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Relative roles of heart rate and ventricular stroke volume for the regulation of cardiac output during controlled hypotension with sodium nitroprusside in man
Author(s) -
ZIMPFER M.,
FITZAL S.,
SEMSROTH M.
Publication year - 1982
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1982.tb00933.x
Subject(s) - sodium nitroprusside , stroke volume , cardiology , medicine , cardiac output , stroke (engine) , heart rate , anesthesia , hemodynamics , nitric oxide , blood pressure , mechanical engineering , engineering
. The effects of N‐allyl clonidine (St 567, alinidine), (0.5 mg/kg i.v.), a substance with specific bradycardic action at the sinus node, were studied on a total of thirteen patients in neuroleptanaesthesia and during controlled hypotension with sodium nitroprusside (SNP). Invariably, the fall in blood pressure was associated with an increase in heart rate (20.0 ± 4.3%; P < 0.01), presumably due to an activation of the arterial baroreceptor reflex. Alinidine decreased heart rate to the original level but no fall in cardiac output occurred as ventricular stroke volume and the calculated left ventricular stroke work were increased compensatorily (35.9 ± 7.2% and 35.9 ± 6.7%, P < 0.01, respectively). In patients who received alinidine before the onset of controlled hypotension ( n = 5) SNP failed to elicit an increase in heart rate. It is concluded that in patients under neuroleptanaesthesia tachycardia does not play an important role for the maintenance of an adequate cardiac output during controlled hypotension with SNP.