Arterial Blood Gas Tensions Research Articles

Cardiovascular, Respiratory, and Analgesic Effects of Fentanyl in Unanesthetized Rhesus Monkeys

To determine the suitability of the rhesus monkey as a model for investigation of opioids, we examined the analgesic, respiratory, and cardiovascular effects of fentanyl in six adult male rhesus monkeys. Fentanyl was administered in sequential bolus injections of 2, 4, 16, 64, and 128 micrograms/kg, with 10 min between each dose. Arterial plasma fentanyl concentrations and blood gas tensions were measured 3 and 9 min after each dose and 1, 2, 5, 20, 60, and 120 min after the final dose. At the same time periods, mean systemic arterial, pulmonary arterial, central venous, and pulmonary capillary wedge pressures, cardiac output, heart rate, and respiratory rate were measured. Analgesia was quantified as the time required for tail withdrawal from a standardized noxious stimulus. Tail latency response time increased significantly after the 4-microgram/kg dose (plasma fentanyl concentration = 2.7 +/- 0.9 ng/mL). Maximum tail latency response time was attained after the 64-micrograms/kg dose (43.4 +/- 26.0 ng/mL). Respiratory rate decreased significantly after the 2-microgram/kg dose, and PaCO2 increased significantly after the 4-microgram/kg dose. All animals became apneic, requiring tracheal intubation and controlled ventilation, after the 64-micrograms/kg dose. Also, mean arterial pressure and cardiac output decreased significantly after the 64-micrograms/kg dose. There were no other significant cardiovascular changes. Peak plasma fentanyl concentration after the 128-micrograms/kg dose was 117.0 +/- 49.6 ng/mL. It appears that plasma concentrations of approximately 40 ng/mL are sufficient to reach the full cardiovascular, respiratory, and analgesic effects of fentanyl in the rhesus monkey. Significant respiratory and analgesic effects are evident at concentrations as low as 3 ng/mL.(ABSTRACT TRUNCATED AT 250 WORDS)

Oral dexmedetomidine attenuates hemodynamic responses during emergence from general anesthesia in chronically instrumented dogs.

This investigation evaluated the hemodynamic effects of orally administered dexmedetomidine in chronically instrumented dogs in the conscious state, during enflurane anesthesia, and after emergence. Four experimental groups (n = 9 each) were completed. In groups 1 and 2, dexmedetomidine (10 or 20 micrograms/kg, respectively) was administered orally, and hemodynamics, arterial blood gas tensions, and plasma norepinephrine concentrations were monitored for 6 h. Animals in groups 3 and 4 were given dexmedetomidine (20 micrograms/kg) or placebo orally, and hemodynamics, arterial blood gas tensions, and plasma norepinephrine concentrations were measured 1 h later with animals in the conscious state, after 30 min of enflurane anesthesia (1.0 MAC), and 2 and 7 min after extubation. Oral administration of dexmedetomidine resulted in sedation with significant decreases in heart rate (76 +/- 4 to 49 +/- 4 beats per min), rate-pressure product (11,500 +/- 650 to 6,100 +/- 600 mmHg. beats per min), cardiac output (2.2 +/- 0.2 to 1.2 +/- 0.4 l/min), and plasma norepinephrine concentrations (290 +/- 50 to 135 pg/ml). Peak effects occurred within 30 min and lasted approximately 3 h. No reduction in coronary blood flow velocity, decrease in regional contractile function, or respiratory depression was observed. Administration of dexmedetomidine before enflurane anesthesia also was associated with a reduction in heart rate and rate-pressure product, and dexmedetomidine prevented the increase in heart rate (146 +/- 9 vs. 60 +/- 7 beats per min) and arterial pressure (117 +/- 7 vs. 98 +/- 7 mmHg) during emergence from anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of negative pressure ventilation on arterial blood gas pressures and inspiratory muscle strength during an exacerbation of chronic obstructive lung disease.

