Effect of arterial carbon dioxide tension on regional myocardial tissue oxygen tension in the dog]

We investigated the effects of arterial carbon dioxide tension on the myocardial tissue oxygen tensions of subepicardium and subendocardium in the anesthetized dogs. The study was done in fourteen open-chest mongrel dogs, weighing 13 +/- 1 kg, anesthetized with sodium pentobarbital (30 mg.kg-1 iv), and mechanically ventilated with 100% oxygen to maintain normocapnia. End tidal CO2 fraction (FECO2) was monitored continuously by capnograph. Regional myocardial tissue PO2 was measured using a monopolar polarographic needle electrode. Two pairs of combined needle sensors were carefully inserted, one in the epicardial and the other in the endocardial layer of the beating heart. Electromagnetic blood flow probe was applied on the left anterior descending artery (LAD). After a stable normocapnic ventilation, hypocapnia was induced by increasing the respiratory rate, and this mechanical hyperventilation was kept fixed throughout the experiments. To induce hypercapnia, exogenous carbon dioxide was added to the inspired gas step-wise until FECO2 reached 10%. Hypocapnic hyperventilation (PaCO2: 22 mmHg) invariably resulted in a significant reduction of coronary blood flow (LADBF) and left ventricular myocardial tissue PO2 in both epicardial and endocardial layers, while addition of carbon dioxide to the inspired gas (hypercapnic hyperventilation) reversed the change by increased LADBF and arterial PaCO2 in a dose-dependent manner. These results indicate that injudicious and severe hypocapnic hyperventilation may induce impaired myocardial tissue perfusion and oxygenation although normal cardiac output and arterial blood oxygenation are maintained.     

Evaluation of noninvasive monitoring of preoxygenation

Administration of 100% oxygen before a "rapid-sequence" induction of anesthesia is recommended to prevent hypoxemia during induction. In the present study, we used a laser scattering analyzer to study the effectiveness of nitrogen washout from the lungs with oxygen wash into the lungs under two different preoxygenation regimens; 4 times of maximal breathing of 100% oxygen in one minute and normal tidal breathing of 100% oxygen for 3 minutes. The volunteers were healthy, ASA physical status 1, 22 to 33 years of age (26 +/- 3), 167 +/- 5 cm tall, and weighing 60 +/- 5 kg. Arterial blood saturation measured by a pulse oximeter was 97 while breathing 21% oxygen, and 99% while breathing 100% oxygen. Arterial oxygen tensions were 98 mmHg while breathing 21% oxygen, and over 480 mmHg while breathing 100% oxygen. Arterial carbon dioxide and end tidal carbon dioxide concentrations indicated that 4 time of maximal breathing in a minute leads to hyperventilation. The end-tidal oxygen concentration was not significantly different between before and after oxygen administration in two different regimens. End-tidal nitrogen concentration after tidal volume ventilation was lower than that of 4 breath in a minute. These results indicate that end-tidal nitrogen and oxygen could reflect arterial nitrogen and oxygen tensions during preoxygenation.     

Effects of Hyperventilation and Hypocapnic/Normocapnic Hypoxemia on Renal Function and Lithium Clearance in Humans

Background: Using the renal clearance of lithium as an index of proximal tubular outflow, this study tested the hypothesis that acute hypocapnic hypoxemia decreases proximal tubular reabsorption to the same extent as hypocapnic normoxemia (hyperventilation) and that this response is blunted during normocapnic hypoxemia.

Methods: Eight persons were studied on five occasions: (1) during inhalation of 10% oxygen (hypocapnic hypoxemia), (2) during hyperventilation of room air leading to carbon dioxide values similar to those with hypocapnic hypoxemia, (3) during inhalation of 10% oxygen with the addition of carbon dioxide to produce normocapnia, (4) during normal breathing of room air through the same tight-fitting face mask as used on the other study days, and (5) during breathing of room air without the face mask.

Results: Hypocapnic and normocapnic hypoxemia and hyperventilation increased cardiac output, respiratory minute volume, and effective renal plasma flow. Glomerular filtration rate remained unchanged on all study days. Calculated proximal tubular reabsorption decreased during hypocapnic hypoxemia and hyperventilation but remained unchanged with normocapnic hypoxemia. Sodium clearance increased slightly during hypocapnic and normocapnic hypoxemia, hyperventilation, and normocapnic normoxemia with but not without the face mask.     

