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Hypermetabolism after coronary artery bypass
J THORAC CARDIOVASC SURG 1991;101:598-600
Hypermetabolism after coronary artery bypass We measured the changes in energy expenditure in the early postoperative phase after coronary artery bypass operations and the ventilatory response to the increased demand for respiratory gas exchange. Breathing pattern and gas exchange were measured noninvasively by respiratory inductive plethysmography and indirect calorimetry with a canopy. Eighteen patients were studied after weaning from mechanical ventilation. Energy expenditure increased by 18.3%, which is comparable to the response to major injury. Carbon dioxide production increased from 162 ± 20 to 195 ± 36 mljmin in the supine position (p < 0.001~ and similar changes were observed in the half-sitting position. Arterial carbon dioxide tension increased marginally (37.5 ± 2.96 rom Hg preoperatively versus 39.7 ± 4.87 rom Hg postoperatively; p < O.O~ while oxygen tension decreased from 89.9 ± 17.3 rom Hg to 62.9 ± 13.4 rom Hg (p < 0.001). Minute ventilation increased by 34% in the supine position (p < 0.01) and by 28 % in the half-sitting position (p < O.~ while tidal volume remained unchanged. We conclude that coronary artery bypass operations induce hypermetabolism and substantially increase ventilation and risk of arterial hypoxemia during the phase of compromised cardiovascular reserves.
Ham Tulla, MD, Jukka Takala, MD, PhD, Esko Alhava, MD, PhD, Heikki Huttunen, MD, PhD, and Aarno Karl, MD, PhD, Kuopio, Finland
Increased oxygen consumption and carbon dioxide production caused by postoperative hypermetabolism after coronary artery bypass operations impose demand for increased performance of the cardiorespiratory system, and myocardial and respiratory reserves are compromised during the early postoperative recovery.' Factors that may modify the postoperative energy expenditure after cardiac operations include increased work of breathing.? the metabolic requirements of recovery from hypothermia.' and anesthetic techniques used to minimize the myocardial stress." Elective abdominal operations increase the energy expenditure by 0% to 10%.5 The effect of coronary artery bypass operations on energy expenditure has not been systematically documented. The aim of the study was to measure the effect of cardiac operations on energy metabolism and to document the changes in breathing pattern used to compensate for the increased demand for gas exchange.
From the Critical Care Research Program and the Departments of Surgery and Anesthesiology, Kuopio University Central Hospital, Kuopio, Finland. Received for publication Nov. 1,1989. Accepted for publication April 10, 1990. Addressfor reprints:Jukka Takala, MD, Associate Professor of Anesthesiology, Critical Care Research Program, Intensive Care Unit, KuopioUniversity Central Hospital, SF-7021O Kuopio, Finland.
12/1/21571
598
Patients and methods We measured respiratory gas exchange and breathing pattern in 18 patients before and after elective coronary artery grafting operations (Table I). The study was approved by the ethical committee of the hospital, and informed consent was obtained from each patient. The measurements were made both in the supine position and with the head of the bed elevated 30 degrees. On the day before operation the preoperative measurement was performed in the afternoon after 4 to 6 hours' fasting, and the patients were kept supine for a minimum of 15 minutes before the measurements were started. The postoperative measurements were done on the first postoperative day in the intensive care unit 15.0 ± 4.8 hours after weaning from mechanical ventilation. Supplementary oxygen was withdrawn during the measurement, and no analgesics were given 1 hour preceding the measurement. The respiratory gas exchange was studied by an indirect calorimetry device (Deltatrac TM metabolic monitor, Datex/Instrumentarium Corp., Helsinki, Finland). The Deltatrac monitor is an open system indirect calorimetry device for measurements of carbon dioxide production ("Ve02) and oxygen consumption (V0 2). Energy expenditure is calculated from the measured rates or vco, and V0 2. Measurements during spontaneous breathing are made by suctioning air through a