Gerald A. Maccioli

Anesthesia advanced circulatory life support

PurposeThe constellation of advanced cardiac life support (ACLS) events, such as gas embolism, local anesthetic overdose, and spinal bradycardia, in the perioperative setting differs from events in the pre-hospital arena. As a result, modification of traditional ACLS protocols allows for more specific etiology-based resuscitation.Principal findingsPerioperative arrests are both uncommon and heterogeneous and have not been described or studied to the same extent as cardiac arrest in the community. These crises are usually witnessed, frequently anticipated, and involve a rescuer physician with knowledge of the patient’s comorbidities and coexisting anesthetic or surgically related pathophysiology. When the health care provider identifies the probable cause of arrest, the practitioner has the ability to initiate medical management rapidly.ConclusionsRecommendations for management must be predicated on expert opinion and physiological understanding rather than on the standards currently being used in the generation of ACLS protocols in the community. Adapting ACLS algorithms and considering the differential diagnoses of these perioperative events may prevent cardiac arrest.RésuméObjectifLe grand ensemble d’événements liés à la réanimation cardiaque avancée (ACLS) tels que les embolies gazeuses, les surdosages d’anesthésiques locaux et la bradycardie sinusale dans un contexte périopératoire est différent des événements que l’on observe à l’extérieur de l’hopital. En conséquence, une modification des protocoles traditionnels d’ACLS permet une réanimation plus spécifique, en fonction de l’étiologie.Constatations principalesLes arrêts cardiaques en période périopératoire sont à la fois rares et hétérogènes; ils n’ont pas été décrits ou étudiés avec la même ampleur que les arrêts cardiaques survenant hors de l’hôpital. Ces crises sont habituellement vécues en direct, souvent anticipées et impliquent l’intervention d’un médecin connaissant les comorbidités du patient ainsi que la physiopathologie en rapport avec l’intervention et les anesthésiques utilisés. Lorsque le professionnel de la santé identifie la cause probable de l’arrêt cardiaque, le praticien a la possibilité d’entreprendre rapidement une prise en charge médicale.ConclusionsDes recommandations pour la prise en charge doivent être fondées sur les avis d’experts et sur la compréhension de la physiologie plutôt que sur des normes actuellement utilisées pour la création de protocoles d’ACLS hors du milieu hospitalier. L’adaptation des algorithmes d’ACLS et la prise en compte des diagnostics différentiels de ces événements périopératoires peuvent prévenir les arrêts cardiaques.

Response of lower esophageal contractility to changing concentrations of halothane or isoflurane: A multicenter study

A multiple-center study was performed to determine the relationship between lower esophageal contractility, clinical signs, and anesthetic concentration as expressed by minimum alveolar concentration (MAC). One hundred four American Society of Anesthesiologists Class I through III patients were exposed to isoflurane (with and without nitrous oxide) or halothane in concentrations of 0.5, 1.0, and 1.5 MAC. Heart rate and systolic blood pressure were continuously monitored. Both the amplitude and frequency of spontaneous and provoked lower esophageal contractions were measured in situ by using a 24-F probe equipped with provoking and measuring balloons. Combined results demonstrated statistically significant correlations (P<0.001) between lower esophageal contractility and MAC. Spontaneous lower esophageal contractions decreased from 1.10±0.12 (SEM) contractions per minute (0.5 MAC) to 0.42±0.05 (1 MAC) to 0.18±0.05 (1.5 MAC). Provoked lower esophageal contractility values decreased from 45±4 mm Hg (0.5 MAC) to 29±3 (1 MAC) to 19±2 (1.5 MAC). Heart rate changes did not correlate with MAC, and systolic blood pressure correlated in only one of three centers. Intracenter and intercenter analyses failed to demonstrate a significant relationship between lower esophageal contractility and heart rate or systolic blood pressure. No intracenter differences in either amplitude or frequency of lower esophageal contractions were observed, despite differences in volatile agents, induction techniques and agents, patient populations, and duration of anesthesia. Our studies indicate that lower esophageal contractility may be an indicator of anesthetic depth as reflected by MAC, but further studies are needed to quantify the effects of surgical stimulus, intravenous anesthetics, vasodilators, anticholinergics, calcium channel blockers, beta-adrenergic agonists, and the presence of a nasogastric tube.

Advances in oral anti-arrhythmic therapy: implications for the anaesthetist

Surgical patients often are receiving antiarrhythmic therapy. Thus, because anaesthetic agents can affect cardiac function and may interact with concurrent antiarrhythmic medications, the anaesthetist should be aware of the electrophysiology associated with dysrhythmias and their management. Tocainide, flecainide, mexiletine, encainide and amiodarone have been introduced recently and each has an unique pattern of bioavailability, metabolism and toxicity. Patients treated with these drugs need special concern as they have abnormal cardiovascular systems and may be at increased risk for perioperative morbidity. In addition, unexpected untoward reactions and toxicity can result from interactions of anaesthetic agents and these drugs. This review discusses normal cardiac electrophysiology, common dysrhythmias and the electrophysiological effects of the newer oral antiarrhythmic drugs.RésuméPlusieurs candidats à une intervention chirurgicale sont sous thérapie antiarythmique. Les tocaïnide, flécainide, mexilétine, eucaïnide et amiodarone sont des antiarythmiques oraux relativement nouveaux avec chacun des caractéristiques d’absorption, de biotransformation et de toxicité qui leurs sont propres. Les patients qui en prennent peuvent voir leur risque de morbidité périopératoire augmenter non seulement à cause de leur maladie cardio-vasculaire sous-jacente mais aussi, à cause des interactions possibles avec les agents anesthésiques. Il est done important que l’anesthésiste connaisse l’électrophysiologie cardiaque normale, celle des arythmies communes et l’effet des nouveaux antiarythmiques oraux.