The effects of intermittent negative pressure ventilation have been studied in 20 patients with chronic obstructive pulmonary disease during an exacerbation of their disease. Measurements of arterial blood gas tensions and maximal inspiratory pressure (MIP) were performed before and after six hours of negative pressure ventilation or standard treatment (control day) given in random order on two consecutive days. After negative pressure ventilation the mean (SD) value of MIP increased from 68.1 (21.5) to 74.8 (20) cm H2O;* arterial oxygen tension (PaCO2) fell from 60.6 (12.2) to 50.9 (8.9) mm Hg* but PaO2 changed little (from 48.4 (7.4) to 47.6 (8.2) mm Hg). There were no significant changes on the control day in arterial blood gas tensions (PaO2 47.8 (8.1) and 48.9 (9.4) and Paco2 59.8 (10.9) and 57.5 (8.06) mm Hg) or in MIP (69.4 (22.4) and 70.9 (22.9) cm H2O). Six patients tolerated negative pressure ventilation poorly and these patients showed less improvement after negative pressure ventilation. Our results suggest that intermittent negative pressure ventilation can increase alveolar ventilation in patients with an exacerbation of chronic obstructive lung disease, particularly in those who tolerate the procedure well. Most subjects showed a fall in PaCO2 and an increase in MIP. The fact that PaO2 was unchanged despite the fall in PaCO2 suggests that gas exchange may deteriorate with negative pressure ventilation in these patients.

Arterial blood sample collection from the newborn calf

Measurements of arterial blood gas tensions and acid-base status provide a means of assessing how well the respiratory system is functioning. This information is essential for thorough evaluation of a compromised neonatal calf but arterial blood sampling is difficult immediately after birth. A technique for collecting blood from the brachial artery of the newborn calf is described. This technique, which uses an easily located site, has been successfully used in field studies to determine arterial blood gas values in such calves.

Mechanics of breathing during strenuous exercise in thoroughbred horses

The changes induced by exercise on the mechanics of breathing, as well as the simultaneous changes occuring in arterial blood gas tensions and in respiratory gas exchange were investigated in 6 healthy thoroughbred, performing a treadmill exercise of increasing intensity. Respiratory airflow and tidal volume (Vt) were measured with ultrasonic flowmeters. Pleural pressure changes were measured by an oesophageal balloon catheter. Gas concentration of the expired air was analysed with a mass spectrometer; the oxygen consumption (V̇O2) and the carbon dioxide output (V̇CO2) were computed breath-by-breath. Arterial blood gas values were obtained by sampling from the carotid artery. Between rest and fast gallop Vt, respiratory frequency, expired minute ventilation (V̇e),V̇O2,V̇CO2, total pulmonary resistance (Rl), mechanical work of breathing (Ẇrm) and PaCo2 increased significantly while PaO2 decreased significantly. TheW˙rm·V˙O2−1 ratio in galloping horses increased exponentially withV̇e. This is together with the relationship between the changes in PaO2 and in PaCO2 and the increase in the ventilatory mechanics parameters, suggests that the mechanics of breathing may be one of the factors constraining further increase in ventilation in exercising healthy horses.

Effect of Premedication on Arterial Blood Gases Prior to Cardiac Surgery

The effect of premedication on arterial blood gas tensions was studied in thirty adult surgical patients with valvular disease. They were divided into three groups, each group having a different premedication regimen. Blood gas tensions were compared in these patients when awake on the night before surgery, asleep, after premedication and just prior to induction of anaesthesia. Samples were taken while the patient breathed air and each patient acted as his/her own control. The patients were randomised into one of three premedication regimens: 1. intramuscular lorazepam, 2. intramuscular morphine and hyoscine (scopolamine) and 3. oral lorazepam plus intramuscular morphine and hyoscine. There was a statistically significant though not clinically significant rise in PaCO2 and fall in pH following premedication with lorazepam, morphine and hyoscine. There was also a significant fall in PaO2 associated with morphine and hyoscine premedication which was greater than that which occurred with unsedated sleep. Patients who are to undergo cardiac valvular surgery should receive supplementary oxygen following premedication and during transfer to the operating room.

CARBOXYHAEMOGLOBIN CONCENTRATIONS, PULSE OXIMETRY AND ARTERIAL BLOOD-GAS TENSIONS DURING JET VENTILATION FOR Nd-YAG LASER BRONCHOSCOPY

Oxygen saturation measured with pulse oximetry (SpO2) is overestimated in the presence of carboxyhaemoglobin (COHb). Smoke produced during laser resection of tracheobronchial malignancies may increase concentrations of COHb. We have measured COHb concentrations in 14 patients undergoing laser resection and compared SpO2 with functional oxygen saturation (SaO2) to ascertain if pulse oximetry is an accurate monitor of oxygen saturation. During the procedure frequent changes occur in ventilatory mechanics. Arterial blood-gas tensions were measured to see if gas exchange was satisfactory. Mean preoperative COHb was 1.4%. There was no significant change in COHb in any patient at any stage during treatment. The highest value was 2.05%. The mean difference between SaO2 and SpO2 was 1.13% (95% confidence interval 0.70-1.56%). Oxygen saturation may therefore safely be monitored by pulse oximetry in patients managed by our technique. Empirical setting of a jet ventilator provided acceptable blood-gas tensions, although sometimes it was necessary to increase the FlO2 to greater than 0.3 to maintain oxygenation.

