Arteriovenous O2 Content Difference Research Articles

Changes in oxygen uptake-work rate relationship as a compensatory mechanism in patients with heart failure.

To assess the compensatory change in oxygen uptake (VO2) kinetics during exercise in patients with heart failure, we performed cardiopulmonary exercise testing using a cycle ergometer in 29 cardiac patients and 18 normal subjects. The work rate increased linearly (1w/6sec) after a 4 min, 20w warm-up. The ratio of increase in VO2 to increase in work rate (delta VO2/delta WR) was determined by linear regression of VO2 plots. Cardiac output by dye dilution method and plasma norepinephrine concentration (NE) were measured at rest and 20w warm-up. VO2 at rest and at 20w warm-up and delta VO2/delta WR decreased significantly with increasing severity in NYHA functional classification. delta VO2/delta WR showed significant negative correlation to the difference in NE levels at rest and at 20w (r = -0.69, p less than 0.001). The delta values of arteriovenous O2 content difference, calculated using Fick's principle, and cardiac index from rest to 20w warm-up failed to show significant relationship to delta VO2/delta WR. These results suggest that the decrease in VO2 requirement in heart failure patients is due probably to blood redistribution during exercise as a compensatory mechanism for exercise intolerance.

Effect of phentolamine on the relationship between O2 consumption and delivery in sheep

The oxygen flux challenge test (OFT) has recently been used in critically ill patients as a dynamic test for assessment of the response in oxygen consumption (VO2) to an increase in O2 delivery (QO2). Such a test may indicate whether a patient demonstrates delivery-dependent VO2. However, the increase in whole body VO2 following an increase of QO2 might be due to the agents used for the OFT. In this study, we examined the possibility of obtaining false positive OFT with an alpha-adrenergic antagonist. Five normothermic thiopentone-anaesthetised and mechanically-ventilated (inspired O2 fraction, 0.3; expired CO2 fraction, 0.045-0.055) adult sheep (25-31 kg) were investigated. The QO2 was increased in a stepwise fashion from 200 to 850 ml.min-1 by vasodilatation with intravenous infusion of phentolamine. The VO2 was calculated at each step from the product of arteriovenous. O2 content difference (CO2, a-v) and cardiac output (Qc), the latter being continuously measured with a transit-time ultrasonic flow probe placed around the main pulmonary artery. The VO2 (y) was linearly related to QO2 (x), y = 0.034 (SD 0.024) x + 29.3 (SD 3.9). The relationship between Qc (y) and CO2, a-v (x) was y = 4.6x(-1.12) (n = 69; r2 = 0.75; P = NS compared to the expected relationship for isoconsumption conditions, i.e. where Qc = VO2.(CO2, a-v)(-1). Our data suggested that under stable conditions, an infusion of phentolamine did not sufficiently alter the relationship between Qc and CO2, a-v to invalidate its use for OFT in normal sheep.

Diaphragmatic Energetics during Prolonged Exhaustive Exercise

The present study was carried out to examine diaphragmatic O2 extraction and lactate and ammonia production during prolonged exhaustive exercise. Experiments were performed on nine healthy exercise-conditioned ponies in which catheters had been implanted in the phrenic vein previously. Blood-gas variables and lactate and ammonia concentrations were determined on simultaneously obtained arterial and phrenic-venous blood samples at rest and during 30 min of exertion at 15 mph + 7% grade (heart rate, 200 beats/min; approximately 90% of maximum). Arterial O2 tension and saturation were maintained near resting value but CO2 tension decreased markedly with exercise, and because of increased hemoglobin concentration, arterial O2 content rose. Concomitantly, phrenic venous O2 tension, saturation and content decreased markedly (23.6 +/- 1 mm Hg, 24.5 +/- 2%, 5.2 +/- 0.3 ml/dl at 3 min of exertion) and significant fluctuations did not occur as exercise duration progressed to 30 min. Diaphragmatic arteriovenous O2 content difference and O2 extraction rose from 4 +/- 0.3 to 16 +/- 0.5 ml/dl and from 30 +/- 3 to 75 +/- 1% at 3 min of exercise, and significant deviations did not occur as exercise duration progressed. Arterial lactate and ammonia levels increased during exercise, indicating their release from working limb muscles. Phrenic-venous values of lactate and ammonia did not exceed arterial values. Ponies sweated profusely and were unable to keep up with the belt speed in the last 4 to 5 min of exercise. Constancy of phrenic arteriovenous O2 content difference in exercise indicated ability to adjust perfusion in diaphragm so as to adequately meet its O2 needs.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output and Oxygen Delivery during Exercise in Sickle Cell Anemia

