The hemodynamic effects of anesthetic induction in vascular surgical patients chronically treated with angiotensin II receptor antagonists

The use of angiotensin II receptor subtype-1 antagonists (ARA), recently introduced as antihypertensive drugs, is becoming more prevalent. We studied the prevalence and severity of hypotension after the induction of general anesthesia in 12 patients treated with ARA until the morning of surgery. The hemodynamic response to induction was compared with that of patients treated with beta-adrenergic blockers (BB) and/or calcium channel blockers (CB) (BB/CB group, n = 45) and angiotensin-converting enzyme inhibitors (ACEI) (ACEI group, n = 27). A standardized anesthesia induction protocol was followed for all patients. Hypotension occurred significantly (p < or = 0.05) more often in ARA-treated patients (12 of 12) compared with BB/CB-treated patients (27 of 45) or with ACEI-treated patients (18 of 27). There was a significantly (P < or = 0.001) increased ephedrine requirement in the ARA group (21+/-3 mg) compared with the BB/CB group (10+/-6 mg) or the ACEI group (7+/-4 mg). Hypotension refractory to repeated ephedrine or phenylephrine administration occurred significantly (P < or = 0.05) more in the ARA group (4 of 12) compared with the BB/CB group (0 of 45) or the ACEI group (1 of 27), but it was treated successfully by using a vasopressin system agonist. Treatment with angiotensin II antagonism until the day of surgery is associated with severe hypotension after the induction of anesthesia, which, in some cases, can only be treated with an agonist of the vasopressin system. IMPLICATIONS: Hypotensive episodes occur more frequently after anesthetic induction in patients receiving Angiotensin II receptor subtype-1 antagonists under anesthesia than with other hypotensive drugs. They are less responsive to the vasopressors ephedrine and phenylephrine. The use of a vasopressin system agonist was effective in restoring blood pressure when hypotension was refractory to conventional therapy.     

Isoflurane-induced hypotension in orthognathic surgery

The effect of isoflurane-induced hypotension on reduction of blood loss, improvement of surgical field, and postoperative edema was investigated in 52 patients undergoing combined maxillary and mandibular osteotomies. Anesthesia was maintained with fentanyl, N2O, O2, and isoflurane. Deliberate hypotension was induced by increasing isoflurane inspired concentration. Blood loss in the hypotensive group (MAP 55-65 mm Hg) was significantly less than that in the control group (MAP 75-85 mm Hg); 454.0 +/- 211.3 mL versus 755.3 +/- 334.6 mL (P less than 0.001). Fewer patients had to be transfused in the hypotensive group, 12.0% versus 44.4% (P less than 0.02). The surgical field was significantly improved by the hypotensive technique, but operative time was not shortened. Subjective and objective measurements of postoperative edema failed to show any effect of deliberate hypotension. Our data suggest that isoflurane-induced hypotension effectively reduces blood loss and the number of transfusions in orthognathic surgery.     

Treatment of intraoperative refractory hypotension with terlipressin in patients chronically treated with an antagonist of the renin-angiotensin system.

The goal of the present study was to determine whether terlipressin, an agonist of the vasopressin system, could counteract perioperative hypotension refractory to common vasopressor therapy and to analyze its circulatory effects. We enrolled 51 consecutive vascular surgical patients chronically treated with angiotensin-converting enzyme inhibitors or antagonists of the receptor of angiotensin II, who received a standardized opioid-propofol anesthetic. Of these 51 patients, 32 had at least one episode of hypotension, which responded to epinephrine or phenylephrine. In 10 other patients, systolic arterial pressure (SAP) did not remain above 100 mm Hg for 1 min, despite three bolus doses of ephedrine or phenylephrine. In these patients, we injected a bolus of 1 mg of terlipressin, repeated twice if necessary. Hemodynamic and echocardiographic variables were recorded every 30 s over 6 min. In eight patients, arterial pressure was restored with one injection of terlipressin; in two other patients, three injections were necessary. One minute after the last injection of terlipressin, the SAP increased from 88+/-3 to 100+/-4 mm Hg and reached 117+/-5 mm Hg (P = 0.001) 3 min after the injection and remained stable around this value. This increase in SAP was associated with significant changes in left ventricular end-diastolic area (17.9+/-2 vs 20.2+/-2.2 cm2; P = 0.003), end-systolic area (8.1+/-1.3 vs 9.6+/-1.5 cm2; P = 0.004), end-systolic wall stress (45+/-8 vs 66+/-12; P = 0.001), and heart rate (60+/-4 vs 55+/-3 bpm; P = 0.001). Fractional area change and velocity of fiber shortening did not change significantly. No additional injection of vasopressor was required during the perioperative period. No change in ST segment was observed after the injection. IMPLICATIONS: Terlipressin is effective to rapidly correct refractory hypotension in patients chronically treated with antagonists of the renin-angiotensin system without impairing left ventricular function.     

