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Lecture

BIOC33H3 Lecture Notes - T Cell, Pulmonary Vein, Perfusion


Department
Biological Sciences
Course Code
BIOC33H3
Professor
Stephen Reid

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Chapter 35: Heart Failure
ETIOLOGY AND PATHOPHYSIOLOGY
Heart failure (HF) is an abnormal clinical condition involving impaired cardiac pumping
that results in the characteristic pathophysiologic changes of vasoconstriction and fluid
retention.
HF is characterized by ventricular dysfunction, reduced exercise tolerance, diminished
quality of life, and shortened life expectancy.
Risk factors include coronary artery disease (CAD) and advancing age. Hypertension,
diabetes, cigarette smoking, obesity, and high serum cholesterol also contribute to the
development of HF.
CLASSIFICATION
Heart failure is classified as systolic or diastolic failure.
o Systolic failure, the most common cause of HF, results from an inability of the
heart to pump blood.
o Diastolic failure is an impaired ability of the ventricles to relax and fill during
diastole. Decreased filling of the ventricles will result in decreased stroke volume
and cardiac output (CO).
CLINICAL MANIFESTATIONS
HF can have an abrupt onset or it can be an insidious process resulting from slow,
progressive changes. Compensatory mechanisms are activated to maintain adequate CO.
To maintain balance in HF, several counter regulatory processes are activated, including
the production of hormones from the heart muscle to promote vasodilation.
Cardiac compensation occurs when compensatory mechanisms succeed in maintaining an
adequate CO that is needed for tissue perfusion.
Cardiac decompensation occurs when these mechanisms can no longer maintain adequate
CO and inadequate tissue perfusion results.
The most common form of HF is left-sided failure from left ventricular dysfunction. Blood
backs up into the left atrium and into the pulmonary veins causing pulmonary congestion
and edema. HF is usually manifested by biventricular failure.
Acute decompensated heart failure (ADHF) typically manifests as pulmonary edema, an
acute, life-threatening situation.
Clinical manifestations of chronic HF depend on the patient’s age and the underlying type
and extent of heart disease. Common symptoms include fatigue, dyspnea, tachycardia,
edema, and unusual behavior.

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Pleural effusion, atrial fibrillation, thrombus formation, renal insufficiency, and
hepatomegaly are all complications of HF.
DIAGNOSTIC STUDIES
The primary goal in diagnosis of HF is to determine the underlying etiology of HF.
o A thorough history, physical examination, chest x-ray, electrocardiogram (ECG),
laboratory data (cardiac enzymes, b-type natriuretic protein (BNP), serum
chemistries, liver function studies, thyroid function studies, and complete blood
count), hemodynamic assessment, echocardiogram, stress testing, and cardiac
catheterization are performed.
NURSING AND COLLABORATIVE MANAGEMENT: ADHF AND PULMONARY
EDEMA
The goals of therapy for both ADHF and chronic HF are to decrease patient symptoms,
reverse ventricular remodeling, improve quality of life, and decrease mortality and
morbidity.
Treatment strategies should include the following:
o Decreasing intravascular volume with the use of diuretics to reduce venous return
and preload.
o Decreasing venous return (preload) to reduce the amount of volume returned to
the LV during diastole.
o Decreasing afterload (the resistance against which the LV must pump) improves
CO and decreases pulmonary congestion.
o Gas exchange is improved by the administration of IV morphine sulfate and
supplemental oxygen.
o Inotropic therapy and hemodynamic monitoring may be needed in patients who
do not respond to conventional pharmacotherapy (e.g., diuretics, vasodilators,
morphine sulfate).
o Reduction of anxiety is an important nursing function, since anxiety may increase
the SNS response and further increase myocardial workload.
COLLABORATIVE CARE: CHRONIC HEART FAILURE
The main goal in the treatment of chronic HF is to treat the underlying cause and
contributing factors, maximize CO, provide treatment to alleviate symptoms, improve
ventricular function, improve quality of life, preserve target organ function, and improve
mortality and morbidity.
Administration of oxygen improves saturation and assists greatly in meeting tissue
oxygen needs and helps relieve dyspnea and fatigue.
Physical and emotional rest allows the patient to conserve energy and decreases the need
for additional oxygen. The degree of rest recommended depends on the severity of HF.
Nonpharmacologic therapies used in the management of HF patients who are receiving
maximum medical therapy, continue to have NYHA Functional Class III or IV
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symptoms, and have a widened QRS interval include the following:
o Cardiac resynchronization therapy (CRT) or biventricular pacing. Involves pacing
both the right and left ventricles to achieve coordination of right and left ventricle
contractility.
o Cardiac transplantation. Strict criteria are used to select the few patients with
advanced HF who can even hope to receive a transplanted heart.
o Intraaortic balloon pump (IABP) therapy. The IABP can be useful in the
hemodynamically unstable HF patient because it decreases SVR, PAWP, and
PAP as much as 25%, leading to improved CO. However, the limitations of bed
rest, infection, and vascular complications preclude long-term use.
o Ventricular assist devices (VADs). VADs provide highly effective long-term
support for up to 2 years and have become standard care in many heart transplant
centers. VADs are used as a bridge to transplantation.
o Destination therapy. The use of a permanent, implantable VAD, known as
destination therapy, is an option for patients with advanced NYHA Functional
Class IV HF who are not candidates for heart transplantation.
General therapeutic objectives for drug management of chronic HF include: (1)
identification of the type of HF and underlying causes, (2) correction of sodium and
water retention and volume overload, (3) reduction of cardiac workload, (4) improvement
of myocardial contractility, and (5) control of precipitating and complicating factors.
o Diuretics are used in HF to mobilize edematous fluid, reduce pulmonary venous
pressure, and reduce preload.
Thiazide diuretics may be the first choice in chronic HF because of their
convenience, safety, low cost, and effectiveness. They are particularly
useful in treating edema secondary to HF and in controlling hypertension.
Loop diuretics are potent diuretics. These drugs act on the ascending loop
of Henle to promote sodium, chloride, and water excretion. Problems in
using loop diuretics include reduction in serum potassium levels,
ototoxicity, and possible allergic reaction in the patient who is sensitive to
sulfa-type drugs.
Spironolactone (Aldactone) is an inexpensive, potassium-sparing diuretic
that promotes sodium and water excretion but blocks potassium excretion.
This aldosterone receptor antagonist also blocks the harmful
neurohormonal effects of aldosterone on the heart blood vessels.
Spironolactone adds to the benefits of angiotensin-converting
enzyme (ACE) inhibitors, and is appropriate to use while renal
function is adequate.
Spironolactone may also be used in conjunction with other
diuretics, such as furosemide.
Vasodilator drugs have been shown to improve survival in HF. The goals
of vasodilator therapy in the treatment of HF include (1) increasing venous
capacity, (2) improving EF through improved ventricular contraction, (3)
slowing the process of ventricular dysfunction, (4) decreasing heart size,
(5) avoiding stimulation of the neurohormonal responses initiated by the
compensatory mechanisms of HF, and (6) enhancing neurohormonal
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