UNIVERSITY OF NUEVA CACERES

COLLEGE OF NURSING

J. Hernandez Ave., Naga, Camarines Sur

Assignment:

1. Differentiate characteristic of ulcer in venous and arterial

- Attach an image of venous and arterial ulcer

- Identify cause, risk factors, wound characteristic and nursing management.

2. 4 compensatory mechanism of heart failure

Venous Ulcer Arterial Ulcer

The venous system normally decreases in Arterial ulcers are caused by reduced arterial
pressure during exercise or when the calf blood supply to the lower limbs secondary to
muscle pump is in use. When muscles are atherosclerotic disease of the larger arteries.
relaxed, the valves in the perforating veins When there is concurrent hypertension in the
should prevent reflux and maintain a low intimal layer of an artery, further damage will
pressure in the deep venous circulation. If there occur. Results of poor circulation or decreased
is damage to the veins, pressure remains high, arterial blood supply are tissue hypoxia and
and therefore valves are deemed incompetent. tissue damage.
Sustained venous hypertension leads to venous
leg ulcers caused by chronic venous
insufficiency.

Causes: Causes:
Venous ulcers occur when oxygen-poor blood  There are a number of reasons why
can’t flow from your extremities back to your arteries may be blocked resulting in
heart. Instead, it pools, creating pressure in your arterial issues. Some of the most
veins. This damages skin tissue and leads to an common causes of arterial blockage
ulcer. may include:
 High cholesterol
Your veins contain tiny valves that keep blood  Chronic kidney issues
circulating throughout your body. These valves  Atherosclerosis (arterial thickening) due
snap open and shut to move blood against the to deposits of cholesterol and other
force of gravity back to your heart. lipids on vessel walls
In some people, venous diseases affect valve  Smoking that weakens arterial walls
functioning. Other medical conditions, like  Diabetes
diabetes, can also put you at risk for leg and foot  High Blood Pressure (Hypertension)
ulcers.  Vasculitis
 Limited Mobility (sitting or lying in one
Other venous ulcer causes include: position for too long)
 High blood pressure (hypertension)  Restrictions to blood vessels due to
which damages blood vessel walls. peripheral vascular disease
 Venous obstruction, a vein blockage  Trauma
that’s sometimes due to blood clots.  Increased age
 Venous reflux, when blood flows  Comorbidities like sickle cell anemia
backward through weak or damaged and rheumatoid arthritis
valves.  Foot deformities
 Poor footwear

Risk Factors: Risk Factors:

 Advanced Age Reversible:
 Obesity  Hypertension
 Pregnancy  Diabetes
 Family history of venous disease  Cigarette smoking
 Systemic Inflammation  Obesity
 Venous thromboembolism  Sedentary lifestyle
 Varicose veins
 Pulmonary embolism Irreversible:
 Sedentary lifestyle  Male
 Smoking  Strong family history of ulcer
 Paralysis
 Trauma/leg fractures
 Family hx of venous disease
 Previous wound
 Injection drug user
 Impair calf muscle pump
 Restricted range of motion of the ankle
 Surgery, such as a knee replacement.
 Varicose
 Spider veins.

Wound Characteristics: Wound Characteristics:

Pedal Pulse: Pedal Pulse:
 Strong  Weak or absent
 May seem week due to edema
Pain:
Pain:  Typically, severe (but absent if the
 Possibly dull and achy patient also has peripheral neuropathy)
 Improved by elevating the leg  Improved by dangling the leg
(increasing blood flow)
Location:
  Distal medial calf and ankle Location:
 On or between the toes
Depth:  Lateral Ankle
 Shallow  Tibia

Border: Depth:
 Irregular  Deep

Skin: Border:
 Allegator like  Round
 Scaly  Raised
 Edema  Regular, well-defined
 Weepy wound
 Varicose vein Skin:
 Cracked
 Dry
 Cold

Nursing Management: Nursing Management:

