Intravenous nitroglycerin administration during infrarenal aortic clamping

Twenty-five patients requiring infrarenal abdominal aortic clamping were studied during halothane, nitrous oxide anaesthesia. Aortic clamping caused reductions in cardiac index (CI), stroke volume index (SVI) and left ventricular stroke work index (LVSWI). Systemic vascular resistance (SVR) increased. In seven patients CI was less than 1.81 X min-1 X m-2. Intravenous administration of nitroglycerin, 1 microgram X kg-1 X min-1, for 20 minutes, accompanied by volume loading to maintain pulmonary capillary wedge pressure, resulted in a significant improvement in haemodynamic parameters. CI increased 24 per cent as a result of a 14 per cent increase in SVI and an eight per cent increase in heart rate. LVSWI increased 13 per cent and SVR decreased 21 per cent. The plasma nitroglycerin concentration at the time of these measurements was 2.9 +/- 1.0 ng X ml-1. Aortic unclamping resulted in a mean maximum decrease of 14 +/- 2 torr mean arterial pressure. Epinephrine, norepinephrine and plasma renin activity gradually increased during the period of the anaesthetic.     

Peripheral vascular and cardiac effects of nitrous oxide in the bovine.

Peripheral vascular and myocardial effects of increasing concentrations of nitrous oxide (0 to 70 per cent) in oxygen were determined in 15 unanaesthetized calves before and after replacement in their natural heart (NH) with a pneumatically driven artificial heart (AH). Nitrous oxide produced concentration-related decreases in arterial and mixed venous pH and increases in minute ventilation and arterial and mixed venous carbon dioxide tensions in both NH and AH calves. Nitrous oxide resulted in significant increases in cardiac output, stroke volume and mean aortic, pulmonary artery and right atrial pressures in NH and AH calves, but did not significantly change systemic vascular resistance in either group of animals. Heart rate was increased in NH calves but was fixed in AH calves. Elevations in heart rate and cardiac output at nitrous oxide concentrations greater than 30 per cent and aortic pressure at 70 per cent nitrous oxide were significantly greater in NH than AH animals (P less than 0.05). These data demonstrate that nitrous oxide stimulates the cardiovascular system in spontaneously breathing mammals and that the changes result from improved venous return and an increase in myocardial chronotropy. Our findings also suggest that cardiovascular stimulation during nitrous oxide breathing may be related to increased concentrations of arterial and/or venous carbon dioxide.     

Intravenous nitrogly-cerin administration during infrarenal aortic clamping

Twenty-five patients requiring infrarenal abdominal aortic clamping were studied during halothane, nitrous oxide anaesthesia. Aortic clamping caused reductions in cardiac index (CI), stroke volume index (SVI) and left ventricular stroke work index (LVSWI). Systemic vascular resistance (SVR) increased. In seven patients CI was less than 1.8 l·min^-1m^-2. Intravenous administration of nitroglycerin, 1μg·kg^-1min^-1, for 20 minutes, accompanied by volume loading to maintain pulmonary capillary wedge pressure, resulted in a significant improvement in haemodynamic parameters. CI increased 24 per cent as a result of a 14 per cent increase in SVI and an eight per cent increase in heart rate, LVSWI increased 13 per cent and SVR decreased 21 per cent. The plasma nitroglycerin concentration at the time of these measurements was 2.9 ± 1.0ng·ml^-1, Aortic unclamping resulted in a mean maximum decrease of 14 ± 2 torr mean arterial pressure. Epinephrine, norepinephrine and plasma renin activity gradually increased during the period of the anaesthetic.     

Left ventricular performance and pulmonary circulation following addition of nitrous oxide to morphine during coronary-artery surgery.

