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Cor pulmonale

INTRODUCTION

Cor pulmonale is the alteration of right ventricular structure or function that is due to pulmonary hypertension caused by diseases affecting the lung or its vasculature. Right-sided heart disease resulting from primary disease of the left side of the heart or from congenital heart disease is not considered within this constellation of disorders [1,2].

Although most of the conditions that cause cor pulmonale are chronic and slowly progressive, patients may also present with acute and life-threatening symptoms. Such abrupt decompensation occurs when the right ventricle is unable to compensate for the imposition of sudden additional demands, resulting either from progression of the underlying disease or a superimposed acute process.

The etiology, clinical characteristics, and treatment of cor pulmonale will be reviewed here. Detailed discussions of the clinical characteristics and treatment of both primary and secondary causes of pulmonary hypertension are presented separately. (See "Overview of pulmonary hypertension" and "Diagnostic evaluation of pulmonary hypertension" and "Pathogenesis of pulmonary hypertension" and "Treatment of pulmonary hypertension".)

ETIOLOGY

Cor pulmonale is a state of cardiopulmonary dysfunction that may result from several different etiologies and pathophysiologic mechanisms (table 1). (See "Overview of pulmonary hypertension".) Possible mechanisms include [3]:

  • Pulmonary vasoconstriction (secondary to alveolar hypoxia or blood acidosis)
  • Anatomic reduction of the pulmonary vascular bed (emphysema, pulmonary emboli, etc)
  • Increased blood viscosity (polycythemia, sickle-cell disease, etc)
  • Increased pulmonary blood flow.
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References Top
  1. MacNee, W. State of the art: Pathophysiology of cor pulmonale in chronic obstructive pulmonary disease (Parts 1 & 2). Am J Respir Crit Care Med 1994; 150:833.
  2. Wiedemann, HP, Matthay, RA. Cor pulmonale. In: Decision Making in Emergency Medicine, Callaham, ML, Barton, CW, Schumaker, HM (Eds), Philadelphia, BC Decker, Inc 1990. p.120.
  3. Wiedemann, HP, Matthay, RA. The management of acute and chronic cor pulmonale. In: Heart-Lung Interactions in Health and Disease, Scharf, SM, Cassidy, SS (Eds), Marcel Dekker, Inc, New York, 1989, p. 915.
  4. Wiedemann, HP, Matthay, RA. Cor pulmonale in chronic obstructive pulmonary disease: circulatory pathophysiology and management. Clin Chest Med 1990; 11:523.
  5. Salvaterra, CG, Rubin, LJ. Investigation and management of pulmonary hypertension in chronic obstructive pulmonary disease. Am Rev Respir Dis 1993; 148:1414.
  6. Morrison, DA, Klein, C, Welsh, C. Relief of right ventricular angina and increased exercise capacity with long term oxygen therapy. Chest 1991; 100:534.
  7. Mesquita, SM, Castro, CR, Ikari, NM, et al. Likelihood of left main coronary artery compression based on pulmonary trunk diameter in patients with pulmonary hypertension. Am J Med 2004; 116:369.
  8. Kawut, SM, Silvestry, FE, Ferrari, VA, et al. Extrinsic compression of the left main coronary artery by the pulmonary artery in patients with long-standing pulmonary hypertension. Am J Cardiol 1999; 83:984.
  9. Weitzenblum, E, Apprill, M, Oswald, M, et al. Pulmonary hemodynamics in patients with chronic obstructive pulmonary disease before and during an episode of peripheral edema. Chest 1994; 105:1377.
  10. Campbell, EJM, Short, DS. The cause of oedema in cor pulmonale. Lancet 1960; 1:1184.
  11. Richens, JM, Howard, P. Oedema in cor pulmonale. Clin Sci 1982; 62:255.
