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Carbon dioxide production, metabolism, and anesthesia
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).
... A BRIEF OVERVIEW ON METABOLISM, MITOCHONDRIA, AND ROS In our body, nutrients and oxygen are transformed into energy, water, carbon dioxide, and other by-products as ROS. The amounts of O 2 consumed, and CO 2 produced reflect the body's metabolism and metabolized nutrients (14). In biological systems, energy is mainly provided by the controlled oxidation of carbohydrates and fatty acids, where the oxidizer is the limiting reagent. ...
Dysregulation of the immune system is associated with an overproduction of metabolic reactive oxygen species (ROS) and consequent oxidative stress. By buffering excess ROS, cerium oxide (CeO2) nanoparticles (NPs) (nanoceria) not only protect from oxidative stress consequence of inflammation but also modulate the immune response towards inflammation resolution. Immunomodulation is the modulation (regulatory adjustment) of the immune system. It has natural and human-induced forms, and it is part of immunotherapy, in which immune responses are induced, amplified, attenuated, or prevented according to therapeutic goals. For decades, it has been observed that immune cells transform from relative metabolic quiescence to a highly active metabolic state during activation(1). These changes in metabolism affect fate and function over a broad range of timescales and cell types, always correlated to metabolic changes closely associated with mitochondria number and morphology. The question is how to control the immunochemical potential, thereby regulating the immune response, by administering cellular power supply. In this regard, immune cells show different general catabolic modes relative to their activation status, linked to their specific functions (maintenance, scavenging, defense, resolution, and repair) that can be correlated to different ROS requirements and production. Properly formulated, nanoceria is highly soluble, safe, and potentially biodegradable, and it may overcome current antioxidant substances limitations and thus open a new era for human health management.
... However, the authors also stated that the model is valid for a specific given activity task and should be repeated and re-developed for different activities. On the other hand, researchers showed that carbon dioxide production of the human body reflects the rate of body metabolism [25][26][27][28]. For instance, Na et al. [29] developed a deep learning system which predicts the M with the parameters of CO2 concentration apart from the HR. ...
Thermal comfort depends on four environmental parameters such as air temperature, mean radiant temperature, air velocity and relative humidity and two personal parameters, including clothing insulation and metabolic rate. Environmental parameters can be measured via objective sensors. However, personal parameters can be merely estimated in most of the studies. Metabolic rate is one of the problematic personal parameters that affect the accuracy of thermal comfort models. International thermal comfort standards still use a conventional metabolic rate table which is tabulated according to different activity tasks. On the other hand, ISO 8996 underestimates metabolic rates, especially when the time of activity level is short and rest time is long. To this aim, this paper aims to determine metabolic rates from physical measurements of heart rate, mean skin temperature and carbon dioxide variation by means of nineteen sample activities. 21 male and 17 female subjects with different body mass indices, sex and age are used in the study. The occupants are subjected to different activity tasks while heart rate, skin temperature and carbon dioxide variation are measured via objective sensors. The results show that the metabolic rate can be estimated with a multivariable non-linear regression equation with high accuracy of 0.97.
... Une augmentation de l'activité métabolique accroît le taux de CO 2 sanguin (p. ex., lors d'une activité physique, d'une fièvre, d'une infection, de convulsions)(Casey, 2015;Willner et Weissman, 2011). ...
Despite the fact that the arms are used extensively in daily life and that some of the muscles of the shoulder girdle share both a respiratory and a positional function for the arms, surprisingly little is known about the respiratory response to unsupported upper extremity activity. To determine the respiratory consequences of simple arm elevation during tidal breathing, we measured minute ventilation (VE), tidal volume (VT), respiratory rate (f), heart rate (HR), oxygen uptake (VO2), and carbon dioxide production (VCO2) in 22 normal subjects seated with arms elevated in front of them to shoulder level (AE) for 2 min and down at the sides (AD) for the same time period. The sequence was randomized. Compared with AD, during AE there were significant increases in VO2 (336 +/- 18 vs 289 +/- 14 ml/min, p less than 0.001), VCO2 (315 +/- 23 vs 245 +/- 16 ml/min, p less than 0.001), HR (84 +/- 6 vs 73 +/- 4 beats/min, p less than 0.05), VE (11.5 +/- 0.9 vs 9.3 +/- 0.6 L/min, p less than 0.001), and VT (868 +/- 66 vs 721 +/- 48 ml, p less than 0.001). In 11 subjects, breath-by-breath metabolic and ventilatory parameters were studied with AD for 2 min, AE for 2 min, and with AD for 3 min while also recording gastric (Pg), pleural (Ppl), and transdiaphragmatic pressures (Pdi). With AE, there was a significant increase in Pg at end inspiration (PgI, 15.4 +/- 3.2 vs 11.9 +/- 2.7 cm H2O, p less than 0.01) and in Pdi (26.5 +/- 3.4 vs 21.4 +/- 2.4 cm H2O, p less than 0.01) with no change in Pg at end expiration (PgE) or in Ppl. The increases in VO2, VCO2, VE, and VT during arm elevation persisted for 2 min after arm lowering, whereas Pgi and Pdi abruptly dropped as the arms were lowered. We conclude that simple arm elevation during tidal breathing results in significant increases in metabolic and ventilatory requirements. These increased demands are associated with higher PgI and Pdi suggesting an increased diaphragmatic contribution to the generation of ventilatory pressures. The sudden drop in Pg with arm lowering indicate a change in ventilatory muscle and or torso recruitment independent of the metabolic drive and ventilatory needs. These findings may help explain the limitation that has been reported in some normal subjects and in many patients with lung disease during unsupported upper extremity activity.