The effects of nitrous oxide on ventricular performance and pulmonary circulation were studied in 12 patients with angiographically demonstrated coronary-artery disease and normal ventricular contractility who had received 2 mg/kg morphine intravenously. Seventeen studies were performed intraoperatively, five before and 12 after cardiopulmonary bypass and myocardial revascularization. Recordings were obtained during oxygen breathing and during nitrous oxide administration. Fifty per cent nitrous oxide significantly decreased mean arterial pressure (P less than 0.05), cardiac index (P less than 0.01), stroke index (P less than 0.01), left ventricular stroke work index (P less than 0.01), peak left ventricular dP/dt (P less than 0.05) and dP/dt/P (P less than 0.01), and heart rate-systolic arterial pressure product (P less than 0.01). Mean pulmonary arterial pressure (P less than 0.05), pulmonary artery occluded pressure (P less than 0.01), left ventricular end-diastolic pressure (P less than 0.01) and pulmonary vascular resistance (P less than 0.05) increased. Heart rate, right atrial pressure and systemic vascular resistance remained unchanged. When nitrous oxide was discontinued, all variables returned to control except mean pulmonary arterial pressure and pulmonary vascular resistance. Responses were similar before and after cardiopulmonary bypass and myocardial revascularization. These findings suggest that nitrous oxide depresses left ventricular performance when administered intraoperatively to patients who have received large doses of morphine for coronary-artery surgery. Nitrous oxide also increases pulmonary vascular resistance, possibly via alpha-adrenergic stimulation.     

The Influence of Hyperoxic Ventilation during Sodium Nitroprusside-induced Hypotension on Skeletal Muscle Tissue Oxygen Tension

Background: Increasing inspired oxygen concentrations might provide a simple and effective intervention to increase oxygen tension in tissues during controlled hypotension. To test this hypothesis, the influence of hyperoxic ventilation (100% O2) on skeletal muscle oxygen partial pressure (Ptio2) in patients receiving sodium nitroprusside-induced controlled hypotension was studied.

Methods: Forty-two patients undergoing radical prostatectomy were prospectively studied and randomly divided into three groups as follows: (1) Controlled hypotension induced by sodium nitroprusside (mean arterial blood pressure, 50 mmHg) and hyperoxic ventilation (CH-100%; n = 14); (2) controlled hypotension and ventilation with 50% O2 in nitrous oxide (CH-50%; n = 14); and (3) standard normotensive anesthesia with 50% O2 in nitrous oxide (control; n = 14). Ptio2 values were measured continuously in all patients using implantable polarographic microprobes. Arterial blood gases and lactate concentrations were analyzed in 30-min intervals.

Results: Surgical blood loss and transfusion requirements were significantly reduced in both groups receiving hypotensive anesthesia. During surgery, arterial partial pressure of oxy-gen and arterial oxygen content were significantly higher in patients of the CH-100% group. Baseline values of Ptio2 were comparable between the groups (CH-50%: 25.0 +/- 0.7 mmHg; CH-100%: 25.2 +/- 0.2 mmHg; control: 24.5 +/- 0.2 mmHg). After a transient increase in Ptio2 in the CH-100% group during normotension, Ptio2 values returned to baseline and remained unchanged in the control group. Ptio2 decreased significantly during the hypotensive period in the CH-50% group. The lowest mean Ptio2 values were 15.0 +/- 4.1 mmHg in the CH-50% group, 24.2 +/- 4.9 mmHg in the CH-100% group, and 23.5 +/- 3.8 mmHg in the control group. There were no significant changes in lactate plasma concentrations in any group throughout the study period.     

Nitrous oxide added to halothane reduces coronary flow and myocardial oxygen consumption in patients with coronary disease

The haemodynamic and myocardial metabolic effects of adding 50 per cent nitrous oxide to 0.5 per cent halothane were studied in 13 patients, before the surgical incision for coronary artery vein grafts. Cardiac output and coronary sinus blood flow were determined by thermodilution, along with haemodynamic measurements. Measurements 15 minutes after addition of nitrous oxide revealed a significant decrease in heart rate, arterial pressure, cardiac index, coronary sinus blood flow and myocardial oxygen consumption. There was a significant increase in coronary sinus lactate content, and a significant decrease, from 27 to 11 per cent, in myocardial lactate extraction. We conclude that these circulatory changes were likely to be due to a depression of ventricular function by the nitrous oxide. The myocardia of these patients with severe coronary disease were becoming globally ischaemic while they were receiving 50 per cent oxygen, in the presence of hypotension. Nitrous oxide should be turned off when hypotension occurs in coronary patients.     

