Karl A. Poterack

Who uses transesophageal echocardiography in the operating room

A survey was made of 155 anesthesiology residency programs in the United States to determine the patterns of use, responsibility for interpretation, and training of those responsible for intraoperative transesophageal echocardiography (TEE).Survey questions included numbers and types of cases for which TEE is used, who interprets TEE data and how they are trained, the extent of resident training in TEE, and beliefs about the utility of TEE. One hundred eight completed surveys were returned (70% response). Of those responding, 98 (91%) use intraoperative TEE. In 53 of those 98 institutions (54%), an anesthesiologist was primarily responsible for the interpretation of TEE data, whereas a cardiologist was responsible in the remainder. Approximately 35% of anesthesiologists using TEE had training in its use during residency or fellowship; the remainder were trained after finishing residency or fellowship. Forty-two percent of anesthesiologists who use TEE leave a formal interpretation on the chart apart from the anesthesia record, and 43% bill specifically for performing TEE. Although 69% of those responding thought that formal credentials should be required for anesthesiologists to use intraoperative TEE, only 32% reported that their institutions actually mandated this. 38% of those responding stated that they offer a dedicated TEE rotation to their residents, and 13% thought that their graduating residents were trained well enough to use TEE on their own. Among academic institutions responding, the use of intraoperative TEE is nearly universal, responsibility for its interpretation is split almost evenly between cardiologists and anesthesiologists, and there is a disparity between opinions and reality with regard to TEE credentialing for anesthesiologists. (Anesth Analg 1995;80:454-8)

A comparison of transfusion requirements between living donation and cadaveric donation liver transplantation: relationship to model of end-stage liver disease score and baseline coagulation status.

The use of living donation is an important option for patients in need of liver transplant. We retrospectively reviewed the preoperative Model for End-Stage Liver Disease (MELD) score, baseline coagulation laboratory results, and intraoperative transfusion of red blood cells and component therapy for 27 living donation transplants and 69 cadaveric donation transplants during a 3-yr period (2001–2004). Patients undergoing living donation transplantation had significantly lower MELD scores and preserved coagulation function compared with cadaveric donation transplantation recipients (P < 0.001). The living donation transplant patients also received significantly fewer transfusions of red blood cells and component therapy compared with the cadaveric donation transplant patients (P < 0.001). For the combined population of both cadaveric donation transplant and living donation transplant patients, there were significant associations between MELD score and preoperative coagulation tests (P < 0.001) and intraoperative transfusion of blood and component therapy. MELD score and preoperative fibrinogen concentration were identified as independent predictors of transfusion exposure. In conclusion, we detected significant differences in severity of disease at time of transplantation, degree of impairment of coagulation function, and need for transfusion of red blood cells and component therapy between patients undergoing living donation transplantation compared with patients undergoing cadaveric donation transplantation.

Effects of Isoflurane, Midazolam, and Etomidate on Cardiovascular Responses to Stimulation of Central Nervous System Pressor Sites in Chronically Instrumented Cats

