Auscultation

Question 0

Major components of heart sounds.

Answer 0

Vibrations associated with the abrupt acceleration or deceleration of blood.

Question 1

Events in the cardiac cycle that can help determine timing of a heart sound or murmur.

Answer 1

Carotid arterial pulse, JVP and apical impulse

Question 2

Factors that influence the intensity of S1

Answer 2

(1) the position of the mitral leaflets at the onset of ventricular systole; (2) the rate of rise of the left ventricular pressure pulse; (3) the presence or absence of structural disease of the mitral valve; (4) the amount of tissue, air, or fluid between the heart and the stethoscope.

Question 3

Causes of a loud S1

Answer 3

(1) Diastole is shortened because of tachycardia (2) AV flow is increased because of high cardiac output or prolonged because of mitral stenosis (3) Atrial contraction precedes ventricular contraction by an unusually short interval, reflected in a short PR interval

Question 4

Cause of loud S1 in mitral stenosis

Answer 4

Open valve at the onset of isovolumetric

contraction because of the elevated left atrial pressure.

Question 5

Causes of a soft S1

Answer 5

(1) Poor conduction of sound through the chest wall (2) Slow
rise of the left ventricular pressure pulse (3) Long PR interval (4) Imperfect closure (5) Anterior mitral leaflet is immobile because of rigidity and calcification, even in the presence of predominant mitral stenosis

Question 6

What is normal splitting of S1?

Answer 6

Split of 10-30 ms. First component is MV closure and second is TV.

Question 7

Most common cause of a widened, split S1.

Answer 7

Complete right bundle branch block which causes delay in onset of RV pressure pulse.

Question 8

Cause of split S2

Answer 8

Increased RV stroke volume during inspiration.

Question 9

Why does A2 occur before P2?

Answer 9

Pulmonary arterial pressure is less than aortic pressure (i.e, pulmonary resistance to forward flow from ventricles is less than aortic resistance ). Therefore as pulmonary impedance is less, even after right ventricular systolic contraction, blood continues to flow through valve until pulmonary arterial pressure increases more than right ventricle). But as aortic impedance is more ,it stops blood flow through the aortic valve before itself. Due to the above reasons ,right ventricular ejection begins prior to left ventricular ejection, has a slightly longer duration, and terminates after left ventricular ejection, resulting in P2 normally occurring after A2

Question 10

What is hangout interval?

Answer 10

It is a measure of impedance in the artery system into which blood is being ejected. In the highly compliant pulmonary vascular bed, it is a determinant of RV ejection. May vary from 30 to 120 msec. The pulmonary valve is suppose to close at the point of cross-over of ventricular pressure and arterial pressure but this is not the case in reality. The time interval from cross-over of pressures to actual occurance of sound is called hangout interval. The duration of the hangout interval is inversely related to the vascular impedance. In contrast, hangout interval is negligible because the high impendance of the aorta causes the valve to close.

Question 11

What conditions affect hangout time?

Answer 11

The interval is prolonged, and physiologic splitting of S2 is accentuated, in conditions associated with right ventricular volume overload and a distensible pulmonary vascular bed. In patients with an increase in pulmonary vascular resistance, the hangout time is markedly reduced, and narrow splitting of S2 is present.

Question 12

Splitting that persists with expiration (heard best at the pulmonic area or left sternal border) is usually abnormal when the patient is in the upright position. What are some causes?

Answer 12

Delayed activation of the right ventricle (right bundle branch block); left ventricular ectopic beats; a left ventricular pacemaker; prolongation of right ventricular contraction with an increased right ventricular pressure load (pulmonary embolism or pulmonic stenosis); or delayed pulmonic valve closure because of right ventricular volume
overload associated with right ventricular failure or diminished impedance of the pulmonary vascular bed and a prolonged hangout time (atrial septal defect).

Question 13

Changes in P2 and splitting in pulmonary hypertension.

Answer 13

P2 is loud, and splitting of S2 may be diminished, normal, or accentuated, depending on the cause of the pulmonary hypertension, the pulmonary vascular resistance, and the presence or absence of right ventricular decompensation.

Question 14

Effect of mitral regurgitation and VSD in S2 splittting.