Cerebral Effects of Fentanyl in Dogs

We have studied the cerebral haemodynamic and metabolic effects of fentanyl 50 μg kg−1 and 100 μg kg−1 in dogs undergoing ventilation with oxygen and nitrogen at normocapnia. Cerebral blood flow was measured continuously by direct measurement of the outflow of the posterior sagittal sinus. Arterial and sagittal sinus bloodgas tensions were measured intermittently for calculation of cerebral metabolism. Systemic pressures were measured continuously with intermittent measurements of cardiac output. These doses of fentanyl had minimal effect on cerebral blood flow, cerebral oxygen consumption and the energy state of the brain reflected by the normal concentration of cerebral metabolites at the end of the study. There was also little effect on systemic haemodynamics. It is concluded that, in the absence of other anaesthetic agents which might influence cerebral haemodynamics and metabolism, large doses of fentanyl have little effect on the cerebral circulation.

Cardiopulmonary effects of xylazine sedation in the foal

Six healthy foals underwent instrumentation for measurement of the cardiopulmonary effects of sedation with 1.1 mg/kg bodyweight xylazine hydrochloride given intravenously. Responses to xylazine in foals at 10 and 28 days of age were not significantly different. Foals became sedate and markedly ataxic, and four of the six foals became recumbent. Heart rate decreased significantly but no arrhythmias were detected. Arterial blood pressure increased initially and then fell significantly below pre-injection values. Changes in respiratory airflow, upper airway obstruction and respiratory noise were noted in the initial 20 mins of sedation, after which respiratory rate fell, tidal volume increased, and minute volume decreased gradually. Arterial blood gas tensions and pH did not change significantly during the 120 mins following xylazine administration. Control studies showed no significant changes. All foals recovered uneventfully.

Cardio respiratory responses to electrical stimulation of the buccal mucosa in ponies

The cardiovascular and respiratory responses to electrical stimulation of the buccal mucosa under general anaesthesia in ponies were measured in order to provide some insight into the cardiorespiratory effects of anaesthesia in equidae. This knowledge may be useful for reducing morbidity during clinical anaesthesia in horses. Anaesthesia was induced with intravenous thiopentone and maintained with 1·3 per cent inspired halothane in oxygen. Arterial blood pressure, heart rate, minute volume, tidal volume, respiratory rate, arterial blood gas tensions and clinical signs of anaesthetic depth were recorded while the buccal mucous membrane was stimulated electrically. A rise in arterial blood pressure was the most consistent response detected along with clinical signs. The response of individual animals varied considerably. Alterations of respiratory pattern sometimes occurred during stimulation but there was no consistent pattern of change in any animal.

Cerebrospinal Fluid Pressure in Patients With Brain Tumors

The effects on the cerebrospinal fluid pressure (CSFP) of alfentanil and fentanyl were compared during nitrous oxide-oxygen (N2O-O2) anesthesia in 24 patients who had brain tumors. Monitored variables included CSFP (lumbar subarachnoid catheter), heart rate from electrocardiographic lead II, mean radial arterial blood pressure, and arterial blood gas tensions. General anesthesia was induced with thiopental, 5 mg/kg IV in divided doses, and maintained with 70% N2O in O2; ventilation was held constant (PaCO2 = 37.4 +/- 1.6 mm Hg [mean +/- SEM]). After baseline data were recorded, 16 subjects were randomly assigned to receive either 5 micrograms/kg fentanyl as an intravenous bolus or 50 micrograms/kg alfentanil as an intravenous bolus, followed by an infusion of alfentanil at 1 micrograms.kg-1.min-1. Monitored variables were continuously recorded for 15 min after opioid injection. A third group of 8 patients was studied subsequently; they received only N2O-O2 during a 15-min observation period and served as controls. Blood pressure was held constant with an intravenous infusion of 0.1% phenylephrine, as needed; noxious stimulation was carefully avoided. Cerebrospinal fluid pressure remained unchanged both in patients who received N2O-O2 alone and in those who received fentanyl-N2O-O2. By contrast, those who received alfentanil-N2O-O2 had a gradual increase in CSFP, reaching 30% above baseline values after 10 min and stabilizing thereafter. Although the absolute increase in CSFP during normocarbic alfentanil-N2O anesthesia was relatively small (9.5 +/- 1.3 mm Hg to 13.0 +/- 1.3 mm Hg [mean +/- SE], P less than 0.05), the absence of a similar effect after fentanyl administration suggests that precautionary measures such as hyperventilation are advisable if alfentanil is used for potentiating normocarbic N2O-O2 anesthesia in neurosurgical patients with intracranial mass lesions.

