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Carbon dioxide production, metabolism, and anesthesia

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Abstract

The human body is fueled by nutrients and oxygen (O2) that are metabolized to energy, carbon dioxide (CO2), and waste products (see Figure 25.1). The amounts of O2 consumed and CO2 produced reflect the rate of body metabolism and the types of nutrients metabolized. The tasks of the respiratory and cardiovascular systems are to ensure that the cells of the body receive sufficient O2 and adequate amounts of CO2 are removed. The result of these interactions is tight coupling between the respiratory, cardiovascular, and metabolic systems. Therefore, when interpreting measurements of CO2 production and O2 consumption, it is important to consider the interaction of these systems. The overall amount of O2 consumed and CO2 produced by the human body depends on the rate of metabolism, while the proportion of O2 consumed to CO2 produced depends on the type of nutrients being metabolized or synthesized. Each cell type and organ system has a different metabolic function and, as a result, has different metabolic rates and nutrient requirements. Therefore, measurements of whole-body O2 consumption and CO2 production reflect the sum of the quantity and types of O2-consuming and CO2-producing activities of the various cell and organ systems of the body. The cells of the body metabolize carbohydrates, lipids, and proteins to produce energy in the form of high-energy phosphates (adenosine triphosphate, ATP).

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Article
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Article
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The mechanisms responsible for the marked increase in ventilation at the onset of exercise are incompletely defined. A conditioned response to exercise anticipation has been suggested as an influencing factor, but systematic measurements have not been made during the transition from rest to the time when exercise is anticipated but has not yet commenced. We tested the hypothesis that cortical activity associated with the anticipation of exercise causes hyperpnea, which is at least partly responsible for the increased ventilation at the onset of exercise. To assess the influence of continuous cortical activity in the absence of exercise anticipation the subjects performed mental arithmetic tasks. Fifteen subjects performed the two experiments in a random order. Ventilation was measured noninvasively using a calibrated respiratory inductive plethysmograph and end-tidal CO2 concentration (FETCO2) was monitored at the nasal vestibule. Both exercise anticipation and mental arithmetic caused an increase in minute ventilation (VI) (P less than 0.01) and mean inspiratory flow (VT/TI, P less than 0.01), which reflects respiratory center drive, although the derivation differed in that the former was volume based, whereas the latter was due to alteration in timing. Despite the increase in VI, FETCO2 remained constant in both instances. In a complementary study the constant FETCO2 in the face of increased VI was shown to be due to increased CO2 output. The results show that the mere anticipation of exercise causes an increase in ventilation. The mechanism responsible for this hyperpnea cannot be due solely to respiratory center activation because of the constancy of FETCO2 and the associated alterations in cardiac and metabolic behavior.
Article
Eighteen patients undergoing alloplastic surgery of the hip were divided into three groups, each consisting of six patients. All operations were performed under endotracheal intubation using halothane N2O-O2 anaesthesia. After a steady state as to CO2-production had been obtained, suxamethonium 1 mg kg-1 was given intravenously to the patients in Group I. A maximum rise in CO2-production of 14.8% (range: 12.9-16.8) was observed after 5 min. In Group II, patients were pretreated with pancuronium 0.01 mg kg-1: no increase in CO2-production was observed. The third group received a continuous infusion of suxamethonium. In this group there was an increase in CO2-production of 17.6% (range: 6.7-22.0) 5 min after start of infusion. The CO2-production then fell to the preinfusion level over the next 10 min.
Article
Recent investigation suggests that both ventilation (VE) and the chemical sensitivity of the respiratory control system correlate closely with measures of metabolic rate [O2 consumption (VO2) and CO2 production (VCO2)]. However, these associations have not been carefully investigated during sleep, and what little information is available suggests a deterioration of the relationships. As a result we measured VE, ventilatory pattern, VO2, and VCO2 during sleep in 21 normal subjects (11 males and 10 females) between the ages of 21 and 77 yr. When compared with values for awake subjects, expired ventilation decreased 8.2 +/- 2.3% (SE) during sleep and was associated with a 8.5 +/- 1.6% decrement in VO2 and a 12.3 +/- 1.7% reduction in VCO2, all P less than 0.01. The decrease in ventilation was a product primarily of a significant decrease in tidal volume with little change in frequency. None of these findings were dependent on sleep stage with results in rapid-eye-movement (REM) and non-rapid-eye-movement sleep being similar. Through all sleep stages ventilation remained tightly correlated with VO2 and VCO2 both within a given individual and between subjects. Although respiratory rhythmicity was somewhat variable during REM sleep, minute ventilation continued to correlate with VO2 and VCO2. None of the parameters described above were influenced by age or gender, with male and female subjects demonstrating similar findings. Ten of the subjects demonstrated at least occasional apneas. These individuals, however, were not found to differ from those without apnea in any other measure of ventilation or metabolic rate.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
This study characterizes the pattern of caloric expenditure of a group of 19 mechanically ventilated critically ill patients after surgery. Continuous measurements of metabolic rate were used to examine the total energy expended over an eight-hour period (10 AM to 6 PM) on 21 occassions. This allowed for determination of the energy expended during activity, rest, and sleep. The patients were observed to be resting, defined as lying motionless with eyes open and responsive to surrounding events, for 44 +/- 4 percent (SE) of the studied period. Sleeping, a state where the patient was not aroused by surrounding events, was observed for 17 +/- 3 percent of the studied period. Total energy expenditure was 4.8 +/- 1.8 percent greater than resting energy expenditure (REE). The REE was 13.1 +/- 2.3 percent above sleeping energy expenditure (awakeness factor), while activity energy expenditure was 17.1 +/- 2.9 percent above REE (activity factor). The respiratory quotient (RQ) during activity in the 15 patients receiving infusions of physiologic saline solution or 5 percent dextrose solution was significantly less (p less than 0.02) than the RQ during rest. This appears to be due to increased fat oxidation during activity.
