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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, pericarditis, chronic sleep apnea, croup, and obstructive lung disease (e.g. asthma, COPD).
The paradox in pulsus paradoxus is that, on clinical examination, one can also detect beats on cardiac auscultation during inspiration that cannot be palpated at the radial pulse.
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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, pericarditis, chronic sleep apnea, croup, and obstructive lung disease (e.g. asthma, COPD).
The paradox in pulsus paradoxus is that, on clinical examination, one can also detect beats on cardiac auscultation during inspiration that cannot be palpated at the radial pulse. 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 slightly increased, due to decreased left ventricular output.
Mechanism of reduced blood pressure during inspiration in normal conditions
During inspiration, systolic blood pressure decreases slightly, and pulse rate goes up slightly. 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 blood capacity 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.
An alternative and more plausable explanation to the decrease in blood pressure during inspiration compared to the ** idea above, is that: A) increased negative intrathoracic pressure causes, B) increased right sided venous return, C) to the right atrium, and then right ventricle during diastole, D) which causes an increase in right ventricular filling pressures because of increased volume and stretch leading to E) a buldging of the intraventricular septum towards the left ventricle, F) decreasing the left ventricular size and filling volume, G) with subsequent decreased left sided stroke volume and therefore a lower systolic blood pressure. Note that this ventricular septal deviation from right to left can be visually seen during cardiac echocardiography real time and the decreased pressures can be measured.
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. Pulsus paradoxus is an inspiratory reduction in systolic pressure >10 mmHg. Pulsus paradoxus can also be measured by listening to Korotkoff sounds during blood pressure measurement -- slowly decrease cuff pressure to the systolic pressure level where sounds are first heard during expiration. Then, cuff pressure is slowly lowered further until Korotkoff sounds are heard throughout the respiratory cycle, during both inspiration and expiration. If the pressure difference between hearing the first sounds and hearing them throughout the respiratory cycle is >10mmHg, it can be classified as pulsus paradoxus.
Predictive value for tamponade
PP has been shown to be predictive of the severity of cardiac tamponade.
Causes
Pulsus paradoxus can be caused by several physiologic mechanisms. Anatomically, these can be grouped into:
- 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:
See also
External links
- - Mechanism, pathophysiology, detection and management of patient with pulsus paradoxus.
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