VARIATION IN ARTERIAL PRESSURE DURING ANAESTHESIA WITH HALOTHANE IN DIFFERENT GAS MIXTURES

Seventeen patients were anaesthetized with halothane vaporizedin oxygen, air, and 75 per cent nitrous oxide in oxygen,forthe performance of prolonged superficial operations. With oxygenthere was an average fall in arterial pressure of 17 per centfrom pre-operative value. When air was next substituted foroxygen in seven patients pressure changes were negligible, butsubstitution of nitrous oxide then resulted in falls averaging20 per cent. When oxygen was followed first by nitrous oxidein ten patients falls averaging 23 per cent were observed whichwere substantially reversed on return to anas the vaporizingmedium.     

Haemodynamic and biochemical variables after induction of anaesthesia with fentanyl and nitrous oxide in patients undergoing coronary artery by-pass surgery

The effects on the haemodynamic and biochemical parameters of three different anaesthetic induction regimes, namely fentanyl (4.1 μg · kg^-1 or 15 μg · kg^-1) plus 60 percent nitrous oxide with oxygen and fentanyl 15 μg · kg^-1 plus 60 per cent nitrogen with oxygen, were studied in patients undergoing coronary artery surgery. Fentanyl 15 μg · kg^-1 with nitrous oxide and oxygen produced simultaneous reductions in oxygen uptake, cardiac index and left ventricular stroke work with an unaltered oxygen extraction. Diastolic blood pressure (an index of coronary artery perfusion) was only slightly reduced, and there were no changes in arterial lactate, glucose and free fatty acids. The lower dose of fentanyl (4.1 μg · kg^-1) with nitrous oxide produced no haemodynamic changes but decreased the oxygen uptake and extraction. The patients receiving fentanyl 15 μg · kg^-1 with nitrogen and oxygen showed increases in heart rate, blood pressure, cardiac index and left ventricular stroke work, together with a significant fall in oxygen extraction. Moreover, in the patients who received fentanyl 4.1 μg · kg^-1 with nitrous oxide and oxygen and fentanyl 15 μg · kg^-1 with nitrogen and oxygen there were significant increases in blood lactate, glucose and free fatty acids, indicating increased sympathetic activity. We conclude that fentanyl 15 μg · kg^-1, together with 60 per cent nitrous oxide with oxygen provides a satisfactory haemodynamic and biochemical state during induction of anaesthesia in patients with myocardial function prejudiced by coronary artery insufficiency.     

Effects of alfentanil on intracranial pressure in children undergoing ventriculoperitoneal shunt revision.

The effects of alfentanil on intracranial pressure in patients with diminished intracranial compliance has not been established. Ten patients with hydrocephalus of varying etiologies, ages 16 months to 20 yr, presenting for ventriculoperitoneal shunt revision were studied. Following induction of anesthesia with thiopental, nitrous oxide/oxygen, and isoflurane, the trachea was intubated and anesthesia was maintained with isoflurane (0.5%), nitrous oxide (70%), and oxygen. After a minimum of 30 min and after the new shunt was placed, alfentanil was administered in increments of 10, 20, and 40 micrograms/kg at 3-min intervals, and intracranial pressure was measured over 12 min via the new shunt. In these unstimulated, normocapnic (PETCO2 32-38 mmHg) patients, heart rate, mean arterial pressure, and cerebral perfusion pressure declined from 110 +/- 26 beats/min, 90 +/- 11 mmHg, and 71 +/- 14 mmHg, to 84 +/- 25 beats/min, 66 +/- 11 mmHg, and 45 +/- 16 mmHg (mean +/- SD), respectively, by 3 min after the third dose (P less than 0.001). Intracranial pressure did not change from baseline (19 +/- 14 mmHg vs. 21 +/- 11) after any dose of alfentanil. Contrary to earlier studies in adult patients with brain tumors, the authors found that alfentanil, in pediatric patients with hydrocephalus anesthetized with oxygen, nitrous oxide, and isoflurane, did not increase intracranial pressure within a 9-min study period. The significant decreases in cerebral perfusion pressure observed merit concern and further study.     

The effects of nitrous oxide and oxygen on transient hyperemic response in human volunteers.

