume of inspired VA

air which fills the airways and is breathed out unchanged. In terms of partial pressure,
Air entering alveoli which have no blood perfusing them,

VO
also does not take part in gas exchange and is breathed PiO2 – PAO2 = 2
× 0.863
out unchanged. This is wasted ventilation and constitutes VA
alveolar dead space. The sum of the anatomical dead space
and the alveolar dead space is termed the physiological dead We have already defined V· A (under Alveolar Ventilation) in
space, though admittedly there is nothing physiological about terms of PaCO2.
this dead space. Figure 8 illustrates the concept of anatomical
.
and alveolar dead space. VO2
PAO2 = PiO2 – PaCO2 × . × 0.863
Effective alveolar ventilation is only that ventilation VCO2
entering perfused alveoli. Hyperventilated alveoli will cont
· / VCO
·
ribute to the overall concept of alveolar dead space. The ratio VO 2 2 is in fact the respiratory exchange
Ordinarily as much as 30% of tidal volume is dead space ratio R, and R in a steady state equals the metabolic respiratory
ventilation. This may increase considerably in patients with quotient (RQ). Thus
diseased lungs. The quantum of dead space can be calculated PAO2 = PiO2 – PaCO2 × 1/R
by the following equation:
on blood gas measurements. If the value of the measured

PaCO2 is taken as correct, the alveolar equation allows one
to compute the PAO2. If the PaO2 reported by the laboratory
is higher than the PAO2, it is obviously incorrect.
The Alveolar-Arterial Oxygen Gradient

The normal range of the alveolar-arterial oxygen gradient
has already been mentioned. An increased alveolar-arterial
oxygen gradient denotes an impairment of gas exchange
across the alveolar capillary membrane. When however a
low PaO2 is due to hypoventilation, or is related to breathing
at high altitudes, then there is no increase in the alveolar-
arterial oxygen gradient since the PAO2 is also proportionately
low. A lowered PaO2 from any other cause (V/Q mismatch,
Fig. 9: O2-CO2 diagram. The slope of the line depends on the Respiratory
increased shunt, impaired diffusion), is always associated
Quotient (RQ, normally 0.8). For any given PaCO2, the alveolar PO2
with an increased alveolar-arterial oxygen gradient. Also
3
can be read, and for any given PAO2, PaCO2 can be read. The line to
the left illustrates the PAO2-PaCO2 relationship in the alveoli when the greater the alveolar-arterial oxygen gradient, the
breathing air (PiO2 = 149 mm Hg). The circle marked on this line shows greater the disturbance in gas exchange within the lungs.
the normal alveolar PO2 when breathing air (RQ = 0.8). The line to the This observation should however be viewed in its proper
right illustrates the PAO2-PaCO2 relationship with an RQ of 0.8 when perspective. Thus an alveolar-arterial gradient of 20 mm Hg
breathing 40% oxygen (PiO2 = 285 mm Hg) (upper limit of normal), when it occurs on the steep part of
Source: From Udwadia FE. Diagnosis and Management of Acute Respiratory the oxygen dissociation curve will denote a gross disturbance
Failure. Mumbai: OUP; 1979. in pulmonary gas exchange.
Let us consider a patient with chronic bronchitis in severe
hypercapnic respiratory failure. If the PAO2 of this patient is 50
If carbohydrates are preponderantly burnt as fuel, R = 1; if mm Hg and the PaO2 is 30 mm Hg, the gradient of just 20 mm
fats are burnt as fuel R = 0.7; if carbohydrates and fats are both Hg (upper limit of normal) would suggest that the hypoxia is
burnt as fuel, as is usually the case, R = 0.8. chiefly due to alveolar hypoventilation. However, at a PO2 of 50
mm Hg the oxygen saturation is 85%; at a PO2 of 30 mm Hg the
The above equation is a simplified form of the alveolar air oxygen saturation is about 55%. Thus the oxygen saturation
equation. It is of great use because— has fallen 30% between the alveoli and the arterial blood.
TT It allows a quick determination of alveolar oxygen pressure Normally the fall in oxygen saturation does not exceed 2%. It
(PAO2) if the PiO2 and the PaCO2 are known. is evident that there is a serious disturbance in gas exchange in
TT If the PAO2 is known and the PaO2 is available through this patient, even though the alveolar-arterial oxygen gradient
an arterial blood gas measurement, the alveolar-arterial is not unduly increased.
oxygen gradient can be calculated as the difference
between PAO2 and PaO2. The upper normal of this gradient Venous Admixture
is 15 to at most 20 mm Hg. In most normal individuals it If deoxygenated blood perfuses atelectatic alveoli and
averages 10 mm Hg. bypasses ventilated alveoli, the oxygen content of the blood
TT The alveolar equation points to a linear relationship leaving the lungs will be less than that leaving ventilated
between PAO2 and PaCO2. The O2-CO2 diagram or line is alveoli. This constitutes the concept of venous admixture
further elaborated upon in the chapter Acute Respiratory (Figs 10A to C). Venous admixture at the bedside has two
Failure in Adults (Fig. 9). From this diagram one can components—a true right to left shunt due to perfusion of
quickly plot the expected PAO2 if the PaCO2 is known for totally atelectatic alveoli, and a shunt effect observed in alveoli
any given inspired oxygen concentration. If the alveolar- which are hypoventilated in relation to blood perfusing them
arterial oxygen gradient is taken as 10–15 mm Hg, then i.e. alveoli with low ventilation-perfusion ratios. A true right to
for any given PaCO2 one can read off the PaO2. This is left shunt (also called a true venous admixture) is unchanged
true provided the alveolar-arterial oxygen gradient is not by increasing inspired concentration of oxygen. The shunt
abnormally increased. effect produced by alveoli with lowered ventilation-perfusion
TT A consideration of the alveolar air equation shows that at ratios will however be abolished by suitably increasing the
a given inspired oxygen concentration and a given RQ, the inspired oxygen concentration. The simple bedside test of
alveolar PO2 is dependent on alveolar ventilation. A lower noting the degree of rise in PaO2 with 100% inspired oxygen,
alveolar ventilation would thus lead to a lowered alveolar thus distinguishes between a true right to left shunt within the
PO2, and hence a lowered arterial PO2. lungs, and a shunt effect produced by ventilation-perfusion
The alveolar air equation helps the physician to check inequalities. More often than not, a right to left shunt as
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Large ships had two decks, an upper one and a gun-deck
underneath. Towards the end of the sixteenth century, a third deck,
called a false orlop was laid in the hold to carry cabins and stores.
The ship was divided transversely on both upper and lower decks by
means of bulkheads where the forecastle and poop ended. Gravel
ballast was used to such an extent that but little room was left for
stores. A large portion of the space left in the hold of the ship in the
waist was taken up by the cooking-galley which was a solid structure
of bricks and mortar. Raleigh[77] complains of the heat “that comes
from the cook roome” as well of the risk of fire which it afforded,
and of the unsavoury smells which emanated from this part of the
ship. He therefore recommends that the “cook roomes” be placed in
the forecastle instead, as was the custom already adopted by many
of the merchant ships.
When Elizabeth came to the throne, the Henri Grace à Dieu had
been accidentally burnt five years before. Apart from the Jesus of
Lubeck (700 tons), the Triumph was the largest English ship afloat.
Built in 1561, her tonnage was over a thousand, and her crew
numbered 500. Until the launching of the Prince Royal in 1610, she
was the finest English ship afloat. But though there were
improvements going on in regard to the building of the ships, the lot
of the sailor was not entirely a happy one. Musty rations, want of
clothes, and the harmful effects of the bilge water collecting in the
bottom of the ship and emitting an unwholesome stench, caused
scurvy and dysentery; and the sailors of both the English ships and
the Spanish Armada suffered terribly from these. But on the other
hand, we find that as early as the year 1601, Lancaster, during his
first voyage for the East India Company, kept the crew of his flagship
in comparatively good health by serving out lime-juice.[78]
Fig. 50. The “Ark Royal,” Elizabeth’s Flagship. Built in 1587.
The illustration in Fig. 50 is of the Ark Royal, from a contemporary

