Signs of myocardial ischaemia after injection of oxytocin: a randomized double-blind comparison of oxytocin and methylergometrine during Caesarean section.

BACKGROUND: ECG changes, similar to those seen during myocardial ischaemia, together with symptoms of chest pain, are common during Caesarean section (CS). We hypothesized that oxytocin administration has cardiovascular effects leading to these symptoms and ECG changes. METHODS: Forty women undergoing elective CS under spinal anaesthesia were given an i.v. bolus of either 10 IU of oxytocin (Group OXY-CS, n=20) or 0.2 mg of methylergometrine (Group MET-CS, n=20), in a double-blind, randomized fashion after delivery. Ten healthy, non-pregnant, non-anaesthetized women were used as normal controls (Group OXY-NC, n=10) and were given 10 IU of oxytocin i.v. Twelve-lead ECG, on-line, computerized vectorcardiography (VCG), and invasive arterial pressure were recorded. RESULTS: Oxytocin produced a significant increase in heart rate, +28 (SD 4) and +52 (3) beats min(-1) [mean (SEM); P<0.001], decreases in mean arterial pressure, -33 (2) and -30 (3) mm Hg (P<0.001), and increases in the spatial ST-change vector magnitude (STC-VM), +77 (12) and +114 (8) microV (P<0.001), in CS patients and controls, respectively. Symptoms of chest pain and subjective discomfort were simultaneously present. Methylergometrine produced mild hypertension and no significant ECG changes. CONCLUSIONS: Oxytocin administered as an i.v. bolus of 10 IU induces chest pain, transient profound tachycardia, hypotension, and concomitant signs of myocardial ischaemia according to marked ECG and STC-VM changes. The effects are related to oxytocin administration and not to pregnancy, surgical procedure, delivery, or sympathetic block from spinal anaesthesia.

Hemodynamics, cerebral circulation, and oxygen saturation in Cheyne-Stokes respiration.

Because cardiovascular disorders and stroke may induce Cheyne-Stokes respiration, our purpose was to study the interaction among cerebral activity, cerebral circulation, blood pressure, and blood gases during Cheyne-Stokes respiration. Ten patients with heart failure or a previous stroke were investigated during Cheyne-Stokes respiration with recordings of daytime polysomnography, cerebral blood flow velocity, intra-arterial blood pressure, and intra-arterial oxygen saturation with and without oxygen administration. There were simultaneous changes in wakefulness, cerebral blood flow velocity, and respiration with accompanying changes in blood pressure and heart rate approximately 10 s later. Cerebral blood flow velocity, blood pressure, and heart rate had a minimum occurrence in apnea and a maximum occurrence during hyperpnea. The apnea-induced oxygen desaturations were diminished during oxygen administration, but the hemodynamic alterations persisted. Oxygen desaturations were more severe and occurred earlier according to intra-arterial measurements than with finger oximetry. It is not possible to explain Cheyne-Stokes respiration by alterations in blood gases and circulatory time alone. Cheyne-Stokes respiration may be characterized as a state of phase-linked cyclic changes in cerebral, respiratory, and cardiovascular functions probably generated by variations in central nervous activity.

Impairment of cerebral perfusion during obstructive sleep apneas.

Cerebral circulation was studied in six patients with obstructive sleep apnea (OSA) by transcranial Doppler. Cerebral blood flow velocity (CBFV), pulsatility index (Pi), intra-arterial radial blood pressure, transcutaneous blood gases, and respiration were recorded during sleep with or without apneas. There was a concomitant increase of mean arterial pressure (Pa) and CBFV by 11 +/- 6% (p < 0.001) and 15 +/- 6% (p < 0.001) compared with baseline at 5.1 +/- 2.4 and 5.3 +/- 2.6 s, respectively, after apnea termination. Pa and CBFV decreased to a minimum of -8 +/- 2% (p < 0.001) and -23 +/- 8% (p < 0.001), respectively, below baseline at 19.8 +/- 5.0 and 19.4 +/- 4.5 s after apnea. Values returned to baseline within 60 s, except during repetitive apneas, which were associated with prolonged periods of reduced Pa and CBFV. Pi changed inversely to CBFV and rose to 34 +/- 15% (p < 0.001) above baseline 19.5 +/- 5.5 s after the end of apnea because of a decrease in diastolic CBFV. There was a close correlation between Pa and CBFV (r = 0.67, p < 0.001), indicating that cerebral autoregulation is insufficient to protect the brain from rapid systemic pressure changes in OSA. The findings suggest that apneas during sleep are associated with profound changes in cerebral blood flow. Apnea-induced hypoxemia combined with reduced cerebral perfusion may predispose to nocturnal cerebral ischemia in patients with OSA.