Desaturation in patients with sickle cell anemia (SCA) can lead to intravascular sickling and vascular occlusion. The increased metabolic demands of exercise tend to increase oxygen extraction, giving rise to a fall in saturation in the capillary bed that may predispose to sickling. This could be minimized with an increase in cardiac output. The aims of this study were to assess the role of increased stroke volume (SV) in augmenting cardiac output (Q) and to estimate the role of enlarged arteriovenous O2 content difference in maintaining O2 transport in children with SCA. A group of 30 children with SCA (Hb 65 to 133 g/L) and 16 healthy controls of the same racial group and of similar height and weight performed incremental and steady-state exercise at 50% Wmax. Cardiac output (Q) was measured by the indirect (CO2) Fick method during steady state. The slope of delta HR/delta VO2 during incremental exercise was higher in SCA subjects compared with controls (4.01 +/- 1.73 versus 2.80 +/- 0.61 bpm per ml/min/kg VO2, p = 0.001). Q for VO2 was abnormally high in patients, particularly older ones with lower Hb levels. HR (% predicted) was higher in patients than in controls (106 +/- 11 versus 92 +/- 8% predicted, p less than 0.0001), as was SV (113 +/- 16 versus 98 +/- 14% predicted, p = 0.002). Multiple linear regression of Q % predicted and SV % predicted on Hb and age showed a positive correlation with age and a negative correlation with Hb (r = 0.84 for Q and r = 0.76 for SV).(ABSTRACT TRUNCATED AT 250 WORDS)

O2 metabolism of the sheep diaphragm during flow resistive loaded breathing.

To determine whether O2 availability limited diaphragmatic performance, we subjected unanesthetized sheep to severe (n = 11) and moderate (n = 3) inspiratory flow resistive loads and studied the phrenic venous effluent. We measured transdiaphragmatic pressure (Pdi), systemic arterial and phrenic venous blood gas tensions, and lactate and pyruvate concentrations. In four sheep with severe loads, we measured O2 saturation (SO2), O2 content, and hemoglobin. We found that with severe loads Pdi increased to 74.7 +/- 6.0 cmH2O by 40 min of loading, remained stable for 20-30 more min, then slowly decreased. In every sheep, arterial PCO2 increased when Pdi decreased. With moderate loads Pdi increased to and maintained levels of 40-55 cmH2O. With both loads, venous PO2, SO2, and O2 content decreased initially and then increased, so that the arteriovenous difference in O2 content decreased as loading continued. Hemoglobin increased slowly in three of four sheep. There were no appreciable changes in arterial or venous lactate and pyruvate during loading or recovery. We conclude that the changes in venous PO2, SO2, and O2 content may be the result of changes in hemoglobin, blood flow to the diaphragm, or limitation of O2 diffusion. Our data do not support the hypothesis that in sheep subjected to inspiratory flow resistive loads O2 availability limits diaphragmatic performance.

Rate of decrease of myocardial O2 consumption due to cardiac arrest in anesthetized goats.