Ephedrine, dopamine, or doubtamine to treat hypotension with propofol during epidural anesthesia

PURPOSE: To compare the efficacy of ephedrine, dopamine and dobutamine for circulatory support during thoracic epidural anesthesia after anesthetic induction with propofol. METHODS: Forty patients undergoing lobectomy or mastectomy were divided into four groups of 10: a control group received no vasopressor; an ephedrine group received 5 mg ephedrine when the mean arterial pressure (MAP), measured every 2.5 min, decreased by 10% from baseline; dopamine and dobutamine groups received 5 microg x kg(-1) x min(-1) dopamine or 3 microg x kg(-1) x min(-1) dobutamine from five minutes after epidural injection of local anesthetic to the end of tracheal intubation. Anesthesia was induced with 2 mg x kg(-1) propofol. The MAP and heart rate (HR) were measured at baseline, 20 min after epidural injection, three minutes after propofol, and one minute after tracheal intubation. RESULTS: In the control group, MAP and HR decreased from 86+/-9 mmHg, 74+/-8 bpm to 62+/-9 mm Hg; P<0.0001, 60+/-8 bpm; P = 0.0003 after propofol. After tracheal intubation, MAP was restored to (81+/-13 mmHg, 70+/-13 bpm). In the ephedrine, dopamine, and dobutamine groups, MAP and HR remained unchanged during epidural anesthesia and propofol induction. However, after tracheal intubation, MAP and HR increased in the ephedrine (104+/-11 mm Hg; P = 0.004, 87+/-11 bpm; P<0.0001) and dobutamine (117+/-13 mm Hg; P = 0.0005, 100+/-11 bpm; P<0.0001) groups, but not in the dopamine group compared with baseline. CONCLUSION: Dopamine is preferable to ephedrine and dobutamine in providing hemodynamic stability during propofol induction and tracheal intubation following epidural anesthesia.     

Patients with severe preeclampsia experience less hypotension during spinal anesthesia for elective cesarean delivery than healthy parturients: a prospective cohort comparison

In this prospective cohort study, we compared the incidence and severity of spinal anesthesia (SA)-associated hypotension in severely preeclamptic (n = 30) versus healthy (n = 30) parturients undergoing cesarean delivery. After the administration of IV fluids, SA was performed with hyperbaric 0.5% bupivacaine, sufentanil, and morphine. Blood pressure (BP) was recorded before and at 2-min intervals for 30 min after SA. Clinically significant hypotension was defined as the need for ephedrine (systolic BP decrease to <100 mm Hg in healthy parturients or 30% decrease in mean BP in both groups). Despite receiving a smaller fluid volume (1653 +/- 331 mL versus 1895 +/- 150 mL; P = 0.005) and a larger bupivacaine dose (10.5 +/- 0.9 mg versus 10.0 +/- 0.7 mg; P = 0.019), the severely preeclamptic patients had a less frequent incidence of clinically significant hypotension (16.6% versus 53.3%; P = 0.006), which was less severe and required less ephedrine. The risk of hypotension was almost six times less in severely preeclamptic patients (odds ratio, 0.17; 95% confidence interval, 0.05-0.58; P = 0.006) than that in healthy patients.     

The influence of nicardipine-, nitroglycerin-, and prostaglandin E(1)-induced hypotension on cerebral pressure autoregulation in adult patients during propofol-fentanyl anesthesia.