print in the Print Room of the British Museum. Built for Sir Walter
Raleigh in 1587, she was sold while on the stocks to Queen Elizabeth
for £5000. Her name was to have been the Ark Ralegh, but on being
purchased it was changed as above. Her name was, after the end of
this reign, changed to the Anne Royal, and in 1625, while returning
from Cadiz, she began to leak like the proverbial lobster-pot and only
reached home with difficulty. In 1636, while lying in the Thames, she
bilged on her own anchor and sank. It was this Ark Royal that was
Elizabeth’s flagship of the fleet that defeated the Armada, and for
this reason, if for no other, she is deserving of a more complete
consideration than we have room to devote to other ships of this
period. Sir William Monson,[79] who was already a captain by 1587,
gives her tonnage as 800, and the number of her crew as 400.
Happily the complete inventory of the Ark Royal is still in existence,
and the reader is referred to the “State Papers Relating to the Defeat
of the Spanish Armada, anno 1588.”[80] It was compiled in
September 1588 after the Ark Royal had come in for a survey,
having been out in the Channel in the memorable victory. All the
tackle and spars and sails, every item of the inventory down to the
kettles for the cooking-room is mentioned. From this list we find that
the spritsail, besides its yard, had clew lines, braces, sheets,
halyards, and “a false tye.” Sir Henry Manwayring, who also fought
in the fleet against the Armada, in his “Seamen’s Dictionary” defines
ties as four-strand ropes, hawser-laid, being the ropes by which the
yards hang. But the spritsail yard having no ties, was made fast by a
pair of slings to the bowsprit. Among the items of the rigging of the
foremast are included the “fore pennants,” and both the falls and
pennants of the “swifters.” Referring to Manwayring’s “Dictionary,”
we find that “swifters doe belong to the maine and foremast, and
are to succour the shrowdes and keep stiffe the mast. They have
pendants, which are made fast under the shrowdes at the head of
the mast with a double block, through which is reeved the swifter.”
Mention must be made of the “forebolings” and main bowlines. Our
ancestors made great use of these bowlines in order that these
great square sails might set quite flat. Until the triangular head sails
came in about the middle of the eighteenth century, the foremast
was stepped very far forward, for the spritsail was only used off the
wind and when getting under way. The manner in which the spritsail
in this illustration of the Ark Royal is shown in the head stowed is
quite correct.
The inventory mentions also the clew-garnets and martnets
(leech-lines) of the foresail, and the “fore-puttocks” (i.e., futtock
shrouds) of the foretopmast. The fall of the martnets of the topsails
led down into the fighting-top where it was hauled, and the
expression “top the martnets” was the order for hauling the
martnets up. The yards were hoisted by jeers or halyards.
Manwayring defines “jeere” as a hawser, made fast to the main or
fore yard close to the ties of great ships only. It came through a
block which was seized close to the top and led down to another
block at the bottom of the mast close to the deck. Great ships had
one on either side of the ties. Apart from the use of the jeer to hoist
or lower the yards, it was especially serviceable for taking some of
the weight off the ties, and to hold the yard from falling down if the
ties should break. In fights, when the sickle-shaped shear-hooks
already mentioned were used by the enemy, the opponent would
sling his yards in chains “for feare least the ties should be cut, and
so the yards fall downe, and these chaines are called slings”
(Manwayring). The lateen yards on the mizzen and bonaventure-
mizzen had parrals to secure them to the masts.
The Ark Royal carried three bower anchors of 20 cwt. as well as
three others and a grapnel. She had fifty fathoms of 15-inch cable,
three compasses, four running glasses, three flags of St. George and
two of the Queen’s arms, as well as a silk ensign. In the illustration
before us the St. George’s flags will be noticed flying at the fore and
bonaventure mizzen; at the main is the royal standard, and at the
main-mizzen the Tudor Rose. From the spritsail yard flies a pennant
surcharged with a St. George’s cross, from the foretop a pennant
bearing a foul anchor, being the pennant of the Lord High Admiral.
This flag will also be noticed on the foremast of the ship of Charles
II.’s time of the frontispiece. In fact, as the reader is probably aware,
this is still used as the Admiralty’s flag. From the fore topgallant yard
is a streamer bearing a lion rampant, of Lord Howard of Effingham,
Lord High Admiral of England; from the maintop another streamer,
striped, whilst at the waist is a large banner with Howard’s arms
thereon. The inventory includes ballast baskets for carrying the
gravel on board, or in which it would be stowed; netting for the
forecastle, the waist and the half-deck, as well as cloths for the waist
and top armours for the mizzen top, but we shall refer to these later.
Touching the sails of the Ark Royal, she had a bonnet to her
spritsail laced on in the manner adopted to-day by the wherry-man
of the Norfolk Broads. The mainsail and foresail and main mizzen
also had the bonnet, but the others had not, although a topsail
bonnet was found rarely. The foresail had a double bonnet with a
single drabbler, likewise the mainsail. In the case of the main mizzen
the bonnet was a double one. The inventory only includes one
topgallant sail, although three are shown in this engraving. This fact
is certainly an argument for those who assert that the illustration
represents not the Ark Royal, although the rest of the evidence is
against this assertion. Much more likely is it that the other topgallant
sails were added at a later date.
The inventory includes a sail for the ship’s boat, and two for the
pinnesse. A longboat with a brass sheave in the head and supplied
with oars, a pinnesse and a “cocke” (derived from the French coque)
which was a ship’s boat, as well as an older pinnesse, were carried
on board the Ark Royal. During the survey at Chatham it was
decided to have her overlop in the waist made less curved and more
level for the sake of placing the guns in better position, a lesson that
had been impressed on them even more forcibly by the ill-success of
the fire of the Spaniards. In our illustration it will be noticed that the
curve has disappeared. I therefore conclude that this engraving was
made after the ship had been altered at Chatham. It seems very
probable that it was during this overhaul that the other topgallant
sails were added, in which case the argument against the veracity of
this engraving is rebutted.
Elizabeth’s own royal ships were undoubtedly fine able vessels for
their time. They were seaworthy, and at any rate during the time of
the Armada did not suffer from leaks. But the same statement
cannot be made of the merchant ships that joined the royal fleet
from the various English ports. These were far from sound and
leaked badly. In a letter from Howard to Walsyngham[81] we find
that the merchants besought the former that he and the rest of Her
Majesty’s fleet would carry less sail for they could not endure it,
while “we,” writes Howard, “made no reckoning of it.” This inferiority
is confirmed also by Seymour, who writes to say that the merchant
ships in the English fleet were not as good sea-boats as the Queen’s.
Before we leave the Ark Royal, let us call to the reader’s attention
a detail that, if he is a sailorman, he will have already noticed. The
furling of the sails, correctly shown here, is very clumsy and
bungling. The custom was when the sails were furled to bind them
to the yard with rope yarns, and these yarns were cut to loose the
sail when getting under way. Thus Sir William Wynter, writing on
February 28, 1587, concludes his letter: “Written aboard the
Vanguard, being in the Downs, ready to cut sail.”[82]
Centuries ago, when England had only her Viking-like craft, she
had bravely claimed for herself the Sovereignty of the Seas. It was
to the foreigner an insolent, arrogant boast. She had fought for the
distinction many times. Spain had grown up to be the first maritime
nation of the world, but just as in after years the Dutch and the
French had, not without a severe tussle, to be prevented from
usurping this distinction, so England had to smash the Armada—the
greatest aggregation of naval power the world had ever seen on one
sea—and with this defeat England was again, for a time at least, the
mistress of the sea. Drake’s voyage round the world with a squadron
of five ships, the largest of which did not exceed 100 tons, set the
final seal on the abilities of English seamanship and navigation. The
victory over the Armada settled their superiority in ships, strategy
and shooting.
Before we pass from the story of the fight that never grows old—
and there is no more stirring reading than the plain narrative
included in Hakluyt—let us not forget that capable as were the royal
ships of Elizabeth, they could never have been victorious had not the
West countrymen of England come to help with their ships and their
crews. The former may have been leaky, the latter may have been
not as skilled as Howard’s men in the finer arts of war, but they did
their duty, in spite of a thousand drawbacks, and did it well. Where
had they learned their seamanship? How was it that they had even
such good ships as they possessed but a hundred years after Henry
VII. had come to the throne? As Mr. Blackmore points out,[83] ever
since the discovery of Newfoundland the men of Cornwall and Devon
had gone forth year after year to fish for cod off the Banks. Kipling,
Connolly, and others, have sung the epic of the brave fishermen who
to-day race out to the same banks from Gloucester, U.S.A. Most
readers of fiction know that cruising about there is no latitude for a
fair-weather sailor, yet three hundred years before them, when the
arts of shipbuilding and navigation were not what they are now,
Englishmen in ships built at Dartmouth and elsewhere were making
regular voyages across the broad Atlantic to those fishing banks. Big
vessels and brave capable seamen were essential for these trips.
Both, at the summons of necessity, had gradually evolved from the
West Country, and, at the hour of need, placed themselves at the
service and in the defence of their fatherland.
Fig. 51. Elizabethan Man-of-war.
What were the kinds of ships that sailed in English waters during
the reign of Elizabeth? As far as historical research will suffer us let
us try and obtain a general idea as to their rig and appearance. Fig.
51, which is taken from the Rawlinson MSS. in the Bodleian, affords
an excellent example of an Elizabethan man-of-war. The flags flying
are the green and white Tudor colours on the ensign staff and the
St. George at the main, which was the national flag, but it was men-
of-war only that were allowed to fly it at the main. According to
Manwayring the Elizabethan ships, when running before a wind or
with the wind on the quarter in the case of a fair fresh gale, often
unparralled the mizzen lateen yard from the mast, and launched out
the yard and sail over the quarter on the lee side, fitting guys at the
further end to keep the yards steady. A boom also appears to have
been used in this case. If a ship gripe too much, says Manwayring,
then the mizzen was stowed, for otherwise “she will never keep out
of the wind.” The mizzen was sometimes used when at anchor to
back the ship astern in order to keep her from fouling her anchor on
the turn of the tide.
Perhaps in the mind of the general reader the one type of ship of
this age that he has any vague knowledge of is the galleon. He
associates her with the Armada and with the Spanish nation
exclusively. He has not forgotten that he learned in the days of his
youth that the ships of the Armada were of enormous size, and that
the English ships were victorious because they were small and
nimble. It is perfectly true to say that our vessels were light and
comparatively handy, but we must not omit to throw into the
balance the superiority of our seamanship and gunnery, as we
pointed out just now. The English had a natural taste for the sea;
the Spaniards, in spite of all their trading and exploring across the
ocean, had for it an equal distaste. They were admittedly bad
seamen.[84] I am not expressing an opinion but asserting a fact, and
this was as much the cause of their defeat as anything else. But the
English ships were not particularly small. At least seven were of
between 600 and 1100 tons. There were in the whole Spanish
Armada only four ships larger than our Triumph, whilst of the English
merchantmen the Leicester and the Merchant Royal were each of
400 tons.
Nor did the word “galleon” necessarily denote a Spanish ship. It is
perfectly true that the Spanish Armada contained a number of
cumbrous galleons, but it must not be inferred from this that a
galleon was necessarily clumsy. In point of fact, Spain was the last
of the great maritime nations to adopt the galleon. In England the
galleon denoted a vessel built expressly for war, as distinguished
from the adapted merchantmen. She was essentially a ship built with
finer lines, and in every way smarter than the ordinary vessel. The
type had been first introduced into the English service by Henry VIII.
long before Spain had adopted it, although, as we mentioned earlier,
there was considerable confusion as to the actual names. Thus
Henry VIII.’s ships were classed as “great ships,” “galleasses,” and
“galleys,” while for a long time, both in England and France, the
galleon was called indifferently “galleon,” “galleasse,” “galley,” and
“galliot.” By the outbreak of the Spanish war practically all the men-
of-war in our country were galleons, and were thus described by
foreigners. Nevertheless, as Mr. Corbett points out,[85] English
seamen never took kindly to the word galleon. They continued to
confuse “galleasse” and “galleon” in describing the ships of
foreigners. But for all that English shipwrights understood perfectly
the technical characteristics, and in official building programmes
after the middle of Elizabeth’s reign the three terms “galleon,”
“galleasse,” and “galley” appear correctly. The galleon, as Mr.
Masefield well describes her, was roughly the prototype of the ship
of the line, the galleasse the prototype of the frigate, and the
pinnace of the sloop or corvette. The galleon was low in the waist
with a square forecastle and a high quarter-deck just abaft the
mainmast, rising to a poop above the quarter-deck. Reckoning
upwards, the two decks, according to Manwayring, were called lower
orlop or first orlop, and the next the second orlop. But if a ship had
three decks they never called the uppermost—the third—by the
name of orlop, but simply “upper deck.” The wooden bulkheads that
separated the stern from the waist were pierced with holes for small
quick-firing guns.
The length of the galleon was three times that of her beam,
whereas the ordinary merchantman was only twice her own beam,
thus preserving the old distinction that we saw in classical time
existing between the long ship and the round ship. Yet the newer
class of Elizabethan merchantman was getting longer, influenced by
the experience gained on the long voyages across the Atlantic. It
had been in Italy, the great home of maritime matters in earlier
days, that the galleon had first been built. The galleon was in fact
the child of necessity. The Mediterranean possessed the galley-type
from very early times as we have already seen; she had, as we have
also seen, the “round” merchant type. But as time went on a
demand arose for a compromise between the two. Able to hold as
much cargo, and more, than the old rounships, yet not utterly
helpless like them in calms and narrow waters, the galleons were yet
to be of such a kind as to be capable of acting with the galleys in
war time. So they were made not as long but with more beam than
the galleys, with a built-up structure fore and aft and—let us note
this carefully—though they were sailing ships they had at first
auxiliary oar-propulsion. The smaller English galleons also retained
their oars for a long time.
Fig. 52. The Spanish Armada coming up Channel.
The immediate ancestor of the English galleon was the Italian

