Pulsus paradoxus
| Pulsus paradoxus | |
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| Classification and external resources | |
| DiseasesDB | 11041 |
In medicine, a pulsus paradoxus (PP), also paradoxic pulse or paradoxical pulse, is an exaggeration of the normal variation during the inspiratory phase of respiration, in which the blood pressure declines as one inhales and increases 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).[1]
The paradox in pulsus paradoxus is that, on clinical examination, one can detect beats on cardiac auscultation during inspiration that cannot be palpated at 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 slightly increased,[2] due to decreased left ventricular output.[3]
Contents
Mechanism of reduced blood pressure during inspiration in normal conditions
Normally during inspiration, systolic blood pressure decreases ≤10 mmHg.[1], 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. Also the increased venous return to the right side of the heart expands the right heart and directly compromises filling of 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.
Another explanation is that: the increased negative intrathoracic pressure causes increased right sided venous return to the right atrium and, subsequently, to the right ventricle during diastole. This causes an increase in right ventricular filling pressures because of increased volume and stretch, leading to a bulging of the intraventricular septum towards the left ventricle, thus decreasing the left ventricular size and filling volume due to this protrusion. Thus, there is a subsequently 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 echocardiography real time and the decreased pressures can be measured.
Although one or both of these mechanisms may occur, a third may additionally contribute. The large negative intrathoracic pressure increases the pressure across the wall of the left ventricle (increased transmural pressure, equivalent to [pressure within ventricle] - [pressure outside of ventricle]). This pressure gradient, resisting the contraction of the left ventricle, causes an increase in afterload. This results in a decrease in stroke volume, contributing to the decreased pulse pressure and increased heart rate as described above.
Measurement of PP
PP is quantified using a blood pressure cuff and stethoscope (Korotkoff sounds), by measuring the variation of the systolic pressure during expiration and inspiration. Inflate cuff until no sounds (as is normally done when taking a BP) slowly decrease cuff pressure until systolic sounds are first heard during expiration but not during inspiration, (note this reading), slowly continue decreasing the cuff pressure until sounds are heard throughout the respiratory cycle, (inspiration and expiration)(note this second reading). If the pressure difference between the two readings 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.[4]
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 lung hyperinflation (e.g. asthma, COPD) and anaphylactic shock.
List of causes
Cardiac:
Pulmonary:
Non-pulmonary and non-cardiac:
- anaphylactic shock
- superior vena cava obstruction
See also
References
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- Clinical signs in medicine: pulsus paradoxus - Mechanism, pathophysiology, detection and management of patient with pulsus paradoxus.
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- ↑ 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
- ↑ 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.
- ↑ 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.
