Weaning injured patients with prolonged pulmonary failure from mechanical ventilation in a non-intensive care unit setting.

BACKGROUND: Injured patients with pulmonary failure often require prolonged length of stay in an intensive care unit (ICU), which includes weaning from ventilatory support. In the last decade, noninvasive ventilation modes have been established as safe and effective. One method for accomplishing this mode of ventilation uses a simple bilevel ventilator. Because this ventilator has been successfully used in hospital wards, we postulated that bilevel ventilators could provide sufficient support during weaning from mechanical ventilation of injured patients in a non-ICU setting. METHODS: A retrospective review of trauma patients (August 1996-January 1999) undergoing bilevel positive pressure ventilation as the final phase of weaning was conducted. Before ward transfer with bilevel ventilation, conventionally ventilated ICU patients were changed to bilevel ventilation and were required to tolerate this mode for at least 24 hours. All patients had a tracheostomy as a secure airway. Outcomes analyzed included ICU length of stay, hospital length of stay, duration of mechanical ventilation, weaning success, complications, and survival. RESULTS: Fifty-one patients (39 men, 12 women) with a mean age of 53 received more than 24 hours of bilevel positive pressure ventilation. Mean Injury Severity Score was 29, with blunt mechanisms of injury occurring in 90%. Chest or spinal cord injuries that affected pulmonary mechanics were present in 75% of patients. Ventilator-associated pneumonia was treated in 43% of patients. Mean ICU length of stay and hospital length of stay were 21 and 34 days, respectively. Weaning was successful in 89% of patients, whereas 11% were discharged to skilled nursing facilities still receiving bilevel positive pressure ventilation. Two patients died, neither from a pulmonary nor airway complication. Of the remaining 49 patients, 12 were weaned in the ICU and 37 were transferred to the ward with bilevel ventilatory support. The average length of ward ventilation was 6.5 +/- 5.4 days (n = 37). CONCLUSIONS: Implementation of a program using bilevel ventilation to support the terminal phase of weaning seriously injured patients from mechanical ventilation was successful. After initiating this mode in the ICU, it was satisfactorily continued in standard surgical wards. Because this method enabled the withdrawal of ventilatory support in a non-ICU setting, its major advantage was reducing ICU length of stay.

Procedural anesthesia at the bedside.

Procedural anesthesia at the bedside offers patients relief from anxiety, discomfort, and pain and may expedite the procedure by increasing patient cooperation. Prospective planning requires knowledge of the condition of the patient and an assessment of the anesthetic requirements of the proposed procedure. The spectrum of anesthetic options includes sedation and analgesia, monitored anesthesia care, to total intravenous anesthesia (see Fig. 1). Identification of the at-risk patient and modifying the anesthetic should reduce complications (see Box 3). The choice of pharmaceuticals varies depending on the level of anticipated anesthesia. Personnel requirements also vary. Although an anesthesiologist is not required to administer medications and monitor the patient for sedation and analgesia or monitored anesthesia care, TIVA requires the services of an anesthesiologist. Costs are influenced by the personnel requirements and length of the procedure, which sets the drug requirements and drug costs. In the end, personal experience combined with knowledge should guide the provider to offer efficacious and cost-effective procedural anesthesia in the ICU.

Cardioprotection provided by adenosine receptor activation is abolished by blockade of the KATP channel.

Adenosine agonists and openers of the ATP-sensitive potassium (KATP) channel have been reported to limit infarct size (IS). We tested the hypothesis that these phenomena are interdependent. Anesthetized swine underwent 60 min of coronary artery occlusion and 90 min of reperfusion. Preconditioning was elicited by two cycles comprising 10 min of occlusion and 10 min of reperfusion (n = 7 swine). An intracoronary infusion of adenosine (Ado; n = 10) or (-)-N6-(2-phenylisopropyl)-adenosine (R-PIA; n = 7) replaced preconditioning ischemia. KATP channels were blocked with sodium 5-hydroxydecanoate (5-HD) in the absence (n = 6) or presence (n = 8) of R-PIA. Control pigs (n = 7) received saline vehicle. IS was assessed with tetrazolium and normalized as percentage of area at risk. Preconditioning resulted in a reduced IS compared with Control (3.9 +/- 1.8 vs. 43.5 +/- 6.9%, respectively; P < 0.0005). Ado and R-PIA also reduced IS [21.1 +/- 6.8 (P < 0.01) and 11.2 +/- 7.4% (P < 0.005), respectively]. 5-HD alone did not alter IS, but it abolished R-PIA-induced cardioprotection (IS 5-HD + R-PIA = 48.6 +/- 13.2%). Thus Ado A1-receptor agonists mimicked the cardioprotection of ischemic preconditioning. The Ado-induced limitation of IS was abolished by blockade of the KATP channel. We conclude that both Ado A1 receptors and KATP channels may be involved in ischemic preconditioning.

Analysis of trauma intubations.