merchantman that traded between Venice and London. This had
three masts with a square sail on the foremast, but lateen on the
main and mizzen. She carried also oars as auxiliaries. Afterwards, by
degrees the oars were dispensed with, so that by the end of the
sixteenth century the galleon was a purely sailing vessel with
sometimes two and sometimes three decks, while the galleasse had
oars as well. Her special claim was that she was both faster and
more weatherly than the older type of warship. English shipwrights
understood a galleasse to be similar to a galleon but with more
length in proportion to her beam, though strictly speaking the
galleasse should designate a large ship with high freeboard, using
oars as well as sails. The ships, however, that fitted this description
were known to them by the name of “bastard galleasses.” The
galleasse was sometimes flush-decked and minus both poop and
forecastle and never so highly charged (i.e., with such high decks at
stern and bow) as the galleon. A good illustration will be found in
the foreground of Fig. 52, which contains two of these with their
oars out. This picture represents the Spanish Armada coming up
channel when first sighted off the Lizard. The illustration has been
taken from one of the plates in “The Tapestry Hangings of the House
of Lords,” engraved by John Pine, London, in 1739. If the reader will
pardon a short digression it may not be out of place to say a few
words in explanation of these engravings.
After he had defeated the Armada in 1588, Lord Howard of
Effingham, later raised to an earldom, determined to commemorate
the victory by depicting the scenes he had so recently passed
through. Accordingly Hendrik Corneliszoon Vroom, who had at this
time obtained a European reputation as a marine artist, was invited
from Haarlem to paint the pictures. From these Francis Speiring, an
eminent craftsman, wove the designs into tapestry. Howard, or, as
he now was, the Earl of Nottingham, sold them in his old age to
James I., who hung them in the precincts of the House of Lords.
When, during the Commonwealth, the House of Lords was
abolished, the tapestries were fitted into brown wooden frames and
hung on the walls of the chamber which had been used for the
Upper House. Here they remained until the House was burned down
in 1834, when the ten tapestries perished. Fortunately, however,
even in the inartistic eighteenth century, an artist, John Pine, and a
friend of Hogarth, had the inspiration to reproduce them by
engraving, But for this we should lack what is a most valuable
record. It is so easy to fall into inaccuracies a century after an event,
but since Pine copied from the tapestries, and the tapestries were
executed under Howard’s own supervision, there cannot be much
room left for anything incorrect in respect of the ships. Howard had
fought against the Spanish ships night and day in that memorable
month of July, and had every opportunity of noting the rigging and
lines of his enemy’s vessels, so that when he had left the sea and,
not unnaturally, devoted his attention to his own memorial, he would
be the ideal person to see that accuracy was insisted upon. These
engravings are still to be picked up occasionally in some of the
London print-sellers, but the illustration here given is from the
collection in the Print Room of the British Museum.[86]
The reader who is familiar with Elizabethan literature must have
found considerable confusion existing in his mind as to what a
“pinnesse” really was. Let us say at once, then, that the name was
indiscriminately given to two distinct classes of craft. One class was
a kind of galleasse, only smaller; that is to say, she relied on both
oars and sails. She was a sea-going ship and decked. Under this
heading came also row-barges, and at various times also galleots,
galleys, frigates, and shallops. The point to notice is that this class
comprised really big craft. The other “pinnesses” were ships’ boats.
The modern use of the word pinnace expresses pretty clearly its
relation to the mother ship. The greatest critics are unable to define
exactly what a “bark” was, but from an early Venetian print I gather
that she was smaller than the prevailing Mediterranean galley. At the
same time the word seems to have included also vessels ranging
from fifty, to a hundred and fifty tons. Thus they were sometimes
small ships, and sometimes large pinnaces. Whilst Elizabethan
seamen included all sailing vessels fit to take their place in the line
of battle under the generic term of ship, the shipwrights divided
them according to their design into “ships,” “galleons,” “galleasses”;
“barks” being a convenient term for vessels of smaller ability.
Fig. 53. The “Black Pinnesse,” which brought Home the Body of Sir Philip
Sidney.
The “brigandine” or “brigantine” was a Mediterranean type of

