Prophylactic nitroglycerin did not reduce myocardial ischemia during accelerated recovery management of coronary artery bypass graft surgery patients.

OBJECTIVE: To evaluate the use of a high dose of nitroglycerin (NTG) for prophylaxis against myocardial ischemia and infarction in patients undergoing coronary artery bypass graft (CABG) surgery with accelerated recovery. DESIGN: Prospective, double-blind, placebo-controlled randomized study. SETTING: A university-based medical center. PARTICIPANTS: Forty adult patients presenting for elective CABG surgery. INTERVENTIONS: Forty patients were divided into 2 blinded study groups. Twenty patients received 2 microg/kg/min of NTG starting before induction of anesthesia and continuing for 6 hours after extubation in the intensive care unit. The placebo group (n = 20) received normal saline during this same interval. MEASUREMENTS AND MAIN RESULTS: Hemodynamics, incidence and severity of myocardial ischemia, and myocardial infarction rates were determined. There were no differences in hemodynamic parameters between groups. The incidence of ischemia was approximately 35% in each group. Myocardial infarction (as determined by elevated creatine kinase-MB fraction, troponin I, and electrocardiogram criteria) was 10% in the placebo group and 5% in the NTG group (p = 0.234). CONCLUSIONS: This study shows a high incidence of myocardial ischemia and infarction in patients presenting for CABG surgery with an accelerated recovery management scheme. NTG was well tolerated clinically; however, it was not found to be protective against myocardial ischemia or infarction in this setting.

Thoracic epidural analgesia: its role in postthoracotomy atrial arrhythmias.

OBJECTIVE: To determine the effects of thoracic epidural analgesia (TEA) management on the incidence of atrial arrhythmias (AAs) after thoracotomy for lung resection. DESIGN: Retrospective. SETTING: A major university medical center. PARTICIPANTS: The medical records of 185 consecutive patients who underwent thoracotomy between 1993 and 1997 were reviewed; patients with TEA only were included in the analysis. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: There was a 20% incidence of AAs after thoracotomy. Preoperative predictors of AAs were age >65 years, cardiac history, and an abnormal electrocardiogram (ECG). There was a temporal relationship between epidural catheter removal and occurrence of AAs. Fourteen patients developed AAs before TEA catheter removal, whereas 29 patients developed AAs after TEA catheter removal (p = 0.01). There was no relationship between anatomic site of epidural catheter placement or choice of epidural agent and AAs. CONCLUSIONS: AAs after thoracotomy were common. These AAs were associated with increased age, cardiac history, abnormal ECG, increased cost, increased length of hospital stay, and time of epidural catheter removal. Although a cause-and-effect relationship cannot be inferred from this study, the presence or absence of TEA was found to have a temporal relationship with the incidence of AAs.

Thoracic epidural anesthesia reduces infarct size in a canine model of myocardial ischemia and reperfusion injury.

OBJECTIVE: To determine the effects of thoracic epidural anesthesia on myocardial infarct size, regional myocardial blood flow (RMBF), and plasma norepinephrine in an anesthetized canine model of ischemia reperfusion injury with infarction. DESIGN: Blinded, randomized, placebo-controlled animal study. SETTING: Experiments were performed in the cardiothoracic research laboratory at Wake Forest University Baptist Medical Center. PARTICIPANTS: Anesthetized, open-chest mongrel dogs were used in these studies. METHODS: Dogs were instrumented for measurement of aortic pressure (AP) and left ventricular systolic pressure (LVSP), dP/dt, and RMBF Epidural catheters were inserted at thoracic segment T5. Three groups received epidural 0.5% bupivacaine: low-dose (n = 7; 0.3 mg/kg bolus, 0.15 mg/kg/ h), mid-dose (n = 7; 0.6 mg/kg bolus, 0.3 mg/kg/h), high-dose (n = 7; 1.2 mg/kg bolus, 0.6 mg/kg/h). The vehicle (VEH) group received epidural saline. Bolus followed by maintenance infusions began 30 minutes before the onset of ischemia (60 min) and continued through reperfusion (180 min). RESULTS: Myocardial infarct size was significantly reduced in the high-dose group versus the VEH and low-dose groups (p < 0.05). After initiation of the mid and high dose, AP, LVSP, and dP/dt decreased 7% to 16% (high vVEH; p < 0.05). VEH dogs showed a 130% increase from control in early postischemic RMBF. There was a dose-dependent attenuation in this reflow response: 72%, 31%, and 6% increase in RMBF in the low, mid, and high groups, relative to controls (p < 0.05 high v VEH). Although there was no significant difference in plasma norepinephrine, fewer surges occurred in the high-dose group. CONCLUSIONS: Thoracic epidural anesthesia reduces infarct size and postischemic hyperemia in a model of ischemia reperfusion injury.