Effects of carbon dioxide (hypocapnia and hypercapnia) on tissue blood flow and oxygenation of liver, kidney and skeletal muscle in the dog

We investigated the effects of carbon dioxide on the splanchnic visceral organs (liver and kidney) as well as skeletal muscle in the anesthetized dog. Thirty two adult mongrel dogs were anesthetized with sodium pentobarbital, intubated and ventilated mechanically with 100% oxygen to maintain normocapnia. After laparotomy, miniature Clark-type polarographic oxygen electrodes were placed on the surfaces of liver, kidney and rectus femoris muscle. Electromagnetic blood flow (BF) probes were also applied to hepatic artery (HA), portal vein (PV), left renal artery (RA) and left femoral artery (FA). After a stable normocapnic ventilation, the hypocapnia was produced by increasing respiratory rate, and the hypercapnia was induced by adding the exogenous carbon dioxide. Results: Hyperventilation resulted in a significant decrease in HABF, PVBF, liver surface PO2 and kidney surface PO2 in parallel with the decreased PaCO2, but these parameters increased dose dependently when the carbon dioxide was added to the inspired gas (hypercapnic hyperventilation). On the contrary, FABF and skeletal muscle surface PO2 increased by hypocapnia and decreased during hypercapnia. Neither PaCO2 or cardiac output showed any significant change during the entire experiment. Arterial PCO2 appears to exert significant effects on both splanchnic and skeletal muscle perfusion as well as corresponding changes in tissue oxygenations. It is possible that injudicious and prolonged hypocapnic hyperventilation may seriously compromise splanchnic organ perfusion and oxygenation.     

Comparison of the effects of inhaled ipratropium bromide and salbutamol on the bronchoconstrictor response to hypocapnic hyperventilation in normal subjects.

A double blind, placebo controlled comparison was made of the effects of nebulised ipratropium bromide (0.05 and 0.5 mg) and salbutamol (0.25 and 2.5 mg) on lung function and the airway response to hyperventilation in eight normal subjects. Both agents at both doses caused similar baseline bronchodilatation, confirming the presence of resting bronchomotor tone. The overall mean increases as percentages of control were 33% in specific airway conductance (sGaw), 10% in maximal flow after expiration of 50% of vital capacity, and 3.7% in FEV1. Hypocapnia (mean end tidal carbon dioxide tension 2.2 kPa) was produced by three minutes of voluntary hyperventilation and resulted in a mean fall in sGaw of 0.49 s-1 kPa-1 (20%). After inhalation of 0.25 mg salbutamol hypocapnic hyperventilation still produced a mean fall in sGaw of 0.55 s-1 kPa-1, whereas salbutamol 2.5 mg reduced this response to 0.15 s-1 kPa-1 (6%). After both doses of ipratropium the decrease in sGaw caused by hyperventilation was similar to the control. This suggests that bronchoconstriction in response to hypocapnic hyperventilation in normal subjects is not mediated via a cholinergic reflex.     

The effects of different mouth-to-mouth ventilation tidal volumes on gas exchange during simulated rescue breathing.

