Bolus Doses Of Phenylephrine Research Articles

Independent responses of baroreceptors and blood pressure to low bolus dose of phenylephrine in fully conscious human volunteers

Independent responses of baroreceptors and blood pressure to low bolus dose of phenylephrine in fully conscious human volunteers

The effects of prophylactic bolus phenylephrine on hypotension during low-dose spinal anesthesia for cesarean section

BackgroundContinuously infused phenylephrine is frequently used to reduce the incidence of hypotension in women undergoing cesarean section under spinal anesthesia, but less is known about the prophylactic bolus method. We evaluated three prophylactic bolus doses of phenylephrine during low-dose spinal anesthesia for cesarean section. MethodsOne-hundred-and-eighty-four patients were randomized to receive 0.9% saline 2mL (Control Group) or phenylephrine 1.0μg/kg (PHE1 Group), 1.5μg/kg (PHE1.5 Group), or 2.0μg/kg (PHE2 Group) immediately after induction of combined spinal-epidural anesthesia. Maternal blood pressure and heart rate were recorded at 1-min intervals until delivery. Hypotension, defined as systolic blood pressure <80% of baseline, was treated with rescue doses of phenylephrine 100μg at 1-min intervals until hypotension resolved. The incidence of nausea, vomiting, bradycardia, and hypertension, as well as Apgar scores and umbilical blood gases, were recorded. ResultsThe incidence of hypotension was 71.7% (33/46) in the Control Group, 68.9% (31/45) in the PHE1 Group, 37.0% (17/46) in the PHE1.5 Group and 45.7% (21/46) in the PHE2 Group (P=0.001). The total rescue dose of phenylephrine was greater in the Control Group than those in the PHE1.5 Group (P<0.05) and PHE2 Group (P<0.05). The incidence of hypertension increased as the dose of prophylactic phenylephrine increased (P<0.001) and was highest in the PHE2 group (37%). Other variables did not differ among the four groups. ConclusionsUnder the conditions of this study, prophylactic bolus injection of phenylephrine 1.5μg/kg was a suitable alternative method for reducing the incidence of hypotension during low-dose spinal anesthesia for cesarean section.

Determination of the 90% effective dose (ED90) of phenylephrine for hypotension during elective cesarean delivery using a continual reassessment method

ObjectiveThe purpose of this study was to determine, by continual reassessment, the 90% effective dose (ED90) of phenylephrine for hypotension after combined spinal–epidural anesthesia. Study designTerm pregnant women scheduled for elective cesarean delivery received combined spinal epidural anesthesia. Subjects received phenylephrine at one of 6 incremental doses ranging from 60 to 160μg (n=3 for each dose). While the first cohort received a conservative, predetermined dose of 60μg, subsequent cohorts received phenylephrine doses determined using Bayesian-based software. One of the predetermined bolus doses of phenylephrine was given in the event of both hypotension [defined as systolic blood pressure (SBP)<80% of baseline or below 100mmHg] and tachycardia [defined as heart rate >120% of baseline or >100beatsmin−1]. Treatment was considered successful if SBP returned to within 80% of the baseline or ≥100mmHg within 2min. ResultsTwenty-four subjects with hypotension and tachycardia were included. T6 block was achieved within 15min in 20 patients and after additional epidural chloroprocaine in the remaining four. The estimated ED90 was 100μg, with a response probability of 90.7% (95% CI 74.1–99.5%). Treatment was successful in 20 patients. Probability of success at each bolus dose (in μg) was as follows: 60, 58.9%; 80, 80.3%; 100, 90.7%; 120, 95.5%; 140, 98.3%; and 160, 99.2%. ConclusionsThe ED90 of a phenylephrine bolus dose for hypotension in term pregnant women is approximately 100μg, based on continual reassessment.