Article
Rewarming in the postoperative period after hypothermic cardiopulmonary bypass is often associated with hemodynamic and ventilatory instability. Temperature changes, PaCO2 values, and delivered mechanical ventilation were observed for the first 12 hr in the intensive care unit in 73 patients who had undergone cardiac surgery with hypothermic cardiopulmonary bypass. Mean rectal temperature increased from 34.7 to 38.3 degrees C over the first 8 hr after admission to the intensive care unit (P less than 0.001). The temperature curve was sigmoid rather than linear, and the most rapid rate of temperature increase occurred 2-4 hr after admission. During rewarming, the most common abnormality of PaCO2 on mechanical ventilation was acute respiratory acidosis (PaCO2 greater than 45 mm Hg, pH less than 7.35), which occurred in 42% of patients. This suggests that ventilatory management in the early postoperative period after hypothermic cardiopulmonary bypass should be carefully adjusted to the increased metabolic rate during rapid rewarming.
Article
Intraoperative hypothermia has become a common occurrence. Postoperative rewarming often is accompanied by shivering and results in increased metabolic and circulatory demands. We examined the metabolic, hemodynamic, and biochemical variables in 2 groups of hypothermic (greater than 35.8 degrees C) patients requiring mechanical ventilation after a major operation. One was observed during routine medical management whereas the other group received 40 mg of metocurine iodide and then observed during routine medical management. All patients were allowed to rewarm passively. O2 consumption (VO2, ml/min, STPD), CO2 production (VCO2, ml/min, STPD) and respiratory quotient (RQ) measurements were made every 15 min using a Beckman Metabolic Measurement Cart. Esophageal temperature, arterial blood pressure, heart rate (HR), rate pressure product, CVP, arterial blood gases, serum lactate concentration, and duration of shivering also were recorded. Suppression of the shivering by metocurine increased rewarming time significantly and decreased VCO2, VO2, HR, rate pressure product, mean arterial pressure (MAP), and the O2 cost of rewarming. Thus, the elimination of shivering during postoperative rewarming is associated with a decrease in caloric, metabolic demands and myocardial work (as assessed by the rate pressure product) while rewarming time is prolonged. In the postoperative, hypothermic, critically ill patient, suppression of the shivering response in selected patients may be indicated.
Article
The alterations in metabolic (oxygen consumption [VO2] and carbon dioxide production [VCO2]) and hemodynamic (heart rate and blood pressure) parameters caused by various common intensive care activities were examined in a group of 23 mechanically-ventilated critically-ill patients. The observed variations in metabolic rate can be classified into four categories as follows: (a) the lowest energy expenditure, which was associated with sleeping in the majority (83 percent) of instances; (b) resting, which was defined as a state where the patient was lying motionless with eyes open and responding to surrounding events, where VO2 and VCO2 averaged 9.1 +/- 7.5(SD) percent and 7.5 +/- 7.3 percent, respectively, above the lowest values; (c) a variety of routine daily care activities (eg, bathing, performing a physical examination) that although not particularly painful, caused arousal from the resting state. During these situations, VO2 and VCO2 averaged about 20 percent above lowest values; and (d) chest physical therapy, which was associated with metabolic increases of 35 percent above lowest values as well as increases in both heart rate and blood pressure. This study demonstrates that routine daily ICU activities can significantly alter metabolic rate, and thus, it is important to couple such measurements with astute observations of the patients' activity state. In addition, we have defined an activity state--resting--that can be used in the calculation of energy expenditure as well as for intrapatient and interpatient comparisons.