Measurement with an infrared analyzer of CO2 given off by the hands of human volunteers under laboratory conditions showed that they continuously produced CO2 at the rate of 1.0-1.8 ml/h. Increased production of CO2 was observed with increase in temperature for all subjects. Treatment of subjects with three insect repellents or ethanol resulted in a short-term drop in CO2 production, after which it returned to pretreatment levels. Olfactometer studies showed no correlation between the amount of CO2 produced by hands and the attractancy of the subjects to host-seeking female Ae. aegypti (L.). The supplemental addition of five times the amount of CO2 given off by the hands did not affect attractancy of subjects to mosquitoes. The amount of CO2 released by hands is negligible compared to ambient levels of 300 ppm, and it is unlikely to be attractive at this level of release by itself.
Oxygen consumption (VO2), carbon dioxide production (VCO2), end-tidal carbon dioxide partial pressure (PETCO2), mixed venous oxygen saturation (SvO2) and haemodynamic variables were recorded every 30 min for four hours in 15 patients recovering from hypothermic cardiopulmonary bypass (CPB). All patients had been anaesthetised with fentanyl 40 micrograms.kg-1, supplemented with isoflurane, and pancuronium 0.15 mg.kg-1 for muscle relaxation. Three of the 15 patients (20 per cent) shivered, defined as intermittent or continuous, vigorous movements of chest or limb muscles. Patients who shivered had a VO2 of 159 +/- 16.4 ml.min-1.m-2 on arrival in the ICU which rose to a maximum value of 254 +/- 28.3 ml.min-1.m-2 by 150 min post-CPB. In contrast, patients who did not shiver had a significantly lower VO2 of 93.1 +/- 6.9 ml.min-1.m-2 on arrival in the ICU which rose to a maximal value of only 168 +/- 11.5 ml.min-1.m-2 by 180 min post-CPB. Maximal VO2 in both groups was reached when the nasopharyngeal temperature (NPT) was approaching normal. VCO2 paralleled the increase in VO2 in both groups. By four hours there was no significant difference between the two groups; however, the VO2 in both groups (160.5 +/- 21.3 ml.min-1.m-2 and 173.9 +/- 12.3 ml.min-1.m-2 respectively) was approximately twice values commonly measured in anaesthetized patients. Patients who shivered had a significantly higher heart rate and cardiac index and significantly lower SvO2. We conclude that the high VO2 and VCO2 associated with shivering causing increased myocardial work may be detrimental to patients who have impaired cardiac function post-coronary artery surgery (CAS).
To assess the effect of colonic fermentation on respiratory gas exchanges, six methane-nonproducing healthy volunteers ingested in the postabsorptive state 1 wk apart either 90 mL lactulose syrup containing 60 g lactulose, 4 g lactose, and 7 g galactose or the same solution but without lactulose (control solution). Six patients with short bowel and remnant colon (SBS) also ingested 90 mL lactulose syrup. Carbon dioxide production (VCO2), oxygen consumption (VO2), respiratory quotient (RQ), and hydrogen excreted in breath were measured basally and for 4 h after the ingestion of solutions. In healthy volunteers within 4 h after ingestion of the control solution, VCO2 and the RQ decreased whereas VO2 remained unchanged. In contrast, in healthy volunteers and patients with SBS, VCO2 and the RQ increased after lactulose ingestion, whereas VO2 did not change. The increase in VCO2 appeared to be accounted for mainly by bacterial production of carbon dioxide and was significantly related to breath-hydrogen concentration (r = 0.56, P < 0.02 for healthy subjects; r = 0.59, P < 0.01 for SBS subjects). A breath-hydrogen test should be performed in conjunction with indirect calorimetry to determine whether colonic fermentation is taking place and, if so, to correct appropriately the VCO2 value in calorimetric equations.
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 alpha2-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 [micro sign]g/kg) and midazolam (70 [micro sign]g/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 IV. 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.
