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Pulsus Alternans in Effusive Pericarditis
Thorac SurK 15:210, 1973 2 Gopalrao T, Ford WB: A simple tag to localize aorta-to(:oronary artery saphenous vein graft ostiwn. Ann Thorae Surg 14:217, 1972 3 Elias DO, Burman SO: A radiopaque suture to identify the aortosaphenous vein graft orifice. J Thorac Cardiovasc Surg 67 :282-284, 1974
Pulsus Alternans
In
RIGHT VENTRICULAR PRESSURE
Effusive
Pericarditis To the Editor: The report of Calick and Berger! on pulsus alternans (PA) in the November, 1973 issue of Chest, may be supplemented by the following case, which adds an additional etiologic factor to the known causes of pulsus alternans. We recently saw a patient with pneumococcal effusive pericarditis and pulsus alternans. To our knowledge, effusive pericarditis has not yet been reported among the causes of PA.2.3 This condition in our patient was confirmed by right heart catheterization, including right atrial angiography, and by surgery. The systolic pressure in the right ventricle (Fig 1) and pulmonary artery alternated between 23 and 32 nun Hg. The higher systolic pressure was preceded by an end-diastolic pressure of 7.0 mm Hg, and the lower systolic pressure was followed by a lower enddiastolic pressure of 5.0 mm Hg. The mean right atrial pressure was slightly elevated (7.0 mm Hg). Although the exact mechanism of PA in our patient was not clear, there may have been three possible causes: a) myopericarditis;4 b) tachycardia;5.6 and c) decreased venous return. 7 Any inBammatory process of the pericardium can extend to the myocardium, but if myopericarditis involves the myocardium without producing heart failure, it is probably not severe enough to cause PA. An increased heart rate and a decreased venous return could be factors causing pulsus alternans.5-7 Pulsus alternans has indeed been reported in various supraventricular tachyarrhythmias, usually at the beginning of the paroxysm. 6 The mechanism of tachycardia induced PAis not completely understood. Saunders and Ord6 believe that in addition to tachycardia, decreased venous return may contribute to the PAin these patients. Decreased venous return, even without tachycardia, can elicit PA in patients with organic heart disease. 7 The recent report describing pulsus alternans in pulmonary artery hypertension secondary to pulmonary embolism, also lists several other known causes 506 COMMUNICATIONS TO THE EDITOR
FIGURE
1
for PA, but does not include effusive pericarditis among the etiologic factors encountered in the literature. 7 The heart rate in our patient when PA was present was 120/min, and more than 400 ml of purulent Buid was found in the pericardial sac. This amount of Buid may contribute to impairment of diastolic filling of the heart. In conclusion, our findings show that a combination of tachycardia and decreased venous return, with or without concomitant myopericarditis, contributed to the appearance of PAin a patient with purulent pericarditis. Paul Schweitzer, M.D. Jersey City Medical Center Jersey City, New Jersey REFERENCES
1 Calick A, Berger S: Pulmonary artery pulsus a1temans associated with pulmonary embolism. Chest 64:5,663-664, 1973 2 Hurst JW, Logue RB: The Heart (3rd ed). New York, McGraw-Hill, 1974, p 176 3 Harris LC, Nghiem QX, Schreiber MH, et al: Severe pulsus altemans associated with primary myocardial disease in children. Observation on clinical features, hemodynamic findings, mechanism and prognosis. Circulation 34:948-961, 1966 4 Gardiner AJS, Short D: Four faces of acute myopericarditis. Br Heart J 35:433-442, 1973 5 Lewis T: The Mechanism and Graphic Registration of the Heart Beat. London, Shaw and Sons, 1920, p 373 6 Saunders DE, Ord JW: The hemodynamic effects of paroxysmal supraventricular tachycardia in patients with Wolff-Parkinson-White Syndrome. Am J Cardiol 9:223236, 1962 7 Friedman B, Daily WM, Sheffield R: Orthostatic factors in pulsus altemans. Circulation 6:864-873, 1953
CHEST, 67: 4, APRil, 1975
Pulsus Alternans
In
RIGHT VENTRICULAR PRESSURE
Effusive
Pericarditis To the Editor: The report of Calick and Berger! on pulsus alternans (PA) in the November, 1973 issue of Chest, may be supplemented by the following case, which adds an additional etiologic factor to the known causes of pulsus alternans. We recently saw a patient with pneumococcal effusive pericarditis and pulsus alternans. To our knowledge, effusive pericarditis has not yet been reported among the causes of PA.2.3 This condition in our patient was confirmed by right heart catheterization, including right atrial angiography, and by surgery. The systolic pressure in the right ventricle (Fig 1) and pulmonary artery alternated between 23 and 32 nun Hg. The higher systolic pressure was preceded by an end-diastolic pressure of 7.0 mm Hg, and the lower systolic pressure was followed by a lower enddiastolic pressure of 5.0 mm Hg. The mean right atrial pressure was slightly elevated (7.0 mm Hg). Although the exact mechanism of PA in our patient was not clear, there may have been three possible causes: a) myopericarditis;4 b) tachycardia;5.6 and c) decreased venous return. 7 Any inBammatory process of the pericardium can extend to the myocardium, but if myopericarditis involves the myocardium without producing heart failure, it is probably not severe enough to cause PA. An increased heart rate and a decreased venous return could be factors causing pulsus alternans.5-7 Pulsus alternans has indeed been reported in various supraventricular tachyarrhythmias, usually at the beginning of the paroxysm. 6 The mechanism of tachycardia induced PAis not completely understood. Saunders and Ord6 believe that in addition to tachycardia, decreased venous return may contribute to the PAin these patients. Decreased venous return, even without tachycardia, can elicit PA in patients with organic heart disease. 7 The recent report describing pulsus alternans in pulmonary artery hypertension secondary to pulmonary embolism, also lists several other known causes 506 COMMUNICATIONS TO THE EDITOR
FIGURE
1
for PA, but does not include effusive pericarditis among the etiologic factors encountered in the literature. 7 The heart rate in our patient when PA was present was 120/min, and more than 400 ml of purulent Buid was found in the pericardial sac. This amount of Buid may contribute to impairment of diastolic filling of the heart. In conclusion, our findings show that a combination of tachycardia and decreased venous return, with or without concomitant myopericarditis, contributed to the appearance of PAin a patient with purulent pericarditis. Paul Schweitzer, M.D. Jersey City Medical Center Jersey City, New Jersey REFERENCES
1 Calick A, Berger S: Pulmonary artery pulsus a1temans associated with pulmonary embolism. Chest 64:5,663-664, 1973 2 Hurst JW, Logue RB: The Heart (3rd ed). New York, McGraw-Hill, 1974, p 176 3 Harris LC, Nghiem QX, Schreiber MH, et al: Severe pulsus altemans associated with primary myocardial disease in children. Observation on clinical features, hemodynamic findings, mechanism and prognosis. Circulation 34:948-961, 1966 4 Gardiner AJS, Short D: Four faces of acute myopericarditis. Br Heart J 35:433-442, 1973 5 Lewis T: The Mechanism and Graphic Registration of the Heart Beat. London, Shaw and Sons, 1920, p 373 6 Saunders DE, Ord JW: The hemodynamic effects of paroxysmal supraventricular tachycardia in patients with Wolff-Parkinson-White Syndrome. Am J Cardiol 9:223236, 1962 7 Friedman B, Daily WM, Sheffield R: Orthostatic factors in pulsus altemans. Circulation 6:864-873, 1953
CHEST, 67: 4, APRil, 1975