Pulsus paradoxus describes an abnormal, exaggerated fall in arterial pressure during inspiration, conventionally defined as a fall in systolic pressure more than 10 mm Hg. Pulsus paradoxus was first described in 1873 by Adolf Kussmaul, the German pathologist who saw a "paradox" in three patients with constrictive pericarditis; their palpated pulse would disappear during inspiration and reappear during expiration, despite the uninterrupted presence of a precordial cardiac impulse.

In healthy individuals, quiet inspiration decreases intrathoracic pressure by 5 to 10 mm Hg, which is transmitted to the atria and ventricles. This augments venous return to the right heart, leading to maximal RV SV during inspiration. LV SV respiratory variation also occurs, influenced by both the lungs and the RV. During inspiration, lung expansion exerts radial traction on the pulmonary vasculature and increases its capacitance. This decreases LV filling and SV, with the reverse occurring in expiration. Changes in RV SV affect LV filling with a delay of several seconds as blood crosses the pulmonary circulation to the left heart. If both ventricles are "out of phase" with respect to pulmonary transit time, the effect of inspiration-augmented RV SV on LV filling is increased, increasing LV SV and systemic arterial pressure respiratory variation. The opposite can occur if the two ventricles are "in phase." This accounts for the respiratory variation in arterial pressure in healthy individuals with fluctuations in systolic arterial pressure of 10 mm Hg or less. This is more prominent when both ventricles are preload sensitive (ie, on the steep part of the Starling curve when the LV is constrained and made small by cardiac tamponade).

In cardiac tamponade, elevated pericardial pressure is transmitted to all cardiac chambers, increasing their filling pressures relative to extrapericardial structures including the vena cava. Furthermore, increasing pericardial constraint on the cardiac chambers exaggerates parallel and series ventricular interdependence. Both factors lead to an augmentation of the phasic rise and fall in LV SV.

Pulsus paradoxus is not a sensitive or specific sign of cardiac tamponade. It can also be seen in patients with respiratory distress due to increased negative intrathoracic pressures during inspiration, constrictive pericarditis, and RV failure. It can be absent, even in cardiac tamponade, in patients who cannot generate negative intrathoracic pressure (eg, neuromuscular disease, chest wall trauma) or in patients with aortic regurgitation or an atrial septal defect. Patients who are ventilated with positive pressure can display a "reversed" pulsus paradoxus, that is, an exaggerated increase in systolic arterial pressure with inspiration due to increased RV afterload causing a leftward septal shift during positive inspiratory pressure.

References

• Ramachandran D, Luo C, Ma TS, Clark JW Jr. Using a human cardiovascular-respiratory model to characterize cardiac tamponade and pulsus paradoxus. Theor Biol Med Model. 2009 6;6:15.
• Swami A, Spodick DH. Pulsus paradoxus in cardiac tamponade: a pathophysiologic continuum. Clin Cardiol. 2003;26:215-217.
• Wong FW. Pulsus paradoxus in ventilated and non-ventilated patients. Dynamics. 2007;18:16-18.