Article
We address the question of whether an oxygen debt develops during a period of abdominal aortic cross-clamping that may explain observed hemodynamic changes. Group 1 received morphine sulfate (1 mg/kg) during induction of anesthesia. Group 2 received same dose of morphine sulfate. Group 3 received 4 mg/kg of morphine sulfate. We measured the oxygen consumption (VO2) and the carbon dioxide production levels (VCO2), as well as hemodynamic and biochemical parameters. In groups 1 and 3, VO2 and VCO2 decreased 10% to 13% following abdominal aortic cross-clamping compared with values measured before cross-clamping. In group 2, VO2 and VCO2 decreased 3% and 7%, respectively. On unclamping, the greatest increase in VO2 was observed in group 3 (26%), while in groups 1 and 2, VO2 rose 18% and 5%, respectively. In all three groups, metabolic changes were not paralleled by hemodynamic or temperature changes. Results indicate that oxygen debt developed during abdominal aortic cross-clamping, but this has no effect on hemodynamic changes seen after unclamping. Higher dosage of narcotic administered during anesthetic induction did not temper increase in metabolic rate observed after unclamping.
Article
Critically ill patients are subjected to routine clinical activities that increase oxygen demand. This results in increased heart rate, blood pressure, minute ventilation, and oxygen delivery in patients with often already compromised cardiopulmonary systems. This study examines whether the benzodiazepine, midazolam, could attenuate the increase in metabolism, respiration, and circulation seen during chest physical therapy. Two groups of mechanically ventilated postoperative patients were studied. One group (n = 15) received, in random order, 0.015 mg/kg of midazolam and placebo prior to two consecutive chest physical therapy sessions, while the other (n = 13) received 0.030 mg/kg and placebo. Both doses of midazolam significantly attenuated the increases in oxygen consumption, heart rate, and systemic blood pressure observed during placebo administration. The cardiac output increase was also attenuated. Although midazolam reduced minute ventilation and respiratory rate, no excess CO2 retention occurred when the drug was administered likely as the result of reduced CO2 production. The administration of midazolam (0.015 mg/kg and 0.030 mg/kg) prior to chest physical therapy reduces metabolic, hemodynamic, and ventilatory responses to chest physical therapy.
Article
Twelve healthy, unpremedicated women scheduled for total abdominal hysterectomy were given either isoflurane (n = 6) or halothane (n = 6) anaesthesia. They all received general anaesthesia for a period of 3 h, with surgery being carried out only in the last hour. The anaesthesia consisted of thiopentone, pancuronium and a mixture of oxygen-enriched air (FiO2 = 34%) supplemented with 1 MAC of either isoflurane or halothane. The patients were maintained normothermic, and with an arterial SaO2 above 95% throughout the period of the study. The following measurements were made before, during and after anaesthesia (with and without surgery): oxygen consumption (VO2), carbon dioxide production (VCO2); circulating concentrations of various hormones (insulin, growth hormone and cortisol); various metabolites; selected amino acids and albumin; forearm arterio-venous concentration difference of glucose, lactate, free fatty-acids and selected amino acids (four patients in each group). Whole body VO2 decreased significantly by over 20% during anaesthesia (with or without surgery), P < 0.05). Although the circulating concentration of most amino acids showed little or no change during anaesthesia alone, there was a tendency for the flux of most metabolites to decrease, and this persisted during surgery (P < 0.05). During anaesthesia alone there was a twofold reduction in the plasma cortisol concentration (P < 0.05), and a decrease in albumin concentration (P < 0.01). With the onset of surgery, plasma cortisol concentration increased rapidly (in association with several other hormones and metabolites) but hypoalbuminemia persisted.
Article
We examined end-tidal CO2 tension (PETCO2) and pulmonary CO2 elimination of CO2 (VECO2) during CO2 insufflation under general anesthesia for three surgical procedures: gynecologic laparoscopy (intraperitoneal CO2 insufflation for 43 +/- 4 min), laparoscopic cholecystectomy (intraperitoneal CO2 insufflation for 125 +/- 14 min), and pelviscopy (extraperitoneal CO2 insufflation for 45 +/- 3 min). All patients (10 in each group) underwent controlled mechanical ventilation. Oxygen consumption (VO2) and VECO2 were measured at 2-min intervals by a system using a mass spectrometer. For the three surgical procedures, VO2 remained stable, whereas VECO2 and PETCO2 increased in parallel from the 8th to the 10th min after the start of CO2 insufflation. A plateau was reached 10 min later in patients having intraperitoneal insufflation, whereas VECO2 and PETCO2 continued to increase slowly throughout CO2 insufflation during pelviscopy. During pelviscopy, the maximum increase in VECO2 and PETCO2 (76 +/- 5% and 71 +/- 7%) was significantly more pronounced than that observed during cholecystectomy (25 +/- 4% and 25 +/- 4%) and gynecologic laparoscopy (15 +/- 3% and 12 +/- 2%). The authors conclude that CO2 diffusion into the body is more marked during extraperitoneal than during intraperitoneal CO2 insufflation but is not influenced markedly by the duration of intraperitoneal insufflation.
