Haemodynamic Dose-Response Effects of a Transdermal Nitrate Delivery System in Acute Myocardial Infarction With and Without Left Heart Failure

1988 ◽  
Vol 11 (2) ◽  
pp. 151-157
Author(s):  
S. P. Verma ◽  
B. Silke ◽  
G. W. Reynolds ◽  
M. Hafizullah ◽  
G. I.C. Nelson ◽  
...  
1985 ◽  
Vol 109 (3) ◽  
pp. 720-722 ◽  
Author(s):  
Marc Renard ◽  
Philippe Jacobs ◽  
Isabelle Liebens ◽  
Alain Friart ◽  
Roland Bernard

Gerontology ◽  
1984 ◽  
Vol 30 (6) ◽  
pp. 408-413 ◽  
Author(s):  
Marc Renard ◽  
Roland Bernard ◽  
Christian Melot ◽  
Ph. Jacobs ◽  
Marc Englert

1980 ◽  
Vol 59 (2) ◽  
pp. 115-121 ◽  
Author(s):  
H. Clarke ◽  
S. Dhingra ◽  
N. R. Anthonisen

1. In 18 patients with acute myocardial infarction, we measured ventilation, frequency, inspiratory duration and the pressure at the mouth 0.1 s after the onset of inspiration against an occluded airway; mean inspiratory flow and the fraction of the breathing cycle devoted to inspiration were calculated. Measurements were made on 2–3 consecutive days soon after admission and repeated 4–10 days after admission. 2. Eight patients showed no clinical evidence of left heart failure at any time; in these patients no changes in breathing pattern, ventilation or occlusion pressure were observed. 3. Ten patients were in heart failure, as judged by the presence of râles and/or hypoxaemia on day 1 of the study, and all had recovered on the last day. When in failure these patients demonstrated increased minute ventilation, occlusion pressure was increased more than was mean inspiratory flow and their breathing pattern was altered. Tidal volume was similar to that in patients without failure and did not change with time, but frequency was initially high and fell as recovery from failure occurred. The duration of inspiration was decreased during failure, so mean inspiratory flow was increased. The fraction of the breathing cycle devoted to inspiration was constant and similar to that in patients without failure. 4. While in failure no patients were acidotic and not all patients were hypoxaemic; administration of oxygen did not influence results in two patients during failure. 5. These results indicate that clinically detectable pulmonary oedema is associated with increased ventilatory drive, which cannot be explained on the basis of hypoxaemia or hypercapnia. The observed changes in breathing pattern were probably due at least in part to vagal reflexes, and these may have contributed to the increase in drive.


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