We investigated the influence of drug-induced hypotension at a mean arterial pressure (MAP) of 60-70 mm Hg on cerebral pressure autoregulation in 45 adult patients during propofol-fentanyl anesthesia. Time-averaged mean blood flow velocity in the right middle cerebral artery (Vmca) was continuously measured at a PaCO(2) of 39-40 mm Hg by using transcranial Doppler ultrasonography. Hypotension was induced and maintained with a continuous infusion of nicardipine, nitroglycerin, or prostaglandin E(1). Cerebral autoregulation was tested by a slow continuous infusion of phenylephrine to induce an increase in MAP of 20-30 mm Hg. From the simultaneously recorded data of Vmca and MAP, cerebral vascular resistance (CVR) was calculated as MAP/Vmca. Furthermore, the index of autoregulation (IOR) was calculated as DeltaCVR/DeltaMAP, where DeltaCVR = change in CVR and DeltaMAP = change in MAP. The test was performed twice for each condition on each patient: baseline and hypotension. The IOR during baseline was similar among the groups. During nitroglycerin- and prostaglandin E(1)-induced hypotension, IOR was not different from baseline. In contrast, during nicardipine-induced hypotension, IOR significantly decreased compared with baseline (0.37 +/- 0.08 versus 0.83 +/- 0.07, P < 0.01). In conclusion, nicardipine, but not nitroglycerin or prostaglandin E(1), significantly attenuates cerebral pressure autoregulation during propofol-fentanyl anesthesia. IMPLICATIONS: Vasodilators may influence cerebral autoregulation by changing cerebral vascular tone. Nicardipine, but not nitroglycerin or prostaglandin E(1), attenuated cerebral pressure autoregulation in normal adult patients during propofol-fentanyl anesthesia.     

Spinal versus epidural anesthesia for cesarean delivery in severe preeclampsia: a prospective randomized, multicenter study

In this randomized, multicenter study we compared the hemodynamic effects of spinal and epidural anesthesia for cesarean delivery in severely preeclamptic patients. The epidural group (n = 47) received 2% lidocaine with epinephrine 1:400,000, 18-23 mL, followed by 3 mg of morphine after delivery. The spinal group (n = 53) received 2.2 mL of 0.5% hyperbaric bupivacaine plus 0.2 mg morphine. We hypothesized that the lowest MAP (mean arterial blood pressure, the primary outcome) during the delivery period would have to be at least 10 mm Hg less in the spinal group to be of clinical importance. We found that there was a statistically significant difference in MAP, with more patients in the spinal group exhibiting hypotension (P < 0.001). Although the incidence of hypotension (systolic arterial blood pressure, SAP < or =100 mm Hg) was more frequent in the spinal group than in the epidural group (51% versus 23%), the duration of significant hypotension (SAP < or =100 mm Hg) was short (< or =1 min) in both groups. There was more use of ephedrine in the spinal group than in the epidural group (median, 6 versus 0 mg) but hypotension was easily treated in all patients. Neonatal outcomes assessed by Apgar scores and the umbilical arterial blood gas analysis were similar in both groups. Adverse neonatal outcomes (5-min Apgar score < 7 and umbilical arterial blood pH < 7.20) were found in only 2 premature newborns (weight < 1500 g) who were born without maternal hypotension after regional anesthesia. We conclude that the results of this large prospective study support the use of spinal anesthesia for cesarean delivery in severely preeclamptic patients.     

Prevention of hypotension by a single 5-mg dose of ephedrine during small-dose spinal anesthesia in prehydrated cesarean delivery patients

To evaluate the effectiveness of prophylactic ephedrine for the prevention of hypotension associated with spinal anesthesia, 50 parturients undergoing cesarean delivery received either ephedrine 5 mg or saline IV in a double-blinded fashion immediately after the induction of spinal anesthesia. Spinal anesthesia was performed with hyperbaric bupivacaine 6.6 mg combined with sufentanil 3.3 microg as part of a combined spinal-epidural technique. All patients received 1000 mL of lactated Ringer's solution and 500 mL of hydroxyethylstarch 6% before the spinal injection. Additional ephedrine boluses (5 mg) were administered IV when the systolic blood pressure or heart rate decreased by more than 30% from baseline values, when systolic blood pressure became <100 mm Hg, or when patients complained of nausea or feeling faint. The height of the block was equal in the groups; however, more patients in the placebo group were found to develop hypotension (58% vs 25%, P < 0. 05). Only 2 (8%) patients in the ephedrine group developed hypotension with systolic blood pressure values <90 mm Hg, whereas 10 patients (42%) in the saline group experienced hypotension of this severity (P < 0.05). In addition, there was a higher incidence of nausea in the placebo-treated patients. The total amount of ephedrine administered did not differ between groups. These findings suggest that the incidence and severity of hypotension are significantly reduced by the IV administration of a prophylactic dose of 5 mg ephedrine in patients receiving small-dose spinal anesthesia for cesarean delivery. IMPLICATIONS: Ephedrine is the drug most often used to correct hypotension during spinal anesthesia for cesarean delivery in healthy patients. A single IV dose of 5 mg decreases the occurrence and limits the severity of hypotension in prehydrated subjects receiving a small-dose spinal local anesthetic-opioid combination.     