Article
Our objective was to determine the effect of perioperative epidural anaesthesia and analgesia on the increase in energy expenditure which accompanies major elective abdominal surgery in a prospective, randomized study. Eight patients undergoing elective resections of the colon and/or rectum received general anaesthesia alone (nitrous oxide, oxygen, and isoflurane, supplemented with intravenous fentanyl to a maximum of 10 micrograms.kg-1), and 12 patients received perioperative epidural anaesthesia and analgesia using lidocaine (carbonated lidocaine 2% with epinephrine 1:200,000, 20 ml over 30 min) and morphine (preservative-free morphine 0.10 mg.kg-1 after catheter insertion and 0.05 to 0.10 mg.kg-1 every 12 hr as needed until the morning following surgery) via a lower lumbar catheter in addition to general anaesthesia. Respiratory gas exchange was measured using a metabolic cart and canopy system early on the morning of surgery, six hours postoperatively, and on the first and second postoperative mornings. Parenteral analgesic administration (P < 0.001) and visual analogue pain scores (P < 0.05) were lower in the patients receiving epidural anaesthesia and time to first parenteral analgesia was longer (P < 0.005). Oxygen consumption, carbon dioxide production, and energy expenditure increased after surgery (all P < 0.001) but were very similar in the two groups (all P > or = 0.8) before and after surgery. Despite substantial effects on postoperative pain, we conclude that oxygen consumption and energy expenditure following major abdominal surgery are not diminished by perioperative epidural anaesthesia and analgesia.
Article
Colonic fermentation produces short-chain fatty acids (SCFA). In humans, the amount of energy produced from the oxidation of these compounds is unknown and could modify the metabolic utilization of energetic fuels (eg, carbohydrates and lipids). If it were so, the equations used to evaluate the oxidation of nutrients from indirect calorimetry data should include the contribution of SCFA, which is not usually the case. Indeed, this fermentation process is usually considered as a minor and neglected energetic pathway. In this study, we have addressed the reliability of this assumption. Six normal subjects received orally either 50 g glucose or 50 g glucose plus 20 g lactulose. Their respiratory gas exchanges, breath hydrogen, methane, and 13CO2 concentrations, and plasma glucose, insulin, and free fatty acid (FFA) concentrations were monitored for 8 hours. CO2 production and breath hydrogen concentration were significantly greater with lactulose. No differences in oxygen consumption, breath 13CO2 production, or plasma concentrations of blood glucose, FFA, and insulin could be found between the two experiments. This suggests that the fermentation process induced by lactulose generates extra fuels going through an oxidation pathway. Therefore, the classic equations used to calculate carbohydrate and lipid oxidation and energy expenditure (EE) from indirect calorimetry data are probably not valid when fermentation is taking place. Indeed, in this experiment we could have overestimated glucose oxidation (12.5%) if the fermentation process were not considered. In conclusion, colonic fermentation in humans of nondigestible carbohydrates produces energetic substrates that could be used and oxidized as energetic fuels.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
In pneumoperitoneum, carbon dioxide eliminated in expired gas (carbon dioxide output) contains both metabolic and absorbed carbon dioxide from the peritoneal cavity. When elimination of carbon dioxide is much higher than carbon dioxide output, storage of tissue carbon dioxide and arterial carbon dioxide concentrations change. Finally, the rate of carbon dioxide eliminated in expired gas is not a match for the real rate of metabolic production and absorbed carbon dioxide from the peritoneal cavity. During and after insufflation of carbon dioxide, changes in carbon dioxide output were elucidated under constant arterial carbon dioxide pressure (PaCO2), the same as the preinduction level. We studied patients undergoing elective laparoscopic cholecystectomy. Carbon dioxide output, oxygen uptake, respiratory exchange ratio (RER), expired minute ventilation (VE), deadspace to tidal volume ratio (VD/VT ratio) and arterial to end-tidal carbon dioxide partial pressure difference (PaCO2-PE'CO2) were determined before induction, and during anaesthesia, pneumoperitoneum and recovery. By controlling ventilatory frequency (f) every 1 min, PaCO2 was adjusted to concentrations before induction. Constant monitoring of end-tidal carbon dioxide partial pressure (PE'CO2) and intermittent measurement of (PaCO2-PE'CO2) (15-min intervals) were conducted to predict PaCO2). Carbon dioxide output and oxygen uptake decreased significantly from mean values of 83.5 (SEM 5.2), 101.6 (5.1) to 68.5 (4.2), 81.1 (4.6) ml min-1 m-2 (ATPS, P < 0.05) with sevoflurane anaesthesia, and RER did not change. During carbon dioxide pneumoperitoneum (intra-abdominal pressure 8 mm Hg), carbon dioxide output increased by 49% (102.4 (5.0) ml min-1 m-2) (P < 0.05) while oxygen uptake remained stable and RER increased from 0.84 (0.02) to 1.16 (0.03) (P < 0.05). It was necessary to increase VE during pneumoperitoneum by 1.54 times that during anaesthesia to maintain individual PaCO2 values constant. After removal of carbon dioxide from the abdominal cavity, the regression equation of excess carbon dioxide output/BSA best fitted a two-compartment model. The time constants of the rapid and slow compartments were 8.2 and 990 min, respectively. Excess carbon dioxide output/BSA was still 5.5 ml min-1 m-2, 30 min after pneumoperitoneum.
