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Paroxysmal nocturnal dyspnea in CHF: Mechanisms and aminophyline therapy
Volume Number
103 2
Letters
possibly consequent to the marked decline in BP with critical reduction of coronary perfusion. The impressive BP reduction induced by a single dose of nifedipine, either sublingual or oral, demonstrates the potency and efficacy of the drug in the treatment of hypertension. Nevertheless, the observed ECG changes suggest the need for close supervision and monitoring of the initial response in possible coronary patients with severe acute and chronic hypertension.
Hadassah
Y. Yagil, M.D. I. Kobrin, M.D. B. Leibel, R.N. and D. Ben-Ishay, M.D. Dept. of Medicine University Hospital-Mt. Scopus P.0. Box 24035 il-91240 Jerusalem Israel
REFERENCES
1. Guaxzi M, Olivari MT, Polese A, Fiorentini C, Magrini F, Moruzzi P: Nifedipine, a new anti-hypertensive with rapid action. Clin Pharmacol Ther 22:528, 1977. 2. Olivari MT, Bartorelli C, Polese A, Fiorentini C, Moruzzi P, Guazzi M: Treatment of hypertension with nifedipine, a calcium antagonist agent. Circulation 59~1056, 1979. 3. Goldberg S, Reicheck N, Wilson J, Hirshfeld JW, Muller J, Kastor JA: Nifedipine in the treatment of Prinzmetal’s angina. Am J Cardiol 44~804, 1979. 4. Jariwalla AG, Anderson EG: Production of ischemic cardiac pain by nifedipine. Br Med J 1:1181, 1978. 5. McMahon FG: Management of essential hypertension. New York, 1978, Futura Publishing Co, p 229, 383, 386.
to the Editor
311
hyperventilation phase. By careful questioning or by observation of the patient at night, this may be distinguished from the more severe dyspnea associated with pulmonary edema. Such paroxysmal nocturnal dyspnea may respond to aminophylline, since such therapy often relieves Cheyne-Stokes breathing in patienta.3,4 P. J. Rees, M.A., M.R.C.P. T.J.H. Clark, M.D., F.R.C.P. Respiratory Function Unit Clinical Science Laboratories Guy’s Hospital, St. Thomas Street London SE1 9RT, United Kingdom REFERENCES
Harrison TR, King CE, Calhoun JA, Harrison WG: Congestive-heart failure. Cheyne-Stokes respiration as the cause of paroxysmal dyspnoea at the onset of sleep. Arch Intern Med 53:891, 1934. Webb P: Periodic breathing during sleep. J Appl Physiol 372399, 1974. Dowel1 AR, Heyman A, Sieker HO, Tripathy K: Effect of aminophylline on respiratory centre sensitivity in CheyneStokes respiration and in pulmonary emphysema. N Engl J Med 273:1447, 1965. Moyer JH, Miller SI, Tashnek AB, Bowman R: Effect of theophylline with ethylenediamine (aminophylline) on cerebral haemodynamics in the presence of cardiac failure with and without Cheyne-Stokes respiration. J Clin Invest 31:267, 1952.