Predictors of hypotension after induction of general anesthesia

Hypotension after induction of general anesthesia is a common event. In the current investigation, we sought to identify the predictors of clinically significant hypotension after the induction of general anesthesia. Computerized anesthesia records of 4096 patients undergoing general anesthesia were queried for arterial blood pressure (BP), demographic information, preoperative drug history, and anesthetic induction regimen. The median BP was determined preinduction and for 0-5 and 5-10 min postinduction of anesthesia. Hypotension was defined as either: mean arterial blood pressure (MAP) decrease of >40% and MAP <70 mm Hg or MAP <60 mm Hg. Overall, 9% of patients experienced severe hypotension 0-10 min postinduction of general anesthesia. Hypotension was more prevalent in the second half of the 0-10 min interval after anesthetic induction (P < 0.001). In 2406 patients with retrievable outcome data, prolonged postoperative stay and/or death was more common in patients with versus those without postinduction hypotension (13.3% and 8.6%, respectively, multivariate P < 0.02). Statistically significant multivariate predictors of hypotension 0-10 min after anesthetic induction included: ASA III-V, baseline MAP <70 mm Hg, age > or =50 yr, the use of propofol for induction of anesthesia, and increasing induction dosage of fentanyl. Smaller doses of propofol, etomidate, and thiopental were not associated with less hypotension. To avoid severe hypotension, alternatives to propofol anesthetic induction (e.g., etomidate) should be considered in patients older than 50 yr of age with ASA physical status > or =3. We conclude that it is advisable to avoid propofol induction in patients who present with baseline MAP <70 mm Hg.     

Terlipressin versus norepinephrine to counteract anesthesia-induced hypotension in patients treated with renin-angiotensin system inhibitors: effects on systemic and regional hemodynamics

BACKGROUND: Terlipressin has been suggested as the ideal drug to treat anesthesia-induced hypotension in patients under long-term renin-angiotensin system inhibitor treatment for arterial hypertension. The authors compared the effects of terlipressin and norepinephrine on systemic hemodynamic parameters and gastric mucosal perfusion using a laser Doppler flowmetry technique in patients treated with renin-angiotensin system inhibitors who experienced hypotension at induction of anesthesia. METHODS: Thirty-two patients scheduled for carotid endarterectomy under general anesthesia and treated with renin-angiotensin system inhibitors had hypotension after induction of general anesthesia. They were randomized to receive 1 mg of terlipressin (n = 16) or norepinephrine infusion (n = 16) to counteract anesthesia-induced hypotension. A laser Doppler probe was introduced into the gastric lumen. All measurements were performed just before surgery, during hypotension, at 30 min, and at 4 h. RESULTS: Terlipressin produced an increase in mean arterial pressure and a decrease in gastric mucosal perfusion detected by laser Doppler flowmetry (P < 0.05) over 30 min that were sustained for 4 h. During the infusion, norepinephrine produced an increase in mean arterial pressure and in gastric mucosal perfusion detected by laser Doppler flowmetry (P < 0.05). If compared to norepinephrine, terlipressin reduced oxygen delivery and oxygen consumption (P < 0.05) and increased arterial lactate concentrations (P < 0.05). CONCLUSION: This study showed the efficacy of terlipressin in the treatment of hypotension episodes in anesthetized patients chronically treated with renin-angiotensin system inhibitors, angiotensin converting-enzyme inhibitors, and angiotensin II receptor antagonists. However, the negative effects on gastric mucosal perfusion and the risk of iatrogenic oxygen supply dependency of terlipressin need to be taken into account.     

Survival with full neurologic recovery after prolonged cardiopulmonary resuscitation with a combination of vasopressin and epinephrine in pigs