The rate of change of myocardial O2 consumption, MVO2, has been measured during the transition from beating to cardiac arrest. Cardiac arrest was achieved by destruction of the bundle of His by injection of formalin and induced by 25 s interruption of pacing. The left main coronary artery was perfused under constant pressure and the great cardiac vein was drained under controlled pressure. The arterio-venous O2 content difference, [O2](a-v), and coronary arterial and venous flows, CAF resp CVF, were continuously measured. The MVO2 transient was calculated using the following equation based on a 3 compartment model: MVO2 = CAF . [O2](a-v) - (Vc + Vv) . d[O2]v/dt - (Vc . Vv/CVF) . d2[O2]v/dt2 where Vc and Vv are the capillary and the venous blood volume as function of time and [O2]v is the venous oxygen content. A 7th order polynoma was fit to the [O2]v-data and the fitted equation was differentiated analytically to obtain the first and second order derivatives. The MVO2 decreased from 94 +/- 5 microliters O2/s/100 g (mean +/- SE) before cardiac arrest to 15.4 +/- 5 microliters O2/s/100 g after 15 s of cardiac arrest. The change in MVO2 (50% in 3.8 +/- 0.3 s) preceded the change in venous oxygen content (50% in 12.7 +/- 0.5 s) and the change in coronary resistance (50% in 14.9 +/- 0.9). These results are in accordance with the hypothesis that interstitial O2 concentration is a major determinant of coronary resistance.

Diaphragmatic O2 and lactate extraction during submaximal and maximal exertion in ponies.

Diaphragmatic O2 and lactate extraction were studied in 10 healthy ponies at rest and during treadmill exercise. The phrenic vein was aseptically catheterized via a lateral thoracotomy 8-35 days before the study. Arterial and phrenic venous blood samples were obtained simultaneously at rest and at 30-s intervals during 4 min of exertion. Three levels of exertion were studied (moderate, 10 mi/h; heavy, 15 mi/h; maximal, 20 mi/h), and a rest period of at least 90 min was allowed between them. Each pony was studied twice at least 2-3 days apart. At rest the diaphragmatic venous PO2, O2 saturation, arteriovenous O2 content difference, and O2 extraction were 43.2 +/- 2.0 Torr, 76.1 +/- 3.2%, 3.14 +/- 0.43 ml/dl, and 23.60 +/- 3.61%, respectively. Significant decrease in phrenic venous PO2 and O2 saturation occurred within 30 s of exercise. Phrenic venous PO2 decreased to 20.3 +/- 1.0, 18.9 +/- 1.1, and 15.4 +/- 0.9 Torr at 120 s of moderate, heavy, and maximal exercise, respectively. Corresponding values of phrenic venous O2 saturation were 33.6 +/- 2.2, 25.8 +/- 2.1, and 17.9 +/- 0.5%, respectively. Diaphragmatic arteriovenous O2 content difference expanded to 13.11 +/- 0.49, 15.00 +/- 0.60, and 16.90 +/- 0.60 ml/dl at 120 s of moderate, heavy, and maximal exercise, respectively, as O2 extraction rose to 65.93 +/- 1.98, 73.90 +/- 1.99, and 80.95 +/- 0.47%, respectively. During heavy and maximal exercise, the diaphragmatic venous lactate concentration remained similar to the arterial concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

O2 transport in the horse during rest and exercise.

We studied mechanisms of O2 transport in 6 adult (2-5 year old) horses at rest and during steady-state exercise on a treadmill (0% slope) at 12 m/s (a submaximal gallop). Oxygen consumption was measured using an open-flow system. Arterial and mixed venous blood samples were simultaneously obtained for measurement of O2 content and hemoglobin concentration. VO2 increased from 1.5 +/- 0.2 L/min at rest to 46.2 +/- 4.8 L/min during exercise. HR increased from a resting value of 36.9 +/- 2.5 bpm to 196.5 +/- 10.9 bpm and the arterio-venous O2 content difference (a-v O2) increased from 4.2 +/- 0.8 ml O2/100 ml blood to 20.3 +/- 1.6 ml O2/100 ml blood. The 30.4-fold increase in oxygen consumption in the horse at submaximal VO2 versus only a 10-fold increase in man at VO2 max demonstrates the marked ability of the horse to transfer O2 at each step in the O2 transport pathway.

