Approach to Cardiac Disease Diagnosis-3

Approach to Cardiac Disease Diagnosis
CURRENT Diagnosis & Treatment in Cardiology

Approach to Cardiac Disease Diagnosis

Michael H. Crawford, MD

Physical Findings(cont'd)

5. Cardiac auscultation—Heart sounds are caused by the acceleration and deceleration of blood and the subsequent vibration of the cardiac structures during the phases of the cardiac cycle. To hear cardiac sounds, use a stethoscope with a bell and a tight diaphragm. Low-frequency sounds are associated with ventricular filling and are heard best with the bell. Medium-frequency sounds are associated with valve opening and closing; they are heard best with the diaphragm. Cardiac murmurs are due to turbulent blood flow, are usually high-to-medium frequency, and are heard best with the diaphragm. Low-frequency atrioventricular valve inflow murmurs, such as that produced by mitral stenosis, are best heard with the bell, however. Auscultation should take place in areas that correspond to the location of the heart and great vessels. Such placement will, of course, need to be modified for patients with unusual body habitus or an unusual cardiac position. When no cardiac sounds can be heard over the precordium, they can often be heard in either the subxiphoid area or the right supraclavicular area.
Auscultation in various positions is recommended because low-frequency filling sounds are best heard with the patient in the left lateral decubitus position, and high-frequency murmurs, such as that of aortic regurgitation, are best heard with the patient sitting.
a. Heart sounds—The first heart sound is coincident with mitral and tricuspid valve closure and has two components in up to 40% of normal individuals. There is little change in the intensity of this sound with respiration or position. The major determinant of the intensity of the first heart sound is the electrocardiographic PR interval, which determines the time delay between atrial and ventricular contraction and thus the position of the mitral valve when ventricular systole begins. With a short PR interval, the mitral valve is widely open when systole begins, and its closure increases the intensity of the first sound, as compared to a long PR-interval beat when the valve partially closes prior to the onset of ventricular systole. Certain disease states, such as mitral stenosis, also can increase the intensity of the first sound.
The second heart sound is coincident with closure of the aortic and pulmonic valves. Normally, this sound is single in expiration and split during inspiration, permitting the aortic and pulmonic components to be distinguished. The inspiratory split is due to a delay in the occurrence of the pulmonic component because of a decrease in pulmonary vascular resistance, which prolongs pulmonary flow beyond the end of right ventricular systole. Variations in this normal splitting of the second heart sound are useful in determining certain disease states. For example, in atrial septal defect, the second sound is usually split throughout the respiratory cycle because of the constant increase in pulmonary flow. In patients with left bundle branch block, a delay occurs in the aortic component of the second heart sound, which results in reversed inspiratory splitting; single with inspiration, split with expiration.
A third heart sound occurs during early rapid filling of the left ventricle; it can be produced by any condition that causes left ventricular volume overload or dilatation. It can therefore be heard in such disparate conditions as congestive heart failure and normal pregnancy. A fourth heart sound is due to a vigorous atrial contraction into a stiffened left ventricle and can be heard in left ventricular hypertrophy of any cause or in diseases that reduce compliance of the left ventricle, such as myocardial infarction.
Although third and fourth heart sounds can occasionally occur in normal individuals, all other extra sounds are signs of cardiac disease. Early ejection sounds are due to abnormalities of the semilunar valves, from restriction of their motion, thickening, or both (eg, a bicuspid aortic valve, pulmonic or aortic stenosis). A midsystolic click is often due to mitral valve prolapse and is caused by sudden tensing in midsystole of the redundant prolapsing segment of the mitral leaflet. The opening of a thickened atrioventricular valve leaflet, as in mitral stenosis, will cause a loud opening sound (snap) in early diastole. A lower frequency (more of a knock) sound at the time of rapid filling may be an indication of constrictive pericarditis. These early diastolic sounds must be distinguished from a third heart sound.
b. Murmurs—Systolic murmurs are very common and do not always imply cardiac disease. They are usually rated on a scale of 1 to 6, where grade 1 is barely audible, grade 4 is associated with palpable vibrations (thrill), grade 5 can be heard with the edge of the stethoscope, and grade 6 can be heard without a stethoscope. Most murmurs fall in the 1–3 range, and murmurs in the 4–6 range are almost always due to pathologic conditions; severe disease can exist with grades 1–3 or no cardiac murmurs, however. The most common systolic murmur is the crescendo/decrescendo murmur that increases in intensity as blood flows early in systole and diminishes in intensity through the second half of systole. This murmur can be due to vigorous flow in a normal heart or to obstructions in flow, as occurs with aortic stenosis, pulmonic stenosis, or hypertrophic cardiomyopathy. The so-called innocent flow murmurs are usually grades 1–2 and occur very early in systole; they may have a vibratory quality and are usually less apparent when the patient is in the sitting position (when venous return is less). If an ejection sound is heard, there is usually some abnormality of the semilunar valves. Although louder murmurs may be due to pathologic cardiac conditions, this is not always so. Distinguishing benign from pathologic systolic flow murmurs is one of the major challenges of clinical cardiology. Benign flow murmurs can be heard in 80% of children; the incidence declines with age, but may be prominent during pregnancy or in adults who are thin or physically well trained. The murmur is usually benign in a patient with a soft flow murmur that diminishes in intensity in the sitting position and neither a history of cardiovascular disease nor other cardiac findings.