The aim of this study was to determine the effects of breathing 100% oxygen or 50% nitrous oxide in oxygen on the indices of cerebral autoregulation derived from the transient hyperemic response (THR) test in human volunteers. Data were analyzed from nine healthy subjects. Middle cerebral artery (MCA) blood flow velocity (FV) was measured by transcranial Doppler ultrasound, and the THR test was performed using 10-s compression of the common carotid artery. Continuous measurement of P(ETCO2) and expired fractions of oxygen (F(ETO2)) and nitrous oxide (F(ETN2O)) was established, and mean arterial pressure (MAP) was recorded at 2-min intervals. All measurements were performed while the volunteers were breathing room air and were repeated 10 min after achieving F(ETO2) >0.95 and 10 min after achieving F(ETN2O) 0.48-0.52. Two indices derived from the THR test, the transient hyperemic response ratio (THRR) and strength of autoregulation (SA), were used to assess cerebral autoregulation. P(ETCO2) and mean arterial pressure did not change significantly throughout the study period. Breathing 100% oxygen did not change MCA FV, THRR, or SA. Inhalation of nitrous oxide resulted in a marked and significant increase in the MCA FV (from 48+/-9 to 72+/-8 cm/s; mean +/- SD) and a significant decrease in the THRR (from 1.5+/-0.2 to 1.2+/-0.1) and the SA (from 1.0+/-0.1 to 0.8+/-0.1) (P<0.05 for all). We conclude that breathing 50% nitrous oxide in oxygen results in both a significant increase in MCA FV and impairment of transient hyperemic response. IMPLICATIONS: Our study suggests that nitrous oxide impairs cerebral autoregulation and may have implications for its use in neurosurgical anesthesia and for interpretation of the results from studies of anesthetics in which nitrous oxide is used in the background.     

Protective effects of the Hemopump left ventricular assist device in experimental cardiogenic shock.

The efficacy of the new cable-driven rotating left ventricular assist device Hemopump in cardiogenic shock was examined in experiments with adult sheep (n = 14; body weight 50-71 kg). Shock was induced by high frequency ventricular pacing. Aortic, pulmonary, central venous and left ventricular pressures as well as electromagnetic measurements of coronary blood flow were recorded continuously; cardiac output was measured by thermodilution technique. Blood samples for determination of oxygen content, electrolytes and lactate were taken under control conditions, in shock, and during pump intervention at different levels of pump speed. Vascular resistance, total body and myocardial oxygen consumption as well as myocardial uptake and release of lactate were calculated. High frequency pacing led to a significant decrease in cardiac output (from 3.8 +/- 0.8 to 2.2 +/- 1.6 l/min), mean aortic pressure (89.1 +/- 14.4 to 47.6 +/- 7.2 mmHg), and total body oxygen consumption (2.6 +/- 0.3 to 1.4 +/- 0.7 ml/min per kg), as well as myocardial release of lactate (arterial coronary-venous difference of lactate: 0.27 +/- 0.26 to -0.32 +/- 0.72 mmol/l). Hemopump assist in this condition resulted in a significant increase in cardiac output (to 2.8 +/- 0.6 l/min), mean aortic pressure (to 65.6 +/- 13.9 mmHg), and myocardial perfusion pressure (from 25.5 +/- 11.0 to 59.0 +/- 14.7), and led to nearly normal total body oxygen consumption (2.5 +/- 0.7 ml/min per kg), a decrease in myocardial oxygen consumption (from 6.1 +/- 2.1 in shock, to 4.8 +/- 1.7 ml/min per 100 g), and to normal arterial coronary-venous difference of lactate (0.24 +/- 0.26 mmol/l).(ABSTRACT TRUNCATED AT 250 WORDS)     

The influence of hyperoxic ventilation during sodium nitroprusside-induced hypotension on skeletal muscle tissue oxygen tension