Abnormal tissue oxygenation in patients with cirrhosis and liver failure

Systemic haemodynamic and hepatic venous pressures, arterial and mixed venous gases and arterial lactate concentration were measured in 35 patients with histologically proven alcoholic cirrhosis who had been classified into three groups (A, B and C). Eight alcoholic patients without cirrhosis on liver biopsy were also studied. Compared with group A patients, group C patients had significantly higher hepatic venous pressure gradient, cardiac index, O2 transport and arterial lactate concentration and significantly lower systemic vascular resistance, arteriovenous O2 content difference and O2 uptake. In group B patients, corresponding values fell between those of groups A and C. Group A patients, unlike group C patients, were not significantly different from patients without cirrhosis with respect to cardiac index, systemic vascular resistance, O2 uptake and arterial lactate concentration. Our results suggest that in patients with cirrhosis, liver failure-associated hyperdynamic circulation may be accompanied by an abnormal tissue oxygenation.

Effect of intestinal denervation on intestinal vascular response to severe arterial hypoxia in newborn swine.

We examined the effects of alpha-adrenergic blockade (phentolamine) and intestinal denervation on the circulatory response of the newborn swine intestine to severe arterial hypoxia. Intestinal vascular resistance significantly increased during severe arterial hypoxia in the control group, whereas no change in intestinal vascular resistance was observed in the phentolamine or denervation groups at this time. Intestinal perfusion pressure increased in the control group but decreased in the phentolamine and denervation groups during severe arterial hypoxia. Despite the difference in intestinal vascular resistance, intestinal blood flow decreased in a similar manner in all groups during severe arterial hypoxia. Intestinal arteriovenous O2 content difference [(a-v)O2] and O2 uptake were greater during severe arterial hypoxia in the phentolamine and denervation groups than in the control group. We speculate that the sympathetic stimulation mediates the increase in intestinal vascular resistance in newborn swine during severe arterial hypoxia; and sympathetic stimulation limits the increase in intestinal (a-v)O2, which occurs during severe arterial hypoxia in the newborn swine intestine.

Changes in cardiac output during sustained maximal ventilation in humans.

To determine the increment in cardiac output and in O2 consumption (Vo2) from quiet breathing to maximal sustained ventilation, Vo2 and cardiac output were measured using an acetylene rebreathing technique in five subjects. Cardiac output and Vo2 were measured multiple times in each subject at rest and during sustained maximal ventilation. During maximal ventilation subjects breathed 5% CO2 to prevent hypocapnia. The increase in cardiac output from rest to maximal breathing was taken as an estimate of respiratory muscle blood flow and was used to calculate the arteriovenous O2 content difference across the respiratory muscles from the Fick equation. Cardiac output increased by 4.3 +/- 1.0 l/min (mean +/- SD), from 5.6 +/- 0.7 l/min at rest to 9.9 +/- 1.1 l/min, during maximal ventilations ranging from 127 to 193 l/min. Vo2 increased from 312 +/- 29 to 723 +/- 69 ml/min during maximal ventilation. O2 extraction across the respiratory muscles during maximal breathing was 9.6 +/- 1.0 vol% (range 8.5 to 10.7 vol%). These values suggest an upper limit of respiratory muscle blood flow of 3-5 l/min during unloaded maximal sustained ventilation.

Perfluorochemical Artificial Blood as a Volume Expander in Hypoxemic Respiratory Failure in Dogs

The perfluorochemical O2-transport fluid, Fluosol-DA 20 percent (PFC), is being clinically evaluated as a volume expander in patients who are unable to receive blood products. Since patients treated with Fluosol-DA may be at risk of developing adult respiratory distress syndrome (ARDS) as a complication of the original disorder for which they were transfused, we examined central hemodynamics and gas exchange in anesthetized O2-ventilated dogs with oleic-acid induced pulmonary edema before and after transfusion with 400 ml of either PFC (n = 5) or whole blood (n = 5). Transfusion produced similar increases in cardiac output, pulmonary and systemic vascular pressures and intrapulmonary shunt in the two groups. Arterial O2 tension, however, fell from 209 +/- 117 to 172 +/- 81 mmHg in the blood transfused group but increased from 219 +/- 145 to 302 +/- 138 mmHg in the PFC group. Arterial O2 content, on the other hand, increased in the blood transfused group due to an increase in hematocrit, but fell with PFC because of hemodilution. This lower total arterial O2 content in the PFC group was, however, compensated for by more efficient O2 transport by the PFC in that the PFC arteriovenous O2 content difference accounted for 26 percent of the total arteriovenous O2 content difference, making it about four times as efficient as hemoglobin in tissue O2 delivery. Fluosol DA, 20 percent, is an effective volume expander in this model of hypoxemic respiratory failure, and it can transport significant amounts of O2 even in the presence of a substantial intrapulmonary shunt.