Ischemic preconditioning reduces neurologic injury in a rat model of spinal cord ischemia.

BACKGROUND: Ischemic preconditioning (IPC) is an endogenous cellular protective mechanism whereby brief, noninjurious periods of ischemia render a tissue more resistant to a subsequent, more prolonged ischemic insult. We hypothesized that IPC of the spinal cord would reduce neurologic injury after experimental aortic occlusion in rats and that this improved neurologic benefit could be induced acutely after a short reperfusion interval separating the IPC and the ischemic insult. METHODS: Forty male Sprague-Dawley rats under general anesthesia were randomly assigned to one of two groups. The IPC group (n = 20) had 3 minutes of aortic occlusion to induce spinal cord ischemia 30 minutes of reperfusion, and 12 minutes of ischemia, whereas the controls (n = 20) had only 12 minutes of ischemia. Neurologic function was evaluated 24 and 48 hours later. Some animals from these groups were perfusion-fixed for hematoxylin and eosin staining of the spinal cord for histologic evaluation. RESULTS: Survival was significantly better at 48 hours in the IPC group. Sensory and motor neurologic function were significantly different between groups at 24 and 48 hours. Histologic evaluation at 48 hours showed severe neurologic damage in rats with poor neurologic test scores. CONCLUSIONS: Ischemic preconditioning reduces neurologic injury and improves survival in a rat model of spinal cord ischemia. The protective benefit of IPC is acutely invoked after a 30-minute reperfusion interval between the preconditioning and the ischemic event.

Cloricromene reduces infarct size and alters postischaemic blood flow defects in dog myocardium.

1. The aim of the present investigation was to evaluate the effect of cloricromene on myocardial infarct size, regional myocardial blood flow and neutrophil accumulation in a canine model of ischaemia-reperfusion. 2. Dogs were instrumented to measure blood pressure, left anterior descending (LAD) coronary flow (flow probe) and regional myocardial blood flow (coloured microspheres). Two groups were studied: (i) CLO (n = 8) received an infusion of cloricromene (15 micrograms/kg per min); and (ii) VEH (n = 8) received saline. Infusions began at the onset of ischaemia (60 min) and continued through reperfusion (180 min). 3. Haemodynamic responses were not different between groups. Cloricromene reduced the area of necrosis expressed as a percentage of the area at risk from 35 +/- 3% in the VEH group to 23 +/- 4% in the CLO group (P < 0.05). Regional myocardial blood flow in the ischaemic region was different between groups; VEH dogs showed an early reperfusion hyperaemia followed by a progressive reduction in flow, while CLO dogs exhibited a gradual increase in reflow in the absence of an early hyperaemic response (P < 0.05). Left anterior descending flow was enhanced during the reperfusion period in the CLO group compared with VEH (P < 0.05). Cloricromene reduced polymorphonuclear neutrophil (PMN) infiltration (myeloperuxidase activity) in all myocardial regions when compared with VEH (non-ischaemic zone, 0.34 +/- 0.54 vs 0.05 +/- 0.01 IU/100 mg; ischaemic zone, 2.03 +/- 0.80 vs 0.24 +/- 0.08 IU/100 mg; and necrotic zone, 0.56 +/- 0.04 vs 3.59 +/- 1.09 IU/100 mg for VEH vs CLO groups, respectively; P < 0.01). In a separate in vitro preparation, cloricromene reduced adherence of platelet-activating factor (PAF)-stimulated PMN to canine coronary endothelium. Stimulation of PMN by 100 nmol/L PAF resulted in adherence of 176 +/- 36 compared with 48 +/- 12 cells/mm2 in PAF-stimulated PMN treated with 100 mumol cloricromene (P < 0.001). 4. These data indicate that cloricromene reduces myocardial infarct size in a canine model of ischaemia-reperfusion injury. Postischaemic blood flow patterns are significantly different in cloricromene-treated dogs. Cloricromene-mediated reductions in infarct size, neutrophil accumulation and adherence may play a role in this effect.

Anesthetic considerations of cardiovascular risk during electroconvulsive therapy.