EARLY MOBILIZATION AFTER UNCOMPLICATED MYOCARDIAL INFARCTION To the Editor:
PAROXYSMAL NOCTURNAL DYSPNEA IN CHF: MECHANISMS AND AMINOPHYLLINE THERAPY To the Editor:
Nocturnal breathlessness occurs in a number of conditions including congestive heart failure (CHF), asthma, and chronic airflow obstruction. In CHF such breathlessness may be caused by pulmonary edema, but not all episodes of nocturnal dyspnea in cardiac patients can be attributed to pulmonary edema. Harrison et al.’ observed in 1934 that, during the first two hours of sleep, CHF patients may wake with dyspnea related to Cheyne-Stokes respiration. To study this further, we monitored breathing at night in four CHF patients using pairs of magnetometer coils to detect chest wall and abdominal movement and thermistors to register airflow at nose and mouth. These four patients had various degrees of CHF and all complained of sleep disturbance with nocturnal breathlessness. They were all found to have a periodic pattern of respiration during sleep with apneic periods lasting up to 60 seconds. This produced a disturbance of sleep during the hyperventilation phase of the periodic respiration in all four patients. This disturbance varied from mild restlessness to repeated awakenings with marked dyspnea every 2 to 3 minutes. These studies indicate that periodic breathing may produce a range of sleep disturbances in CHF. In some patients there may be paroxysmal dyspnea, while in others there may be mild sleep disturbance contributing to tiredness and sleepiness during the day. Although periodic breathing occurs in normal subjects,2 the decreased lung compliance in CHF is likely to lead to dyspnea during the
A policy of early mobilization after myocardial infarction (MI) has been supported by a number of retrospective studies and controlled trials which have shown no adverse effects.‘” The present trial’ expands on previous investigations in that it was multicenter, employed relatively early mobilization, involved more patients, and provided long follow-up. During 1973 and 1974,34 physicians in 13 hospitals throughout Wales collaborated in a multicenter randomized trial of mobilization at 5 days compared with 10 days after uncomplicated MI.’ Eligible patients were those with acute MI aged under 70 years and admitted to hospital within 48 hours of initial cardiac pain. Patients with uncomplicated MI were randomly selected to be mobilized on the fifth or tenth day after MI onset. Patients considered to have complicated MI (thromboembolic complications, persistence of heart failure, hypotension, arrhythmias or cardiac pain) were excluded on day 5 at their physician’s discretion. Mobilization consisted of sitting out of bed and walking on the level after 1 week. Details of mobilization and total hospital stay were not controlled but guidelines were given and average hospital stay was 13 and 16 days in the two trial groups, respectively. Selected clinical information was recorded on days 0, 5, and 10 for each patient and follow-up was planned for 12 months but chronic assessment was up to 4 years later; median follow-up time was I3 months. Mortality was calculated using life table survivorship to 3 years and the two mobilization groups were compared by Mantel Haenzel test. Of 1039 patients, 293 (28%) were excluded because of complications and 746 were entered into the trial; 4 were lost to follow-up. Results were compared in 742 patients; 347 (47% ) mobilized on day 5 and 395 (53% ) on day 10. The two groups were well matched for age, sex, past-history (including MI, angina and
103 2
Letters
possibly consequent to the marked decline in BP with critical reduction of coronary perfusion. The impressive BP reduction induced by a single dose of nifedipine, either sublingual or oral, demonstrates the potency and efficacy of the drug in the treatment of hypertension. Nevertheless, the observed ECG changes suggest the need for close supervision and monitoring of the initial response in possible coronary patients with severe acute and chronic hypertension.
Hadassah
Y. Yagil, M.D. I. Kobrin, M.D. B. Leibel, R.N. and D. Ben-Ishay, M.D. Dept. of Medicine University Hospital-Mt. Scopus P.0. Box 24035 il-91240 Jerusalem Israel
REFERENCES
1. Guaxzi M, Olivari MT, Polese A, Fiorentini C, Magrini F, Moruzzi P: Nifedipine, a new anti-hypertensive with rapid action. Clin Pharmacol Ther 22:528, 1977. 2. Olivari MT, Bartorelli C, Polese A, Fiorentini C, Moruzzi P, Guazzi M: Treatment of hypertension with nifedipine, a calcium antagonist agent. Circulation 59~1056, 1979. 3. Goldberg S, Reicheck N, Wilson J, Hirshfeld JW, Muller J, Kastor JA: Nifedipine in the treatment of Prinzmetal’s angina. Am J Cardiol 44~804, 1979. 4. Jariwalla AG, Anderson EG: Production of ischemic cardiac pain by nifedipine. Br Med J 1:1181, 1978. 5. McMahon FG: Management of essential hypertension. New York, 1978, Futura Publishing Co, p 229, 383, 386.
