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Blood gas tensions and acid-base status were determined in six patients with tetanus before and after the onset of severe muscle spasms. Hypoxaemia and metabolic acidosis present in all the patients, were worsened by muscle spasms. It is suggested that frequent measurements of blood gases should be carried out where such facilities are available.
Cerebral blood flow (CBF) and cerebral venous blood gases were studied in seven patients before, during and after intravenous sodium nitroprusside infusion. The 133Xe intra-arterial injection method was used for the CBF measurements. A dose of sodium nitroprusside (mean 1.0 mg, mean infusion time 20 min), which reduced mean arterial blood pressure by a mean of 17%, resulted in a 13% decrease in CBF (P less than 0.05). Measurements obtained 5 and 20 min after termination of the sodium nitroprusside infusion showed no signs of a hyperaemic rebound effect. Arterial PCO2, metabolic rate of oxygen, arterio-venous oxygen difference and venous PO2 remained unchanged during and after infusion. It is concluded that sodium nitroprusside has a minor effect on cerebral haemodynamics, an effect that might be mediated by the sympathetic nervous system.
Cerebral blood flow (CBF) and cerebral venous blood gases were investigated in seven awake patients during hypotension induced with sodium nitroprusside. Infusion of the drug into the internal carotid artery produced no changes in cerebral haemodynamics. Intravenous nitroprusside infusion resulted in a decrease in both CBF and jugular venous PO2 (P less than 0.01, respectively). Reducing mean arterial blood pressure by 18% and 43% produced a mean CBF fall of 6% and 27% respectively. Arteriovenous oxygen difference increased in consonance with the CBF decrease (P less than 0.01). Arterial PCO2 fell during the infusion (P less than 0.01). At 18% blood pressure reduction, the observed PCO2 decrease of 0.25 kPa could account for the 6% CBF decrease. At 43% blood pressure reduction, PCO2 fell by 0.53 kPa, a decrease which could not explain the observed CBF fall of 27%. Dizziness and incipient fainting occurred in the patients at this point. It is concluded that sodium nitroprusside has a minor but significant effect on cerebral haemodynamics in normal awake man.
Liquid propane and similar coolants are used in the rapid freezing of biological specimens. These coolants form explosive gas mixtures with air, with a 14,000-fold increase in volume over that of the liquid. The liquefied gases have high vapour pressures and, unless they are maintained below their flashpoint, the vapour above them will reach ignitable concentrations. The flashpoint of liquid propane is -104 degrees C. Ethane has a higher vapour pressure, and vapour mixed with air above liquid ethane can be ignited at a coolant temperature of -130 degrees C. The danger is minimized if the coolant is maintained near its freezing point and under a nitrogen atmosphere, in a fume cupboard. Liquid nitrogen evaporates to a 690-fold increase in volume at room temperature. It is important to ventilate the working area, especially when cryo-sectioning in a small room, otherwise there is a possibility of asphyxiation.
Thirty-four patients with gallbladder disease, but otherwise healthy, were studied in connection with cholecystectomy. For postoperative analgesia, 22 patients were given a posterior splanchnic blockade with 0.5% plain lidocaine, and 12 were injected intramuscularly with fentanyl in a dose of 3.5 mug/kg b.w. Postoperatively, before administration of the analgesic agent, the cardiac output, mean arterial blood pressure, heart work and estimated hepatic blood flow were increased and the total peripheral resistance, splanchnic vascular resistance, arterial oxygen tension and base excess values were decreased. Fentanyl, in addition to its analgesic effect, also decreased the arterial oxygen tension and pH and increased the arterial carbon dioxide tension. There was little change in cardiac output, mean arterial blood pressure and estimated hepatic blood flow. Following splanchnic blockade, on the other hand, pain relief was accompanied by a decrease in cardiac output, mean arterial blood pressure and heart work to about the preoperative level, while the estimated hepatic blood flow remained unchanged and the splanchnic vascular resistance decreased rapidly. Neither total peripheral resistance nor blood gases altered as a result of splanchnic blockade.
Halothane and nitrous oxide (N2O) concentrations were measured in operating theatres, in the areas corresponding to theinhalation zones of the anaesthetists and operating nurses. The measurements were performed in an operating theatre with a non-recirculating air exchange rate of 20/h. This was performed partly in model experiments and partly during the administration of anaesthesia by intubation. In the model experiments. the measurements were taken both with and without a specially constructed scavenging system. During anaesthesia, the measurements were taken exclusively with the scavenging system, although well-defined leakages were fitted into the otherwise gas-tight anaesthetic system. The results were supplemented by smoke experiments which showed the air distribution patterns. The investigation showed that the gases were concentrated over and around the operating table. Activities during surgery diluted this concentration. Furthermore, it was shown that leakage in the anaesthetic system significantly influences the achieving of a low gas-air mixture. Halothane concentrations in the inhalation zone of the anaesthetist and operating nurse can be reduced to 0.02 and 0.01 p.p.m. respectively, if the anaesthetic system is completely gas-tight.