BACKGROUND: Increasing inspired oxygen concentrations might provide a simple and effective intervention to increase oxygen tension in tissues during controlled hypotension. To test this hypothesis, the influence of hyperoxic ventilation (100% O2) on skeletal muscle oxygen partial pressure (Ptio2) in patients receiving sodium nitroprusside-induced controlled hypotension was studied. METHODS: Forty-two patients undergoing radical prostatectomy were prospectively studied and randomly divided into three groups as follows: (1) Controlled hypotension induced by sodium nitroprusside (mean arterial blood pressure, 50 mmHg) and hyperoxic ventilation (CH-100%; n = 14); (2) controlled hypotension and ventilation with 50% O2 in nitrous oxide (CH-50%; n = 14); and (3) standard normotensive anesthesia with 50% O2 in nitrous oxide (control; n = 14). Ptio2 values were measured continuously in all patients using implantable polarographic microprobes. Arterial blood gases and lactate concentrations were analyzed in 30-min intervals. RESULTS: Surgical blood loss and transfusion requirements were significantly reduced in both groups receiving hypotensive anesthesia. During surgery, arterial partial pressure of oxy-gen and arterial oxygen content were significantly higher in patients of the CH-100% group. Baseline values of Ptio2 were comparable between the groups (CH-50%: 25.0 +/- 0.7 mmHg; CH-100%: 25.2 +/- 0.2 mmHg; control: 24.5 +/- 0.2 mmHg). After a transient increase in Ptio2 in the CH-100% group during normotension, Ptio2 values returned to baseline and remained unchanged in the control group. Ptio2 decreased significantly during the hypotensive period in the CH-50% group. The lowest mean Ptio2 values were 15.0 +/- 4.1 mmHg in the CH-50% group, 24.2 +/- 4.9 mmHg in the CH-100% group, and 23.5 +/- 3.8 mmHg in the control group. There were no significant changes in lactate plasma concentrations in any group throughout the study period. CONCLUSIONS: Hyperoxic ventilation improved skeletal muscle tissue oxygenation during sodium nitroprusside-induced hypotension. This improved local tissue oxygenation seems to be most likely due to an increase in convective oxygen transport and the attenuation of hyperoxemia-induced arteriolar vasoconstriction by sodium nitroprusside.     

Pulmonary gas exchange effects of nitroglycerin in canine edematous lungs

The authors determined the effects of nitroglycerin on pulmonary edema induced by oleic acid injury. Measurements of venous admixture (QVA/Qt) and shunt (Qs/Qt) using both oxygen and inert-gas-elimination methods were done before, during, and after nitroglycerin infusion, first during air ventilation and then during ventilation with 100 per cent oxygen. Nitroglycerin reduced mean blood pressure (MAP) approximately 30 per cent (P less 0.01) during both air and oxygen ventilation. During air ventilation, nitroglycerin caused PVR to decrease by 29 per cent (P less than 0.01) but caused no change in PVR during oxygen ventilation. Pa02 decreased from 64 +/- 8 torr (mean +/- SD) to 55 +/- 9 torr (P less than 0.01) with nitroglycerin infusion during air ventilation. The decrease in Pa02 was primarily due to an increase in QVA/Qt which increased from 28 +/- 12 per cent to 36 +/- 14 per cent (oxygen method) (P less than 0.05). Similarly, the inert gas QVA/Qt increased from 31 +/- 10 to 37 +/- 14 per cent (P less than 0.05). During oxygen ventilation, the effect of nitroglycerin on gas exchange was similar in direction but less in magnitude. These results provide evidence that nitroglycerin may cause significance impairment of pulmonary gas exchange when abnormal lung function is present and FI02 is low. The mechanism is most likely due to inhibition of hypoxic pulmonary vasoconstriction.     

Treatment of cardiac and renal effects of PEEP with dopamine in patients with acute respiratory failure.

The hemodynamic and renal effects of mechanical ventilation with positive end-expiratory pressure (PEEP) were studied with and without continuous dopamine administration in ten patients who had acute pulmonary failure. The application of 20 cm H2O PEEP during mechanical ventilation resulted in improvements in arterial blood oxygen tension, from 63 +/- 6 to 81 +/- 12 torr (mean +/- SE), and intrapulmonary shunt fraction, from 29 +/- 3 to 21 +/- 3 per cent, whereas cardiac output, systemic oxygen transport and renal function were impaired by 20, 19 and 47 per cent, respectively. Dopamine infusion at a rate of 5 +/- 0.05 micrograms/kg/min reversed the deleterious effects of PEEP on cardiovascular and renal function: cardiac output increased from 4.5 +/- 0.3 to 6.0 +/- 0.51, urinary output from 1.0 +/- 0.3 to 1.7 +/- 0.4 ml/min, sodium excretion and creatinine clearance by 50 per cent. Systemic oxygen transport was improved from 680 +/- 44 to 925 +/- ml, arterial oxygen tension from 81 +/- 12 to 102 +/- 14 torr, and total deadspace to tidal volume ratio from 0.49 +/- 0.02 to 0.44 +/- 0.03 with dopamine. The authors conclude that the depression of cardiovascular and renal functions that may occur in patients who need high levels of PEEP for the treatment of acute pulmonary failure can be treated successfully with dopamine infusion. This represents a valuable alternative to expansion of blood volume for the improvement of systemic oxygen transport and arterial blood oxygen tension in critically ill patients.     