light, transparent canopy, placed over the head of the patient, at a known, constant rate of approximately 40 L/min. The difference between the inspired and expired oxygen fractions (Fi02, FOO2) is measured with a fastresponse, paramagnetic differential oxygen sensor. The expired carbon dioxide fraction (Fec02) is measured with an infrared carbon dioxide sensor. A microcomputer controls a set of magnetic valves for the automatic control of the absolute Fi02 and Fie02 and gas analyzer baselines. The device has been extensively validated in our laboratory, and relative error of Ve02 and V02 is within ± 5%.6 The gas exchange monitor was calibrated
Volume 101 Number 4 April 1991
before each study with a standardized, certified gas mixture (oxygen and carbon dioxide). The first 10 minutesof each measurement were discarded, and data collection was started after achieving a stable gas exchange. Data were collected for 20 minutes in each position. The expected energy expenditurewas calculated according to the Harris-Benedict formula," Simultaneously with the gas exchange measurement the breathing pattern was studied with a respiratory inductive plethysmograph (RespigraphTM NIMS, Miami Beach,Fla.).8 Therespiratory inductiveplethysmographconsistsof two elastictransducer bands wornaround the rib cage and the abdomen formeasurement of motion and volumechanges in the respiratory system. The signalsof the two transducers are electronicallysummed to givea third signal that is proportionalto tidal volume (VT). The respiratory inductive plethysmograph was calibrated semiquantitatively by firstcollectingbaselinebreathing 5 minutes and thereafter by calibration against a known volume reference. A heated pneumotachometer (Hans Rudolf, Inc., Kansas City, Mo.) was used as a volumereference,and at least five breaths were sampled for calibration. The calibration was checked witha validationand acceptedonlyif the measured error ofsampleof breaths was in the range of ± 5%.9 Breathing pattern was measured for 20 minutes in each position. Measurements included frequency, tidal volume (VT), and minute ventilation (VE). No data were obtained from two patients in 3D-degree position. Afterthe measurements arterial blood was sampled for the analysis of blood gases with a standard blood gas analyzer (IL 1302, Instrumentation Laboratories, Lexington, Mass.) Standardanesthesia technique with high-dose fentanyl was used inall patients. Postoperatively the patients were treated in theintensive care unit for 2 days. The patients were mechanically ventilated until the first postoperative morning. No oral intake exceptwater was allowedbefore the postoperativestudy, and allpatientsreceived intravenousdextrose infusionat a rate of400 kcaljday. Resultsfrom the properativeand postoperative measurements in each positionand between the positions were compared by the paired t test. Differences were considered as statistically significant, when the p value was less than 0.05.
Results Gasexchange. There were only minor changes in gas exchange betweenthe supine and the 30-degreepositions, but when the preoperative and the postoperative measurements werecompared marked changes were found in most parameters. V C02 and V0 2 increased significantly by 19.3% and 17.3%, respectively (p < 0.001) (Table II), whereas respiratoryquotient (RQ) remained unchanged. Energy expenditure postoperatively was 18.3% higher than preoperatively (p < 0.001). The measured energy expenditure was 96% of the expected preoperative measurement and 114% postoperatively. The preoperative energy expenditure (normalized for body weight) was similar in male and female patients (20 ± 2.4 versus 19.8 ± 2.9kcaljkgjday, NS*). The postoperativeenergy expenditure was slightly higher in male patients (24.7 ± 3.1 versus 21.4 ± 2.2 kcaljkgjday; p < 0.01). *NS = Not significant.
Hypermetabolism after coronary artery bypass 5 9 9
Table I. Patient characteristics Patients Age (yr) Weight (kg) Body surface area (m-) NYHA classification (I-IV) Operation time(min) Interval between operation and postoperative study (hr) Range (hr) Interval between extubation and postoperative study (hr) Range (hr)
9 M;9 F 55.9 ± 5.1 69.8 ± 11.8 1.75 ± 0.15 2/1, 13/III, 3/1V 414 ± 75 28.3 ± 4.9 23.0-41.0 15.0 ± 4.8 8.7-23.9
NYHA, New York Heart Association.
