Aggressive use of intra-aortic balloon pump and emergency coronary bypass surgery. Enhanced survival in acute evolving MI.

This report describes our experience with prophylactic and therapeutic use of IABPs prior to and following coronary artery bypass grafting (CABG) in 39 patients experiencing acute evolving myocardial infarctions (AEMI). All patients showed objective evidence of coronary thrombosis (contrast angiography) followed by later evidence of streptokinase (SK)-induced restoration of antegrade blood flow in the infarct-related coronary artery (as determined by repeat angiography). In these 39 high-risk patients, 38 survived and were discharged. One patient died (2.6 per cent) on the twelfth postoperative day.

Hemodynamic status following regional and general anesthesia for carotid endarterectomy.

We prospectively studied 23 patients undergoing carotid endarterectomy under regional (n = 13) or general (n = 10) anesthesia to determine the hemodynamic basis of increased frequency in the need for postoperative vasopressor support when regional anesthesia was used. Anesthesia and postoperative care were conducted without reference to hemodynamic data from pulmonary artery catheterization. Although mean arterial pressure was similar in the two groups postoperatively, 11 of the 13 patients undergoing regional anesthesia and 3 of the 10 patients undergoing general anesthesia required phenylephrine postoperatively. No patient required therapy postoperatively to reduce a systolic pressure exceeding 160 mm Hg. Mean arterial pressure remained below the preoperative baseline value in both groups (p < 0.05 with general anesthesia; p = 0.06 with regional anesthesia) during follow-up. In the general anesthesia group, systemic vascular resistance declined significantly below baseline (p < 0.05) following the operation, accompanied by a decline in mean arterial pressure (p < 0.05) and a higher cardiac output. Intraoperative fluid requirements were greater during general anesthesia than during regional anesthesia (p < 0.01). Pulmonary artery occlusion pressure was lower postoperatively than at baseline in both groups (p < 0.05). Pulmonary artery occlusion pressure was higher in the general anesthesia group despite the greater use of phenylephrine in the regional anesthesia group.

Sternal retraction and pulmonary artery catheter compromise.

Forty-one consecutive open-chest cardiac procedures requiring sternal retractors for visualization were prospectively studied. Chest x-rays demonstrating the course of the introducer sheaths and pulmonary artery catheters (PACs) were taken before and after sternal retractor expansion. Five different introducer sheath insertion sites were monitored (right internal jugular, left internal jugular, left subclavian, right subclavian, and right supraclavicular). The incidence of permanent loss of pulmonary artery (PA) and central venous pressure (CVP) waveforms was recorded after retractor expansion. Forty-five percent of both the left and right subclavian groups suffered loss of the PA and CVP waveforms, whereas none of the other insertion site groups was affected. Therefore, it is recommended that PACs inserted for surgery requiring sternal retractors be placed via nonsubclavian routes.

Coronary artery bypass grafting within 24 hours after intracoronary streptokinase thrombolysis.

Little specific information currently exists describing the management of patients with an evolving acute myocardial infarction (AMI) treated with direct intracoronary infusion of streptokinase (SK) followed by emergency coronary artery bypass grafting (CABG). A total of 194 patients with an evolving AMI underwent emergency coronary artery angiography with infusion of SK. Thirty-four of these patients with partial restoration of orthograde blood flow in the infarct-related coronary artery (as determined by clinical and objective evidence of myocardial salvage) were referred for emergency CABG. Problems related to the surgical and anesthetic care of these high-risk patients involved: (1) management of resuscitation of patients with AMI, (2) SK-induced coagulopathy and ongoing thrombolysis, and (3) timely CABG to preserve myocardial salvage. To highlight comparisons of SK-CABG management, data regarding 34 consecutive patients having routine non-SK-CABG surgery were collected simultaneously during the study. Data collected retrospectively included: anesthetic drug summaries, time frame of events from admission to the emergency room until commencing bypass, use of invasive monitoring and hemodynamic assist devices, induction complications, operative complications, coagulation derangements, volume replacement, and blood loss. Results revealed no deaths up to 24 hours postoperatively in the 34 emergency SK-CABG patients, even though complications were frequent intraoperatively. Furthermore, there were no statistically significant differences in SK patients v non-SK patients in blood lost, banked blood and cell saver blood administered, or platelet transfusions. However, in comparison to the non-SK-CABG patients, the SK patients received significantly larger amounts of fresh frozen plasma, cryoprecipitate, and aminocaproic acid.

