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Exam (elaborations)

BSNC 2000 Module 4 Test Questions and Answers

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  • Course
  • BSNC 2000
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  • BSNC 2000

BSNC 2000 Module 4 Test Questions and Answers Key mechanisms causing systolic dysfunction - Answer-1. Myocardial damage 2. Excessive workload 3. Impaired contractility Key mechanisms causing diastolic dysfunction - Answer-1. Decreased compliance 2. Obstructed filling 3. Impaired relaxation ...

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  • August 15, 2024
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  • Exam (elaborations)
  • Questions & answers
  • BSNC 2000
  • BSNC 2000
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BSNC 2000 Module 4 Test Questions
and Answers

Key mechanisms causing systolic dysfunction - Answer-1. Myocardial damage
2. Excessive workload
3. Impaired contractility

Key mechanisms causing diastolic dysfunction - Answer-1. Decreased compliance
2. Obstructed filling
3. Impaired relaxation

Compensatory Response to decreased CO due to HF: Sympathetic Activation -
Answer-- Increased HR and contractility leading to increased CO
- Vasoconstriction causes increase in vascular resistance and preload
- Arteriolar constriction leading to an increased BP
- Attempted to increase CO and decrease BP

Compensatory Response to decreased CO due to HF: RAAS - Answer-- Angiotensin II
is a potent arteriolar vasoconstrictor which increases BP
- Aldosterone stimulates sodium and fluid retention, and increases blood volume and
preload

Myocardial Remodeling - Answer-Occurs in response to excessive preload/afterload

Ventricular Dilation - Answer-- Ventricles enlarge (muscle fibres increase in length) in
response to conditions that increase preload
- Initially allows the heart to accommodate an increased volume while maintaining wall
tension
- The ventricles (and whole heart) become more spherical; eventually, overstretching
impairs contractility

Ventricular Hypertrophy - Answer-- Ventricular walls thicken (muscle fibres increase in
width) in response to conditions that increase afterload (improves pumping)
- Muscle mass increases to pump blood against increased resistance
- Initially maintains systolic function
- Eventually decreases wall compliance and increases oxygen demand

Detrimental effects of persistent activation of compensatory responses: Chronic
Increase in Preload - Answer-- Stretches ventricle, increases blood volume which
increases edema, can cause ventricular dilation (muscle fibres incerase in length)

, - Initially this allows the heart to accommodate an incerased volume while maintaining
wall tension, but eventually the heart becomes more spherical and overstretching
impairs contractility

Detrimental effects of persistent activation of compensatory responses: Chronic
Increase in Afterload - Answer-- Increases the workload of the heart, can cause
ventricular hypertrophy as ventricle walls to thicken (muscle fibres increase in width)
- Muscle mass increases to pump blood against increased resistance which initially
maintains systolic function but eventually decreases wall compliance and increases
oxygen demand
- Increase in sympathetic discharge = increase in force, rate and preload of the heart
which increases CO
- Increase in renin release leads to an increased in angiotensin II = increased afterload
and remodelling

Compensatory responses are ________ short term but _______ long term - Answer-
GOOD

BAD

Heart Failure Assessment: Subjective Data - Answer-- Focussed interview related to
cardiovascular and peripheral vascular disease
- Ask relevant questions related to chest pain, SOB, edema, cough, fatigue, and cardiac
risk factors, leg pain, skin changes, swelling in limbs, history of past illnesses, history of
diabetes, injury

Heart Failure Assessment: Objective Data - Answer-Inspect:
- Face, lips, and ears for colour (cyanosis)
- Chest for deformities, scars
- Bilateral arms/hands noting CWMS, edema, colour of nail beds
- Bilateral legs, noting CWMS, edema to lower legs and feet, and presence of superficial
distended veins
- Compare calf size/pain for signs of DVT

Auscultate:
- Apical pulse for one minute (rate/rhythm)

Palpate:
- Radial/brachial/dorsalis pedis and posterior tibialis

Left-Sided HF Assessment Data - Answer-- Pulmonary interstitial edema and gas
exchange
- Dyspnea
- Cough
- Fatigue
- Pulmonary crackle

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