Arterial blood gas analysis. Arterial oxygen tension was reduced from 89.9 ± 17.3 mm Hg to 62.9 ± 13.4 mm Hg (p < 0.001), whereas arterial carbon dioxide tension increased from 37.5 ± 2.96 mm Hg to 39.7 ± 4.87 mm Hg (p < 0.05) postoperatively. Breathing pattern. Breathing frequency increased postoperatively in both positions(p < 0.001) (Table III). VT remained practically unchanged. Accordingly, VE increased and was higher in the 3O-degree position than in the supine positionboth in the preoperative and in the postoperative measurements. Discussion Modem equipment has made bedside noninvasive studiesof gas exchangeand breathing patterns possiblein the early postoperativephase when the cardiorespiratory status is compromised.We found marked hypermetabolism after weaning from the respirator early after coronary artery bypass operations. This has not been documented before. The increment of energy expenditure is similar to the responseto radical cystectomy or multiple injury.S,1O Factors contributing to the hypermetabolism include metabolic demand for the recovery from hypothermia;' the neuroendocrine response to operative trauma.U: 12 and the increased work of breathing.I Our results clearly demonstrate that although efforts have been focusedon reducing the operative stress on the cardiovascular system by "stress-free" anesthesia, for example.P the immediate postoperativephase is characterized by metabolic changes comparable to stress after major injury. Hypermetabolism was associated with marked respiratory changes. The demand for alveolar ventilation was increased because of increased VC02. The ventilatory responseto the demand was to increase VE by higher frequency with an unchanged VT. The resulting alveolar ventilationwas sufficient to compensate for the increased VC02 because arterial carbon dioxide tension was relatively well maintained. The slight, but significant,
600
The Journal of Thoracic and Cardiovascular Surgery
Tulia et al.
Table II. Gas exchange studies Postoperative
Preoperative
odegrees VC02 (ml/min) v02 (ml/rnin) EE (kcaljday)
RQ
162 203 1381 0.82
± ± ± ±
30 degrees
20 23 157 0.08
165 202 1381 0.82 37.5 89.9
PaC02 (mm Hg) Pa02 (mm Hg)
± ± ± ± ± ±
22 27 188 0.05 2.96 17.3
odegrees 195 239 1639 0.82
30 degrees
± 36* ± 42* ± 295* ± 0.05
195 236 1628 0.82 39.7 62.9
± 35* ± 44* ± 301*
± 0.06 ± 4.87t
± 13.4*
Ve02. Carbon dioxide production; V0 2• oxygen consumption; EE, energy expenditure; RQ, respiratory quotient; Pae02, arterial carbon dioxide tension; Pa02, arterial oxygen tension . •p < 0.001.
tp < 0.05.
Table III. Breathing pattern Before operation
Frequency (breaths/min) VT (ml) VE (Lj'min)
After operation
odegrees
30 degrees
odegrees
30 degrees
11.6 ± 3.6 527 ± 170 5.73 ± 1.37
12.8 ± 3.3 534 ± 167 6.36 ± 1.14t
16.7 ± 3.9* 455 ± 153 7.67 ± 3.08t
17.2 ± 3.6* 476 ± 153 8.15 ± 3.22§t
VT, Tidal volume; VE. minute ventilation. *p < 0.001 (before versus after operation). tp < 0.05 (0 degrees versus 30 degrees). :j:p < 0.01 (before versus after operation). §p < 0.05 (before versus after operation).
increase in arterial carbon dioxide tension was probably due to postanestheticdepression of the respiratorycenter. Regardless of the increased YE, marked hypoxemia was observed in the postoperative state. The impairedarterial oxygenationin conjunctionwithincreasedYEand normal arterial carbon dioxidetensionis likelydue to altered distribution of ventilationand perfusionin the lung and formation of atelectasis.Worsenedmechanicalpropertiesof the lungs and the chest wall increasethe work of breathing and probably contribute to impaired gas exchange. The postoperative hypermetabolism, together with the changes in breathing pattern and gas exchange,imposes additional stress on patients during the early postoperative recovery from coronary artery bypass operations. REFERENCES 1. Chiara 0, Giomarelli PP, Biagioli B, Rosi R, Gattinoni L. Hypermetabolic response after hypothermic cardiopulmonary bypass. Crit Care Med 1987;15:995-1000. 2. Wilson RS, Sullivan SF, Maim JR, Bowman FO Jr. The oxygen cost of breathing following anesthesia and cardiac surgery. Anesthesiology 1973;39:387-93. 3. Rodriguez JL, Weissman Ch, Damask MC, Askanazi J, Hyman AL, Kinney JM. Physiologic requirements during rewarming: suppression of the shivering response. Crit Care Med 1983;11:490. 4. Paton Be. Intraoperative myocardial preservation. Adv Cardiol 1979;26:86-93.