The American Heart Association recommends tidal volumes of 700 to 1000 mL during mouth-to-mouth ventilation, but smaller tidal volumes of 500 mL may be of advantage to decrease the likelihood of stomach inflation. Because mouth-to-mouth ventilation gas contains only 17% oxygen, but 4% carbon dioxide, it is unknown whether 500-mL tidal volumes given during rescue breathing may result in insufficient oxygenation and inadequate carbon dioxide elimination. In a university hospital research laboratory, 20 fully conscious volunteer health care professionals were randomly assigned to breathe tidal volumes of 500 or 1000 mL of mouth-to-mouth ventilation gas (17% oxygen, 4% carbon dioxide, 79% nitrogen), or room air control (21% oxygen, 79% nitrogen) for 5 min. Arterial blood gases were taken immediately before, and after breathing 5 min of the experimental gas composition. When comparing 500 versus 1000 mL of mouth-to-mouth ventilation tidal volumes with 500 mL of room air, 500 mL of mouth-to-mouth ventilation tidal volume resulted in significantly (P < 0.05) lower mean +/- SEM arterial oxygen partial pressure (70 +/- 1 versus 85 +/- 2 versus 92 +/- 3 mm Hg, respectively), and lower oxygen saturation (94 +/- 0.4 versus 97 +/- 0.2 versus 98 +/- 0.2%), but increased arterial carbon dioxide partial pressure (46 +/- 1 versus 40 +/- 1 versus 39 +/- 1 mm Hg, respectively). Sixteen of 20 volunteers had to be excluded from the experiment with 500 mL of mouth-to-mouth ventilation gas after about 3 min instead of after 5 minutes as planned because of severe nervousness, sweating, and air hunger. We conclude that during simulated mouth-to-mouth ventilation, only large (approximately 1000 mL), but not small (approximately 500 mL) tidal volumes were able to maintain both sufficient oxygenation and adequate carbon dioxide elimination. IMPLICATIONS: To provide efficient mouth-to-mouth ventilation, it is important to administer tidal volumes of 1000 mL; tidal volumes of 500 mL were not adequate.     

Lung function, breathing pattern, and gas exchange in interstitial lung disease.

BACKGROUND: The aim of this study was to determine the relation between the severity of abnormalities in ventilatory function tests and tidal breathing pattern and gas exchange indices in interstitial lung disease. METHODS: Pulmonary function, ventilation, carbon dioxide production, oxygen consumption, arterial blood gas tensions, and pH were measured during resting steady state conditions in 60 patients with proved interstitial lung disease. Patients were categorised by forced vital capacity (FVC) (percentage of predicted values) as having a mild, moderate, or severe restrictive defect with means (SD) of 71% (4%), 57% (4%), and 41% (7%) of predicted values, respectively. RESULTS: FVC varied from 29% to 79% of predicted values and from 0.99 l to 4.32 l. The two measurements of FVC correlated strongly with most static lung volumes and with transfer factor for carbon monoxide. Mean respiratory rates (per minute) and tidal volumes (ml) were 17 (4) and 484 (131), 20 (4) and 460 (139), and 23 (5) and 377 (109) in mild, moderate, and severe restrictive defects, respectively. FVC correlated negatively with respiratory rate and positively with tidal volume. Arterial carbon dioxide tension ranged from 30 to 49 mm Hg; only two patients were hypercapnic. Mean arterial oxygen tensions were not significantly different among the three groups, and there were no significant correlations between forced expiratory volume in one second or FVC and arterial carbon dioxide tension or carbon dioxide production. CONCLUSION: Low values of FVC were associated with increased respiratory rate and decreased tidal volume; this pattern of breathing mimics external elastic loading, suggesting that mechanoreceptors may contribute to the rapid and shallow pattern of breathing in interstitial lung disease. Hypercapnia seems to be rare in interstitial lung disease even when functional impairment is severe and tidal volume is small. The increased respiratory rate is important in maintaining adequate ventilation. In the face of a severe restrictive defect carbon dioxide production did not increase, which also contributed to the maintenance of eucapnia.     

Accumulation of carbon dioxide under ophthalmic drapes during eye surgery: a comparison of three different drapes

Carbon dioxide accumulation under ophthalmic drapes is caused by their impaired permeability to exhaled carbon dioxide in spontaneously breathing patients. Three different ophthalmic drapes were examined under clinical conditions. Sixty unpremedicated patients of each gender, aged over 60 years and with an ASA status of I-III undergoing cataract surgery under retrobulbar anaesthesia were included in the study. Patients with known pulmonary diseases were excluded. The patients were divided into three groups of 20 patients each. In all groups, oxygen was insufflated under the drapes at a constant flow of 21.min-1. Carbon dioxide concentration in the inspired air, transcutaneous carbon dioxide pressures, respiratory rate and oxygen saturation by pulse oximetry were measured. Accumulation of carbon dioxide under the drapes, increase of partial pressure of transcutaneous carbon dioxide and hyperventilation were observed in all three groups. An oxygen supply of 21.min-1 prevented hypoxaemia but not hypercapnia. Therefore, producers of ophthalmic drapes are encouraged to look for further ways to increase the carbon dioxide permeability of their drapes with the aim of reducing carbon dioxide accumulation and hyperventilation in spontaneously breathing patients undergoing eye surgery.     