Effects of resuscitation from hemorrhagic shock on cerebral hemodynamics in the presence of an intracranial mass.

This study compares intracranial pressure, cerebral blood flow, and cerebral oxygen transport during hemorrhagic shock and following fluid resuscitation with crystalloid or colloid solution in a canine model with an epidural mass lesion. After placement of an epidural balloon, intracranial pressure was increased to 30 mm Hg for 5 minutes and then permitted to vary without further manipulation. Hemorrhagic shock was produced by the rapid removal of blood to achieve a mean arterial pressure of 55 mm Hg for 30 minutes. Resuscitation then was performed with intravenous lactated Ringer's solution, 60 ml/kg, or with 6.0% hetastarch, 20 ml/kg. Following both solutions mean arterial pressure and cardiac output were increased and hemoglobin concentration was reduced. Intracranial pressure was significantly lower immediately after resuscitation in the hetastarch group; it then gradually increased so that the difference was much less 1 hour later. Cerebral blood flow decreased during shock and was not restored by either fluid; cerebral oxygen transport fell further with resuscitation in both groups due to hemodilutional reductions in hemoglobin. Although colloid resuscitation improved systemic hemodynamics and maintained lower intracranial pressure, it failed, as did crystalloid resuscitation, to restore cerebral oxygen transport to prehemorrhagic shock levels.

Cerebral hemodynamics after hemorrhagic shock: effects of the type of resuscitation fluid.

Cerebral blood flow (CBF), cerebral oxygen delivery, and intracranial pressure were measured in 12 dogs subjected to hemorrhagic shock and then resuscitated with lactated Ringer's solution or 6% hetastarch. Hemorrhagic shock was produced by the rapid removal of blood to achieve a mean arterial pressure (MAP) of 40 mm Hg with BP maintained at that level for 30 min. Six animals were resuscitated with lactated Ringer's solution, 60 ml/kg iv, and six with 6% hetastarch, 20 ml/kg iv. Both solutions effectively restored systemic hemodynamic stability, increasing cardiac output and MAP. Intracranial pressure was significantly (p less than .05) lower after resuscitation in the hetastarch group, but CBF, which had decreased during shock, was not normalized by either fluid, and cerebral oxygen transport fell further with resuscitation secondary to a hemodilutional reduction of hemoglobin. Although 6% hetastarch may improve systemic hemodynamics and maintain a low intracranial pressure during resuscitation, it fails, as does lactated Ringer's solution, to restore cerebral oxygen transport to prehemorrhagic shock levels.

Effects of hypertonic saline versus lactated Ringer's solution on cerebral oxygen transport during resuscitation from hemorrhagic shock.

Hypertonic saline successfully restores systemic hemodynamics in dogs and humans with severe hemorrhagic shock and, in contrast to lactated Ringer's solution, does not increase intracranial pressure (ICP). This study compares cerebral oxygen delivery in 12 dogs subjected to hemorrhagic shock by the rapid removal of blood (mean arterial pressure of 40 mm Hg maintained for 30 minutes), and then resuscitated with lactated Ringer's solution (six dogs) or 7.5% saline solution (six dogs) to restore systolic arterial pressure. Both solutions effectively restored systemic hemodynamic stability, increasing cardiac output and systolic blood pressure while decreasing mean and diastolic arterial pressure and systemic vascular resistance. The ICP was significantly lower after resuscitation in the hypertonic saline group (p less than 0.05), but cerebral blood flow, which had decreased during shock, was not restored by either fluid, and cerebral oxygen transport fell further secondary to a hemodilutional reduction of hemoglobin. Although hypertonic saline may improve systemic hemodynamics and maintain a low ICP during resuscitation, it fails, as does Ringer's solution, to restore cerebral oxygen transport to prehemorrhagic shock levels.

