Anesthesia and analgesia
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Anesthesia and analgesia · Feb 1999
Comparative StudyThe effect of nitroglycerin on pacing-induced changes in myocardial oxygen consumption and metabolic coronary vasodilation in patients with coronary artery disease.
In the present study, we assessed the potential effect of nitroglycerin IV (NTG), a donor of exogenous nitric oxide, on metabolic coronary flow control in patients with coronary artery disease. In 12 patients scheduled for coronary artery surgery, arterial blood pressure, pulmonary capillary wedge pressure, coronary sinus blood flow (continuous thermodilution), myocardial oxygen supply (DVO2), and myocardial oxygen consumption (MVO2) were measured at sinus rhythm and in response to atrial pacing at 30 bpm greater than baseline sinus rate. These measurements were repeated during infusion of NTG 1 and 2 microg x kg(-1) x min(-1). At control, in the absence of NTG, MVO2 increased from 13.7 +/- 3.4 mL O2/min during sinus rhythm to 19.3 +/- 5.5 mL O2/min during pacing. NTG 1 and 2 microg x kg(-1) x min(-1) blunted the pacing-induced increase in MVO2 dose-dependently. During NTG 1 microg x kg(-1) x min(-1), MVO2 increased from 12.9 +/- 3.3 mL O2/min at sinus rhythm to 17.3 +/- 4.7 mL O2/min during pacing (P = 0.01 versus control pacing); during NTG 2 microg x kg(-1) x min(-1), MVO2 increased from 13.4 +/- 3.3 mL O2/min to 15.9 +/- 3.7 mL O2/min (P = 0.008 versus control pacing). However, the pacing-induced increase in DVO2 per mL O2/min increase in MVO2 (delta DVO2/delta MVO2), was significantly greater during the infusion of NTG 2 microg x kg(-1) x min(-1) (1.85 +/- 0.56; P = 0.023) compared with control (1.51 +/- 0.22). This was associated with an increase in coronary sinus hemoglobin oxygen saturation (30% +/- 5% at control pacing and 34% +/- 6% during pacing with NTG 2 microg x kg(-1) x min(-1); P = 0.018), which indicates that during the infusion of NTG, there was more metabolic coronary vasodilation than achievable solely on the basis of the metabolic stimulus. ⋯ Our findings suggest that nitroglycerin, a donor of exogenous nitric oxide, reduces pacing-induced increases in myocardial oxygen consumption and enhances metabolic coronary vasodilation in patients with coronary artery disease, in whom endogenous nitric oxide activity may be reduced.
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Anesthesia and analgesia · Feb 1999
Drug therapy before coronary artery surgery: nitrates are independent predictors of mortality and beta-adrenergic blockers predict survival.
We conducted this study to evaluate whether there is an association between preoperative drug therapy and in-hospital mortality in patients undergoing coronary artery graft surgery. We collected data on 1593 consecutive patients undergoing coronary artery surgery. The relative risk of in-hospital mortality was determined by logistic regression with in-hospital mortality as the dependent variable, and independent variables that included known risk factors and preoperative cardioactive or antithrombotic drug treatment, i.e., age; left ventricular function; left main coronary artery disease; urgent priority; gender; previous cardiac surgery; concurrent cardiovascular surgery; chronic lung disease; creatinine concentration; hemoglobin concentration; diabetes; hypertension; cerebrovascular disease; recent myocardial infarction; prior vascular surgery; number of arteries bypassed; and regular daily treatment with beta-blockers, aspirin within 5 days, calcium antagonists, angiotensin converting enzyme (ACE) inhibitors, digoxin, or warfarin. In-hospital mortality was 3.3%. The relative risk of in-hospital mortality (with 95% confidence intervals of the relative risk) associated with the following drug treatments was: nitrates 3.8 (1.5-9.6), beta-blockers 0.4 (0.2-0.8), aspirin within 5 days 1.0 (0.5-1.9), calcium antagonists 1.1 (0.6-2.1), ACE inhibitors 0.8 (0.4-1.5), digoxin 0.7 (0.2-1.8), and warfarin 0.3 (0.1-1.6). We conclude that in-hospital mortality is positively associated with preoperative nitrate therapy and negatively associated with beta-adrenergic blocker therapy. A significant association between in-hospital mortality and the preoperative use of calcium antagonists, ACE inhibitors, aspirin, digoxin, and warfarin was not confirmed. ⋯ We examined the association between common drug treatments for ischemic heart disease and short-term survival after cardiac surgery using a statistical method to adjust for patients' preoperative medical condition. Death after surgery was more likely after nitrate therapy and less likely after beta-blocker therapy.
