Anesthesia and analgesia
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Anesthesia and analgesia · Sep 1999
Cardiac output is a determinant of the initial concentrations of propofol after short-infusion administration.
Indicator dilution theory predicts that the first-pass pulmonary and systemic arterial concentrations of a drug will be inversely related to the cardiac output. For high-clearance drugs, these first-pass concentrations may contribute significantly to the measured arterial concentrations, which would therefore also be inversely related to cardiac output. We examined the cardiac output dependence of the initial kinetics of propofol in two separate studies using chronically instrumented sheep in which propofol (100 mg) was infused IV over 2 min. In the first study, steady-state periods of low, medium, and high cardiac output were achieved by altering carbon dioxide tension in six halothane-anesthetized sheep. The initial area under the curve and peak value of the pulmonary artery propofol concentrations were inversely related to cardiac output (R2 = 0.57 and 0.66, respectively). For the systemic arterial concentrations, these R2 values were 0.68 and 0.71, respectively. In our second study, transient reductions in cardiac output were achieved in five conscious sheep by administering a short infusion of metaraminol concurrently with propofol. Cardiac output was lowered by 2.2 L/min, and the area under the curve to 10 min of the arterial concentrations increased to 143% of control. ⋯ The initial arterial concentrations of propofol after IV administration were shown to be inversely related to cardiac output. This implies that cardiac output may be a determinant of the induction of anesthesia with propofol.
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Anesthesia and analgesia · Sep 1999
Nitrous oxide increases normocapnic cerebral blood flow velocity but does not affect the dynamic cerebrovascular response to step changes in end-tidal P(CO2) in humans.
We sought to clarify the effect of nitrous oxide (N2O) on the immediate responses of cerebral vasculature to sudden changes in arterial carbon dioxide tension in healthy humans. By use of a transcranial Doppler ultrasonography, blood flow velocity in the middle cerebral artery (V(MCA)) was measured during a step increase followed by a step decrease in end-tidal CO2 tension (PET(CO2)) between normo- and hypercapnia while subjects inspired gas mixtures containing 70%O2 + 30% N2 (control) and 70% O2 + 30% N2O (N2O) separately. During the control condition, both step increase and decrease in PET(CO2) produced rapid exponential changes in V(MCA). An increase in V(MCA) produced by the step increase in PET(CO2) was smaller (P < 0.001) and slower (P < 0.001) than a decrease in V(MCA) induced by the step decrease in PET(CO2). These general features of the dynamic cerebrovascular response were not affected by substitution of N2O for N2 in the inspired gases although N2O increased baseline V(MCA) by 15% (P < 0.001) compared with the control condition. We conclude that N2(O) in itself does not affect the dynamic cerebrovascular response to arterial CO2 changes, although it produces static mild cerebral vasodilation. ⋯ This study suggests that nitrous oxide does not affect the dynamic cerebrovascular reactivity to acute arterial carbon dioxide (CO2) changes, i.e., exponential changes in cerebral blood flow in response to step changes in alveolar CO2 tension, although it does produce a mild increase in normocapnic cerebral blood flow velocity.
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Anesthesia and analgesia · Sep 1999
Adverse cardiac outcomes after noncardiac surgery in patients with prior percutaneous transluminal coronary angioplasty.
In this retrospective cohort study, we compared adverse cardiac outcomes after noncardiac surgery among patients with prior percutaneous transluminal coronary angioplasty (PTCA), patients with nonrevascularized coronary artery disease (CAD), and normal controls. Inpatient hospital discharge abstracts from all nonfederal acute care hospitals in Washington State linked to death certificates were evaluated. Patients > or =45 yr old with prior PTCA who underwent noncardiac surgery from 1987 to 1993 were matched by age, sex, surgery type, and discharge year to 686 patients with CAD and to 2155 normal controls (no CAD). We compared risk for adverse cardiac outcomes (death, myocardial infarction, angina, congestive heart failure, malignant dysrhythmia, cardiogenic shock, coronary artery bypass graft, or PTCA) within 30 days. Patients with PTCA had twice the risk of adverse cardiac outcome as normal controls (odds ratio [OR] 1.98; P < 0.001), with a higher risk of angina (OR 7.84), congestive heart failure (OR 2.06), and myocardial infarction (OR 3.86) but a lower risk of death (OR 0.46; P < 0.001). Patients with PTCA had half the risk of adverse cardiac outcome as patients with CAD (OR 0.50; P < 0.001), including less risk of angina (OR 0.51) and congestive heart failure (OR 0.40; P < 0.001), but no difference in myocardial infarction (P = 0.304) or death (P = 0.436). No difference was found between 142 patients with recent PTCA (< or =90 days before noncardiac surgery) matched to patients with CAD (OR 0.90; P = 0.396). Patients revascularized by PTCA >90 days before noncardiac surgery seem to have a lower risk of poor outcome than nonrevascularized patients, although not as low as normal controls. For recent PTCA patients, the lack of difference compared with CAD patient outcomes requires a larger sample size for verification. Present findings do not lend support to a role for prophylactic PTCA to improve noncardiac surgery outcomes. This investigation did not control for CAD severity, medical management, or comorbidities. Study of these factors is needed before the clinical implications of PTCA for noncardiac surgical risk can be completely assessed. ⋯ Hospital records showed patients with prior percutaneous transluminal coronary angioplasty were twice as likely as healthy patients to have an adverse cardiac outcome after noncardiac surgery, although their risk was reduced by half compared with patients with untreated coronary artery disease. Further study of the role of percutaneous transluminal coronary angioplasty in modulating noncardiac surgery risk is needed.
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Anesthesia and analgesia · Sep 1999
Clinical TrialLack of rapid development of opioid tolerance during alfentanil and remifentanil infusions for postoperative pain.
Studies in animals and volunteers have suggested the development of acute tolerance to opioid analgesics. In this article, we present data from patients who regulated their own target-controlled infusions of alfentanil and remifentanil to provide analgesia in the immediate postoperative period. Fifty-one patients received alfentanil for 24 h after cardiac surgery, and 30 patients received remifentanil for 6 h after orthopedic surgery. Satisfactory analgesia, defined as a rating of < or =3 on an 11-point visual analog scale, was obtained by patients after each type of surgery. The target concentrations of the opioids required to produce postoperative analgesia and the cumulative opioid doses administered over the course of the clinical observation suggest there was no tolerance to the analgesic effects of the opioids. The requirements for both analgesic drugs in individual patients had a large variation (>200%). We conclude that our results may indicate an absence of tolerance to opioids in postoperative analgesia. Nonetheless, our data show that the postoperative requirement for these rapidly acting drugs is qualitatively similar to that for other opioids in that dosage escalation does not occur. ⋯ The development of acute tolerance to opioid analgesics has been suggested based on experimental studies in animals and volunteers. Our report from patients who self-controlled their analgesic requirements by using target-controlled infusions of alfentanil and remifentanil for postoperative analgesia provides no evidence of tolerance to opioids.