HEART SOUNDS

DEFINITION
Brief auditory sounds of variable intensity , frequency and quality.

Mechanism
Due to the sudden closure of valves there will be turbulence of fluid for a very short period which will produce the heart sounds

Important points to remember

Normal heart sounds dont rule out a pathological heart Extra sounds dont confirm a pathological heart Third heart sound is normal in some children and adolascents Fourth sound rarely audible

s1
The s1 is best heard at the apex. The main component of s1 is mitral component. The speed of closure of valves is proportional to the intensity of the heart sound. S1 has two components m1 and t1

Splitting of s1
RBBB with pulmonary hypertension Left ventricular pacing Ebsteins anamoly

Reverse splitting of s1
Right ventricular pacing Ectopic beat from right ventricle

Soft s1
Mitral regurgitation Tricuspid regurgitation Prolonged PR interval Left ventricular dysfunction

Loud s1
Hyperdynamic states Decreased PR interval Large cardiac output Large stroke volume Mitral stenosis

variable
Atrial fibrillation Heart blocks Extra systoles

Second heart sound

Produced by two components aortic and pulmonic
Loud A2 hypertension Loud p2 Pulmonary hyertension Delayed A2 Complete LBBB Early P2 WPW syndrome

Aortic aneurysm
atherosclerosis

Pulmonary artery dilatation

Eisenmenger complex
arteriosclerosis

Syphilitic Aortic regurgitation

Left ventricular outflow obstruction

Splitting of S2
wide slit s2 variable Wide fixed split Mitral regurgitation VSD Constrictive pericarditis Left ventricular ectopics and pacemaker ASD Right ventricular failure Massive acute pulmonary embolism Partial anamolous pulmonary venous connection Reverse splitting WPW syndrome Aoritc stenosis HOCM

Latent PDA

LBBB Right ventricular ectopics

Third heart sound

Low pitched sound heard best at the apex in the early diastole Determinants volume and velocity of inflow and completeness of ventricular relaxation Some also say it due to the rotation of the heart With the above said determinants two theories were put internal and external production theory respectively

 Physiological S3

children Young adults athletes pregnancy

Pathological S3
High output states ASD , VSD ,PDA AR , MR , TR hyertension HOCM IHD Constrictive pericarditis Pulmonary hypertension

Fourth heart sound

Low pitched sound best heard at the apex in the end diastole or presystole S4 is due to regurgitation or transient valve movement occuring at the time of atrial contraction due to transient raise of pressure gradient in the ventricle. Causes are HOCM , HTN , MI , angina ,ventricular aneurysm

Atrial gallop-S1 ,S2 , S4 Ventricular gallop-S1,S2,S3 Summation gallop-S1 , S2 , merged S3 ,S4 Quadruple rhythm-presence of the four heart sounds

ADDITIONAL SOUNDS
Tumor plop-diastolic sound heard due to long pedicle rt or lt atrial myxomas Pericardial knock-high pitched diastolic sound heard in constrictive pericarditis due to stopping of diastolic filling abruptly Mid systolic click or non valvular click-MVP , Tricuspid valve prolapse , ebsteins anamoly ,severe AR

 Valvular click-aortic stenosis and pulmonary stenosis in systole Vascular clicksaortic dilatation Pulmonary hyertension Pulmonary dilatation Systemic hypertension

 Opening snap is a high pitched additional sound heard after the A2 (aortic) which is due to the forceful opening of the AV valves Mitral stenosis , tricuspid stenosis MR , TR ,VSD ,ASD and PDA

 Opening snap and mitral stenosis Absent or soft in congenital ,calcific ,mild and very severe and when associated with AS OR AR

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