THE EFFECT OF NEUROLEPTANALGESIA WITH INNOVAR ON THE METABOLIC RATE OF MAN

The metabolic rate of eight healthy adults did not change significantlyafter the introduction of neuroleptanalgesia with Innovar. Averageoxygen consumption decreased from the control value of 133 ml/min/sq.m±22(standard deviation) which is 98.6 per cent of predicted basalmetabolic rate, to 127±37 8 minutes after the injectionof Innovar (93.2 per cent), and was 141±17 25 to 30 minutesafter injection (105.5 per cent). Ventilation was controlled,keeping end-tidal carbon dioxide constant. Carbon dioxide excretionand the respiratory quotient did not change. Anatomical deadspaceand the ratio of deadspace to tidal volume both rose after induction.This study offers no support for the theory that Innovar "protects"by reducing metabolic demand for oxygen in man.     

Respiratory depression in children at different end tidal halothane concentrations

Respiratory motor function and timing were investigated at end tidal halothane concentrations of 1.5%, 1.0% and 0.5% before and during 4% carbon dioxide stimulation in 10 spontaneously breathing children who weighed between 10.2 and 25.2 kg, during hypospadias repair under halothane anaesthesia. Their tracheas were intubated and all received a caudal block to eliminate surgical stimulation. Pneumotachography and capnography were used and in three cases movements of ribcage and abdomen were also studied by magnetometers. Respiratory drive was evaluated by occlusion tests. Ventilation was depressed at an end tidal halothane concentration of 1.5%, with smaller tidal volumes, higher respiratory rates, higher end tidal carbon dioxide tensions and a weaker respiratory drive compared with 1.0% and 0.5% halothane. Paradoxical breathing was noted at 1.5% as well as at 1.0% but not at 0.5% halothane anaesthesia; the ribcage moved inwards during inspiration. Respiratory compensation during periods of 4% carbon dioxide stimulation was inadequate at 1.5% halothane, as indicated by higher end tidal carbon dioxide tensions, less negative occlusion pressures and movements of ribcage and abdomen that were unresponsive to 4% carbon dioxide, when compared with 1.0% and 0.5% halothane. Respiratory rates were higher and duration of inspiration longer at 1.5% than at 1.0% and 0.5% halothane. Respiratory timing was unaltered by carbon dioxide stimulation. It is concluded that the ventilatory motor response to carbon dioxide is dose dependent and improves at more superficial anaesthetic levels, while respiratory timing is unresponsive to carbon dioxide stimulation irrespective of the halothane concentration used. Paradoxical breathing existed at end tidal halothane concentrations higher than 1%.     

Hypoxic Pulmonary Vasoconstriction in Man: Effects of Hyperventilation

The pulmonary vasoconstriction response to hypoxia was studied in eight anaesthetized supine subjects. One lung was made hypoxic while the other was ventilated with 100% oxygen. This was achieved by separating the tidal gas-distribution to the lungs by means of a double-lumen tracheal catheter. The hypoxic pulmonary vasoconstriction (HPV) response was estimated from the blood flow diversion away from the hypoxic lung. Blood flow distribution between the lungs was calculated from the regional expired carbon dioxide production, assuming regional carbon dioxide production to be proportional to blood flow. The subjects were studied during six different conditions. Firstly, when ventilated with 100% oxygen to both lungs at a PaCO2 of about 6 kPa. Secondly, with 100% oxygen to the left lung and 5% oxygen in nitrogen to the right (test) lung. The ratio between carbon dioxide output from right and left lung was calculated. These measurements were repeated during two states of hyperventilation (PaCO2 of about 4.5 kPa and 3.5 kPa, respectively) with and without hypoxia (conditions 3-6). During normoventilation, blood flow distribution between the lungs was equal. During hypoxia, blood flow distribution to the hypoxic lung decreased by 35% of the pre-hypoxic value. Furthermore, a decrease in arterial oxygen tension from 51.5 +/- 4.5 to 11.5 +/- 2.1 kPa was observed. During excessive hyperventilation (PaCO2 3.2 +/- 0.2 kPa), blood flow distribution to the hypoxic right lung decreased by only 10% of its pre-hypoxic value. A further decrease in arterial oxygen tension to 8.5 +/- 1.8 kPa was observed. This decrease in PaO2 was possibly due to an increased venous admixture caused by an abolished HPV response. It is concluded that hyperventilation counteracts hypoxic pulmonary vasoconstriction in man.     

