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Showing posts with label cardiac tamponade. Show all posts
Showing posts with label cardiac tamponade. Show all posts

Pulses paradoxus or Kussmaul's pulse

Pulses paradoxus is defined as an exaggerated narrowing of the pulse volume due to fall of systolic BP during inspiration, as evidenced by inspiratory fall of systolic BP > 10 mm Hg during quiet breathing.
The difference in pressure between expiration and inspiration is < 10 mm Hg normally In pulses paradoxus, it is >10 mm Hg.
In normal individuals also, inspiratory filling of left ventricle is less, stroke volume is less, pulse volume is less, but may not be clinically detectable.
In pulses paradoxus the pulse volume decreases with inspiration and volume increases with expiration (it not truly the opposite of sinus arrhythmia which denotes the changes in pulse rate only). The paradox in this situation is that the heartsounds may still be heard on auscultation over the cardiac apex at a time when no pulse is palpable at the radial artery. 
It is commonly seen in.
  • Acute severe asthma.
  • Cardiac tamponade (rapidly developing pericardial effusion).
  • Chronic constrictive pericarditis..
  • Restrictive cardiomyopathy.
The probable mechanisms of pulses paradoxus is 
  • Intrapericardial pressure rises more during inspiratiory phase due to the traction on the pericardium which in turn decreases cardiac output by causing obstruction in venous return seen in cardiac tamponade.
  • Anti-Bernhelm effect is seen in inspiration, more blood comes in the right ventricle which will pushe the interventricular septum to the left side hence diminish the left ventricular cavity and resulting in low cardiac output.
  • Pulsus paradoxus is the exaggeration of normal physiological phenomenon, ie. an exaggerated inspiratory fall in systolic BP of more than 10 mm of Hg during quiet breathing.
What are the mechanism of pulses paradoxus?
  • In pericardial diseases like constrictive pericarditis, cardiac chambers are held in rigid pericardium, inspiratory increased filling of RV is taking place at the expense of the LV volume. Thus LV volume is decreased left ventricular filling is decreased, stroke volume is decreased  pulse volume is decreased. Ventricles cannot,increase its size during diastole due to thickened pericardium or due to increase in intrapericardial pressure as in pericardial effusion.
  • During inspiration, there is a fall in negativity of pressure in all the structures inside the chest. The fall in pressure is more in pulmonary vein than in left atria which is kept inside the rigid pericardium, thus the pressure gradient between pulmonary vein and left atrium is increased left atrial  filling is reduced LV filling is reduced and stroke volume and pulse volume is reduced.
  • During inspiration as there is stretch of pericardium by the downward movement of diaphragm, this will further reduce  the volume of the cardiac chambers including left ventricle impeding the filling further resulting in further reduction of stroke volume and pulse volume
How will you demonstrate Pulses paradoxus?
This can be demontrated accurately by using sphygmomanometer demonstrating systolic pressure fall > 10n Hg during inspiration. Patient should be in quiet breathing, by raising the pressure You should now occlude the arterial pulse, then slowly release the pressure initially one will hear the korotkoff sound
Expiration - Korotkoff sounds 
11111 11111 11111
Inspiration - Korotkoff sounds 
11111 11111 11111 11111 11111
Difference in systolic pressure in expiration  and inspiration > 10 mm Hg
Reverse pulses paradoxus 
Inspiratory rise in pulse volume and arterial pressure.
Causes are:
  • HOCM
  • Isorhythmic AV dissociation
  • Intermittent positive pressure ventilatior