Mechanism of Pulsus Paradoxus in Clinical Shock

Jay N. Cohn; Alan L. Pinkerson; Felix E. Tristani

doi:10.1172/JCI105665

Mechanism of Pulsus Paradoxus in Clinical Shock

Jay N. Cohn, Alan L. Pinkerson, and Felix E. Tristani

Published November 1, 1967 - More info

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Abstract

An inspiratory fall in systolic arterial pressure of more than 10 mm Hg (pulsus paradoxus) was noted in 30 of 61 patients with shock. Inspiratory right atrial pressures and total blood volumes were significantly lower in patients with pulsus paradoxus. Rapid infusion of dextran in 22 patients usually was effective in reversing the exaggerated inspiratory fall in systolic pressure. Total peripheral vascular resistance tended to be higher in the patients with pulsus paradoxus and administration of vasoconsrictor drugs often accentuated the respirator pressure variation.

Respiratory effects on blood flow in the aorta, pulmonary artery, and venae cavae were studied in anesthetized, closed-chest dogs. In the control state, pulmonary arterial flow increased during inspiration but aortic flow remained nearly constant. After hemorrhage a sharp inspiratory fall in aortic flow was associated with decreased central blood volume and attenuation of the usual inspiratory increase in venae caval and pulmonary arterial flows. The respiratory changes in aortic flow after hemorrhage could be attributed both to depletion of the pulmonary reservoir and to alterations in pulmonary inflow related to changes in systemic venous return.

These data indicate that blood volume depletion may precipitate pulsus paradoxus both in the anesthetized dog and in the critically ill patient. The occurrence of pulsus paradoxus may aid in the clinical recognition of the common syndrome of occult hypovolemia in patients with shock in the absence of signs of blood loss.

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