Effect of Different Phenylephrine Bolus Doses for Treatment of Hypotension during Spinal Anaesthesia in Patients Undergoing Elective Caesarean Section

The efficacy of phenylephrine might be improved by giving doses higher than that traditionally used (100 µg). This study compared the effects of three initial bolus doses of intravenous phenylephrine; 100 µg (group P100), 125 µg (group P125) and 150 µg (group P150), for the treatment of post-spinal hypotension in patients undergoing elective caesarean delivery. If hypotension was not corrected by this dose, additional boluses of 25 µg were given every minute. Further hypotensive episodes were treated with half the initial bolus dose, followed by 25 µg boluses, as required. Umbilical arterial and venous blood samples were obtained for blood gas analysis and Apgar scores recorded. One hundred and twenty subjects (40 per group) who developed post-spinal hypotension (75%) were included in this randomised, double blind trial. Although systolic blood pressure was higher at certain time-points after 150 µg phenylephrine, there were no statistically significant differences in the effectiveness of the first bolus of phenylephrine to treat hypotension (85%, 95% and 95% in groups P100, P125 and P150, respectively, P=0.215); the additional dose of phenylephrine after the first bolus (P=0.810); the number of additional boluses (P=0.318) or of hypotensive episodes (P=0.118). There were no significant differences in the number of patients developing reactive hypertension or bradycardia, in maternal side-effects or in neonatal outcomes. Although the study may have been underpowered, initial phenylephrine bolus doses of 100 µg, 125 µg and 150 µg did not significantly differ in efficacy to treat post-spinal hypotension in these patients.

Anaesthetic management for drainage of frontoparietal abscess in a patient of uncorrected Tetralogy of Fallot.

Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease, characterised by aortic overriding, right ventricular hypertrophy, pulmonary stenosis (PS) and ventricular septal defect (VSD). When left untreated, survival to adulthood is rare.[1] Brain abscesses can occur in them because of paradoxical embolism and absence of pulmonary phagocytic clearance of pathogens. There are few case reports of uncorrected TOF surviving to adulthood and then presenting for non-cardiac surgeries.[1,2,3] We present a case of drainage of a large left fronto-parietal abscess under general anaesthesia, in a patient of uncorrected TOF.

A randomised comparison of the effects of low-dose spinal or general anaesthesia on umbilical cord blood gases during caesarean delivery of growth-restricted foetuses with impaired Doppler flow

Hypotension following spinal anaesthesia for caesarean delivery may decrease uteroplacental perfusion and produce foetal acidosis. The optimal anaesthetic technique for mothers with foetal growth restriction and impaired Doppler flow is unclear. To compare the effects of low-dose spinal anaesthesia and general anaesthesia on neonatal outcome and maternal haemodynamics. Prospective, randomised clinical trial. Tertiary care hospital. Forty pregnant women with foetal growth restriction and impaired Doppler flow scheduled for elective caesarean delivery. The women were allocated randomly to receive a low-dose spinal anaesthetic (8-mg hyperbaric bupivacaine 0.5% with fentanyl 20 μg) or standard general anaesthesia for elective caesarean delivery. SBP was maintained between 80 and 100% of baseline using bolus doses of phenylephrine. The total duration of hypotension, dose of phenylephrine used and any incidence of hypotension, nausea or vomiting were recorded. The primary outcome variable was arterial and venous umbilical cord base deficit. Neonatal outcome and maternal haemodynamics were analysed as secondary endpoints. The mean umbilical artery pH was significantly lower in the low-dose spinal anaesthesia group than in the general anaesthesia group (7.23 ± 0.06 vs. 7.27 ± 0.04, P = 0.01). Cord base deficit was similar in the two groups. Higher partial pressures of oxygen occurred in the general anaesthesia group (20.9 ± 6.5 kPa) than in the low-dose spinal anaesthesia group (13.6 ± 6.1 kPa, P = 0.001). No difference was observed between groups in 1 and 5-min Apgar scores. There appeared to be a greater need for immediate resuscitation of neonates in the general anaesthesia group, but the difference was not statistically significant (P = 0.51). Low-dose spinal anaesthesia was associated with hypotension of short duration (0.7 ± 1.1 min). In this study, there was no difference in umbilical cord base deficit between the groups. Larger studies would be required to assess whether the mode of anaesthesia influences the incidence of clinically important neonatal acidosis in neonates with foetal growth restriction.