The holosystolic, or pansystolic, murmur is almost always associated with cardiac pathology. The most common cause of this murmur is atrioventricular valve regurgitation, but it can also be observed in conditions such as ventricular septal defect, in which an abnormal communication exists between two chambers of markedly different systolic pressures. Although it is relatively easy to determine that these murmurs represent an abnormality, it is more of a challenge to determine their origins. Keep in mind that such conditions as mitral regurgitation, which usually produce holosystolic murmurs, may produce crescendo/decrescendo murmurs, adding to the difficulty in differentiating benign from pathologic systolic flow murmurs.
Diastolic murmurs are always abnormal. The most frequently heard diastolic murmur is the high-frequency decrescendo early murmur of aortic regurgitation. This is usually heard best at the upper left sternal border or in the aortic area (upper right sternal border) and may radiate to the lower left sternal border and the apex. This murmur is usually very high frequency and may be difficult to hear. Although the murmur of pulmonic regurgitation may sound like that of aortic regurgitation when pulmonary artery pressures are high, it is usually best heard in the pulmonic area (left second intercostal space parasternally). If structural disease of the valve is present with normal pulmonary pressures, the murmur usually has a midrange frequency and begins with a slight delay after the pulmonic second heart sound. Mitral stenosis produces a low-frequency rumbling diastolic murmur that is decrescendo in early diastole, but may become crescendo up to the first heart sound with moderately severe mitral stenosis and sinus rhythm. The murmur is best heard at the apex in the left lateral decubitus position with the bell of the stethoscope. Similar findings are heard in tricuspid stenosis, but the murmur is loudest at the lower left sternal border.
A continuous murmur implies a connection between a high- and a low-pressure chamber throughout the cardiac cycle, such as occurs with a fistula between the aorta and the pulmonary artery. If the connection is a patent ductus arteriosus, the murmur is heard best under the left clavicle; it has a machine-like quality. Continuous murmurs must be distinguished from the combination of systolic and diastolic murmurs in patients with combined lesions (eg, aortic stenosis and regurgitation).
Traditionally, the origin of heart murmurs was based on five factors: (1) their timing in the cardiac cycle, (2) where on the chest they were heard, (3) their characteristics, (4) their intensity, and (5) their duration. Unfortunately, this traditional classification system is unreliable in predicting the underlying pathology. A more accurate method, dynamic auscultation, changes the intensity, duration, and characteristics of the murmur by bedside maneuvers that alter hemodynamics.
The simplest of these maneuvers is observation of any changes in murmur intensity with normal respiration because all right-sided cardiac murmurs should increase in intensity with normal inspiration. Although some exceptions exist, the method is very reliable for detecting such murmurs. Inspiration is associated with reductions in intrathoracic pressure that increase venous return from the abdomen and the head, leading to an increased flow through the right heart chambers. The consequent increase in pressure increases the intensity of right-sided murmurs. These changes are best observed in the sitting position, where venous return is smallest, and changes in intrathoracic pressure can produce their greatest effect on venous return. In a patient in the supine position, when venous return is near maximum, there may be little change observed with respiration. The ejection sound caused by pulmonic stenosis does not routinely increase in intensity with inspiration. The increased blood in the right heart accentuates atrial contraction, which increases late diastolic pressure in the right ventricle, partially opening the stenotic pulmonary valve and thus diminishing the opening sound of this valve with the subsequent systole.
Changes in position are an important part of normal auscultation; they can also be of great value in determining the origin of cardiac murmurs (Table 1–2). Murmurs dependent on venous return, such as innocent flow murmurs, are softer or absent in upright positions; others, such as the murmur associated with hypertrophic obstructive cardiomyopathy, are accentuated by reduced left ventricular volume. In physically capable individuals, a rapid squat from the standing position is often diagnostically valuable because it suddenly increases venous return and left ventricular volume and accentuates flow murmurs but diminishes the murmur of hypertrophic obstructive cardiomyopathy. The stand- squat maneuver is also useful for altering the timing of the midsystolic click caused by mitral valve prolapse during systole. When the ventricle is small during standing, the prolapse occurs earlier in systole, moving the midsystolic click to early systole. During squatting, the ventricle dilates and the prolapse is delayed in systole, resulting in a late midsystolic click.