small galley, rowed by its own fighting crew and without slaves.
Sometimes she was classed as a “pinnesse” and sometimes as a
bark, but never as a galley. Whether or not she possessed sails she
was primarily a rowed boat. The illustration in Fig. 53 represents a
big sea-going pinnesse as distinct from the ship’s boat. This was the
vessel that carried home the body of Sir Philip Sydney, and is taken
from “Sequitur celebritas et pompa funeris...” (of Sir Philip Sydney)
by Thomas Lant, printed in 1587. The Elizabethan deep-sea pinnaces
were from eighty to fifteen tons. The present illustration shows the
vessel with her waist-cloths rigged up to prevent boarding, and with
nettings[87] drawn over the waist to intercept the missiles dropped
from the fighting-tops of the enemy. Mr. Masefield says that this
cloth was of canvas two bolts (three feet six inches) deep. It was
gaily painted with designs of red, yellow, and the Tudor green and
white. It was of no protection against the enemy’s guns, yet it
helped the sail trimmers on board from being aimed at. But against
the enemy’s arrows sent from the tops it was efficacious, for though
they penetrated the texture they were caught. We have already
called attention to the additional protection of the shields or
pavesses that ran around the outside of the deck.
Fig. 54. A Galleon of the Time of Elizabeth.
The illustration in Fig. 54 shows a galleon with decorated sails, a

