Class Notes (835,600)
Canada (509,275)
BIOC33H3 (127)
Lecture

Heart Failure

8 Pages
114 Views
Unlock Document

Department
Biological Sciences
Course
BIOC33H3
Professor
Stephen Reid
Semester
Fall

Description
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.  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 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 blockade.  ACE inhibitors (e.g., captopril [Capoten], benazepril [Lotensin], enalapril [Vasotec]) are useful in both systolic and diastolic HF, and they are the first-line therapy in the treatment of chronic HF.  Angiotensin II receptor blockers (e.g., losartan [Cozaar], valsartan [Diovan]) may be used in patients who are ACE inhibitor intolerant.  Nitrates are used to treat HF by acting directly on the smooth muscle of the vessel wall. Major effects include a decrease in preload and vasodilation of coronary arteries.  Nesiritide, a synthetic form of human BNP, being studied for its use in the ongoing treatment of patients with chronic HF.  -Adrenegic blockers, specifically carvedilol (Coreg) and metoprolol (Toprol-XL), have improved survival of patients with HF.  Positive inotropic agents improve cardiac contractility and CO, decrease LV diastolic pressure, and decrease SVR.  Digitalis glycosides [e.g., digoxin (Lanoxin)] remain the mainstay in the treatment of HF, however, they have not been shown to prolong life.  Calcium sensitizers are novel positive inotropic agents in the treatment of HF. They improve cardiac performance by interacting directly with contractile proteins without affecting intracellular calcium concentrations or increasing myocardial oxygen demand.  BiDil, a combination drug containing isosorbide dinitrate and hydralazine, approved only for the treatment of HF in African Americans who are already being treated with standard therapy. o Diet education and weight management are critical to the patient’s control of chronic HF.  Diet and weight management recommendations must be individualized and culturally sensitive if the necessary changes are to be realized.  A detailed diet history should be obtained and should include the
More Less

Related notes for BIOC33H3

Log In


OR

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


OR

By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.


Submit