Magometschnigg D, Hörtnagl H, Gassner A, Hammerle A F, Kleinberger G, Lenzhofer R, Lochs H, Pall H, Pichler M
Clin Cardiol. 1981 Sep-Oct;4(5):238-42. doi: 10.1002/clc.4960040505.
The use of neuroleptanalgesia in acute myocardial infarction offers the possibility of reducing pain and emotional stress. The influence of such treatment on hemodynamic parameters (heart rate, cardiac output, stroke volume, peripheral resistance, systemic blood pressure, and pulmonary pressure) and on the plasma level of adrenaline and noradrenaline has been studied in 6 patients with acute myocardial infarction. This results demonstrate that during neuroleptanalgesia the already elevated levels of noradrenaline and adrenaline further increase. This increase was most pronounced in the patients with the highest initial levels of catecholamines. Since the peripheral resistance and systolic and diastolic blood pressures decrease concomitantly, it is concluded that the increase in levels of noradrenaline and adrenaline further increase. This increase was most pronounced in the plasma catecholamines is due to a reaction of the sympathetic nervous system to the alpha-adrenergic receptor blocking activity of droperidol causing vasodilation. The data indicate that pain, emotional stress, and anxiety in the acute phase of myocardial infarction do not play the expected essential role for the activation of the sympathetic nervous system generally observed in acute myocardial infarction. Additionally, the data demonstrate that drugs producing a vasodilation can have a deteriorating effect on the hemodynamic situation and that a reduction of the afterload by vasodilating drugs can result in a further increase in the release of catecholamines.
