Cardiac sounds are often at the threshold of audibility. The human ear can only perceive sounds between 20 and 20,000   Hz: it can neither reach beyond (as dolphins and whales do) nor go below it (as elephants often do). Yet, in this range, it has a preferential bandwidth of 1000–5000   Hz, corresponding to that of the human voice. Yet, most cardiac sounds are <500   Hz. In fact, many are so low pitched to be almost inaudible (S₃ or S₄ can be <100   Hz).

Cardiac sounds are crammed in a very little time interval. At a rate of 70/minute, a cycle of 0.8 seconds can easily harbor four to five sounds, many barely detectable.

Hospital rooms are noisy.

Patients’ hair and respiration create misleading artifacts.

The obesity epidemic has given many patients a much fattier chest muffler.

Pathology has shifted from rheumatic to coronary, thus reducing the pool of teaching patients.

Our ever-increasing fascination with the inanimate and the machine (and the sophistication of technology), compounded by:

Medicolegal issues (which have made imaging a self-protecting necessity)

Patients’ demands and expectations

Reduced emphasis on bedside skills during training andreduced availability of teachers

Time constraints (which make resorting to technology an ever-increasing need)

Take your time.

Be thorough.

Control noise in the room.

Separate systole from diastole (easily done in normal rates by recognizing the acoustic differences of S₁ and S₂ plus the long and short intervals; in faster hearts, it may require simultaneous assessment of the arterial pulse or precordial impulse).

“Inch” (move your stethoscope inch by inch, from auscultatory area to auscultatory area).

Know how to use your tool: (1) bell versus diaphragm; (2) patient’s position (supine, seated, and left lateral decubitus); (3) changes with respiration; and (4) dynamic bedside maneuvers (straight-leg raising, squatting-standing, Valsalva, hand-gripping, exercise).

When challenged by feeble and crammed signals, focus on one sound at a time.

Develop pattern recognition. This means practice, practice, practice…. In fact, you may need to hear an individual acoustic event as many as 500 times before you can master it.

Aortic area: Second right parasternal interspace

Pulmonic area: Second left parasternal interspace

Erb’s point: Third left parasternal interspace (area of left ventricular outflow)

Mitral area: Apex (fifth interspace left midclavicular line)

Tricuspid area: Fourth to fifth left parasternal space, at times extending into the epigastrium/subxiphoid

1. Closure of the atrioventricular (A-V) valves

2. Opening of the semilunar valves. This in turn leads to two separate sounds, caused by:

Opening of the semilunar valves per se

Blood being ejected into the large vessels

S₂ is indeed louder than S₁ (usually as a result of either pulmonary or systemic hypertension).

S₂ is normal, whereas S1 is softer.

1. The rate of rise in left ventricular pressure: This is a function of ventricular contractility, with stronger contractions causing a faster rise in left ventricular pressure and thus brisker and more forceful A-V closure. Hence, a loud S₁ is typical of the hyperkinetic heart syndrome, whereas a soft (muffled) S₁ is instead common in congestive heart failure, whose failing ventricles can only generate a slow rise in systolic pressure.

2. The separation between atrioventricular leaflets at the onset of ventricular systole: The closer the leaflets, the softer S₁ is; conversely, the wider apart the leaflets, the louder S₁ is. This mechanism feeds into two other important variables:

The duration of the P-R interval: A short P-R forces the ventricles to contract while the leaflets are still widely separated, so that their closure occurs on a steeper part of the left ventricular pressure curve. This, in turn, means a more forceful and louder closure. Conversely, a long P-R provides enough time for the leaflets to come close to each other, thus softening S₁. A muffled S₁ used to be quite common in rheumatic fever with first- degree A-V block. The progressive P-R lengthening of the Wenckebach phenomenon may also gradually (and increasingly) soften S₁.

The atrioventricular pressure gradient: A large A-V pressure gradient keeps the leaflets widely separated until ventricular pressure rises high enough to shut them close. Since the closure takes place on a steeper part of the left ventricular pressure curve, it will be forceful and loud. Hence, the longer the ventricle has to contract in order to close the A-V valve, the louder S₁ will be. This is quite common in mitral stenosis, where it contributes to the loudness of S₁.

3. The thickness of the atrioventricular leaflet: The thicker the leaflets, the louder S₁ is (banging hardbacks against each other generates more noise than banging paperbacks). Still, a soft S₁ may indicate leaflets that are too rigid. Hence, a thickened and stenotic mitral valve may generate a booming S₁ early on in the disease, but a softer (or absent) S₁ when the leaflets get eventually calcified and fixed.