The systemic hemodynamic actions of isoflurane (a volatile anesthetic) and etomidate and midazolam (intravenous anesthetics) have been well documented. However, few studies have investigated the actions of these agents on central cardiovascular control sites. The present investigation examined the actions of these agents on the responses of systolic arterial pressure (SAP), heart rate, infrarenal aortic blood flow, and lower body vascular resistance to central nervous system pressor site stimulation in chronically instrumented cats. Male and female cats (n = 23) were chronically instrumented with bipolar stimulating electrodes in the regions of the ventrolateral hypothalamus (anterior, 10.0 mm; lateral, 2.5 mm; depth, −4.0 mm) and mesencephalic reticular formation (anterior, 2.0 mm; lateral, 2.0 mm; depth, −1.0 mm). Control experiments consisted of stimulation sequences at 1×, 2×, and 4× threshold current levels to elicit pressor responses. Stimulation of the hypothalamic site produced current-dependent increases in SAP (6–85 mm Hg), in heart rate (3–56 beats/min), and in infrarenal aortic blood flow (0–85 mL/min). Reticular formation site stimulation produced graded increases in SAP (6–129 mm Hg) only. Isoflurane (1.5%, 2.5%, and 3.0%), etomidate (3.0-mgkg bolus and 0.4-mg·kg−1·h−1 infusion), and midazolam (7.5-mg/kg bolus and 0.2-mg·kg−1·h−1 infusion) were then administered in separate experimental groups. After a steady hemodynamic state was established with each agent, stimulation sequences were repeated. Isoflurane produced an attenuation of the responses of SAP (from 85.1 ± 8.2 to 17.8 ± 6.1 mm Hg at 1.5%, to 7.2 ± 2.0 mm Hg at 2.5%, and to 4.7 ± 2.0 mm Hg at 3%, all P < 0.05), heart rate (from 41.1 ± 13.0 to 12.5 ± 2.7 beats/min at 2.5% and to 6.2 ± 1.7 beats/min at 3%, all P < 0.05), and of the infrarenal aortic blood flow (from 72.6 ± 14.3 to 11.8 ± 4.2 mL/min at 1.5%, to 10.2 ± 5.6 mL/min at 2.5%, and to 3.2 ± 1.5 mL/min at 3%, all P < 0.05) to the highest level of hypothalamic site stimulation. Isoflurane similarly produced an attenuation of the SAP response (from 128.7 ± 10.3 to 15.4 ± 8.1 mm Hg at 1.5%, to 0.2 ± 1.1 mm Hg at 2.5%, and to 0.3 ± 0.5 mm Hg at 3.0%, all P < 0.05) to the highest level of reticular formation site stimulation. Etomidate administration attenuated SAP responses to the highest level of hypothalamic site stimulation (from 50.6 ± 6.8 to 24.4 ± 10.8 mm Hg, P < 0.05) and to the highest level of reticular formation site stimulation (from 92.7 ± 14.0 to 23.8 ± 12.6 mm Hg). Heart rate and blood flow responses were not changed by etomidate. Similarly, midazolam administration blunted the SAP responses to the highest level of hypothalamic site stimulation (from 73.0 ± 8.9 to 38.0 ± 7.2 mm Hg, P < 0.05) and to the highest level of reticular formation site stimulation (from 108.0 ± 17.9 to 54.7 ± 17.7 mm Hg, P < 0.05). Blood flow responses were not changed by midazolam, and only heart rate change at the highest level of hypothalamic stimulation was decreased (from 56.7 ± 7.9 to 32.0 ± 6.4 beats/min, P < 0.05). During emergence from isoflurane, occasional conversion of pressor to depressor responses was observed. The results suggest that disruption of central nervous system cardiovascular control centers may contribute to the alterations in hemodynamic stability produced by these anesthetic agents.

Dexmedetomidine and halothane produce similar alterations in electroencephalographic and electromyographic activity in cats

Dexmedetomidine, an alpha2-adrenergic agonist, produces sedation and reduces volatile anesthetic requirements. This investigation compared the actions of dexmedetomidine and halothane on the processed EEG and on the electromyogram (EMG) which has not been previously described. Chronically instrumented cats were prepared with arterial and venous cannulae, quadriceps EMG electrodes and EEG electrodes in the lateral geniculate nucleus and over the frontal and occipital cortices. Hemodynamics, EEG and EMG were recorded in the conscious state and after randomly administered halothane or intravenous dexmedetomidine (on separate days). Blink and tail-clamp responses also assessed level of consciousness. Halothane resulted in unconsciousness and a lack of response to tail clamping, while dexmedetomidine produced profound sedation, with preservation of tail-clamp responses. Both agents similarly decreased (P < 0.05) the median power frequency from 9.5 +/- 0.9 to 5.7 +/- 0.4 Hz (2% halothane) and from 9.6 +/- 0.7 to 5.9 +/- 0.8 Hz (20 microg/kg dexmedetomidine), and 95% power frequency from 23.0 +/- 0.2 to 18.2 +/- 0.6 Hz (2% halothane) and from 23.0 +/- 0.2 to 19.1 +/- 0.8 Hz (20 microg/kg dexmedetomidine). Both agents increased the total spectral power and delta band power of the EEG and reduced integrated EMG activity. Halothane and dexmedetomidine produced differing effects on level of consciousness as assessed by response to tail clamping. The results suggest that conventional processing of EEG and EMG parameters are inadequate to assess anesthetic depth in the presence of alpha2-adrenergic agonists.

The Effect of Halothane on Thermosensitive Neurons in the Preoptic Region of the Anterior Hypothalamus in Acutely Instrumented Cats