Regional Cerebral Blood Flow after Hemorrhagic Hypotension in the Preterm, Near-Term, and Newborn Lamb

Developmental changes in regional cerebral blood flow (CBF) responses to hemorrhagic hypotension during normoxia and normocapnia were determined using radioactively labeled microspheres to measure flow to the cortex, brainstem, cerebellum, white matter, caudate nucleus, and choroid plexus in three groups of chronically catheterized lambs: 90- to 100-d preterm fetal lambs (n = 9); 125- to 136-d near-term fetal lambs (n = 9); and newborn lambs 5- to 35-d-old (n = 8). Heart rate, central venous pressure, and arterial blood pressure were monitored continuously and arterial blood gas tensions, pH, Hb, and oxygen saturation together with regional CBF were measured periodically. Hemorrhagic hypotension produced a mean decrease in arterial blood pressure of 27 +/- 4, 23 +/- 2, and 41 +/- 4% in the three groups, respectively, whereas reinfusion of the lamb's blood resulted in a return to control blood pressure within 3% in all three groups. In the pre-term fetal lamb, CBF decreased significantly in all regions during hypotension. In the near-term fetal lamb, only blood flow to the cortex decreased significantly during hypotension. In the newborn lamb, only the choroid plexus demonstrated a significant decrease in blood flow during hypotension. The lower limit of regional CBF autoregulation was identical to the resting mean arterial pressure in fetal life but significantly lower in newborn lambs. These experiments demonstrate for the first time that vulnerability to hypotension decreases with increasing maturity and that the brainstem, the phylogenetically oldest region of the brain, is the least vulnerable to the effects of hypotension at any age in the lamb model.

Ionization and Hemodynamic Effects of Calcium Chloride and Calcium Gluconate in the Absence of Hepatic Function

Serial serum ionized calcium concentrations were measured before and after administration of either calcium chloride or calcium gluconate during the anhepatic stage of liver transplantation in 15 patients to determine the release of ionized calcium in the absence of hepatic function. When hypocalcemia (Ca++ less than 0.8 mM) occurred during the anhepatic stage, patients were randomly assigned to treatment with chemically equivalent doses of either calcium chloride (10 mg/kg, n = 8) or calcium gluconate (30 mg/kg, n = 7). Serum concentrations of ionized calcium and citrate, hematocrit, arterial blood gas tensions, acid-base state, and hemodynamic profiles were determined before and up to 10 min after calcium therapy. In both groups of patients initial similar and rapid increases in Ca++ (0.98 +/- 0.14 mM in the calcium chloride group and 1.05 +/- 0.10 mM in the calcium gluconate group) were followed by gradual decreases over the next 10 min. Measured hemodynamic values were similar in the two groups, and neither group showed improvement in cardiovascular function after calcium therapy, possibly because of the decrease in preload that occurred during the anhepatic stage. Equally rapid increases in Ca++ after administration of calcium chloride and gluconate in the anhepatic state suggest that calcium gluconate does not require hepatic metabolism for the release of Ca++ and is as effective as calcium chloride in treating ionic hypocalcemia in the absence of hepatic function.

