ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundSpinal anesthesia for surgical repair of hip fracture in the elderly is associated with a high incidence of hypotension. The synergism between intrathecal opioids and local anesthetics may make it possible to achieve reliable spinal anesthesia with minimal hypotension using a minidose of local anesthetic.MethodsTwenty patients aged ≥ 70 yr undergoing surgical repair of hip fracture were randomized into two groups of 10 patients each. Group A received a spinal anesthetic of bupivacaine 4 mg plus fentanyl 20 &mgr;g, and group B received 10 mg bupivacaine. Hypotension was defined as a systolic pressure of < 90 mmHg or a 25% decrease in mean arterial pressure from baseline. Hypotension was treated with intravenous ephedrine boluses 5–10 mg up to a maximum 50 mg, and thereafter by phenylephrine boluses of 100–200 &mgr;g.ResultsAll patients had satisfactory anesthesia. One of 10 patients in group A required ephedrine, a single dose of 5 mg. Nine of 10 patients in group B required vasopressor support of blood pressure. Group B patients required an average of 35 mg ephedrine, and two patients required phenylephrine. The lowest recorded systolic, diastolic, and mean blood pressures as fractions of the baseline pressures were, respectively, 81%, 84%, and 85%versus64%, 69%, and 64% for group Aversusgroup B.ConclusionsA “minidose” of 4 mg bupivacaine in combination with 20 &mgr;g fentanyl provides spinal anesthesia for surgical repair of hip fracture in the elderly. The minidose combination caused dramatically less hypotension than 10 mg bupivacaine and nearly eliminated the need for vasopressor support of blood pressure.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundThe current study investigates the effects of morphine and fentanyl upon intracranial pressure and cerebral blood flow estimated by cerebral arteriovenous oxygen content difference and transcranial Doppler sonography in 30 consecutive patients with severe head injury in whom cerebrovascular autoregulation previously had been assessed.MethodsPatients received morphine (0.2 mg/kg) and fentanyl (2 &mgr;g/kg) intravenously over 1 min but 24 h apart in a randomized fashion. Before study, carbon dioxide reactivity and autoregulation were assessed. Intracranial pressure, mean arterial blood pressure, and cerebral perfusion pressure were repeatedly monitored for 1 h after the administration of both opioids. Cerebral blood flow was estimated from the reciprocal of arteriovenous oxygen content difference and middle cerebral artery mean flow velocity using transcranial Doppler sonography.ResultsAlthough carbon dioxide reactivity was preserved in all patients, 18 patients (56.7%) showed impaired or abolished autoregulation to hypertensive challenge, and only 12 (43.3%) had preserved autoregulation. Both morphine and fentanyl caused significant increases in intracranial pressure and decreases in mean arterial blood pressure and cerebral perfusion pressure, but estimated cerebral blood flow remain unchanged. In patients with preserved autoregulation, opioid-induced intracranial pressure increases were not different than in those with impaired autoregulation.ConclusionsThe authors conclude that both morphine and fentanyl moderately increase intracranial pressure and decrease mean arterial blood pressure and cerebral perfusion pressure but have no significant effect on arteriovenous oxygen content difference and middle cerebral artery mean flow velocity in patients with severe brain injury. No differences on intracranial pressure changes were found between patients with preserved and impaired autoregulation. Our results suggest that other mechanisms, besides the activation of the vasodilatory cascade, also could be implicated in the intracranial pressure increases seen after opioid administration.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundInvestigations to determine the incidence of venous air embolism in children undergoing craniectomy for craniosynostosis repair have been limited, although venous air embolism has been suspected as the cause of hemodynamic instability and sometimes death. A precordial Doppler ultrasonic probe is an accepted method for detection of venous air embolism and is readily available at most institutions.MethodsA prospective study was conducted using a precordial Doppler ultrasonic probe in children undergoing craniectomy for craniosynostosis repair. The Doppler signal was continuously monitored intraoperatively for characteristic changes of venous air embolism. A recording was made of the precordial Doppler probe pulses, which was later reviewed by a neuroanesthesiologist, blinded to the intraoperative events. This information was