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Anesthesia and analgesia · Feb 1999
The effect of halothane on the amplitude and frequency characteristics of heart sounds in children.
Although continuous auscultation has been used during surgery as a monitor of cardiac function for many years, the effect of anesthetics on heart sounds has never been quantified. We determined the root mean squared amplitude and frequency characteristics (peak frequency, spectral edge, and power ratios) of the first (S1) and second (S2) heart sounds in 19 healthy children during induction of anesthesia with halothane. In all patients, halothane decreased the amplitude of S1 (R2 = 0.87 +/- 0.12) and S2 (R2 = 0.66 +/- 0.33) and the high-frequency components (>80 Hz) of these sounds. These changes were clearly audible and preceded decreases in heart rate and blood pressure. The spectral edge decreased for S1 in 18 patients (R2 = 0.73 +/- 0.24) and for S2 in 13 patients (R2 = 0.58 +/- 0.25). Peak frequency did not change. The rapidity with which myocardial depression and its associated changes in heart sound characteristics occurred confirms that continuous auscultation of heart sounds is a useful clinical tool for hemodynamic monitoring of anesthetized infants and children. ⋯ Heart sound characteristics can be used to monitor cardiac function during halothane anesthesia in children. The changes occur rapidly and precede noticeable changes in heart rate and blood pressure.
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Anesthesia and analgesia · Feb 1999
Comparative StudyDynamic cerebral autoregulation during sevoflurane anesthesia: a comparison with isoflurane.
We investigated dynamic cerebral pressure autoregulation awake and during 1.5 minimum alveolar anesthetic concentration (MAC) sevoflurane or isoflurane anesthesia in 16 patients undergoing nonintracranial neurosurgical procedures. All patients received a standardized anesthetic, and their lungs were ventilated with 1.5 MAC volatile anesthetic in 100% oxygen to normocapnia. Routine monitors included electrocardiogram, pulse oximetry, end-tidal capnography, and continuous noninvasive blood pressure. In addition, middle cerebral artery blood velocity (Vmca) was measured continuously using transcranial Doppler ultrasonography. Dynamic cerebral autoregulation was tested by inducing a rapid transient decrease in mean arterial pressure by deflation of large thigh cuffs, which were placed around both thighs and inflated to 100 mm Hg above systolic pressure. The Vmca response to the decrease in blood pressure was fitted to a series of curves to determine the rate of dynamic cerebral autoregulation (dRoR). Awake dRoR values were similar in the isoflurane and sevoflurane groups, 32 +/- 2%/s and 29 +/- 2%/s, respectively. dRoR decreased to 5 +/- 1%/s during isoflurane anesthesia but to only 24 +/- 2%/s during sevoflurane anesthesia. We conclude that dynamic cerebral autoregulation is better preserved during sevoflurane than isoflurane anesthesia in humans. ⋯ We investigated the effect of sevoflurane and isoflurane on dynamic cerebral pressure autoregulation using transcranial Doppler ultrasonography. At 1.5 minimum alveolar anesthetic concentration, dynamic autoregulation was better preserved during sevoflurane than isoflurane anesthesia.
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Anesthesia and analgesia · Feb 1999
Endobronchial intubation causes an immediate increase in peak inflation pressure in pediatric patients.
Our purpose was to determine whether endobronchial intubation always causes an immediate increase in peak inflation pressure and, if so, the magnitude of the increase. Fourteen children scheduled for central line placement for prolonged antibiotic administration comprised the study group. After routine premedication and induction of anesthesia (halothane in oxygen), an endotracheal tube was inserted, and its position was verified by auscultation and fluoroscopy. Children were mechanically ventilated using a preset volume pressure-limited ventilator with a 5-L fresh gas flow. All children received a constant tidal volume using a similar circuit, similar tubing, and a similar compression volume. The lowest peak inflation pressure to deliver a tidal volume of 15 mL/kg was used. After adjusting the respiratory rate (end-tidal CO2 30 mm Hg) and anesthetic level (halothane end-tidal 1.2%), the peak inflation pressure at this endotracheal position was recorded. The endotracheal tube was advanced into a bronchus, the position was verified as above, and peak inflation pressure was recorded. The endobronchial tube was then pulled back into the trachea, and placement of the central line proceeded. The peak inflation pressure at the endobronchial position was significantly greater than the peak inflation pressure at the endotracheal position (P < 0.0001). The increase was instantaneous at the endobronchial position. Monitoring peak inflation pressure while inserting an endotracheal tube and during anesthesia can help to diagnose endobronchial intubation. ⋯ Monitoring peak inflation pressure while inserting an endotracheal tube and during anesthesia can help to diagnose endobronchial intubation.