Copyright © 1990 by the European Society of Cardiology.
© 1990 The European Society of Cardiology
Acute haemodynamic effects of intravenous infusion of adenosine in conscious man
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Departments of Pharmacology and Therapeutics, University of Wales College of Medicine Health Park, Cardiff CF4 4XN, United Kingdom
*Department of Cardiology, University of Wales College of Medicine Health Park, Cardiff CF4 4XN, United Kingdom
Received 20 July 1989; revised 26 January 1990; .
Address for correspondence: Dr P. G. Reid, Department of Cardiology, Freeman Hospital, Freeman Road, Newcastle-upon-Tyne, NE77DN, United Kingdom
Abstract
The acute haemodynamic effects of intravenous infusion of adenosine, a dilator of most vascular beds, were studied in 16 patients (seven with coronary artery disease, nine with normal coronary arteries) undergoing cardiac catheter ization for investigation of chest pain.
At the lowest dose used (4.3 mg min'1) adenosine increased minute ventilation by 44% (P <0.01, n = 11) and reduced pulmonary vascular resistance by 20% (P<0.05) without causing other significant haemodynamic changes. Symptoms, including chest discomfort in 14 patients and dyspnoea in 11, limited the maximum dose to 8.5 ±2.3 mg min–1 (mean±SD, 108 ±24 µg kg–1 min–1). At this dose, adenosine reduced pulmonary and systemic vascular resistance (by 38% and 34%, respectively) and increased heart rate (by 34%), stroke index (by 12%) and cardiac index (by 52%). Systemic blood pressure and right atrial pressure did not change. Unexpectedly, adenosine increased left ventricular end-diastolic pressure (LVEDP) (from 5 ±6 to 14 ± 10 mmHg, n = 8), pulmonary capillary wedge pressure (from 3 ±2 to 10 ±5 mmHg, n= 16) and consequently mean pulmonary artery pressure (from 10 ±2 to 16 ±5 mmHg). Minute ventilation increased by 84% (n= 11), resulting in hypocapnia (Pco: 31 ±3mmHg, n-8) andalkalosis (pH: 7.46±0.02, n = 8). Oxygen consumption was unchanged during the infusion, but increased by 21% 5 minpost infusion. All effects were similar in patients with and without coronary artery disease.
Adenosine therefore causes pulmonary and systemic vasodilation and respiratory stimulation. Symptoms and an increase in L VEDP of uncertain cause, which occur with high doses, may limit the use of adenosine as a systemic vasodilator in conscious subjects. However at lower doses adenosine causes selective pulmonary vasodilation which merits further study.
Key Words: Adenosine • myocardial contraction • pulmonary circulation • respiration • vasodilator agents
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