Contemporary anesthesia practice最新文献

Disorders of the thyroid gland are frequently unrecognized and untreated by the attending physician and present the anesthesiologist with a diagnostic and therapeutic challenge. Very large goiters distort and compress the larynx and require an experienced anesthesiologist for safe intubation. If surgery is elective and can be postponed in patients suspected of being hypo- or hyperthyroid, there is sufficient time to permit the anesthesiologist and the attending physician to obtain appropriate tests of thyroid function and institute appropriate therapeutic measures to restore the metabolic rate to normal. When there is insufficient time to confirm a clinical diagnosis of thyroid disease, the anesthesiologist is faced with important therapeutic decisions. It is the author's opinion that therapeutic intervention is, in most instances, preferable to therapeutic nihilism. In the case of a patient suspected of hypothyroidism, it is usually safe to administer a physiologic replacement dose of thyroxine to support the patient intraoperatively or postoperatively. If hypothyroidism is associated with cardiovascular disease, other debilitating illness, or advanced age, thyroxine must be given with extreme caution in order to avoid dangerous tachyarrhythmias or too rapid acceleration of the metabolic rate. The hyperthyroid patient facing nonelective surgery represents a very serious challenge to the anesthesiologist, since marked accentuation of clinical hyperthyroidism (thyroid storm) is a major risk of such surgery. In such a situation, intravenous propranolol and intravenous iodine are the optimal drugs for a safe and uncomplicated clinical course during and following surgery. In both instances, the anesthesiologist must use skillful clinical judgment in making the appropriate diagnosis and selecting appropriate therapy. Careful and continuous supervision of the patient is necessary during and following surgery and appropriate treatment and support of the patient should be provided until it is safe to discontinue therapy, if necessary, to confirm the diagnosis of thyroid disease. Careful clinical judgment and judicious use of appropriate medication should provide the patient with a smooth and safe intraoperative course and a rapid and uncomplicated postoperative recovery.

Arginine vasopressin, the antidiuretic hormone in man, in low concentrations increases reabsorption of water in the collecting ducts of the kidney, producing a concentrated urine. It is also a potent vasoconstrictor because of its direct effect on arteriolar smooth muscle, particularly the splanchnic, renal, and coronary vascular beds. This appears to be a dose-dependent response. In very high concentrations it is capable of producing a diuresis with increased urinary sodium excretion. The preponderance of evidence today has failed to show any significant increase in antidiuretic hormone levels with anesthesia alone, provided significant hemodynamic changes do not occur. It seems unlikely, then, that the inhalation anesthetics or high-dose narcotic anesthesia are a direct stimulus to ADH release. If a decrease in urine flow does occur, it is more likely caused by either the renal hemodynamic effects of the anesthetic or a secondary release of ADH. Surgical stimulation is capable of significantly increasing ADH levels. This apparently is a stress response that can be attenuated by the depth of anesthesia. Such a response to operation may produce ADH levels that can indeed decrease urinary flow, but more importantly may succeed in achieving levels that can exert a significant vasopressor effect. In unusual circumstances, vasopressin levels can occur that are capable of producing a diuresis and increased urine sodium excretion.

Prophylactic pacemakers should be recommended for all preoperative patients with second- and third-degree heart block, regardless of whether the block is in the AV node or the trifascicular conduction system. Symptomatic patients with potential for trifascicular block should also have a transvenous pacemaker. Those without symptoms should be monitored during anesthesia and the postoperative recovery period.

The suggested anesthetic management of patients with potentially ischemic myocardium is as follows: 1. Careful work-up before proceeding if angina is present preoperatively. 2. Heavy premedication, attention to factors of preoperative anxiety, and avoidance of unnecessary painful procedures in the awake patient. Do not stop propranolol. 3. Monitoring of ST segments via V5 lead during anesthesia. Do not permit large fluctuations in systolic blood pressure or large increases in heart rate. 4. Maintenance of patient's temperature to obviate postoperative shivering. 5. Treatment of increased heart rate and ST segment changes with propranolol in 0.25-mg I.V. increments every 1 to 3 minutes until improvement noted (reasonable acute dose limit is 2 to 3 mg). 6. Treatment of ventricular arrhythmias with lidocaine bolus (50 to 100 mg) and infusion if more than one bolus is required (1 to 2 mg/70 kg/min), plus usual blood gases and electrolytes.