We sought to determine the effects of a combination of vasopressin and epinephrine on neurologic recovery in comparison with epinephrine alone and saline placebo alone in an established porcine model of prolonged cardiopulmonary resuscitation (CPR). After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive, every 5 min, either a combination of vasopressin and epinephrine (vasopressin [IU/kg]/epinephrine [ micro g/kg]: 0.4/45, 0.4/45, and 0.8/45; n = 6), epinephrine alone (45, 45, and 200 micro g/kg; n = 6), or saline placebo alone (n = 5). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve the return of spontaneous circulation. Aortic diastolic pressure was significantly (P < 0.01) increased 90 s after each of 3 vasopressin/epinephrine injections versus epinephrine alone versus saline placebo alone (mean +/- SEM: 69 +/- 3 mm Hg versus 45 +/- 3 mm Hg versus 29 +/- 2 mm Hg, 63 +/- 4 mm Hg versus 27 +/- 3 mm Hg versus 23 +/- 1 mm Hg, and 52 +/- 4 mm Hg versus 21 +/- 3 mm Hg versus 16 +/- 3 mm Hg, respectively). Spontaneous circulation was restored in six of six vasopressin/epinephrine pigs, whereas six of six epinephrine and five of five saline placebo pigs died (P < 0.01). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait and was normal 5 days after the experiment in all vasopressin/epinephrine-treated animals. In conclusion, in this porcine model of prolonged CPR, repeated vasopressin/epinephrine administration, but not epinephrine or saline placebo alone, ensured long-term survival with full neurologic recovery. IMPLICATIONS: We present a study to evaluate the effects of a combination of vasopressin and epinephrine during prolonged cardiopulmonary resuscitation on neurological outcome in pigs. We found that all pigs treated with a combination of vasopressin and epinephrine could be resuscitated and had full neurologic recovery observed over an entire period of 5 days.     

Terlipressin versus Norepinephrine to Counteract Anesthesia-induced Hypotension in Patients Treated with Renin-Angiotensin System Inhibitors: Effects on Systemic and Regional Hemodynamics

Background: Terlipressin has been suggested as the ideal drug to treat anesthesia-induced hypotension in patients under long-term renin-angiotensin system inhibitor treatment for arterial hypertension. The authors compared the effects of terlipressin and norepinephrine on systemic hemodynamic parameters and gastric mucosal perfusion using a laser Doppler flowmetry technique in patients treated with renin-angiotensin system inhibitors who experienced hypotension at induction of anesthesia.

Methods: Thirty-two patients scheduled for carotid endarterectomy under general anesthesia and treated with renin-angiotensin system inhibitors had hypotension after induction of general anesthesia. They were randomized to receive 1 mg of terlipressin (n = 16) or norepinephrine infusion (n = 16) to counteract anesthesia-induced hypotension. A laser Doppler probe was introduced into the gastric lumen. All measurements were performed just before surgery, during hypotension, at 30 min, and at 4 h.

Results: Terlipressin produced an increase in mean arterial pressure and a decrease in gastric mucosal perfusion detected by laser Doppler flowmetry (P < 0.05) over 30 min that were sustained for 4 h. During the infusion, norepinephrine produced an increase in mean arterial pressure and in gastric mucosal perfusion detected by laser Doppler flowmetry (P < 0.05). If compared to norepinephrine, terlipressin reduced oxygen delivery and oxygen consumption (P < 0.05) and increased arterial lactate concentrations (P < 0.05).     

Hemodynamic effects of spinal anesthesia and simultaneous intravenous bolus of combined phenylephrine and ephedrine versus ephedrine for cesarean delivery

BACKGROUND: Hypotension following spinal anesthesia for cesarean delivery can produce adverse maternal symptoms and neonatal acid-base effects. Single-agent prophylaxis, most notably with ephedrine, does not reliably prevent spinal anesthesia-induced hypotension; recently, however, the prophylactic use of phenylephrine with ephedrine as an infusion was observed to be effective. We postulated that this combination, when given as an intravenous bolus for prophylaxis and rescue treatment, could be similarly effective. METHOD: Forty-three term parturients were randomized to receive a bolus of ephedrine 10 mg +/- phenylephrine 40 microg (groups E and EP, respectively) simultaneously with spinal anesthesia. Hypotension was defined as a systolic blood pressure below 100 mmHg or a decrease of 20% from a baseline value. Rescue boluses comprised of ephedrine 5 mg +/- phenylephrine 20 microg. RESULTS: For groups E and EP, respectively, the incidence of hypotension was 80% vs. 95% (P=0.339), with the mean number of rescue boluses being 3.85+/-3.7 and 3.05+/-1.7 and the mean umbilical artery pH being 7.246+/-0.081 vs. 7.244+/-0.106. All comparisons were not significant (NS). CONCLUSION: The combination of ephedrine and phenylephrine given as an intravenous bolus at the doses selected is not superior to ephedrine alone in preventing or treating hypotension in healthy parturients undergoing cesarean delivery.     

