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R A Kates

Publications and source records attributed to R A Kates.

18 recordsLinked to original sources
PubMed1989

General anesthesia during percutaneous transluminary coronary angioplasty for acute myocardial infarction: results of a randomized controlled clinical trial.

Acutely ill patients with myocardial infarction may require immediate cardiac catheterization and coronary angioplasty to achieve myocardial reperfusion. To determine the feasibility of using general anesthesia under these circumstances, a randomized clinical trial was performed. Of 50 patients, 25 received anesthesia and 25 receive intravenous sedation. There were transient increases in heart rate and blood pressure after tracheal intubation in the anesthetized patients, followed by significant and sustained decreases below baseline values once steady state anesthesia was attained. Arterial oxygenation was significantly improved in anesthetized patients. There were no serious complications due to anesthesia, but the small sample size limited the power of the study to detect differences in morbidity or mortality. Patients strongly preferred anesthesia. These results show that general anesthesia is feasible in patients undergoing interventional cardiac catheterization during acute myocardial infarction, when pain, anxiety or agitation do not respond adequately to conventional measures.

Anesthesia, General↗
PubMed1988

Anesthetic implications for the management of patients with acute myocardial infarction: a matched cohort study of patients undergoing emergency myocardial revascularization.

Emergency coronary artery bypass grafting (CABG) is advocated as a treatment of acute myocardial infarction (AMI). To attempt to define anesthetic management problems in this patient group, a retrospective study was conducted comparing the perioperative courses of 23 patients undergoing emergency CABG during AMI with 23 elective patients, individually matched for gender, operating surgeon, ejection fraction, and aortic crossclamp time. The 23 AMI patients were anesthetized 5.98 +/- 3.0 (range 1.5 to 11.0) hours after the onset of chest pain. Anesthetic agents were similar for both groups. Induction of anesthesia was well tolerated by AMI patients. Tolerance of cardioplegic arrest was impaired in the AMI group as evidenced by the sharp increase in frequency of inotropic support required to discontinue bypass in the AMI group compared to elective patients (12/23 v 3/23; P less than .005). Fifteen AMI patients who received preoperative streptokinase had greater postoperative bleeding. Three AMI patients died postoperatively. The number of patients requiring prolonged postoperative ventilation and extended ICU care was higher in the AMI group. It is concluded that patients undergoing emergency CABG during AMI represent a greater risk than elective patients. They have a higher incidence of myocardial dysfunction following cardioplegic arrest during bypass. Those who receive preoperative thrombolytic therapy exhibit greater bleeding tendencies.

Anesthesia, Intravenous↗
PubMed1988

alpha 1-Adrenergic responsiveness during coronary artery bypass surgery: effect of preoperative ejection fraction.

Elevated catecholamines and beta-adrenergic receptor hyporesponsiveness (or desensitization) have been demonstrated in failing human myocardium, but the role of the alpha-adrenergic receptor remains unclear. The authors tested the hypothesis that alpha 1-adrenergic responsiveness decreases in patients with impaired ventricular function undergoing coronary artery revascularization. Impaired ventricular function was defined prospectively by left ventricular ejection fraction less than or equal to 40% (group I, n = 12), and normal ventricular function by ejection fraction greater than 40% (group II, n = 22). Phenylephrine (Phe) pressor dose-response curves were established prior to anesthesia, during fentanyl anesthesia, and during fentanyl anesthesia plus hypothermic cardiopulmonary bypass at the time of aortic cross-clamp (anes + CPB/AXC). Polynomial regression of the Phe dose response curve estimated the Phe dose required to increase mean arterial blood pressure 20%, designated PD20. Although pre-anesthesia PD20 and anes + CPB/AXC PD20 values were not affected by ejection fraction, significant differences in PD20 (P less than 0.05) between groups occurred during fentanyl anesthesia (group I = 2.28 +/- 1.60 micrograms.kg-1, group II 1.57 +/- 0.98 micrograms.kg-1; mean +/- SD). Anes + CPB/AXC was associated with a significant reduction in PD20 in both groups compared with pre-anesthesia (P less than 0.01). Our results suggest impairment of alpha 1-adrenergic responsiveness occurs during fentanyl anesthesia in patients with ejection fractions less than or equal to 40% (evidenced by greater PD20 values). Although this impairment may be due to altered Phe pharmacokinetics, these results also support the possible existance of alpha 1-adrenergic receptor desensitization in this group. Reduction in PD20 during anes + CPB/AXC in all patients points to more powerful effects than fentanyl anesthesia alone; such influencing effects may include hemodilution, hypothermia, elevated plasma catecholamines, exclusion of the pulmonary circulation, or altered Phe pharmacokinetics.

