Anesthesia Vetilators 101
Anesthesia Vetilators 101
Anesthesia Vetilators 101
There are numerous indications for ventilating the anesthetized patient. First and
foremost, it is important to realize that all anesthetized patients’ hypoventilate due to abnormal
alveolar ventilation. The decision to institute mechanical ventilation can vary greatly and range
from the presence of thoracic trauma, such as flail chest or diaphragmatic hernia, to the use of
neuromuscular blocking agents. Furthermore, hypoventilation can be associated with gross
obesity, and is known as pickwickian syndrome. Ventilatory assistance should also be
considered for any surgical procedure lasting > 90 minutes. Regardless of the presence or
absence of disease, the goal of ventilation is to maintain normal end-tidal carbon dioxide
(ETCO2) tensions in arterial blood.
Classifications of Ventilators
The power source for mechanical ventilators may be comprised of electricity, compressed
gas (pneumatic), or both. Most anesthesia ventilators have pneumatic drive mechanisms
meaning that the drive mechanism is most commonly compressed gas, even when electric
controls used. The cycling mechanism may consist of TIME PLUS electronic, pressure, or fluidic
(older models) mechanisms, but most modern ventilators are usually time-cycled and
electronically controlled. The direction that the bellows moves during expiration (ascending
versus descending) also helps to characterize anesthesia ventilators. Most anesthesia ventilators
control ventilation.
The tidal volume (VT) is the amount of gas exchanged in one respiratory cycle, and the
minute volume (Vm) is the total amount of gas (expressed in liters) exchanged in one minute.
Therefore, Vm = VT X BPM (breaths per minute.)
I. Hook up
All anesthetic machines compatible with the ventilator should be modified with the
appropriate extra connections and clearly labeled.
*Connect breathing system hose (clear) to the rebreathing bag connection
*Attach the Airway Pressure Sensing Tee to the inhalation side of the anesthetic
machine
*Close the Pop-off valve
* Plug in ventilator and hook up scavengers
**It is very important to use a leak free anesthetic machine while using the ventilator.
Do check for leaks prior to hooking up the ventilator. To check the ventilator and
anesthetic machine for leaks simultaneously, see instructions on the side of the ventilator.
II. Controls
There are 4 control knobs on the front panel of the ventilator. Two controls, the Rate and
Volume, are used to directly set ventilation parameters. The third control is used to set a
maximum pressure limit, and the last one is used to pause cycling.
*I/O Power Switch- A toggle switch to turn the ventilator ON. Green LED
indicates power is ON.
*Rate Control- A potentiometer. Use to set the respiratory rate in BPM.
* Volume Control- A needle valve regulating inspiratory flow. Use to adjust the
minute ventilation of the patient, more or less. Since the inspiratory;expiratory (I:E) ratio
is held constant at 1:2, this is the only control that will effect minute ventilation.
*Maximum Working Pressure Limit Control (MWPL)- A potentiometer. Use to
adjust an upper limit above which you wish the pressure to never exceed. In general, for
a healthy patient, the peak inspiratory pressure (PIP) should be kept in the range of 15 to
20 cm of H2O.
III. Alarms
*Maximum Working Pressure Limit-The ventilator will terminate the inspiratory
phase of the breathing cycle and begin an expiratory phase when the pressure transducer
senses a pressure above the MWPL. The MWPL is settable over a range of 10 to 60 cm
H2O. When the airway pressure reaches the set limit, the yellow light on the front panel
blinks and a short tone is heard. If the excessive pressure is not immediately relieved,
cycling is paused and the alarm sounds continuously. Note that the INSpiratory HOLD
feature is designed not to function when the MWPL setting is exceeded.
*Low Breathing System Pressure Alarm (LO BSP)- The LO BSP alarm is
activated at the end of Inspiration is there is not at least 5 cm of H2O pressure sensed by
the pressure transducer. This alarm is sometimes referred to as the “Disconnect” alarm;
however, it should be understood that a patient disconnect is not always nor the only
cause of low breathing system pressure. Typically, the alarm will sound if the oxygen
tank is running out. During the alarm condition a yellow light is illuminated on the front
panel and the sound of a raspy siren is heard. The alarm automatically resets at the end
of the next inspiratory phase in which there is a minimum of 5 cm of H2O pressure
(PEEP) sensed by the transducer.
Capnography
Measuring ETCO2 is paramount to ensuring adequate ventilation in the anesthetized
patient, especially when utilizing mechanical ventilation. End-tidal carbon dioxide is the result of
expired gases from the alveoli. The site of gas exchange occurs in the alveolar capillary beds
lying between the blood and air within the lungs. In addition to assessing the adequacy of patient
ventilation in a variety of clinical situations, end-tidal carbon dioxide analysis can be used to
help assess acid/base status. Furthermore, an abrupt decrease in ETCO2 can be an early and
reliable indication of an impending cardiovascular collapse or cardiac arrest. Since delivery of
carbon dioxide from the lungs requires blood flow, cellular metabolism, and alveolar ventilation,
assessing ETCO2 can also be used to assess the effectiveness of cardio-pulmonary-resuscitation
(CPR) techniques.
