Anesthesia and analgesia
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Anesthesia and analgesia · Apr 2003
The effect of the interval between blood pressure determinations on the delay in the detection of changes: a computer simulation.
The frequency of automated noninvasive blood pressure (NIBP) measurements during routine anesthesia is a balance between potentially deleterious effects of frequent cycling and a delay in detecting changes caused by a long cycle time. A computer model generated systolic blood pressures that changed to a new, random value after a period of stability. We sampled these data at intervals between 1 and 10 min to simulate NIBP measurements. A separate algorithm, based on Trigg's Tracking Variable, indicated when a change had been detected. For each set of variables, the simulation was repeated 1000 times, and the average time to detect a change was recorded. The mean time to detect a change was 8.0 min with a 1-min cycle, 8.9 min with a 2-min cycle, 10.8 min with a 5-min cycle, and 13.0 min with a 10-min cycle. As the cycle time increased, the delay in detecting changes increased but only by approximately half the increase in the cycle time. The optimum variables for the trend detection algorithm also changed as the NIBP interval increased. Provided that abrupt changes in blood pressure are not anticipated, a 1- or 2-min cycle time for NIBP offers little advantage over a longer period. ⋯ We used a computer model to study the effect of increasing noninvasive blood pressure (NIBP) sampling interval on the detection of blood pressure changes. The detection time increased only 50% of the increase in the sampling interval. This information may help optimize NIBP intervals in different circumstances.
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Anesthesia and analgesia · Apr 2003
Cerebral blood flow is not altered in sheep with Pseudomonas aeruginosa sepsis treated with norepinephrine or nitric oxide synthase inhibition.
The origin of cerebral dysfunction in patients with sepsis is still unclear. However, altered cerebral perfusion may play an important role in its pathogenesis. Using an established, chronic model of hyperdynamic ovine sepsis, we examined cerebral perfusion in 20 sheep subjected to a continuous infusion of live Pseudomonas aeruginosa. After 24 h of sepsis, the hypotensive sheep (reduction in mean arterial blood pressure by 16%; P < 0.05) received the nitric oxide synthase inhibitor N(G)-mono-methyl-L-arginine (L-NMMA; 7 mg. kg(-1). h(-1); n = 7), norepinephrine (NE; n = 7), or normal saline (control; n = 6). NE infusion was individually targeted to achieve the same increase in mean arterial blood pressure as that observed in matched sheep of the L-NMMA group. Regional perfusion was measured by using colored microspheres. Although L-NMMA caused a significant increase in systemic vascular resistance index (1167 +/- 104 versus 793 +/- 59 dyne. cm(-5). m(2); P < 0.05), it caused a change neither in cerebrovascular resistance nor in cerebral blood flow. When related to systemic blood flow, a redistribution of blood flow to the brain became obvious. The NE-associated increase in systemic blood pressure (98 +/- 5 versus 83 +/- 5; P < 0.05) was accompanied by an increase in cardiac output (7.8 +/- 0.5 versus 6.7 +/- 0.6; P < 0.05) and, hence, systemic perfusion. However, blood flow to the brain remained unaffected. Although detrimental vasoconstrictive effects of NE and L-NMMA, including cerebral hypoperfusion, are discussed, neither drug had any effect on cerebral perfusion during experimental hyperdynamic sepsis. ⋯ Cerebral dysfunction is often found in septic patients. In this regard, it is debated whether vasopressor drugs, such as norepinephrine and L(G)-mono-methyl-L-arginine, have harmful effects on the cerebral circulation. During experimental hyperdynamic sepsis, however, neither drug altered cerebral vascular resistance or cerebral blood flow.
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Anesthesia and analgesia · Apr 2003
The effect of inhaled colforsin daropate on contractility of fatigued diaphragm in dogs.
We studied the effect of inhaled colforsin daropate, a water-soluble forskolin derivative, on the contractility of fatigued diaphragm in dogs. Animals were divided into 3 groups of 8. In each group, diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20-Hz stimulation applied for 30 min. Immediately after the end of the fatigue-producing period, Group 1 received inhaled vehicle, Group 2 received inhaled colforsin daropate 0.1 mg/mL, and Group 3 received inhaled colforsin daropate 0.2 mg/mL. We assessed diaphragmatic contractility by transdiaphragmatic pressure (Pdi). After fatigue was produced, in each group, Pdi at low-frequency (20-Hz) stimulation decreased from baseline values (P < 0.05), and there was no change in Pdi at high-frequency (100-Hz) stimulation. In Groups 2 and 3, during colforsin daropate inhalation, Pdi at both stimuli increased from fatigued values (P < 0.05). The increase in Pdi was significantly larger in Group 3 than in Group 2. The integrated electrical activity of the diaphragm did not change in any group. We conclude that inhaled colforsin daropate causes an increase in contractility of fatigued canine diaphragm in a dose-related fashion. ⋯ Diaphragmatic fatigue may contribute to the development of respiratory failure. Inhaled colforsin daropate improves, in a dose-dependent manner, the contractility of fatigued diaphragm in dogs.