INFLUENCE OF PREOPERATIVE BETA-ADRENOCEPT OR BLOCKADE ON POSTOPERATIVE SENSITIVITY TO ADRENERGIC-STIMULATION WITH ADRENALINE IN CARDIOSURGICAL PATIENTS

For the prebypass period various authors have shown that patients on o ral or intravenous beta blocking therapy respond to catecholamine trea tment 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 t o whether beta-blocking agents, administered orally on the morning of the operation, can still have negative effects during this phase of th e procedure. Patients and Methods: 20 patients (NYHA classification II to III) undergoing coronary artery bypass grafting, half of them havi ng been on chronic beta-adrenoceptor blocking therapy, were treated wi th 0,1 mu g/kg/min adrenaline as an infusion, when following cardiopul monary bypass cardiac index was < 2,4 l/min/m(2) with left and/or righ t ventricular filling pressures being normal or raised. Haemodynamic m onitoring consisted of EGG, direct arterial pressure, a pulmonary arte ry catheter and of an additional thermodilution catheter placed direct ly into the coronary sinus. The parameters looked at were mean arteria l pressure (MAP), heart rate (HR), cardiac index (CI), coronary perfus ion pressure (CPP), total peripheral resistance (TPR), pulmonary capil lary wedge pressure (PCWP), right atrial pressure (RAP), pressure work index (PWI), myocardial blood flow (MBF) and myocardial oxygen consum ption (MVO(2)). Arterial and myocardial lactate levels were measured a nd from that myocardial lactate extraction and production were calcula ted. Measurements were made immediately following termination of cardi opulmonary bypass and then after 15, 30, 45 and 60 minutes under conti nuous infusion of adrenaline. In addition left ventricular pressure wa s measured via transseptal needle for calculation of myocardial contra ctility dp/dt(max) directly after termination of cardiopulmonary bypas s 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 lev els within the therapeutic range prior to induction of anaesthesia. Fo llowing 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 increa se of pressure work index (Figure 5), myocardial blood flow (Figure 6) and myocardial oxygen consumption (Figure 7) in both groups. Effect o n afterload was significantly different. In both groups MAP was increa sed 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 i ncreased by 100 dyn . s . cm(-5) on average (Figure 4). As a consequen ce 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 group s in the prebypass period on patients treated with beta blocking agent s, which demonstrate dramatic increases in afterload with no improveme nt in cardiac index following catecholamine administration do not hold true for the postbypass period. The reason could be a wash out effect of the Bretschneider cardioplegia on cardiac beta receptors. The incr ease in MAP, TPR and CPP can be explained by remaining peripheral effe cts of beta blockade as plasma levels of the beta blocking drugs in th e postbypass period were, with 2 exceptions, still within the therapeu tic range. In both groups the increase in myocardial oxygen consumptio n and myocardial blood flow was accompanied by significantly raised ar terial and myocardial lactate levels. Myocardial lactate production wa s observed only in the group without beta blockade. This suggests a re maining protective effect of beta blockade in the postbypass period on myocardial metabolism and against reperfusion injury. This effect is not sufficiently high to reduce sensitivity to adrenergic stimulation.