Heart Sound

  • Abnormal heart sounds heard shortly after S2 includes opening snap, pericardial knock and tumor plop.
  1. Opening snap is a crisp, sharp sound heard during early diastole in the mid precordial location, usually in the area from the left sternal border to just inside the apex. It is heard when the AV valve is thickened and deformed mostly due to rheumatic heart disease. 
  2. Tumor plop is a characteristic low-pitched sound, heard during early or mid-diastole. It result from the impact of the tumor against the mitral valve or ventricular wall.
  3. Pericardial knock is an abnormal S3 heard in patients with constrictive pericarditis. This sound occur closer to S2.
  • Systolic ejection clicks are heard just after S1 and may be due to abrupt opening of semi lunar valves or rapid distension of proximal aorta or pulmonary artery at the onset of ejection.
  • The mitral valve can be auscultated in the left 5th intercostal space, slightly below the nipple.
  • The aortic valve can be auscultated in the 2nd right intercostal space, just lateral to sternal angle.
  • The pulmonary valve can be auscultated in the 2nd left intercostal space, just lateral to sternal angle.
  • The tricuspid valve can be auscultated in the 4th left intercostal space, just lateral to sternum.
  • First heart sound is a low, slightly prolonged lub caused by vibrations set up by the sudden closure of mitral or tricuspid valves at the start or ventricular systole and it occurs during the period of Isovolumetric contraction..
  1. Short PR interval is associated with a Loud S1.
  2. Left Bundle Branch Block, and Atrial myxoma are causes of reverse splitting of First Heart Sound (S1)
  • ASD ,Pulmonic Stenosis, RBBB are associated with a wide physiological (non-paradoxical) split of second heart sound due to delayed pulmonic closure (Delayed P2) while VSD is associated with a wide physiological (non-paradoxical) split second heart sound from early aortic closure (Early A2).
  1. Left Bundle Branch Block (LBBB) is typically associated with Reversed or Paradoxical Splitting of S2.
  2. TOF, Pulmonary Atresia and severe pulmonic stenosis are associated with single S2 as one component of S2 is either absent or inaudible in these conditions.
  3. Loud P2 suggests the presence of pulmonary Arterial Hypertension..Eisenmerger's syndrome is associated with pulmonary arterial hypertension and hence also causes a loud P2.
  • The third heart sound (S3) is a low pitched sound produced in the ventricle 0.14 to 0.16s after A2, at the termination of rapid filling.
  1. Physiologic S3 seen in Children, High cardiac output ,Atheletes, Fever, Pregnancy.
  2. Pathologic S3 seen in Ventricular dysfunction (LVF/RVF), Idiopathic dilated cardiomyopathy ,Ischemic/Valvular/congenital heart disease , Systemic and pulmonary hypertension ,Excessively rapid early diastolic ventricular filling - Hyperkinetic states - Anemia - Thyrotoxicosis - Arteriovenous fistula - Atrioventricular valve incompetence ,Left to right shunts (VSD, PDA and ASD) ,Restrictive myocardial or pericardial disease , Constrictive pericarditis (pericardial knock) ,Restrictive and Hypertrophic cardiomyopathy.
  3. Pericardial knock is S3 that occurs earlier (0.1 to 0.12 after A2) and is higher pitched than normal. It often occurs in patients with constrictive pericarditis. Its presence depends upon the restrictive effect of the adherent pericardium, which halts diastolic filling abruptly. 
  • The fourth heart sound (S4) is a low pitched presystolic sound produced in ventricles during ventricular filling. It is heard over the apex when the patient is in supine or left semi lateral position. It is a low pitched heart sound heard at late diastole or early systole. It increases with forced inspiration, exercise, elevation of legs and with increased venous return.
  • As the severity of the pulmonary stenosis progresses :
  1. The interval between SI and the systolic ejection click becomes shorter
  2. S2 becomes widely split
  3. P2 diminishes or disappears
  4. Systolic ejection murmur lengthens and peaks later in systole, often extending beyond A2
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