Prophylactic effects of systemic oral ephedrine in spinal anesthesia-induced hypotension during transurethral prostatectomy

OBJECTIVE: We investigated the prophylactic effects of systemic oral ephedrine in spinal anesthesia-induced hypotension during transurethral prostatectomy. MATERIAL AND METHODS: Sixty American Society of Anesthesiologists Grade II and III patients scheduled for spinal anesthesia were randomized into one of two groups. Patients in Group I (n = 30) received oral ephedrine 50 mg in addition to premedication whilst those in Group II (n = 30) received only premedication 30 min before spinal anesthesia. Pre-infusion values were measured in order to obtain baseline readings after oral ephedrine administration in Group I and after premedication in Group II. Systolic arterial pressure (SAP) and heart rate (HR) were recorded before and after infusion, during and 5 min after spinal anesthesia and intraoperatively. Hypotension was defined as SAP <100 mmHg and <20% of baseline value. Hypotension was treated with 3 mg ephedrine and bradycardia was corrected with atropine 0.5 mg, given as an i.v. bolus. RESULTS: SAP values were significantly lower in Group II during the spinal anesthesia, post-spinal and intraoperative periods (p < 0.0001). Fifteen patients received ephedrine in Group II and seven in Group I. Supplemental ephedrine was used at doses of 3.42 +/- 0.97 mg in Group I and 8.86 +/- 1.24 mg in Group II. The incidence of hypotension was halved in Group I compared to Group II (23.33% vs 50%, p = 0.003). Six patients received atropine in Group II because of severe bradycardia. Mean HR values were lower in Group II than Group I during the spinal anesthesia, post-spinal and intraoperative periods. CONCLUSIONS: We conclude that a prophylactic oral dose of ephedrine 50 mg is effective for minimizing and managing spinal anesthesia-induced hypotension during transurethral prostatectomy.     

Terlipressin versus norepinephrine to correct refractory arterial hypotension after general anesthesia in patients chronically treated with renin-angiotensin system inhibitors

BACKGROUND: Terlipressin, a precursor that is metabolized to lysine-vasopressin, has been proposed as a drug for treatment of intraoperative arterial hypotension refractory to ephedrine in patients who have received long-term treatment with renin-angiotensin system inhibitors. The authors compared the effectiveness of terlipressin and norepinephrine to correct hypotension in these patients. METHODS: Among 42 patients scheduled for elective carotid endarterectomy, 20 had arterial hypotension following general anesthesia that was refractory to ephedrine. These patients were the basis of the study. After randomization, they received either 1 mg intravenous terlipressin (n = 10) or norepinephrine infusion (n = 10). Beat-by-beat recordings of systolic arterial blood pressure and heart rate were stored on a computer. The intraoperative maximum and minimum values of blood pressure and heart rate, and the time spent with systolic arterial blood pressure below 90 mmHg and above 160 mmHg, were used as indices of hemodynamic stability. Data are expressed as median (95% confidence interval). RESULTS: Terlipressin and norepinephrine corrected arterial hypotension in all cases. However, time spent with systolic arterial blood pressure below 90 mmHg was less in the terlipressin group (0 s [0-120 s] vs. 510 s [120-1011 s]; P < 0.001). Nonresponse to treatment (defined as three boluses of terlipressin or three changes in norepinephrine infusion) occurred in zero and eight cases (P < 0.05), respectively. CONCLUSIONS: In patients who received long-term treatment with renin-angiotensin system inhibitors, intraoperative refractory arterial hypotension was corrected with both terlipressin and norepinephrine. However, terlipressin was more rapidly effective for maintaining normal systolic arterial blood pressure during general anesthesia.     

Prophylactic IM small-dose phenylephrine blunts spinal anesthesia-induced hypotensive response during surgical repair of hip fracture in the elderly