Anesthesia, Intravenous↗
PubMed1987

Effects of preoperative calcium entry blocker therapy on alpha-adrenergic responsiveness in patients undergoing coronary revascularization.

Calcium entry blocking drugs (CaEBs) produce vasodilation and, in high doses, modify alpha adrenergic receptor function. Previous laboratory data suggested that CaEBs might alter the response to alpha-adrenergic stimulation. The authors tested the hypothesis that CaEB therapy altered alpha-adrenergic responsiveness in patients chronically treated with CaEBs. Twenty-six consenting patients with coronary artery disease were given a phenylephrine challenge before anesthesia induction and during cardiopulmonary bypass while the aorta was cross-clamped. A log dose response curve was constructed for each patient, and the ED30 (dose producing 30% increase in systemic vascular resistance) was calculated. Nine patients not treated with CaEB served as controls, and 17 patients were treated with nifedipine (n = 7) or diltiazem (n = 10). Mean ED30 was increased approximately three-fold in the CaEB treated groups compared to the control group. However, there was no statistical difference in the ED30 or phenylephrine dose response slopes between CaEB treated and untreated patients. In awake patients, ED30 correlated with nifedipine levels (R = 0.953, P = 0.01). There was a significant (P less than .02) shift in the ED30 from prior to anesthesia to during aortic cross-clamp and cardiopulmonary bypass; ED30 was approximately 50% less and correlated with CaEB level (R = 0.713, P = 0.03). Hemodynamic variables were not different between groups at any interval. Our data suggest that vascular responsiveness to phenylephrine in patients treated with CaEBs is diminished, but similar to that in untreated patients. Vascular responsiveness decreases in awake patients with increasing nifedipine levels.

Adult↗
PubMed1986

Verapamil and myocardial preservation in patients undergoing coronary artery bypass surgery.

The value of verapamil hydrochloride as a myocardial preservative when administered prior to or during periods of myocardial ischemia was studied in patients with normal preoperative cardiac function during elective coronary artery bypass grafting. Myocardial protection included systemic hypothermia (28 degrees C) and hypothermic hyperkalemic cardioplegia. Patients were randomly divided into four groups. Group 1 received intravenous administration of verapamil prior to aortic cross-clamping. Group 2 received intravenous verapamil plus verapamil in the cardioplegic solution. Group 3 received verapamil in the cardioplegic solution only. Group 4 was given no verapamil. Oxygen extraction during the reperfusion period was greatest in Group 4. However, the incidence of pacing was 50 to 78% in Groups 2 and 3, who were given verapamil in the cardioplegic solution. These groups also had a greater need for inotropic agents for discontinuation of cardiopulmonary bypass (CPB). This study indicates that verapamil may be a useful pretreatment prior to CPB and ischemia, but is not effective and may even be detrimental when administered during ischemic periods to patients with good myocardial function.

Adult↗
PubMed1984

Massive transfusion in a neonate.

We have presented a case in which a neonate suffered massive intracranial hemorrhage during surgery. Despite what appeared to be a fatal insult, the patient responded to massive transfusion therapy and all its associated problems and survived.

Blood Transfusion↗
PubMed1984

Hyperkalemia and cardiovascular collapse after verapamil and dantrolene administration in swine.

