Posts Tagged ‘pericardial knock’

A  patient who presents with predominantly right  heart failure  is  an interesting clinical challenge . Constrictive pericarditis (CP)  remains  a popular diagnosis in this setting. However  in the bed side clinical  examination (and in cardiology Board exams )  the following  differential diagnoses are  to be  considered .( And ruled out one by one)

  1. Restrictive cardiomyopathy* especially Right  sided .In India endo myocardial fibrosis tops the list
  2. Primary Tricuspid valve disease( Tricuspid stenosis / Carcinoid etc)
  3. Chronic cor-pulmonale in terminal RV failure
  4. Silent Mitral stenosis with right heart failure
  5. Ebstein anomaly
  6. Severe forms of valvular pulmonary stenosis with RV dysfunction
  7. SVC obstruction
  8. Cirrhosis of liver
  9. Porto pulmonary hypertension

( The list is not complete , readers may contribute )

Bed side clues

  • Remember  a deep “y” descent  is  the bed side counter part of   Square root sign  recorded by  invasive RV pressure study
  • Similarly , pericardial knock is the auditory   equivalent (You hear the square root !  . . .yes  )as the ventricle thuds the rigid thickened pericardial shell in very early diastole !)
  • Pulsus paradoxus and kussmal sign can occur in both CP and RCM.
  • If a good LV apex , is  palpated it  goes against CP .
  • Please be reminded , even restrictive cardiomyopathy  will ultimately dilate their chamber pre-terminal and clinical features may be confounded with that of DCM.
  • Silent heart would suggest CP.
  • AV valve regurgitation would favor RCM
  • Features of  Pulmonary hypertension will help confirm Mitral valve disease , Cor pulmonale,
  • Deep  “y”descents  are against  any form of  Tricuspid stenosis.
  • Opening snap of mitral valve is to be distinguished from pericardial knock.( Opening snap high pitched  and occur later than   pericardial knock in diastole   , best heard in expiration )
  • Cirrhosis liver with hypo- proteinimic   fluid retention is  a traditionally close mimicker  .It  may be ruled out by the careful history taking as exertional dyspnea is an exception , if  at all , it is a very late event  in cirrhosis.
  • The issue gets further weird   as chronic constriction can lead on to chronic congestive liver and cardiac cirrhosis .
  • Severe  forms of constriction can invade the myocardium and result in features of myocardial dysfunction .It is more common than we recognise.

How to confirm ?

Following should be performed in that order

  • ECG
  • X -Ray
  • Echocardiogram
  • CT scan
  • MRI

*Cath study is no longer done (Only for academic purpose )

Final message

Even in this era of sophisticated  medical  imaging  , clinical examination  remains the key . One should  realise the importance  of  meticulous  clinical history  ,  sequential examination and interpretation .It  will   “rule out  or rule in”  majority of  cardiac disorders .

The hi tech imaging  modalities should be used only to confirm , risk stratify and  plan management . If you skip the clinical  part , one  may still arrive at a correct  diagnosis  but there is  high chances of erring in  management.

(Cardiac pearls lie in the bed side not in cath labs !   Here is  one such pearl  . Not every constriction  require surgery !

Please note about 20 % of constrictive pericarditis are  transient !)

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Third heart sound is a unique heart sound  because its   perfect physiology  to hear it  in the young  ,  while the same may denote  serious LV dysfunction in patients with myocardial disease.

It is a low pitched  early diastolic sound usually correspond to  the end of rapid filling phase.The mechanism of genesis of this sound has been debated for many years .(Still I think it is unsettled !)

We know genesis of intracardiac sound is contributed  by three factors

  • The blood flow
  • The valve motion
  • The myocardial contractile and  relaxyl  property

The above  three is collectively  called cardio-hemic system . When this system vibrates heart sounds are generated .In  the genesis of S3 all the three may be important . The only difference is ,  in physiological S3 the valvular and hemic component play a major role . In pathological S3 the  myocardial component has a pivotal  role .The distended LV facilitates chest wall impact during the rapid filling phase . It is now  accepted  LV S3 is  generated outside the LV  . It  was proved elegantly by Shaver et all with sound recording on either side of  LV /Chest wall.

It is to be emphasized  the mechanism of genesis of S3 is diagonally opposite in  physiology vs  pathological  S3 in some conditions . Rapid AV filling  can  rarely be  responsible for pathological  S3  associated with severe LV dysfunction , while chest wall  impact can contribute in both physiological as well as pathological S 3 .

 One can understand the complexity of genesis of  S 3  , as  there are  too many  determinants  that contribute in  varying degree of acoustics.

Factors determining the intensity of S3 is complex 

  1. Age,
  2. Atrial pressure,
  3. Rapidity of  flow across the atrio-ventricular valve,
  4.  Rate of early  diastolic relaxation 
  5.  Distensibility of the ventricle,
  6.  Blood  volume,
  7. Ventricular cavity size,
  8.  Diastolic momentum of the  heart,
  9. Degree of contact (coupling) with the chest wall, thickness
  10. Character of the chest wall
  11.  The position of the  patient.


It is ironical, pathological   S3 which is a  diastolic  sound  though ,  still  its genesis  is largely  determined by the systolic function of the heart .This mystery is partially solved as we recognise  now ,  LV S3 is equally common in  severe degrees of diastolic dysfunction. In fact ,  while we were studying the relationship  of LVS3 in DCM  , it  has strongly predicted the  presence of   severe restrictive pattern in them .




1.Multimedia of S3


2.Importance of  S3 in cardiology NEJM 2001 article


3.Chest wall impact theory of S3  by Shaver

Shaver JA, Salerni R. Auscultation of the heart. In: Hurst, ed. Heart. 8th ed. New York, NY: McGraw-Hill, Inc; 1994:291.

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