Article
Systemic metabolism results in a production of not only carbon dioxide, water and urea but also bicarbonate ions. Most of these bicarbonate ions are generated during the catabolism of glutamine. In order to be eliminated as carbon dioxide in the lungs bicarbonate ions must be protonised. This protonisation of the bicarbonate ion seems to take place in a number of tissue compartments in which acid-base balance is maintained. One of the most important processes for protonisation of the bicarbonate ion is the hepatic ureagenesis from ammonia/ammonium ions. A substantial part of the ammonia/ammonium ions are generated during the catabolism of amino acids. Terminal oxidation of glutamine in the gut seems to be of great significance for this process. In certain conditions the enteric generation of ammonium ions seems so important that an ATP-driven enterohepatic recirculation of ammonium ions/urea constituting an amplifying mechanism for the protonisation of the bicarbonate ion is motivated.
Article
Propofol is formulated in an emulsion similar to 10% Intralipid, and several authors have suggested that fat accumulates during its infusion. In this study we used indirect calorimetry to measure lipid metabolism during abdominal surgery in patients anesthetized with propofol, using midazolam as a control. Thirty patients were randomly divided into three groups: Group P (propofol 2 mg/kg + 5 mg.kg-1.h-1, n = 13); Group M (midazolam, n = 9), and Group I (midazolam + 10% Intralipid at rates similar to those infused in Group P, n = 8). They were monitored with an indirect calorimeter for 90 min. Data including oxygen consumption (VO2), CO2 production (VCO2), energy expenditure (EE), respiratory quotient (RQ), and lipid utilization were obtained every 15 min. VO2 increased in all groups at 45 min in respect to basal measurements with no differences between them. VCO2 decreased significantly only in Groups P and I, although no differences between the three groups were observed. EE did not vary in any of the groups. RQ decreased in all groups at 30 min, being significantly higher in Group M than in Groups P and I. Lipid oxidation increased in all groups from the beginning of the study reaching a plateau at 45 min. The lipid oxidation was higher in Groups P and I than in Group M, and coincided (80-100 g/24 h) with the amount of fat administered exogenously (85.4 g/ 24 h for a patient of 70 kg). Compared to VO2, VCO2, and EE, propofol behaves as other anesthetics. The fat administered in its formulation is metabolized in a preferential way, although it is likely that larger doses than those studied in our patients partially accumulate.
Article
In this double-blind placebo controlled study the preoperative cardiovascular and metabolic effects of intramuscular (i.m.) clonidine and midazolam are assessed. Forty-five ASA Grade I patients (n = 15 per group) undergoing plastic surgical procedures were randomly allocated to receive either placebo, clonidine 4 micrograms kg-1 or midazolam 70 micrograms kg-1. Drugs were administered into the deltoid muscle approximately 90 min prior to the scheduled induction of anaesthesia. The metabolic measurements were performed using an indirect calorimetry device. Heart rate and blood pressure were measured noninvasively. Pre-operative subjective anxiety, dryness of mouth and tiredness were assessed using visual analogue scales (VAS). Clonidine increased subjective tiredness significantly more than placebo. Clonidine also induced moderate decreases in blood pressure and heart rate. Oxygen consumption (VO2), CO2 production and energy expenditure (EE) decreased significantly after clonidine and midazolam. The decrease in VO2 and EE was maximally 11-14% on average from the base-lines after clonidine and midazolam. These effects were of longer duration after clonidine and lasted until the end of the 90 min study period. In conclusion, both clonidine and midazolam are effective as a means of decreasing pre-operative VO2 and EE.
Article
The aim of the study was to investigate whether oxygen consumption and carbon dioxide production changed in the early postoperative period in the same manner in patients who underwent coronary artery bypass graft (CABG) surgery or abdominal aortic surgery (AAS). Prospective clinical study. Single community hospital. Twenty-four patients (ASA II to III) who underwent elective abdominal aortic surgery and 49 patients (NYHA II, III) who underwent elective CABG surgery. In the ICU, oxygen consumption (VO2), carbon dioxide production (VCO2), and respiratory quotient (RQ) were continuously monitored with an indirect calorimetric device. Hemodynamic and metabolic parameters were measured during the first 3 hours. In the early postoperative course, VO2 and VCO2 in the AAS group were significantly higher (p < 0.001), and the RQ was significantly lower during the first 90 minutes (p < 0.001). In the AAS patients, VO2 decreased with the postoperative increase of body temperature; whereas in the CABG patients, VO2 slightly increased. The high VO2 in the AAS patients observed during the early postoperative course can be explained by an oxygen debt that occurred as a result of clamping the aorta. It was presumed that the repayment of the debt was delayed and extended to the ICU stay because of thermoregulatory vasoconstriction. Abnormally low RQ values are probably a clue to repayment of an oxygen debt.