(Anesth Analg 1998;87:161-7)
• 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 (V̇o2) and the carbon dioxide production levels (V̇co2), as well as hemodynamic and biochemical parameters. In groups 1 and 3, V̇o2 and V̇co2 decreased 10% to 13% following abdominal aortic cross-clamping compared with values measured before cross-clamping. In group 2, V̇o2 and V̇co2 decreased 3% and 7%, respectively. On unclamping, the greatest increase in V̇o2 was observed in group 3 (26%), while in groups 1 and 2, V̇o2rose 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.(Arch Surg 1984:119:1332-1337)
Propofol is formulated in an emulsion similar to 10% Intralipid Registered Trademark, 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 centered dot kg-1 centered dot h-1, n = 13); Group M (midazolam, n = 9), and Group I (midazolam + 10% Intralipid Registered Trademark 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 (VCO (2)), 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. (Anesth Analg 1996;83:837-43)
• This study examines the oxygen consumption (Vo2) and carbon dioxide production (Vco2) occurring before, during, and after cardiopulmonary bypass (CPB) and whether they correlate with changes in cardiac output. Twenty-three patients undergoing open heart surgery were studied. Group 1 (N =11) received fentanyl citrate, 50 μg/kg, intravenously during the induction of anesthesia. Group 2 (N=12) received 100 μg/kg of fentanyl citrate intravenously. We measured Vo2, Vco2, as well as hemodynamic and biochemical factors. Initial statistical analyses failed to show any differences in the Vo2, Vco2, hemodynamic, or biochemical factors between groups 1 and 2. Therefore, the data from both groups were combined. In comparing the average (for all data) of the post-CPB with the pre-CPB periods in both groups for the metabolic factors, there were 9.0%, 11.5%, and 2.4% increases in the Vo2, Vco2, and respiratory quotient, respectively. There was an 80% increase in total serum lactate levels seen in the post-CPB periods when compared with the pre-CPB periods. Serum triglyceride and free fatty acid levels measured in the post-CPB period decreased 39% and 25%, respectively, when compared with the pre-CPB periods. Although there were no changes in the cardiac outputs following CPB, the post-CPB periods showed a 37% increase in central venous pressure when compared with the pre-CPB periods. These data suggest that although there are significant metabolic and biochemical sequelae to CPB, the modest increases in post-CPB Vo2, and Vco2 did not affect cardiac output following cardiovascular surgery. Increasing doses of narcotic do not have an effect on those relationships.
(Arch Surg 1987;122:1026-1031)
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 attentuated. 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.
Twelve healthy, unpremedicated women scheduled for total abdominal hysterectomy were given either isoflurane (n = 6) or halothane (n = 6) anaesthesia. They all 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.
The CO2-production and degree of relaxation after increasing doses of suxamethonium were measured in seven patients undergoing alloplastic surgery of the hip. The study indicates that the CO2-production rises following the injection of increasing doses of suxamethonium. Another group of patients received diazepam 0.1 mg kg-1 before the injection of suxamethonium 1 mg kg-1. CO2-production was significantly reduced compared to CO2 production when suxamethonium was not preceded by diazepam. It is suggested that diazepam in doses larger than 0.1 mg kg-1 might be effective in preventing fasciculations and postoperative muscle pains before the injection of suxamethonium in a dose of 0.5 mg kg-1.
The requirements for fresh gas inflow with the Bain breathing circuit in children was examined by determining the PaCO2 in 46 children during controlled ventilation with a total fresh gas inflow of 3.5 l/min and by measuring the carbon dioxide output in 83 children under anaesthesia. It could be shown that all children below 40 kg body weight had a PaCO2 below 40 torr (5.32 kPa) and the PaCO2 paralleled the body weight, i.e., the lowest carbon dioxide tension was seen in children under 10 kg. As expected, the highest carbon dioxide output was found in children below 5 kg body weight; the carbon dioxide output per kilogram decreased with increasing body weight up to 30-35 kg and remained at that level in larger children. Children in their teens, although they may have attained adult body weight, had a higher carbon dioxide output than adults. Based on these findings, our recommendation of a total fresh gas inflow of 3.5 1/min for all children would appear adequate for a body weight up to 35 kg on controlled ventilation. In children under 10 kg body weight, a reduction of the total fresh gas flow to two litres per minute will avoid marked respiratory alkalosis. For children over 35 kg, a fresh gas flow of 100 ml/kg/min should be satisfactory during controlled ventilation.
