Decreased oxygen saturation as a result of haemoglobin Titusville.

INTRODUCTION: Our patient was admitted to the hospital due to shortness of breath. Although partial pressure of oxygen in arterial blood was normal, oxygen saturation measured with pulse oximetry (SpO(2)) was markedly decreased. SpO(2) and oxygen saturation of arterial blood (SaO(2)) stayed low during monitoring even with an increased fraction of oxygen in inspired air. METHODS: Report of a case. RESULTS: After extensive investigations, a rare haemoglobin variant, haemoglobin Titusville, with decreased oxygen binding capacity was discovered. This is the first haemoglobin Titusville case reported in Scandinavian countries.

Cardiovascular changes after naloxone administration in propofol-sedated piglets during opioid overdose.

BACKGROUND: Naloxone is an opioid receptor antagonist. Even when used in modest doses, it has been associated with serious cardiopulmonary side-effects. In this experimental porcine study, we examined the cardiac effects of naloxone during an opioid overdose. METHODS: Cardiac parameters, changes in the left ventricular compliance and the magnitude of catecholamine release were evaluated in eight spontaneously breathing piglets under propofol sedation. Cardiac parameters were recorded every 30 s and transthoracic echocardiography was used for the continuous assessment of cardiac performance. Respiratory arrest was induced by morphine (8 mg/kg). Ten minutes after morphine administration, naloxone (80 microg/kg) was injected intravenously. Every 5 min, arterial blood gases were measured and, every 10 min, a sample for the analysis of plasma catecholamines was drawn. RESULTS: There were no statistically significant changes in left ventricular ejection fraction and no signs of pulmonary hypertension. There was a statistically significant increase in the mean arterial pressure immediately after naloxone administration and in norepinephrine concentration before naloxone administration. After naloxone administration, the plasma catecholamine levels decreased in all but one animal. Two animals developed cardiac arrest (pulseless electrical activity and ventricular fibrillation) shortly after receiving naloxone. Although they were both administered naloxone prematurely due to hypoxic bradycardia, naloxone could have contributed to the development of ventricular fibrillation. CONCLUSION: Naloxone did not cause changes in ejection fraction or mean pulmonary artery pressure in hypoxic and hypercarbic conditions. After naloxone administration, the plasma catecholamine levels returned to baseline in all but one animal, and two animals developed cardiac arrest.

Measurement of systemic oxygen uptake during low-flow anaesthesia with a standard technique vs. a novel method.

We assessed agreement between measurement of systemic oxygen uptake using the Fick-derived method, and a novel method described by Biro, based on the difference in oxygen concentrations of the delivered fresh gas and the gas circulating in the circle system. Twenty-nine patients undergoing elective cardiac surgery were studied during stable haemodynamic and ventilatory conditions. Systemic oxygen uptake was measured using the two methods in each patient before and after cardiopulmonary bypass. Limits of agreement were found to be wide (-162 to 311 ml.min-1 before bypass, and -257 to 401 ml.min-1 after bypass), indicating poor agreement between the methods. No significant difference was found between the pre- and post cardiopulmonary bypass values for each method. We conclude that the Biro method, although attractive in terms of its simplicity, is an unreliable measure of systemic oxygen uptake under these conditions.

Nitecapone as an additive to crystalloid cardioplegia in patients who had coronary artery bypass grafting.

BACKGROUND: Nitecapone has been shown to have a protective effect against ischemia-reperfusion injury in experimental heart transplantation and in Langendorff preparations. This prospective, randomized study assessed the effects of nitecapone in patients who had coronary artery bypass grafting. METHODS: Thirty patients with normal myocardial function were randomly divided into control patients (n = 15), who received crystalloid (Plegisol) cardioplegia, and nitecapone patients, who received nitecapone in a 50 microM solution (n = 15) in Plegisol. Cardioplegia was administered as an initial dose of 15 mL/kg of body mass after cross-clamping and 2 mL/kg every 15 minutes. Simultaneous coronary sinus and aortic blood samples, and myocardial biopsies were taken at 1, 5, and 10 minutes after unclamping. Hemodynamics were measured invasively for 24 hours and with transesophageal echocardiography for 3 hours after cardiopulmonary bypass. RESULTS: There were no adverse effects. The incidence of ventricular arrhythmias was significantly lower in the treatment group during the recovery period (p = 0.02). Cardiac output and stroke volume did not differ significantly between the groups. The conjugated dienes gradient between the aorta and the coronary sinus increased significantly during the first minute of reperfusion in the control group (p = 0.02) compared with the nitecapone group. Myeloperoxidase activity in myocardial biopsies was higher in the control group (2.3 times higher at 5 minutes and 3.2 times higher at 10 minutes) than in the nitecapone group (p = 0.13). CONCLUSIONS: Nitecapone did not exert any significant hemodynamic effects in patients with normal ejection fraction.

