Michael R. Hodges

Ventilatory pattern, intrapleural pressure, and cardiac output.

Continuous positive-pressure ventilation may decrease cardiac output. However, a few reports have separated the effects of positive and end-expiratory pressure (PEEP) from those of mechanical ventilation. Ten surgical patients requiring mechanical ventilatory support had catheters inserted for measurement of right atrial pressure (RAP), pulmonary artery occlusion pressure (PAOP), intrapleural, radial artery, airway, and atrial filling pressures, and cardiac output. All patients breathed spontaneously between mechanical breaths delivered every 30 seconds by intermittent mandatory ventilation (IMV). Measurements were made with 0, 5, and 10 cm H2O PEEP, and during intermittent positive-pressure ventilation (IPPV) with 12 breaths/min without PEEP. Airway pressure (Paw), intrapleural pressure, RAP, and PAOP were increased by PEEP and IPPV. Intrapleural pressure increased most during IPPV (p less than 0.001). Atrial filling pressures and cardiac output were unaffected by PEEP but decreased during IPPV (p less than 0.001). Patients receiving IMV maintained negative intrapleural pressure, atrial filling pressure, cardiac output and, therefore, O2 delivery, regardless of PEEP level. The authors conclude that patients requiring mechanical respiratory support, with or without PEEP, may maintain better cardiopulmonary function when allowed some spontaneous ventilatory activity.

Comparison of venous air embolism monitoring methods in supine dogs.

The sensitivities and durations of positive responses of routinely used methods for detecting venous air embolism and physiologic variables reflecting changes accompanying air embolism were compared in ten anesthetized dogs receiving incremental venous injections of 0.1, 0.25, 0.5, 0.75, 1.0, 1.5, and 2.0 ml/kg air. These doses of air produced a spectrum of changes ranging from subtle alterations in Doppler frequency to dramatic, life-threatening cardiovascular depression. Precordial Doppler ultrasound monitoring was the most sensitive detection method, but failed to reflect embolus size. Mean pulmonary arterial pressure and end-tidal carbon dioxide concentration (FETCO2), while slightly less sensitive than the Doppler device, reliably detected 0.25-0.5 ml/kg of injected air and quantitatively reflected the size of the embolus. Changes in Doppler, and FETCO2 were predictably positive at air volumes one fourth of those producing decreases in arterial blood pressure and cardiac output. Other frequently monitored signs of air embolism, such as a millwheel murmur and cardiac arrhythmias, were late manifestations and were seen only with injection of 1.5–2.0 ml/kg air. and FETCO2 remained altered the longest after air injections (20–30 min at 2.0 ml/kg), while changes in Doppler-transmittcd signals at the same dose lasted 15 min. Positive responses with other methods of air embolus detection, although dose-related, were significantly shorter-lasting than and FETCO2 alterations. Cardiac murmurs and arrhythmias were transient after air injection, lasting less than a minute, even with emboli of 2.0 ml/kg. The data indicate that the combination of application of a Doppler device with cither end-tidal carbon dioxide measurement or a flowdirected pulmonary-artery catheter with display provides the desired combination of sustained, sensitive and reliable detection of air embolism and quantitative evaluation of embolus size.

Change in pulmonary venous admixture with varying inspired oxygen.

Pulmonary venous admixture (&OV0422;sp/&OV0422;t) was analyzed as a function of fractional concentration of inspired O2 (Fio2) in 30 patients who required postoperative mechanical ventilation. Pulmonary and radial artery blood-gas tensions and pH were measured and &OV0422;sp/&OV0422;t was calculated with Fio2 ranging from 0.21 to 1. In all patients, &OV0422;sp/&OV0422;t decreased when Fio2 was increased from 0.21 to 0.4 and then stabilized to an Fio2 of approximately 0.6. As the Fio2 was increased to 1, &OV0422;sp/&OV0422;t increased. Since the inhalation of gas mixture with Fio2 ≥ 0.6 increased right-to-left intrapulmonary shunting of blood, we recommend respiratory function be evaluated during inhalation of a clinically useful concentration of O2 rather than at an Fio2 of 1.