The use of protriptyline for respiratory failure in patients with chronic airflow limitation

Treatment of nocturnal hypoventilation in patients with restrictive chest wall disease and respiratory failure, results in improved daytime arterial blood gas tensions, increase in functional ability and longer survival. Success has been achieved with the use of protriptyline which reduces the duration of rapid eye movement (REM) sleep during which nocturnal hypoventilation occurs. Eighteen patients with severe chronic airflow limitation (CAL), took part in a randomized, double-blind, crossover trial of protriptyline and placebo. Seventeen patients completed the study. The use of protriptyline was associated with a fall in the median percentage of total sleep time spent in REM from 16 to 8.8% (p less than 0.01). This was associated with a reduction in the median daytime arterial carbon dioxide tension from 6.4 kPa (range 5.2-8.5 kPa) to 5.8 kPa (range 5.0-8.1 kPa) (p less than 0.01); increased respiratory muscle strength (p less than 0.05), and increased six minute walking distance from a median of 258 m (range 58.5-585 m) to 275 m (range 171-598 m) (p less than 0.02). We found pharmacological treatment of REM-related nocturnal hypoventilation in patients with CAL to be effective, but anticholinergic side-effects, particularly in older male patients, might preclude long-term treatment.

Dexmedetomidine, an ??2-Adrenergic Agonist, Decreases Cerebral Blood Flow in the Isoflurane-Anesthetized Dog

The purpose of this study was to examine the effects of dexmedetomidine, an alpha 2-adrenergic agonist, on cerebral blood flow and metabolic rate in dogs anesthetized with 0.64% isoflurane. After intubation and institution of mechanical ventilation, arterial, venous, pulmonary artery, and sagittal sinus catheters were inserted. Measurements of cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRo2), mean arterial pressure, cardiac output, and blood gas tensions were made at various levels of isoflurane anesthesia (0.64%, 1.9%, and 2.8%), after the administration of 10 micrograms/kg of dexmedetomidine (a dose that has been shown to reduce anesthetic requirements in dogs by greater than 90%) and finally after 0.3 micrograms/kg of the alpha 2-adrenergic antagonist idazoxan. Despite an increase in arterial pressure, dexmedetomidine caused a marked reduction (greater than 45%, P less than 0.05) in CBF when compared with all preceding concentrations of isoflurane. The administration of dexmedetomidine had no effect on the CMRo2. The electroencephalogram showed a loss of high-frequency activity in a pattern similar to that seen with 1.90% isoflurane. Administration of dexmedetomidine was associated with a 57% decrease in cardiac output (to 0.89 L/min). Administration of idazoxan (an alpha 2-adrenergic antagonist) resulted in an increase in cardiac output and a reversal of the electroencephalogram effects. This experiment indicates that 10 micrograms/kg of dexmedetomidine in isoflurane-anesthetized dogs is associated with a profound decrease in CBF and cardiac output in the face of an unaltered CMRo2. Despite the large reduction in the CBF/CMRo2 ratio, there was no evidence of global cerebral ischemia.

Respiratory failure and sleep in neuromuscular disease.

Sleep hypoxaemia in non-rapid eye movement (non-REM) and rapid eye movement (REM) sleep was examined in 20 patients with various neuromuscular disorders with reference to the relation between oxygen desaturation during sleep and daytime lung and respiratory muscle function. All the patients had all night sleep studies performed and maximum inspiratory and expiratory mouth pressures (PI and Pemax), lung volumes, single breath transfer coefficient for carbon monoxide (KCO), and daytime arterial oxygen (PaO2) and carbon dioxide tensions (PaCO2) determined. Vital capacity in the erect and supine posture was measured in 14 patients. Mean (SD) PI max at RV was low at 33 (19) cm H2O (32% predicted). Mean PE max at TLC was also low at 53 (24) cm H2O (28% predicted). Mean daytime PaO2 was 67 (16) mm Hg and PaCO2 52 (13) mm Hg (8.9 (2.1) and 6.9 (1.7) kPa). The mean lowest arterial oxygen saturation (SaO2) was 83% (12%) during non-REM and 60% (23%) during REM sleep. Detailed electromyographic evidence in one patient with poliomyelitis showed that SaO2% during non-REM sleep was maintained by accessory respiratory muscle activity. There was a direct relation between the lowest SaO2 value during REM sleep and vital capacity, daytime PaO2, PaCO2, and percentage fall in vital capacity from the erect to the supine position (an index of diaphragm weakness). The simple measurement of vital capacity in the erect and supine positions and arterial blood gas tensions when the patient is awake provide a useful initial guide to the degree of respiratory failure occurring during sleep in patients with neuromuscular disorders. A sleep study is required to assess the extent of sleep induced respiratory failure accurately.