  12. Farber, MO, Roberts, LR, Weinberger, MH, et al. Abnormalities of sodium and H2O handling in chronic obstructive lung disease. Arch Intern Med 1982; 142:1326.
  13. Schafer, JA. Mechanism coupling the absorption of solutes and water in the proximal nephron. Kidney Int 1984; 25:708.
  14. Reihman, DH, Farber, MO, Weinberger, MH, et al. Effect of hypoxemia on sodium and water excretion in chronic obstructive lung disease. Am J Med 1985; 78:87.
  15. Wiedemann, HP, Matthay, RA. Cor pulmonale. In: Heart Disease: Textbook of Cardiovascular Medicine, 5th ed, Braunwald, E (Ed), WB Saunders, Philadelphia, 1997, p. 1604.
  16. Klinger, JR, Hill, NS. Right ventricular dysfunction in chronic obstructive pulmonary disease. Chest 1991; 99:715.
  17. Incalzi, RA, Fuso, L, De Rosa, M, et al. Electrocardiographic signs of chronic cor pulmonale: A negative prognostic finding in chronic obstructive pulmonary disease. Circulation 1999; 99:1600.
  18. Jardin, F, Dubourg, O, Bourdarias, JP. Echocardiographic pattern of acute cor pulmonale. Chest 1997; 111:209.
  19. Mikami, T, Kudo, T, Sakurai, N, et al. Mechanisms for development of functional tricuspid regurgitation determined by pulsed Doppler and two dimensional echocardiography. Am J Cardiol 1984; 53:160.
  20. Yock, PG, Popp, RL. Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation 1984; 70:657.
  21. Otto, C. Textbook of clinical echocardiography. In: Pearlman, S (Ed), Saunders, Philadelphia, 1995.
  22. Berger, M, Haimowitz, A, Van Tosh, A, et al. Quantitative assessment of pulmonary hypertension in patients with tricuspid regurgitation using continuous wave Doppler ultrasound. J Am Coll Cardiol 1985; 6:359.
  23. Himelman, RB, Struve, SN, Brown, JK, et al. Improved recognition of cor pulmonale in patients with severe chronic obstructive pulmonary disease. Am J Med 1988; 84:891.
  24. Singh, H, Ebejer, MJ, Higgens, DA, et al. Acute hemodynamic effects of nifedipine at rest and during maximal exercise in patients with chronic cor pulmonale. Thorax 1985; 40:910.
  25. Dal Nogare, AR, Rubin, LJ. The effects of hydralazine on exercise capacity in pulmonary hypertension secondary to chronic obstructive pulmonary disease. Am Rev Respir Dis 1986; 133:385.
  26. Agostoni, P, Doria, E, Galli, C, et al. Nifedipine reduces pulmonary pressure and vascular tone during short- but not long-term treatment of pulmonary hypertension in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1989; 139:120.
  27. Biernacki, W, Prince, K, Whyte, K, et al. The effect of six months of daily treatment with the beta-2 agonist oral pirbuterol on pulmonary hemodynamics in patients with chronic hypoxic cor pulmonale receiving long-term oxygen therapy. Am Rev Respir Dis 1989; 139:492.
  28. Bratel, T, Hedenstierna, G, Nyquist, O, Ripe, E. Long-term treatment with a new calcium antagonist, felodipine, in chronic obstructive lung disease. Eur J Respir Dis 1986; 68:351.
  29. Mahler, DA, Matthay, RA, Snyder, PE, et al. Sustained-release theophylline reduces dyspnea in non-reversible obstructive airway disease. Am Rev Respir Dis 1985; 131:22.
  30. Bell, RC, Mullins RC III, West LG, et al. The effect of almitrine bismesylate on hypoxemia in chronic obstructive pulmonary disease. Ann Intern Med 1986; 105:342.
  31. MacNee, W, Connaughton, JJ, Rhind, GB, et al. A comparison of the effects of almitrine or oxygen breathing on pulmonary arterial pressure and right ventricular ejection fraction in hypoxic chronic bronchitis and emphysema. Am Rev Respir Dis 1986; 134:559.
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