Hernodynamic Responses to Endotracheal Extubation After Coronary Artery Bypass Grafting Robert Paulissian, MD, M. Ramez Salem, MD, Ninos J. Joseph, BS, Berton Braverman, PhD, Howard C. Cohen, MD, George J. Crystal, PhD, and Harold J. Heyman, MD Department of Anesthesiology, Illinois Masonic Medical Center, Chicago, Illinois
After coronary artery bypass grafting (CABG) surgery, patients may remain at risk for myocardial ischemia and infarction and ventricular dysrhythmias. The hemodynamic responses to endotracheal extubation and the efficacy of intravenous lidocaine pretreatment were studied after CABG surgery and overnight mechanical ventilation. Twenty-five patients were divided into two groups: group l ( n = 13) patients who had tracheal extubation after pretreatment with a placebo; group 2 patients who received lidocaine (1 mg/kg IV) before tracheal extubation. Hemodynamic data, electrocardiographic tracings, and arterial blood gases were obtained before tracheal extubation, during suctioning, and 1, 5, and 20 min after tracheal extubation. Group 1 patients displayed significant increases in heart rate, arterial blood pressure, rate-pressure product, right atrial pressure, and cardiac index during suctioning and within 1 min of tracheal extubation, returning to preextubation level
A
fter coronary artery bypass grafting (CABG) surgery, patients may remain at risk for myosardial ischemia and infarction (1) and ventricular dysrhythmias (2). This has been attributed to several factors. First, some vessels with >70% occlusion are not surgically bypassed (3) and, in the absence of adequate collateral blood flow, the areas of the myocardium perfused by these vessels might remain vulnerable to ischemia. Second, distal coronary disease may prevent adequate runoff in those vessels surgically bypassed (3). Third, zones surrounding areas of prior myocardial infarction may trigger ventricular dysrhythmias, particularly during stress-induced catecholamine release (4).Thus, measures to prevent imbalances between myocardial supply and demand after CABG surgery may be important. Accepted for publication April 21, 1991. Address correspondence to Dr. Paulissian, Department of Anesthesiology, Illinois Masonic Medical Center, 836 West Wellington Avenue, Chicago, IL 60657.
10
by 5 min. There were no significant changes in pulmonary and systemic resistance indices. Hemodynamic changes in group 2 patients were similar to those in group 1. Both in the absence and presence of lidocaine, tracheal extubation caused hemodynamic responses that were small in magnitude and brief in duration. These responses were not associated with electrocardiographic or enzymatic evidence of myocardial ischemia or infarction, or with ventricular dysrhythmias. Compared with the well-documented hemodynamic responses to tracheal intubation, we found that extubation of the trachea after CABG surgery was associated with less pronounced responses. This may be related to avoidance of laryngoscopy and possibly accommodation to the endotracheal tube. These modest hemodynamic responses of extubation of the trachea after CABG surgery were not modified by intravenous lidocaine. (Anesth Analg 1991;73:1&5)
Although the hemodynamic responses to endotracheal intubation have been extensively studied (5-8), the hemodynamic consequences of extubation have received little attention. Coughing during suctioning and endotracheal extubation may cause tachycardia, hypertension, and excessive catecholamine release, thus increasing myocardial oxygen demands. Bidwai and associates (9, 10) investigated the heart rate (HR) and arterial blood pressure (MAP) response to extubation in essentially healthy patients undergoing elective general, orthopedic, and gynecologic operations. They found significant increases in HR and MAP that persisted for 6-8 min and that these responses were attenuated by the intravenous administration of lidocaine before extubation (9). Comparable increases in HR, MAP, or other hemodynamic alterations might be detrimental in patients after CABG surgery. The present study was undertaken to examine the hemodynamic and electrocardiographic (ECG) responses associated with endotracheal extubation after CABG surgery. In light of the findings of Bidwai et al. that prior treatment with intravenous 01991 by the International Anesthesia Research Society 0003-2999/91/$3.50
ANESTH ANALG 1991;73:1M
lidocaine blunted the increase in HR and MAP, the efficacy of prior treatment with intravenous lidocaine was also evaluated.
