We studied the haemodynamic response to cessation of mechanical ventilation and removal of the tracheal tube in 84 patients after coronary artery bypass grafting. Patients were sedated on the ICU with propofol 1-3 mg kg-1 h-1, and randomly allocated to extubation while awake or while still sedated. Systolic and diastolic blood pressures and heart rate increased significantly faster in the awake group as mechanical ventilation was stopped; systolic blood pressure 6.1 (3.0) vs 0.7 (1.8) mm Hg min-1, diastolic blood pressure 2.1 (1.6) vs 0.2 (0.9) mm Hg min-1, heart rate 2.1 (1.7) vs 0.2 (0.5) beats min-2; P < 0.01 in each case. Treatment was required for systolic hypertension during discontinuation of mechanical ventilation in 20 patients (53%) in the awake group and in three patients (7.5%) in the sedated group (P < 0.001). No patient in the sedated group had any new ischaemic ECG changes. Significant new ST segment changes did not occur in the sedated group but were present in five patients in the awake group (P = 0.013), one of whom suffered a perioperative myocardial infarction. Removal of the tracheal tube while patients are still sedated after coronary artery bypass grafting is safe, and reduces the incidences of haemodynamic disturbance and myocardial ischaemia during extubation.
For patients with mild lung dysfunction, a leucocyte-depleting arterial line filter improves postoperative oxygenation, reduces extravascular lung water accumulation, and reduces time on artificial ventilator after CPB. There may be an economic argument for the routine use of leucocyte-depleting filters for every patient during CPB.
Fifty patients undergoing elective coronary revascularisation were prospectively randomised to receive either a leucocyte-depleting or a control filter inserted into the arterial line of the cardiopulmonary bypass (CPB) circuit. The concentration of exhaled nitric oxide (NO) was measured 15 min before and 30 min after CPB using a real-time chemiluminescence analyser (Logan Research, Northampton, UK). The baseline rate of exhaled NO production was 2.14 +/- 0.83 ppb/s in the control group, and 2.58 +/- 0.53 ppb/s in leucocyte-depleted group (p = 0.17). Following CPB, the mean rate of exhaled NO production in the control group had increased by 1.51 +/- 0.45 ppb/s to 3.65 +/- 0.81 ppb/s and in the leucocyte- depletion group had increased by 1.05 +/- 0.45 ppb/s to 3.64 +/- 0.62 ppb/s. The increase in exhaled NO production was significantly lower in the leucocyte depleted group (p = 0.002), indicating that leucocyte depletion suppressed the increase in exhaled NO production seen following CPB.
Skin--electrode impedance was determined at 100 Hz and 1 kHz between two disposable electrodes, 5 cm apart, at current densities < 65 microA.cm-2. Measurements were made on the volar skin of the forearm during cooling on cardiopulmonary bypass, and on the dorsum of the foot in the absence of skin blood flow during aortic aneurysm repair. Both the resistive and reactive components of the skin-electrode impedence showed an inverse linear relationship to temperature between 26 and 36 degrees C. The magnitude of the impedance change was different for each patient studied; resistance changes ranged from 0.03 to 23.2 k omega. Degrees C-1 at 100 Hz and from 0.03 to 2.7 k omega. Degrees C-1 at 1 kHz, while reactance changes ranged from 0.4 to 2.1 k omega. Degrees C-1 at 100 Hz and from 0.04 to 0.18 k omega. Degrees C-1 at 1 kHz. Changes in skin-electrode impedance were not due to changes in skin blood flow. There was no consistent change in offset potential with temperature. Although the skin-electrode impedance increases as temperature falls, it is concluded that temperature effects at the skin-electrode interface are not responsible for the observed failure of evoked electromyography during clinical monitoring of neuromuscular function.
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