Seizure-associated pulmonary edema and cerebral oxygenation in the rat

Cerebral partial pressure of O2 (PO2), relative changes in the ratio of reduced/oxidized cytochrome aa3, blood flow, and the arteriovenous difference in O2 content were measured during seizures with and without pulmonary edema. Seizures were induced with bicuculline (0.2-1.2 mg/kg iv) in rats anesthetized with 70% N2O and paralyzed with curare. Briefer seizures were accompanied by increased cerebral PO2 and increased oxidation of cytochrome aa3. Lung water content and arterial O2 partial pressure (PaO2) remained normal. Longer duration seizures were also accompanied initially by increases in cerebral oxygenation. Within minutes, however, PaO2 fell from a mean of 118 to 51 mmHg, and lung water content increased from 76.2 to 83.6%. Cerebral PO2 fell but most often rose back to or above control levels, while cytochrome aa3 became markedly reduced. Simultaneously, cerebral blood flow increased more than 300% above preseizure values and O2 delivery increased more than O2 consumption. The reductive shift of cytochrome aa3 was greater than that produced by lowering PaO2 to equivalent values in seizure-free rats. The reductive shift of cytochrome aa3, despite increased O2 delivery, may be indicative of derangements in cerebral O2 diffusion or energy metabolism.

A method for estimating contact time of red cells in lung capillaries from O2 and CO2 concentrations in rebreathing air in man.

In a previous paper (Mochizuki et al., 1986) we described the relation between alveolar- and venous-Pco2 and the contact time (tc). However, at that time, Pco2-dependency of the arterio-venous difference in O2 content ((a-v)Co2), the contact-time-dependency of the Haldane effect, and linearity of the relation between the experimental gas exchange ratio and Pco2 (R-Pco2 line) in rebreathing air were not taken into account. Recently, we have precisely analysed the above correlations from the numerical solutions of the simultaneous O2 and CO2 diffusions in the red blood cell (RBC). Based upon the results we have derived a corrected contact time equation. When the time constant of the reaction rate of the extracellular dehydration reaction was less than 0.2 sec, good agreement was observed between the contact time obtained from the pulmonary diffusing capacity for CO (Uchida, Shibuya and Mochizuki, 1986) and that from the present method.

Uteroplacental O2 uptake: continuous measurements during uterine quiescence and contractions.

To determine the constancy of uteroplacental O2 uptake (VO2) during uterine quiescence and both spontaneous and oxytocin-induced uterine contractions, we have developed a method to measure VO2 continuously and reproducibly. In seven ewes during uterine quiescence, total uterine blood flow (Qut) averaged 200 ml X min-1 X kg uterine contents-1, with intra-animal SD of 18 min X min-1 X kg-1 and interanimal SD of 86 ml X min-1 X kg-1. Uterine arteriovenous O2 content difference averaged 4.2 +/- 0.5 ml X dl-1. VO2 averaged 8.2 +/- 1.2 ml X min-1 X kg-1, with interanimal SD of 3.6 ml X min-1 X kg-1. During 21 spontaneous prelabor contractions, VO2 decreased 3.8% to 8.7 +/- 0.3 ml X min-1 X kg-1 (NS) during the contraction and subsequently increased 12.3% to 10.1 +/- 0.3 ml X min-1 X kg-1 (P less than 0.05) near the end of the contraction. With oxytocin-induced contractions, VO2 fell 10% to 6.4 +/- 0.2 ml X min-1 X kg-1 at the contraction onset (P less than 0.05) but by the end of the contraction had increased 6.1% to 7.6 +/- 0.2 ml X min-1 X kg-1 (NS). In conclusion, uteroplacental VO2 was measured continuously and reproducibly using relatively straightforward methodology; uteroplacental blood flow, arteriovenous O2 content difference, and uteroplacental O2 uptake were normally distributed with coefficients of variation less than 15%; and during both spontaneous and oxytocin-induced uterine contractions Qut decreased significantly, while VO2 initially decreased moderately and then showed an overshoot, during the contraction.