Association between R-wave amplitude of the electrocardiogram and myocardial function during coronary artery bypass grafting.

OBJECTIVE: The recovery of R-wave amplitude in the V5 lead of the electrocardiogram (ECG) was recently found to be worse in nonsurvivors than in survivors after coronary artery bypass grafting (CABG). On the contrary, an increase in R-wave amplitude has been found to reflect myocardial dysfunction in exercise testing. The purpose of this study was to examine whether the changes in R-wave amplitude are associated with changes of myocardial function during CABG. DESIGN: A prospective clinical study. SETTING: Cardiothoracic division of surgery in a university hospital. PARTICIPANTS: Ten consecutive patients undergoing CABG. MEASUREMENTS: R-wave amplitude was measured at eight different time points. Left ventricular end-systolic wall tension, wall stress at isovolumic contraction (afterload), end-diastolic wall stress (preload), end-systolic wall stress per end-systolic area (contractility), and stroke work were calculated using transesophageal echocardiography and arterial pressure. MAIN RESULTS: Linear regression was calculated between changes in R-wave amplitude and echo parameters. A weak positive association within subjects was noted among R amplitude and all measured cardiac function parameters except preload. R2 value varied from 0.101 to 0.266, and R2 for preload was 0.017. CONCLUSIONS: These results suggest that only 10% to 27% of variation in R-wave amplitude can be explained by left ventricular function indices measured by echocardiography in patients with CABG. Thus, R-wave amplitude changes in an individual patient undergoing CABg have very limited utility as a noninvasive measure of left ventricular function.

Improved gas exchange during exercise after weight loss in morbid obesity.

The aim of this study was to determine the effect of weight loss induced by 6 weeks very-low-calorie-diet (VLCD) and behavioural intervention on pulmonary gas exchange during exercise in non-smoking morbid obese (BMI>40 kg/m2) otherwise healthy patients. Seven obese patients underwent a maximal bicycle ergometer test with continuous analysis of expired air and arterial blood sampling before and after a mean weight loss of 18% (25.7 kg, range: 10-50 kg). Body mass index (BMI) decreased with weight loss from 46.6 (6.3) kg/m2 to 38.0 (4.7) kg/m2 (P<0.01). Oxygen consumption (VO2) at low and submaximal exercise levels decreased after weight reduction, but the change was not statistically significant. The peak oxygen consumption related to body weight (VO2/kg) increased 22% from the initial 16.2 (3.6) ml/min/kg to 19.8 (3.1) ml/min/kg (P<0.05). Decrease in VCO2 was significant at submaximal exercise level. Ventilatory equivalent for CO2 increased significantly after weight reduction (P<0.05). Standing up and light exercise resulted in a significant increase in the mean arterial oxygen tension (PaO2) (P<0.05) and a significant decrease in the mean alveolar-arterial difference P(A-a)O2 (P<0.05) when compared to supine values. The mean increase in PaO2 with weight loss was not significant. The peak P(A-a)O2 decreased significantly after weight reduction. In conclusion, weight reduction induced by VLCD and behavioural intervention without exercise therapy can improve gas exchange during exercise in morbid obesity. Increased wasted ventilation, and a tendency to alveolar hyperventilation, after weight loss may reflect a delay in the adaptation of regulation of breathing to rapid weight loss.

Effect of weight loss and body position on pulmonary function and gas exchange abnormalities in morbid obesity.

