Cardiovascular depression and thermoregulatory disruption caused by pentothal/halothane anesthesia in the harbor seal, Phoca vitulina.

Anesthesia was induced in the harbor seal (Phoca vitulina) with an intravenous injection of 10 mg/kg thiopental sodium; this was followed by halothane (1%) anesthesia for up to 9.5 h. Cardiac output was reduced to 30% of the pre-anesthesia value (from an average of 11.5 1/min to 3.5 1/min) while systemic blood pressure fell from an average of 150/110 to 80/60. Arterial oxygen partial pressures were somewhat depressed (58-72 Torr) during ventilation with air. Heart rate became stable at 90-100 beats/min. Hypothermia was an occasional problem during the first hour of anesthesia, but this trend reversed and gave way to hyperthermia during prolonged anesthesia.

Blunted hypoxic pulmonary vasoconstriction by increased lung vascular pressures.

We tested the hypothesis that increased pressures within the lung vessels would inhibit hypoxic pulmonary vasoconstriction at all levels of alveolar CO2 tension. Selective hypoxia of the left lower lobe of the lung in open chested dogs caused the electromagnetically measured blood flow to the lobe to decrease 51 plus or minus 4 (SE) percent and its vascular resistance to increase 132 plus or minus 13 percent. Pressure and blood flow in the main pulmonary artery and left atrial pressure did not change during the hypoxic response. Stepwise increments in left artrial and pulmonary arterial pressures induced either by inflating a left atrial balloon or infusing dextran, progressively diminished the vasoconstrictive response to hypoxia. The response was usually abolished when left atrial pressure reached 25 mmHg. For all vascular pressures, hypoxic vasoconstriction was blunted by hypocapnic alkalosis but not enhanced by hypercapnia. We conclude that the redistribution of blood flow away from an hypoxic lobe of the lung to lobes with high Po2 was greatly attenuated by increasing pressures within lung vessels or by inducing respiratory alkalosis.

Local effects of anesthetics on regional hypoxic pulmonary vasoconstriction.

The hypothesis that halogenated anesthetics and N2O locally inhibit hypoxic pulmonary vasoconstriction (HPV) was tested. Selective ventilation of the left lower lobe of the lung with N2 in dogs anesthetized with pentobarbital caused blood flow to the lobe to decrease 55.5 +/- 2.0 per cent and lobar vascular resistance to increase 148 +/- 8 per cent. Responses to hypoxia were remeasured during administration of various MAC multiples of inhalation anesthetics to the left lower lobe and following systemic administration of intravenous anesthetics. Isoflurane and fluorexene progressively inhibited and finally almost extinguished the vasoconstriction response as anesthetic concentration increased to 3 MAC. N2O moderately diminished HPV. Halothane had little, and intravenous anesthetics had no, significant effect on HPV. It is concluded that N2O, isoflurane, and fluroxene locally inhibit regional HPV and via this mechanism may increase total venous admixture.

Dependency of hypoxic pulmonary vasoconstriction on temperature.

We studied the effect of temperature change on hypoxic pulmonary vasoconstriction. Selective hypoxia on the left lower lobe of the lung in open-chested dogs at 37 degrees C caused the electromagnetically measured blood flow to the lobe to decrease 51 +/- 5 (SE)% and its vascular resistance to increase 155 +/- 25%. Testing hypoxic response. The hypoxic response at 31.1 +/- 0.4 degrees C was only a 26 +/- 6% decrease in lobar blood flow compared to the hypoxic response at 40.0 +/- 0.5 degrees C which was a 60 +/- 5% decrease in lobar blood flow. Hypothermia itself was associated with a significant increase in pulmonary vascular resistance. We conclude that hypothermia inhibits and hyperthermia enhances hypoxic pulmonary vasoconstriction. The mechanism of inhibition may involve prehypoxic vasoconstriction.

Acute effects of hypercapnia and hypoxia on minute ventilation in unrestrained Weddell seals.

We studied the ventilatory response to hypoxia and hypercapnia in five freely diving juvenile Weddell seals (age = 2 years) at McMurdo Station, Antarctica. The ventilatory response to CO2 was brisk, with minute ventilation increasing as a linear function of end tidal CO2 with an average slope of 3.1 L X (min X mm Hg)-1. The ventilatory response to hypoxia was small and variable. End tidal PO2 values as low as 28 mm Hg provoked at most a doubling of minute ventilation. These results were supported by the observation that elevated end tidal CO2 always inhibited voluntary diving whereas low PO2 values did not. Comparison of the Weddell seals' CO2 responsiveness to that of other mammals reveals similar CO2 sensitivity. We conclude that CO2 is the major determinant of ventilatory drive in wild Weddell seals.

Pulmonary circulation of the harbor seal.