The effect of isoflurane-induced hypotension on cerebral blood flow and cerebral metabolic rate for oxygen in humans.

Deliberate hypotension was induced with isoflurane (mean inspired concentration 2.3 +/- 1.0%) in 12 patients undergoing craniotomy for clipping of cerebral aneurysms. Global cerebral blood flow (CBF) was measured before, during, and after hypotension. Arterio-venous O2 content difference was measured concomitantly, and the cerebral metabolic rate for oxygen (CMRO2) was calculated from these data. Mean arterial pressure (MAP) was reduced from 78 +/- 5 mmHg to 51 +/- 7 mmHg and then returned to 82 +/- 8 mmHg. Mean CBF before hypotension was 49 +/- 14 ml X 100 g-1 X min-1 and was unchanged during (45 +/- 12 ml X 100 g-1 X min-1) and after (49 +/- 15 ml X 100 g-1 X min-1) hypotension. The CMRO2 before hypotension was 2.0 +/- 0.6 ml X 100 g-1 X min-1. This was statistically significantly (P less than 0.025) reduced to 1.5 +/- 0.5 ml X 100 g-1 X min-1 during hypotension and then returned to 2.2 +/- 0.6 ml X 100 g-1 X min-1 on return to normotension. This indicates that the global cerebral O2 supply-demand balance was favorably influenced by isoflurane. No complications could be attributed to the hypotensive technique. We conclude that, with regard to global cerebral oxygenation, isoflurane is a safe agent with which to induce hypotension during neurosurgery.

Physiological and metabolic response to isolated closed-head injury. Part 1: Basal metabolic state: correlations of metabolic and physiological parameters with fasting and stressed controls.

Studies of the metabolic and physiological response to closed-head injury have intimated the presence of persistent hypermetabolism. To more fully define and evaluate the metabolic response to head trauma, a prospective study was conducted in patients with isolated closed-head injuries. Metabolic and cardiopulmonary data were obtained for a 7-day period. Patients with multiple injuries or infections, or those who received steroids, were excluded. The basic treatment regimen utilized hyperventilation, bed rest with head elevation, intracranial pressure monitoring, mild fluid restriction, and mannitol as needed. No exogenous nutritional support was given. Intrastudy trends and comparsion with data from unstressed fasting patients and stressed patients were noted. Mean Glasgow Coma Scale scores were 4.4 +/- 1.5 initially, but rose to a mean of 8.2 +/- 3.7 by Day 7. While the responses of cardiac index, CO2 production, lactate/pyruvate ratio, and arteriovenous O2 content difference (AVO2D) were initially elevated, these parameters declined over the course of 7 days. The AVO2D was equivalent to the fasting level by Day 5. Metabolic data, including most amino acid levels in plasma, showed an initial equivalence to stress control levels and a pattern similar to that in non-stressed control subjects by Day 7. Nitrogen and 3-methyl histidine excretion were persistently elevated for the full 7 days. Patients with isolated closed-head injury seemed to be initially hypermetabolic, but this process appeared to resolve by 1 week; the persistent nitrogen excretion may reflect equilibration of muscle mass to the existing level of activity (bed rest). After the first few days, nitrogen excretion may give an erroneous index of the level of metabolic stress and the type or amount of nutritional support needed.

Theoretical analysis of oxygen transport during hypothermia.

