Class notes
NURS 4183 Chapter 34 Lecture Notes
- Course
- NURS 4183
- Institution
- Prairie View A&M State University
This is a comprehensive and detailed lecture note on chapter 34; heart attack for NURS 4183.
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Ch.34- Heart Failure Complex clinical syndrome that resulting in the
inability of the heart to provide sufficient blood to
meet the O2 needs of tissues and organs
A defect in either ventricular filling (diastolic
dysfunction) or ventricular ejection (systolic
dysfunction)
Ejection fraction (EF) amount of blood pumped by
the left ventricular w/ each heart beat
American Academy of Cardiology Foundation (ACCF) has adapted the terms HF w/ reduce EF (HFrEF) and HF w/
preserved EF (HFpEF) to described systolic and diastolic HF
Associated w/ numerous CV diseases, particularly
long-standing HTN, CAD, and MI
Etiology
o Risk factors: HTN and CAD (primary risk
factors); DM; metabolic syndrome; advanced
age; tobacco use; obesity; and high serum
cholesterol
o HF may be caused by any interference w/ the
normal mechanisms regulating CO
o CO depends on (1) preload, (2) afterload, (3)
myocardial contractility, and (4) HR any
changes in these factors can lead to ↓
ventricular function and HF.
o The major causes of HF may be divided into
two subgroups: (1) primary causes and (2)
precipitating causes
o Precipitating causes often ↑ the workload of
the ventricles, resulting in an acute condition
and ↓ heart function.
Genetic Link
o Specific genes and gene mutations have
been linked to the development of HTN, CAD, and cardiomyopathy (weakening of the heart muscle)
o Cardiomyopathy may be attributed to as many as 40 different defective genes
o Body’s largest protein is a muscle protein called titin, which is found in cardiac sarcomeres (part of the
heart muscles that contracts)
Mutations in titin gene are the most common known genetic cause of dilated cardiomyopathy
Patho
o Left-Sided HF
Systolic Failure or HF w/ Reduced EF
Systolic failure results from an inability of the heart to pump blood effectively.
Hallmark: ↓ in EF
o Normal EF is 55% to 60%. Pts w/ systolic HF generally have an EF < 45% (can be
as low as 10%)
Caused by impaired contractile function (e.g., MI), ↑ afterload (e.g., HTN),
cardiomyopathy, and mechanical abnormalities (e.g., valvular heart disease).
LV in systolic failure loses its ability to generate enough pressure to eject blood forward
through the aorta over time it becomes dilated and hypertrophied.
, Weakened heart muscle cannot generate adequate stoke volume, which affect CO end
diastolic volumes and pressures in the LV ↑
When LV fails, blood backs up into the left atriumfluid accumulates in lungs ↑
pulmonary hydrostatic pressure causes fluid leakage from the pulmonary capillary bed
into the intersistium and then the alveoli pulmonary congestion and edema
Diastolic Failure or HF w/ Preserved EF
Inability of the ventricles to relax and fill during diastole.
LV is stiff and noncompliant
↓ filling of the ventricles results in ↓ stroke volume and CO.
Characterized by high filling pressures bc of stiff ventricles ↓ filling in ventricles↓
stroke volume and CO end result pulmonary congestion
Venous engorgement in both the pulmonary and systemic vascular systems.
Diastolic failure is usually the result of left ventricular hypertrophy from HTN (most
common), myocardial ischemia, valve disease (e.g., aortic, mitral), or cardiomyopathy.
However, many pts do not have an identifiable heart disease.
Diastolic failure occurs more frequently in older adults, women, and people who are
obese
Diagnosed by the following: s/s of HF; normal EF; evidence of LV diastolic dysfunction by
echocardiography or cardiac catheterization
Mixed Systolic and Diastolic Failure
Seen in disease states such as dilated cardiomyopathy (DCM).
DCM is a condition in which
poor systolic function is
further compromised by
dilated LV walls that are
unable to relax
Pts often have extremely low
EFs (< 35%), high pulmonary
pressures, and biventricular
failure (both ventricles are
dilated and have poor filling
and emptying capacity).
Pt w/ ventricular failure of
any type may have low BP,
low CO, and poor renal
perfusion.
Poor exercise tolerance and
heart dysrhythmias are also
common.
o Right-Sided HF
Occurs when the right ventricle (RV)
falls to pump effectively, allowing
fluid to back up into the venous
system causing movement of fluid
into the tissues and organs (e.g.,
peripheral edema, ab ascites,
hepatomegaly, jugular venous
distention)
Most common cause is from left-sided HF
, As the LV fails, fluid backs up into the pulmonary system, causing ↑ pressures in the
lungs
RV has to work harder to push blood to the pulmonary system over time, this ↑
workload weakens the RV gradually fails
Other cause (independent of LV): RV infarction, pulmonary embolism, and cor pulmonale (RV
dilation and hypertrophy caused by pulmonary disease)
o Compensatory Mechanisms
HF can have an abrupt onset as w/ acute MI, or it can be a subtle process resulting from slow,
progressive changes.
Overloaded heart uses compensatory mechanisms to try to maintain adequate CO
Neurohormonal Response
Renin-angiotensin-aldosterone system (RAAS)
o Regulatory system that works to maintain normal homeostasis
o Activation results in BP control and fluid and electrolyte balance
o In response to stress, its role is to promote retention of fluid and Na+ and cause
vasoconstriction to raise BP
o However, recurrent activation of RAAS in HF is what is responsible for s/s that
develop
o As the CO falls, blood flow to the kidneys ↓ sensed by the juxtaglomerular
apparatus in the kidneys as ↓ volume.
o In response, the kidneys release renin, which converts angiotensinogen to
angiotensin I
o Angiotensin I is subsequently converted to angiotensin II by a converting enzyme
made in the lungs.
o Angiotensin II causes
(1) Activation of the SNS to ↑ BP and HR
(2) Adrenal cortex to release aldosterone, which results in Na+ and
water retention
(3) ↑ peripheral vasoconstriction, which ↑ BP.
(4) Stimulation of the pituitary gland, which releases antidiuretic
hormone (ADH) aka vasopressin, which results in water reabsorption)
Result from low CO causes a ↓ in cerebral perfusion pressure.
o The outcome of the cascade results in further water and Na+ retention in an
already overloaded state and ↑ workload of the failing heart
o The production of endothelin, a potent vasoconstrictor produced by the
vascular endothelial cells, is stimulated by ADH, catecholamines (Nor, Epi, Dop),
and angiotensin II.
Endothelin results in further arterial vasoconstriction and an ↑ in
cardiac contractility and hypertrophy.
o Locally, proinflammatory cytokines are released by heart cells in response to
various forms of cardiac injury (e.g., MI).
Two cytokines, tumor necrosis factor (TNF) and interleukin-1 (IL-1),
further depress heart function by causing hypertrophy, contractile
dysfunction, and cell death over time, a systemic inflammatory
response also occurs.
o This accounts for the cardiac and skeletal muscle myopathy and fatigue that
accompany advanced HF.
SNS Activation
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