Arterial-to-end-tidal carbon dioxide tension difference in children with congenital heart disease

OBJECTIVES: This study estimated the arterial-to-end-tidal carbon dioxide tension difference (deltaPaCO2-PE'CO2) in children with congenital heart disease; evaluated whether hyperventilation can reduce this difference; and analyzed the relationship between the difference and the oxygen saturation (SaO2) and hemoglobin level. DESIGN: Prospective clinical study. SETTING: Tertiary health care center. PARTICIPANTS: One hundred patients scheduled for correction of their underlying cardiac defect with either right-to-left or left-to-right intracardiac shunts were divided into 4 groups (n = 25 each): (1) N1, cyanotic with severe pulmonary artery hypertension; (2) N2, cyanotic with normal or decreased pulmonary artery pressure (PAP); (3) N3, acyanotic with normal or mild increases in PAP and severe increases in pulmonary blood flow (PBF); and (4) N4, acyanotic with normal PAP and normal or mild increase in PBF. INTERVENTIONS: All the patients received the same anesthetic regimen. The initial settings for tidal volume, respiratory rate, and inspiratory-to-expiratory (I:E) ratio were 10 mL/kg, 15 to 30 breath/min, and inspired time 40% of the total respiratory period with a 10% end-inspiratory pause. After the measurement of oxygen saturation, PO2, Hb, and deltaPaCO2-PE'CO2, all the children were hyperventilated (tidal volume: 14-15 mL/kg, respiratory rate: 5-6 breaths/min more than the initial rate, I:E ratio: same) to observe its effects on the deltaPaCO2-PE'CO2. MEASUREMENTS AND RESULTS: The deltaPaCO2-PE'CO2, when predicted from the oxygen saturation, hemoglobin concentration, and PaO2, was found to be greater than the observed value in the first 3 groups (p < 0.001); whereas in group N4 these 2 values were comparable. It was also found that the gradient was higher when there was a decrease in SaO2 and an increase in the hemoglobin level. After hyperventilation, in groups N1 and N3, deltaPaCO2-PE'CO2 was decreased when compared with their baseline values; this reduction was not as much as predicted (p = 0.363 and 0.236, respectively). However, in groups N2 and N4 posthyperventilation, the deltaPaCO2-PE'27 CO2 was decreased significantly below their baseline measurements. These decreases were as much predicted. CONCLUSION: The deltaPaCO2-end-tidal carbon dioxide (PE'CO2) can be increased both in cyanotic and acyanotic children. Increased PAP is as important as increased PBF or right-to-left shunting in producing disorders in carbon dioxide homeostasis. Hyperventilation is of little use in reducing deltaPaCO2-PE'CO2 in children with high PAPs and pulmonary hyperperfusion.     

Intraperitoneal oxygen and carbon dioxide tensions in experimental adhesion disease and peritonitis.

Intraperitoneal oxygen and carbon dioxide tensions were studied in rats during silica-induced adhesion formation or fecal peritonitis. Measurements of PO2 and PCO2 in the abdominal cavity were performed by means of an implanted Silastic tonometer. During active adhesion formation one to three weeks after administration of silica, the intra-abdominal PO2 decreased by 50 per cent from normal whereas the intra-abdominal PCO2 and the rate of oxygen consumption in the peritoneum were elevated. Progressing peritonitis also resulted in decreased intraperitoneal PO2 and increased accumulation of carbon dioxide in the peritoneal cavity. In rats with peritonitis the rate of oxygen consumption in the peritoneal exudate clearly exceeded that in the peritoneal membrane.     

