What is the cause of pulsus paradoxus in cardiac tamponade?

From the Guidelines

Pulsus paradoxus in cardiac tamponade occurs due to the exaggerated respiratory variation in cardiac filling and output, resulting from the increased intrapericardial pressure and ventricular interdependence, as described in the 2015 European Society of Cardiology guidelines 1. The pathophysiology of pulsus paradoxus in cardiac tamponade can be explained by the following mechanisms:

• During normal inspiration, intrathoracic pressure decreases, increasing venous return to the right heart while simultaneously decreasing left ventricular filling.
• In cardiac tamponade, fluid accumulates in the pericardial space, creating a fixed pericardial volume that restricts cardiac filling.
• This restriction means the heart chambers must compete for space within the pericardium, leading to ventricular interdependence.
• During inspiration, the increased right ventricular filling further compromises left ventricular filling due to ventricular interdependence and the fixed pericardial constraint.
• This leads to a significant drop in left ventricular stroke volume and systolic blood pressure during inspiration, exceeding the normal physiologic decrease of 10 mmHg. Some key points to consider in the diagnosis of cardiac tamponade include:
• Clinical signs such as tachycardia, hypotension, pulsus paradoxus, raised jugular venous pressure, and muffled heart sounds.
• Echocardiographic findings, including cyclic compression, inversion, or collapse of the right atrium, diastolic RV collapse, and dilatation of the inferior vena cava without change during deep inspiration.
• The use of pulsed wave Doppler to provide additional information in the diagnosis of tamponade, as described in the European Association of Cardiovascular Imaging and the Acute Cardiovascular Care Association recommendations 1. The diagnosis of cardiac tamponade should be based on a combination of clinical and echocardiographic findings, and treatment should involve drainage of the pericardial fluid, preferably by needle pericardiocentesis with echocardiographic guidance, as recommended in the 2015 ESC guidelines 1.

From the Research

Mechanism of Pulsus Paradoxus in Cardiac Tamponade

• Pulsus paradoxus in cardiac tamponade occurs due to the inspiratory reduction in left heart filling, which leads to a decrease in the output of the left ventricle during inspiration 2.
• The reduced filling of the left ventricle during inspiration is caused by underfilling of the left heart, which is the most likely cause of this combination of events 2.
• Inspiratory increases in right heart filling and output are necessary for pulsus paradoxus to occur, and inspiration causes decreases in left ventricular dimensions and aortic and mitral velocities and left ventricular diastolic compliance 3.

Clinical Presentation and Diagnosis

• Cardiac tamponade is characterized by an impairment of the diastolic filling of the ventricles, causing a reduction of cardiac output, and usually produces signs and symptoms of cardiac arrest if untreated 4.
• The diagnosis of cardiac tamponade is a clinical diagnosis based on a suggestive history and clinical presentation with worsening dyspnea, distended jugular veins, muffled heart sounds, and pulsus paradoxus, and should be confirmed by echocardiography 4.
• Echocardiographic findings in pericardial tamponade include a pericardial effusion, diastolic right ventricular collapse, systolic right atrial collapse, a plethoric non-collapsible inferior vena cava, and sonographic pulsus paradoxus 5.

Pathophysiology and Echocardiographic Correlates

• Pulsus paradoxus is complex and multifactorial in origin, and may be absent in cardiac tamponade when certain conditions, such as left ventricular dysfunction, coexist 3.
• Doppler studies of pulmonary venous inflow confirm that an inspiratory fall in left atrial filling is necessary for pulsus paradoxus 3.
• Understanding the accuracy of pulsus paradoxus for a diagnosis of cardiac tamponade requires a consideration of the mechanisms underlying its genesis, and a knowledge of its presence in other conditions and its variable absence in cardiac tamponade with associated disease states 3.