We studied the effects of elective hip surgery, performed under either spinal (SA, n = 10) or general anesthesia (GA, n = 10), on breathing pattern and gas exchange. Measurements were made with respiratory inductive plethysmograph and indirect calorimetry in two positions before and after surgery. The method of anesthesia had no effect on the severity of postoperative hypoxemia. Reduced arterial oxygenation (PaO2; P less than 0.001, SA from 12.5 +/- 2.37 kPa to 10.5 +/- 1.38 kPa, GA from 12.5 +/- 2.95 kPa to 10.5 +/- 1.75 kPa) despite increased alveolar ventilation (P less than 0.01; from 2.30 +/- 0.37 l/min to 2.39 +/- 0.43 l/min in SA, 2.27 +/- 0.56 l/min to 2.57 +/- 0.35 l/min in GA) and reduced arterial carbon dioxide partial pressure (PaCO2; SA from 5.20 +/- 0.22 kPa to 4.95 +/- 0.33 kPa, P less than 0.01, GA from 5.07 +/- 0.36 kPa to 4.72 +/- 0.41 kPa, P less than 0.05) indicated maldistribution of ventilation and perfusion. Changes in breathing pattern and gas exchange and differences between the groups were minimal. Minute ventilation, tidal volume and mean inspiratory flow remained unchanged in both groups. The contribution of rib cage to tidal volume increased postoperatively in the supine position (P less than 0.001; SA from 32.6% +/- 10.3 to 46.3% +/- 7.5, GA from 36.5 +/- 16.4 to 48.5% +/- 15.4). CO2 production, oxygen consumption and energy expenditure remained unchanged. The postoperative changes in breathing pattern are related to the operation, not to the type of anesthesia and do not explain the alterations in gas exchange.
Oxygen consumption (VO2), carbon dioxide elimination (VCO2), and respiratory exchange ratio (RQ) were continuously measured in 15 male and 15 female adults during knee surgery, with the leg exsanguinated by an inflatable tourniquet around the thigh. Arterial blood was also intermittently sampled for blood gas analysis, electrolytes, and lactate content before and after tourniquet deflation. There was a significant increase in VO2 and VCO2 after tourniquet deflation, which was more pronounced in the male (aged 29.5 +/- 14.8 yr, mean +/- SD) than the female (aged 56.9 +/- 15.6 yr) patients, both in terms of maximal increase (P less than 0.001) and percent of increase from values before deflation (P less than 0.001 and P = 0.01). The body weights and tourniquet inflation times were not significantly different between the male and female patients. Excess VO2 (O2 debt) and excess VCO2 over 12 min after deflation of the tourniquet were also significantly higher for male (593.5 +/- 222.9 mL and 714.9 +/- 463.8 mL, respectively) than for female patients (302 +/- 73.3 mL and 196 +/- 162.22 mL, respectively; P less than 0.01). There was no correlation between the duration of tourniquet inflation time and peak increase in VO2, peak increase in VCO2, and O2 debt over 12 min after deflation of the tourniquet; however, tourniquet time was weakly correlated with excess VCO2 over 12 min after tourniquet deflation (r = 0.55, P = 0.002). There was a significant decrease in pHa (P less than 0.001) from release of PaCO2 and lactate after tourniquet deflation. Plasma potassium levels also increased significantly after tourniquet release (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Shivering after cardiac surgery can produce adverse haemodynamic and metabolic sequelae. In this study, the metabolic effects of shivering and the efficacy of treatment with meperidine or pancuronium were studied, using a metabolic cart, in 61 patients who had undergone cardiac surgery. The patients received premedication with morphine, perphenazine and diazepam or lorazepam, and were anaesthetised with fentanyl or sufentanil and diazepam. Muscle relaxation was achieved with pancuronium. Patients were monitored with a radial arterial line, pulmonary artery catheter and oesophageal and urinary bladder temperature probes. Rewarming to an oesophageal temperature of 38 degrees C was achieved before the termination of CPB and was maintained for a minimum of 15 min reperfusion time. Every 15 min after surgery, the patients' temperature at three sites (pulmonary artery, oesophagus, bladder) and shivering scores were monitored. Hourly measurements were made of haemodynamic variables (MAP, PAOP, CVP, SVR, PVR, CI), carbon dioxide production, oxygen consumption and respiratory quotient. If the patient shivered, the measurements were recorded prior to drug treatment and repeated 30 min later following randomization to either: meperidine 0.25 mg.kg-1 (Group 1), meperidine 0.5 mg.kg-1 (Group 2) or pancuronium 0.06 mg.kg-1 intravenously (Group 3). Thirty-two patients shivered and mean VO2 and VCO2 values were greater in the shivering group than in the nonshivering patients (VO2 334.8 +/- 17.6 vs. 240.5 +/- 8.8 ml.min-1; VCO2 238.8 +/- 17.2 vs 199.2 +/- 8.4 ml.min-1, P = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