The investigation includes measurement of the N2O-concentration in the recovery rooms of three hospitals with different room ventilation systems. The amount of ventilation determines the elimination of the gas exhaled by the patients and, therefore, is related to the number of patients in the recovery rooms. The investigation has shown that non-recirculating room ventilation of 500 m3/pt./hour in recovery rooms gives personnel the same protection against inhalation of anaesthetic gases as is afforded to personnel in operating theatres with scavening equipment.
Aggregate anaphylaxis was induced by intravenous injection of the specific antigen in eight ovalbumin-sensitized monkeys. Changes in respiratory mechanics, acid-base status and blood gases were studied during the following half hour. Within 1 minute after challenge, a short period of respiratory depression, probably reflex-mediated, was observed. This was followed by hyperventilation, and arterial PCO2 decreased. There was a rapid increase in pulmonary resistance (Rpulm) and a concomitant decrease in pulmonary dynamic compliance (Cdyn), suggesting constriction of smooth muscles in the lung. Rpulm returned to the control value but Cdyn remained depressed, as a result of constriction of small airways and pulmonary congestion. Oxygen saturation in arterial blood decreased slightly due to a marked desaturation of mixed venous blood and increased venous admixture. Progressive metabolic acidosis developed, indicating poor tissue oxygenation and perfusion. The changes observed in this study were not severe enough to cause any major disturbance of the gas exchange in the lungs, despite a severe anaphylactic shock.
The effect on cerebral haemodynamics of arterial hypotension induced by sodium nitroprusside infusion was studied in nine patients at the end of operations for intracranial aneurysms under N2O-O2-halothane anaesthesia. Cerebral blood flow (CBF), using the intraarterial 133Xe injection method, and cerebral jugular venous blood gases were monitored before, during and after the induced hypotension. CBF and jugular venous oxygen tension (PvO2) remained constant during the hypotensive period. Following its termination, a 13% increase in CBF occurred (P less than 0.05) and PvO2 showed the same trend, a 5% increase (P less than 0.30). Regional CBF recordings (rCBF) in 16 small areas within the cerebral hemisphere were obtained at each measurement. In four of the patients, rCBF abnormalities were present in the form of hyperaemic regions, probably induced by the operation or the disease itself. The focal abnormalities were not accentuated during hypotension nor were ischaemic regions disclosed. It is concluded that sodium nitroprusside has only a minor influence on cerebral haemodynamics in the anaesthetized state.
The effects of repeated doses of benzodiazepines, diazepam and midazolam in combination with meperidine on arterial blood gases and transcutaneous PO2 were studied in eight healthy volunteers. The study was designed to mimic a clinical situation. Initially two doses of either midazolam 0.05 mg/kg or diazepam in fat emulsion 0.15 mg/kg were given in a randomized crossover fashion with a 20-min interval, followed by meperidine 0.5 mg/kg another 20 min later. The opioid effects were then antagonized by naloxone 0.4 mg. The initial doses of benzodiazepines caused an increase in PaCO2 and a decrease in PaO2. The changes in PaO2 were of short duration and recovered to baseline levels between injections. However, they came sooner and were more pronounced after midazolam. The changes in PtcO2 paralleled those in PaO2. The PtcO2 index as a measure of cardiac output and peripheral blood flow adequacy was increased immediately after the first injection of midazolam but was otherwise not different from control. There were no differences between the drugs concerning PtcO2 index. PaCO2 increased after the first benzodiazepine injection and remained so throughout the study. Addition of meperidine caused only small changes in PaO2 and PaCO2. These changes were reversed by naloxone. In spite of different elimination kinetics there was no difference in the duration of respiratory depression between the two benzodiazepines.
Prior to the start of supportive therapy at the site of the accident, arterial blood samples from 47 patients with acute head injury were taken for blood gas analysis. At the same time, the degree of unconsciousness was assessed using the Glasgow-Coma-Scale. After transport to the hospital, arterial blood gases and the level of unconsciousness were again determined. A very close correlation was found between the initial depth of unconsciousness and the degree of hypercapnia (R = -0.90). Patients with head injury and other multiple injuries did not differ in this report (R = -0.95) from those with isolated head injury. The correlation between PaO2 and the degree of unconsciousness was less well defined, and the results showed a greater degree of scatter (R = 0.54). The acidosis observed resulted mainly from the rise in PaCO2. The absence of any correlation between the base excess and the Glasgow-Coma-Scale levels (R = -0.27) makes a common metabolic derangement unlikely. As a result of intubation and controlled ventilation, the hypercapnia of the comatose patients had been corrected, and a correlation could no longer be found between the Glasgow-Coma-Scale level and the PaCO2. In order to avoid hypoventilation, which carries with it the danger of a rise in intracranial pressure, all patients with severe head injury should be intubated and ventilated as soon as possible after the accident.