Methods The experimental protocol was approved by the institutional review board, and informed consent was obtained from 40 patients scheduled to undergo elective CABG surgery. Patients with valvular heart disease, cardiac dysrhythmias, and pacemakers were excluded from the study. Demographic data, preoperative cardiac medications, indices of cardiac function (left ventricular end-diastolic pressure and ejection fraction), and number of diseased vessels (>70% occlusion) reported during preoperative cineangiocardiography were obtained from the patients’ charts. All cardiac medications were continued throughout the intraoperative period. On arrival to the operating suite, intravenous, radial artery, and triple-lumen thermodilution pulmonary artery catheters were percutaneously inserted under local anesthesia. Anesthesia was induced intravenously with 50-75 pglkg of fentanyl and 0.1 mg/kg of pancuronium followed by endotracheal intubation with an appropriately sized, cuffed orotracheal tube. Anesthesia was maintained with additional doses of fentanyl (total dose = 100-150 pg/kg IV) and pancuronium. The operation then progressed in a routine fashion. After the completion of the operation, the patients were transferred to the Surgical Intensive Care Unit and were mechanically ventilated overnight using a Bennett MA I respirator in a synchronized intermittent mandatory ventilatory (SIMV) mode. The tidal volume, SIMV rate, and inspired oxygen fraction (Fro,) were set to maintain the arterial carbon dioxide tension (Paco,) between 35 and 43 mm Hg and the arterial oxygen tension (Pao,) 290 mm Hg. Sedatives and narcotics were administered as needed to facilitate ventilatory support during the early hours after operation but were discontinued approximately 6 h before anticipated endotracheal extubation. The FIO, was gradually reduced from 0.6 to 0.4, the FIO, at which tracheal extubation was attempted. On the morning of the first postoperative day, the hemodynamic status and ventilatory variables were evaluated. Patients who required circulatory support (intravenous inotropes or vasodilators or intraaortic balloon counterpulsation) on the morning of the first postoperative day were excluded from the study. If the circulatory status of the patient appeared stable, arterial blood gas values, portable chest radiographs, and respiratory variables were used to evaluate the feasibility of weaning from respiratory support. The criteria to begin weaning from mechanical ventilation
CARDIOVASCULAR ANESTHESIA PAULISSIAN ET AL. HEMODYNAMIC RESPONSES T O EXTUBATION AFTER CABC
11
included a fully awake patient, no abnormal findings on chest radiograph, Paco, between 35 and 45 mm Hg, Pao, 2 90 mm Hg (FIo, = 0.4), a negative inspiratory force 2 25 cm H,O, and a vital capacity 2 1 0 mL/kg. When the patient met the above criteria for weaning, the mandatory breaths during SIMV were progressively decreased from 8 to 4 breaths/ min, and serial analysis of arterial blood gases was performed. Endotracheal extubation was considered feasible if the patient was hemodynamically stable, Paco, remained between 35 and 45 mm Hg, Pao, 2 90 mm Hg (Fro, = 0.4), negative inspiratory force z 25 cm H,O, and vital capacity L 15 mL/kg at an SIMV rate of 4 breathdmin. After the criteria for tracheal extubation were met, the patients were randomly assigned to one of two groups. In group 1 (n = 13), a placebo injection of 0.9% sodium chloride was administered 2 min before endotracheal extubation. The respirator was disconnected then and was replaced by assisted ventilation with a self-inflating bag (15-L 0, flow) for several large breaths before the endotracheal tube and oropharynx were suctioned. The self-inflating bag was then reconnected for several more large breaths while the endotracheal tube cuff was deflated and the endotracheal tube was withdrawn. After tracheal extubation, 0, with heated aerosol was administered by mask at 5-L flow for the remainder of the study period. In group 2 (n = 12), the patients received an intravenous bolus injection of 2% lidocaine (1 mg/kg) 2 min before suctioning followed by extubation in the manner described above. The persons performing the extubation and recording hemodynamic and respiratory data were not informed as to whether a placebo or lidocaine was administered. The following variables were measured or derived from appropriate formulas: HR, MAP, cardiac index (CI), rate-pressure product (RPP), right atrial pressure (RAP), mean pulmonary artery pressure (MPAP), pulmonary capillary wedge pressure (PCWP), stroke volume index (SVI), systemic vascular resistance index (SVRI), and pulmonary vascular resistance index (PVRI). Electrocardiographic tracings, leads I1 and V,, were obtained at each measurement period. All measurements were recorded at (a) 5 min before extubation, (b) during suctioning of the airway, (c) immediately after extubation, (d) 5 min after extubation, and (e) 20 min after extubation. In addition, arterial and mixed venous blood gas samples were drawn before tracheal extubation and 5 and 20 min after extubation. The ECG tracings obtained at each measurement interval were evaluated by a cardiologist who was not informed as to whether the patient received lidocaine. Electrocardiographicevidence of new myocardial ischemia was defined as ST-segment changes
12
ANESTH ANALG 1991;73:10-5
CARDIOVASCULAR ANESTHESIA PAULISSIAN ET AL. HEMODYNAMIC RESPONSES TO EXTUBATION AFTER CABG
Table 1. Demographic Data Group 1 n Age (yr) Sex Male Female BSA (m’) LVEDP (mm Hg) Ejection fraction No. of diseased vessels Preoperative pblockade
Group 2 12
13 60.6
&
3.1
57.7
2
2.8
7
10 3
5
1.91 2 0.04 11.1 r 1.2 53.9 & 4.1 3.2 2 0.2 12
1.90 2 0.06 9.9 2 1.5 55.6 -+ 4.7 3.1 2 0.2 11
BSA, body surface area; LVEDP, left ventricular end-diastolic pressure. All values except n, sex, and preoperative pblockade are mean ? SEM.
of 21.0 mm measured 80 ms beyond the J point (11-13). Perioperative myocardial infarction (MI) was suspected when any of the following was present: acute ST-segment elevation with or without T-wave abnormalities unresponsive to nitrates or calcium channel blockers; appearance of new Q-waves >0.04 s, or ST-segment depression with deeply inverted T-waves in the absence of Q-waves (14). Confirmation of suspected MI was obtained if creatinine phosphokinase (CPK) was >500 U/L and the isoenzyme CPK-MB was >3% (15). These CPK measurements were done within the first 3 h immediately postoperatively and daily during the intensive care stay. Significant differences between and within groups were identified by a multivariate analysis of variance for repeated measures and the Student-NewmanKeuls test. Demographic differences between groups were analyzed with the Student’s t-test for continuous variables and the Mann-Whitney U-test for discrete data. Statistical significance was accepted when P < 0.05.
Results Of the original 40 patients who consented to the study, 25 patients met all the criteria for tracheal extubation and inclusion in the study on the morning of the first postoperative day. These patients were randomly assigned to group 1 (placebo, 13 patients) or group 2 (lidocaine, 12 patients). Demographic data including age, sex, body surface area (BSA), preoperative cardiac medications, preoperative cardiac status, and number of grafts were not different between the two groups and are shown in Table 1. Hemodynamic and blood gas data appear in Tables 2 and 3. Group 1 patients had slightly higher preextubation values for RAP, MPAP, and PCWP and lower SVRI as compared with those in group 2 patients (Table 2).
In group 1, HR was increased modestly during suctioning and immediately after tracheal extubation. Heart rate returned to the preextubation level by 5 min after extubation and remained essentially unchanged at 20 min. Mean arterial blood pressure, RPP, and CI increased in parallel with HR during suctioning and immediately after tracheal extubation, returning to control level by 5 min after tracheal extubation. There were no changes in PCWP, SVI, SVRI, PVRI, pHa, Paco,, or Pao, (Tables 2 and 3). In the lidocaine-treated patients (group 2), HR also increased during suctioning and immediately after extubation. By 5 min after tracheal extubation, the HR had returned to the preextubation level. Mean arterial blood pressure was significantly increased during extubation. Mean pulmonary artery pressure, PCWP, and RAP were increased during suctioning and extubation, respectively. Rate-pressure product, CI, SVI, SVRI, PVRI, pHa, Paco,, and Pao, did not change during the study in group 2 (Tables 2 and 3). No patients in either group required reintubation or showed ECG or enzymatic evidence of myocardial ischemia or infarction intraoperatively or postoperatively. All patients had uneventful recovery and were discharged from the hospital.