5. Kinney JM, Duke JH Jr, Long CL, Gump FE. Tissue fuel and weight loss after injury. Proceedings from symposium on the pathology of trauma. J Clin Pathol·1970;4:65-72. 6. Takala J, Keinanen 0, Vaisanen P, Kari A. Measurement of gas exchange in intensive care: laboratory and clinical validation of a new device. Crit Care Med 1989;10:1041-7. 7. Harris JA, Benedict FG. A biometric study of basal metabolism in man. Publication No. 297, Carnegie Institute of Washington, D.C., 1919. 8. Cohn MA, Rao ASY, Broudy M, et al. The respiratory inductive plethysmograph: a new non-invasive monitor of respiration. Bull Eur Physiopathol Respir 1982;18:64358. 9. Sackner MA, Watson H, Belsito AS, et al. Calibration of respiratory inductive plethysmography during natural breathing. J Appl PhysioI1989;66:41O-20. 10. Hensle TW, Askanazi J, Rosenbaum LH, Bernstein G, Kinney JM. Metabolic changes associated with radical cystectomy. J UroI1985;134:1032-6. 11. Cryer PE. Physiology and pathophysiology of the human sympatho-adrenal neuroendocrine system. N Engl J Med 1980;303:436-44. 12. Hine IP, Wood WG, Mainwaring-Burton JM, et al. The adrenergic response to surgery involving cardiopulmonary bypass, as measured by plasma and urinary catecholamine concentrations. Br J Anaesth 1976;48:355-62. 13. Bovill JG, Sebel PS, Stanley TH. Opioid analgesics in anesthesia: with special reference to their use in cardiovascular anesthesia. Anesthesiology 1984;61:731-55.
Hypermetabolism after coronary artery bypass We measured the changes in energy expenditure in the early postoperative phase after coronary artery bypass operations and the ventilatory response to the increased demand for respiratory gas exchange. Breathing pattern and gas exchange were measured noninvasively by respiratory inductive plethysmography and indirect calorimetry with a canopy. Eighteen patients were studied after weaning from mechanical ventilation. Energy expenditure increased by 18.3%, which is comparable to the response to major injury. Carbon dioxide production increased from 162 ± 20 to 195 ± 36 mljmin in the supine position (p < 0.001~ and similar changes were observed in the half-sitting position. Arterial carbon dioxide tension increased marginally (37.5 ± 2.96 rom Hg preoperatively versus 39.7 ± 4.87 rom Hg postoperatively; p < O.O~ while oxygen tension decreased from 89.9 ± 17.3 rom Hg to 62.9 ± 13.4 rom Hg (p < 0.001). Minute ventilation increased by 34% in the supine position (p < 0.01) and by 28 % in the half-sitting position (p < O.~ while tidal volume remained unchanged. We conclude that coronary artery bypass operations induce hypermetabolism and substantially increase ventilation and risk of arterial hypoxemia during the phase of compromised cardiovascular reserves.
Ham Tulla, MD, Jukka Takala, MD, PhD, Esko Alhava, MD, PhD, Heikki Huttunen, MD, PhD, and Aarno Karl, MD, PhD, Kuopio, Finland
Increased oxygen consumption and carbon dioxide production caused by postoperative hypermetabolism after coronary artery bypass operations impose demand for increased performance of the cardiorespiratory system, and myocardial and respiratory reserves are compromised during the early postoperative recovery.' Factors that may modify the postoperative energy expenditure after cardiac operations include increased work of breathing.? the metabolic requirements of recovery from hypothermia.' and anesthetic techniques used to minimize the myocardial stress." Elective abdominal operations increase the energy expenditure by 0% to 10%.5 The effect of coronary artery bypass operations on energy expenditure has not been systematically documented. The aim of the study was to measure the effect of cardiac operations on energy metabolism and to document the changes in breathing pattern used to compensate for the increased demand for gas exchange.