Normal thermoregulatory processes are significantly impaired by halothane anesthesia. However, the direct effects of halothane on thermosensitive neurons in the preoptic region of the anterior hypothalamus, a major thermoregulatory site, have not been previously investigated. Thirty-eight cats were anesthetized with alpha-chloralose (60 mg/kg) and urethane (600 mg/kg) and placed in stereotactic restraint. Stainless steel thermodes for highly selective local heating and cooling were stereotactically placed into the preoptic region with thermocouples used to monitor regional temperature. Using tungsten microelectrodes, 148 single neurons in the preoptic region were identified and subjected to local heating (to 42 degrees C) and cooling (to 30 degrees C). Eighteen percent (n = 27) in 15 different cats were classified as thermosensitive by accepted criteria (change in firing rate per degree centigrade of greater than 0.8 spikes.s-1.degrees C-1 or less than -0.6 spikes.s-1.degrees C-1). Thermosensitve units were then subjected to graded concentrations of halothane (0.25-1.0% end-tidal), and local heating and cooling were repeated. The spontaneous firing rate (spikes per second) at 37 degrees C of 21 warm-sensitive neurons was significantly (P less than 0.05) reduced, to 65.5 +/- 8.3, 42.6 +/- 10.7, 28.0 +/- 9.5, and 18.1 +/- 6.0% of control at 0.25, 0.50, 0.75, and 1% halothane, respectively. Spontaneous firing rate returned to 99.5 +/- 19.8% of control within 30 min after discontinuation of halothane. Thermosensitivity (change, per degree centigrade, in spikes per second) was also significantly reduced, to 33.3 +/- 5.6, 28.5 +/- 14.6, and 13.9 +/- 6.6% of control at 0.50, 0.75 and 1.0% halothane (all P less than 0.05 compared to control).(ABSTRACT TRUNCATED AT 250 WORDS)

The Effects of Halothane, Isoflurane, and Enflurane on Thermoregulatory Responses in the Neuraxis of Cats

Background:Normal thermoregulatory function is believed to be modulated by thermosensitive neurons in the preoptic region of the anterior hypothalamus and other sites within the central nervous system including the spinal cord. Previous evidence has demonstrated modulation of segmental spinal cord thermoregulatory mechanisms from more rostral central nervous system sites. The ability of the volatile anesthetics to disrupt normal thermoregulatory function and produce shivering-like activity during emergence is well documented. The purpose of the current investigation was to examine the action of the volatile anesthetics halothane, isoflurane, and enflurane on thermoregulatory responses produced at the preoptic region and spinal cord. Methods:Cats were chronically instrumented with bilateral cannulas allowing selective heating and cooling of the preoptic region. Electrodes were implanted in hindlimb and forelimb muscles for electromyographic (EMG) analysis. Animals underwent selective heating and cooling of the preoptic region in the awake state, during volatile agent anesthesia and during emergence. In a separate series of animals, pontine-transected cats with epidural thermodes and a thermocouple underwent alternate heating and cooling of the spinal cord. Heating and cooling was performed in the nonanesthetized state, at graded concentrations of halothane, and during emergence. In all animals, deep core peritoneal temperature, epidural spinal cord temperature, forelimb and hindlimb EMG activity were continuously recorded and digitally processed. EMG responses in both experiments were quantitated and analyzed for power spectral density. Results:In the chronically prepared animals, heating and cooling of the preoptic region in the conscious state resulted in appropriate thermoregulatory responses, including shivering-like activity and increased EMG power with preoptic region cooling. Halothane, isoflurane, and enflurane each abolished these thermoregulatory responses. During emergence from anesthesia, however, the typical spontaneous increases in EMG power observed at normothermia were significantly attenuated by heating of the preoptic region and augmented by cooling of the preoptic region. In the acutely prepared animals, cooling of the spinal cord produced graded increases in EMG activity. Increased concentrations of halothane dose-dependenstly diminished this response to cooling of the spinal cord. During emergence, cooling of the spinal cord resulted in a shivering response similar to those observed during control conditions. Conclusions:The ability of preoptic region heating and cooling to modulate postanesthetic shivering implies that while thermoregulatory pathways remain intact, volatile anesthetics produce an imprecision in the control of thermoregulatory responses at the level of the anterior hypothalamus. Attenuation of shivering-like responses generated at spinal cord levels in pontine-transected cats implies a significant blunting action of thermoregulatory response mechanisms at the level of the spinal cord or lower brain stem.