A new method for clinical assessment of the negative inotropic action of anaesthetics--with special reference to isoflurane and its effect on myocardial oxygenation.

A new method for maintaining the peripheral determinants of myocardial oxygen demand constant is described. Intravenously administered phenylephrine and nitroglycerin were used to control afterload and preload. Heart rate was kept constant with atrial pacing. The method was used to establish the in vivo negative inotropic effect of 1% end-tidal isoflurane in eight patients with ischaemic heart disease during positive pressure ventilation (IPPV). Stroke volume measured during steady-state isoflurane anaesthesia and IPPV with preload, afterload, and heart rate kept constant was 23% below awake control. The decrease in myocardial oxygen consumption was 22% and correlated well (r = 0.891) with the fall in left ventricular performance (stroke volume).

In vitro analysis of thermal transport in coronary sinus thermodilution catheters.

The continuous thermodilution technique for measuring blood flow in the range 50-300 ml/min was evaluated in vitro. Experiments indicated that thermotransport within the catheter from the indicator line to the mixing thermistor exists. The resulting error in calculated thermodilution flow will increase with increasing flow rate. A correction factor for thermal transport, Ft, obtained from a blood circulation model was incorporated in a modified formula for calculation of thermodilution flow. Flows derived with the standard Ganz formula were significantly lower than timed volumetric flows, whereas flows obtained with the modified formula agreed with volumetric flow. The coefficient of variation for four consecutive measurements was 3.4%.

Droperidol inhibits the effects of intravenous ketamine on central hemodynamics and myocardial oxygen consumption in patients with generalized atherosclerotic disease.

A 2-mg/kg dose of ketamine was administered intravenously to 16 patients with generalized atherosclerotic disease. Eight patients were given 200 mu/kg of droperidol intravenously 10 min before ketamine administration; eight patients not given droperidol served as controls. Central hemodynamics, coronary flow (thermodilution technique) and myocardial oxygen, lactate, hypoxanthine, and catecholamine balances were studied. In control patients, ketamine increased mean blood pressure by 42%, pulmonary capillary wedge pressure by 144%, mean right atrial pressure by 60%, heart rate by 15%, and systemic vascular resistance by 40% without changes in cardiac index, stroke volume index, or left ventricular stroke work index. These data indicate that cardiac performance did not increase in parallel with the rise in afterload. However, the 50% increase in myocardial oxygen demand was associated with a 48% increase in coronary blood flow without changes in coronary vascular resistance or myocardial oxygen extraction. Augmented sympathetic activity was manifested by 397% and 164% increases in plasma levels of epinephrine and norepinephrine, respectively. The hemodynamic and cardiometabolic effects of ketamine were abolished when patients were pretreated with droperidol. The increase in plasma epinephrine levels was likewise inhibited by droperidol; significantly lower plasma norepinephrine levels also were observed. These findings suggest that droperidol inhibits the cardiovascular effects of ketamine by a centrally mediated reduction in sympathetic activity and by peripheral alpha receptor blockade.

Effects of halothane on coronary haemodynamics and myocardial metabolism in patients with ischaemic heart disease and heart failure.