Bilateral subclavian artery stenosis found by inter-arm blood pressure difference during distal pancreatectomy

Bilateral subclavian artery stenosis found by inter-arm blood pressure difference during distal pancreatectomy

Effect of Phenylephrine and Ephedrine Bolus Treatment on Cerebral Oxygenation in Anaesthetized Patients

Meng, L.*; Cannesson, M.*; Alexander, B.S.*; Yu, Z.†; Kain, Z.N.*; Cerussi, A.E.‡; Tromberg, B.J.‡; Mantulin, W.W.‡ Author Information

A role for xanthine oxidase in the control of fetal cardiovascular function in late gestation sheep

Virtually nothing is known about the effects on fetal physiology of xanthine oxidase inhibition. This is despite maternal treatment with the xanthine oxidase inhibitor allopurinol being considered in human complicated pregnancy to protect the infant’s brain from excessive generation of ROS.We investigated the in vivo effects of maternal treatment with allopurinol on fetal cardiovascular function in ovine pregnancy in late gestation. Under anaesthesia, pregnant ewes and their singleton fetus were instrumented with vascular catheters and flow probes around an umbilical and a fetal femoral artery at 118±1 dGA (days of gestational age; termca. 145 days). Five days later, mothers were infused I.V. with either vehicle (n =11) or allopurinol (n =10). Fetal cardiovascular function was stimulated with increasing bolus doses of phenylephrine (PE) following maternal vehicle or allopurinol. The effects of maternal allopurinol on maternal and fetal cardiovascular function were also investigated following fetal NO blockade (n =6) or fetal β1-adrenergic antagonism (n =7). Maternal allopurinol led to significant increases in fetal heart rate, umbilical blood flow and umbilical vascular conductance, effects abolished by fetal β1-adrenergic antagonism but not by fetal NO blockade. Maternal allopurinol impaired fetal α1-adrenergic pressor and femoral vasopressor responses and enhanced the gain of the fetal cardiac baroreflex. These effects of maternal allopurinol were restored to control levels during fetal NO blockade. Maternal treatment with allopurinol induced maternal hypotension, tachycardia and acid–base disturbance. We conclude that maternal treatment with allopurinol alters in vivo maternal, umbilical and fetal vascular function via mechanisms involving NO and β1-adrenergic stimulation. The evidence suggests that the use of allopurinol in clinical practice should be approached with caution.

Comparison between phenylephrine and ephedrine in preventing hypotension during spinal anesthesia for cesarean section

Background: Maternal hemodynamic changes are common during spinal anesthesia for cesarean delivery. Many agents are used for treating hypotension. In this study we compared the efficacy of ephedrine and phenylephrine in preventing and treating hypotension in spinal anesthesia for cesarean section and their effect on fetal outcome. Materials and Methods: A total of 100 ASA Grade I patients undergoing elective cesarean section under spinal anesthesia with a normal singleton pregnancy beyond 36 weeks gestation were randomly allocated into two groups of 50 each. Group I received prophylactic bolus dose of ephedrine 10 mg IV at the time of intrathecal block with rescue boluses of 5 mg. Group II received prophylactic bolus dose of phenylephrine 100 μg IV at the time of intrathecal block with rescue boluses of 50 μg. Hemodynamic variables like blood pressure and heart rate was recorded every 2 minutes up to delivery of baby and then after every 5 minutes. Neonatal outcome was assessed using Apgar score at 1 and 5 minutes and neonatal umbilical cord blood pH values. Results: There was no difference found in managing hypotension between two groups. Incidence of bradycardia was higher in phenylephrine group. The differences in umbilical cord pH, Apgar score, and birth weight between two groups were found statistically insignificant. Conclusion: Phenylephrine and ephedrine are equally efficient in managing hypotension during spinal anesthesia for elective cesarean delivery. There was no difference between two vasopressors in the incidence of true fetal acidosis. Neonatal outcome remains equally good in both the groups.