practice that died out about the close of Elizabeth’s reign.[88] This
decoration was effected by stitching on to the canvas cut-out pieces
of cloth with twine. Most of the sails were woven in Portsmouth on
hand looms, and the stuff was of good quality. But during the reign
of James II. when the Huguenots took refuge in England, among the
many new trades which the settlers brought over was that of the
manufacture of sail-cloth. A French refugee, Bonhomme, who had
settled down at Ipswich, taught the secret of its manufacture.
Previously, England had imported her sail-cloth from France. The
new factory was assisted in every possible way, but was finally
destroyed by French agents, who bribed the artisans to return once
more to France. Another factory was set up in London during the
reign of William III., but as late as the time of George I. sail-cloth
was imported from abroad.
As to the rigging of Elizabethan ships: the shrouds of the fore and
main masts led outside the ship to chains to which they were made
fast. The platforms in the “chains” of the ships of this time were of
no small size as we shall see when we come to consider the Spanish
vessels. The shrouds of the mizzen and bonaventure were set up
usually from inside the bulwarks on deck. The fighting-tops were of
elm, being entered through a lubber’s hole in the floor.
Contemporary prints show sheaves of arrows projecting from the
tops. At a later date light guns were placed here, but as this
necessitated the use of lighted matches there was always the risk of
setting fire to the sails. The shrouds and stays were of thick nine-
stranded hemp. We see from old prints of this time that those parts,
as for instance where the foresail came into contact with the
bowsprit, which were liable to suffer from chafing were protected by
matting made of rope or white line plaited, and then tarred. Masts
were made of pine or fir. In dirty weather the fore-yard and fore-
topsail yard could be sent on deck. Parrals of course kept the yard to
the mast. There is not so very much difference between the sailor
language of Elizabeth’s time and that in use on board a modern
sailing ship. Mr. Bullen in an essay on “Shakespeare and the Sea”
reminds us that “Elizabethan England spoke a language which was
far more studded with sea-terms than that which we speak ashore
to-day.” In such plays as Twelfth Night, Comedy of Errors, Macbeth,
King Henry VI., and The Tempest, we have instances of this. Thus in
Act III. Scene I. of the latter the first sailor commands the other to
“slack the bolins there.” Modern bowlines are slight ropes leading
from forward to keep the leach or weather edge of the courses flat
and rigid in light winds when on a wind. But in olden times the
bowline was of far greater importance, as we have seen, and led
well out on to the bowsprit. Not merely the lower course, but topsail
and topgallant sails possessed them.
When the English fleet opposed the Armada it consisted of 197
vessels made up as follows: 34 of Elizabeth’s own royal ships, 34
merchant vessels, 30 ships and barks paid by the City of London, 33
ships and barks (with 15 victuallers not reckoned in the total
number), 23 coasters varying from 160 to 35 tons, 20 other coasters
and 23 voluntary ships. Of the merchant ships the Galleon Leicester
and the Merchant Royal are each given as of 400 tons and carrying
160 men. The smallest was the small caravel of 30 tons with 20
men. But we have spoken at some length of the English ships. Let us
now turn to consider the ships of other nations of this period.
The Armada consisted of 130 vessels if we add up the list given in
Hakluyt. This number was made up of the following types: galleons,
patasses or pataches, galleasses, zabras, galleys and hulks. Besides
these there were 20 “caravels rowed with oares, being appointed to
Performe necessary services unto the greater ships,” making a total
of 150. The tonnage of the fleet came to 60,000. There were 64
galleons “of an huge bignesse” and “so high that they resembled
great castles,” but in attacking ability “farre inferiour unto the English
and Dutch ships, which can with great dexteritie weild and turne
themselves at all assayes.” It was this “bignesse” and the high
castles at bow and stern that caused the prevailing fallacy to arise
that the Armada ships were far larger than ours. The former were
very high but very short on the keel, and in consequence equally
unseaworthy. Ours were, as we pointed out above, long on the keel
and not highly “charged” with castles. The Hakluyt account says the
upperworks of the galleons were so thick and strong as to resist
musket shot. The lower part of the hull and its timbers also were
“out of measure strong, being framed of plankes and ribs foure or
five foote in thicknesse, insomuch that no bullets could pierce them,
but such as were discharged hard at hand: which afterward prooved
true, for a great number of bullets were founde to sticke fast within
the massie substance of those thicke plankes. Great and well-pitched
cables were twined about the masts of their shippes, to strengthen
them against the battery of shot.”
The galleasses “were of such bigness, that they contained within
them chambers, chapels, turrets, pulpits, and other commodities of
great houses. The galliasses were rowed with great oares, their
being in eche one of them 300 slaves for the same purpose, and
were able to do great service with the force of their ordinance.[89]
All these together with the residue aforenamed were furnished and
beautified with trumpets, streamers, banners, war-like ensignes, and
other such like ornaments.” The various vessels also carried 12,000
pipes of fresh water and plentiful supplies of bacon, cheese, biscuit,
fish, rice, beans, peas, oil, vinegar and wine. Among their stores
were candles, lanterns, hemp, ox-hides and lead sheathing to be
used to stop the holes that should be made by the enemy’s guns.
The Spanish ships had been built unnecessarily strong by very
heavy scantlings. They were, according to Mr. Oppenheim,[90] of
light draught with broad floors and were both crank and leewardy.
The seams opened in spite of the strength with which they had been
put together. They were bolted with iron spikes and it was not long
before these ships became “nail-sick.” Their masts and spars were
too heavy and their standing rigging too weak; in fact, whilst the
demand had to be met for big ocean-going ships, the Spanish
shipwrights and naval architects were not sufficiently advanced at
this time to deal with such enormous masses of material.
Fig. 55. Spanish Galleons.
We have mentioned above that Spain was the last of the great
maritime Powers to adopt the galleon. In Fig. 55 the reader will see
a representation of her galleons. It was not till about 1550, Mr.
Oppenheim states, that the great galleon was introduced. The print
here reproduced is in the British Museum, and the date the
authorities assign to it is about 1560, so that we have every reason
for supposing that this illustration is a correct one. The reader will at
once notice the high-charged stern immediately abaft the mainmast.
The Spanish ships were notorious for their wall-like sides; and for
the height to which the bowsprit was “steeved,” both of which
details will be noticed in the illustration before us. We mentioned in
this chapter that in her origin the galleon owed something to the
galley. Now, one of the chief characteristics of the galley type was
the ram which was handed down from ancient times. Here, then, in
this picture will be seen the survival of the ram affixed to the
galleon. But it is here no longer entirely for the purpose of attacking
the enemy’s ships but for boarding the fore-tack when by the wind.
The bowlines are clearly seen on the vessel to the right of the print,
leading from both the foresail to the bowsprit and from the mainsail.
On both the fore and main courses, the martnets or leach lines are
shown very clearly in the print; it is a little difficult to indicate these
so clearly in reproduction. Notice, too, that both foresail and main
have got both bonnet and drabbler laced on. Below the bowsprit is
seen the spritsail. The main-mizzen topsail is stowed, and the
bonaventure does not carry a topsail above her lateen. The under
portion of the hull of these Spanish ships was painted white, but
ochre was frequently used for the stern. They had lids to their
portholes, nettings and waist-cloths, and “blinders” to avert the
arrows and musket fire. The armament of the Spanish merchantman
was, in the case of vessels of 100 tons, four heavy iron guns and
eight hand guns aside as well as eight other hand guns; but after
about 1550 the armament became heavier.
Fig. 56. Spanish Treasure-Frigate of about 1590.
We pass now to speak of the Spanish treasure-frigates. These