In a double-blinded, placebo-controlled, randomized study, we evaluated the effect of prophylactic IM phenylephrine at doses of 1.5 and 3 mg on hyperbaric tetracaine spinal anesthesia-induced hypotension in 90 normotensive and hypertensive patients aged >65 yr undergoing surgery for hip fracture. Thirty normotensive patients received 1.5 or 3 mg of phenylephrine IM (N/P-1.5 and N/P-3.0 groups; n = 15 in each), whereas controls received saline (N/C group; n = 15), and 45 hypertensive patients were treated in a similar manner (H/P-1.5, H/P-3.0, and H/C groups; n = 15 in each). All groups had a peak sensory block height of T9, with a range of T8 to T10. The incidence of hypotension (>25% decrease in mean arterial blood pressure [MAP] from baseline) was significantly lower in the patients who received phenylephrine 1.5 or 3 mg than in the controls, both in the normotensive and hypertensive groups (P < 0.01). The N/P-3.0 and N/P-1.5 groups and the H/P-3.0 group had significantly lower percentage reductions in MAP (P < 0.05) and required significantly smaller doses of rescue IV ephedrine (P < 0.05) than did the N/C group or the H/C group. The H/P-1.5 group also required significantly less rescue IV ephedrine (P < 0.05), although it was not sufficient to significantly attenuate the percentage decrease in MAP compared with that in the H/C group. Bradycardia (heart rate <50 bpm) as an adverse effect after IM administration of phenylephrine was not observed in any of the groups. Hypertension (MAP >20% increase from baseline) after medication occurred in the N/P-3.0 and H/P-3.0 groups, but not in the N/P-1.5 and H/P-1.5 groups. We conclude that prophylactic IM injection of 1.5 mg of phenylephrine is a safe (defined as the inhibition of bradycardia and hypertension) and effective means of reducing the incidence of hypotension associated with spinal anesthesia in normotensive and hypertensive elderly patients. IMPLICATIONS: We evaluated the efficacy and safety of small-dose IM phenylephrine for prophylaxis against spinal anesthesia-induced hypotension in normotensive and hypertensive elderly patients. Phenylephrine 1.5 mg IM was effective for reducing the incidence of hypotension and avoided adverse effects.     

Morphine-induced cardiovascular stimulation: the effects of two doses on healthy subjects

In humans, morphine induces hypotension, probably because of histamine liberation. Earlier animal studies have, however, suggested that morphine can induce immediate cardiovascular stimulation when given as a sole medication. The aim of this study was to evaluate the initial effects of morphine on circulation, oxygen consumption, and plasma histamine and catecholamine concentrations. Oxycodone was used as a reference drug. Eight healthy volunteers received, in a random, cross-over, double-blinded fashion: 0.07 mg/kg morphine (M1); 0.14 mg/kg morphine (M2); 0.14 mg/kg oxycodone (O); and placebo (P) as a 2-min IV injection for pain. Mean arterial blood pressure (MAP), heart rate (HR), and oxygen consumption (VO(2)) were recorded. Plasma histamine and catecholamine concentrations were determined. Both M1 and M2 elicited an initial, but transient, increase in MAP from 84 +/- 5 to 96 +/- 9 mm Hg (P < 0.05) and from 83 +/- 8 to 100 +/- 10 mm Hg (P < 0.05), respectively. A parallel increase in HR was also seen after M1 (from 62 +/- 12 to 70 +/- 10 bpm, P < 0.05) and M2 (from 67 +/- 9 to 78 +/- 8 bpm, P < 0.05). After M2, this was accompanied by a simultaneous increase in VO(2) from 295 +/- 39 mL/min to 322 +/- 61 mL/min (P < 0.05). After O, as well as P, no increase in MAP or HR was detected. Plasma histamine and catecholamine concentrations were not clearly affected by any of the treatments. We conclude that the immediate effect of morphine on the hemodynamics of healthy volunteers was stimulation, not hypotension. This effect was not seen in conjunction with oxycodone, a morphine-like mu-receptor agonist. IMPLICATIONS: In this double-blinded, randomized study, we evaluated whether morphine could induce immediate cardiovascular stimulation, as seen previously in animal studies. In healthy volunteers, during a painful stimulus, morphine caused an initial, transient hemodynamic stimulation, accompanied by increased oxygen consumption, without detectable release of histamine or catecholamines into the plasma. Oxycodone caused only minor hemodynamic alterations.     

Hydroxyethylstarch 10% is superior to Ringer’s solution for preloading before spinal anesthesia for Cesarean section

PURPOSE: To compare the preloading effect of 500 ml hydroxyethylstarch (HES) 10% with 1 L Lactated Ringer's solution (LR). METHODS: In 40 healthy women undergoing elective Cesarean section HES, 500 ml (n = 20), or LR, IL (n = 20), was administered during 10 min before spinal anesthesia. The incidence of hypotension, (systolic blood pressure < 80% of baseline and < 100 mm Hg), and the amount of ephedrine used to treat it were compared. Also, the incidence of nausea and/or vomiting were recorded. Neonatal outcome was assessed using Apgar scores and umbilical venous and arterial blood gases. RESULTS: The incidence of hypotension was higher in the LR than in HES group (80% vs 40%). Mean minimum systolic blood pressure was lower in the LR than in the HES group (86.1 +/- 12.7 mm Hg vs 99.6 +/- 9.7 mm Hg P < 0.05). Systolic blood pressure < 90 mmHg occurred in two of 20 patients (10%) who received HES vs 11 of 20 patients (55%) who received LR (P < 0.05). More doses of ephedrine were required to treat hypotension in the LRthan in the HES group (35.3 +/- 18.4 mg vs 10.6 +/- 8.6 mg; P < 0.05). The incidence of nausea and/or vomiting was lower in the HES than in the crystalloid group. Neonatal outcome was good and similar in both groups. CONCLUSION: Preloading patients undergoing elective Cesarean section with 500 ml HES 10%, decreases the incidence and severity of spinal-induced hypotension more than preloading with 1 L of LR solution.     