Oxygen transport and delivery to peripheral tissues during hypothermia are analyzed theoretically, taking into consideration various conditions observed both in nature and clinically. With decreasing temperature, P50 (the oxygen tension [PO2] at 50% hemoglobin saturation with oxygen) decreases, thereby leading to low mixed venous oxygen tension (PvO2) and thus low tissue PO2 values. On cooling from 37 degrees C to 25 degrees C at pH 7.4, the P50 decreases from a normal 26.8 mm Hg to 13.2 mm Hg. In the intact animal, as well as in a patient on cardiopulmonary bypass, oxygen consumption (Vo2) and cardiac output (QT, or recommended pump flow rate) decrease. If the ratio of Vo2/QT remains constant, then the arteriovenous O2 content difference, C(a-v)O2, must remain constant. If C(a-v)O2 is 5 ml/dl, we calculate that the PvO2 must decrease from a normal 40 mm Hg to 26.8 mm Hg at 25 degrees C. Clinically induced hypothermia is usually accompanied by hemodilution of the patient's blood to 50% normal hematocrit, which would reduce PvO2 to 13.7 mm Hg. Use of constant relative alkalinity (pH = 7.58 at 25 degrees C) further reduces the P50 to 10.8 mm Hg and the PvO2 to 10.9 mm Hg. Other clinical situations are also discussed. Sensitivity analysis predicts that during hypothermia PvO2 (and thus tissue PO2) is very dependent on P50, hemoglobin concentration, and QT, and less dependent on oxygen solubility and arterial PO2. We conclude that monitoring of mixed venous or tissue PO2 might be advisable, and that blood flow is the component of oxygen transport most amenable to manipulation by the clinician to ensure adequate tissue oxygenation during induced hypothermia.

Change in O2 uptake during rebreathing in hyperoxia in man.

In pertaining to PO2 dependency of the pulmonary CO diffusing capacity during rebreathing, the O2 uptake (VO2) and cardiac output (Q) were measured at three different PO2 levels between 100 and 500 Torr. Since the VO2 measured by an O2 injection method is strongly influenced in hyperoxia by a gas exchange ratio (R), a simulation method using a R-PCO2 relation during rebreathing was developed. Gas volume in the lung-bag-system needed in the computation was measured from the difference in O2 concentration between before and after injecting a known amount of O2 into the rebreathing circuit. The accuracy of the volume was checked by comparing it with the volume measured successively with a body box. The VO2 was determined by comparing the simulated O2 and CO2 concentrations in rebreathing gas with the measured ones. The VO2 significantly increased by rebreathing in hyperoxia. To analyze the VO2 increase, the Q was computed by dividing the VO2 by the arteriovenous O2 content difference, which in turn was obtained by dividing the slope of the CO2 dissociation curve by that of the R-PCO2 line. The Q was almost linearly related to the VO2. Since there was no difference in VO2 in steady state breathing between normoxia and hyperoxia, the increase in VO2 and Q seemed to occur transiently. This finding is very important in evaluating the PO2 dependency of the pulmonary diffusing capacity for CO.

Mechanism of transient nocturnal hypoxemia in hypoxic chronic bronchitis and emphysema.

In five patients with hypoxic chronic bronchitis and emphysema we measured ear O2 saturation (SaO2), chest movement, oronasal airflow, arterial and mixed venous gas tensions, and cardiac output during nine hypoxemic episodes (HE; SaO2 falls greater than 10%) in rapid-eye-movement (REM) sleep and during preceding periods of stable oxygenation in non-REM sleep. All nine HE occurred with recurrent short episodes of reduced chest movement, none with sleep apnea. The arterial PO2 (PaO2) fell by 6.0 +/- 1.9 (SD) Torr during the HE (P less than 0.01), but mean arterial PCO2 (PaCO2) rose by only 1.4 +/- 2.4 Torr (P greater than 0.4). The arteriovenous O2 content difference fell by 0.64 +/- 0.43 ml/100 ml of blood during the HE (P less than 0.05), but there was no significant change in cardiac output. Changes observed in PaO2 and PaCO2 during HE were similar to those in four normal subjects during 90 s of voluntary hypoventilation, when PaO2 fell by 12.3 +/- 5.6 Torr (P less than 0.05), but mean PaCO2 rose by only 2.8 +/- 2.1 Torr (P greater than 0.4). We suggest that the transient hypoxemia which occurs during REM sleep in patients with chronic bronchitis and emphysema could be explained by hypoventilation during REM sleep but that the importance of changes in distribution of ventilation-perfusion ratios cannot be assessed by presently available techniques.