were an important class of vessel during the last quarter of the
sixteenth century. The length on their upper deck was nearly four
times the beam, and they possessed considerable speed. They were
not properly cargo ships, but built in order to carry the valuable
treasures from the Spanish Main across the Atlantic to Spain.
Specially designed by Pero Menendez Marquez about the year 1590,
to get across from the West Indies with the utmost despatch, they
carried 150 men with soldiers and marines. Hakluyt[91] contains
“certaine Spanish letters intercepted by shippes ... containing many
secrets touching” South America and the West Indies. The extremely
interesting drawing in Fig. 56 was sent home by an English spy and
is now preserved in the Records Office, by whose permission it is
reproduced here. This illustration shows very clearly that she had
evolved from a galley. She has three masts of which the main and
mizzen are seen to possess topmasts that lower. These two masts
also have topsails. The yards of the mainsail and foresail have also
affixed to their extremities crescent-shaped shear-hooks for tearing
the enemy’s rigging. The forestay and foretopmast stay are well
indicated. The mizzen has a lateen as usual, and the ram still
survives. The artist has also shown the netting mentioned just now.
As to the hull, we see from the spy’s handwriting that she was “104
foote by the keele” and “34 foote in breadth.” She has three tiers of
guns, these being mounted also forward, so as to be able to fire
straight ahead. She appears to have as many as six decks aft—main,
upper, spar and four poop decks. The greatest precaution was taken
by the Spanish government to ensure seaworthiness in the ships
leaving their shores for the West Indies. Three times they had to be
inspected before being allowed to set forth: once when empty, then
when laden, and lastly, immediately before departure. No cargo was
allowed to be carried on deck except water, provisions and
passengers’ luggage. In the huge “channels” which were mentioned
above were stowed such commodities as wool, small casks of water,
and straw. Mr. Oppenheim mentions that an ancient “Plimsoll” mark
was ordered by the inspectors in the year 1618, although the
Genoese statutes had ordained this as early as 1330.
When in 1592 the English captured the “huge carak” called the
Madre de Dios belonging to Portugal, there were found stowed in
her capacious channels about 200 tons of goods. This will give some
idea of the extent to which these channels grew in size. Hakluyt
contains a long and detailed account of the capture and dimensions
of this carack, which was the largest the English seamen had yet
encountered. She was 1600 tons, having between 600 and 700 souls
aboard, besides her rich cargo of jewels and spices and silks and
other goods. She was eventually brought into Dartmouth, and is said
never again to have left the harbour. When surveyed, Hakluyt says
that she measured from beak-head to the stern, 165 feet, extreme
beam, 46 feet 10 inches. Her draught when laden had been 31 feet,
which, being about the draught of one of the largest modern liners,
would seem exaggerated did not the account definitely state that the
survey was exactly made by “one M. Robert Adams, a man in his
faculty of excellent skill.” When, after being lightened, she was taken
into Dartmouth, she drew only 26 feet, which is still enormous. Her
decks at the stern comprised a main orlop and three closed decks.
At the bows she had a forecastle and a spar-deck “of two floors
apiece.” The length of her keel was 100 feet, of the mainmast 121
feet, while the circuit at the partners was 10 feet 7 inches, the main
yard being 106 feet long. The following year another enormous
carack was fired and sunk by the English. Her name was Las Cinque
Llagas (“The Five Wounds”), and she is said by some to have been
bigger even than the Madre de Dios.
Fig. 57. Mediterranean Galley.
One of the most memorable of naval battles was that which was
fought on the Adriatic Sea in 1571. On the one side were the allied
forces of Venice, Spain, and the Papal States: on the other, the Turks
who were defeated. Galleys and galleasses played an important part
in obtaining this victory. To what development the galley had
attained since the times of the early Greeks and Romans will be seen
in Figs. 57 and 58. But in spite of all that history had added to them,
it is surprising how little they differ in essentials. Fig. 57 has been
sketched from a model in the South Kensington Museum. It is quite
old, and is said to have belonged to the Knights of Malta. Her
dimensions if built to scale would work out at about 165 feet long,
by 22 feet beam, with extreme beam from gunwale to gunwale, 31
feet. The depth would be 9·9 feet, and the number of sweeps 44. In
the United Service Museum there is also an instructive Maltese galley
model of a large size which, though of the eighteenth century,
differed so little as to be closely similar to the excellent illustration
which we give in Fig. 58. This has been taken from an important
publication, of the beginning of the seventeenth century, by Joseph
Furttenbach, entitled “Architectura Navalis,” printed at Ulm in 1629.
As will be seen, each oar is still worked by a gang of men. At the
stern the captain sits with his knights by his side, while at the
extreme stern is the pilot. Along the corsia or gangway down the
ship walk two men with long poles with which to beat the lazy
oarsmen. The principal armament was carried in the bows and so
was unable to be used for broadside fire. Notice also the survival of
the trumpeters. The length of this vessel was 169 feet from beak to
stern, with an extreme beam of about 20 feet. The word antennæ is
still found at this time as applied to the yards. In spite of the
handiness of the galley and her consequent popularity in the
Mediterranean, she was thoroughly despised by Elizabethan seamen.
Much more after their own heart was the nave or ship shown in Fig.
59, and also taken out of Furttenbach. The reader will notice a wise
restriction of high-charged structures. This vessel, in fact, shows a
steady improvement in naval architecture. Thus, besides the lateen
mizzen she carries a square topsail above, while in addition to the
spritsail seen furled to its yard on the bowsprit, there has now been
added a sprit topsail whose yard is seen to hoist up a sprit topmast.
When we compare this vessel with the wooden walls of the
eighteenth century, she will be seen to be wonderfully modern. The
last traces of crude mediævalism are disappearing. Science in design
has fast begun to supplant rule of thumb and guess-work based only
on ignorance. Skill has taken the place of inexperience in the work of
the shipwright, and both design and construction have been based
on the knowledge obtained not only in long and tedious voyages,
but in the brisk fighting between nation and nation and privateer
against treasure ship and trader. In the same volume of Furttenbach
a useful plan of the lines of this ship is given, from which we see
that whilst the mainmast is stepped at the keelson, the fore and
mizzen are stepped on the main deck.
Fig. 58. An Early Seventeenth-century Galley.
A favourite vessel with the Turkish pirates who infested the