This article focuses on anesthetic considerations of cardiovascular risk for electroconvulsive (ECT) therapy. Preoperative evaluation, intraoperative management, and postoperative care are reviewed. Although the anesthetic risk to ECT patients is quite low, elderly patients or those presenting with known cardiovascular disease may be at increased risk and need special intervention or management during ECT.

The effect of esmolol on ST-segment depression and arrhythmias after electroconvulsive therapy.

Electroconvulsive therapy (ECT) induces sympathetically mediated hemodynamic alterations that can be associated with myocardial ischemia and arrhythmia generation. Esmolol, a short-acting beta-blocker, blunts the hypertension and tachycardia seen with ECT. The purpose of this study is to determine whether esmolol use during ECT reduces the incidence of myocardial ischemia or arrhythmias after ECT. In a randomized, double-blind, placebo-controlled protocol, with each patient acting as his/her own control, the effects of esmolol on the incidence of myocardial ischemia and arrhythmias were studied using two-lead Holter monitoring for at least 2 h post-ECT. Nineteen patients underwent 71 ECT treatments (34 placebo, 37 esmolol), recording 746 h of Holter data. The esmolol group had significantly reduced heart rate and mean arterial pressure immediately after ECT. There was no difference in the incidence of ECG defined ischemia post-ECT between groups, with 7 of 19 (36.8%) patients in the esmolol group showing ST-segment depression compared with 5 of 19 (26.3%) in the placebo group. There was no difference between groups in arrhythmia detection. This experiment demonstrates that (a) ECT is associated with a significant incidence of ST-segment depression, (b) esmolol blunts the sympathetic discharge during ECT, and (c) esmolol does not reduce the incidence of post-ECT ischemia or arrhythmia.

Effect of esmolol pretreatment on EEG seizure morphology in RUL ECT.

Intravenous beta-blockers are an effective means of controlling heart rate and blood pressure during electroconvulsive therapy (ECT), but have been shown to decrease seizure duration. While the importance of seizure duration to the antidepressant response of ECT grows less certain, there is growing evidence that seizure morphology predicts the antidepressant effect of ECT. This study examined the impact of esmolol pretreatment on seizure morphology. Eighteen depressed patients (6 men, 12 women; 69 +/- 12.8 years old) received ECT with and without esmolol pretreatment in a randomized, blinded crossover design. The seizures were blindly rated for duration of motor convulsion, duration of electroencephalogram (EEG) seizure, degree of seizure regularity, and degree of postictal EEG suppression. Esmolol shortened the duration of the motor convulsion and degraded the quality of the ictal regularity. Routine administration of intravenous esmolol before ECT may cause a decrease in ictal regularity. Careful consideration should be given to the potential benefits of esmolol versus the deleterious effect on the electrophysiologic process. Esmolol may still be indicated on a case-by-case basis for extreme tachycardia or hypertension associated with ECT, and presumably poses no problem for the therapeutic effect of ECT if given after the seizure is over.

Topical ice slurry prevents brain rewarming during deep hypothermic circulatory arrest in newborn sheep.

OBJECTIVES: To measure the effect of ice slurry topical cooling on brain surface temperature during deep hypothermic circulatory arrest. DESIGN: This was a prospective, controlled experiment. SETTING: Animal laboratory at a university hospital. PARTICIPANTS: Five control lambs, five treatment (ice slurry) lambs. INTERVENTIONS: Animals were studied in two groups: the study group had topical cooling of the head with ice slurry started immediately before circulatory arrest and continued throughout the period of circulatory arrest; control group lambs received no supplemental topical cooling. MEASUREMENTS AND MAIN RESULTS: Brain surface temperature, scalp, nasopharyngeal, and rectal temperatures were measured at 5-minute intervals during 45 minutes of circulatory arrest. Lambs receiving topical cooling of the head with ice slurry had a statistically significant decrease in brain surface temperature of 2.2 +/- 1.2 degrees C during circulatory arrest, whereas brain surface temperature increased 1.2 +/- 0.3 degrees C, in control lambs. Equilibration of temperature between the scalp and brain in control lambs produced rewarming of the brain surface. CONCLUSIONS: Topical cooling of the head with ice slurry in newborn lambs lowers brain surface temperature during deep hypothermic circulatory arrest. Surrogate temperature monitoring locations such as nasopharyngeal and rectal temperatures varied significantly and do not accurately reflect changes in brain surface temperature.