Continuous Arterial PO(2) and PCO(2) Measurements in Swine during Nitrous Oxide and Xenon Elimination: Prevention of Diffusion Hypoxia

Background: During nitrous oxide (N2 O) elimination, arterial oxygen tension (PaO(2)) decreases because of the phenomenon commonly called diffusive hypoxia. The authors questioned whether similar effects occur during xenon elimination.

Methods: Nineteen anesthetized paralyzed pigs were mechanically ventilated randomly for 30 min using inspiratory gas mixtures of 30% oxygen and either 70% N2 O or xenon. The inspiratory gas was replaced by a mixture of 70% nitrogen and 30% oxygen. PaO(2) and carbon dioxide tensions were recorded continuously using an indwelling arterial sensor.

Results: The PaO(2) decreased from 119 +/- 10 mmHg to 102 +/- 12 mmHg (mean +/- SD) during N2 O washout (P < 0.01) and from 116 +/- 9 mmHg to 110 +/- 8 mmHg during xenon elimination (P < 0.01), with a significant difference (P < 0.01) between baseline and minimum PaO(2) values (Delta PaO(2), 17 +/- 6 mmHg during N2 O washout and 6 +/- 3 mmHg during xenon washout). The PaCO(2) value also decreased (from 39.3 +/- 6.3 mmHg to 37.6 +/- 5.8 mmHg) during N2 O washout (P < 0.01) and during xenon elimination (from 35.4 +/- 1.6 mmHg to 34.9 +/- 1.6 mmHg; P < 0.01). The Delta PaCO(2) was 1.7 +/- 0.9 mmHg in the N2 O group and 0.5 +/- 0.3 mmHg in the xenon group (P < 0.01).     

STUDIES OF ANAESTHESIA IN RELATION TO HYPERTENSION IH: PULMONARY GAS EXCHANGE DURING SPONTANEOUS VENTILATION

Ventilation, pulmonary gas exchanges and oxygen transport werestudied in a group of treated and untreated hypertensive elderlypatients, before, during and after nitrous oxide-halothane anaesthesiawith spontaneous ventilation. During anaesthesia minute andalveolar ventilation were depressed (— 30 per cent) outof proportion to the decrease in oxygen uptake (-18 per cent)and carbon dioxide production (— 19 per cent), and moderatehypercapnia ensued (mean Paoo3 50.3 mm Hg). All these variablesreturned to the pre-anaesthetic levels within 1 hour of terminatinganaesthesia. VD/VT was increased following induction of anaesthesiaas a result of decreased tidal volumes (— 47 per cent),but did not change progressively during the course of anaesthesia.Total deadspace (VD) was reduced by an average of 44 ml as aresult of intubation. Based on measurements of arterial Poaand the alveolar-arterial Poj difference, mean pulmonary venousadmixture was 10.4 per cent before anaesthesia, 10.9 per centduring anaesthesia but before surgery, 13.1 per cent after surgery,and 15.6 per cent 1 hour after the termination of anaesthesia.Although the average postoperative arterial Poa was slightlylower ( - 7.4 rnm Hg) than before anaesthesia, the differencewas due to many factors, and no evidence of a deteriorationin the over-all pulmonary gas exchange could be found. The conceptof "airway closure" in the supine elderly subject as a causefor the increased pulmonary venous admixture at rest is discussed.Impairment of pulmonary function during anaesthesia in hypertensiveelderly patients causes less concern than the severe changesin cardiovascular function ^*Present address: Hospital Notre Dame, Montreal133, P.Q., Canada     

Cardiovascular response of a continuous variable rate alfentanil infusion for abdominal aortic surgery