Effects on cerebral hemodynamics of resuscitation from endotoxic shock with hypertonic saline versus lactated Ringer's solution.

This study was carried out to determine whether 7.5% hypertonic saline (HSS) and lactated Ringer's solution restore cerebral hemodynamics comparably when used for resuscitation from endotoxic shock. Endotoxic shock was produced in 13 dogs by the iv administration of 1.5 mg/kg Escherichia coli endotoxin. After 90 min of shock, seven animals were resuscitated with lactated Ringer's solution, 60 ml/kg iv, and six with 7.5% HSS, 6 ml/kg iv. Both solutions increased cardiac output and mean arterial pressure. With HSS, intracranial pressure was lower immediately after resuscitation (p less than .001) and one hour later (p less than .01). However, cerebral blood flow was not increased by either fluid and, due to hemodilution, cerebral oxygen transport decreased during resuscitation in both groups of animals. Thus, HSS restored systemic hemodynamics and maintained a lower intracranial pressure during resuscitation from endotoxic shock, but failed, as did lactated Ringer's solution, to restore cerebral blood flow and oxygen transport.

Effects on intracranial pressure of resuscitation from hemorrhagic shock with hypertonic saline versus lactated Ringer's solution.

Hypertonic saline (2400 mOsm/L) has been used successfully for fluid resuscitation of dogs subjected to severe hemorrhagic shock. This study compared the effects of resuscitation with hypertonic saline vs. lactated Ringer's solution on intracranial pressure (ICP) in dogs subjected to 30 min of sustained hypovolemic shock. Hypotension was produced by rapid withdrawal of blood until mean arterial pressure was 50 mm Hg, maintained at that level by withdrawal or infusion of blood over the next 30 min as necessary. Eight animals were resuscitated with hypertonic saline solution and nine with lactated Ringer's solution. Both solutions restored systolic blood pressure and cardiac output to control values. However, diastolic blood pressure and mean arterial pressure did not return to control values. The most prominent difference between the two groups was in ICP measured after resuscitation. ICP was lower in dogs resuscitated with hypertonic saline than in dogs resuscitated with lactated Ringer's solution (p = .029). Hypertonic saline fluid resuscitation may represent a potential alternative when aggravation of intracranial hypertension during resuscitation would place a patient at greater risk.

Implications of nimodipine prophylaxis of cerebral vasospasm on anesthetic management during intracranial aneurysm clipping.

Nimodipine, a calcium entry blocking agent similar in structure to nifedipine but with selective cerebrovascular dilating effects, has potential use in the therapy and prevention of cerebral vasospasm after intracranial hemorrhage. The authors summarize the effects of calcium entry blockers, review the pharmacology of nimodipine, and discuss both the known and possible interactions of oral nimodipine with physical and pharmacological interventions that neuroanesthesiologists employ for patients with cerebral vasospasm during craniotomy for aneurysm clipping. In a series of 26 patients undergoing aneurysm clipping, the authors found that intraoperative blood pressure tended to be reduced by nimodipine. Although the number of patients was limited by the fact that they were enrolled in a multi-center nimodipine aneurysm study and thus had to meet the criteria for that study, it is concluded that prophylaxis of cerebral vasospasm with nimodipine in patients with ruptured intracranial aneurysm results only in a favorable tendency toward lower systemic blood pressure during craniotomy.

Electroencephalographic evidence of arousal in dogs from halothane after doxapram, physostigmine, or naloxone.

