Charles E. Whitcher

Cardiovascular Effects of Halothane in Man

The author examined the cardiovascular effect of halothane in 15 unmedicated volunteers under moditions of constant arterial carbon dioxide tension and body temperature. Compared with awake measurements, the effects during the first hour of anesthesia included depression of enrdiac output, stmke volume, arterial pressure, left ventricular minute and stroke work, and myocardial contractility (as evidenced by the ballistocardiogram IJ-wave amplitude), muscle blood flow, and total body oxygen consumption. Mean right atrial pressure incrensed. These efeect were directly related to halothane concentration. Total peripheral resistance and heart rate were unchnnged and, at lighter anesthetic levels, skin blood flow increased. After five hours of anesthesia saveral values returned to towards or above awake values. These were: cardiac output, stroke volume, left ventricular work or stroke work, IJ-wave amplitude, muscle blood flow, and mean right atrial pressure. Told peripheral resistance fell and heart rate increased with progressive duration of anesthesia.

Chronic exposure to anesthetic gases in the operating room.

Halothane present in the ambient atmosphere was continuously measured in each of two operating rooms during the conduct of surgical anesthesia. Concentrations were determined on-line with a mass spectrometer and found to vary with sampling site, breathing system used, and the scavenging system employed to remove overflow anesthetic gases. Concentrations of halothane measured within a 3-foot radius of the anesthesia equipment averaged 8.7 ppm when a nonrebreathing circuit was used (flow 10 l/min), and 4.9 ppm with a semiclosed circle system (flow 4–5 l/min). End-tidal concentrations of halothane averaged 0.21 ppm in 81 samplings from operating room nurses and 0.46 ppm in 36 samplings from anesthetists. Residual concentrations were present in many individuals 16 hours after exposure. A significant reduction in atmospheric contamination of the operating room was obtained by use of appropriate scavenging equipment. The implications of these findings are discussed.

Exposure to Nitrous Oxide and Neurologic Disease among Dental Professionals

Questionnaires, mailed to approximately 30,000 dentists and an equal number of dental assistants requesting information regarding professional exposure to anesthetics and health problems, showed an increased incidence of neurologic complaints in dental professionals who worked with nitrous oxide. The most striking differences were noted in individuals reporting symptoms of numbness, tingling, and/or muscle weakness. For dentists heavily exposed to nitrous oxide, the rate of these complaints was 4-fold greater than for nonanesthetic-exposed dentists. For dental assistants heavily exposed to nitrous oxide, a 3-fold increase in these same complaints was noted. In view of recent evidence that nitrous oxide abuse may lead to polyneuropathy, the results suggest that occupational exposure to nitrous oxide by both dentists and dental assistants may be associated with similar neuropathy.

Distribution of waste anesthetic gases in the operating room air.

Epidemiologic and animal studies identify a relationship between chronic exposure to anesthetic gases and health hazards. Efforts to reduce exposure of personnel require an understanding of the distribution of anesthetic waste gases in the operating room air. Concentrations ol nitrous oxide and halothane were measured at numerous stations throughout an operating room and a delivery room in the absence of personnel. Air conditioning flow rates and flow patterns were varied, as was the height of the anesthetic gas source. Air flow patterns were found to dominate the anesthetic gas distribution, while buoyaney effects were neligible. Venting waste gases at the floor does not significantly reduce exposure of personnel. Areas of high concentration were observed; their occurrences and locations varied strongly with air flow patterns. The exhaust grille is the best location for a single measurement of the average room concentration. Recirculating air-conditioning systems reduce energy costs; however, only the non-recirculating portion of the air exchanges reduces waste gas concentrations.

Monitoring occupational exposure to inhalation anesthetics.

Air monitoring, an essential feature of the waste gas control program, is best based on measurement of total leakage in time-weighted sampling of N2O present in the anesthetists breathing zone during clinical anesthesia. Leakage in the high-pressure N2O system is measured separately in a survey of the empty rooms. The infrared N2O analyzer used for these measurements is also useful as a teaching device and in enhancing the safety of the patient.

Reflex Cardiovascular Responses to Simulated Diving

Submersion produces profound cardiovascular responses in diving mammals and birds. This &dquo;diving reflex&dquo; consists of bradycardia, decreased cardiac output and a marked decrease in peripheral blood flow.’ Studies of land mammals such as man suggest these mammals possess a modified diving reflex. In man, the method of study have been necessarily limited. We have taken advantage of two techniques to assess more thoroughly the diving reflex in man. First is the method of Whayne and Killip which allows diving to be simulated by a cold

Acute Hemodynamic Effects of Methoxamine in Man

The circulatory effects of single intravenous injections of 0.065 mg./kg methoxamine were investigated in 5 healthy volunteer subjects. Ninety minutes after the first injection, atropine 1–2 mg. was administered intravenously and the injection of methoxamine repeated. Cardiovascular parameters were evaluated by ballistocardiographic and dye-dilution methods, the former data continuously calculated by an analog computer. Methoxamine briefly, but markedly, depressed heart rate, cardiac output, and left ventricular work. Stroke volume decreased moderately, while mean arterial pressure increased moderately, and total peripheral resistance increased markedly. A preliminary partial vagal block with atropine permitted a greater increase in mean arterial pressure, with lesser changes in all other parameters except stroke volume, thus making methoxamine a “better” vasopressor.It is suggested that some of the depressant effects of methoxamine are related to intense arteriolar constriction, venous pooling of blood, reflex vagal depression of the atria and ventricles, and direct beta-adrenergic blocking, and excitation-contraction uncoupling actions.