Pulsus paradoxus, also paradoxic pulse or paradoxical pulse, is an abnormally large
decrease in systolic blood pressure and pulse wave amplitude during inspiration. The normal
fall in pressure is less than 10 mmHg or 10 torr. When the drop is more than 10mm Hg,
it is referred to as pulsus paradoxus. Pulsus paradoxus has nothing to do with pulse rate
or heart rate. The normal variation of blood pressure during breathing/respiration is a
decline in blood pressure during inhalation and an increase during exhalation. Pulsus
paradoxus is a sign that is indicative of several conditions, including cardiac tamponade,
pericarditis, chronic sleep apnea, croup, and obstructive lung disease.
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.
It results from an accentuated decrease of the blood pressure, which leads to the pulse
not being palpable and may be accompanied by an increase in the jugular venous pressure
height. 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 and in tamponade
Normally during inspiration, systolic blood pressure decreases ≤10 mmHg., and pulse
rate goes up slightly. This is because inspiration makes intrathoracic pressure more negative
relative to atmospheric pressure. The negative pressure in the thorax increases 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 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, 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. 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 and croup. The mechanism, at least
with severe tamponade, is likely very similar to those of hypertrophic and restrictive cardiomyopathies,
where a decrease in Left Ventricular 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. 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.
Measurement of PP PP is quantified using a blood pressure cuff
and stethoscope, by measuring the variation of the systolic pressure during expiration
and inspiration. Inflate cuff until no sounds slowly decrease cuff pressure until systolic
sounds are first heard during expiration but not during inspiration,, slowly continue decreasing
the cuff pressure until sounds are heard throughout the respiratory cycle,(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.
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 lung
hyperinflation and anaphylactic shock. List of causes
Cardiac: constrictive pericarditis. One study found
that pulsus paradoxus occurs in less than 20% of patients with constrictive pericarditis.
pericardial effusion, including cardiac tamponade cardiogenic shock
Pulmonary: pulmonary embolism
tension pneumothorax asthma
chronic obstructive pulmonary disease Non-pulmonary and non-cardiac:
anaphylactic shock hypovolemia
superior vena cava obstruction pregnancy
obesity See also
List of paradoxes Precordial exam
Pulsus alternans References
External links Clinical signs in medicine: pulsus paradoxus
- Mechanism, pathophysiology, detection and management of patient with pulsus paradoxus.
Another definition of Pulsus Paradoxus Hamzaoui, O; Monnet, X; Teboul, JL. "Pulsus
paradoxus.". The European respiratory journal 42: 1696–705. doi:10.1183/09031936.00138912.
PMID 23222878.