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Physical Examination of the Heart

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Updated: Thursday, Mar 19,2009, 11:19:51 AM
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1. Jugular venous pulse (JVP). Two types of information are obtained from the JVP: the quality of the wave form and the central venous pressure (CVP).
 

(1) Technique of examination. The JVP is best observed in the right internal jugular vein. With normal CVP, the JVP is assessed with the patient's trunk raised less than 30 degrees. With elevated CVP the patient's trunk must be raised higher, sometimes to as much as 90 degrees. The JVP is accentuated by turning the patient's head away from the examiner and shining a flashlight obliquely across the skin overlying the vein.
 
(2) Wave form of the JVP. Two waves per heartbeat are generally visible in the JVP: the A wave and the V wave. The A wave appears as a brief "flicker" and represents increased venous pressure resulting from atrial contraction. The V wave is a longer surge that follows the A wave and represents increased venous pressure transmitted during ventricular contraction. The drop in pressure following the A wave is called the X descent, and the fall in pressure after the V wave is denoted as the Y descent. The JVP waves should be timed with simultaneous palpation of the carotid artery. The A wave immediately precedes the carotid pulse; the V wave follows the pulse. The diagnosis of a variety of pathologic states is assisted by observation of abnormalities in the JVP wave forms (Table 1-1).
 

 
(3) Determination of CVP. CVP can be estimated by observing the vertical distance from the top of the V wave to the right atrium. In the individual with normal CVP, the V wave rises 1-2 cm above the sternal angle. When the V wave rises to more than halfway to the angle of the jaw in a patient who is not recumbent, elevated CVP is present. In some pathologic conditions (e.g., cardiac tamponade, constrictive pericarditis), CVP may be so high that A and V waves are above the angle of the jaw. In this setting, exaggerated X and Y descents may suggest the diagnosis. As a rule of thumb, for a patient sitting upright, a JVP visible at the sternal angle represents a CVP of approximately 10 mm Hg.
 
 
 
During inspiration the height of the JVP typically declines (although amplitude of the X and Y descents will increase). In certain pathologic conditions such as chronic constrictive pericarditis and occasionally tricuspid stenosis, congestive heart failure, right ventricular dysfunction, or infarction the JVP actually increases with inspiration. This important clinical finding is known as Kussmaul's sign.

 
2. Arterial pressure pulse. The central arterial pressure pulse is characterized by a rapid rise to a rounded shoulder peak with a less rapid decline. Information about the adequacy of ventricular contraction and possible obstruction of the left ventricular outflow tract may be assessed by palpation of the carotid artery. By the time the pulse wave is transmitted to peripheral arteries, much of this initial information is lost; however, pulsus alternans is best evaluated in peripheral arteries.
 
A variety of pathologic conditions alters the characteristics of the carotid pulse. These conditions, and the corresponding modifications of the carotid pulse, are listed in Table 1-2. In patients with unexplained hypertension, simultaneous palpation of radial and femoral arterial pulses helps to rule out coarctation of the aorta.
 
 
 
3. Precordial palpation. Information concerning the location and quality of the left ventricular impulse is available through precordiat palpation. In addition, intensity of murmurs may be gauged by palpating associated thrills. Palpation is best accomplished using the fingertips, with the patient either supine or in the left lateral decubitus position. Simultaneous auscultation can aid in the timing of events. A list of abnormalities detected by precordial palpation and their significance is found in Table 1-3.
 

Auscultation
 
 
1. Sl. The first heart sound (SI) occurs at the time of closure of the mitral and tricuspid valves. It is probably generated by the closure of the valves. Si is frequently split (with mitral closure preceding tricuspid), but this event is often hard to appreciate and of little clinical relevance. More important is variation in intensity of the first sound. S1 varies with the P-R interval of the ECG. The shorter the P-R interval, the louder the Si. The best example of S1 variation with P-R interval occurs in complete heart block, in which atrial and ventricular contractions are dissociated.
 
 
S1 may be loud and "snapping" in quality in mitral stenosis, indicating both that the valve is pliable and that it remains wide open at the beginning of isovolumic contraction. Conversely, a diminished or absent S1 in mitral stenosis suggests a rigidly calcified valve that cannot "snap" shut.
 