Halothane was administered at an end-tidal concentration of 1% to 10 patients with stable ischaemic heart disease and clinical and haemodymanic signs of moderate heart failure. Measurements of central haemodynamic variables, coronary sinus blood flow and oxygen, lactate and hypoxanthine balances over the myocardium were done before and at steady state during halothane anaesthesia. Halothane induced marked haemodynamic changes with decreases in mean arterial pressure (-43%), mean pulmonary arteriolar occlusion pressure (-42%), systemic vascular resistance (-31%), cardiac index (-20%) stoke volume index (-31%) and left and right stroke work indices (-62% and -55%, respectively). Heart rate and pulmonary vascular resistance did not change. Coronary sinus blood flow decreased in parallel with perfusion pressure, and myocardial oxygen consumption decreased (-40%), as did myocardial oxygen extraction. Rate pressure product and triple product correlated better with changes in myocardial oxygen consumption in the present subset of patients than in healthy volunteers during halothane anaesthesia. The findings suggest that halothane, through its systemic vasodilatory effect, unloads the failing left ventricle and that this peripheral action predominates over the direct cardiodepressant action of the agent. The combined findings of unchanged coronary vascular resistance, decreased myocardial oxygen extraction and absence of increasing or pathological levels of lactate and hypoxanthine in coronary sinus blood imply a direct dilatory effect of halothane on the coronary vasculature.

Myocardial oxygen consumption and coronary haemodynamics during fentanyl-droperidol-nitrous oxide anaesthesia in patients with ischaemic heart disease.

Eight patients with stable ischaemic heart disease were investigated to determine the effects of fentanyl (15 micrograms/kg) - droperidol (150 micrograms/kg) - nitrous oxide (75%) anaesthesia, without concomitant fluid challenge, on myocardial oxygen consumption and lactate uptake, and central and coronary haemodynamics. Anaesthesia induced reductions in mean arterial pressure (--35%, P less than 0.01), systemic vascular resistance (--30%, P less than 0.01), left ventricular stroke work index (--50%, P less than 0.01) and total body oxygen consumption (--23%, P less than 0.01), with no changes in heart rate, cardiac output or mean pulmonary arteriolar occlusion pressure. Mixed venous oxygen content increased (P less than 0.05). Systemic vasodilatation, circulatory adaptation to an overall lower metabolic rate, and clinically negligible cardiodepression are the likely mechanisms behind the central haemodynamic response to this form of anaesthesia. Coronary sinus blood flow (measured by the continuous thermodilution technique) decreased (P less than 0.01) in parallel with the decrease in coronary perfusion pressure. Thus coronary vascular resistance remained unchanged. As expected from the haemodynamic findings, myocardial oxygen consumption decreased (--37%, P less than 0.01). Coronary sinus oxygen content and myocardial oxygen extraction did not change, nor was myocardial lactate uptake affected. No ST-T-segment depressions or dysrhythmias were recorded. These observations indicate that myocardial oxygenation was adequate in spite of the reduction in coronary perfusion pressure. There was poor correlation between changes in myocardial oxygen consumption and rate pressure product (R = 0.455) or triple produce (R - 0.375).

Effects of thiopentone on cardiac performance, coronary hemodynamics and myocardial oxygen consumption in chronic ischemic heart disease.

Thiopentone was administered as induction agent for general anesthesia to eight patients with stable ischemic heart disease; 6 mg/kg of the drug induced decrease in arterial blood pressure (-27%), systematic vascular resistance (-20%), stroke volume index (-14%), mean pulmonary arteriolar occlusion pressure (-15%) and left ventricular stroke work index (-38%), while heart rate increased by 10% and cardiac output remained unchanged. Total body oxygen consumption decreased by 30%. Myocardial oxygen consumption decreased by 39% with unchanged or decreased myocardial oxygen extraction and myocardial lactate uptake decreased by 40%. Arterial and coronary sinus hypoxanthine levels were unchanged and no ST-T-segment changes or dysrhythmias were recorded. In the present experimental setting, the results indicate that thiopentone substantially decreased myocardial oxygen requirements. In spite of the marked reduction in coronary perfusion, myocardial oxygen demand was matched by supply, myocardial dysoxia was not induced and cardiodepression was clinically negligible. Rate pressure product was a poor indicator of changes in myocardial oxygen consumption after thiopentone administration.