[Does chronic oral treatment with beta-receptor blockers have an effect on positive inotropic therapy of coronary patients with adrenaline after extracorporeal circulation?].

UNLABELLED: For the prebypass period various authors have shown that patients on oral or intravenous beta blocking therapy respond to catecholamine treatment with marked increase in afterload and no change in cardiac index. Since positive inotropic therapy is usually not necessary until, but after termination of cardiopulmonary bypass, the question arises as to whether beta-blocking agents administered orally on the morning of the operation, can still have negative effects during this phase of the procedure.

PATIENTS AND METHODS: 20 patients (NYHA classification II to III) undergoing coronary artery bypass grafting, half of them having been on chronic beta-adrenoceptor blocking therapy, were treated with 0.1 micrograms/kg/min adrenaline as an infusion, when following cardiopulmonary bypass cardiac index was < 2.4 l/min/m2 with left and/or right ventricular filling pressures being normal or raised. Haemodynamic monitoring consisted of ECG, direct arterial pressure, a pulmonary artery catheter and of an additional thermodilution catheter placed directly into the coronary sinus. The parameters looked at were mean arterial pressure (MAP), heart rate (HR), cardiac index (CI), coronary perfusion pressure (CPP), total peripheral resistance (TPR), pulmonary capillary wedge pressure (PCWP), right atrial pressure (RAP), pressure work index (PWI), myocardial blood flow (MBF) and myocardial oxygen consumption (MVO2). Arterial and myocardial lactate levels were measured and from that myocardial lactate extraction and production were calculated. Measurements were made immediately following termination of cardiopulmonary bypass and then after 15, 30, 45 and 60 minutes under continuous infusion of adrenaline. In addition left ventricular pressure was measured via transseptal needle for calculation of myocardial contractility dp/dtmax directly after termination of cardiopulmonary bypass and 15 minutes later with adrenaline therapy. Prior to induction of anaesthesia and following termination of cardiopulmonary bypass blood samples were taken to measure plasma levels of the beta blocking drug.

RESULTS: All 10 patients on oral beta blocking therapy had plasma levels within the therapeutic range prior to induction of anaesthesia. Following cardiopulmonary bypass the plasma levels had fallen by 50% on average, but with 2 exceptions, they were still within the therapeutic range (Table 2). Irrespective of the fact whether preoperatively beta blockers had been taken, adrenaline caused a significant increase in contractility (Table 3), mean arterial pressure (Figure 1), heart rate (Table 3) and cardiac index (Figure 2). There was a comparable increase of pressure work index (Figure 5), myocardial blood flow (Figure 6) and myocardial oxygen consumption (Figure 7) in both groups. Effect on afterload was significantly different. In both groups MAP was increased but that was more marked in the presence of beta blockade (Figure 1). Total peripheral resistance fell in the group without preoperative beta blockade whereas in patients on preoperative beta blockade TPR increased by 100 dyn.s.cm-5 on average (Figure 4). As a consequence adrenaline infusion caused an increase in CPP only in the presence of beta blockade (Figure 3). In both groups adrenaline infusion caused an increase in arterial and myocardial lactate levels (Tables 6 and 7). Some patients without preoperative beta blockade showed myocardial lactate production whereas in the presence of beta blockade myocardial lactate extraction was found at all points of measurement (Figure 8).

CONCLUSION: Our results show, that observations made by various groups in the prebypass period on patients treated with beta blocking agents, which demonstrate dramatic increases in afterload with no improvement in cardiac index following catecholamine administration do not hold true for the post-bypass period. The reason could be a wash out effect of the Bretschneider cardioplegia on cardiac beta receptors.