Answer 14

Early aortic valve closure may also produce splitting that persists during expiration.

Question 15

What is the cause of fixed splittig in ASD?

Answer 15

The proportion of right atrial filling contributed by the left atrium and the venae cavae varies reciprocally during the respiratory cycle, so that right atrial inflow remains relatively constant.
Therefore, the volume and duration of right ventricular ejection are not significantly increased by inspiration, and there is little inspiratory exaggeration of the splitting of S2.

Question 16

What is paradoxic splittig of S2?

Answer 16

P2 is heard before A2. Splitting is then maximal in expiration and decreases during inspiration with the normal delay of pulmonic valve closure.

Question 17

What are some causes of paradoxic split of S2?

Answer 17

Most common causes of reversed splitting of S2 are left bundle branch block and delayed excitation of the left ventricle from a right ventricular ectopic beat. Mechanical prolongation of left ventricular systole, resulting in reversed splitting of S2, may
also be caused by severe aortic outflow obstruction, a large aorta-to-pulmonary
artery shunt, systolic hypertension, and ischemic heart disease or cardiomyopathy with left ventricular failure.

Question 18

Intensity of P2 compared to A2.

Answer 18

P2 is normally softer than A2 in the second left intercostal space; a P2 that is greater
than A2 in this area suggests pulmonary hypertension (except in patients with atrial septal defect).

Question 19

What systolic sounds may be present on auscultation?

Answer 19

Ejection sound: A sharp, high-pitched event occurring in early systole and closely following the first heart sound. Ejection sounds occur in the presence of semilunar valve stenosis and in conditions associated with dilation of the aorta or pulmonary artery. Nonejection clicks, or midsystolic clicks: Occurring with or without a late systolic murmur, often denote prolapse of one or both leaflets of the mitral valve.

Question 20

What diastolic sounds may be present on auscultation?

Answer 20

Opening snap (OS): A brief, highpitched, early diastolic sound, which is usually due to stenosis of an AV valve, most often the mitral valve. It is generally heard best at the lower left sternal border and radiates well to the base of the heart. The OS of tricuspid stenosis occurs later in diastole than the mitral OS and is often overlooked. A tumor plop in patients with left atrial myxoma may have the timing of an opening snap, but it is usually lower-pitched. Third heart sound (S3): A low-pitched sound produced in the ventricle after A2, at the termination of rapid filling. Frequent in normal children and in patients with high cardiac output. In patients over 40 years, an S3 usually indicates impairment of ventricular function, AV valve regurgitation, or other conditions that increase the rate or volume of ventricular filling. The left-sided S3 is best heard with the bell at the left ventricular apex during expiration and with the patient in the left lateral position. The right-sided S3 is best heard at the left sternal border or just beneath the xiphoid and is usually louder with inspiration. Third heart sounds often disappear with treatment of heart failure. An S3 that is earlier (0.10–0.12 s after A2) and higher pitched than normal (a pericardial knock) often occurs in patients with constrictive pericarditis; its presence depends on the restrictive effect of the adherent pericardium, which abruptly halts diastolic filling. Fourth heart sound (S4): A low-pitched, presystolic sound produced in the ventricle during ventricular filling; it is associated with an effective atrial contraction and is best heard with the bell piece of the stethoscope. The sound is absent in patients with atrial fibrillation. Frequently present in patients with systemic hypertension, aortic stenosis, hypertrophic cardiomyopathy, ischemic heart disease, and acute mitral regurgitation.

Question 21

Heart sound most often heard in patients who acute MI and sinus rhythm?

Answer 21

S4. The S4 is loudest at the left ventricular apex when the patient is in the left lateral position and is accentuated by mild isotonic or isometric exercise in the supine position. An S4 frequently accompanies delayed AV conduction, even in the absence of clinically detectable heart disease. The incidence of an audible S4 increases with increasing age. Whether an audible S4 in adults without other evidence of cardiac disease is abnormal remains controversial.

Question 22

Cause of right-sided S4.

Answer 22

Right ventricular hypertrophy secondary to either pulmonic stenosis or pulmonary hypertension and frequently accompanies a prominent presystolic a wave in the JVP.