to the Editor
311
hyperventilation phase. By careful questioning or by observation of the patient at night, this may be distinguished from the more severe dyspnea associated with pulmonary edema. Such paroxysmal nocturnal dyspnea may respond to aminophylline, since such therapy often relieves Cheyne-Stokes breathing in patienta.3,4 P. J. Rees, M.A., M.R.C.P. T.J.H. Clark, M.D., F.R.C.P. Respiratory Function Unit Clinical Science Laboratories Guy’s Hospital, St. Thomas Street London SE1 9RT, United Kingdom REFERENCES
Harrison TR, King CE, Calhoun JA, Harrison WG: Congestive-heart failure. Cheyne-Stokes respiration as the cause of paroxysmal dyspnoea at the onset of sleep. Arch Intern Med 53:891, 1934. Webb P: Periodic breathing during sleep. J Appl Physiol 372399, 1974. Dowel1 AR, Heyman A, Sieker HO, Tripathy K: Effect of aminophylline on respiratory centre sensitivity in CheyneStokes respiration and in pulmonary emphysema. N Engl J Med 273:1447, 1965. Moyer JH, Miller SI, Tashnek AB, Bowman R: Effect of theophylline with ethylenediamine (aminophylline) on cerebral haemodynamics in the presence of cardiac failure with and without Cheyne-Stokes respiration. J Clin Invest 31:267, 1952.
EARLY MOBILIZATION AFTER UNCOMPLICATED MYOCARDIAL INFARCTION To the Editor:
PAROXYSMAL NOCTURNAL DYSPNEA IN CHF: MECHANISMS AND AMINOPHYLLINE THERAPY To the Editor:
Nocturnal breathlessness occurs in a number of conditions including congestive heart failure (CHF), asthma, and chronic airflow obstruction. In CHF such breathlessness may be caused by pulmonary edema, but not all episodes of nocturnal dyspnea in cardiac patients can be attributed to pulmonary edema. Harrison et al.’ observed in 1934 that, during the first two hours of sleep, CHF patients may wake with dyspnea related to Cheyne-Stokes respiration. To study this further, we monitored breathing at night in four CHF patients using pairs of magnetometer coils to detect chest wall and abdominal movement and thermistors to register airflow at nose and mouth. These four patients had various degrees of CHF and all complained of sleep disturbance with nocturnal breathlessness. They were all found to have a periodic pattern of respiration during sleep with apneic periods lasting up to 60 seconds. This produced a disturbance of sleep during the hyperventilation phase of the periodic respiration in all four patients. This disturbance varied from mild restlessness to repeated awakenings with marked dyspnea every 2 to 3 minutes. These studies indicate that periodic breathing may produce a range of sleep disturbances in CHF. In some patients there may be paroxysmal dyspnea, while in others there may be mild sleep disturbance contributing to tiredness and sleepiness during the day. Although periodic breathing occurs in normal subjects,2 the decreased lung compliance in CHF is likely to lead to dyspnea during the
A policy of early mobilization after myocardial infarction (MI) has been supported by a number of retrospective studies and controlled trials which have shown no adverse effects.‘” The present trial’ expands on previous investigations in that it was multicenter, employed relatively early mobilization, involved more patients, and provided long follow-up. During 1973 and 1974,34 physicians in 13 hospitals throughout Wales collaborated in a multicenter randomized trial of mobilization at 5 days compared with 10 days after uncomplicated MI.’ Eligible patients were those with acute MI aged under 70 years and admitted to hospital within 48 hours of initial cardiac pain. Patients with uncomplicated MI were randomly selected to be mobilized on the fifth or tenth day after MI onset. Patients considered to have complicated MI (thromboembolic complications, persistence of heart failure, hypotension, arrhythmias or cardiac pain) were excluded on day 5 at their physician’s discretion. Mobilization consisted of sitting out of bed and walking on the level after 1 week. Details of mobilization and total hospital stay were not controlled but guidelines were given and average hospital stay was 13 and 16 days in the two trial groups, respectively. Selected clinical information was recorded on days 0, 5, and 10 for each patient and follow-up was planned for 12 months but chronic assessment was up to 4 years later; median follow-up time was I3 months. Mortality was calculated using life table survivorship to 3 years and the two mobilization groups were compared by Mantel Haenzel test. Of 1039 patients, 293 (28%) were excluded because of complications and 746 were entered into the trial; 4 were lost to follow-up. Results were compared in 742 patients; 347 (47% ) mobilized on day 5 and 395 (53% ) on day 10. The two groups were well matched for age, sex, past-history (including MI, angina and