Discussion The reported incidence of postoperative MI after CABG surgery varies between 2.8% and 31% (16). The wide disparity seems to depend on the sensitivity of the diagnostic techniques used to detect MI (16). Force and associates (l),studying risk stratification of postoperative MI after CABG surgery, found that low postoperative ejection fraction (
After coronary artery bypass grafting (CABG) surgery, patients may remain at risk for myocardial ischemia and infarction and ventricular dysrhythmias. The hemodynamic responses to endotracheal extubation and the efficacy of intravenous lidocaine pretreatment were studied after CABG surgery and overnight mechanical ventilation. Twenty-five patients were divided into two groups: group l ( n = 13) patients who had tracheal extubation after pretreatment with a placebo; group 2 patients who received lidocaine (1 mg/kg IV) before tracheal extubation. Hemodynamic data, electrocardiographic tracings, and arterial blood gases were obtained before tracheal extubation, during suctioning, and 1, 5, and 20 min after tracheal extubation. Group 1 patients displayed significant increases in heart rate, arterial blood pressure, rate-pressure product, right atrial pressure, and cardiac index during suctioning and within 1 min of tracheal extubation, returning to preextubation level
A
fter coronary artery bypass grafting (CABG) surgery, patients may remain at risk for myosardial ischemia and infarction (1) and ventricular dysrhythmias (2). This has been attributed to several factors. First, some vessels with >70% occlusion are not surgically bypassed (3) and, in the absence of adequate collateral blood flow, the areas of the myocardium perfused by these vessels might remain vulnerable to ischemia. Second, distal coronary disease may prevent adequate runoff in those vessels surgically bypassed (3). Third, zones surrounding areas of prior myocardial infarction may trigger ventricular dysrhythmias, particularly during stress-induced catecholamine release (4).Thus, measures to prevent imbalances between myocardial supply and demand after CABG surgery may be important. Accepted for publication April 21, 1991. Address correspondence to Dr. Paulissian, Department of Anesthesiology, Illinois Masonic Medical Center, 836 West Wellington Avenue, Chicago, IL 60657.
10
by 5 min. There were no significant changes in pulmonary and systemic resistance indices. Hemodynamic changes in group 2 patients were similar to those in group 1. Both in the absence and presence of lidocaine, tracheal extubation caused hemodynamic responses that were small in magnitude and brief in duration. These responses were not associated with electrocardiographic or enzymatic evidence of myocardial ischemia or infarction, or with ventricular dysrhythmias. Compared with the well-documented hemodynamic responses to tracheal intubation, we found that extubation of the trachea after CABG surgery was associated with less pronounced responses. This may be related to avoidance of laryngoscopy and possibly accommodation to the endotracheal tube. These modest hemodynamic responses of extubation of the trachea after CABG surgery were not modified by intravenous lidocaine. (Anesth Analg 1991;73:1&5)
Although the hemodynamic responses to endotracheal intubation have been extensively studied (5-8), the hemodynamic consequences of extubation have received little attention. Coughing during suctioning and endotracheal extubation may cause tachycardia, hypertension, and excessive catecholamine release, thus increasing myocardial oxygen demands. Bidwai and associates (9, 10) investigated the heart rate (HR) and arterial blood pressure (MAP) response to extubation in essentially healthy patients undergoing elective general, orthopedic, and gynecologic operations. They found significant increases in HR and MAP that persisted for 6-8 min and that these responses were attenuated by the intravenous administration of lidocaine before extubation (9). Comparable increases in HR, MAP, or other hemodynamic alterations might be detrimental in patients after CABG surgery. The present study was undertaken to examine the hemodynamic and electrocardiographic (ECG) responses associated with endotracheal extubation after CABG surgery. In light of the findings of Bidwai et al. that prior treatment with intravenous 01991 by the International Anesthesia Research Society 0003-2999/91/$3.50
ANESTH ANALG 1991;73:1M
lidocaine blunted the increase in HR and MAP, the efficacy of prior treatment with intravenous lidocaine was also evaluated.