Cloricromene reduces myocardial infarct size in rabbits when administered during the early reperfusion period.

Cloricromene is a coumarin derivative without anticoagulant activities that has recently been found to decrease myocardial infarct size after an ischemic-reperfusion injury. This study seeks to determine when the cardioprotective action of cloricromene is exerted in an in vivo rabbit model of ischemic-reperfusion injury. Forty-nine rabbits subjected to 30 min of coronary occlusion and 120 min of reperfusion were randomized into five groups: VEH (n = 11) received saline vehicle; IR (n = 9) received an infusion of cloricromene starting at the onset of ischemia at 8 micrograms.kg-1.min-1; R(-5)(n = 9) and R(+30)(n = 9) received an infusion of cloricromene at 8 micrograms.kg-1.min-1 starting 5 min before reperfusion and 30 min after reperfusion, respectively; and RB(-5)(n = 11) received 300 micrograms/kg bolus of cloricromene 5 min before reperfusion followed by an infusion of 8 micrograms.kg-1.min-1. All infusions were continued until the end of the reperfusion period. Myocardial infarct size was significantly reduced in groups IR, R(-5), and RB(-5). We conclude that cloricromene's effective time of action occurs prior to the first 30 min of the reperfusion period.

A comparison of isoflurane versus fentanyl as primary anesthetics for mitral valve surgery.

We conducted a randomize study of fentanyl compared to isoflurane anesthesia in patients with pulmonary hypertension undergoing mitral valve surgery. Patients were premedicated and randomly assigned to one of two groups: 21 patients had anesthesia induced with thiopental and maintained with isoflurane; 23 patients had anesthesia induced with a fentanyl bolus and maintained with a fentanyl infusion. Adjustments of fentanyl infusion and isoflurane concentration, as well as fentanyl boluses and vasoactive/positive inotropic medication, were administered to maintain preoperative arterial blood pressure. Both groups exhibited similar demographics, similar duration of cardiopulmonary bypass (CPB) surgery, anesthesia, and time from entrance into the surgical intensive care unit (SICU) to endotracheal extubation. However, the time from entrance into the SICU to awake was significantly (P < 0.05) shorter in patients given isoflurane anesthesia. Hemodynamic variables were recorded at baseline and 12 surgical events and compared between and within groups. Significant changes from baseline were demonstrated in both groups upon institution and discontinuation of CPB. Patients receiving isoflurane anesthesia exhibited cardiovascular depression as compared to their baseline. There were no deaths in either patient group. Adequate hemodynamic profiles were achieved in both groups with comparable use of inotropic and vasoactive medication, with the exception of norepinephrine that was administered intraoperatively to significantly (P < 0.05) more patients in the isoflurane-based anesthesia group. Neither technique was associated with acute improvement of right heart performance or pulmonary hypertension, in large part because of morphologic changes of the pulmonary arterial bed, occurring with long-standing mitral valve disease. We conclude that isoflurane-based anesthesia is adequate for this type of surgery, although there is a higher anesthetic algorithm failure rate than with fentanyl-based anesthetic technique.

The importance of the postoperative anesthetic visit: do repeated visits improve patient satisfaction or physician recognition?

This study evaluates whether repeated postoperative visits by the anesthesiologist improve patient ability to recall the anesthesiologist's name and the patient's perception of and satisfaction with anesthesia services. In a randomized, prospective trial, 144 patients with an anticipated postoperative length of stay of at least three days were enrolled in three groups: Group A patients (n = 48) had one postoperative visit, Group B (n = 48) had two postoperative visits, and Group C (n = 48) had three postoperative visits. All postoperative visits were performed by the attending anesthesiologist on consecutive postoperative days. Patients were contacted two days after their last postoperative visit to complete a study questionnaire. Patients were able to recall the anesthesiologist's name significantly less frequently than the surgeon's name, and there was no difference in name recall among groups. Recall was not affected by patient age, sex, or ASA physical status; the mode of contact (telephone versus personal visit); the anesthesiologist's gender; the presence of preoperative medication; or the identity of the preoperative evaluator. Patients could identify the anesthesiologist's gender approximately 85% of the time, regardless of group, and were more likely to identify female anesthesiologists (P = 0.026, odds ratio 3.3). Patient evaluation of hospital, surgical, and anesthesia care was favorable in all groups and did not vary with group. Increasing the number of postoperative visits does not improve patient name recognition of the anesthesiologist or increase patient satisfaction with or perception of anesthesia services.