Central venous air embolism without a catheter

Venous air embolism is a well-recognized complication of central venous catheterization. Although previous reports have documented venous air embolism occurring in a number of ways, including during initial catheterization, when catheters crack or are disconnected, and after catheter removal, no reports mention the possibility of air embolism occurring when a guide wire without a catheter was in place. A patient is presented who displayed signs and symptoms of venous air embolism (tachypnoea, chest pain, and arterial hypoxaemia) during central venous catheter manipulation while a guide wire alone was in place. Pulse oximetry was used to detect hypoxaemia and suggest an aetiology for the patient’s clinical symptoms. It is postulated that a previously described gasp reflex or some sort of sustained negative pressure manoeuvre caused venous air embolism around the guide wire and accounted for the patient’s signs and symptoms. During central venous catheter placement, a high index of suspicion for venous air embolism should be maintained, pulse oximetry should be used, the skin entrance site should be kept covered by an occlusive dressing, and the patient should be positioned head-down.RésuméL’embolie veineuse aérienne est une complication bien reconnue de la cathétérisation du système veineux central. Même si des rapports préalables ont documenté que l’embolie veineuse gazeuse peut survenir de différentes façons incluant lors de la cathétérisation initiate, lors d’un bris de cathéter ou lors de la disconnection des cathéters, ainsi qu’après l’extraction de catheter, aucun rapport ne mentionne la possibilité d’embolie gazeuse quand la broche-guide sans cathéter est en place. Un patient qui a démontré des signes et symptômes d’embolie gazeuse veineuse (tachypnée, douleur thoracique, et désaturation artérielle) durant la manipulation d’un cathéter veineux central est présenté alors que la broche-guide seule était en place. L’oxymetrie de pouls fut utilisée afin de détecter l’hypoxémie et suggérer l’étiologie des symptômes cliniques du patient. On présume qu’une inspiration profonde réflexe ou une pression négative soutenue lors de la manoeuvre a occasionné l’embolie gazeuse autour de la broche-guide. Durant l’installation d’un cathéter veineux central, on doit maintenir un haut degré de suspicion face à l’embolie gazeuse veineuse, l’oxymétrie de pouls doit être utilisée et le site d’entree doit être recouvert par un pansement occlusif, le patient doit être en position de Trendelenburg.

Preoperative Midodrine Use Does Not Predict Intraoperative HypotensionDuring Orthotopic Liver Transplantation

Background: Complications of liver transplantation undermine long term benefits for patients with end-stage liver disease. Some patients awaiting liver transplantation are treated with midodrine, an oral α1 agonist. We hypothesized that preoperative use of midodrine would predict increased intraoperative hypotension with associated vasopressor and blood product administration and deleterious effects on graft survival. Methods: We performed a retrospective, matched case control study examining patients receiving midodrine versus those not before undergoing liver transplantation. Sixty-four patients were examined and analyzed. Primary outcomes were total intraoperative vasopressor use and minutes of intraoperative hypotension. Results: For the primary outcomes, no statistically significant difference was found between the groups. No significant differences were seen in one year patient or graft survival. Statistically significant differences were noted in American Society of Anesthesiologists (ASA) physical status, Model for End-Stage Liver Disease (MELD) scores, preoperative blood pressure metrics, use of continuous renal replacement therapy intraoperatively, cryoprecipitate, and cell saver use. Conclusions: Preoperative use of midodrine in patients undergoing liver transplantation did not predict increased intraoperative hypotension or concomitant need for vasopressors or blood products. Midodrine use was associated with higher ASA and MELD scores, renal replacement therapy, and decreased preoperative blood pressure, but not altered graft survival.

Adult Live Donor Hepatectomy: A Retrospective Pilot Study Comparing Four Strategies of Perioperative Pain Control

Purpose: To compare the post operative pain control of four distinct management strategies in adult live donor hepatectomy. Methods: Sixty-two ASA physical status I and II patients undergoing live donor hepatic resection from 2001 to 2008 were retrospectively organized into four groups for post-operative pain control. Group A received epidural catheter, Group B received PCA, Group C received intraoperative dexmedetomidine and PCA, and Group D received perioperative gabapentin, intraoperative dexmedetomidine, and PCA. Four day postoperative visual analog pain scores (VAS), intravenous morphine equivalent use, duration of hospitalization, and time until return of bowel function was measured. Results: Mean visual analog pain score for a cumulative four day postoperative interval demonstrated 2.2 (± 0.73) for epidural catheter, 3.4 (± 1.13) for patient controlled analgesia (PCA), 3.0 (± 1.42) for intraoperative dexmedetomidine infusion plus PCA, and 2.3 (± 1.09) for perioperative gabapentin, intraoperative dexmedetomidine, combined with PCA. These results achieved statistical significance with p = 0.0443. Total intravenous morphine equivalent use was similar between the three non-epidural groups. There was no difference in length of hospitalization or time until return of bowel function amongst the four groups. Conclusions: Both epidural infusion and a three drug regimen of perioperative gabapentin, intraoperative dexmedetomidine, and PCA produced superior postoperative pain control compared with PCA alone or a combination of PCA and dexmedetomidine. The three drug regimen represents a preferred strategy as it provides optimal pain control without the theoretic risk of epidural hematoma in patients with a predictable postoperative coagulopathy. This pilot study serves as a template for future prospective examination of this three drug regimen versus epidural in major non-hepatic open abdominal surgery where post operative coagulopathy is less of a concern.