Methods The experimental protocol was approved by the institutional review board, and informed consent was obtained from 40 patients scheduled to undergo elective CABG surgery. Patients with valvular heart disease, cardiac dysrhythmias, and pacemakers were excluded from the study. Demographic data, preoperative cardiac medications, indices of cardiac function (left ventricular end-diastolic pressure and ejection fraction), and number of diseased vessels (>70% occlusion) reported during preoperative cineangiocardiography were obtained from the patients’ charts. All cardiac medications were continued throughout the intraoperative period. On arrival to the operating suite, intravenous, radial artery, and triple-lumen thermodilution pulmonary artery catheters were percutaneously inserted under local anesthesia. Anesthesia was induced intravenously with 50-75 pglkg of fentanyl and 0.1 mg/kg of pancuronium followed by endotracheal intubation with an appropriately sized, cuffed orotracheal tube. Anesthesia was maintained with additional doses of fentanyl (total dose = 100-150 pg/kg IV) and pancuronium. The operation then progressed in a routine fashion. After the completion of the operation, the patients were transferred to the Surgical Intensive Care Unit and were mechanically ventilated overnight using a Bennett MA I respirator in a synchronized intermittent mandatory ventilatory (SIMV) mode. The tidal volume, SIMV rate, and inspired oxygen fraction (Fro,) were set to maintain the arterial carbon dioxide tension (Paco,) between 35 and 43 mm Hg and the arterial oxygen tension (Pao,) 290 mm Hg. Sedatives and narcotics were administered as needed to facilitate ventilatory support during the early hours after operation but were discontinued approximately 6 h before anticipated endotracheal extubation. The FIO, was gradually reduced from 0.6 to 0.4, the FIO, at which tracheal extubation was attempted. On the morning of the first postoperative day, the hemodynamic status and ventilatory variables were evaluated. Patients who required circulatory support (intravenous inotropes or vasodilators or intraaortic balloon counterpulsation) on the morning of the first postoperative day were excluded from the study. If the circulatory status of the patient appeared stable, arterial blood gas values, portable chest radiographs, and respiratory variables were used to evaluate the feasibility of weaning from respiratory support. The criteria to begin weaning from mechanical ventilation
CARDIOVASCULAR ANESTHESIA PAULISSIAN ET AL. HEMODYNAMIC RESPONSES T O EXTUBATION AFTER CABC
11
included a fully awake patient, no abnormal findings on chest radiograph, Paco, between 35 and 45 mm Hg, Pao, 2 90 mm Hg (FIo, = 0.4), a negative inspiratory force 2 25 cm H,O, and a vital capacity 2 1 0 mL/kg. When the patient met the above criteria for weaning, the mandatory breaths during SIMV were progressively decreased from 8 to 4 breaths/ min, and serial analysis of arterial blood gases was performed. Endotracheal extubation was considered feasible if the patient was hemodynamically stable, Paco, remained between 35 and 45 mm Hg, Pao, 2 90 mm Hg (Fro, = 0.4), negative inspiratory force z 25 cm H,O, and vital capacity L 15 mL/kg at an SIMV rate of 4 breathdmin. After the criteria for tracheal extubation were met, the patients were randomly assigned to one of two groups. In group 1 (n = 13), a placebo injection of 0.9% sodium chloride was administered 2 min before endotracheal extubation. The respirator was disconnected then and was replaced by assisted ventilation with a self-inflating bag (15-L 0, flow) for several large breaths before the endotracheal tube and oropharynx were suctioned. The self-inflating bag was then reconnected for several more large breaths while the endotracheal tube cuff was deflated and the endotracheal tube was withdrawn. After tracheal extubation, 0, with heated aerosol was administered by mask at 5-L flow for the remainder of the study period. In group 2 (n = 12), the patients received an intravenous bolus injection of 2% lidocaine (1 mg/kg) 2 min before suctioning followed by extubation in the manner described above. The persons performing the extubation and recording hemodynamic and respiratory data were not informed as to whether a placebo or lidocaine was administered. The following variables were measured or derived from appropriate formulas: HR, MAP, cardiac index (CI), rate-pressure product (RPP), right atrial pressure (RAP), mean pulmonary artery pressure (MPAP), pulmonary capillary wedge pressure (PCWP), stroke volume index (SVI), systemic vascular resistance index (SVRI), and pulmonary vascular resistance index (PVRI). Electrocardiographic tracings, leads I1 and V,, were obtained at each measurement period. All measurements were recorded at (a) 5 min before extubation, (b) during suctioning of the airway, (c) immediately after extubation, (d) 5 min after extubation, and (e) 20 min after extubation. In addition, arterial and mixed venous blood gas samples were drawn before tracheal extubation and 5 and 20 min after extubation. The ECG tracings obtained at each measurement interval were evaluated by a cardiologist who was not informed as to whether the patient received lidocaine. Electrocardiographicevidence of new myocardial ischemia was defined as ST-segment changes
12
ANESTH ANALG 1991;73:10-5
CARDIOVASCULAR ANESTHESIA PAULISSIAN ET AL. HEMODYNAMIC RESPONSES TO EXTUBATION AFTER CABG
Table 1. Demographic Data Group 1 n Age (yr) Sex Male Female BSA (m’) LVEDP (mm Hg) Ejection fraction No. of diseased vessels Preoperative pblockade
Group 2 12
13 60.6
&
3.1
57.7
2
2.8
7
10 3
5
1.91 2 0.04 11.1 r 1.2 53.9 & 4.1 3.2 2 0.2 12
1.90 2 0.06 9.9 2 1.5 55.6 -+ 4.7 3.1 2 0.2 11
BSA, body surface area; LVEDP, left ventricular end-diastolic pressure. All values except n, sex, and preoperative pblockade are mean ? SEM.