The clinical impressions of enhanced arousal from halothane anesthesia and improvement of postanesthesia recovery scores after doxapram, physostigmine, or naloxone have not been verified in laboratory studies based on the effect of these drugs on MAC. With induction of anesthesia, a shift in the amplitude of the EEG from low to high occurs at anesthetic concentrations well below MAC and appears to coincide with the loss of consciousness. The authors examined the effect of arousal agents on the end-tidal halothane concentration required to produce this shifting EEG. In 24 unmedicated dogs, the end-tidal halothane concentration was elevated to 20 per cent above the shift point concentration (from 0.61 +/- 0.03 to 0.73 +/- 0.03 per cent) and maintained at this level for 30 min. Doxapram, 1 mg/kg, iv, and physostigmine, 0.03 mg/kg, iv, converted the EEG from a high amplitude to a low amplitude tracing in 22 +/- 3 s in eight of eight, and 225 +/- 37 s in seven of eight dogs, respectively. The end-tidal halothane concentration required to restore the shifting EEG was elevated above control for 50 +/- 7 min and 109 +/- 7 min, respectively. Naloxone, 0.06 mg/kg, iv, produced an awake EEG in two of eight dogs in 233 +/- 18 s which persisted for 22 +/- 4 min, and a transiently shifting EEG in three of eight dogs between 200 and 240 s. Naloxone 0.006, mg/kv, iv, produced an awake EEG in 80 +/- 8 s in four of four dogs who had previously received doxapram 3 h earlier. In this model doxapram and physostigmine paralleled the clinically observed onset and duration of arousal. The inconstant arousal from halothane anesthesia induced by naloxone was interpreted in terms of an opiate receptor independent action.

Dibutyryl cyclic adenosine monophosphate effects in the ischemic-hypoxic cat.

The effects of dibutyryl cyclic adenosine monophosphate (dB-cAMP) were studied in fifty cats, twenty anesthetized with pentobarbital and thirty with halothane. Nasopharyngeal temperature and Paco2 were maintained at normal values. Somatosensory evoked response was monitored and used as an indicator of cerebral cortical function. Ischemic hypoxic injury was produced by an orthopedic tourniquet snugly applied around the animal's neck and inflated for a period of fifteen minutes. This method produces a reliable and reproducible injury. Times for recovery of the evoked response to 10% of control value, as well as immediate and long-term animal survival, were noted. The dBcAMP was administered at the end of the hypoxic insult. Treated animals recovered the evoked response earlier than the untreated controls and had better immediate and long-term survival rates.

The nonlinear responses of cerebral metabolism to low concentrations of halothane, enflurane, isoflurane, and thiopental.

The relationship between cerebral oxygen consumption (CMRO2) and anesthetic concentration has been assumed (based upon isolated measurements) to be approximately linear at concentrations less than 1 MAC. The shapes of the anesthetic dose-response curves for both CMRO2 and cerebral blood flow (CBF) were examined by multiple measurements made at small, progressive concentration increments from 0 to 2 MAC halothane (six dogs), enflurane (six dogs), and isoflurane (six dogs), and during a constant 23 mg/kg/hr infusion of thiopental (six dogs). The EEG was continuously recorded and changes in EEG patterns from "awake" to "anesthetic" were correlated with changes in anesthetic concentration, CBF, and CMRO2. The significance of changes in the slopes of regression lines for CMRO2 before, during and after changes in EEG patterns from "awake" to "anesthetic" were then determined. Contrary to previous inferences, CMRO2 dose-response curves were found to be nonlinear at anesthetic concentrations less than 1 MAC for all anesthetics studied. CMRO2 decreased precipitously until a stable "anesthetic" pattern was observed on the EEG; thereafter, CMRO2 decreased at a markedly reduced rate. The onset of this change occurred at concentrations well below MAC for the inhalational anesthetics. With the thiopental infusion, CMRO2 decreased most rapidly during the first 25 minutes. With halothane and enflurane, CBF was maximal during the period of transition in the EEG from an "awake" to an "anesthetic" pattern. CBF was elevated at all concentrations of isoflurane studied. CBF decreased rapidly during thiopental infusion until the EEG pattern changed from "awake" to "anesthetic" and then more slowly. The results demonstrate that the change in the EEG to an "anesthetic" pattern, which occurs at concentrations well below MAC, is accompanied by an abrupt metabolic depression. It is speculated that these events coincide with the onset of functional depression.

