Single-breath measurements of pulmonary oxygen uptake and gas flow rates for ventilator management in ARDS.

Monitoring data in critical care and anesthesiology should be displayed to present a rapid and easily comprehensible definition of the patient's clinical status. A graphic computer display of the analog output of gas flow rates and the O(2) and CO(2) concentrations of respiratory gases profiles the expired breath for an estimation of pulmonary function and gas exchange. An estimate of pulmonary perfusion, cardiac output, and the general adequacy of cardiovascular circulation is obtained from the computer calculation of O(2) uptake and CO(2) elimination, dead space, and alveolar ventilation. Adjunctive data from the spirometric measurements of airway pressures, volumes, and compliance, supplemented by hemodynamic monitoring, aids in the diagnosis of physiologic changes. For > 10 years, we have used this system to monitor patients who are anesthetized, sedated, and receiving mechanical ventilation during anesthesia and surgery, and recently have extended the technique to intensive care areas. Our experience has shown good correlation of changes in the computer-assisted expired breath analysis with coinciding clinical events, including upper airway obstruction, bronchospasm, and alveolar volume/pulmonary capillary blood flow impairment. To demonstrate the use of this system, we describe the ventilator management for a patient with severe ARDS. In this patient, changes in ventilator management, including pressure control ventilation, improved pulmonary O(2) uptake (mean, 18.7 vs 8.5 mL/breath), CO(2) elimination (mean, 17 vs 13 mL/breath), and compliance (mean, 29.7 vs 19.0 mL/cm H(2)O), were compared with intermittent mandatory ventilation.

Sedation in the critically ill patient.

The goal of critical care medicine is to support organ function and maintain homeostasis until healing can occur. Sedation and analgesia may blunt the physiologic and psychologic sequelae of intensive care unit stress, and support homeostasis. Although a wide variety of agents have been used empirically, the recognition of analgesia, amnesia, and hypnosis as discrete elements comprising the sedated state has facilitated an individualized approach to therapy. Because intensive care unit patients are a highly heterogeneous population with varying levels of end-organ compromise, the development of specific, easily titratable, parenteral agents has made intensive care unit sedation safer. A trend toward refining dosage regimens in order to minimize the total dose of drug administered and to reduce the occurrence of residual sedation is driven by utilization and cost concerns. The capability for simple bedside electrophysiologic monitoring of the level of sedation is expected to improve the ability to provide optimal therapy.

Portable power supply for continuous mechanical ventilation during intrahospital transport of critically ill patients with ARDS.

Patients with respiratory failure and poor pulmonary compliance requiring high levels of positive pressure ventilation are at high risk during intrahospital transportation. Most ICU ventilators currently do not have a built-in power supply. Manual bag-valve ventilation frequently is used but often without optimum mean airway pressures or minute ventilation guarantees. Transport ventilators also are limited in their ability to provide high positive end-expiratory pressure, variable inspiratory-expiratory ratios, or pressure-controlled ventilation. The 3M SARNS HELP (Hospital Emergency Limited Power) 115, a portable battery, provides continuous power to ICU ventilators and eliminates ventilator circuit interruption for the critical period of patient transportation.

Use of the activated coagulation time and heparin dose-response curve for the determination of protamine dosage in vascular surgery.

The activated coagulation time (ACT) can be used to construct a two-point heparin dose-response curve (HDRC) from the ACT values at baseline and 5 minutes after heparin administration. The ACT value at any subsequent time interval can then be used to estimate the residual heparin activity from the HDRC. The protamine dose is calculated to be the amount of residual heparin multiplied by a correction factor (1.3 was suggested for cardiac surgery). In vascular surgery, heparin and protamine dosing remain empirical, ACT monitoring is not standard, and use of the HDRC has not been previously investigated. Forty-five patients were prospectively randomized to one of three groups. ACT was measured before heparinization (1 mg/kg, 1 mg = 100 U), 5 minutes later, and then every 30 minutes until just prior to and after protamine administration. Group I received 1 mg/kg of protamine. In Groups II and III the residual heparin activity was interpolated from the HDRC and multiplied by 1.3 or 1.0, respectively, to derive the protamine dosage. Randomization created balanced groups with respect to demographic data. The individual peak effect of heparin ranged from 177% to 401% of control. The ACT returned to control after protamine in all groups. The protamine dose was significantly less when the HDRC was used (P < 0.05). Group III received the least protamine (0.64 +/- 0.07 mg/kg, P < 0.05). No adverse protamine reactions or postoperative bleeding occurred. It is concluded that ACT monitoring and use of the HDRC provides a safe and easy method to individualize protamine dosage in vascular surgery.

Acute adrenal insufficiency resulting from adrenal hemorrhage as indicated by post-operative hypotension.

We examined the incidence, diagnosis and therapy of acute adrenal insufficiency, secondary to adrenal hemorrhage. This insufficiency resulted in temperature irregularities. hemodynamic instability, and a large volume resuscitation requirement post-operatively. The case illustrates that a high level of suspicion should be maintained in a clinical scenario that mimics sepsis or myocardial insufficiency in the intensive care unit.