From the Critical Care Research Program and the Departments of Surgery and Anesthesiology, Kuopio University Central Hospital, Kuopio, Finland. Received for publication Nov. 1,1989. Accepted for publication April 10, 1990. Addressfor reprints:Jukka Takala, MD, Associate Professor of Anesthesiology, Critical Care Research Program, Intensive Care Unit, KuopioUniversity Central Hospital, SF-7021O Kuopio, Finland.
12/1/21571
598
Patients and methods We measured respiratory gas exchange and breathing pattern in 18 patients before and after elective coronary artery grafting operations (Table I). The study was approved by the ethical committee of the hospital, and informed consent was obtained from each patient. The measurements were made both in the supine position and with the head of the bed elevated 30 degrees. On the day before operation the preoperative measurement was performed in the afternoon after 4 to 6 hours' fasting, and the patients were kept supine for a minimum of 15 minutes before the measurements were started. The postoperative measurements were done on the first postoperative day in the intensive care unit 15.0 ± 4.8 hours after weaning from mechanical ventilation. Supplementary oxygen was withdrawn during the measurement, and no analgesics were given 1 hour preceding the measurement. The respiratory gas exchange was studied by an indirect calorimetry device (Deltatrac TM metabolic monitor, Datex/Instrumentarium Corp., Helsinki, Finland). The Deltatrac monitor is an open system indirect calorimetry device for measurements of carbon dioxide production ("Ve02) and oxygen consumption (V0 2). Energy expenditure is calculated from the measured rates or vco, and V0 2. Measurements during spontaneous breathing are made by suctioning air through a light, transparent canopy, placed over the head of the patient, at a known, constant rate of approximately 40 L/min. The difference between the inspired and expired oxygen fractions (Fi02, FOO2) is measured with a fastresponse, paramagnetic differential oxygen sensor. The expired carbon dioxide fraction (Fec02) is measured with an infrared carbon dioxide sensor. A microcomputer controls a set of magnetic valves for the automatic control of the absolute Fi02 and Fie02 and gas analyzer baselines. The device has been extensively validated in our laboratory, and relative error of Ve02 and V02 is within ± 5%.6 The gas exchange monitor was calibrated
Volume 101 Number 4 April 1991
before each study with a standardized, certified gas mixture (oxygen and carbon dioxide). The first 10 minutesof each measurement were discarded, and data collection was started after achieving a stable gas exchange. Data were collected for 20 minutes in each position. The expected energy expenditurewas calculated according to the Harris-Benedict formula," Simultaneously with the gas exchange measurement the breathing pattern was studied with a respiratory inductive plethysmograph (RespigraphTM NIMS, Miami Beach,Fla.).8 Therespiratory inductiveplethysmographconsistsof two elastictransducer bands wornaround the rib cage and the abdomen formeasurement of motion and volumechanges in the respiratory system. The signalsof the two transducers are electronicallysummed to givea third signal that is proportionalto tidal volume (VT). The respiratory inductive plethysmograph was calibrated semiquantitatively by firstcollectingbaselinebreathing 5 minutes and thereafter by calibration against a known volume reference. A heated pneumotachometer (Hans Rudolf, Inc., Kansas City, Mo.) was used as a volumereference,and at least five breaths were sampled for calibration. The calibration was checked witha validationand acceptedonlyif the measured error ofsampleof breaths was in the range of ± 5%.9 Breathing pattern was measured for 20 minutes in each position. Measurements included frequency, tidal volume (VT), and minute ventilation (VE). No data were obtained from two patients in 3D-degree position. Afterthe measurements arterial blood was sampled for the analysis of blood gases with a standard blood gas analyzer (IL 1302, Instrumentation Laboratories, Lexington, Mass.) Standardanesthesia technique with high-dose fentanyl was used inall patients. Postoperatively the patients were treated in theintensive care unit for 2 days. The patients were mechanically ventilated until the first postoperative morning. No oral intake exceptwater was allowedbefore the postoperativestudy, and allpatientsreceived intravenousdextrose infusionat a rate of400 kcaljday. Resultsfrom the properativeand postoperative measurements in each positionand between the positions were compared by the paired t test. Differences were considered as statistically significant, when the p value was less than 0.05.
