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Pulsus paradoxus in pericardial disease

Author
Barry A Borlaug, MD
Section Editor
Martin M LeWinter, MD
Deputy Editor
Brian C Downey, MD, FACC

INTRODUCTION

Systemic blood pressure is not constant but varies slightly from heart beat to heart beat and between inspiration and expiration. Normally, the systolic blood pressure decreases by less than 10 mmHg during inspiration, but a decline of this magnitude is not detectable on examination of the peripheral pulse. Moderate to severe cardiac tamponade, and occasionally constrictive pericarditis, induce hemodynamic changes that enhance the inspiratory fall in systolic blood pressure. This exaggerated drop in systemic blood pressure during inspiration is termed pulsus paradoxus (waveform 1 and waveform 2).

Although Kussmaul named this phenomenon pulsus paradoxus, the paradox to which he referred was not the change in blood pressure but rather that the pulse palpated on examination is of variable strength, while precordial activity is regular [1]. The name is somewhat misleading, since the direction of systolic blood pressure change is the same as in normal subjects (albeit more exaggerated in pathologic instances) and is therefore not paradoxical.

Pulsus paradoxus will be discussed here, including its proper measurement, pathophysiology, and clinical conditions in which it may be present. Specific clinical conditions in which pulsus paradoxus may be present are discussed in greater detail separately. (See "Cardiac tamponade" and "Constrictive pericarditis".)

PATHOPHYSIOLOGY OF PULSUS PARADOXUS IN CARDIAC TAMPONADE

Pulsus paradoxus can be thought of as a direct result of competition (ie, enhanced chamber interaction) between the right and left sides of the heart for limited space; for the right heart to fill more, the left heart must fill less. The interaction of multiple forces results in the excessive inspiratory fall in systemic blood pressure, but enhanced chamber interaction, especially in cardiac tamponade, is by far the principal mechanism.

Although enhanced chamber interaction is the most important mechanism, several other complex mechanisms contribute [2].

       

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Literature review current through: Jan 2015. | This topic last updated: Feb 5, 2015.
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References
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  1. Kussmaul A. Über schwielige Mediastino-Pericarditis und den paradoxen Puls. Berliner Klinische Wochenschrift 1878; 10:461.
  2. Shabetai R, Fowler NO, Fenton JC, Masangkay M. Pulsus paradoxus. J Clin Invest 1965; 44:1882.
  3. Reddy PS, Curtiss EI, O'Toole JD, Shaver JA. Cardiac tamponade: hemodynamic observations in man. Circulation 1978; 58:265.
  4. Santamore WP, Heckman JL, Bove AA. Right and left ventricular pressure-volume response to elevated pericardial pressure. Am Rev Respir Dis 1986; 134:101.
  5. Reddy PS, Curtiss EI, Uretsky BF. Spectrum of hemodynamic changes in cardiac tamponade. Am J Cardiol 1990; 66:1487.
  6. Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation 1989; 79:357.
  7. GOLINKO RJ, RUDOLPH AM. The mechanism of pulsus paradoxus during acute pericardial tamponade. J Clin Invest 1963; 42:249.
  8. McGregor M. Current concepts: pulsus paradoxus. N Engl J Med 1979; 301:480.
  9. Spodick DH. Acute pericarditis: current concepts and practice. JAMA 2003; 289:1150.
  10. Roy CL, Minor MA, Brookhart MA, Choudhry NK. Does this patient with a pericardial effusion have cardiac tamponade? JAMA 2007; 297:1810.
  11. Curtiss EI, Reddy PS, Uretsky BF, Cecchetti AA. Pulsus paradoxus: definition and relation to the severity of cardiac tamponade. Am Heart J 1988; 115:391.
  12. Gollapudi RR, Yeager M, Johnson AD. Left ventricular cardiac tamponade in the setting of cor pulmonale and circumferential pericardial effusion. Case report and review of the literature. Cardiol Rev 2005; 13:214.
  13. Antman EM, Cargill V, Grossman W. Low-pressure cardiac tamponade. Ann Intern Med 1979; 91:403.
  14. Appleton CP, Hatle LK, Popp RL. Cardiac tamponade and pericardial effusion: respiratory variation in transvalvular flow velocities studied by Doppler echocardiography. J Am Coll Cardiol 1988; 11:1020.
  15. Swami A, Spodick DH. Pulsus paradoxus in cardiac tamponade: a pathophysiologic continuum. Clin Cardiol 2003; 26:215.
  16. Cohn JN, Pinkerson AL, Tristani FE. Mechanism of pulsus paradoxus in clinical shock. J Clin Invest 1967; 46:1744.
  17. Yalamanchili K, Summer W, Valentine V. Pectus excavatum with inspiratory inferior vena cava compression: a new presentation of pulsus paradoxus. Am J Med Sci 2005; 329:45.
  18. Settle HP Jr, Engel PJ, Fowler NO, et al. Echocardiographic study of the paradoxical arterial pulse in chronic obstructive lung disease. Circulation 1980; 62:1297.
  19. Shiomi T, Guilleminault C, Stoohs R, Schnittger I. Leftward shift of the interventricular septum and pulsus paradoxus in obstructive sleep apnea syndrome. Chest 1991; 100:894.
  20. Lee JC, Atwood JE, Lee HJ, et al. Association of pulsus paradoxus with obesity in normal volunteers. J Am Coll Cardiol 2006; 47:1907.
  21. Cohen SI, Kupersmith J, Aroesty J, Rowe JW. Pulsus paradoxus and Kussmaul's sign in acute pulmonary embolism. Am J Cardiol 1973; 32:271.