Effect of phenylephrine and ephedrine bolus treatment on cerebral oxygenation in anaesthetized patients

How phenylephrine and ephedrine treatments affect global and regional haemodynamics is of major clinical relevance. Cerebral tissue oxygen saturation (Sct(O2) )-guided management may improve postoperative outcome. The physiological variables responsible for Sct(O2) changes induced by phenylephrine and ephedrine bolus treatment in anaesthetized patients need to be defined. A randomized two-treatment cross-over trial was conducted: one bolus dose of phenylephrine (100-200 µg) and one bolus dose of ephedrine (5-20 mg) were given to 29 ASA I-III patients anaesthetized with propofol and remifentanil. , mean arterial pressure (MAP), cardiac output (CO), and other physiological variables were recorded before and after treatments. The associations of changes were analysed using linear-mixed models. The CO decreased significantly after phenylephrine treatment [▵CO = -2.1 (1.4) litre min(-1), P<0.001], but was preserved after ephedrine treatment [▵CO = 0.5 (1.4) litre min(-1), P>0.05]. The was significantly decreased after phenylephrine treatment [▵ = -3.2 (3.0)%, P<0.01] but preserved after ephedrine treatment [▵ = 0.04 (1.9)%, P>0.05]. CO was identified to have the most significant association with (P<0.001). After taking CO into consideration, the other physiological variables, including MAP, were not significantly associated with (P>0.05). Associated with changes in CO, decreased after phenylephrine treatment, but remained unchanged after ephedrine treatment. The significant correlation between CO and implies a cause-effect relationship between global and regional haemodynamics.

Altered sympathetic reflexes and vascular reactivity in rats after exposure to chronic intermittent hypoxia

Exposure to chronic intermittent hypoxia (CIH) yields persistent elevations in sympathetic nerve activity (SNA) and mean arterial pressure(MAP)with exaggerated sympathetic chemoreflexes. We examined the impact of CIH upon other sympathoexcitatory reflexes and a potential central mechanism underlying the altered regulation of SNA.Male Sprague-Dawley rats were exposed to CIH for 2 weeks (40 s at 6% O2 every 9 min, 8 h day⁻¹). After exposure to CIH, urethane-anaesthetized, vagotomized, ventilated, paralysed rats had significantly elevated MAP, splanchnic SNA, and rate of phrenic nerve discharge (PND; P<0.05). Elimination of SNA by ganglionic blockade produced a larger fall in MAP in rats exposed to CIH (P<0.05). Like acute hypoxia, stimulation of the sciatic nerve or the nasal mucosa evoked greater increases in SNA after exposure to CIH (P<0.05). In addition, acute hypoxia promoted exaggerated increases in PND amplitude after CIH (P<0.05). In contrast, the nasopharyngeal reflex evoked exaggerated increases in SNA during apnoea. These sympathoexcitatory reflexes are mediated by glutamatergic activation of the rostral ventrolateral medulla (RVLM), and accordingly, microinjections of glutamate into RVLM evoked larger increases in SNA after CIH (P<0.05). Paradoxically, none of these exaggerated acute rises in SNA was accompanied by enhanced pressor responses. Reduced adrenergic vascular reactivity may contribute to the blunted sympathetically mediated pressor responses, because bolus doses of phenylephrine evoked attenuated pressor responses after CIH (P<0.01).These data suggest exposure to CIH facilitates activation of SNA, potentially by changes within the RVLM. However, the exaggerated rises in SNA are not dependent upon stimulation of inspiratory drive. Although elevated SNA may contribute to CIH-induced hypertension, reduced adrenergic vascular reactivity buffers the cardiovascular impact of exaggerated acute rises in SNA.

