Pulsus paradoxus
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In medicine, a pulsus paradoxus (PP), also paradoxic pulse and paradoxical pulse, is an exaggeration of the normal variation in the pulse 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]
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,[1] due to increased venous return.[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.
Measurement of PP
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.
Predictive value for tamponade
PP has been shown to be predictive of the severity of cardiac tamponade.[1]
Causes
Pulsus paradoxus can be caused by several physiologic mechanisms. Anatomically, these can be grouped into:[1]
- cardiac causes,
- pulmonary causes and
- non-pulmonary and non-cardiac causes.
Considered physiologically, PP is caused by:
- decreased right heart functional reserve, e.g. myocardial infarction and tamponade,
- right ventricular inflow or outflow obstruction, e.g. superior vena cava obstruction and pulmonary embolism, and
- decreased blood to the left heart due to pulmonary vasodilation/hyperinflation, e.g. asthma, COPD and anaphylactic shock.
List of causes
Cardiac:
Pulmonary:
Non-pulmonary and non-cardiac:
- anaphylactic shock
- superior vena cava obstruction
Complete Differential Diagnosis
In alphabetical order: [1] [1]
- Adhesive pericarditis
- Cardiac Tamponade
- Constrictive pericarditis
- Endocardial fibrosis
- Hypovolemia
- Mitral stenosis with right heart failure
- Myocardial amyloidosis
- Paramediastinal effusion
- Pericardial effusion
- Pulmonary embolism
- Pulmonary emphysema
- Scleroderma
- Severe asthma
- Tricuspid stenosis
References
See also
External links
- Clinical signs in medicine: pulsus paradoxus - Mechanism, pathophysiology, detection and management of patient with pulsus paradoxus.
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