Article
Because deliberate hypothermia is becoming commonly used during neurosurgery, this study was performed to investigate the effects of a progressive reduction of body core temperature (T) on whole body oxygenation variables in patients undergoing elective intracranial surgery. In 13 patients (Hypothermic Group), T was reduced to 32.0 degrees C using convective-based surface cooling. In six patients (Control Group), T was maintained at 35.5 degrees C during the entire study period. The cardiac index (CI) was determined with a pulmonary artery catheter by thermodilution. Whole body oxygen delivery (DO2) was calculated from CI and arterial oxygen content. Whole body oxygen consumption (VO2), carbon dioxide production (VCO2), and energy expenditure (EE) were determined by ventilation gas analysis (indirect calorimetry). Mixed venous oxygen tension at 50% saturated hemoglobin (P50), and whole body oxygen extraction ratio (O2ER) were calculated. Repeated-measures analysis of variance and the Mann-Whitney test were used for statistical analysis. Data are expressed as means +/- SD. VO2 (from 100 +/- 13 to 77 +/- 11 ml.min-1.m-2), VCO2 (from 75 +/- 7 to 57 +/- 7 ml.min-1. m-2), EE (from 667 +/- 67 to 509 +/- 66 kcal.d-1.m-2), P50 (from 23.8 +/- 1.7 to 20 +/- 0.9 mm Hg), and O2ER (from 0.29 +/- 0.05 to 0.22 +/- 0.03%) decreased significantly in the Hypothermic Group between 35.5 and 32.0 degrees C (p < 0.05). None of these variables changed in the Control Group and at 32.0 degrees C VO2, VCO2, EE, P50, and O2ER were significantly lower in the Hypothermic Group than in the Control Group. DO2 remained unchanged in both groups. We conclude that progressive hypothermia in anesthetized patients reduces metabolic rate but does not change DO2. The significant decrease in O2ER may partly be related to a leftward shift of the oxyhemoglobin dissociation curve, as evidenced by the decrease in P50.
Article
Unlabelled: To examine whether the degree of the changes in metabolic variables correlates with the duration of tourniquet inflation or other factors in spontaneously breathing patients undergoing unilateral lower-limb surgery under epidural anesthesia, we measured changes in metabolic variables. Metabolic variables consisted of oxygen consumption (VO2), carbon dioxide elimination (VCO2), and respiratory quotient (RQ). The patients (n = 30) received continuous epidural anesthesia with 1.5% lidocaine with epinephrine solution (5 micrograms/mL). The averaged values of VO2 and VCO2 for 10 min after tourniquet release increased significantly from 171.2 +/- 34.5 mL/min to 262.7 +/- 90.0 mL/min and from 202.0 +/- 33.1 mL/min to 250.5 +/- 64.2 mL/min, respectively. They returned to the baseline values within 10 min after deflation. Therefore, rapid response to changes in metabolic condition can be anticipated after tourniquet release in patients breathing spontaneously under epidural anesthesia. The percent increases in the averaged values of VO2 and VCO2 for 10 min after tourniquet release were correlated with body surface area but not with tourniquet inflation time. We conclude that the changes in metabolic variables after tourniquet release are dependent on body size, i.e., muscle mass, but not on the duration of tourniquet inflation. Implications: We measured changes in metabolic variables, i.e., oxygen consumption and carbon dioxide elimination, after tourniquet release in patients undergoing lower-limb surgery under epidural anesthesia. We found that the extent of changes in these variables was dependent on body size but not on the duration of inflation. These results have implications as to how long a tourniquet can be inflated during surgery.
Article
Unlabelled: The use of ketamine as a sole anesthetic induces marked central sympathetic stimulation, causing increased heart rate, blood pressure (BP), and oxygen consumption (VO2). Both alpha 2-agonists and benzodiazepines have been used to attenuate these potentially harmful ketamine-induced responses. This double-blind, randomized, placebo-controlled study was designed to compare the perioperative metabolic, hemodynamic, and sympathoadrenal responses to IM clonidine (2 micrograms/kg) and midazolam (70 micrograms/kg) premedication during ketamine anesthesia. VO2 was measured continuously using indirect calorimetry in 30 ASA physical status I patients. The patients received ketamine, mivacurium, and fentanyl for the induction of anesthesia. Anesthesia was maintained using a ketamine infusion and fentanyl boluses i.v. Preoperatively, both VO2 and BP decreased significantly after the administration clonidine and midazolam compared with placebo (P < 0.01). Intraoperatively, VO2 was higher in the midazolam group than in the placebo and clonidine groups (P < 0.05). Postoperatively, there were no significant differences in BP and VO2, although they stayed at lower level in the clonidine group during the whole postoperative period. Clonidine decreased pre- and postoperative plasma catecholamine concentrations (P < 0.05). Our results indicate that a midazolam-ketamine combination may induce potentially harmful metabolic stimulation, whereas the sympatholytic effects of clonidine on ketamine-anesthetized patients may be beneficial, as perioperative VO2 was decreased. Implications: Ketamine causes sympathetic stimulation with an ensuing increase in oxygen consumption. Anticipating that clonidine might attenuate this response, we measured oxygen consumption in patients undergoing surgery during ketamine anesthesia. Patients treated with a clonidine-ketamine combination had lower intra- and postoperative oxygen consumption than those treated with a midazolam-ketamine combination.