Capnometers and capnographs monitor ETCO2 by evaluating samples of the patient’s
exhaled gases taken from the anesthetic circuit via an adapter placed on the end of the patient’s
endotracheal tube. This adapter must be placed precisely at the end of the patient’s nose to
eliminate excessive dead space and prevent rebreathing of carbon dioxide. Cutting the
endotracheal tube to shorter lengths allows the adapter to be located at the end of the nose while
still allowing the cuff to sit immediately distal to the larynx, but no further than the thoracic inlet.
Capnometers provide only minimum and maximum ETCO2 values, while capnographs also
provide a capnogram, which is a graphic display of the carbon dioxide content of each breath.
(See Figures 1-5) Recognizing abnormalities in ventilation or anesthetic circuit function are
easier utilizing capnograms.
Normal ETCO2 values are 35-45 mmHg. Under normal circumstances, ETCO2 typically
underestimates the arterial carbon dioxide partial pressure (PaCO2) by a clinically insignificant
2-5 mmHg. End-tidal carbon dioxide disparity during open thoracotomy is ~6 mmHg greater
than the PaCO2. End tidal carbon dioxide values above 45 mmHg indicate inadequate
ventilation, necessitating ventilatory assistance via manual or mechanical means. Conversely, by
allowing modest increases in ETCO2 (up to 50 mmHg) the anesthetist can bolster arterial blood
pressure via endogenous catecholamine release. Nonetheless, the highest ETCO2 permissible
should be <60 mmHg.
There are caveats to ETCO2 monitoring: Esophageal intubation, occlusion of the
endotracheal tube, inadequate seal on the endotracheal tube, anesthetic circuit
dysfunction/disconnects, moisture within the sampling line, hyperventilation, or respiratory
and/or cardiac arrest are all potential causes of failure to detect carbon dioxide. Elevated ETCO2
levels may occur as a result of hypoventilation due to airway obstruction, pneumothorax, body
positioning, or lung disease, or during periods of acutely increased metabolism (e.g., malignant
hyperthermia, thyroid storm, or catecholamine release). Significant disparities between PaCO2
and ETCO2 indicate an inefficiency of gas exchange (e.g., dead space ventilation), which may be
secondary to pulmonary embolism, thromboembolism, decreased cardiac output, or perhaps as a
result of mechanical ventilation (intermittent positive pressure ventilation). Explanations for
elevated ETCO2 and inspiratory carbon dioxide may include anesthetic machine malfunction
(e.g., malfunctioning valves within the breathing circuit), unsuitable fresh gas flow rates (e.g.,
non-rebreathing circuits), or exhausted carbon dioxide granules. Therefore, end-tidal carbon
dioxide is best analyzed in conjunction with an arterial blood gas sample to yield the most
complete status of respiratory function.
Ventilator Weaning
The respiratory drive is regulated via oxygen and carbon dioxide tension in the blood. To
stimulate spontaneous respiration upon the completion of mechanical ventilation, it is easiest to
manipulate the carbon dioxide tension. This can be done in one of two ways: 1.) The ‘cold
turkey’ method involves turning the ventilator off for a period of one minute. If spontaneous
respiration does not return, give another ventilator-generated breath and repeat the process until
movement of the bellows or the capnogram indicates spontaneous breathing. 2.) The second
method is more gradual. Turn the ventilator rate and volume settings down as low as possible
(just enough to avoid inciting an alarm), and observe the bellows for spontaneous respirations to
occur between the ventilator-generated breaths, at which point ventilation can be discontinued.
Other methods that may be necessary to hasten a patient’s removal from mechanical
ventilation include reversing neuromuscular agents, antagonizing drugs causing respiratory
depression (e.g., opioids), or physical manipulations (e.g., toe pinching, rolling the patient.)
Extreme care should be taken when utilizing mechanical ventilation. Improper use of
ventilators can result in severe damage to the lungs such as barotrauma, a result of pressure-
induced lung injury, or volutrauma due to volume-induced lung injury. Furthermore, long-term
ventilation has also been associated with oxygen toxicity (>12-16+ hours), atelectotrauma,
pneumonia, and biotrauma secondary to sepsis and/or SIRS.
References:
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1996.
Glerum L: Anesthetic Monitoring: Interpreting the Data, Proc Am College Vet Surgeons, pp
652-655, 2005.
Greene S: Veterinary Anesthesia and Pain Management Secrets, Philadelphia, PA, Hanley &
Belfus, Inc.; pp 113-119, 2002.
Lukasik V: Anesthesia of the Pediatric Patient, NAVTA Journal, pp 52-57, Fall 2006.
Muir W, Hubbell J, Skarda R, Bednarski R: Handbook of Veterinary Anesthesia, ed 3. St.
Louis, MO, Mosby, pp 232-251, 455-474, 2000.
Seahorn J: Monitoring the Anesthetized Small Animal Patient, NAVTA Journal, pp 53-58,
Winter 2004.
Tefend M: Hemodynamic Monitoring in the Postoperative Patient, Proc Am College Vet
Surgeons, 2003.
Thurmon J, et.al, Lumb and Jones Vet Anes (3rd Ed), Baltimore, Lippincott Williams &
Wilkins; pp 411-414, 535-549, 553, 859,1996.
Weil A: Anesthetic Emergencies, NAVTA Journal, pp 42-48, Spring 2005.
Carbon dioxide capnograms courtesy of Mele Tong.