Carbon dioxide tensions during anesthesia in the prone position.
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Biomedical subjects
Publications and source records attributed to R W Wahba.
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PURPOSE: A direct relationship between cardiac index (CI) and end-tidal PCO2 (PETCO2) shortly after decreased CI was reported, but arterial PCO2 was not measured. Our purpose was to supply the missing information on the immediate effects of alterations in CI on PaCO2, PETCO2 and thus on Pa-PETCO2. METHODS: We measured CI, Pa and PETCO2 and calculated the difference in 20 patients scheduled for elective heart surgery just before and immediately after the sternotomy. The measurements were made using standard methods: thermodilution for CI, infra-red and blood gas analysis for PET and PaCO2 respectively. The results were analyzed by linear regression. RESULTS: Very significant, direct and immediate changes in PET and PaCO2 with changes in CI were noted. The ratios were 3.8 and 4.2 mmHg L-1 respectively. The calculated values of r were 0.75 (P < 0.001) for PETCO2 and 0.64 (P < 0.005) for PaCO2. The magnitude of individual change in PCO2 varied considerably such that the alterations in Pa-PETCO2 were also variable, without any correlation with the direction or magnitude of change in CI. CONCLUSION: Our results explain the reported wide variations in Pa-PETCO2 that accompany perturbations of cardiac output. Our observations pertain to the unsteady state only. The results suggest that PETCO2 can be used to estimate changes in CI with a reasonable degree of confidence.
PURPOSE: The aim of this study was to determine if the literature supported the assumption that the values and changes in end-tidal PCO2 (PETCO2) during anaesthesia accurately reflect the values and changes in arterial PCO2 (PaCO2) is tenable. METHODS: The information was obtained by (a) a Medline literature search and the appropriate references quoted in the list generated; (b) appropriate abstracts in recent issues of the annual meeting supplements of Anesth Analg, Anesthesiology, Br J Anaesth and Can J Anaesth. We specifically sought information obtained during major operations, in sick patients, and reports of serial measurements. The information obtained is summarized in graphic form, with a discussion of the mechanisms and clinical implications. RESULTS: (1) Patients with systemic disease, or when placed in the lateral position, or with haemodynamic instability have an increased Pa-PETCO2 gradient. The values during surgery are probably due to marked alterations of ventilation: perfusion relationships. (2) In a number of reports, the gradient varied widely during the procedure. (3) The gradient may be reduced due to an alteration of the configuration of the alveolar plateau. (4) The magnitude and direction of change in PaCO2 and PETCO2 can be disproportionate and in the opposite direction. CONCLUSION: End-tidal PCO2 is often not indicative of PaCO2. Also, changes in PETCO2 do not always accurately indicate the direction and extent of the change in PaCO2.
PURPOSE: This article examines and summarizes the published reports dealing with subcutaneous emphysema, pneumothorax and carbon dioxide (CO2) embolism during laparoscopic upper abdominal surgery. The purpose is to describe the expected clinical picture, the differential diagnosis and the management of these complications. SOURCE: The information was obtained from a Medline literature search and the annual meeting supplements of Anesthesiology, Anesth Analg, Br J Anaesth and Can J Anaesth. PRINCIPAL FINDINGS: An abrupt increase in PETCO2 is the first sign of subcutaneous emphysema and of pneumothorax. Desaturation and increased airway pressure occur with pneumothorax, but not with subcutaneous emphysema alone. Desaturation and increased airway pressure also occur with bronchial intubation. The preliminary diagnosis is made by verifying the position of the tube, examination of the patient for swelling and crepitus and auscultation for air entry. Chest radiography and paracentesis confirm the diagnosis of pneumothorax, which frequently occurs with subcutaneous emphysema but is rarely of the tension type. Pulmonary embolism due to CO2 during LUAS has not been reported, but the available data suggest that small, haemodynamically inconsequential CO2 embolism occurs without change in PETCO2. Massive embolism is possible and will markedly decrease PETCO2, arterial O2 saturation (SpO2) and blood pressure. CONCLUSION: The immediate recognition of the three complications requires continuous monitoring of PETCO2, arterial saturation, airway pressure, and an index of pulmonary compliance.
