NUR325 Final Exam
Study online at https://quizlet.com/_evc69a
1. What is HF? - HF = impaired cardiac pumping or filling or both
What is it charac- - characterized by ventricular dysfunction, reduced exer-
terized by? cise tolerance, diminished QOL, and shortened life ex-
pectancy
2. What are the - causes: CAD, HTN, valvular heart disease, cardiomy-
causes and risk opathy
factors of HF? - risk factors: diabetes, smoking, obesity, dyslipidemia
3. What are the 2 1. Heart failure with reduced ejection fraction:
types of HF? - most common form
- results from inability of heart to pump blood effectively
(d/t MI, HTN, valvular heart disease)
- L ventricle loses ability to generate enough pressure to
eject blood forward through the aorta
- EF = 40% or lower (normal = 55%)
2. Heart failure with preserved ejection fraction:
- inability of the ventricles to relax and fill during diastole
which results in decreased SV and CO
- characterized by high filling pressures - results in venous
engorgement in the pulmonic and systemic vascular sys-
tems
- usually the result of L ventricular hypertrophy from HTN
(most common), MI, valve disease, or cardiomyopathy
- Dx = presence of HF symptoms with an EF of 50% or
greater
4. What are the 1. activation of the SNS
4 compensatory 2. neurohormonal response
mechanisms of 3. ventricular dilation
HF? 4. ventricular hypertrophy
5. Explain the com- - in response to low SV and CO, SNS activity increases
pensatory mech- which results in the release of epi and norepi
anism of the acti- - this causes increase in HR, contractility, and peripheral
vation of the SNS vasoconstriction
in HF - initially this improves CO, but over time these effects are
harmful because they increase the heart's workload when
it's already working hard
, NUR325 Final Exam
Study online at https://quizlet.com/_evc69a
6. Explain the com- (1) RAAS activation:
pensatory mech- - as CO decreases, renal perfusion decreases which
anism of the neu- causes the kidneys to release *renin* (converts an-
rohormonal re- giotensin to angiotensin I which gets converted to II via
sponses in HF ACE) - this results in sodium and water retention
- angiotensin II causes adrenal cortex to release *aldos-
terone* which results in increased peripheral vasocon-
striction and increased BP
(2) ADH:
- as CO decreases, cerebral perfusion decreases which
causes the posterior pituitary gland to secrete ADH which
results in water retention
(3) endothelin:
- the release of ADH, catecholamines, and angiotensin II
stimulates the production of endothelin which results in
further arterial vasoconstriction, increased cardiac con-
tractility, and hypertrophy
(4) cytokines:
- proinflammatory cytokines (tumor necrosis factor and
interleukin-1) are released by the heart cells in response
to cardiac injury which further depresses heart function
by causing hypertrophy, contractile dysfunction, and cell
death
- over time, a systemic inflammatory response also oc-
curs which accounts for the cardiac and skeletal myopa-
thy and fatigue that accompany advanced HF
(5) combination:
- activation of the SNS and neurohormonal response lead
to elevated levels of norepi, angiotensin II, aldosterone,
ADH, endothelin, and proinflammatory cytokines
- together, these factors result in increased cardiac work-
load, myocardial dysfunction, and ventricular remodelling
- ventricular remodelling = altered geometric shape of
the ventricles which results in increased ventricular mass,
increased wall tension, increased oxygen consumption,
and impaired contractility
- ventricular remodelling is a risk factor for life-threatening
dysrhythmias and sudden cardiac death
, NUR325 Final Exam
Study online at https://quizlet.com/_evc69a
7. Explain the com- - dilation = enlargement of the chambers of the heart
pensatory mech- which happens when the pressure in the heart chambers
anism of ventric- becomes chronically elevated
ular dilation in - muscle fibres stretch in response to the volume of blood
HF in the heart at the end of diastole
- initially, this is an adaptive mechanism to cope with
increasing BV and the increased contraction leads to
increased CO and maintenance of arterial BP and per-
fusion
- over time, it becomes inadequate because the elastic
elements of the muscle fibres are overstretched and can't
contract effectively so CO diminishes
8. Explain the com- - hypertrophy = increase in muscle mass and cardiac wall
pensatory mech- thickness in response to overwork and strain
anism of ventric- - develops slowly
ular hypertrophy - initially, the increased contractile power of the muscle
in HF fibres leads to an increase in CO and maintenance of
tissue perfusion
- over time, hypertrophic heart muscle has poor contrac-
tility and requires more oxygen to perform work, coronary
artery circulation becomes poor, and the heart is prone to
dysrhythmias d/t altered electrical pathways
9. What is - natriuretic peptides ANP and BNP (atrial and brain na-
the counterreg- triuretic peptides) are hormones produced by the heart
ulatory mecha- muscles in response to increased bv in the heart
nism seen in HF - they have renal, CV, and hormonal effects
as a response to - renal: increased GFR and diuresis, excretion of sodium
the compensato- - CV: vasodilation and decreased BP
ry mechanisms? - hormonal: inhibition of aldosterone and renin secretion,
interferes with ADH release
- combined effects of ANP and BNP counter the effects
of the SNS and RAAS
10. What are the 2 1. Left-sided heart failure:
types of heart - most common form
failure? - results from ventricular dysfunction causing blood to
