[The cardiovascular effects of the inspiratory N2O-concentration during piritramide anaesthesia in the dog (author's transl)].

Administration of nitrous oxide following large doses of narcotics has been reported to impair myocardial performance. In this investigation the effect of the inspiratory N2O-concentration (F1N2O = 0.0; 0.2; 0.4; 0.6; 0.8) upon haemodynamics, inotropism of the heart, coronary blood flow and myocardial oxygen consumption was studied in 8 dogs, which were normoventilated and narcotized with piritramide infused continuously (2.5 mg/kg-h). While 40% N2O(F1N2O = 0.4) decreased cardiac index (18%) and mean arterial pressure (5%) and increased total peripheral resistance (11%) significantly, the remaining inspiratory N2O-concentrations did not affect these parameters considerably. Load data, heart rate and the continuous decrease of LVdp/dtmax from 3170 mm Hg/s (F1N2O - 0.0) to 2175 mm Hg/s (F1N2O = 0.8) indicated negative inotropic properties of high concentrations of nitrous oxide. The myocardial oxygen demand, which was adequately met by the coronary blood flow, decreased with increasing N2O-concentrations initially by 18% (F1N2O = 0.4) due to bradycardia, slight hypotension and reduction in inotropism. Inhalation of 80% N2O, however, returned the energy demand of the heart to control levels (F1N2O = 0.0) resulting from increased myocardial wall-tension (increase in left ventricular end-diastolic pressure by 30%). The efficiency of left ventricular external work decreased from 18.6% (F1N2O = 0.0) to 14.7% (F1N2O - 0.8) indicating that myocardial performance was uneconomically influenced by high inspiratory N2O-concentrations and large doses of narcotics. The clinical implications of the results were discussed.