The cardiovascular and neuromuscular interactions of verapamil and dantrolene were evaluated in 20 chloralose-anesthetized swine. The animals were randomly divided into three groups. Group I, ten animals, received a bolus intravenous injection of 0.1 mg . kg-1 of verapamil followed by the continuous infusion of 5 micrograms . kg-1 . min-1. This group was then randomly divided into two equal subgroups. Five of these animals, Group Ia, continued to receive the verapamil infusion alone. The other five animals, Group Ib, received dantrolene in incremental doses of 1.0, 3.3, and 5.6 mg . kg-1 while the verapamil infusion was continued. An additional group of five animals, Group II, received the same incremental doses of dantrolene but did not receive verapamil. Five control animals, Group III, received the alpha-chloralose anesthetic without dantrolene or verapamil. Neuromuscular function, as measured by twitch height, was affected only by dantrolene, which produced a dose-dependent depression. Verapamil resulted in initial decreases in heart rate, arterial blood pressure, cardiac output, left ventricular dP/dt, and an increase in PR interval. Dantrolene alone produced a mild increase in arterial blood pressure. Dantrolene administration to verapamil-pretreated animals resulted in a profound depression in cardiac function, marked elevation in serum K+ (8.0 +/- 0.7 mEq . l-1), and no change in arterial pH (7.39 +/- 0.02). Cardiac arrest preceded by complete atrioventricular heart block occurred in one animal before and in four animals after the final dantrolene dose was given to animals pretreated with verapamil. Although we cannot extrapolate data from our porcine model to humans, further studies are indicated to help evaluate a possible fatal drug interaction before verapamil and dantrolene are used concomitantly in a clinical setting.

Animals↗
PubMed1984

Comparative cardiovascular effects of verapamil, nifedipine, and diltiazem during halothane anesthesia in swine.

The cardiovascular effects of the calcium channel blockers verapamil (V), nifedipine (N) and diltiazem (D) were compared in halothane-anesthetized swine. Equipotent hypotensive doses of the three calcium channel blocking drugs were administered randomly by continuous infusion to three groups of six animals each to produce a uniform 25-30% reduction in mean systemic arterial blood pressure (BP). An additional group of six animals received sodium nitroprusside (S) to demonstrate the effects of lowering blood pressure with a pure vasodilator on this experimental preparation. Hemodynamic indices monitored before and after drug administration included ECG, mean systemic and pulmonary artery blood pressure, mean central venous and pulmonary capillary wedge pressure, thermodilution cardiac output, left ventricular pressure, and left ventricular dP/dt. All four study drug infusions reduced BP an average of 28%. V and D reduced BP by decreasing cardiac output (41% and 42%, respectively) without affecting systemic vascular resistance. N and S produced hypotension by decreasing systemic vascular resistance (36% and 21%, respectively) without affecting cardiac output. D reduced heart rate (18%) and both D and V increased the PR interval (60% and 40%, respectively). Calcium chloride (20 mg X kg-1 intravenous bolus) improved indices of myocardial contractility but did not affect drug-induced changes in cardiac electrophysiology. These data demonstrate that in this halothane-anesthetized swine model the administration of equihypotensive doses of verapamil or diltiazem has a more pronounced affect on cardiac conduction and myocardial contractility than does nifedipine, which predominantly reduces systemic vascular resistance with minimal effects on cardiac function.

Anesthesia, General↗
PubMed1983

Hemodynamic interactions of verapamil and isoflurane.

The hemodynamic interactions of verapamil and isoflurane were studied in eight dogs. Left ventricular function was analyzed using a right heart bypass preparation to permit rigid hemodynamic control. Hemodynamic studies were performed at 0.7, 1.05, and 1.40% isoflurane before and during the maintenance of two stable levels of verapamil, administered intravenously by combining a bolus dose (0.2 mg X kg-1) with an infusion (3.0 and 6.0 micrograms X kg-1 X min-1). Isoflurane produced a concentration-dependent depression of left ventricular function as indicated by dP/dt max, per cent systolic shortening, and left ventricular function curves. This depression was enhanced in a dose-plasma concentration-dependent manner by verapamil and was reversed by calcium chloride. Isoflurane alone and the combination of verapamil and isoflurane decreased systemic vascular resistance in a dose-dependent fashion that was antagonized partially by calcium chloride. Therefore, verapamil can enhance the hemodynamic effects of isoflurane in a dose-related manner that needs to be considered when both drugs are administered together.