In second-degree A-V block, there is progressive softening of S₁, while S₂ remains constant. This is due to the increasing P-R lengthening, until a beat is eventually dropped. It is so typical of Mobitz I that Wenckebach could describe it even before electrocardiogram (ECG) availability.

In third-degree A-V block (typical of Morgagni-Adams-Stokes syndrome), the change in S₁ intensity is instead random and chaotic because the atrium and ventricle march to the beat of a different drummer, with rates that are totally independent—when ventricular contraction catches the A-V valves wide apart, S₁ booms; when it catches them partially closed, S₁ softens. The varying S₁ intensity is so typically random to allow the recognition of complete block just on the basis of auscultation (Table 11-1).

Thickening of the mitral leaflets: In the late stages of MS, however, leaflets can become stiff and poorly mobile, which, in turn, softens S₁ and eventually eliminates it.

High atrioventricular pressure gradient: This is produced by the stenotic valve and keeps the A-V leaflets maximally separated at the onset of ventricular contraction.

Hypertrophic ventricles

Holosystolic mitral valve prolapse with regurgitation (where the prolapse delays the tension of the redundant mitral leaflet, thus allowing it to occur at peak of ventricular contraction, which makes it louder). A similar mechanism takes place in:

A left-atrial myxoma. Here it is the tumor that delays the closure of the mitral valve, thus allowing it to occur at peak of ventricular contraction and making it, therefore, louder. As a result, 80% of patients with this condition will have a loud S₁.

Short P-R interval, as in the pre-excitation syndromes of Wolff-Parkinson-White and Ganong-Levine syndromes.

Mitral closure (M₁)

Tricuspid closure (T₁)

Pulmonic opening

Aortic opening

Increased venous return to the right ventricle (due to negative intrathoracic pressure). This delays P₂.

Decreased venous return to the left ventricle (due to pooling of blood in the lungs). This anticipates A₂.

A wide (physiologic) splitting of S₂

A fixed splitting of S₂

A paradoxical splitting of S₂

The late-systolic click varies with bedside maneuvers and is loudest at the apex (conversely, the split S₂ is unchanged with maneuvers and only heard at the base).

The two most common early diastolic extra sounds are the S₃ and the opening snap (OS) of mitral (or tricuspid) stenosis (for a discussion of how to differentiate an opening snap from a widely split S₂ or an S₃, see questions 103, 104, and 130). OS is primarily apical, whereas the split S₂ is basilar. Still, OS can be loud enough to transmit to the base, thus producing a triple lilt in inspiration (OS + split S₂, with a loud P₂ because of pulmonary hypertension). Note that the interval between S₂ and OS is wider than that between the two components of S₂. Finally, an OS is usually (but not necessarily) associated with a diastolic rumble.

Delayed aortic closure. This is indeed the most common reason, usually due to a complete left bundle branch block (where reversed S₂ splitting can occur in 84% of the cases). Other causes include increased impedance to left ventricular emptying (hypertension, AS, coarctation) or left ventricular dysfunction. The latter can occur in acute ischemia and various cardiomyopathies.

Early pulmonic closure. This is a much less common cause of paradoxical splitting, usually due to decreased right ventricular filling—from either tricuspid regurgitation or right atrial myxoma.

Aging: The audible splitting of S₂ decreases in prevalence with age, to the point of becoming absent in most subjects older than 60. This is probably due to the muffling of P₂ by the “physiologic” senile emphysema.

Emphysema: The hyperinflated lungs will muffle P₂ during inspiration, thus making A₂ the only audible sound. Because this phenomenon is less pronounced in exhalation, these patients may be misdiagnosed as having paradoxical splitting of S₂ (while, in fact, they have a pseudo-paradoxical splitting that becomes evident only in expiration).

Reversed (or paradoxical) splitting: In this case, the split will indeed occur only in exhalation.

Pulmonary hypertension: Increased impedance on right ventricular emptying makes the ventricle unable to cope with the increased venous return of inspiration. Hence, there will be no inspiratory lengthening of right ventricular systole and no inspiratory splitting of S₂.

Semilunar valvular disease: Stiffening and reduced mobility of semilunar valves may also lead to the disappearance of either A₂ or P₂, thus making S₂ “single.”