EFFECT OF HIGH THORACIC EXTRADURAL ANAESTHESIA ON VENTILATORY RESPONSE TO HYPERCAPNIA IN NORMAL VOLUNTEERS

We have investigated, in six healthy male volunteers, the effectof high thoracic extradural anaesthesia on the ventilatory patternand hypercapnic ventilatory response. Ventilatory variableswere determined using a respiratory inductive plethysmograph.Duration of inspiration, rib cage excursion and its contributionto tidal volume decreased significantly following extraduralanaesthesia, while mean inspiratory flow rate and minute ventilationincreased. End-tidal PCO₂ and the tidal excursion of the abdomenwere unchanged. Hypercapnic ventilatory response decreased significantlyfollowing extradural anaesthesia, principally because of therib cage component. The slope of the abdominal component didnot change significantly. The results indicate that mechanicalimpairment of rib cage movement can produce decreased ventilatoryresponse to carbon dioxide. The ventilatory impairment and thechanges in breathing pattern induced by the high thoracic extraduralanaesthesia probably reflect blockade of the efferent or afferentpathway (or both) of the intercostal nerve roots.     

Fresh gas flow in the Bain circuit during laparoscopy

Twenty-two women were studied during laparoscopy with abdominal insufflation of carbon dioxide. A bain anaesthetic breathing circuit was used with a fresh gas flow (VFG) of 110 ml.min-1.kg-1, and controlled ventilation was applied with a minute ventilation (VE) of 175 ml.min-1.kg-1. Arterial blood gases were analysed at the end of the operation. Nineteen of the women (86 per cent) were found to have a PaCO2 within the range for normocapnia (i.e., 4.7-5.9 kPa (35-45 mmHg), two were hypocapnic with a PaCO2 of 4.4 and 4.5 kPa (33 and 34 mmHg) respectively and one was found to have a PaCO2 of 6.2 kPa (46.5 mmHg). It was concluded that the carbon dioxide absorbed from the abdomen during laparoscopy demands fresh gas flows that are higher than normally used in the Bain circuit if a PaCO2 within the normal range is to be obtained. A simultaneous increase in VFG and VE of about 45 per cent is sufficient to achieve normocapnia.     

The effect of halothani-nitrous oxide anaesthesia and spontaneous ventilation on arterial blood oxygenation and physiological deadspace.

Arterial blood, inspired and expired gas samples were taken from seven patients anaesthetized with halothane (1-2 per cent) and nitrous oxide in oxygen and who breathed spontaneously. Over a two hour period, the average arterial oxygen tension was 75 mm Hg and carbon dioxide tension 49 mm Hg. No significant deterioration of either blood gas value occurred during the two hours. The dead-space/tidal volume ratio and alveolar-arterial oxygen tension difference did not alter significantly during the period of the study.     

Regional cerebral blood flow responses to hyperventilation during sevoflurane anaesthesia studied with PET

Background: Arterial carbon dioxide tension (PaCO₂) is an important factor controlling cerebral blood flow (CBF) in neurosurgical patients. It is still unclear whether the hypocapnia‐induced decrease in CBF is a general effect on the brain or rather linked to specific brain regions. We evaluated the effects of hyperventilation on regional cerebral blood flow (rCBF) in healthy volunteers during sevoflurane anaesthesia measured with positron emission tomography (PET). Methods: Eight human volunteers were anaesthetized with sevoflurane 1 MAC, while exposed to hyperventilation. During 1 MAC sevoflurane at normocapnia and 1 MAC sevoflurane at hypocapnia, one H₂¹⁵O scan was performed. Statistical parametric maps and conventional regions of interest analysis were used for estimating rCBF differences. Results: Cardiovascular parameters were maintained constant over time. During hyperventilation, the mean PaCO₂ was decreased from 5.5 ± 0.7 to 3.8 ± 0.9 kPa. Total CBF decreased during the hypocapnic state by 44%. PET revealed wide variations in CBF between regions. The greatest values of vascular responses during hypocapnia were observed in the thalamus, medial occipitotemporal gyrus, cerebellum, precuneus, putamen and insula regions. The lowest values were observed in the superior parietal lobe, middle and inferior frontal gyrus, middle and inferior temporal gyrus and precentral gyrus. No increases in rCBF were observed. Conclusions: This study reports highly localized and specific changes in rCBF during hyperventilation in sevoflurane anaesthesia, with the most pronounced decreases in the sub cortical grey matter. Such regional heterogeneity of the cerebral vascular response should be considered in the assessment of cerebral perfusion reserve during hypocapnia.     