Despite the fact that the arms are used extensively in daily life and that some of the muscles of the shoulder girdle share both a respiratory and a positional function for the arms, surprisingly little is known about the respiratory response to unsupported upper extremity activity. To determine the respiratory consequences of simple arm elevation during tidal breathing, we measured minute ventilation (VE), tidal volume (VT), respiratory rate (f), heart rate (HR), oxygen uptake (VO2), and carbon dioxide production (VCO2) in 22 normal subjects seated with arms elevated in front of them to shoulder level (AE) for 2 min and down at the sides (AD) for the same time period. The sequence was randomized. Compared with AD, during AE there were significant increases in VO2 (336 +/- 18 vs 289 +/- 14 ml/min, p less than 0.001), VCO2 (315 +/- 23 vs 245 +/- 16 ml/min, p less than 0.001), HR (84 +/- 6 vs 73 +/- 4 beats/min, p less than 0.05), VE (11.5 +/- 0.9 vs 9.3 +/- 0.6 L/min, p less than 0.001), and VT (868 +/- 66 vs 721 +/- 48 ml, p less than 0.001). In 11 subjects, breath-by-breath metabolic and ventilatory parameters were studied with AD for 2 min, AE for 2 min, and with AD for 3 min while also recording gastric (Pg), pleural (Ppl), and transdiaphragmatic pressures (Pdi). With AE, there was a significant increase in Pg at end inspiration (PgI, 15.4 +/- 3.2 vs 11.9 +/- 2.7 cm H2O, p less than 0.01) and in Pdi (26.5 +/- 3.4 vs 21.4 +/- 2.4 cm H2O, p less than 0.01) with no change in Pg at end expiration (PgE) or in Ppl. The increases in VO2, VCO2, VE, and VT during arm elevation persisted for 2 min after arm lowering, whereas Pgi and Pdi abruptly dropped as the arms were lowered. We conclude that simple arm elevation during tidal breathing results in significant increases in metabolic and ventilatory requirements. These increased demands are associated with higher PgI and Pdi suggesting an increased diaphragmatic contribution to the generation of ventilatory pressures. The sudden drop in Pg with arm lowering indicate a change in ventilatory muscle and or torso recruitment independent of the metabolic drive and ventilatory needs. These findings may help explain the limitation that has been reported in some normal subjects and in many patients with lung disease during unsupported upper extremity activity.
Clinical and metabolic responses to three types of premedication were studied in ASA physical status I patients given any one of the following: (a) 0.5 mg of atropine and 50 mg of meperidine given intramuscularly plus an oral placebo tablet (n = 14), (b) 10 mg of oral diazepam and an intramuscular placebo (2 mL NaCl, concentration = 0.9) (n = 14), or (c) oral and intramuscular placebo (n = 14). Based both on subjective estimates (tiredness, fear, anxiety, dryness of mouth) and, especially, on metabolic responses (energy expenditure, oxygen consumption), oral diazepam appears to be superior to the combination of an opiate (meperidine) plus an anticholinergic (atropine). Atropine plus meperidine significantly increased energy expenditure above predicted values (2061 +/- 365 vs 1714 +/- 361 kcal/24 h, P = 0.004), calculated using the Harris-Benedict equation, based on sex, weight, height, and age, as well as increased oxygen consumption above levels seen with diazepam premedication (160 +/- 29 vs 137 +/- 17 mL.min-1. m-2). These findings indicate an iatrogenic stress factor induced by premedication with atropine plus meperidine.
The metabolic effects of enflurane anaesthesia (1MAC) in air/oxygen were investigated in six healthy unpremedicated women scheduled for total abdominal hysterectomy (TAH). The changes in acid-base status, CO2 production, and circulating concentration of total protein, albumin and a variety of metabolites (glucose, lactate, glycerol and alanine) were measured before and during a 2-h period of anaesthesia alone, during 1 h of anaesthesia plus surgery, and in the recovery period. The subjects were maintained normothermic (36.5 +/- 0.3 degrees C), and with an arterial SaO2 above 95% throughout the period of study. The circulating concentration of all metabolites changed little as a result of anaesthesia alone, but the glucose and lactate levels rose rapidly after the onset of surgery (P less than 0.05). Plasma albumin and total protein concentration decreased during the study, reaching values that were significantly lower than the pre-anaesthetic values (P less than 0.05). CO2 production decreased by 9% during anaesthesia and surgery, but returned towards preoperative values during recovery. This study provides no evidence of any significant effect of enflurane anaesthesia alone on human intermediary metabolism. Most of the changes in circulating metabolite concentrations observed during and after anaesthesia and surgery are likely to be due to the surgical stress.
