Pulsus paradoxus

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Not to be confused with pulsus alternans.
Pulsus Paradoxus
Classification and external resources
DiseasesDB 11041

Pulsus paradoxus (PP), 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 (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's sign). As is usual with inspiration, the heart rate is slightly increased,[2] due to decreased left ventricular output.[3]

Mechanism of reduced blood pressure during inspiration in normal conditions and in tamponade[edit]

Normally during inspiration, systolic blood pressure decreases ≤10 mmHg.,[1] 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.[4] 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.[5]

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.

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 (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.

Measurement of PP[edit]

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[edit]

PP has been shown to be predictive of the severity of cardiac tamponade.[6]

Causes[edit]

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[edit]

Cardiac:

Pulmonary:

Non-pulmonary and non-cardiac:

See also[edit]

References[edit]

  1. ^ a b c d {{cite journal. Pulsus paradoxus >12mmHg is usually indicative of asthma, not COPD. | last = Khasnis | first = A. | last2 = Lokhandwala | first2 = Y. |date=Jan–Mar 2002 | title = Clinical signs in medicine: pulsus paradoxus | journal = Journal of Postgraduate Medicine | volume = 48 | issue = 1 | pages = 46–9 | publisher = 49 | location = Mumbai - 400 012, India | issn = 0022-3859 | pmid = 12082330 | url = http://www.jpgmonline.com/text.asp?2002/48/1/46/153 | accessdate = 21 March 2010 | quote = The “paradox” refers to the fact that heart sounds may be heard over the precordium when the radial pulse is not felt. }}
  2. ^ 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. doi:10.1161/01.res.20.4.381. PMID 6025402.  Abstract
  3. ^ 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.
  4. ^ Reddy, PS; Curtiss, EI; Uretsky, BF (1990). "Spectrum of hemodynamic changes in cardiac tamponade". American Journal of Cardiology 66 (20): 1487–91. doi:10.1016/0002-9149(90)90540-H. PMID 2251997. 
  5. ^ Reddy, PS; Curtiss, EI; O'Toole, JD; Shaver, JA (1978). "Cardiac tamponade: hemodynamic observations in man". Circulation 58 (2): 265–72. doi:10.1161/01.cir.58.2.265. PMID 668074. 
  6. ^ 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.
  7. ^ Talreja, DR; Nishimura, RA, Oh, JK, Holmes, DR (Jan 22, 2008). "Constrictive pericarditis in the modern era: novel criteria for diagnosis in the cardiac catheterization laboratory.". Journal of the American College of Cardiology 51 (3): 315–9. doi:10.1016/j.jacc.2007.09.039. PMID 18206742. 

External links[edit]