A prospective study was undertaken to determine the cardiovascular response of a continuous alfentanil infusion during abdominal aortic surgery (AAS). Each subject (n = 20) received a beta-blocking drug preoperatively, and was premedicated with oral lorazepam. Anaesthesia was induced with alfentanil 50 micrograms.kg-1 and thiopentone 3 mg.kg-1, and was maintained with a variable rate infusion of alfentanil and 66 per cent nitrous oxide in oxygen. During the infusion, boluses of alfentanil, 7.5 micrograms.kg-1, were administered to maintain heart rate and blood pressure within 20 per cent of awake baseline values. Haemodynamic stability during surgery was achieved with infusion rates varying between 0.5 and 2.5 micrograms.kg-1, which resulted in mean alfentanil serum concentrations ranging from 186 +/- 53 to 315 +/- 98 ng.ml-1. The mean cumulative alfentanil dose was 15.4 +/- 6.2 mg.patient-1 for surgery which lasted an average of 141 +/- 41 min. Throughout surgery, no patient required inhalational anaesthetic agents or vasoactive drugs. Fifteen of the 20 patients had perioperative Holter monitoring. No myocardial ischaemia was detected during the intraoperative period. However, there was a 33 per cent incidence of myocardial ischaemia on the first postoperative day. There were no myocardial infarcts and no deaths. We conclude that in beta-blocked patients undergoing aortic reconstructive surgery, a variable rate alfentanil infusion administered with 66 per cent nitrous oxide provides anaesthesia characterized by good haemodynamic control without the need for supplemental agents or vasoactive drugs.     

PULAMONARY GAS EXCHANGE DURING INDUCTION OF ANAESTHESIA WITH NITROUS OXIDE IN SEATED SUBJECTS

During induction of anaesthesia with nitrous oxide and 21 percent oxygen in subjects in the sitting position there was arise in alveolar oxygen tension proportional to the inspirednitrous oxide concentration. The mean rise in alveolar oxygentension was 30 mm Hg after breathing 79 per cent nitrous oxidefor 80 seconds. There was little change in alveolar carbon dioxidetension. There was a rise in arterial oxygen tension in thethree subjects studied; the alveolar/arterial oxygen differenceincreased from 9 to more than 20 mm Hg in two of the subjects.The changes in alveolar and arterial oxygen tensions are dueto lung shrinkage and a greater inspired to expired tidal volumeratio consequent upon nitrous oxide uptake. The increase inalveolar/arterial difference is a consequence of an increasein alveolar oxygen in the presence of non-uniformity of ventilation-perfusionratios. The increase in alveolar/arterial difference was accompaniedby a fall in functional residual capacity. The reduction infunctional residual capacity was found to be proportional tothe inspired nitrous oxide concentration. ^*Present address: Cardiovascular Research Institute, Universityof California, San Francisco Medical Center, San Francisco,California 94122, U.S.A.     

In vivo response time of transcutaneous oxygen measurement to changes in inspired oxygen in normal adults

We examined the in vivo response time of transcutaneous oxygen measurement (PtcO2) to a step increase (100 per cent oxygen) or decrease (air) of inspired oxygen in five normal adults (age 27 +/- SD 4.5 years). The PtcO2 electrode was placed on the upper chest (sensor temperature 44 degrees C). The mean +/- SEM 63 and 95 per cent response times of PtcO2 to a step increase in inspired oxygen were 2.9 +/- 0.2 and 6.8 +/- 0.2 and to a step decrease were 2.4 +/- 0.2 and 5.1 +/- 0.3 minutes. The 63 and 95 per cent response times for the pulmonary washin of oxygen were 1.0 and 2.6 minutes and washout were 0.8 and 2.3 minutes. We conclude that the in vivo response time of the PtcO2 is reproducible but substantially longer than that of the pulmonary washin and washout times and inadequate to monitor rapid changes in arterial oxygenation during anaesthesia, perioperative period or sleep in adults.     

Inhaled nitric oxide to newborns and infants after congenital heart surgery on cardiopulmonary bypass. A dose-response study

Twelve patients (median age 3.8 months) with pulmonary hypertension in the postoperative period after congenital heart surgery on cardiopulmonary bypass were given inhaled nitric oxide. Effects on cardiovascular and respiratory systems were measured. Mean pulmonary artery pressure decreased from 33+/-2 to 28+/-2 mmHg (p < 0.001) and arterial oxygen tension increased from 13.3+/-2.3 to 16.7+/-2.7 kPa (p < 0.05). The mean change in arterial oxygen tension in percent was 29.8+/-6.3% (p < 0.05). The response was significant only in the first step from 0 to 3 or 5 ppm with no further significant changes in mean pulmonary artery pressure or oxygenation at higher doses. The decrease in mean pulmonary artery pressure was concomitant with a significant increase in arterial oxygen tension. No dose-response relationship was found with increasing doses to 80 ppm.