This review analyzes the literature dealing with cardiopulmonary function during and pulmonary function following laparoscopic cholecystectomy in order to describe the patterns of changes in these functions and the mechanisms involved as well as to identify areas of concern and lacunae in our knowledge. Information was obtained from a Medline literature search and the annual meeting supplements of Anesthesiology, Anesth Analg, Br J Anaesth, and Can J Anaesth. The principal findings were that changes in cardiovascular function due to the insufflation are characterized by an immediate decrease in cardiac index and an increase in mean arterial blood pressure and systemic vascular resistance. In the next few minutes there is partial restoration of cardiac index and resistance but blood pressure and heart rate do not change. The pattern is the result of the interaction between increased abdominal pressure, neurohumoral responses and absorbed CO2. Pulmonary function changes are characterized by reduced compliance without large alterations in PaO2, but tissue oxygenation can be adversely affected due to reduced O2 delivery. A major difficulty in maintaining normocarbia is due to the abdominal distention reducing pulmonary compliance and to CO2 absorption. End tidal CO2 tension is not a reliable index of PaCO2, particularly in ASA III-IV patients. The pattern of lung function following LC is characterized by a transient reduction in lung volumes and capacities with a restrictive breathing pattern and the loss of the abdominal contribution to breathing. Atelectasis also occurs. These changes are qualitatively similar to but of a lesser magnitude than those following "open" abdominal operations. It is concluded that the changes in cardiopulmonary function during laparoscopic upper abdominal surgery lead us to suggest judicious invasive monitoring and careful interpretation in ASA III-IV patients. Lung function following extensive procedures in sick patients has not been reported.
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The purpose of this clinical study was to determine: (1) the increase in minute ventilation required to maintain preinsufflation arterial carbon dioxide tension (PaCO2) during laparoscopic cholecystectomy, and (2) whether end-tidal PCO2 (PETCO2) can be used as an index of PaCO2 and, therefore, of the adequacy of minute ventilation during the pneumoperitoneum. We measured PaCO2, PETCO2, expired minute volume (Vexp) standardized for body surface area (SA), airway and intra-abdominal pressure (P(aw), Pabd) during general anaesthesia for laparoscopic cholecystectomy just before and 30 min after the creation of a CO2 pneumoperitoneum in 28 healthy (ASA class 1 and 2) consenting adults. They were in the reverse Trendlenburg position (20 degrees) with a 5 degrees lateral tilt. Expired minute volume was increased from 3.75 (SEM +/- 0.12) to 4.19 (0.15) L.min-1 x m-2 to maintain PaCO2 close to control levels: 38.9 (0.8) vs 40.1 (0.6) mmHg 5.19 (0.1) vs 5.35 (0.08) kPa). In most of the patients (23/28), PETCO2 was less than 41 mmHg with a correlation between PaCO2 and PETCO2. In ten of these patients, (Pa-PET)CO2 was greater than the normal range. In 5/28, (Pa-PET)CO2 was negative. The "driving pressure" (P(aw)-Pabd) increased from 8.7 (1.0) to 10.4 (1.1) cm H2O, without any correlation between the increase in P(aw)-Pabd and that in Vexp. The results indicate the need for extra ventilatory requirement during laparoscopy and that PETCO2 is an imperfect index of PaCO2 under these circumstances.
The literature dealing with the magnitude, mechanism and effects of reduced FRC in the perioperative period is reviewed. During general anaesthesia FRC is reduced by approximately 20%. The reduction is greater in the obese and in patients with COPD. The most likely mechanism is the loss of inspiratory muscle tone of the muscles acting on the rib cage. Gas trapping is an additional mechanism. Lung compliance decreases and airways resistance increases, in large part, due to decreased FRC. The larynx is displaced anteriorly and elongated, making laryngoscopy and intubation more difficult. The change in FRC creates or increases intrapulmonary shunt and areas of low ventilation to perfusion. This is due to the occurrence of compression atelectasis, and to regional changes in mechanics and airway closure which tend to reduce ventilation to dependent lung zones which are still well perfused. Abdominal and thoracic operations tend to increase shunting further. Large tidal volume but not PEEP will improve oxygenation, although both increase FRC. Both FRC and vital capacity are reduced following abdominal and thoracic surgery in a predictable pattern. The mechanism is the combined effect of incisional pain and reflex dysfunction of the diaphragm. Additional effects of thoracic surgery include pleural effusion, cooling of the phrenic nerve and mediastinal widening. Postoperative hypoxaemia is a function of reduced FRC and airway closure. There is no real difference among the various methods of active lung expansion in terms of the speed of restoration of lung function, or in preventing postoperative atelectasis/pneumonia. Epidural analgesia does not influence the rate of recovery of lung function, nor does it prevent atelectasis/pneumonia.