Twenty ASA I patients, undergoing thyroid surgery were allocated randomly to receive at the end of surgery either an isotonic
saline solution or clonidine 2 fig kg−1 i.v. administered over 20 min. Oxygen consumption (VO2) and carbon dioxide production (VCO2) were measured during recovery
in patients breathing spontaneously with a head canopy system. Clonidine was found to attenuate the increase in Vo2 and Vco2
associated with recovery from anaesthesia. The effect of clonidine was associated with a reduction in shivering. Sedative
and analgesic properties of clonidine may also contribute to the reduction in metabolic demand during recovery from anaesthesia.
There is much interest in the relationship between oxygen delivery and oxygen consumption in the critically ill patient. This interest is occasioned by the observation that patients with sepsis and the adult respiratory distress syndrome have a linear or "supply-dependent" relationship instead of the normally observed biphasic or "supply-independent" relationship. These relationships are only valid when subjects are at rest, since during exercise, as VO2 increases, so do DO2 and the oxygen extraction ratio (ER, VO2/DO2). We examined the VO2-DO2 relationship in a group of 16 mechanically-ventilated surgical ICU patients while they were at rest and during activities that increase VO2. At low levels of activity, where mean VO2 increased from 207 +/- 38 (SD) ml/min at rest to 241 +/- 44 ml/min, there were significant increases in mean DO2 but not mean ER. With the greater (greater than 50 percent) increases in VO2 seen with chest physical therapy, there were increases in both DO2 and ER. When the VO2-DO2 relationship during low levels of exercise and rest are plotted, a linear pattern emerges that could be misinterpreted as a "supply dependent" pattern. Therefore, it is important to pay close attention to the activity state of a patient when examining the VO2-DO2 relationship.
In 4 spontaneously breathing, barbiturate-anesthetized dogs, hyperthermia was induced with 2,4-dinitrophenol while rectal temperature, heart rate, mean blood pressure, end-tidal carbon dioxide, and carbon dioxide production (milliliters per minute) were measured continuously. The latter was determined with a pneumotachygraph (to obtain respired volume) and an infrared carbon dioxide analyzer that measured inspired and expired carbon dioxide concentration. Of the five physiologic measurements, the increase in carbon dioxide production preceded the increase in rectal temperature by more than 120 seconds. End-tidal carbon dioxide was an unreliable indicator in the spontaneously breathing animal of approaching hyperthermia during spontaneous breathing due to a transient tachypnea, which decreased end-tidal carbon dioxide. The carbon dioxide production (milliliters per minute) increased immediately and reached three to five times the control value. Blood pressure and heart rate were insensitive indicators of approaching hyperthermia.
The use of uncuffed endotracheal tubes (ETT) in pediatric patients raises concern over the accuracy of indirect calorimetry measurement in the presence of a gas leak around an ETT. We examined the effects of ETT gas leak on respiratory gas measurements in a dog model.
Mongrel dogs (n=12) were sedated, paralyzed, intubated, and placed on mechanical ventilation. Leak was achieved by adjusting cuff volume. Oxygen consumption (VO 2 ), CO 2 production (VCO 2 ), respiratory exchange ratio (RER), and resting energy expenditure (REE) were measured at each leak pressure (Pleak). Peak inspiratory pressure (PIP), Pleak, inspiratory and expiratory tidal volume (VTinsp, VTexp), VE, end tidal CO 2 (ETCO 2 ), and blood gases were recorded at each leak pressure.
VO 2 , VCO 2 , and REE decreased significantly with increasing gas leak. There was a linear relationship between VO 2 , VCO 2 , and REE with both TVratio (VTexp/VTinsp) and Pdiff (PIP‐Pleak). Multiple regression equations based on TVratio and Pdiff were obtained which allowed correction of the measurement error in VO 2 , VCO 2 , and REE, with correlation coefficients ( R ² ) of 0.71, 0.75, and 0.73, respectively.
ETT gas leak affects measurements of VO 2 , VCO 2 , and REE, but not RER. Measurements made with TVratio > 0.80 required no correction. Measurements made with TVratio > 0.45 could be corrected to actual values in our model with regression equations based on TVratio and Pdiff. We conclude that indirect calorimetry measurements can be useful in the presence of tracheal gas leak around an ETT. ( Journal of Parenteral and Enteral Nutrition 14:408–413, 1990)
During exercise, less additional CO2 is stored per kilogram body weight in children than in adults, suggesting that children have a smaller capacity to store metabolically produced CO2. To examine this, tracer doses of [13C]bicarbonate were administered orally to 10 children (8-12 yr) and 12 adults (25-40 yr) at rest. Washout of 13CO2 in breath was analyzed to estimate recovery of tracer, mean residence time (MRT), and size of CO2 stores. CO2 production (VCO2) was also measured breath by breath using gas exchange techniques. Recovery did not differ significantly between children [73 +/- 13% (SD)] and adults (71 +/- 9%). MRT was shorter in children (42 +/- 7 min) compared with adults (66 +/- 15 min, P less than 0.001). VCO2 per kilogram was higher in the children (5.4 +/- 0.9 ml.min-1.kg-1) compared with adults (3.1 +/- 0.5, P less than 0.0001). Tracer estimate of CO2 production was correlated to VCO2 (r = 0.86, P less than 0.0001) and when corrected for mean recovery accurately predicted the VCO2 to within 3 +/- 14%. There was no difference in the estimate of resting CO2 stores between children (222 +/- 52 ml CO2/kg) and adults (203 +/- 42 ml CO2/kg). We conclude that orally administered [13C]bicarbonate can be used to assess CO2 transport dynamics. The data do not support the hypothesis of lower CO2 stores under resting conditions in children.
