closure of the mitral&tricuspid valves at onset of ventricular systole □best heard at the apex
and physiological splitting
closure of the pulmonary and aortic valves at the end of ventricular systole □best heard at the left sternal edge □louder and higher-pitched than S1, the aortic component is normally louder than the pulmonary one.
□Physiological splitting of S2 occurs because LV contraction slightly precedes that of RV so that the aortic valve closes before the pulmonary valve. □splitting ↑ at end-inspiration ← ↑ venous filling of the RV further delays pulmonary valve closure. □separation disappears on expiration □Splitting of S2 is best heard at the left sternal edge. On auscultation, you hear 'lub d/dub' (inspiration) 'lub-dub' (expiration).
□low-pitched □early diastolic
□best heard with the bell at the apex.
□coincides with rapid ventricular filling immediately after opening of the AV valves → heard after S2 as 'lub-dub-dum'.
□normal in children, young adults & during pregnancy.
A S3 is usually pathological after the age of 40 years □commonly due to LV failure (early sign) & mitral regurgitation. ◊In heart failure S3 occurs with a tachycardia and S1 and S2 are quiet (lub-da-dub).
□S4 is less common
□soft and low-pitched
□best heard with the bell at the apex
□occurs just before S1 (da-lub-dub)
□caused by forceful atrial contraction against a non-compliant/ stiff ventricle
□often heard with LV hypertrophy (due to hypertension, aortic stenosis or hypertrophic obstructive cardiomyopathy) □cannot occur when there is AFib.
↑intensity of S1
due to and significance
in mitral stenosis
due to increased Pressure in LA
Wide splitting of S2, but with normal respiratory variation
causes and significance
is in delayed RV emptying ←right bundle branch block
Fixed splitting of S2
significance and causes
i.e. no variation with respiration, → atrial septal defect (RV stroke volume is larger than the left; the splitting is fixed because the defect equalizes the pressure between the two atria throughout the respiratory cycle)
Abnormalities of intensity of S1
Quiet: 1.↓ cardiac output 2. Poor LV function 3.Long P-R interval (1˚ heart block) 4.Rheumatic mitral regurgitation
Loud: 1.↑ cardiac output 2. ↑ stroke volume 3.Mitral stenosis 4. Short P-R interval 5.Atrial myxoma (rare)
Variable : 1.Atrial fibrillation 2. Extrasystoles 3. Complete heart block
Abnormalities in S2
Quiet: 1. ↓ cardiac output 2. Calcific aortic stenosis 3. Aortic regurgitation
Loud: 1.Systemic hypertension (aortic component) 2.Pulmonary hypertension (pulmonary component)
Widens in inspiration (↑physiological splitting):
1. Right bundle branch block 2. Pulmonary stenosis 3.Pulmonary hypertension 4. Ventricular septal defect
Fixed splitting (unaffected by respiration): Atrial septal defect
Widens in expiration (reversed splitting): 1. Aortic stenosis 2.Hypertrophic cardiomyopathy 3.Left bundle branch block 4.Ventricular pacing
causes of a 3rd heart sound
Physiological : 1.Healthy young adults 2. Athletes 3.Pregnancy 4.Fever
Pathological : 1. Large, poorly contracting LV 2.Mitral regurgitation
□mitral (rarely tricuspid) stenosis → sudden opening of a stenosed valve
□early in diastole, just after S2
□best heard at the apex
□early in systole just after S1
□congenital pulmonary or aortic stenosis
□do not occur in calcific aortic stenosis because the cusps are rigid
□mitral valve prolapse □associated with a late systolic murmur □high-pitched and best heard at the apex
○Mechanical heart valves make a sound when they close and open. The closure sound is normally louder, especially with modern valves. The sounds are high-pitched, 'metallic' and often palpable, and may be heard without a stethoscope. A mechanical mitral valve replacement makes a metallic first heart sound and a sound like a loud opening snap. Mechanical aortic valves have loud, metallic second heart sounds and an opening sound like an ejection click. They usually also cause a flow murmur.