Aortic baroreceptor function and depressed baroreflex sensitivity following myocardial infarction

Depressed sinoaortic baroreflex control of heart rate following myocardial infarction (MI) is associated with increased morbidity and mortality. The etiology of this autonomic disturbance is unknown but could potentially occur at several levels of the reflex arc. The purpose of this study was to assess whether depressed baroreflex sensitivity (BRS) post-MI is associated with aortic baroreceptor dysfunction.BRS was measured before and 4–8 weeks after anterior MI in 17 chronically-instrumented, trained, conscious dogs. BRS (ms/mm Hg) was defined as the slope of the relationship between changes in systolic blood pressure (SBP) and heart period in response to a bolus dose of phenylephrine (PE). After the effects of MI on BRS were determined, the animals were anesthetized and the aortic depressor nerves (ADN) were isolated from the cervical vagi. Aortic baroreceptor function was measured by direct recording of ADN activity during gradual elevation of SBP induced by PE infusion.BRS was depressed following MI in 7 of these dogs and preserved in the remaining 10. Aortic baroreceptor sensitivity (ABS) defined as the slope of the relationship between changes in ADN activity and SBP was not significantly different between the dogs with depressed BRS compared to the dogs with preserved BRS post-MI.In conclusion, the response of the aortic baroreceptors to an increase in SBP is similar in dogs with and without depressed BRS post-MI. Based on these data, we conclude that depressed reflex control of heart rate following MI is not related to dysfunction of the afferent limb of the sinoaortic baroreflex.

Nitric Oxide Reduces Vagal Baroreflex Sensitivity in the Late Gestation Fetus

Goals to understand the etiology of essential hypertension have proposed that this problem arises, in part, because of changes within brainstem circuits involved in arterial blood pressure (ABP) control. It has been suggested that nitric oxide (NO) exerts inhibitory influences on the integration of afferent discharge from the arterial baroreceptors. This study tested the hypothesis that the inhibitory influence of NO on the arterial baroreflex is present in fetal life. Fetal baroreflex sensitivity was calculated in fetal sheep, before and during the NO-clamp; a technique that permits NO synthase (NOS) blockade with l-NAME while maintaining basal cardiovascular function with sodium nitroprusside. Under halothane anesthesia, five fetal sheep at 0.8 gestation were instrumented with vascular catheters. Five days later, fetuses received a range of bolus doses of phenylephrine (5-75 microg I.A.) in randomized order either during saline or treatment with the NO clamp. Basal fetal ABP and heart rate before (50 +/- 4 mm Hg, 170 +/- 3 bpm) or during (51 +/- 4 mm Hg, 173 +/- 3 bpm) the NO-clamp were similar. The gradient of the pulse interval-ABP relationship was nearly doubled during NOS blockade (14.2 =/- 2.5 versus 7.8 +/- 1.6 ms/mm Hg). The data provide in vivo evidence that NO attenuates the sensitivity of the cardiac baroreflex during fetal life.

A case of refractory intraoperative hypotension treated with vasopressin infusion

A 56-year-old man, treated with an angiotensin II receptor antagonist for hypertension, presented for placement of a cochlear implant during general anesthesia. Intraoperatively, there was profound hypotension that was resistant to decreasing the anesthetic depth, fluid administration, as well as bolus doses of phenylephrine, ephedrine, and epinephrine. Hypotension was eventually successfully treated with a vasopressin infusion (0.06 U/min). Vasopressin may be a useful agent in such scenarios because its effect is not dependent on either adrenergic or angiotensin receptors, both of which may be affected by angiotensin II receptor antagonists.