Table 1–2. Differentiation of systolic murmurs based on changes in their intensity from physiologic maneuvers.


Valsalva's maneuver is also frequently used. The patient bears down and expires against a closed glottis, increasing intrathoracic pressure and markedly reducing venous return to the heart. Although almost all cardiac murmurs decrease in intensity during this maneuver, there are two exceptions: (1) The murmur of hypertrophic obstructive cardiomyopathy may become louder because of the diminished left ventricular volume. (2) The murmur associated with mitral regurgitation from mitral valve prolapse may become longer and louder because of the earlier occurrence of prolapse during systole. When the maneuver is very vigorous and prolonged, even these two murmurs may eventually diminish in intensity. Therefore, the Valsalva maneuver should be held for only about 10 s, so as not to cause prolonged diminution of the cerebral and coronary blood flow.
Isometric hand grip exercises have been used to increase arterial and left ventricular pressure. These maneuvers increase the flow gradient for mitral regurgitation, ventricular septal defect, and aortic regurgitation; the murmurs should then increase in intensity. Increasing arterial and left ventricular pressure increases left ventricular volume, thereby decreasing the murmur of hypertrophic obstructive cardiomyopathy. If the patient is unable to perform isometric exercises, transient arterial occlusion of both upper extremities with sphygmomanometers can achieve the same increases in left-sided pressure.
Noting the changes in murmur intensity in the heart beat following a premature ventricular contraction, and comparing these to a beat that does not, can be extremely useful. The premature ventricular contraction interrupts the cardiac cycle, and during the subsequent compensatory pause, an extralong diastole occurs, leading to increased left ventricular filling. Because of this, the murmurs of hypertrophic cardiomyopathy and mitral valve prolapse decrease in intensity, and murmurs caused by the flow of blood out of the left ventricle increase in intensity. There is usually no change in the intensity of the murmur of typical mitral regurgitation because blood pressure falls during the long pause and increases the gradient between the left ventricle and the aorta, allowing more forward flow. This results in the same amount of mitral regurgitant flow as on a normal beat with a higher aortic pressure and less forward flow. The increased volume during the long pause goes out of the aorta rather than back into the left atrium. Unfortunately, there is no reliable way of inducing a premature ventricular contraction in most patients; it is fortuitous when a physician is present for one. Atrial fibrillation with markedly varying cycle lengths produces the same phenomenon and can be very helpful in determining the origin of murmurs.
Various rapid-acting pharmacologic agents have been used to clarify the origin of cardiac murmurs. A once-popular bedside pharmacologic maneuver was the inhalation of amyl nitrite. Because this produces rapid vasodilatation and decreases in blood pressure, it diminishes the murmurs of aortic and mitral regurgitation and ventricular septal defect and increases systolic flow murmurs (eg, those caused by aortic stenosis and hypertrophic obstructive cardiomyopathy). Although patients never liked the unpleasant odor of amyl nitrite, it became a popular recreational drug in the 1970s; its popularity has since waned. Other pharmacologic maneuvers have occasionally been used to clarify the origin of a murmur. These include the infusion of synthetic catecholamines to increase blood pressure, isoproterenol to increase the heart rate, and intravenous b-blockers to decrease the heart rate. With the ready availability of echocardiography, these more invasive interventions have also diminished in popularity.

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