correlated with the intraoperative events and episodes of venous air embolism were graded.ResultsTwenty-three patients were enrolled in the study during the 2-yr study period. Nineteen patients (82.6%) demonstrated 64 episodes of venous air embolism; six patients (31.6%) had hypotension associated with venous air embolism. Thirty-two episodes of hypotension were demonstrated in eight patients (34.7%). None of the patients developed cardiovascular collapse.ConclusionThe incidence of venous air embolism in our study of 23 children undergoing craniectomy for craniosynostosis was 82.6%. Though most episodes of venous air embolism during craniosynostosis repair are without hemodynamic consequences, the preemptive placement of a precordial Doppler ultrasonic probe is a noninvasive, economic, and safe method for the detection of venous air embolism. Prompt recognition may allow for the early initiation of therapy, thereby decreasing morbidity and mortality rates related to venous air embolism.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundThe purpose of this prospective study was to examine the effect on cardiac performance of selective increases in airway pressure at specific points of the cardiac cycle using synchronized high-frequency jet ventilation (sync-HFJV) delivered concomitantly with each single heart beat compared with controlled mechanical ventilation in 20 hemodynamically stable, deeply sedated patients immediately after coronary artery bypass graft.MethodsFive 30-min sequential ventilation periods were used interspersing controlled mechanical ventilation with sync-HFJV twice to control for time and sequencing effects. Sync-HFJV was applied using a driving pressure, which generated a tidal volume resulting in gas exchanges close to those obtained on controlled mechanical ventilation and associated with the maximal mixed venous oxygen saturation. Hemodynamic variables including cardiac output, mixed venous oxygen saturation and vascular pressures were recorded at the end of each ventilation period.ResultsThe authors found that in 20 patients, hemodynamic changes induced by controlled mechanical ventilation and by sync-HFJV were similar. Cardiac index did not change (mean ± SD for controlled mechanical ventilation: 2.6 ± 0.7 l · min−1· m−2; for sync-HFJV: 2.7 ± 0.7 l · min−1· m−2;Pvalue not significant). This observation persisted after stratification according to baseline left-ventricular contractility, as estimated by ejection fraction.ConclusionsThe authors conclude that after coronary artery bypass graft, if gas-exchange values are maintained within normal range, sync-HFJV does not result in more favorable hemodynamic support than controlled mechanical ventilation. These findings contrast with the beneficial effects of sync-HFJV, resulting in marked hypocapnia, on cardiac performance observed in patients with terminal left-ventricular failure.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundBurned patients are usually resistant to the neuromuscular effects of nondepolarizing relaxants, mostly because of receptor changes. The magnitude of the resistance is related to burn size and time after burn. Mivacurium is a muscle relaxant, degraded by plasma cholinesterase, whose enzyme activity is decreased in burns. The present study tested the hypothesis that burn-induced depressed plasma cholinesterase activity counteracts the receptor-mediated resistance, resulting in a lack of resistance to mivacurium.MethodsBurned patients (n = 23), aged 2–12 yr, subclassified into burns of 10–30% or > 30% of body surface, were studied at ≤ 6 days and again at 1–12 weeks after burn if possible. Thirteen additional patients served as controls. Neuromuscular variables monitored included onset and recovery following bolus dose, continuous infusion rates required to maintain 95 ± 4% paralysis, and recovery rates following infusion.ResultsThe onset times of maximal twitch suppression were not different between burns and controls, but recovery to 25% of baseline twitch height was prolonged in patients with > 30% burn irrespective of time after injury. The continuous infusion rates to maintain twitch suppression at 95 ± 4% were not different between groups. The recovery indices, including train-of-four to > 75%, 25–75%, or 5–95% in burned patients, were similar or prolonged compared with controls. The prolonged recovery in burned patients was inversely related to plasma cholinesterase activity (R2= 0.86, r = −0.93,P< 0.001), and the decreased plasma cholinesterase activity was related to burn size and time after burn.ConclusionsA normal mivacurium dosage (0.2 mg/kg) effects good relaxation conditions in burned patients, with an onset time similar to that in controls. This finding contrasts with the response seen with other nondepolarizing drugs, higher doses of which are required to effect paralysis. The decreased metabolism of mivacurium, resulting from depressed plasma cholinesterase activity, probably counteracts the receptor-mediated potential for resistance. Because succinylcholine is contraindicated in burned patients, larger doses of nondepolarizing agents are advocated to effect rapid onset of paralysis. This generalization does not hold for mivacurium.