PULMONARY GAS EXCHANGE DURING DELIBERATE HYPOTENSION

Respiratory physiological deadspace may increase from 35 percent of the tidal volume in the normal anaesthetized, normotensiveand supine patient to as much as 80 per cent in the hypotensivepatient in the head-up tilt. Increased mean airway pressure,hypotension, sudden head-up tilt or maintenance of tilt, alltend to increase the respiratory deadspace. Arterial and end-tidalPco² differences parallel the deadspace changes. The averagePco² difference in the supine normotensive patient was 9 mmHg, but during maintained head-up body tilt during hypotension,this difference increased to as much as 25 mm Hg. These dataemphasize the need for careful control of respiration, withhigher than normal tidal volumes and oxygen concentrations duringdeliberate hypotension. They are equally applicable to otherhypotensive states including shock     

Effects of 1 MAC desflurane on cerebral metabolism, blood flow and carbon dioxide reactivity in humans

We investigated the cerebral haemodynamic effects of 1 MAC desflurane anaesthesia in nine male patients scheduled for elective coronary bypass grafting. For the measurement of cerebral blood flow (CBF) a modified Kety-Schmidt saturation technique with argon as inert tracer gas was used. Measurements of CBF were made before induction of anaesthesia and 30 min after induction under normocapnic, hypocapnic and hypercapnic conditions in sequence. Changes in mean arterial pressure after induction of anaesthesia and during the course of the study were minimized using norepinephrine infusion. In comparison with the awake state under normocapnic conditions, desflurane reduced mean cerebral metabolic rate of oxygen (CMRO2) by 51% and mean cerebral metabolic rate of glucose (CMRglc) by 35%. Concomitantly, CBF was significantly reduced by 22%; jugular venous oxygen saturation (SjvO2) increased from 58 to 74%. Hypo- and hypercapnia caused a 22% decrease and a 178% increase in CBF, respectively. These findings may be interpreted as the result of two opposing mechanisms: cerebral vasoconstriction induced by a reduction of cerebral metabolism and a direct vasodilator effect of desflurane. CBF alterations under variation of PaCO2 indicate that cerebrovascular carbon dioxide reactivity is not impaired by application of 1 MAC desflurane.      

The effect of respiratory alkalosis on oxygen consumption in anesthetized patients

Study Objective: To investigate whether hyperventilation significantly altered oxygen consumption in anesthetized and paralyzed patients undergoing surgery.

Design: Open crossover trial with 1 hour of hyperventilation preceded and followed by 1 hour of normoventilation.

Setting: University medical center.

Patients: Eight patients (five men and three women) undergoing lengthy orthopedic surgery with general anesthesia and muscle paralysis.

Interventions: After baseline normoventilationfor 1 hour (Period 1), the anesthetized patients were hyperventilated to an arterial carbon dioxide tension (PaCO₂) of 20 to 25 mmHg for 1 hour (Period 2). Patients then experienced another hour of normoventilation (Period 5).

Measurements and Main Results: Hemodynamic variables, electrocardiography, temperature, end-tidal partial pressure of CO₂ (P_ETCO₂), oxygen consumption (VO₂), carbon dioxide production, and minute ventilation were continuously followed throughout the study, and arterial blood gases were drawn at the beginning and end of each study period. During the period of hyperventilation, pH was significantly higher and P._ETCO₂ and (PaCO₂) significantly lower compared with the periods of normoventilation. (VO₂), was significantly increased during hyperventilation compared with the periods of normoventilation. Hemodynamic variables and temperature were similar in the three study periods.

Conclusions: In anesthetized paralyzed patients, there is an increase in whole-body (VO₂), with hypocapnic alkalosis.