Article
Despite the wide use of hypothermic cardiopulmonary bypass (CPB) during open heart surgery there is little information about the patient metabolism. In particular no complete studies addressed the assessment of the respiratory ratio (RR) during CPB at different core temperatures. Therefore a clinical study was performed in order to evaluate the oxygen consumption (VO2) and carbon dioxide production (VCO2) in adult patients with valvular or coronary heart disease undergoing CPB. Twenty-five patients (16 male, 9 female) aged between 26 and 76 (54.2+/-12.4 mean +/- SD) were the subjects of this study. Measurements (102) were taken at various perfusion flow rates (from 1.6 to 2.9 L/min(-1) x m(-2)) and temperatures (from 24 to 37 degrees C). Arterial and mixed venous gas analyses were performed and O2 and CO2 concentrations were calculated, including the carbamate contribute. We calculated VO2, VCO2 and then RR from artero-venous differences in O2 and CO2 contents. Both VO2 and VCO2 showed a positive linear correlation with temperature (r = 0.82 and r = 0.59 respectively) and with blood flow rate (r = 0.61 and r = 0.29 respectively). The mean RR was 0.78+/-0.28 and more than 84% of RR values fell in the range 0.5-1.2. No significant correlation between RR and temperature and blood flow rate was observed. VCO2 and RR showed a positive linear correlation with the gas to blood flow rate ratio (r = 0.37 and r = 0.49 respectively).
Article
To evaluate the effect of acute changes in minute ventilation (VE) on oxygen consumption (VO2), carbon dioxide production (VCO2), respiratory quotient, and energy expenditure during volume-controlled mechanical ventilation in the critically ill surgical patient. The effects on some oxygen transport variables were assessed as well. Prospective, randomized clinical study Adult surgical intensive care unit of a university teaching hospital. Twenty adult critically ill surgical patients were studied during volume-controlled mechanical ventilation. After a basal period of stability (no changes over time in body temperature, energy expenditure, blood gases, acid-base status, cardiac output, and ventilatory parameters), VE was then randomly either increased or reduced (+/-35%) by a change in tidal volume (VT), while respiratory rate and inspiratory/expiratory ratio were kept constant. Settings were then maintained for 120 mins. During the study, patients were sedated and paralyzed. VO2, VCO2, and respiratory quotient were measured continuously by a Nellcor Puritan Bennett 7250 metabolic monitor (Nellcor Puritan Bennett, Carlsbad, CA). Hemodynamic and oxygen transport parameters were obtained every 15 mins during the study. Despite large changes in VE, VO2 and energy expenditure did not change significantly either in the increased or in the reduced VE groups. After 15 mins, VCO2 and respiratory quotient changed significantly after ventilator resetting. VCO2 increased by 10.5 +/- 1.1% (from 2.5 +/- 0.10 to 2.8 +/- 0.12 mL/min/kg, p< .01) in the increased VE group and decreased by 12.4 +/- 2.1% (from 2.7 +/- 0.17 to 2.4 +/- 0.16 mL/min/kg, p< .01) in the reduced VE group. Similarly, respiratory quotient increased by 16.2% +/- 2.2% (from 0.87 +/- 0.02 to 1.02 +/- 0.02, p< .01) and decreased by 17.2% +/- 1.8% (from 0.88 +/- 0.02 to 0.73 +/- 0.02, p< .01). VCO2 normalized in the reduced VE group, but remained higher than baseline in the increased VE group. Respiratory quotient did not normalize in both groups and remained significantly different from baseline at the end of the study. Cardiac index, oxygen delivery, and mixed venous oxygen saturation increased, while oxygen extraction index decreased significantly in the reduced VE group. Neither of the mentioned parameters changed significantly in the increased VE group. We conclude that, during controlled mechanical ventilation, the time course and the magnitude of the effect on gas exchange and energy expenditure measurements caused by acute changes in VE suggest that VO2 and energy expenditure measurements can be used reliably to evaluate and quantify metabolic events and that VCO2 and respiratory quotient measurements are useless for metabolic purposes at least for 120 mins after ventilator resetting.