Nitrous oxide potentiates succinylcholine neuromuscular blockade in humans.

Sixty ASA physical status I and II adults received 0.3 mg/kg succinylcholine to determine the effect of prolonged administration of thiopental and that of nitrous oxide on succinylcholine neuromuscular blockade. Succinylcholine was administered either 1 min (group 1) or 6 min (groups 2 and 3) after induction of anesthesia with thiopental. In group 2, anesthesia was maintained with thiopental and the patients' lungs were ventilated with oxygen. In group 3, anesthesia was maintained with only 70% nitrous oxide in oxygen. Train-of-four stimulation of the ulnar nerve was started 30 s before the administration of succinylcholine and repeated every 12 s. The force of contraction of the adductor pollicis muscle was measured. Maximum blockade (mean +/- SEM) did not vary significantly between group 1, where thiopental had been administered for 1 min, and group 2, where it had been administered for 6 min (group 1: 61% +/- 6%; group 2: 54% +/- 8%). However, the addition of nitrous oxide increased neuromuscular blockade (group 3: 80% +/- 6%; P less than 0.05 compared with group 2). The degree of twitch augmentation, i.e., greater than maximal response, and times to twitch augmentation and to maximum blockade did not vary significantly among the groups. It is concluded that nitrous oxide increases succinylcholine neuromuscular blockade and that this is manifest within 6 min. This effect is not due to the duration of the anesthetic because thiopental, administered over a similar time period, did not potentiate succinylcholine.

Effect of d-tubocurarine pretreatment on succinylcholine twitch augmentation and neuromuscular blockade.

Subparalyzing doses of d-tubocurarine (dTC) given before succinylcholine decrease the duration of neuromuscular blockade. In animal preparations, they also abolish succinylcholine-induced twitch augmentation, defined as a greater-than-maximal contraction in response to a single stimulus. To determine quantitatively the effect of dTC on succinylcholine potency and on twitch augmentation in humans, 60 adult patients, ASA physical status I or II, were assigned randomly to receive either 0.05 mg/kg of dTC or saline 2 min before induction of anesthesia with fentanyl and thiopental. Train-of-four stimulation was applied every 12 s to the ulnar nerve and the force of contraction of the adductor pollicis muscle was measured. One minute after induction of anesthesia, 0.15, 0.20, 0.25, 0.35, or 0.50 mg/kg of succinylcholine was given. The height of the first twitch (T1) reached 121% +/- 6% (mean +/- SEM) of control without dTC, and was virtually abolished by dTC pretreatment (105% +/- 1%, P less than 0.01). Twitch augmentation was more noticeable with lower doses of succinylcholine, and was not observed in the response to the fourth stimulus of the train of four (T4). The potency of succinylcholine was decreased by approximately one-half in the dTC-pretreated groups. The ED50 was 0.27 +/- 0.04 mg/kg without dTC and 0.50 +/- 0.06 mg/kg with dTC (P less than 0.002). The corresponding values for ED90 were 0.51 +/- 0.07 and 1.02 +/- 0.12 mg/kg, respectively (P less than 0.02). The ED95 values were 0.63 +/- 0.09 and 1.28 +/- 0.15 mg/kg, respectively (P less than 0.02). The slopes of the regression lines did not deviate significantly from parallelism.(ABSTRACT TRUNCATED AT 250 WORDS)

Edrophonium priming for antagonism of atracurium neuromuscular blockade.

Edrophonium administered in divided doses has been reported to accelerate antagonism of neuromuscular blockade, i.e., a "priming" effect. Since measured onset times can be affected by the type of stimulation used, this effect was studied using both train-of-four (TOF) and single twitch (ST) stimulation. During thiopentone-nitrous oxide-enflurane anaesthesia 20 adults were given atracurium 0.5 mg.kg-1. Both ulnar nerves were stimulated with TOF every 12 sec until one per cent recovery of first twitch (T1). At this time, ST stimulation was applied to one arm, selected at random. When the mean value of T1 and ST reached ten per cent of control, edrophonium, 1 mg.kg-1, preceded by atropine was given either as a single dose, or in two doses consisting of 0.2 mg.kg-1 followed by 0.8 mg.kg-1 three minutes later. No statistically significant differences were observed between T1 and ST for the next ten minutes, whether edrophonium had been given in single or divided doses. Giving edrophonium in divided doses did not improve recovery significantly, measured with either T1, ST or train-of-four ratio (T4/T1). Five minutes after the first administration of edrophonium, T1 was (mean +/- SEM) 86 +/- 3 and 86 +/- 2 per cent control in the single and divided dose groups respectively. Corresponding values for ST were 89 +/- 1 and 89 +/- 2 per cent (NS), and for TOF, 49 +/- 3 and 57 +/- 3 per cent (NS), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)