Atrial tachycardia causes hydrops in fetal lambs

The purpose of this project was to study mechanisms responsible for edema formation in fetuses with hydrops. We produced hydrops fetalis in 28 fetal sheep [gestational age of 125 +/- 5 days (mean +/- SD)] by pacing their atria at 300-320 beats/min for 68 +/- 40 (SD) h. All fetuses developed peripheral edema and ascites [volume of ascitic fluid was 134 +/- 75 (SD) ml; total protein concentration was 3.10 +/- 0.6 (SD) g/dl, and total albumin concentration was 1.68 +/- 0.3 (SD) g/dl]. Pacing did not affect aortic pressure but increased venous pressure from 4 +/- 1 to 8 +/- 1 (SE) Torr. Pacing did not affect pH, arterial partial pressure of O2 (PaO2), or Na+ but increased PaCO2 from 53 +/- 1 to 55 +/- 1 (SE) Torr and K+ from 3.9 +/- 0.1 to 4.3 +/- 0.1 (SE) meq/l. Hematocrit increased from 29 +/- 1 to 32 +/- 1 (SE)% acutely with pacing but returned to base line by the last day of the experiment. Plasma protein concentration decreased slightly from 3.7 +/- 0.1 to 3.5 +/- 0.1 (SE) g/dl by the last day of the experiment; plasma albumin concentration did not change. Plasma volume decreased acutely from 271 +/- 19 to 238 +/- 16 (SE) ml and then remained decreased throughout the experiment. Red blood cell mass and the turnover time for albumin were not affected by pacing. We found no consistent relationship between edema formation and changes in arterial blood gas tensions, plasma protein concentrations, or the turnover time for albumin.2

Long term domiciliary oxygen treatment for chronic respiratory failure reviewed.

The use of long term domiciliary oxygen therapy in the Sheffield area from June to August 1987 has been surveyed. Of the 74 patients prescribed long term domiciliary oxygen therapy, 64 were visited at home. These had arterial blood gas tensions or oxygen saturation measured (while breathing oxygen and air), and the indications for long term domiciliary oxygen therapy were examined retrospectively. Fifty two patients had chronic bronchitis and emphysema, the remainder having pneumoconiosis, bronchiectasis, fibrosing alveolitis, and congestive cardiac failure. Of the 54 cases where indications for treatment could be compared with the Department of Health and Social Security (DHSS) guidelines, only 23 (43%) met the full DHSS criteria before the start of treatment. The median length of treatment was 16 months. At follow up 51 patients had an arterial oxygen tension (PaO2) greater than 8.0 kPa when breathing oxygen. They had a significantly higher PaO2 when breathing air than before long term oxygen therapy (6.7 (SD 1.2) kPa before oxygen treatment, 7.6 (1.4) kPa on reassessment). A similar change was seen in the 23 patients assessed as recommended by the DHSS (6.1 (0.8) kPa; 7.2 (1.2]. PaO2 during the breathing of air was less than 7.3 kPa at reassessment in only 21 (33%) patients. Thirteen patients had carboxyhaemoglobin concentrations above 2.5%, the 95th centile of the distribution in nonsmokers in the laboratory.

Cyclic haemodynamic and arterial blood gas changes during Cheyne-Stokes breathing

A 74-year-old patient presented with congestive heart failure and continuous periodic breathing. Left ventricular ejection fraction was 20% and the lung-to-brain circulation time was prolonged to 35 s. We report on the phasic changes of the patient's arterial blood gas tensions and on the periodic fluctuations of pulmonary artery pressures and cardiac output that we observed during Swan-Ganz catheterisation.

Effect of Premedication on Arterial Blood Gases Prior to Cardiac Surgery

The effect of premedication on arterial blood gas tensions was studied in thirty adult surgical patients with valvular disease. They were divided into three groups, each group having a different premedication regimen. Blood gas tensions were compared in these patients when awake on the night before surgery, asleep, after premedication and just prior to induction of anaesthesia. Samples were taken while the patient breathed air and each patient acted as his/her own control. The patients were randomised into one of three premedication regimens: 1. intramuscular lorazepam, 2. intramuscular morphine and hyoscine (scopolamine) and 3. oral lorazepam plus intramuscular morphine and hyoscine. There was a statistically significant though not clinically significant rise in PaCO2 and fall in pH following premedication with lorazepam, morphine and hyoscine. There was also a significant fall in PaO2 associated with morphine and hyoscine premedication which was greater than that which occurred with unsedated sleep. Patients who are to undergo cardiac valvular surgery should receive supplementary oxygen following premedication and during transfer to the operating room.