Medicine (National Medical Series) / Edition 3

Medicine (National Medical Series) / Edition 3

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Lippincott Williams & Wilkins


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Medicine (National Medical Series) / Edition 3

The National Medical Series for Independent Study (NMS) presents an effective system for learning and review. The books in the series are outlines of the basic and clinical sciences with USMLE-type questions and annotated answers.

The National Medical Series has been designed for medical students who want to:

  • Master large amounts of information in a limited amount of time

  • Review specific topics quickly and easily

The books in the basic science group are intended as course supplements and reviews to help students prepare for the United States Medical Licensing Examination (USMLE) Step 1. The clinical science books are intended for use during clinical rotations and to help students prepare for the USMLE Step 2.

Product Details

ISBN-13: 9780683181050
Publisher: Lippincott Williams & Wilkins
Publication date: 01/28/1997
Series: National Medical Series
Edition description: Older Edition
Pages: 752
Product dimensions: 6.99(w) x 9.87(h) x 1.20(d)

Read an Excerpt

Chapter 1: Cardiovascular Diseases

1. Congestive Heart Failure

A. Definition. Congestive heart failure is the inability of the heart, working at normal or elevated filling pressure, to pump enough blood to meet the oxygen requirements of the body tissues. Congestive heart failure should never be considered a diagnosis. Rather, it is a syndrome resulting from many diseases that interfere with cardiac function. In acting as a muscular pump the heart does only two things: it contracts (systole) and it relaxes (diastole). Therefore, heart failure can result from only two broad abnormalities-systolic dysfunction and diastolic dysfunction.

B. Etiology

which the heart must contract.

a. Decreased contractility. Most cases of congestive heart failure occur when an insult to the myocardium reduces its ability to generate force, thus reducing its contractility.

(1) Myocardial infarction. In myocardial infarction, a portion of the myocardium undergoes necrosis and can no longer generate force, resulting in weakening of the ventricle. If extensive areas of the myocardium are infarcted, congestive heart failure results.

(2) Valvular heart disease results in stenosis or regurgitation of the cardiac valves, which places a pressure or volume overload, respectively, on the ventricles. Initially, compensatory mechanisms [see I B 1 c] accommodate these overloads and maintain normal cardiac output at acceptable filling pressure. However, eventually these mechanisms fail and heart failure ensues.

(3) Hypertension. Many patients who develop congestive heart failure have had systemic hypertension at some time in the clinical course of their illness. Persistent severe hypertension is associated with a contractile deficit that leads to congestive heart failure.

(4) Cardiomyopathies are diseases that directly injure the myocardium.

(a) Toxic. Substances directly toxic to the myocardium (e.g., ethanol, cobalt, catecholamines) may damage its force-generating ability. Prolonged exposure to these agents may lead to the development of congestive heart failure.

(b) Idiopathic. When the contractile function of the myocardium fails in the absence of a known etiology, a viral cause often is implied but frequently cannot be proven.

(c) Infiltrative diseases. Infiltration of the myocardium by a variety of substances (e.g., amyloid) may reduce contractility.

b. Increased afterload. Increasing the afterload makes it harder for the ventricular muscle fibers to shorten, reducing cardiac output. Afterload can be quantified by calculating the systolic force on the myocardium using the Laplace equation for stress:

Stress = (pressure x radius)/(2 x thickness)

Thus, disease states that increase either the systolic pressure (hypertension, aortic stenosis) or chamber radius (dilated cardiomyopathy, valvular regurgitation) increase afterload unless the wall thickness increases proportionately.

c. Compensatory mechanisms develop in response to the ventricular pressure and volume overload that accompany decreased contractility.

(1) The Frank-Starling mechanism is activated when reduced ventricular emptying results in more volume retained in the ventricles at the end of systole, which leads to a greater volume at the end of diastole. Increased end-diastolic volume increases sarcomere stretch, which increases the number of systolic actin-myosin crossbridges that develop. The increased number of crossbridges increases the strength of contraction.

(2) Cardiac hypertrophy provides additional muscle mass to bear the burden of various overloads.

(3) Adrenergic stimulation by endogenous catecholamines increases the inotropic state.

2. Diastolic dysfunction. Diastole is governed by active and passive properties. Active relaxation occurs early in diastole as calcium is pumped out of the myocardium, resulting in the near cessation of actin-myosin crossbridge interaction. Passive relaxation occurs as the mitral valve opens, allowing the blood stored in the atria to fill the ventricles.

a. Abnormalities in active relaxation. Active relaxation is impaired when there is delay in calcium reuptake at the beginning of diastole. Myocardial ischemia and ventricular hypertrophy are two common causes of impaired active relaxation.

b. Abnormalities of passive relaxation. Passive relaxation is impaired when the myocardium is stiffer than normal. Stiffness is defined as a change in pressure (AP) per unit change in volume (AV), or dP/dV. When stiffness is increased, any change in volume requires or causes a greater increase in pressure. Thus, in order to fill the heart to an adequate volume, high filling pressure occurs, which in turn leads to pulmonary and systemic congestion. Increased passive stiffness of the ventricles occurs when concentric hypertrophy causes the chamber wall to be thicker than normal as might occur in hypertension or when the myocardium is infiltrated by abnormal substances such as amyloid.