Results Gasexchange. There were only minor changes in gas exchange betweenthe supine and the 30-degreepositions, but when the preoperative and the postoperative measurements werecompared marked changes were found in most parameters. V C02 and V0 2 increased significantly by 19.3% and 17.3%, respectively (p < 0.001) (Table II), whereas respiratoryquotient (RQ) remained unchanged. Energy expenditure postoperatively was 18.3% higher than preoperatively (p < 0.001). The measured energy expenditure was 96% of the expected preoperative measurement and 114% postoperatively. The preoperative energy expenditure (normalized for body weight) was similar in male and female patients (20 ± 2.4 versus 19.8 ± 2.9kcaljkgjday, NS*). The postoperativeenergy expenditure was slightly higher in male patients (24.7 ± 3.1 versus 21.4 ± 2.2 kcaljkgjday; p < 0.01). *NS = Not significant.
Hypermetabolism after coronary artery bypass 5 9 9
Table I. Patient characteristics Patients Age (yr) Weight (kg) Body surface area (m-) NYHA classification (I-IV) Operation time(min) Interval between operation and postoperative study (hr) Range (hr) Interval between extubation and postoperative study (hr) Range (hr)
9 M;9 F 55.9 ± 5.1 69.8 ± 11.8 1.75 ± 0.15 2/1, 13/III, 3/1V 414 ± 75 28.3 ± 4.9 23.0-41.0 15.0 ± 4.8 8.7-23.9
NYHA, New York Heart Association.
Arterial blood gas analysis. Arterial oxygen tension was reduced from 89.9 ± 17.3 mm Hg to 62.9 ± 13.4 mm Hg (p < 0.001), whereas arterial carbon dioxide tension increased from 37.5 ± 2.96 mm Hg to 39.7 ± 4.87 mm Hg (p < 0.05) postoperatively. Breathing pattern. Breathing frequency increased postoperatively in both positions(p < 0.001) (Table III). VT remained practically unchanged. Accordingly, VE increased and was higher in the 3O-degree position than in the supine positionboth in the preoperative and in the postoperative measurements. Discussion Modem equipment has made bedside noninvasive studiesof gas exchangeand breathing patterns possiblein the early postoperativephase when the cardiorespiratory status is compromised.We found marked hypermetabolism after weaning from the respirator early after coronary artery bypass operations. This has not been documented before. The increment of energy expenditure is similar to the responseto radical cystectomy or multiple injury.S,1O Factors contributing to the hypermetabolism include metabolic demand for the recovery from hypothermia;' the neuroendocrine response to operative trauma.U: 12 and the increased work of breathing.I Our results clearly demonstrate that although efforts have been focusedon reducing the operative stress on the cardiovascular system by "stress-free" anesthesia, for example.P the immediate postoperativephase is characterized by metabolic changes comparable to stress after major injury. Hypermetabolism was associated with marked respiratory changes. The demand for alveolar ventilation was increased because of increased VC02. The ventilatory responseto the demand was to increase VE by higher frequency with an unchanged VT. The resulting alveolar ventilationwas sufficient to compensate for the increased VC02 because arterial carbon dioxide tension was relatively well maintained. The slight, but significant,
600
The Journal of Thoracic and Cardiovascular Surgery
Tulia et al.
Table II. Gas exchange studies Postoperative
Preoperative
odegrees VC02 (ml/min) v02 (ml/rnin) EE (kcaljday)
RQ
162 203 1381 0.82
± ± ± ±
30 degrees
20 23 157 0.08
165 202 1381 0.82 37.5 89.9
PaC02 (mm Hg) Pa02 (mm Hg)
± ± ± ± ± ±
22 27 188 0.05 2.96 17.3
odegrees 195 239 1639 0.82
30 degrees
± 36* ± 42* ± 295* ± 0.05
195 236 1628 0.82 39.7 62.9
± 35* ± 44* ± 301*
± 0.06 ± 4.87t
± 13.4*
Ve02. Carbon dioxide production; V0 2• oxygen consumption; EE, energy expenditure; RQ, respiratory quotient; Pae02, arterial carbon dioxide tension; Pa02, arterial oxygen tension . •p < 0.001.
tp < 0.05.
