Normal, transient heart sounds. The normal transient sounds that we recognize include the high-frequency S1 and S2. While these sounds are not produced by simple atrioventricular or semilunar valve cusp closure, we can consider that S1 and S2 coincide with mitral and tricuspid valve closure and aortic and pulmonic valve closure, respectively. Therefore, the association
between mitral valve closure and S1 produces the loudest audible component of S1 over the left apical region of the heart (the location of the mitral valve). Similarly, with an understanding that S2 is associated with aortic and pulmonic valve closure and the sudden deceleration of blood, we most commonly hear S2 loudest at the left heart base (the location of the pulmonic and aortic valves). Recognizing that S1 is loudest at the left apex and S2 is loudest at the left heart base will help you localize cardiac murmurs, no matter the chest conformation. Furthermore,
S1 and S2 mark the beginning and end of systole, respectively, providing a framework around which to recognize and categorize the other
audible transient heart sounds and murmurs (Figure 1).
Figure 1. Electrical events precede mechanical events, so there is a delay between the electrocardiographic deflections and
the individual heart sounds with which they are associated. In this schematic (A), atrial depolarization is associated with
S4, ventricular depolarization with S1, ventricular repolarization with S2, and the period of early rapid ventricular filling with S3. In regard to cardiac auscultation, systole is defined as the period between S1 and S2, while diastole is the period between S2 and S1. Two of the most commonly encountered murmurs include the systolic plateau (regurgitant) and systolic crescendo-decrescendo
(ejection) murmurs (B). Diastolic decrescendo murmurs typically signify aortic insufficiency, while continuous murmurs are
most often identified with a left-to-right shunting patent ductus arteriosus (C).
Alterations of the normal, transient heart sounds. The intensity of S1 primarily depends on the position of the larger anterior mitral valve leaflet at the onset of ventricular systole.2 A more intense S1 is present when the valve is deeply recessed into the left ventricle and may be auscultated in patients with fast heart rates,
short P-R intervals, or high sympathetic tone. Additional contributing factors may include anemia, systemic hypertension,
or thinness.3 Because of acoustic dampening, obese patients, patients with pericardial or pleural effusion, or patients with space-occupying
lesions such as tumors or hernias may display a muted or less distinctive S1. Myocardial failure, a prolonged P-R interval, premature mitral valve closure, various cardiac arrhythmias (including atrial
fibrillation), or shock may also reduce the intensity of S1.2,3