Pulsus Paradoxus - Mechanism of Reduced Blood Pressure During Inspiration in Normal Conditions and In Tamponade

Mechanism of Reduced Blood Pressure During Inspiration in Normal Conditions and In Tamponade

Normally during inspiration, systolic blood pressure decreases ≤10 mmHg., 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 systemic 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.

Although it might be tempting to expect during inspiration that the increased volume of the right ventricle causes the septum to bulge dramatically into the left ventricle, this is unlikely, as there is still a large pressure gradient between the right and left ventricles during inspiration. However, during cardiac tamponade, this is the case. Here, pressure equalizes between all of the chambers of the heart. This means that there is a zero-sum gain and as the right ventricle gets more volume, it can push the septum into the left ventricle and therefore reduce the volume of the left ventricle. This additional loss of volume of the left ventricle that only occurs with equalization of the pressures (as in tamponade) allows for the further reduction in volume, so cardiac output is reduced, leading to a further decline in BP. However, in situations where the left ventricular pressure remains higher than the pericardial sac (most frequently from coexisting disease with an elevated left ventricular diastolic pressure), there is no pulsus paradoxus.

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 - ). 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.

Pulsus paradoxus occurs not only with severe cardiac tamponade, but also with asthma, obstructive sleep apnea, pericarditis and croup. The mechanism, at least with severe tamponade, is likely very similar to those of hypertrophic and restrictive cardiomyopathies (diastolic dysfunction), where a decrease in Left Ventricular (LV) filling corresponds to an increasingly reduced stroke volume. In other words, with these cardiomyopathies, as LV filling decreases, ejection fraction decreases directly, yet non-linearly and with a negative concavity (negative first and second derivatives). Similarly with tamponade, the degree of diastolic dysfunction is inversely proportional to the LV end-diastolic volume. So during inspiration, since LV filling is lesser relative to that during expiration, the diastolic dysfunction is also proportionally greater, so the systolic pressure drops >10 mm Hg. This mechanism is also likely with pericarditis, where diastolic function is chastened.