Heart sounds: S1 & S2.

First heart sound: S1

Within S1 the M1 sound precedes T1 as the left ventricle begins contracting first, but at just 0.01s apart they are usually so close together and the T1 quiet enough that S1 one is heard as one sound. A split first heart occurs when the component T1 and M1 sounds are heard individually, either very closely together or more widely split. This may be associated with non-synchronous ventricular systole, such as in bundle branch blocks, where delayed depolarisation of one ventricle staggers the heart sounds. (Chizner, 2010). A right bundle branch block can cause a significant delay in T1, whilst a left bundle branch block may be heard as one exact sound, or only slightly reverse the order of S1. Continuous variability in the quality of S1 and in any splitting may be seen in premature ventricular contractions (PVCs) and VT, in which cases the slow spread of excitation from the ectopic foci across the ventricles causes non-synchronous contraction. (Alzand & Crijns, 2011; Walsh, O’Rourke, & Shaver, 2011). 

Technique:

• The higher sounds of S1 should be auscultated using firm pressure upon the diaphragm.
• To diagnose a split the quiet T1 must be detected, which is best heard over the tricuspid area at the lower left sternal border.
• For M1 listen at the aortic area at the second right intercostal space.

Findings:

• Increased intensity may be due to:
• A short PR interval, as seen in ventricular pre-excitation.
• Mitral stenosis, as the valve leaflets close more forecfully during systole.
• Hyperkinetic conditions, including fever, fluid overload, exercise, and pregnancy.
• Decreased intensity may result from:
• A long PR interval, reducing 'atrial kick' and force of contraction.
• Ventricular weakness reducing force of contraction, e.g. heart failure, myocardial infarction.
• Diminished sound transmission for reasons including obesity, pericardial effusion, emphysema. 
• Splitting of S1:
• Left bundle branch block may be heard as exactly one S1 sound, or narrowly split with the quieter T1 heard before M1. 
• Delayed depolarisation of one ventricle in right bundle branch block staggers the heart sounds, with M1 clearly occurring before T1.
• Variable S1 sounds:
• During PVCs the wave of depolarisation spreads slowly from its ectopic foci in either ventricle across to the other. This causes split S1 due to the non-synchronous depolarisation.
• Consistently variable S1 during wide complex tachycardia may be indicative of VT.

(Alzand & Crijns, 2011; Chizner, 2008; Walsh, O'Rourke, & Shaver, 2011).

Sounds like:

Click upon the icons to play each example of heart sounds. Audio files are best heard using earphones. When listening to variant heart sounds always go back to compare with the normal sound.

S1 by Hypocaffeinic

Second heart sound: S2

Due to the resistance of the pulmonary capillary bed into which the right ventricular stroke volume is being ejected, right ventricular systole is of longer duration than the left, and so the pulmonic valve usually closes just after the aortic valve. During exhalation the sounds are heard as one, but P2 may be heard slightly after A2 during the peak inspiratory phase, when negative intrathoracic pressure increases venous filling of the right atria and ventricle, increasing preload and extending the duration of ejection. When S2 is split the pulmonic sound heard is much quieter than that of the aortic, reflecting the lower pressures within the pulmonary artery. Bundle branch blocks will cause either widened or reversed splitting of S2 as they do with S1, and wide splits may also be seen with pulmonary embolism and pulmonary hypertension. (Shindler, 2007).

Technique:

• The higher sounds of S1 should be auscultated using firm pressure upon the diaphragm.
• The loud A2 sound may be auscultated across the precordium, and may be palpated over the aortic area of the second right intercostal space.
• The quieter P2 sound is auscultated at the pulmonic area of the mid left sternal border.
• For M1 listen at the aortic area at the second right intercostal space.

Findings:

• A louder, 'ringing' A2 is heard in systemic hypertension due to the increased aortic pressure.
• A loud P2 is heard in pulmonary hypertension, which may result from:
• Congestive heart failure.
• Pulmonary embolism.
• Chronic obstructive pulmonary diseases. 
• Decreased intensity of either A2 or P2 may result from stenosis and the reduced range of movement..
• Splitting of S2 increasing during inspiration is normal and results from increased ventricular filling, but should disappear during expiration. 
• Physiologic splitting of S2 is a wide split that varies with respiration but is still present during expiration, and may result from:
• Right bundle branch block prolonging right ventricular contraction
• Pulmonic valve stenosis extending blood ejection time
• Fixed splitting of S2 that does not vary with respiration may result from atrial septal defect, and is a rare finding.
• S2 splitting that decreases during inspiration is termed paradoxical splitting, being the opposite of normal, and is most frequently seen in left bundle branch blocks.

(Lilly & Jung, 2011; Walsh, O'Rourke, & Shaver, 2011)

Sounds like:

Split sounds can be very subtle, and are best gone over a few times with comparisons to the normal sounds to aid recognition.

S2 by Hypocaffeinic

Split S1 & S2

During bundle branch blocks, both S1 and S2 will be split due to the staggered ventricular contractions affecting both valves on the affected side.

Split S1 & S2 by Hypocaffeinic

Next: Heart sounds S3 and S4.

References

Alzand, B., & Crijns, H. (2011). Diagnostic criteria of broad QRS complex tachycardia: decades of evolution. Europace, 13(4), 465-472.

Chizner, M. (2008). Cardiac auscultation: rediscovering the lost art. Current Problems in Cardiology, 33(7)326-408. 

Lilly, L. & Jung, H. (2011). The cardiac cycle: mechanisms of heart sounds and murmurs. In L. Lilly (Ed.), Pathyphysiology of Heart Disease. (5th ed.). Baltimore, Maryland: Lippincott Williams & Wilkins.

Shindler, D. (2007). Practical cardiac auscultation. Critical Care Nursing Quarterly, 30(2), 166-180.

Walsh, R., O'Rourke, R., & Shaver, J. (2011). The history, physical examination, and cardiac auscultation. In V. Fuster, Walsh, R., & Harrington, R. (Eds.), Hurst's The Heart. (13th ed.). New York, NY: The McGraw-Hill Companies, Inc.