of 21.0 mm measured 80 ms beyond the J point (11-13). Perioperative myocardial infarction (MI) was suspected when any of the following was present: acute ST-segment elevation with or without T-wave abnormalities unresponsive to nitrates or calcium channel blockers; appearance of new Q-waves >0.04 s, or ST-segment depression with deeply inverted T-waves in the absence of Q-waves (14). Confirmation of suspected MI was obtained if creatinine phosphokinase (CPK) was >500 U/L and the isoenzyme CPK-MB was >3% (15). These CPK measurements were done within the first 3 h immediately postoperatively and daily during the intensive care stay. Significant differences between and within groups were identified by a multivariate analysis of variance for repeated measures and the Student-NewmanKeuls test. Demographic differences between groups were analyzed with the Student’s t-test for continuous variables and the Mann-Whitney U-test for discrete data. Statistical significance was accepted when P < 0.05.
Results Of the original 40 patients who consented to the study, 25 patients met all the criteria for tracheal extubation and inclusion in the study on the morning of the first postoperative day. These patients were randomly assigned to group 1 (placebo, 13 patients) or group 2 (lidocaine, 12 patients). Demographic data including age, sex, body surface area (BSA), preoperative cardiac medications, preoperative cardiac status, and number of grafts were not different between the two groups and are shown in Table 1. Hemodynamic and blood gas data appear in Tables 2 and 3. Group 1 patients had slightly higher preextubation values for RAP, MPAP, and PCWP and lower SVRI as compared with those in group 2 patients (Table 2).
In group 1, HR was increased modestly during suctioning and immediately after tracheal extubation. Heart rate returned to the preextubation level by 5 min after extubation and remained essentially unchanged at 20 min. Mean arterial blood pressure, RPP, and CI increased in parallel with HR during suctioning and immediately after tracheal extubation, returning to control level by 5 min after tracheal extubation. There were no changes in PCWP, SVI, SVRI, PVRI, pHa, Paco,, or Pao, (Tables 2 and 3). In the lidocaine-treated patients (group 2), HR also increased during suctioning and immediately after extubation. By 5 min after tracheal extubation, the HR had returned to the preextubation level. Mean arterial blood pressure was significantly increased during extubation. Mean pulmonary artery pressure, PCWP, and RAP were increased during suctioning and extubation, respectively. Rate-pressure product, CI, SVI, SVRI, PVRI, pHa, Paco,, and Pao, did not change during the study in group 2 (Tables 2 and 3). No patients in either group required reintubation or showed ECG or enzymatic evidence of myocardial ischemia or infarction intraoperatively or postoperatively. All patients had uneventful recovery and were discharged from the hospital.
Discussion The reported incidence of postoperative MI after CABG surgery varies between 2.8% and 31% (16). The wide disparity seems to depend on the sensitivity of the diagnostic techniques used to detect MI (16). Force and associates (l),studying risk stratification of postoperative MI after CABG surgery, found that low postoperative ejection fraction (