Animals↗
PubMed1983

Cardiovascular responses to verapamil during coronary artery bypass graft surgery.

The cardiovascular effects of verapamil administration during coronary artery bypass graft surgery were studied in patients with normal left ventricular function. Anesthesia consisted of morphine, diazepam, and nitrous oxide. Before atrial cannulation for cardiopulmonary bypass, 16 patients received either verapamil (N = 8) 0.075 mg X kg-1 or an equal volume of its solvent (N = 8) administered intravenous over 1 min. Hemodynamic functions and serum verapamil levels were measured over the succeeding 10 min. Verapamil produced rapid reductions in systemic vascular resistance, systemic arterial blood pressure, and left ventricular stroke work index. The PR interval increased slightly and two of the patients who had a baseline PR interval of 200 msec developed a mild first degree heart block. Heart rate, cardiac index, pulmonary capillary wedge pressure, central venous pressure, and right ventricular stroke work index did not significantly change. No measured cardiovascular functions changed in the control group. Serum verapamil levels peaked at 346.4 +/- 143.5 ng X ml-1 0.5 min after drug administration and then rapidly declined. Both groups of patients tolerated surgery and the immediate postoperative recovery period without hemodynamic compromise. Verapamil can be safely administered before cardiopulmonary bypass in patient with good left ventricular function during narcotic-based anesthesia.

Aged↗
PubMed1983

Pretreatment with lidoflazine, a calcium-channel blocker. Useful adjunct to heterogeneous cold potassium cardioplegia.

Ten mongrel dogs were studied to determine if pretreatment with lidoflazine would protect the canine myocardium during aortic cross-clamping when circumflex coronary artery occlusion limits the distribution of cold potassium cardioplegia. A canine right heart bypass preparation was used. Regional function was determined with a sonomicrometer. Twenty minutes before aortic cross-clamping, lidoflazine or solvent was administered in a random, blind fashion. A circumflex artery snare prevented the cardioplegic solution from entering the circumflex artery. A 100 minute arrest period with cardioplegic infusion every 20 minutes was followed by 45 minutes of reperfusion before global and regional function were reevaluated. In the group receiving solvent, postarrest function in the circumflex region recovered to only 30% of prearrest values (p less than 0.05), a marked functional deterioration. In the group protected by lidoflazine, function in the circumflex region returned to 90% of prearrest values (NS). Function in the left anterior descending (LAD) regions of both groups demonstrated full recovery after arrest. Global left ventricular function was well preserved in both groups and failed to reflect the damaged, malfunctioning region in the group receiving solvent. These findings suggest that pretreatment with lidoflazine can improve myocardial protection when delivery of cardioplegia is not homogeneous.

Animals↗
PubMed1982

Esophageal lead for intraoperative electrocardiographic monitoring.

The use and safety of the esophageal electrocardiogram for detection and diagnosis of dysrhythmias or ischemia during anesthesia was compared with the conventional electrocardiogram using leads II and V5 in 20 patients undergoing coronary artery bypass graft surgery. Using an intra-atrial electrocardiogram as the standard to provide detection and definitive diagnosis of dysrhythmias, the correct diagnosis from leads II and V5 was made in 53.8% and 42.3% of cases, respectively, whereas 100% of the dysrhythmias were properly diagnosed from the esophageal electrocardiogram (p less than 0.05). In two patients, the presence of a significant dysrhythmia was not detected using standard leads II and V5 alone. Large, distinct P waves, resulting from the proximity of the esophageal lead to the left atrium, clearly established the temporal relationship between atrial and ventricular depolarization. Posterior myocardial ischemia was diagnosed in one patient by ST-segment elevation in the esophageal electrocardiogram, whereas leads II and V5 did not demonstrate ischemic changes. No complications were encountered during the study. The esophageal lead is safe, simple to use, and provides valuable information for detection or diagnosis of dysrhythmias and myocardial ischemia during anesthesia.

Aged↗