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundA new automated system of air tonometry (Tonocap; Datex Ohmeda, Helsinki, Finland) allows for frequent (every 15 min) measurement of gastric luminal partial pressure of carbon dioxide. Its use has not been described in cardiac surgical patients.MethodsOne hundred patients undergoing coronary artery bypass graft or cardiac valve surgery were enrolled in a prospective cohort study. After anesthetic induction and insertion of a TRIP NGS Catheter (Datex Ohmeda), measurements of gastric luminal partial pressure of carbon dioxide were obtained using the Tonocap, and gastric mucosalpH (pHi) was calculated. The main outcome measure was postoperative complication, defined as either in-hospital death or prolonged postoperative hospitalization (> 14 days).ResultsFour patients (4%) died, all of multiple-system organ failure, one each on postoperative days 9, 26, 46, and 121. Postoperative complication occurred in 18 patients (18%), all of whom exhibited persistent dysfunction of at least one organ system. Perioperatively, an abnormalpHi (< 7.32) and gastric luminal minus arterial partial pressure of carbon dioxide gap (> 8 mmHg) occurred in 66% and 70% of patients, respectively. Predictors of postoperative complication included postoperative pHi (P= 0.001), gastric luminal partial pressure of carbon dioxide (P= 0.022), and gastric luminal minus arterial partial pressure of carbon dioxide gap (P= 0.013). In contrast, arterial base excess (P> 0.4) and routinely measured hemodynamic variables (e.g., heart rate, blood pressure) were either less predictive compared with Tonocap-derived variables or not predictive.ConclusionsDespite a low mortality rate, patients undergoing cardiac surgery exhibited high incidences of prolonged hospitalization and postoperative morbidity. The Tonocap was easy to use, particularly compared with saline tonometry. Several Tonocap-derived variables were predictive of postoperative complications consistent with previously published data using saline tonometry.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundHypoxia has a dual effect on ventilation: an initial period of hyperventilation, the acute hypoxic response, is followed after 3–5 min by a slow decline, the hypoxic ventilatory decline. Because of hypoxic ventilatory decline, subsequent acute hypoxic responses are depressed. In this study, the influence of a sedative concentration of propofol on ventilation was studied if hypoxia was sustained and intermittent.MethodsTen healthy young male volunteers performed two hypoxic tests without and with a target controlled infusion of propofol. The sustained hypoxic test consisted of 15 min of isocapnic hypoxia followed by 2 min of normoxia and 3 min of hypoxia. The test of hypoxic pulses involved six subsequent exposures to 3 min hypoxia followed by 2 min of normoxia. The bispectral index of the electroencephalogram was measured to obtain an objective measure of sedation.ResultsBlood propofol concentrations varied among subjects but were stable over time (mean blood concentration 0.6 &mgr;g/ml). The sustained hypoxic test showed that propofol decreased acute hypoxic response by ∼50% and that the magnitude of hypoxic ventilatory decline relative to acute hypoxic response was increased by > 50%. Propofol increased the depression of the acute hypoxic response after 15 min of hypoxia by ∼25%. In control and propofol studies, no hypoxic ventilatory decline was generated during exposure to hypoxic pulses. The bispectral index–acute hypoxic response data suggest that subjects were either awake (with minimal effect on acute hypoxic response) or sedated (with 50–60% reduction of acute hypoxic response).ConclusionsThe depression of acute hypoxic response results from an effect of propofol at peripheral or central sites involved in respiratory control or secondary to the induction of sedation or hypnosis by propofol. The relative increase in hypoxic ventilatory decline is possibly related to propofol’s action at the &ggr;-aminobutyric acid A (GABAA) receptor complex, causing increased GABAergic inhibition of ventilation during sustained (but not intermittent) hypoxia.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID