Pulsus paradoxus: Difference between revisions

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Non-pulmonary and non-cardiac:
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*Adhesive [[pericarditis]]
*Adhesive [[pericarditis]]
*[[Cardiac Tamponade]]
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*[[Constrictive pericarditis]]
*[[Constrictive pericarditis]]
*[[Endocardial fibrosis]]
*[[Endocardial fibrosis]]

Revision as of 19:11, 19 December 2014

Template:Search infobox Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: PP; paradoxic pulse; paradoxical pulse

Overview

Pulsus paradoxus is an exaggeration of the normal variation in the pulse and drop of systolic blood pressure during the inspiratory phase of respiration, in which the pulse becomes weaker as one inhales and stronger as one exhales. It is a sign that is indicative of several conditions including cardiac tamponade and lung diseases (e.g. asthma, COPD).[1]

Mechanism of Reduced Blood Pressure During Inspiration in Normal Conditions

During inspiration, systolic blood pressure decreases, and pulse rate goes up. This is because the intrathoracic pressure becomes more negative relative to atmospheric pressure. This increases systemic venous return, so more blood flows into the right side of the heart. However, the decrease in intrathoracic pressure also expands the compliant pulmonary vasculature. This increase in pulmonary capacitance pools the blood in the lungs, and decreases pulmonary venous return, so flow is reduced to the left side of the heart. Reduced left-heart filling leads to a reduced stroke volume which manifests as a decrease in systolic blood pressure. The decrease in systolic blood pressure leads to a faster heart rate due to the baroreceptor reflex, which stimulates sympathetic outflow to the heart.

Mechanism of Reduced Blood Pressure During Inspiration in Pulsus Paradoxus

A decrease in blood pressure and increase in pulse rate is normally seen with inspiration. As explained above, this is seen normally as a result of increased pulmonary venous capacitance during inspiration, that in turn leads to decrease in blood from lungs to left ventricle resulting in drop of blood pressure and increase in pulse rate during inspiration. Normally the drop in blood pressure is < 10 mm Hg. However, in Pulsus paradoxus there is an abnormally large decrease in systolic blood pressure (>10 mmHg) on inspiration. The reason for the increased fall in blood pressure is the limitation on outward expansion of the right ventricle in tamponade and other conditions. The right ventricular increased pressure during inspiration results in bulging of the interventricular septum into the left ventricle, leading to a large reduction in left ventricular filling that contributes to a large decrease in stroke volume. The paradox in pulsus paradoxus is that, on clinical examination, one can detect extra beats on cardiac auscultation, during inspiration, when compared to the radial pulse.[1] It results from an accentuated decrease of the blood pressure, which leads to the (radial) pulse not being palpable and may be accompanied by an increase in the jugular venous pressure height (Kussmaul sign). As is usual with inspiration, the heart rate is increased,[2] due to increased venous return.[3]

Measurement of Pulsus Paradoxus

PP is quantified using a blood pressure cuff and stethoscope, by measuring the variation of the pressure in systole with respiration. Normal systolic blood pressure variation (with respiration) is considered to be ≤10 mmHg.[1] Pulsus paradoxus is an inspiratory reduction in systolic pressure >10 mmHg. Pulsus paradoxus can also be measured by listening to Korotkoff sounds and hearing the actual sound of the systolic beat. If the pressure gradient is >10mmHg, it can be classified as pulsus paradoxus and shifting of the atrial septum.

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Predictive Value for Tamponade

PP has been shown to be predictive of the severity of cardiac tamponade.[4]

Causes

Common Causes

Pulsus paradoxus can be caused by several physiologic mechanisms. Anatomically, these can be grouped into:[1]

  1. Decreased right heart functional reserve, e.g. myocardial infarction and tamponade,
  2. Right ventricular inflow or outflow obstruction, e.g. superior vena cava obstruction and pulmonary embolism, and
  3. Decreased blood to the left heart due to pulmonary vasodilation/hyperinflation, e.g. asthma, COPD and anaphylactic shock.

Causes by Organ System

Cardiac:

Pulmonary:

Non-pulmonary and non-cardiac:

Causes in Alphabetical Order[5][6]

Related Chapters

References

  1. ↑ 1.0 1.1 1.2 1.3 Khasnis A, Lokhandwala Y. Clinical signs in medicine: pulsus paradoxus. J Postgrad Med. 2002 Jan-Mar;48(1):46-9. PMID 12082330. Free Full Text.
  2. ↑ Guntheroth W, Morgan B, Mullins G (1967). "Effect of respiration on venous return and stroke volume in cardiac tamponade. Mechanism of pulsus parodoxus". Circ. Res. 20 (4): 381–90. PMID 6025402. Abstract
  3. ↑ Soucek M, Kára T, Jurák P, Halámek J, Spinarová L, Meluzín J, Toman J, Rihácek I, Sumbera J, Frána P (2003). "Heart rate and increased intravascular volume". Physiological research / Academia Scientiarum Bohemoslovaca. 52 (1): 137–40. PMID 12625819. Free Full Text.
  4. ↑ Curtiss EI, Reddy PS, Uretsky BF, Cecchetti AA. Pulsus paradoxus: definition and relation to the severity of cardiac tamponade. Am Heart J. 1988 Feb;115(2):391-8. PMID 3341174.
  5. ↑ Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016
  6. ↑ Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:68 ISBN 140510368X

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