The priority of direct monitoring of blood gases in Paediatric Intensive Care Units (PICU) increased substantially after introduction of the Deep Picture method and Oxygen Status Algorithm (OSA) (1) into medical practice. We used the advantages of these methods as a prerequisite for a more detailed and deeper analysis of the blood oxygen profile (2, 3). The aims of the present paper were: 1. To illustrate the applicability of the capacity coefficients beta 1.0, beta 2.3, beta 5-4 of the transported oxygen and the "Useful Ratio" (UR) index of the haemoglobin oxygen, previously described by us, and the benefit derived from differentiation of the states of hyperoxia, normoxia and hypoxia; hyperoxaemia, normoxaemia and hypoxaemia on the Blood Oxygen Binding Curve (BOBC) in critically ill newborns, infants and children. 2. To expand the diagnostic capacity of the Blood Gas Map (BGM) used with the OSA in children and to supplement the arterial oxygen diagnostics with new indices that reflect the relationship between oxygen uptake and oxygen transported in the body. 3. To share our experience in PICU related to the acid-base-electrolytes relationship and to the possibility of assessing the reno-hepatic regulation according to the changes of the acid-base status in critically ill children.
The distribution of respiratory gases, hydrogen ions, glucose and lactate were studied in red cells suspended in SAGM solution and stored undisturbed at +4 degrees C in plastic (PVC) bags. After 42 days' storage there were considerable concentration differences between the supernatant and the red cell layer, as well as concentration gradients within the latter. Thus, pO2, sO2, pH and the glucose concentration were higher in the supernatant and pCO2 and the lactate concentration were higher in the red cell layer. These findings show that sampling from the mixed content of blood which has been stored sedimented in plastic containers will not be representative for the erythrocyte environment at the end of shelf life. This is of importance in attempts to understand storage effects on red cells.
The efficacy of pulmonary gas exchange immediately after delivery is inversely related to the volume of liquid in the lung at birth, but aspiration of as much liquid as possible from the lung before Caesarean delivery fails to improve postnatal oxygenation (Pa,O2) to the level achieved after spontaneous term delivery. We hypothesised that the differing respiratory benefit of aspiration and vaginal delivery results from the differing volume of lung liquid remaining after aspiration (17 ml (kg body weight)-1) and labour (7 ml kg-1). We addressed this hypothesis by reducing lung liquid volume to an estimated 7 ml kg-1 by infusing adrenaline to seven fetal lambs at 140 days gestation (term is 147 days) before performing Caesarean delivery and obtaining postnatal blood gases for comparison with samples from lambs delivered vaginally. Infusion of adrenaline to fetuses caused a progressive decline in arterial O2 saturation (Sa, O2), pH and base excess, but no change in arterial partial pressure of O2 (Pa,O2) or CO2 (Pa,CO2). After birth, Pa,O2 rapidly rose to the same level in adrenaline-treated and vaginal-delivery groups. A severe acidosis occurred in the adrenaline-treated group and this appeared to be related to a higher Pa,CO2 and a transiently lower Sa, O2 in this group. We conclude that adrenaline infusion can enhance postnatal Pa,O2 levels in the newborn lamb, but this beneficial effect may be outweighed by the severe acidosis that develops after prolonged prenatal adrenaline treatment.
Arterial blood gases, physiological dead space and percentage pulmonary venous admixture (physiological shunt) were measured in 31 patients with proteinuric pre-eclampsia. There was no difference in pulmonary function in 22 patients with moderate pre-eclampsia when compared with normal pregnancy, but in 9 patients with severe pre-eclampsia, there was a significant increase in alveolar-to-arterial PO2 difference and physiological shunt, indicating a degree of pulmonary ventilation/perfusion imbalance. There was no accompanying hypoxaemia, suggesting that the impairment was of no clinical importance.
Fetal heart rate (FHR) monitoring and computer-assisted analysis were performed immediately before cordocentesis in 25 severely small-for-gestational age fetuses. There were significant associations between FHR variation and both umbilical vein blood PO2 (r = 0.66) and pH (r = 0.69). However, the wide scatter of values around the regression lines prevented accurate prediction of fetal blood gases from FHR patterns. Nevertheless, FHR variation less than 20 ms was always associated with severe fetal hypoxaemia and acidaemia.
Interpreting arterial blood gases (ABGs) is a common practice in intensive care units. The use of the temperature correction facility, however, is not standardized, and the effects of temperature correction on the ABG result may affect the overall management of the patient. The aim of this study was to discuss the significance of temperature correction. Current practice in the UK and Australia is discussed along with a review of physiological principles of oxygenation and acid-base balance. The alpha-stat and pH-stat methods of blood gas analysis are presented, with arguments for and against using the temperature correction facility for blood gas analysis. The study concludes with recommendations for practice.
Twenty-three psychiatric patients were investigated during electroconvulsive treatment in relaxation. The blood gases, pH and serum bicarbonate levels in blood samples from the internal jugular vein and the femoral artery were measured radiometrically. The LDH fractions were separated electrophoretically and their activity, along with the activity of aldolase, was then determined on test materials. EEG recordings were made during the seizure and also during postconvulsive restitution. The following conclusions were drawn: (1) There was no evidence of anoxic anoxia in the brain during and after seizures. (2) A close relationship was found between the corresponding phases of electrical activity and brain metabolism as indicated by the blood gas changes during postconvulsive restitution. (3) On the basis of the increased glycolytic activity in the sera it is probable that glucose metabolism was shifted in the anaerobic direction during postconvulsive restitution of the brain tissues.