The effects of heparin on recovery from ischemic brain injuries in cats.

Since ischemic anoxia in experimental animals has been reported to produce areas of cerebral postocclusive nonperfusion, the authors studied the effect of heparin on recovery from tourniquet-produced cerebrovascular injury in 41 barbiturate-anesthetized, ventilated cats (PaCO2 30 +/- 2.5 torr). Twenty-four control animals were subjected to 2-to-12-minute ischemic injuries without further treatment. Seven experimental animals were given heparin (1000 u/kg) 1 minute before 4-to-7-minute ischemic injuries, while 10 animals received heparin (1000 u/kg) immediately after 4-to-7-minute injuries. All animals were monitored with continuous arterial and intracranial pressure (ICP) recordings, EEG, and evoked cortical responses. Ischemia and evoked-response recovery times were linearly related in all groups (r = 0.998 control, r = 0.936 heparin preinjury, r = 0.951 heparin postinjury). Regression-line slope comparison indicated shorter evoked response and EEG recovery times in the heparin-treated groups than in the control group. Heparin administration did not effect elevations of ICP seen 6 and 12 hours postinjury in control versus experimental groups. In cats with injuries lasting 5 minutes or more, all control animals were decerebrate and apneic, while 5/12 heparin-treated animals had lesser neurologic deficits.

Anesthesia and subarachnoid intracranial pressure.

Intracranial pressure (ICP) was continuously monitored by the Richmond technic of Vries and Becker in 17 patients undergoing elective craniotomy. This method entails the placement, underlocal anesthesia, of a hollow screw through the cranium into the subarachnoid space. The screw was connected to a Statham P23Db pressure transducer with heavy vinyl tubing and with pressures recorded on a Beckman Dynograph. The effects of 3 anesthetic technice-halothane, enflurane, and nitrous oxide-narcotic-relaxant-on ICP during induction and maintenance were compared with preinduction control pressures. Control ICP in awake, lightly premedicated patients was 15 plus or minus 10 torr. Mask inductions with halothane and enflurane consistently caused significant increases in ICP from preinduction levels in the absence of excitement or airway obstruction. Induction with nitrous oxide-narcotic-relaxant did not increase ICP. Decreases in ICP following barbiturate administration were noted. Addition of halothane and enflurane to the inspired mixture of patients controlled and hyperventilated with nitrous oxide and oxygen caused consistent increases in ICP. With control hyperventilation (Paco2 25 plus or minus 5 torr), the ICP did not return toward preinduction values within 5 minutes with enflurane and halothane.

Intracranial pressure during hypotension and subsequent vasopressor therapy in anesthetized cats.

The effects of vasopressor therapy on intracranial pressure (ICP) during hypotension were evaluated in 45 adult cats anesthetized with pentobarbital and hyperventilated via an endotracheal tube with nitrous oxide, 70 per cent, and oxygen, 30 per cent, to maintain Paco2 25 plus or minus 5 torr. Hypotension was induced by intravenous administration of trimethaphan camsylate or sodium nitroferricyanide and by hemorrhage. Vasopressor (norepinephrine, ephedrine, or isoproterenol) administration in the absence of hypotension caused slight transient increases in ICP. Trimethaphan produced increases in ICP averaging 4.3 mm Hg, while sodium nitroferricyanide caused no change and hemorrhage decreased ICP by 3.9 mm Hg. After hypotension was established, vasopressors caused increases in ICP of 1-21 mm Hg. The greatest increase was seen with norepinephrine administration during sodium nitroferricyanide-induced hypotension. Increases in ICP were pronounced in absolute magnitude and rapidity of rise but were of short duration (2 to 5 minutes). The elevation of pressure might be of clinical significance in patients who have pre-existing intracranial hypertension or space-occupying lesions.