Lithium Carbonate and Neuromuscular Blocking Agents

The effects of lithium carbonate on the responses to five neuromuscular blocking agents were evaluated in dogs anesthetized with halothane (1 per cent) and N2O (60 per cent) in O2. Latency (time from first twitch-height depression to maximal blockade), maximal twitch-height depression, and times to return to 50 per cent and 100 per cent control twitch tension were measured before and after intravenous infusion of lithium carbonate (1 mg/kg/min for one hour) during neuromuscular blockades produced by succinylcholine, decamethonium, gallamine, d-tubocurarine, or pancuronium. Lithium prolonged the latencies of neuromuscular blockades produced by 0.1 mg/kg succinylcholine and 0.1 mg/kg decamethonium by 248.1 per cent and 49.0 per cent, respectively, but had no effect on latency produced by 0.02 mg/kg pancuronium. The times for return to 50 per cent of control twitch height were prolonged by 69.5, 40.0, and 120.1 per cent, respectively. Lithium had no effect on latency or duration of blockades produced by 0.15 mg/kg d-tubocurarine and 0.6 mg/kg gallamine, but enhanced maximal twitch-height depressions produced by 0.9 mg/kg gallamine and 0.02 mg/kg pancuronium by 22.9 and 9.9 per cent, respectively. Twitch tensions decreased 5-10 per cent over three hours in three dogs receiving lithium infusion without relaxants. Twitch tension was depressed 0-2 per cent in three dogs after five hours of anesthesia in the absence of lithium or relaxants. Lithium prolonged the time required for neostigmine to reverse neuromuscular blockade produced by pancuronium in two of three dogs from a mean of 60 seconds to 135 seconds.

Cardiovascular responses to nitrous oxide during light, moderate, and deep halothane anesthesia in man

The cardiovascular effects of addition of 20, 40, and then BO percent N2O or nitrogen during controlled ventilation with light (0.8 percent), moderate (1.2 percent), and deep (1.6 percent) halothane-O2 anesthesia were determined in 39 volunteers and compared to results obtained in 18 additional volunteers who received similar concentrations of halothane-O2 anesthesia alone over the same time interval.Halothane resulted in significant and similar reductions in heart rate at all concentrations studied hut produced concentration-related decreases in mean arterial blood pressure, stroke volume, and cardiac output and increases in right atrial pressure. Halothane did not significantly change peripheral resistance at any concentration. Addition of N2O did not change arterial blood pressure or heart rate at any concentration of halothane but produced increases in right atrial pressure in all groups. Peripheral resistance was reduced and stroke volume and cardiac output increased when N2O was added to 0.8 percent halothane. Subjects anesthetized with 1.2 percent halothane showed no significant change in stroke volume or cardiac output with addition of any concentration of N2O, while those anesthetized with 1.6 per cent halothane sustained reductions in stroke volume and cardiac output with 60 percent N2O. Peripheral resistance remained unaltered during addition of N2O to 1.2 percent halothane but significantly increased with 1.6 percent halothane. Addition of nitrogen to halothane produced changes that were similar to those occurring during continued halothane-O2 administration. These data demonstrate that addition of N2O during halothane-O2 anesthesia produces significant changes in cardiovascular dynamics which are variable and dependent upon the concentrations of halothane and N2O employed. Our findings suggest that N2O blocks the reduction of peripheral vascular resistance and increases in cardiac output, stroke volume, and heart rate seen with continued halothane-O2 administration when added to moderate or deep levels of halothane.

Tracheal pathology following short-term intubation with low- and high-pressure endotracheal tube cuffs.

Histologic sections of dog tracheas were taken from 20 dogs anesthetized and intubated for 5 to 7 hours with high-pressure, low-volume Shiley or low-pressure, high-volume Lanz endo-tracheal tubes. Microscopic examination and measurement showed that while the high-pressure, low-volume cuff produced deeper average mucosal erosion, the large-volume, low-pressure cuff resulted in significantly greater lengths of tracheal mucosa-cuff erosion. Maximal depth of penetration throught the basement membrane was similar in both groups. Grooves in the mucosa were seen in 50% of the high-volume-cuff trachea sections but none of the low-volume-cuff tracheal sections. These findings demonstrate that low-pressure, high-volume endotracheal tube cuffs produce different but significant tracheal damage after short-term intubation when compared to high-pressure, low-volume cuffs.

Comparison of aortic pulse-wave contour analysis and thermodilution methods of measuring cardiac output during anesthesia in the dog.