Table III. Breathing pattern Before operation
Frequency (breaths/min) VT (ml) VE (Lj'min)
After operation
odegrees
30 degrees
odegrees
30 degrees
11.6 ± 3.6 527 ± 170 5.73 ± 1.37
12.8 ± 3.3 534 ± 167 6.36 ± 1.14t
16.7 ± 3.9* 455 ± 153 7.67 ± 3.08t
17.2 ± 3.6* 476 ± 153 8.15 ± 3.22§t
VT, Tidal volume; VE. minute ventilation. *p < 0.001 (before versus after operation). tp < 0.05 (0 degrees versus 30 degrees). :j:p < 0.01 (before versus after operation). §p < 0.05 (before versus after operation).
increase in arterial carbon dioxide tension was probably due to postanestheticdepression of the respiratorycenter. Regardless of the increased YE, marked hypoxemia was observed in the postoperative state. The impairedarterial oxygenationin conjunctionwithincreasedYEand normal arterial carbon dioxidetensionis likelydue to altered distribution of ventilationand perfusionin the lung and formation of atelectasis.Worsenedmechanicalpropertiesof the lungs and the chest wall increasethe work of breathing and probably contribute to impaired gas exchange. The postoperative hypermetabolism, together with the changes in breathing pattern and gas exchange,imposes additional stress on patients during the early postoperative recovery from coronary artery bypass operations. REFERENCES 1. Chiara 0, Giomarelli PP, Biagioli B, Rosi R, Gattinoni L. Hypermetabolic response after hypothermic cardiopulmonary bypass. Crit Care Med 1987;15:995-1000. 2. Wilson RS, Sullivan SF, Maim JR, Bowman FO Jr. The oxygen cost of breathing following anesthesia and cardiac surgery. Anesthesiology 1973;39:387-93. 3. Rodriguez JL, Weissman Ch, Damask MC, Askanazi J, Hyman AL, Kinney JM. Physiologic requirements during rewarming: suppression of the shivering response. Crit Care Med 1983;11:490. 4. Paton Be. Intraoperative myocardial preservation. Adv Cardiol 1979;26:86-93.
5. Kinney JM, Duke JH Jr, Long CL, Gump FE. Tissue fuel and weight loss after injury. Proceedings from symposium on the pathology of trauma. J Clin Pathol·1970;4:65-72. 6. Takala J, Keinanen 0, Vaisanen P, Kari A. Measurement of gas exchange in intensive care: laboratory and clinical validation of a new device. Crit Care Med 1989;10:1041-7. 7. Harris JA, Benedict FG. A biometric study of basal metabolism in man. Publication No. 297, Carnegie Institute of Washington, D.C., 1919. 8. Cohn MA, Rao ASY, Broudy M, et al. The respiratory inductive plethysmograph: a new non-invasive monitor of respiration. Bull Eur Physiopathol Respir 1982;18:64358. 9. Sackner MA, Watson H, Belsito AS, et al. Calibration of respiratory inductive plethysmography during natural breathing. J Appl PhysioI1989;66:41O-20. 10. Hensle TW, Askanazi J, Rosenbaum LH, Bernstein G, Kinney JM. Metabolic changes associated with radical cystectomy. J UroI1985;134:1032-6. 11. Cryer PE. Physiology and pathophysiology of the human sympatho-adrenal neuroendocrine system. N Engl J Med 1980;303:436-44. 12. Hine IP, Wood WG, Mainwaring-Burton JM, et al. The adrenergic response to surgery involving cardiopulmonary bypass, as measured by plasma and urinary catecholamine concentrations. Br J Anaesth 1976;48:355-62. 13. Bovill JG, Sebel PS, Stanley TH. Opioid analgesics in anesthesia: with special reference to their use in cardiovascular anesthesia. Anesthesiology 1984;61:731-55.