Propofol anesthesia enhances the pressor response to intravenous ephedrine

The induction of anesthesia with propofol is often associated with a decrease in arterial blood pressure (BP). Although vasopressors are sometimes required to reverse the propofol-induced hypotension, little is known about the effect of propofol on these drugs. We studied the effects of propofol and sevoflurane on pressor response to i.v. ephedrine. Thirty adult patients were randomly assigned to one of two groups. In the Propofol group (n = 15), patients received propofol 2.5 mg/kg i.v. for induction followed by 100 microg x kg(-1) x min(-1) i.v. for maintenance. In the Sevoflurane group (n = 15), anesthesia was induced with sevoflurane 3%-4% in oxygen and maintained with sevoflurane 2% in oxygen. All patients in both groups received ephedrine 0.1 mg/kg i.v. before and after the anesthetic induction. Ephedrine increased the heart rate significantly (P < 0.05) in awake patients in both study groups. In contrast, there was no increase in heart rate after the ephedrine administration under propofol or sevoflurane anesthesia. In awake patients, transient increases in mean BP were observed after i.v. ephedrine in both groups. In the Propofol group, 2 min after the administration of ephedrine, mean BP increased 16% +/- 10% under anesthesia but increased only 4% +/- 6% when the same patients were awake. The magnitudes of the pressor responses to ephedrine during propofol anesthesia were significantly greater (P < 0.05) than during the awake state. However, ephedrine 0.1 mg/kg i.v. showed no significant increases in BP during sevoflurane anesthesia. We conclude that propofol, not sevoflurane, anesthesia augments the pressor responses to i.v. ephedrine. IMPLICATIONS: The effect of anesthetics on vasopressor-mediated cardiovascular effects is poorly understood. We evaluated the pressor response to ephedrine during propofol or sevoflurane anesthesia. Our study suggests that anesthesia-induced hypotension may be easier to reverse with ephedrine during propofol anesthesia than during sevoflurane anesthesia.     

Hemodynamic effects of anesthesia in patients chronically treated with angiotensin-converting enzyme inhibitors.

Angiotensin-converting enzyme inhibitors (ACEIs) are increasingly used in the treatment of cardiovascular disease, but recent reports have warned of some hemodynamic risk (hypotension and bradycardia) when associated with anesthesia. To assess the hemodynamic effects of induction of anesthesia in patients chronically treated with ACEIs, 16 hypertensive patients scheduled for coronary artery bypass graft surgery (n = 12) or vascular surgery (n = 4) were studied. Eight of them were chronically treated (for at least 1 mo) with ACEIs (ACEI group), and the remaining eight (control group) were treated with other classes of antihypertensive drugs. Induction of anesthesia, which consisted of flunitrazepam (0.03 mg/kg), fentanyl (0.006 mg/kg), and pancuronium (0.1 mg/kg) IV, was followed by a significant decrease in mean arterial blood pressure from baseline in both groups (by 16.8% in controls [P = 0.001] and 33.5% in ACEI-treated patients [P = 0.001] [P = 0.041 between groups]). In control patients, mean arterial blood pressure decrease was only associated with a significant decrease in cardiac index (-18%, P = 0.014). In ACEI-treated patients, the arterial blood pressure decreases were associated with consistent reductions in pulmonary capillary wedge pressure (-26.4%; P = 0.035) and cardiac index (-23.9%; P = 0.001). Systemic vascular resistance index and heart rate were moderately changed (-14.2% and -4.5%, respectively). Rapid restoration of arterial blood pressure was obtained in all ACEI-treated patients, mainly with the intravenous administration of 0.4 to 0.7 L of lactated Ringer's solution. Phenylephrine (0.38 +/- 0.9 mg) was, however, required in four patients when mean arterial blood pressure was less than 60 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)