1. Assess patient history to identify the 1. Assess patient history to identify the
risk factors risk factors
2. Assess the pain location, character, and 2. Assess the pain location, character, and
exacerbating and relieving factors exacerbating and relieving factors
3. Assess the ulcer history to know if the 3. Assess the ulcer history to know if the
patient ulcer is their first or recurrent. patient ulcer is their first or recurrent.
4. Monitor the patient’s blood pressure, 4. Monitor the patient’s blood pressure,
the weight, and urinalysis the weight, and urinalysis
5. Compression therapy (compression 5. Monitor systolic pressure of ankle and
garments, containment devices, Velcro brachial arteries with use of doppler
systems, and short and long stretch-fiber monitor
compression wraps) for edema and pain 6. Patients presenting ulcer should be
reduction, circulation improvement, and screened for arterial disease by doppler
healing enhancement. Compression measurement of ankle-brachial pressure
therapy is contraindicated in arterial index (ABPI)
wounds, so correct diagnosis is 7. Record any unusual appearance and if
required. there is any doubt or concerns refer the
6. Covering the wound with a dressing to patient for specialist medical assessment
promote moist wound healing. Choose 8. Avoid treatments that interfere with
dressings based on wound size, arterial flow (whirlpool, sharps
location, depth, moisture balance, debridement, compression therapy,
presence of infection, allergies, comfort, restrictive footwear, and elevation of the
odor management, ease and frequency limb above heart level)
of dressing changes, cost, and 9. Management of Co-morbid diseases
availability. (ex: diabetes)
7. Removing necrotic tissue by 10. Optimal Nutrition
debridement help expedite wound 11. Advise patient to maintain walking with
healing rest periods when pain occurs
8. Encourage the patient of an hour of leg 12. Treat patient’s pain around the clock
elevation daily may reduce the risk of 13. Assess and treat for infection if needed
venous ulcer recurrence. 14. Maintain patient’s mobility
9. Advise the patient to have mild exercise 15. Maintain patient’s self-esteem through
(such as walking and progressive activity and self-care
resistant exercises) in conjunction with 16. Regularly change the dressing to keep
 compression therapy may aid healing. the wound clean and dry
10. Record any unusual appearance and if 17. Advise patient to avoid tobacco
there is any doubt or concerns refer the products that can harden the arteries
patient for specialist medical assessment 18. Advise patient not to be in one position
11. Management of Co-morbid diseases too long and avoid sitting cross-legged.
(ex: diabetes)
12. Optimal Nutrition
13. Assess and treat for infection if needed
14. Regularly change the dressing to keep
the wound clean and dry
15. Advise the patient to irrigate in the
shower or bathe in buckets or bowls
lined with a clean plastic bag to reduce
the risk of cross-infection.
16. Gently remove the dry skin scales from
the legs, particularly around the ulcer
edges to allow new growth of
epithelium.17
17. Soap substitute products should be used
to cleanse and moisturize the skin.
18. Elevate the leg of the patient at the same
level as the head in order to facilitate
blood circulation.
19. Advise patient not to be in one position
too long and avoid sitting cross-legged.
20. Advise patient to avoid tobacco or
smoking

4 Compensatory Mechanism of Heart Failure

1. Increased sympathetic activity
2. Renin-angiotensin-aldosterone system
3. Ventricular dilation
4. Ventricular hypertrophy
Compensatory Mechanisms and the Cascade of Changes that occur in heart failure:

1. The initial change in heart failure is a reduction in cardiac output.

2. Because of reduced cardiac output, the sympathetic nervous system gets stimulated. This is
the earliest change.
3. This causes peripheral arteriolar constriction, increase in the force of myocardial contraction,
and increase in heart rate which compensate for the decrease in cardiac output.
4. Next the Renin Angiotensin Aldosterone System (RAAS) is activated. This is due to the
relative ischemia of the kidneys combined with sympathetic stimulation of the kidneys.
5. Renin is released from the juxtaglomerular apparatus of the kidneys. This converts
Angiotensinogen produced by the liver to Angiotensin I.
6. Angiotensin I is converted to Angiotensin II by the enzyme Angiotensin Converting Enzyme
(ACE) which is present in tissues like the lungs, heart, and blood vessel walls.
7. Angiotensin II acts on the Angiotensin II type 1 receptors (AT1) present in the heart, kidneys,
and blood vessels.
8. Stimulation of the AT1 receptors cause vasoconstriction, release of aldosterone from the
adrenal glands and release of catecholamines.
9. Aldosterone causes salt and water retention by its action on the kidneys to retain sodium in
exchange for potassium.
10. Angiotensin II also stimulates the release of vasopressin or antidiuretic hormone (ADH) from
the posterior pituitary gland, which plays a role in vasoconstriction as well as water
reabsorption in the kidneys.
11. The long-term effects of Angiotensin II and Aldosterone are also detrimental. Angiotensin
can cause fibrosis in the heart, kidneys, and other organs of the body. Aldosterone can cause
hypertrophy and fibrosis in the ventricular myocardium and the blood vessels. This causes
increased stiffness of the blood vessels and the ventricular muscle.
12. All these long-term changes in the heart due to heart failure led to Ventricular Remodeling
or Dilation which is defined as the change in size, shape, and function of the ventricles due to
 injury or increased load. These changes are brought about by myocardial hypertrophy and
fibrosis. These cause changes to the shape and size of the ventricles. The ventricles become
enlarged (ventricular hypertrophy) and more spherical in shape.

References:

 https://www.medmastery.com/guides/ultrasound-clinical-guide-arteries-legs/how-
differentiate-between-arterial-venous-and-diabetic
 https://westcoastwound.com/arterial-ulcer-treatment-and-wound-care/
 https://www.woundsource.com/blog/venous-vs-arterial-wounds-differential-diagnosis-and-
interventions
 https://slideplayer.com/slide/13675512/
 https://www.myamericannurse.com/venous-ulcer-care/
 https://www.nursinginpractice.com/clinical/managing-leg-ulcers-in-primary-care/
 https://www.ezmedlearning.com/blog/congestive-heart-failure-symptoms-stages-treatment