What is the mechanism of pulsus paradoxus in cardiac tamponade?

Mechanism of Pulsus Paradoxus in Cardiac Tamponade

Pulsus paradoxus in cardiac tamponade is primarily caused by exaggerated ventricular interdependence, where the overall volume of cardiac chambers becomes fixed and any change in the volume of one side of the heart causes opposite changes in the other side during respiration. 1

Pathophysiological Mechanism

• Pulsus paradoxus is defined as an inspiratory decrease in systolic arterial pressure of >10 mmHg during normal breathing, while diastolic blood pressure remains unchanged 1
• During cardiac tamponade, the pericardial space fills with fluid, creating a fixed total heart volume constrained by the stiff pericardium 1
• This creates exaggerated ventricular interdependence, where chambers must compete for space within the confined pericardial sac 1
• During inspiration, there is increased venous return to the right heart, causing the right ventricle to expand 1
• This rightward septal shift reduces left ventricular filling, decreasing left ventricular stroke volume and systolic blood pressure during inspiration 1, 2
• The opposite occurs during expiration, with decreased right heart filling allowing increased left heart filling 1

Hemodynamic Changes

• The stiffness of the pericardium determines how fluid accumulation affects cardiac function, creating a characteristic pressure-volume curve with an initial slow ascent followed by an almost vertical rise 1
• This makes tamponade a "last-drop" phenomenon, where the final increment of fluid produces critical cardiac compression 1
• Underfilling of the left heart during inspiration is the primary mechanism of pulsus paradoxus, as demonstrated by decreased left atrial and ventricular volumes during inspiration 2
• The magnitude of pulsus paradoxus depends on several factors:
  • Rate of fluid accumulation in the pericardial space 1
  • Total amount of pericardial contents 1
  • Distensibility of the pericardium 1
  • Filling pressures and compliance of cardiac chambers 1

Clinical Measurement

• Pulsus paradoxus can be detected by feeling the pulse, which weakens or disappears during inspiration 1
• For accurate measurement using sphygmomanometry:
  • Inflate blood pressure cuff above systolic pressure 1
  • During deflation, note when the first Korotkoff sound appears only during expiration 1
  • Continue deflation until the first Korotkoff sound is audible throughout the respiratory cycle 1
  • The difference between these two pressure points is the measure of pulsus paradoxus 1

Echocardiographic Correlates

• Echocardiographic signs that correlate with pulsus paradoxus include:
  • Exaggerated respiratory variability (>25%) in mitral inflow velocity 1
  • Inspiratory decrease and expiratory increase in pulmonary vein diastolic forward flow 1
  • Respiratory variation in ventricular chamber size 1
  • Abnormal ventricular septal motion 1
  • Flow velocity paradox along the great arteries often precedes clinically detectable pulsus paradoxus 3

Special Considerations and Exceptions

• Pulsus paradoxus may be absent in cardiac tamponade when:
  • Atrial septal defect is present (allowing equalization of pressures between atria) 3
  • Significant aortic regurgitation exists 3
  • Patient has atrial fibrillation (in which case pulse oximetry may help detect the phenomenon) 3
• A pulsus paradoxus >10 mmHg in a patient with pericardial effusion significantly increases the likelihood of tamponade (likelihood ratio 3.3) 4
• Absence of pulsus paradoxus (≤10 mmHg) in a patient with pericardial effusion greatly decreases the likelihood of tamponade (likelihood ratio 0.03) 4

Clinical Significance

• Pulsus paradoxus is a key diagnostic finding in cardiac tamponade, with a pooled sensitivity of 82% 4
• When present alongside other clinical findings (dyspnea, tachycardia, elevated jugular venous pressure), it strongly supports the diagnosis of tamponade 4
• The presence of pulsus paradoxus should prompt immediate echocardiographic evaluation and consideration of pericardiocentesis in unstable patients 1, 5