Development of baroreflex function and hind limb vascular reactivity in the horse fetus

This study investigated, in vivo, the mechanisms underlying the development of cardiovascular function in the horse fetus, with particular relevance to baroreflex function and hind limb vascular arterial reactivity to constrictor agonists. Under general anaesthesia, vascular catheters were inserted and a Transonic flow probe was implanted around one of the metatarsal arteries of 13 horse fetuses, either at 0.6 of gestation (n= 6) or at 0.9 of gestation (n= 7, term approximately 335 days). At least 5 days after surgery, pressor, vasoconstrictor and cardiac chronotropic responses to exogenous bolus doses of phenylephrine, angiotensin II and arginine vasopressin were recorded. Fetal cardiac baroreflex slopes were obtained using the peak pressor and heart rate responses to increasing doses of phenylephrine. Fetal treatment with phenylephrine, angiotensin II and vasopressin produced significant changes in arterial blood pressure, hind limb vascular resistance and heart rate. Pressor and vasopressor responses to all agonists were greater at 0.9 than at 0.6 of gestation; however, fetal cardiac baroreflex sensitivity decreased with advancing gestational age. Correlation analysis revealed that fetal plasma cortisol rather than gestational age was a greater determinant of pressor and vasopressor reactivity. In contrast, gestational age rather than cortisol better determined heart rate and baroreflex responsiveness in the equine fetus. The data show that development of cardiovascular function in the equine fetus occurs via cortisol-dependent and -independent pathways.

Effect of hypothermia on baroreflex control of heart rate and renal sympathetic nerve activity in anaesthetized rats.

The present study investigated the effect of acute hypothermia on baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) by generating baroreflex logistic function curves, using bolus doses of phenylephrine and sodium nitroprusside, in anaesthetized male Wistar rats at a core temperature (T(b)) of 37 degrees C, during acute severe hypothermia at T(b)= 25 degrees C and on rewarming to 37 degrees C. Comparisons were made between rats without (euthermic, n= 6) and with (acclimated, n= 7) prior exposure to lower ambient temperatures and shorter photoperiod, simulating adaptation to winter conditions. In both groups of rats, acute hypothermia to T(b)= 25 degrees C shifted the baroreflex-RSNA curve slightly leftwards and downwards with decreases in the setpoint pressure and maximal gain, whereas it markedly impaired the baroreflex-HR curve characterized by decreases in response range by approximately 90% (P < 0.001), minimum response by approximately 10% (P < 0.05) and maximum gain by approximately 95% (P < 0.001), from that at T(b)= 37 degrees C. All parameters were restored to precooling levels on rewarming. Electrical stimulation of cardiac vagal efferents induced a voltage-related bradycardia, the magnitude of which was partially reduced during acute hypothermia, and there was a significant prolongation of the electrocardiogram intervals indicating a delay in cardiac conduction. Mild suppression of baroreflex control of RSNA could contribute to hypothermic hypotension and may primarily reflect an effect of T(b) on central drive. The marked attenuation of the baroreflex control of HR during hypothermia was likely to be due to an impairment of both the central and peripheral components of the reflex arc. Baroreflex control of RSNA and HR was similar between both groups of rats, which implied that the control was non-adaptive on chronic cold exposure.

Systemic vascular reactivity in an aortic coarctation model of preeclampsia in the rat

Preeclampsia (preECL), a hypertensive disorder of pregnancy, which occurs only in humans, is dangerous for mother and fetus. It may be caused by placental hypoxia triggering the release of a circulating factor that damages the maternal endothelium leading to vasoconstriction and hypertension. Our primary objective was to determine if systemic vascular reactivity is altered in a rat aortic coarctation (ACOR) model of preECL. We hypothesized that reduced blood flow to the rat utero-placental unit would lead to increased responsiveness to vasoconstrictors. On day 8 of pregnancy, rats were anesthetized and subjected to sham (SHAM) or aortic coarctation (ACOR) surgery by placing a 0.4 mm diameter silver clip distal to the renal arteries. Systemic pressor responses to bolus doses of phenylephrine (PE), angiotensin II (AII), and 5-hydroxytryptamine (5-HT) were determined in these animals on gestation days 14–15 (mid-pregnancy) or 19–20 (late pregnancy). Virgin rats were subjected to sham or ACOR surgery and arterial pressure measured 10–11 days after surgery. Arterial pressure was elevated in late pregnant ACOR animals (mean of 120±4 mmHg) compared with SHAM (mean of 101±6), but mid-pregnant and virgin groups were not different. Proteinuria was present more frequently in late pregnant ACOR animals (86%) than in SHAM (41%), but there were no differences in average fetal weight, fetal number, or number of reabsorbed fetuses. Pressor responses were not different in ACOR and SHAM groups in mid- or late pregnancy. These data indicate that the aortic coarctation to 0.4 mm in the rat mimics the clinical presentation of mild preECL in humans.