The timing of trauma patient intubation is dependent on clinical presentation and clinician judgment. We sought to correlate the timing of intubation with the presenting of physiologic parameters and clinical outcome to identify potential quality assurance audit filters. Patients (n = 82) were grouped by timing of intubation: PREHOSPITAL, paramedic intubation; IMMEDIATE, within 10 minutes of arrival; DELAYED, beyond 10 minutes but within 2 hours of arrival; and NONURGENT, beyond 2 hours or at the time of surgery. While mean revised trauma scores and Glasgow Coma Scale (GCS) scores differed for the groups, the mean length of hospital stay and the incidence of aspiration pneumonia were not significantly different. In the DELAYED group, 80% of those who developed aspiration pneumonia had a GCS < or = 13. Patients in the NONURGENT group were older and commonly presented with tachypnea. The survival rate for the NONURGENT group was lower than predicted by the TRISS method (P = .004). A GCS < or = 13 and age greater than 50 years with presenting respiratory rates of more than 25 breaths/min represent potential trauma intubation audit filters.

A comparison of patient-controlled analgesia and bolus PRN intravenous morphine in the intensive care environment.

We compared the use of patient-controlled analgesia (PCA) morphine and p.r.n. intravenous morphine in an intensive care unit setting. Thirty-eight patients scheduled for admission to the Surgical Intensive Care Unit (SICU) were prospectively randomized to either a PCA group or a p.r.n. intravenous morphine group. Assessments included pain and sedation scores, respiratory rates, pulse oximetry, and morphine utilization. PCA was found to be comparable in safety and efficacy to nurse-administered morphine in the intensive care environment. An unexpected finding was the higher initial morphine utilization seen in the patients utilizing PCA.

Isoflurane for the management of status epilepticus.

When conventional therapy fails in status epilepticus, general anesthesia is recommended. We present our experience with isoflurane, an inhalational anesthetic, in the management of a patient with refractory status epilepticus. The seizures were controlled with relatively small concentrations of isoflurane. Hypotension, the only adverse effect of isoflurane, was managed with fluid and dopamine infusions.

The effect of sulfinpyrazone on the response to sympathetic nervous system stimulation.

The purpose of this study was to determine if sulfinpyrazone has a direct action on sympathetic nerve endings to prevent release of the transmitter. Pre-synaptic and post-synaptic events as well as direct sympathetic nervous system stimulation were tested in 15 alpha-chloralose anesthetized cats before and 1 hour after sulfinpyrazone (100 mg . kg-1, i.v.). Heart rate response to cardiac accelerator nerve stimulation or to increasing doses of isoproterenol was not significantly depressed by sulfinpyrazone. In addition, no alteration in the reflex activation of the sympathetic nervous system in response to histamine was observed following sulfinpyrazone. Both norepinephrine and epinephrine levels were similar to those levels reported previously by Smith and Robinson for (7) untreated cats. We conclude sulfinpyrazone has no direct depressing effect on the sympathetic nerve endings and that this mechanism cannot explain the reported beneficial effect of sulfinpyrazone on coronary occlusion induced arrhythmias.

Effect of prostaglandin synthesis inhibition and sympathectomy on ouabain-induced arrhythmia in cats.

The purpose of this study was to examine the importance of endogenous prostaglandins (PGs) and sympathectomy on the arrhythmogenic action of ouabain. Cats, anesthetized with dial-urethane, were infused intravenously with ouabain continuously. The dose of ouabain necessary to produce arrhythmia (AR), ventricular tachycardia (VT), and death was determined. Pretreatment with sulfinpyrazone at 100 mg kg-1 i.v. 1 h before glycoside infusion was used to inhibit PG synthesis. Removal of endogenous PGs with sulfinpyrazone reduced the cardiotoxic dose of ouabain. Sympathetic influences were removed by: (a) destroying sympathetic nerve terminals with 6-hydroxydopamine (6-OHDA); (b) depleting nerve terminal catecholamines with reserpine; or (c) preventing catecholamine release from the nerve terminal with bretylium. Reduction of sympathetic influences with reserpine or bretylium increased the cardiotoxic dose of ouabain; whereas removal of nerve terminals with 6-OHDA did not alter the toxic dose of ouabain from that found in control animals. When endogenous PG synthesis was inhibited with sulfinpyrazone the protective effects of reserpine and bretylium were eliminated. These results suggest that endogenous PGs protect against the arrhythmogenic action of ouabain, not only by interfering with catecholamine influences at the sympathetic nerve terminal, but also by a mechanism independent of sympathetic inhibition. Furthermore, the protective action of agents which diminishes the cardiotoxic action of ouabain by interfering with sympathetic influences is lost when endogenous PGs are removed. Finally, 6-OHDA, which destroys the sympathetic nerve terminals, removes both the arrhythmic influence of the catecholamine as well as the protective influence of the PG, resulting in no net change in the cardiotoxic dose of this glycoside.