Emergent management of the airway. New pharmacology and the control of comorbidities in cardiac disease, ischemia, and valvular heart disease.
Once it is decided that the patient in distress requires tracheal intubation, the primary goal is to secure the airway as quickly and safely as possible to assure adequate oxygenation and ventilation. The clinician should quickly review the patient's history, physical examination findings, and laboratory data to determine the presence of cardiovascular disease, assess intravascular volume status, and formulate a plan for induction of anesthesia. The stresses of hypoxia, hypercarbia, acidosis, and extreme fatigue result in near-maximal sympathetic outflow that is manifest as tachycardia, labile blood pressure, and increased myocardial contractility. The astute clinician should anticipate that the tachycardia and hypertension associated with laryngoscopy and tracheal intubation is followed by a period of hypotension. This postintubation hypotension results from the acute marked attenuation of the sympathetic tone associated with resolution of hypoxia and hypercarbia, direct drug-induced negative inotropic effect, and vasodilation. The decrease in sympathetic vascular tone may result in hypotension by exacerbating the decrease in cardiac preload and afterload from hypovolemia. In addition, the use of positive pressure ventilation and positive end-expiratory pressure (PEEP) in these hypovolemic patients will further decrease ventricular preload by impeding venous return, leading to profound hypotension. Several pharmacologic agents are required to treat effectively the hemodynamic perturbations associated with induction, laryngoscopy, and tracheal intubation. Most sedative hypnotic agents that are administered for induction provide minimal to no analgesia. Patients are most often given a combination of drugs to provide adequate sedation, analgesia to blunt the noxious stimuli, and muscle relaxation to facilitate the laryngoscopy. The major challenge is to choose a combination of drugs that at the appropriate doses, effectively blunt the responses to intubation without contributing to postlaryngoscopy hypotension. One can use several strategies to accomplish these goals; administration of a narcotic analgesic before induction decreases the dose of induction agent and can attenuate the sympathetic response to intubation. Because of the prevalence of cardiovascular disease and hypovolemia in this population of patients, all chosen drugs should have minimal negative effect on cardiac function and patients with hypovolemia should be hydrated. Most clinical studies have been performed in hemodynamically stable patients, so the routine dosages of sedative hypnotics should be reduced substantially and titrated to effect. An additional strategy is to treat significant hemodynamic perturbations with vasopressors, vasodilators, short-acting selective beta-1 blockers, and inotropic agents. The choice of vasoactive agent depends on the magnitude of the hemodynamic response and the presence of specific underlying cardiovascular pathology.
Horak
J
J
Department of Anesthesia, University of Pennsylvania School of Medicine, Philadelphia, USA.
Weiss
S
S
D000402:Airway Obstruction / Q000150:complications* / Q000628:therapy*; D000758:Anesthesia / Q000009:adverse effects / Q000379:methods; D015897:Comorbidity; D006331:Heart Diseases / Q000150:complications* / Q000188:drug therapy* / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D007442:Intubation, Intratracheal / Q000009:adverse effects / Q000295:instrumentation / Q000379:methods*; D007828:Laryngoscopy / Q000009:adverse effects / Q000379:methods; D011175:Positive-Pressure Respiration / Q000295:instrumentation / Q000379:methods; D012151:Resuscitation / Q000009:adverse effects / Q000295:instrumentation / Q000379:methods*; D012307:Risk Factors