Definition: Inspiratory decrease in systolic blood pressure of greater than 10 mm Hg.
History: Adolf Kussmaul coined the term “pulsus paradoxus” in 1873 in three patients with constrictive pericarditis; he described two important physical signs of pericardial disease: pulsus paradoxus and Kussmaul’s sign.
Paradox? The paradox described by Kussmaul was a “pulse simultaneously slight and irregular, disappearing during inspiration and returning upon expiration” despite the continued presence of the cardiac impulse during both respiratory phases. Essentially, the “paradox” was that the peripheral pulse disappeared, while the heart continued to beat. The finding in cardiac tamponade is an exaggeration of normal physiology.
Methods of examination: To measure the inspiratory decrease in systolic blood pressure, the cuff is first inflated 20 mm Hg above the systolic pressure, then deflated until the first Korotkoff sound is heard. Initially the Korotkoff sounds are heard only during expiration. The cuff is deflated until the Korotkoff sounds are heard equally well during inspiration and expiration. If the difference between these two pressures is greater than 10 mm Hg, the patient has a pulsus paradoxus of a magnitude equal to that difference.
Causes of Pulsus Paradoxus:
- Cardiac causes
- Cardiac tamponade
- Pericardial effusion
- Constrictive pericarditis
- Restrictive cardiomyopathy
- Pulmonary embolism
- Acute myocardial infarction
- Cardiogenic shock
- Extracardiac pulmonary causes
- Bronchial asthma
- Tension pneumothorax
- Extracardiac non-pulmonary causes
- Anaphylactic shock (during urokinase administration)
- Volvulus of the stomach
- Diaphragmatic hernia
- Superior vena cava obstruction
- Extreme obesity
Mechanism: Impaired filling of the left ventricle due to inspiratory filling of the right heart in a constricted pericardial space (“ventricular diastolic interdependence”); the right ventricle distends due to increased venous return, the interventricular septum bulges into the left ventricle reducing its size, and increased pooling of blood in the expanded lungs decreases return to the left ventricle, decreasing the stroke volume of the left ventricle.
For more information, check out the Stanford 25 video below: