Specific features of auscultation
Apex
S1 is louder at the apex
S1 is followed by short systolic pause and quiet S2
S2 is followed by a long pause
Base of the heart: predominance of S2
S1 fits in with apex beat and carotid pulse
I и II тоны
Changes of heart sounds
1.Change of loudness
2.Splitting of basic sounds
3.Extra sounds:
S3
S4
Opening snap of mitral stenosis
Systolic click
Physiological causes of cardiac sounds changes
Decrease – thick chest
Increase – thin chest, physical exercise, tachycardia
Extracardiac causes of sound changes
Decrease of S1:
Emphysema;
Left-sided hydrothorax
Increase:
Anemia
Thyrotoxicosis;
Intensity of S1
Increased intensity
•Hyperdynamic circulation:
oTachycardia
oThyrotoxicosis
•Mitral stenosis
Decreased intensity
•Destruction of atrio-ventricular valves
•Low cardiac output
oHeart failure
oMyocardial infarction
•Slow contraction in left ventricular hypertrophy
o Aortic stenosis
•Complete heart block
Влияние длительности интервала PR на
громкость I тона
Changes of S2
Increased intensity (predominance of S2)
•Systemic hypertension
•Pulmonary hypertension
•Dilated aortic root
•Thick valves
o Atherosclerosis
Decreased intensity
•Destruction of semilunar valves
•Heart failure
•Low blood pressure
•Aortic stenosis
Decreased intensity of both sounds
Myocarditis
Low contractility
Splitting of S1
Physiological
In children (in vertical position)
transient: at deep inspirationи and at expiration
Pathological – asynchronous closure of mitral and tricuspid valves
RBBB
More pronounced
At inspiration and expiration
S2
Physiological splitting
–Best Heard At 2nd Left Intercostal Space
–During Inspiration there is Delayed Pulmonic Valve Closure
•Due to Increased Capacitance of Pulmonary Bed
Pathological splitting
•Pulmonary hypertension
•Right ventricular hypertrophy