OBJECTIVE: To determine, whether behavioral management of obesity including very-low-calorie-diet would produce weight loss enough to improve pulmonary mechanics and gas exchange in morbid obesity. DESIGN: Pulmonary function and arterial oxygenation were studied before and after weight loss in 11 patients attending a group therapy with the program of VLCD for 6 weeks and 16 weeks' behavioral intervention. MEASUREMENTS: Spirometry, diffusing capacity, body plethysmograph, closing volume and arterial blood gas analyses. RESULTS: The mean initial BMI was 45.4 kg/m2 (range 39.8-58.7 kg/m2) and decreased to 39.4 kg/m2 (range 31-49.8 kg/m2) (P < 0.01). Expiratory reserve volume (ERV) and functional residual capacity (FRC) improved significantly with weight loss. Closing capacity (CC) exceeded FRC in 10 cases of 11 at the initial stage, but after weight loss only in three patients. The mean arterial oxygen tension with the patients in supine position did not change after weight loss, but standing up improved PaO2 significantly before and after weight loss. CONCLUSION: The dietary treatment of morbid obesity was sufficient to induce improvement in lung volumes, but not enough to improve arterial oxygenation, although ventilatory mechanics was improved significantly and the tendency to early small airway closure was decreased. Hypoxemia was significantly relieved by standing up both before and after weight loss.

Monitoring of CO2 exchange during cardiopulmonary bypass: the effect of oxygenator design on the applicability of capnometry.

The correlation between pCO2 values in blood and in exhaust gas from the oxygenators was examined during cardiopulmonary bypass (CPB) using one bubble oxygenator and three membrane oxygenators. Forty-seven CPBs were performed, 17 with Compactflow (Dideco, Italy), 10 with Maxima (Medtronic Inc., USA), 10 with Cobe CML (Cobe Laboratories, USA) membrane oxygenators and 10 with Hi-Flex (Dideco, Italy) bubble oxygenators. Blood samples were taken both from arterial and venous lines of the oxygenator. A capnometer was connected to the oxygenator gas exhaust port and CO2 fraction was measured at the time of drawing blood samples. CO2 pressure in the gas phase was calculated from the product of the CO2 fraction and water vapour-corrected barometric pressure. Blood gases were measured at 37 degrees C and the pCO2 value was corrected to the temperature of the arterial line. The correlation between blood and exhaust gas pCO2 was good in all the oxygenators examined, ranging from 0.921 to 0.976. The standard error of estimate (SEE) was in the range of about +/- 2 mmHg for all the oxygenators. The systematic error (slope and intercept of the correlation line) varied depending on the construction of the oxygenator, with countercurrent design having the best overall correspondence. Based on the results of this study it can be concluded that arterial or venous CO2 pressure can be monitored with a capnometry device coupled to the oxygenator gas outlet port.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of intramuscularly administered pethidine on the amnesic effects of intravenous diazepam during intravenous regional anaesthesia.

Patients undergoing surgery under regional anaesthesia often receive narcotic analgesics for premedication which may modify the sedative and amnesic effects of intravenously administered diazepam. Sixty-two patients scheduled for upper extremity surgery under intravenous regional anaesthesia received 0.15 mg/kg of diazepam intravenously to supplement the local anaesthesia. Thirty-two of the patients received 0.01 mg/kg of atropine plus 1 mg/kg of pethidine and 30 patients only atropine intramuscularly approximately 1 h before injection of diazepam. Another 30 patients received the same atropine-pethidine premedication and saline intravenously, and served as a reference group. Atropine-pethidine premedication followed by saline did not produce any amnesic effects. Sixty-nine and 38% of patients receiving atropine-pethidine premedication followed by diazepam did not remember a picture shown to them 15 min after diazepam injection or the performance of operation, respectively, the respective figures for patients given atropine premedication followed by diazepam being only 23% and 0% (P less than 0.01 - 0.001 between groups). The anti-recall of painful stimulus (exanguination) was significantly (P less than 0.01) more common when diazepam was given after pethidine premedication (31%) when compared to its injection after atropine alone (7%). The drowsiness produced by the drugs was greatest and the overall patient acceptability of the technique used most satisfactory when pethidine was used for premedication and diazepam for sedation. It is concluded that intramuscularly administered pethidine potentiates the amnesic action of intravenous diazepam for painful stimuli, prolongs the amnesic action of diazepam for visual stimuli and improves the patients' acceptability of intravenous regional anesthesia supplemented by intravenous diazepam.