Oxygen uptake was measured using a mass spectrometer system in 12 patients scheduled for abdominal surgery who intraoperatively were mechanically ventilated with 50% nitrous oxide and given continuous intravenous infusions of methohexital (3.5 mg.kg-1.h-1) plus repeated epidural injections of lidocaine. At the end of the surgical procedure, meperidine (0.7 mg/kg) was epidurally injected in six patients (group A). The other six patients (group B) received no epidural injections during the first 2 h after surgery. Intraoperatively, oxygen uptake decreased in both groups by an average of 28%. Within the first two postoperative hours, clear-cut differences among the two groups arose. Patients in group A had smoother increases in oxygen uptake and core temperatures, greater cardiovascular stability as reflected by the rate-pressure product, and no visible shivering. We suggest that epidural meperidine given immediately at the end of a surgical procedure might be beneficial, especially, perhaps, in patients with impaired cardiac function.
Oxygen consumption (VO2, ml min−1) and carbon dioxide elimination (VCO2, ml min−1), minute ventilation (VE), tidal volume (VT), rate of ventilation (f) and end-tidal carbon dioxide concentration (E' co2 %) were measured in 38 infants and children (body weights 3.6–25 kg). Four children (body weight < 5 kg) had congenital heart
malformations and were studied during controlled mechanical ventilation, where-as the remainder (n = 34) who were healthy,
breathed spontaneously. Anaesthesia was maintained with oxygen in air (FlO2 0.45) and halothane through a non-rebreathing circuit. Minute ventilation was measured by pneumo-tachography, E'CO2 with an in-line infra-red carbon dioxide meter and gas concentrations with a mass spectrometer. There were no differences
in VO2 and VCO2 between children with and without heart disease. VO2 was related to body weight by the equation: VO2 = 5.0×kg+19.8 (r = 0.94) and VCO2 to body weight by the equation: VCO2 = 4.8×kg+6.4 (r = 0.94). There were no differences between VO2 or VCO2 before and after the start of surgery. In 11 of 21 patients weighing less than 10 kg, a reduced VCO2 was noted, giving respiratory quotients of less than 0.7. It is speculated that this age-dependent variation of VCO2 may result from partial inhibition of lipolysis in brown adipose tissue produced by halothane.
Carbon dioxide elimination (VCO2) was measured in 186 anaesthetized, spontaneously breathing infants and children with body weights ranging from 2.8 to 26.5 kg. They all underwent minor paediatric surgical procedures. The influence on VCO2 of age, operation, premedication, caudal anaesthesia, and different volatile anaesthetic agents was investigated. The volume of exhaled gas, during three- to five-minute collection periods, was measured and the fraction of exhaled CO2 was determined by a CO2 meter. Under basal anaesthetic conditions, the average output before operation followed the equation: VCO2 (ml.min-1) = -1.25X + 13.0X2, in which X = lne (body weight, kg). Expressed on a weight basis, the youngest infants (weighing less than 5 kg) had the lowest VCO2. Higher values were measured up to a body weight of 10 kg above which a negative correlation occurred between VCO2 (ml.min-1.kg-1) and body weight. The use of premedication resulted in a more variable VCO2 during operations than when opioid premedication was not used. The combination of a general anaesthetic and caudal anaesthesia stabilized VCO2. Also, children anaesthetized with halothane had a higher VCO2 than those who were anaesthetized with enflurane or isoflurane (P less than 0.05). The variable VCO2 emphasizes the need for increased monitoring of VCO2 during routine anaesthesia and operation in infants and children.
Thirty-three patients undergoing elective myocardial revascularization were prospectively randomized into two study groups (Group S and Group P) to permit evaluation of the effects of shivering on oxygen consumption per minute (VO2), carbon dioxide production per minute (VCO2), and hemodynamic performance. Group S was allowed to shiver during the postoperative rewarming period, and Group P received hourly injections of pancuronium bromide and Metubine (metocurine) sulfate with sedation to block the shivering response. Group S demonstrated significantly higher increases in VO2 and VCO2, lower systolic blood pressure and mixed venous oxygen saturation, and a greater use of inotropic support than the patients in Group P. Suppression of the shivering response minimized increases in VO2 and VCO2, improved hemodynamic stability, and resulted in a decreased need for inotropic support.