Mediterranean at this time was the carramuzzal, classed as a
brigandine. Her sail, says Hakluyt, consisted of “a misen or triangle”
sail, that is of course a lateen. She is shown in Furttenbach
purposely without rigging or sails so as to indicate clearly her
method of firing. The tartana, with her lateen sail, sometimes seen
in contemporary prints, was a Mediterranean fishing vessel.
Fig. 59. A Full-rigged Ship of the Early Seventeenth Century.
In spite of the great interest manifested by England and other

nations recently in Arctic exploration, let us not forget that the first
true polar voyage was undertaken during the reign of Elizabeth by
Dutchmen. Their object was to find the North-East passage to China,
and terrible were the privations and perils endured. The reader who
has become familiar with Franklin’s, McClintock’s, Nansen’s, Scott’s,
Shackleton’s, and other explorers’ travels to the poles, is advised to
compare the experiences which these Dutchmen endured. Many of
them have their counterpart in the accounts written by modern
explorers. Thus one of the ships was tilted over to a dangerous
angle, though ultimately righted. Once one of the ships was caught
in a driving pack of ice, and suddenly freeing herself three of her
crew who were on the ice had barely time to be drawn quickly up
the ship’s sides and saved from drowning. These and the other
incidents mentioned here are all delightfully illustrated in “A true
account of the three new unheard of and strange journeys in ships
... in the years 1594, 1595 and 1596,” by Levinus Hulsius, printed at
Frankfort in 1612. The type of ship used for this expedition appears
to be the galleon. The rigging and sails, the lacing holes for the
drabbler and bonnet, the topsails “goared” out to the clews, and the
bowlines, are all shown. One illustration proves that when close-
hauled these ships stowed both spritsail and sprit topsail.
Unhappily for the navigators, but luckily for us, their big ship stuck
fast in the ice and remained there. Anxious, therefore, to return to
Holland with the approach of summer, they determined to attempt
the journey in open boats. Now much as we sympathise with the
sufferings of these brave men, this unfortunate incident of an
abandoned ship has given us a picture of the men engaged in
adding raised gunwales to their small boats and afterwards sailing
across the sea. Hitherto in this history of the sailing ship, except
when we spoke of the lateen, we have always had in mind the
squaresail rig. Its virtues never grow old when utilised for big ships
and deep-sea sailing. But for small craft and for handiness there is
nothing to beat what is known as the fore and aft rig. Just exactly
when the fore and aft rig originated is not possible to determine,
although its rise and influence have been since very powerful,
especially in the modern yacht and fishing vessel. But it may be
taken as practically certain that the sloop rig (by which I mean a
vessel with a peaked mainsail and a triangular headsail), like many
other good points of ship development, came from the Low
Countries during the first half of the sixteenth century. In a map[92]
sent in 1527 from Seville, in Spain, by M. Robert Thorne to Doctor
Ley we see a Dutch-like sloop depicted. A map of Ireland of 1567
contains two vessels of this rig. H. C. Vroom, whom we referred to
above as the designer of the House of Lords tapestries, painted a
picture entitled The Arrival at Flushing of Robert Dudley, Earl of
Leicester, 1586. The date of Vroom’s birth was 1566. Now this
picture shows about half a dozen small vessels rigged exactly like
the small boat given in Hulsius. This rig consists of a triangular sail
hoisted up the forestay, and with a mainsail having no boom or gaff,
but a large sprit across; in fact, exactly resembling the rig of the
Thames “stumpey” barge to-day. It was only at a later date that the
jib was added to the foresail and a topsail to the sprit mainsail. The
other small boat given in Hulsius is shown square-rigged, with one
course on her main and the same on her fore, but the latter mast is
stepped very far forward and right at the bows. The design of the
latter boat’s hull shows the remnant of the Viking influence, which is
not obliterated even in the modern Dutch schuyt. It should be
mentioned also that the cutter-rigged boat in Hulsius just alluded to
has a yard-tackle coming down from the top of the mast to about
the middle of the sprit, while from the peak of the sail two vangs
lead down aft, just as in the modern barge.
Before we close this eventful period we must not omit to mention
the East India Company, which ranks after the Armada and the
Battle of Lepanto as the most important item to be reckoned with in
connection with the development of the sailing ship. Formed by a
company of merchant-adventurers to trade to the East Indies,
Elizabeth granted its charter in 1600: its first fleet consisted of the
Red Dragon (600 tons and 200 men), the Hector (300 tons and 100
men), the Ascension (200 tons and 80 men), and the Susan (240
tons and 80 men), together with a deep-sea pinnesse of 100 tons
with 40 men.
The Tudor period had seen the most wonderful innovations and
developments in connection with the sailing ship. Under no period
had it altered so much or in so short a space of time. Not, indeed,
until we come to the middle of the nineteenth century did the sea
witness such original craft voyaging across its surface. But let us see
now what happened during the reigns of the Stuarts and their
successors.
CHAPTER VII.
FROM THE ACCESSION OF JAMES I. TO THE

C L O S E O F T H E E I G H T E E N T H C E N T U R Y.
ne of the most lucrative, if exciting, professions