 
Other situations in which S1 may be diminished include mitral regurgitation, slow heart rates (long P-R interval), poor sound conduction through the chest wall, and a slow rise of left ventricular pressure. A summary of clinical information derived from variations in S1 is found in Table 1-4.
 
 
2. S2. In contrast to S1, in which splitting is less important than changes in intensity, S2 reveals variations in both splitting and intensity that provide important clinical information.
 
 
 
The second heart sound (S2) occurs at the time of closure of the aortic and pulmonic valves. In normal circumstances, aortic closure precedes pulmonic closure (A2 followed by P2). Under normal circumstances, the split in S2 is maximal at the end of Inspiration and minimal at the end of expiration. This phenomenon reflects an underlying movement of P2 with respect to a relatively constant A2. During inspiration, right ventricular filling increases and P2 is delayed, causing the widely split S2. During expiration, less right ventricular filling occurs and P2 "closes" toward A2, causing a diminished split in S2. This "normal splitting" of S2 is invariably present in individuals under 30 years of age, provided heart rates are not markedly accelerated. It is best appreciated over the "pulmonic area" and can be heard with either the bell or the diaphragm.
 
 
(1) Fixed splitting of S2. The most common abnormality Of S2 is failure of splitting to close at the end of expiration. This "fixed splitting" occurs for either of two reasons: 1>2 is delayed or A2 is early. A split of S2 on expiration may also represent a normal variant. In the latter setting, however, some difference in the degree of split should occur between inspiration and expiration.
 
 
 
Fixed splitting of S2 due to delayed P2 is found in four clinical settings: acute right-heart pressure overload (e.g., pulmonary embolism), right bundle branch block, atrial septal defect (ASD), and pulmonic stenosis.
 
 
 
(2) Paradoxical splitting of S2. Paradoxical splitting of S2 is said to be present when S2 splits on expiration and closes on inspiration. Although fixed splitting denotes delay in normal closure of the pulmonic valve, paradoxical splitting denotes delayed closure of the aortic valve. This important clinical sign never occurs in the absence of cardiac disease. The most common states in which paradoxical splitting is encountered are aortic stenosis and left bundle branch block. Paradoxical splitting takes place in about 25% of individuals with these conditions.
 
Paradoxical splitting may occur in patients with coronary artery disease or hypertension or both. In these individuals a closely split S2 may be observed to close to a single sound at midinspiration. A similar finding is often made in early stages of aortic stenosis or in incomplete leil bundle branch block.
 
 
Alterations in the intensity of S2 can also yield important clinical information. A2 is frequently decreased in aortic stenosis. The presence of a normal A2 when aortic stenosis is clinically suspected raises the question of outflow obstruction at a site other than the valve. P2 may be augmented in pulmonary hypertension and diminished in pulmonic stenosis. Finally, P2 may appear unusually loud in thin-chested individuals without cardiac disease. A summary of clinical information derived from alterations in S2 is found in Table 1-5.
 

3. S3. The third heart sound (S3, or ventricular gallop) is low-pitched and best heard at the apex with the stethoscope bell. The S3 is probably the result of rapid filling and stretching of an abnormal left ventricle. The cadence of the S3 has been likened to the y in Kentucky. An S3 may be heard in any condition resulting in rapid ventricular filling. It is frequently an early sign of left ventricular failure. Third heart sounds may also be present in atrial septal defect, mitral or aortic insufficiency, ventricular septal defect, and patent ductus arteriosus. An S3 can also be a normal variant, particularly in young adults. A loud, early diastolic sound is often heard in constrictive pericarditis. This "pericardial knock" may be mistaken for an S3.
 
 
4. S4. The fourth heart sound (S4, atrial gallop, presystolic gallop) is also the result of altered ventricular compliance. Its cadence has been likened to the soft a of appendix. It is a low-pitched sound, best heard with the stethoscope bell. It is loudest at the apex and may be accentuated by placing the patient in the left lateral decubitus position. The presence of an S4 implies effective atrial contraction; it is never heard in atrial fibrillation. An S4 may be heard in any condition causing reduced ventricular compliance: aortic stenosis, systemic or pulmonary hypertension, coronary artery disease, hypertrophic cardiomyopathy, acute mitral regurgitation, and myocardial infarction.



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