Article
Postoperative hypothermia is common in cardiac surgery with hypothermic cardiopulmonary bypass (CPB). This trial was designed to evaluate whether rewarming over the normal bladder temperature (over 37 degrees C) at the end of hypothermic CPB combined with passive heating methods after CPB might result in a better heat balance, lower energy expenditure (EE) and decrease of disturbances in oxygen balance compared to only rewarming the patients to a bladder temperature of 35-37 degrees C. A prospective, randomized controlled clinical study was performed in 38 patients scheduled for elective coronary artery bypass surgery. Twenty patients (group C) were rewarmed to a bladder temperature of 35-37 degrees C at the end of hypothermic (28 degrees C) CPB. Eighteen patients (group W) were rewarmed to a bladder temperature of 37-38.5 degrees C. At the end of CPB, the bladder temperature was 36.2+/-0.7 degrees C (mean+/-SD) in group C and 37.9+/-0.5 degrees C in group W. After half an hour's stay in the ICU, the mean body temperature (MBT) was 35.1+/-0.6 degrees C in group C and 36.6+/-0.7 degrees C in group W. During the following five hours, MBT increased to 37.4+/-0.8 degrees C in group C and to 38.0+/-0.6 degrees C in the other group. The peak value of EE in the ICU was 1.73+/-0.44 (group C) vs 1.35+/-0.29 (W/kg) (group W) (P=0.003). EE was significantly (P=0.044) higher in group C than in the other group between 1.5 and 5.5 h in the ICU. The increased energy expenditure due to heat production was associated with an increase in O2 consumption (VO2) 61.6+/-30.4% vs 25.2+/-24.1%, (peak values) compared to the basal values of the two groups measured before anesthesia (between groups P<0.001). Between 1.5 and 5.5 h in the ICU, group C had significantly higher VO2 (P=0.026), CO2 production (P=0.017), venous pCO2 (P<0.001) and minute ventilation (p=0.014) than group W. Venous pH was lower (P<0.001) in group C. The peak value of oxygen extraction was also higher (P=0.045) in group C. On the other hand, the lowest value of venous oxygen saturation was higher (P=0.04) in group W. With rewarming the patients at the end of CPB to a bladder temperature of over 37 degrees C combined with passive heating methods after CPB, it was possible to decrease EE and VO2 compared to the control group (rewarmed to bladder temperature of 35-37 degrees C) after coronary artery bypass surgery with moderate hypothermia.
Article
To interpret correctly the results from studies performed during surgery and anesthesia it is necessary to dissect the separate effect of the anesthetic technique itself. The purpose of this study was to investigate the metabolic effects of epidural blockade (T7-S1) with bupivacaine 0.25% after 12 h fasting and during administration of 4 mg x kg(-1) x min(-1) dextrose in six healthy volunteers. Each volunteer was assigned to randomly undergo a 6-h multiple stable isotope infusion study (3 h fasted, 3 h dextrose infusion) with or without epidural blockade. L-[1-13C]leucine, [6,6-2H2]glucose, and [1,1,2,3,3-2H5]glycerol were infused to measure protein synthesis, breakdown, and amino acid oxidation; glucose production and clearance; and lipolysis. Plasma concentrations of glucose, lactate, glycerol, free fatty acids, insulin, and glucagon were determined. Epidural blockade with bupivacaine had no influence on protein oxidation, breakdown and synthesis, glucose production, glucose clearance and lipolysis in the fasted state. Plasma concentrations of metabolic substrates and hormones also were not affected. Dextrose infusion significantly increased glucose clearance and plasma concentrations of glucose and insulin, while endogenous glucose production and lipolysis decreased to a similar degree in both groups. Protein synthesis, breakdown, and oxidation did not change during dextrose infusion. Epidural blockade with bupivacaine in the absence of surgery has no effect on fasting protein, glucose, and lipid metabolism. Epidural blockade does not modify the inhibitory influence of dextrose administration on endogenous glucose production and lipolysis.
Article
To quantify the effects of neuromuscular blockade (NMB) on energy expenditure for intubated, mechanically ventilated, critically ill children. A prospective, unblinded clinical study. Each subject was studied twice, before and after establishment of NMB. A tertiary care pediatric intensive care unit. Critically ill children undergoing mechanical ventilation and receiving ongoing sedation were eligible, if they had a cuffed endotracheal tube and were physiologically stable. A total of 20 children (age, 1 to 15 yrs) were studied in an unblinded, crossover fashion. All were mechanically ventilated via a cuffed endotracheal tube, with ventilator rate and tidal volume adequate to provide complete ventilation, and F(IO2) <0.6. Absence of gas leak around the endotracheal tube was assured, and all patients were sedated using continuous infusions of midazolam and/or fentanyl; no changes in ventilator settings, nutritional input, or inotropic drug dose were permitted during the study period. Each patient underwent indirect calorimetry immediately before establishment of NMB. NMB was then induced, and indirect calorimetry was repeated. Complete blockade was verified using a peripheral nerve stimulator. In each case, the two sets of measurements were completed within a 1-hr period. Data analyzed included identifying and diagnostic information, oxygen consumption, and carbon dioxide production. Energy expenditure was calculated using standard formulas. Oxygen consumption and energy expenditure values obtained before and after the establishment of NMB were compared by using paired Student's t-test. NMB reduced oxygen consumption from 6.54+/-0.49 mL/kg/min to 5.90+/-0.40 ml/kg/min, and energy expenditure was reduced from 46.5+/-3.7 kcal/kg/24 hrs to 41.0+/-2.8 kcal/kg/24 hrs (p < .001 in each case). The reduction in oxygen consumption was 8.7+/-1.7%, and that in energy expenditure 10.3+/-1.8%, of pre-NMB values, respectively. NMB significantly reduces oxygen consumption and energy expenditure in critically ill children who are sedated and mechanically ventilated; the degree of reduction is small.