Chronic angiotensin converting enzyme inhibition enhances renal vascular responsiveness to acetylcholine in anaesthetized rabbits.

To determine whether 6 weeks continuous treatment with an angiotensin converting enzyme (ACE) inhibitor reduced renal vascular responsiveness in vivo, since this treatment results in extensive phenotypic conversion of afferent arteriolar cells from contractile to endocrine-like, renin secretory cells. Enalapril (10 microg/kg per h s.c.) was delivered continuously for 6 weeks. In anaesthetized rabbits (treated or sham), arterial blood pressure and renal blood flow were measured and renal responsiveness tested by constructing dose-response curves to bolus doses of phenylephrine, angiotensin II and acetylcholine delivered directly into the renal artery. ACE inhibition resulted in a significant shift to the left in the renal vascular conductance responses to acetylcholine (P < 0.005) and angiotensin II (P < 0.05), indicating enhanced, not reduced, responsiveness to these agents. There were no significant effects of chronic ACE inhibition on the conductance responses to phenylephrine. Contrary to our hypothesis, 6 weeks ACE inhibition did not reduce renal vascular responsiveness to three vasoactive agents, suggesting that the phenotypic changes observed in the afferent arterioles and to a lesser extent the interlobular arteries, were either insignificant or compensated for by other changes in renal circulatory control.

The Effects of Clonidine on Sensitivity to Phenylephrine and Nitroprusside in Patients with Essential Hypertension Recovering from Surgery

Clonidine reduces postoperative circulatory instability in patients with essential hypertension.It also increases the sensitivity to vasopressors before and during anesthesia. We investigated blood pressure responses to phenylephrine and nitroprusside pre- vs postoperatively and the effect of clonidine on these responses in patients with essential hypertension. Twenty patients received clonidine 6 [micro sign]g/kg orally 120 min before anesthesia and 3 [micro sign]g/kg IV over the final hour of surgery or an identical placebo. During increasing bolus doses of phenylephrine and nitroprusside (30-300 [micro sign]g), the maximal systolic pressure responses were recorded at baseline on the day before surgery, before the induction of anesthesia, and 1 and 3 h postoperatively. Sensitivity to phenylephrine and nitroprusside was interpolated from linear regression of the data. There was no difference between preoperative and postoperative sensitivity to phenylephrine or nitroprusside in either group. Clonidine increased sensitivity to phenylephrine versus placebo before and after surgery (response to dose of 1.5 [micro sign]g/kg: 42 +/- 14 vs 27 +/- 8 mm Hg preinduction, 37 +/- 10 vs 26 +/- 8 mm Hg 3 h postoperatively; both P < 0.01), but not to nitroprusside (38 +/- 6 vs 37 +/- 10 mm Hg preinduction and 40 +/- 6 vs 39 +/- 8 mm Hg postoperatively). Clonidine increases the sensitivity to phenylephrine but not nitroprusside at baseline and postoperatively in hypertensive patients. Implications: Clonidine increases the sensitivity to bolus injections of the vasoconstrictor phenylephrine, but not the vasodilator sodium nitroprusside, before and after surgery in patients with preexisting hypertension. The doses of vasopressors should be reduced accordingly in hypertensive patients receiving perioperative clonidine. (Anesth Analg 1999;88:1239-43)