Accuracy and reliability of cardiac output (±Qt measurement utilizing computer analysis of the aortic pressure wave (Warner method) were assessed by comparing this technique with a standard thermodilution method in 20 halothane-anesthetized dogs over a wide range of ±Qt and systemic vascular resistance (SVR) values. Five of the dogs also had electromagnetic flow (EMF) probes placed around the ascending aorta. More than 800 pairs of simultaneous ±Qt determinations were performed using pulse-wave and thermodilution methods, and more than 150 triplicate measurements made using all three techniques during changes in inspired halothane concentrations (0.5–2.0 per cent) or during infusions of sodium nitroprusside (SNP) and phenylephrine (PE). Cardiac out±puts ranged from 0.7 to 5.3 1/min, mean aortic blood pressures (BP) ranged from 30 to 200 torr, and SVR varied from 70 per cent below to 200 per cent above control values. Correlation of pulse-wave-computed and thermodilution-calculated ±Qt values was high (r = .91 or better), irrespective of SVR during changes in halothane concentration. Correlation of pulse-wave and EMF methods was equally good during this period (r = .92 or better). Correlation was lower, but still good, with alterations in SVR of 30 per cent or less induced by SNP or PE (r = .90 or better for thermodilution and r = .91 or better for EMF). When SVR was changed from 30 to 50 per cent of control with SNP or PE, correlation between pulse-wave-computed and EMF ±Qt values remained good (r = .85), but correlation between pulse-wave-computed and thermodilution-calculated ±Qt values was only fair (r = .79–.77). Correlation of thermodilution-calculated or EMF and pulse-wave-computed ±Qt values deteriorated significantly with SNP. and PE-induced changes of SVR greater than 50 per cent (r = <.5). These results demonstrate that computer analysis of the aortic pressure wave is a simple and valid method of determining ±Qt during halothane anesthesia, but must be limited to conditions of only moderate alteration of SVR during infusions of vasopressor or vasodilator drugs.

Hypoxemia and hypocarbia following intermittent positive-pressure breathing.

The authors determined the effects of short-term, vigorous intermittent positive-pressure breathing (IPPB) on arterial blood O2 tension (Pao2) in 10 unmedicated preoperative adult patients (ASA class I). Arterial blood was analyzed before and 0.5, 5, 15, and 40 minutes after 12 minutes of IPPB with nebulized 0.9% NaCl and room air. Pao2 increased from 89.1 ± 11 torr (mean ± SD) to 102.1 ± 13.9 torr, and arterial CO2 tension decreased from 29.5 ± 4 torr to 18.4 ± 3 torr, causing significant respiratory alkalosis (pHa 7.62 ± 0.05). Five minutes after IPPB, Pao2 decreased to 69.2 ± 8 torr; alveolar-arterial Po2 difference, breathing 21% O2, increased significantly; and serum K+concentration decreased significantly. All these values returned to baseline levels within 40 minutes. The authors, acknowledging the value of IPPB when specifically indicated, counsel caution in patients with borderline pulmonary reserve and arterial oxygenation.

Correlation of oxygen uptake and cardiovascular dynamics during N2O-fentanyl and N2O-thiopental anesthesia in the dog.

The relationship between changes in whole-body O2 consumption (&OV0312;O2) and cardiovascular dynamics during changing levels of N2O-fentanyl and N2O-thiopental anesthesia was determined in 24 dogs. Dose-dependent reductions in &OV0312;O2, mean blood pressure, and cardiac output occurred with infusion of fentanyl and thiopental. Painful stimuli increased &OV0312;O2 during light anesthesia but not during deeper levels of anesthesia. Deep levels of N2O-fentanyl and N2O-thiopental anesthesia may protect the patient with limited cardiac reserve by reducing &OV0312;O2 and preventing increases in &OV0312;O2 caused by painful stimuli.

Pulmonary Shunt and Cardiovascular Responses to CPAP during Nitroprusside-induced Hypotension

The effects of continuous positive airway pressure (CPAP) on cardiovascular dynamics and pulmonary shunt (QS/QT) were investigated in 12 dogs before and during sodium nitroprusside infusion that decreased mean arterial blood pressure 40-50 per cent. Before nitroprusside infusion, 5 cm H2O CPAP significantly, P < .05, decreased arterial blood pressure, but did not significantly alter heart rate, cardiac output, systemic vascular resistance, or QS/QT- Ten cm H2O CPAP before nitroprusside infusion produced a further decrease in arterial blood pressure and significantly increased heart rate and decreased cardiac output and QS/QT/ Nitroprusside caused significant decreases in arterial blood pressure and systemic vascular resistance and increases in heart rate, but did not change cardiac output or QS/QT. Five cm H2O CPAP during nitroprusside did not further alter any of the above-mentioned variables. However, 10 cm H2O CPAP decreased arterial blood pressure, cardiac output, and QS/QT- These data indicate that nitroprusside infusion rates that decrease mean arterial blood pressure by 40-50 per cent do not change cardiac output or QS/QT. During nitroprusside infusion low levels of CPAP do not markedly alter cardiovascular dynamics, but high levels of CPAP (10 cm H2O), while decreasing QS/QT, produce marked decreases in arterial blood pressure and cardiac output.