which was far from unpopular during Elizabeth’s
reign was that of fitting out a small fleet of two or
three ships, roving about the seas, especially off
the coast of Spain, attacking and, when fortunate,
capturing a ship homeward bound with treasure
from the West Indies. In spite of the distinguished
Englishmen who were engaged in this, in spite of
the excellent training it afforded to our seamen, it can only be
condemned as illegal and piratical, although for a long time it was
winked at. James I., however, on his accession determined to take
away from it any semblance of approval. He did his best to bring an
end to these marauding expeditions, but for all that they went on
persistently though not overtly. Captain John Smith, a distinguished
sailor of this time, who was also the first Governor of Virginia, has
left us a lively account depicting an imaginary engagement to
illustrate the working of a ship of this date. It is to be found in “An
Accidence or The Pathway to Experience necessary for all young
seamen ... written by Captaine John Smith sometimes Governour of
Virginia and Admirall of New England,” printed in London in 1626. As
it shows in actual use the very details of the ship and equipment we
mentioned in the last chapter, I cannot refrain from quoting at length
the following graphic description. I give it just as it was printed,
substituting only modern spelling and punctuation:
“A sail! How stands she? To windward, or leeward? Set him by the
compass. He stands right ahead, or on the weather bow, or lee bow.
Out with all your sails: a steady man to the helm. Sit close to keep
her steady. Give chase or fetch him up. He holds his own. No: we
gather on him. Out goeth his flag and pennants or streamers, also
his colours, his waist-cloths and top-armings. He furles and slings his
mainsail. In goes his spritsail and mizzen. He makes ready his close
fights[93] fore and after: well, we shall reach him by and by. What?
Is all ready? Yea, yea. Every man to his charge. Dowse your topsail.
Salute him for the sea—hail him. ‘Whence your ship?’ ‘Of Spain:
whence is yours?’ ‘Of England.’ ‘Are you merchants or men of war?’
‘We are of the sea.’ He waves us to leeward for the King of Spain
and keeps his luff. Give him a chase piece, a broad side and run
ahead. Make ready to tack about, give him your stern pieces. Be
yare[94] at helm: hail him with a noise of trumpets.
“We are shot through and through, and between wind and water.
Try the pumps. Master, let us breathe and refresh a little. Sling a
man overboard to stop the leak. Done, done! Is all ready again? Yea,
yea. Bear up close with him. With all your great and small shot
charge him. Board him on his weather quarter. Lash fast your
grappling irons and sheer off. Then run stem-lines the midships.
Board and board[95] or thwart the hawse. We are foul on each other.
The ship’s on fire. Cut anything to get clear, and smother the fire
with wet cloths. We are clear, and the fire out. God be thanked. The
day is spent, let us consult. Surgeon, look to the wounded, wind up
the slain. With each a weight or bullet at his head and feet. Give
three pieces for their funerals. Swabber, make clean the ship. Purser,
record their names. Watch, be vigilant to keep your berth to
windward, and that we lose him not in the night. Gunners, spunge
your ordinances. Soldiers, scour your pieces. Carpenters, about your
leaks. Boatswain and the rest, repair the sails and shrouds. Cook,
see you observe your directions against the morning watch. Boy!
Hulloa, master, hulloa! Is the kettle boiled? Yea. Boatswain, call up
the men to prayer and breakfast.
“Boy, fetch my cellar of bottles. A health to you all fore and aft.
Courage, my hearts, for a fresh charge. Master, lay him aboard luff
for luff. Midshipmen, see the tops and yards well manned with
stones and brass balls. To enter them at shrouds and every
squadron else at their best advantage, sound drums and trumpets
and St. George for England. They hang out a flag of truce. Stand in
with him, haul him amain, abaft, or take in his flag. Strike their sails
and come aboard, with the captain, purser and gunner, with your
commission, cocket or bills of loading. Out goes their boat. They are
launched from the ship side. Entertain them with a general cry. God
save the captain, and all the company, with the trumpets sounding.
Examine them in particular, and then conclude your conditions with
feasting, freedom or punishment, as you find occasion. Otherwise if
you surprise him or enter perforce, you may stow the men, rifle,
pillage or sack and cry a prize.”
Perhaps we may be allowed to add a word further in explanation
of the duties of the officers taken also from this little book. The
captain was not necessarily a seaman. His authority was to
command the whole company and keep them in order. The
lieutenant was to assist the captain and—hence the word—in his
absence to take his place. The captain also directed a fight, while
the master was really the sailing master and gave orders to the
sailors, taking charge of the ship as long as she was on the high
seas: but “when they make land” the pilot “doth take charge of the
ship till he bring her to harbour.” The duties of the sailors included
hoisting sails, getting the tacks aboard, hauling the bowlines and
steering the ship. The Yonkers were the young men whose work was
to take in the topsails, furl and sling the mainsail, to do all the
bowsing or tricing, and take their turn at the helm. In the setting of
watches, the master chose one and the mate the other.
As to the ship herself we find that the planking of a vessel of 400
tons was to be four inches thick, ships of 300 tons to have three-
inch planking, and small ships two-inch, but never less than this.
Between the beams of the deck and the orlop there were to be six
feet of head-room, and ten ports on each side upon the lower orlop.

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“And time for all the works and days of hands

Farokh Erach Udwadia

4. Cardiopulmonary Resuscitation and section 7 Cardiovascular Problems

section 3 Basic Cardiorespiratory 19. Acute Coronary Syndromes 213

9. Introduction 93 28. Acute Respiratory Failure in Adults 299

33. Acute Severe Asthma 363 section 14 Surgical Infections

section 9 Mechanical Ventilation in section 15 Organ System Dysfunction

in a Critical Care Setting

section 18 Physical Injuries Requiring section 23 The Critically Ill Child

in the Critically Ill Patient 84. Nutritional Support in the Pediatric

section 21 Critical Care of the 86. Acute Kidney Injury in Infants

73. Critical Care of the Transplant Patient 867

87. End of Life Care in the Intensive Care Unit 945

An Introduction to Critical Care

INTRODUCTION physician or surgeon who can know everything, there is to

Table 2: Trauma score

Table 3: Revised trauma score (RTS)* Box 1: CRAMS scale*

Table 4: APACHE II points (A + B + C below)

*Points are doubled in acute renal failure.

Table 5: sequential organ failure assessment (SOFA) score

Table 6: multiple organ dysfunction score

Cardiopulmonary Resuscitation and

 Cardiopulmonary Resuscitation and Cerebral Preservation in Adults

GENERAL CONSIDERATIONS of symptoms.2 Cardiac arrest is a dreaded complication during

2 TT Advanced Airway Management and Ventilatory Support.

2 ssions even when performed by an expert. Alternative

Stopping Efforts to Resuscitate days after resuscitation. In other words, it is a reperfusion

Management of Post-resuscitation Arrhythmias

Flowchart 3: Management of atrial tachycardia Flowchart 4: Management of post-resuscitation bradycardia

Glucose Control Infection • Prevention and treatment of nosocomial

2 pause on coronary perfusion pressure decay and rescue shock

Basic Cardiorespiratory Physiology in the

 Basic Cardiorespiratory Physiology in the Intensive Care Unit

INTRODUCTION FACTORS REGULATING CARDIAC OUTPUT

impaired or totally absent in patients with cardiac disease.

3 measured, is a function of the length of the muscle fibers.1,2

forward flow and tissue perfusion, without pulmonary

TT Intravascular volume which regulates mean circulatory

0.863 is the correction factor that takes into account the

There is good evidence to show that PaCO2 (pressure of CO2

The PaCO2 is thus inversely related toV· A. A high PaCO2 (>48

gas exchange unit of the lung. It is the volume of inspired VA

Cardiopulmonary Resuscitation and Cerebral Preservation in Adults

Basic Cardiorespiratory Physiology in the Intensive Care Unit