Cardiac output (Q) and pulmonary arterial pressure (Ppa) were measured under various conditions in four harbor seals (Phoca vitulina) weighing 35--52 kg. In seals anesthetized with halothane, Q averaged 3.47 l/min; in awake resting seals, Q averaged 11.5 l/min; and during surface dives (i.e., at atmospheric pressure) Q averaged 1.99 l/min. Stroke volume was one-third and two-thirds of the awake resting value during anesthesia and diving, respectively. Systolic Ppa was usually 40--50 Torr in anesthetized and awake resting seals, but was about 10 Torr lower during both surface and compression (i.e., elevated ambient pressure) dives. Diastolic Ppa was constant and high during anesthesia and quite variable in awake resting seals. During both surface and compression dives the diastolic Ppa often fell to the same level as right atrial pressure. We conclude that Q and Ppa are high in awake resting seals and that pulmonary blood flow may cease between beats during diving.

General anesthetics and regional hypoxic pulmonary vasoconstriction.

Administration of N2O, fluroxene and isoflurane to the left lower lobe (LLL) of dogs anesthetized with pentobarbital was previously shown to inhibit LLL hypoxic pulmonary vasoconstriction (HPV). Using the same experimental model, the present study examined the effect of whole-lung administration of N2O, fluroxene, isoflurane, halothane, and enflurane on left-lower-lobe HPV. Selective ventilation of the LLL with N2 alone caused blood flow to the lobe to decrease 53.3 +/- 3.0 per cent. Responses to LLL hypoxia were remeasured during administration of inhalation anesthetics at 1 and 2 MAC to both the LLL and the rest of the lung. Isoflurane and fluroxene progressively inhibited and at 2 MAC halved lobar HPV. N2O (one third MAC) caused slight but significant inhibition, while halothane and enflurane caused slight and nonsignificant changes in lobar HPV. These effects of whole-lung administration of anesthetics on HPV were almost identical to those obtained when the administration was confined to the test lobe alone. It is concluded that N2O, isoflurane, and fluroxene locally inhibit regional HPV and via this mechanism increase total venous admixture, while halothane and enflurane do not have this effect.

Cyclic hypoxic pulmonary vasoconstriction induced by concomitant carbon dioxide changes.

We examined the stability of acute lobar hypoxic pulmonary vasoconstriction. In 12 mongrel dogs the left lower lobe (LLL) was selectively ventilated with a constant minute molume with nitrogen and the electromagnetically measured fraction of the cardiac output perfusing the LLL and the LLL end-tidal CO2 concentration were observed for 1 h. We found that both the fraction of the cardiac output perfusing the LLL and the LLL end-tidal CO2 concentration initially decreased during LLL hypoxia and then oxcillated in a progressively damped fashion. When LLL end-tidal CO2 was kept constant by CO2 infusion during LLL hypoxia or when LLL hypoxia was induced by LLL atelectasis, no oscillations were observed. We conclude that if minute ventilation of a hypoxic area of lung is kept constant, then decreased regional blood flow decreases regional alveolar PCO2. As a consequence of these two opposing influences, blood flow to an acutely hypoxic area will be oscillatory.

Force, torque, and stress relaxation with direct laryngoscopy.

The anesthetist exerts axial force on the laryngoscope handle to expose the glottis. The anesthetist must also apply a perpendicular force to balance the torque on the laryngoscope. Several studies have measured axial force during direct laryngoscopy, but none has measured torque. This study used a newly designed laryngoscope handle to measure force and torque simultaneously during direct laryngoscopy of ASA grade I and II patients requiring general anesthesia and endotracheal intubation for elective surgery. In 58 patients, peak force averaged 38 +/- 2 newtons. Peak torque averaged 4 +/- 0.2 newton-meters, and the perpendicular force was estimated as 40 +/- 2 newtons. The peak torque that can be balanced by the wrist is approximately 6 newton-meters, suggesting that torque may be a limiting factor for laryngoscopy in some situations. Peak force and torque demonstrated stress relaxation, a viscous property of biologic tissues. Force and torque decreased monoexponentially to approximately 70% of peak values with a half-time of 4 +/- 0.3 s. The phenomenon occurred in spite of administration of muscle relaxants, and was probably due to stress relaxation of pharyngeal tissues that are passively stretched during laryngoscopy.

Force and torque vary between laryngoscopists and laryngoscope blades.

Several studies have examined the effects of patient characteristics on force of laryngoscopy, but little attention has been paid to the importance of technique and equipment. This study investigated whether force, torque, head extension, and view varied significantly between laryngoscopists and compared force and torque using Macintosh 3 and Miller 2 blades. The study population consisted of ASA grade I and II patients requiring general anesthesia and endotracheal intubation for elective surgery. Force, torque, head extension, and laryngeal view were highly reproducible when laryngoscopy was repeated by the same individual, Force and torque showed great variation between laryngoscopies performed by different anesthetists, For example, peak force varied over a range of 56 newtons among patients, but could also vary as much as 30 newtons between different anesthetists repeating laryngoscopy in the same patient. Force and head extension were 30% less with Miller laryngoscope compared to the Macintosh. Thus, laryngoscopic force and torque depend on technique and equipment. Further studies of force and torque may lead to improved techniques. The force-measuring laryngoscope could be a useful tool in teaching laryngoscopy.