C. Descriptive terminology

1. High-output failure is characterized by cardiac output that may be several times higher than normal but still is not adequate to maintain tissue perfusion needs or, if adequate, is maintained with a higher than normal filling pressure. A classic example of high-output failure is chronic severe anemia, which causes a reduced oxygen-carrying capacity. In chronic severe anemia, the following occurs:

a. Compensation is provided by increased forward cardiac output, which is facilitated by cardiac enlargement, decreased total peripheral resistance, and increased venous return to the heart.

b. This causes a volume overload of ventricles.

c. Eventually, the demands on the heart lead to cardiac failure; cardiac output, although high, still is not adequate to meet the circulatory demands placed on the heart by the anemia. Some other causes of high output failure include arteriovenous fistula, beriberi, and thyrotoxicosis.

2. Left-sided failure indicates that the left ventricle is the failing chamber. A disease that primarily affects the left ventricle (e.g., myocardial infarction) may reduce its contractile force, while the right ventricle continues to pump normally. Thus, left ventricular failure can occur without right ventricular failure.

3. Right-sided failure indicates that the right ventricle has failed, either as a result of left ventricular failure, or in isolation from the left ventricle.

a. The most common cause of right ventricular failure is left ventricular failure. When left ventricular failure occurs, the filling pressure in the left ventricle becomes elevated, increasing the work load of the right ventricle (the chamber responsible for filling the left ventricle). Thus overtaxed, the right ventricle eventually fails also.

b. The right ventricle also may fail in isolation from the left ventricle. In the presence of chronic obstructive pulmonary disease (COPD), increased pulmonary vascular resistance develops as a result of architectural changes in the lungs. The increased pulmonary vascular resistance, in turn, produces a pressure overload on the right ventricle, which leads to increased right ventricular work and eventual failure. Pulmonary embolism and primary pulmonary hypertension are some other causes of right-sided failure.

D. Clinical features

1. Symptoms

a. Dyspnea is the most frequently encountered symptom of congestive heart failure.

(1) The feeling of breathlessness is caused by vascular congestion, which reduces pulmonary oxygenation. In addition, the vascular congestion diminishes lung compliance, increasing the work of breathing, thus adding to the feeling of breathlessness.

(2) Dyspnea also results from reduced cardiac output to the periphery, which triggers the symptom through neurohumoral mechanisms. In the early stages of congestive heart failure, dyspnea occurs only with exertion. As heart failure progresses, the amount of exertion required to produce dyspnea becomes progressively less until dyspnea may occur at rest.

b. Orthopnea refers to dyspnea that occurs in the recumbent position and is relieved by elevation of the head. Orthopnea results from volume pooling in the central vasculature during recumbency, which leads to increased cardiac volume and, in turn, to increased left ventricular filling pressure, pulmonary congestion, and the feeling of dyspnea. The physician may gauge the degree of orthopnea by noting the number of pillows the patient uses to sleep. However, it should be recognized that many patients chronically sleep on more than one pillow out of habit, not because of breathlessness. Nocturnal cough, which has the same pathophysiology as orthopnea, may occur together with, or instead of, nocturnal dyspnea.

c. Paroxysmal nocturnal dyspnea is the occurrence of sudden dyspnea that awakens the patient from sleep. Like orthopnea, it occurs during recumbency as a result of pooling in the central vasculature, which increases left ventricular filling pressure. Paroxysmal nocturnal dyspnea may occur in the orthopneic patient who inadvertently slips off the pillows used to elevate the upper body. Usually, the patient awakens from sleep and feels the need to sit upright or to go to an open window for increased ventilation. The symptom usually subsides after the patient has been in the upright position for 5-20 minutes.

d. Nocturia develops in congestive heart failure as a result of increased renal blood flow when the patient is recumbent and asleep.

(1) During the day, when the skeletal muscles are active, limited cardiac output is shifted away from the kidney toward the skeletal musculature. The kidney interprets this reduction in blood flow as hypovolemia and becomes sodium avid via activation of the renin-angiotensin system.

(2) At night, when the patient is at rest, cardiac output is shifted toward the kidney and diuresis ensues.

e. Edema. There are many causes of peripheral edema, several of which are noncardiac. Cardiac edema occurs when the systemic hydrostatic venous pressure is greater than the systemic oncotic venous pressure. Thus, cardiac edema is a sign of right-sided failure; it occurs because of the increased systemic venous pressure that results from right ventricular dysfunction.

f. Anorexia may occur as a late manifestation of congestive heart failure. The exact mechanism leading to anorexia is unknown, but the occurrence of anorexia seems to correlate with hepatic congestion and right-sided failure...

Table of Contents

1 Cardiovascular Diseases
2 Pulmonary Diseases
3 Hematologic Diseases
4 Oncologic Diseases
5 Gastrointestinal Diseases
6 Renal Diseases, Fluid and Electrolyte Disorders, and Hypertension
Part I: Renal Diseases
Part II: Fluid and Electrolyte Disorders
Part III: Hypertension
7 Allergic and Immunologic Disorders
8 Infectious Diseases
9 Endocrine and Metabolic Diseases
10 Rheumatic Diseases

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