Meperidine has been used to suppress postanesthesia shivering. However, its efficacy to date has only been assessed by observation of visible shivering. We measured the effect of meperidine on oxygen consumption (VO2), carbon dioxide production (VCO2) and pulmonary gas exchange in 14 otherwise healthy patients shivering after general anesthesia. Meperidine successfully suppressed visible shivering in all patients and was associated with significant decreases in VO2, and VCO2 and minute ventilation (VE) but not with return to basal levels. Arterial PCO2 levels remained unchanged at normal, whereas significant improvements occurred in pH and bicarbonate levels. Meperidine is an effective method of reducing the elevated metabolic demand of shivering.
This study examines the oxygen consumption (VO2) and carbon dioxide production (VCO2) occurring before, during, and after cardiopulmonary bypass (CPB) and whether they correlate with changes in cardiac output. Twenty-three patients undergoing open heart surgery were studied. Group 1 (N = 11) received fentanyl citrate, 50 micrograms/kg, intravenously during the induction of anesthesia. Group 2 (N = 12) received 100 micrograms/kg of fentanyl citrate intravenously. We measured VO2, VCO2, as well as hemodynamic and biochemical factors. Initial statistical analyses failed to show any differences in the VO2, VCO2, hemodynamic, or biochemical factors between groups 1 and 2. Therefore, the data from both groups were combined. In comparing the average (for all data) of the post-CPB with the pre-CPB periods in both groups for the metabolic factors, there were 9.0%, 11.5%, and 2.4% increases in the VO2, VCO2, and respiratory quotient, respectively. There was an 80% increase in total serum lactate levels seen in the post-CPB periods when compared with the pre-CPB periods. Serum triglyceride and free fatty acid levels measured in the post-CPB period decreased 39% and 25%, respectively, when compared with the pre-CPB periods. Although there were no changes in the cardiac outputs following CPB, the post-CPB periods showed a 37% increase in central venous pressure when compared with the pre-CPB periods. These data suggest that although there are significant metabolic and biochemical sequelae to CPB, the modest increases in post-CPB VO2, and VCO2 did not affect cardiac output following cardiovascular surgery. Increasing doses of narcotic do not have an effect on those relationships.
Improvement in postoperative pulmonary mechanics with epidural analgesia has been described. Data on the hemodynamic effects of this technique are absent from the surgical literature. To provide such data we have evaluated two groups of patients undergoing aortic reconstruction: group I (n = 25), general anesthesia and group II (n = 6), general anesthesia with adjunctive epidural analgesia. The groups were comparable preoperatively as judged by the incidence of cardiac history, preoperative ejection fraction, and measured hemodynamic parameters. Postoperatively there were no significant differences in the pressure-related parameters; however, rate-related factors including heart rate and double product were significantly decreased in group II with no reduction in cardiac index. Postoperative increases in total body oxygen consumption were also markedly attenuated by epidural analgesia. Epidural analgesia reduces the hemodynamic demands on the heart after major surgery and is a useful adjunct, especially in patients with coronary artery disease.
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.
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.
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)
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.
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.
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.
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.
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.
Surgery performed during general anaesthesia has been shown to induce an increase in oxygen consumption. It is postulated that this response might be influenced by the surgical procedure performed. Metabolic gas exchange was continuously measured by indirect calorimetry for 30 min in 45 patients undergoing four different surgical procedures during general anaesthesia with propofol/fentanyl/vecuronium as follows: elective laparotomy (n = 13); emergency laparotomy (n = 10); elective knee joint arthroscopy (n = 10); gynaecological laparoscopy (n = 12). A significant increase in oxygen consumption occurred in all the groups within 5 min of skin incision. The greatest increase was seen in those undergoing elective laparotomy (+13%, p < 0.001 at 15 min), with similar smaller increases in the other three groups (+6 to +7%, p < 0.05). Surgery induced an increase in systolic blood pressure in all four groups, being most pronounced in the elective laparotomy group (+47% 15 min after skin incision, p < 0.001). These patients also experienced a significant rise in heart rate (+14%, p < 0.01 at 15 min). Carbon dioxide production increased both in the laparoscopy patients (+9%, p < 0.05) and, transiently, in the elective laparotomy group (+6% at 15 min, p < 0.01), but decreased in the other two groups (-7 to -15%, p < 0.05). Surgery induced a parallel increase in both oxygen consumption and systolic blood pressure in all types of operations, although the magnitude varied. Continuous measurement of metabolic gas exchange may provide an additional method of evaluating the metabolic response to different types of surgery.
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.
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.
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.
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.
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)