Intravenous Labetalol Research Articles

Antihypertensives

Fifty per cent of pregnancies are unplanned, and 1—6% of young women have pre-existing hypertension. However, no commonly used antihypertensive agent is known to be teratogenic. ACE inhibitors (and angiotensin-receptor antagonists) should be discontinued due to fetotoxicity.Five to 10% of pregnant women have hypertension, of which pre-existing hypertension is but one type. There is consensus that severe maternal hypertension (blood pressure →170/110 mmHg) should be treated to minimize the risk of acute cerebrovascular complications. Parenteral hydralazine may be associated with a higher risk of maternal hypotension, and intravenous labetalol with neonatal bradycardia. There is no consensus that mild-to-moderate hypertension in pregnancy should be treated. Clinical trials indicate that transient severe hypertension, antenatal hospitalization, proteinuria at delivery and neonatal respiratory distress syndrome may be decreased by normalizing blood pressure, but intrauterine fetal growth restriction may be increased. Methodological problems with published trials warrant cautious interpretation of these findings. Methyldopa and β-blockers have been used most extensively, although atenolol may impair fetal growth in particular and should be avoided.

Treating hypertension in women of child-bearing age and during pregnancy.

Hypertension is found among 1 to 6% of young women. Treatment aims to decrease cardiovascular risk, the magnitude of which is less dependent on the absolute level of blood pressure (BP) than on associated cardiovascular risk factors, hypertension-related target organ damage and/or concomitant disease. Lifestyle modifications are recommended for all hypertensive individuals. The threshold of BP at which antihypertensive therapy should be initiated is based on absolute cardiovascular risk. Most young women are at low risk and not in need of antihypertensive therapy. All antihypertensive agents appear to be equally efficacious; choice depends on personal preference, social circumstances and an agent's effect on cardiovascular risk factors, target organ damage and/or concomitant disease. Although most agents are appropriate for, and tolerated well by, young women, another consideration remains that of pregnancy, 50% of which are unplanned. A clinician must be aware of a woman's method of contraception and the potential of an antihypertensive agent to cause birth defects following inadvertent exposure in early pregnancy. Conversely, if an oral contraceptive is effective and well tolerated, but the woman's BP becomes mildly elevated, continuing the contraceptive and initiating antihypertensive treatment may not be contraindicated, especially if the ability to plan pregnancy is important (e.g. in type 1 diabetes mellitus). No commonly used antihypertensive is known to be teratogenic, although ACE inhibitors and angiotensin receptor antagonists should be discontinued, and any antihypertensive drugs should be continued in pregnancy only if anticipated benefits outweigh potential reproductive risk(s). The hypertensive disorders of pregnancy complicate 5 to 10% of pregnancies and are a leading cause of maternal and perinatal mortality and morbidity. Treatment aims to improve pregnancy outcome. There is consensus that severe maternal hypertension (systolic BP > or = 170mm Hg and/or diastolic BP > or = 110mm Hg) should be treated immediately to avoid maternal stroke, death and, possibly, eclampsia. Parenteral hydralazine may be associated with a higher risk of maternal hypotension, and intravenous labetalol with neonatal bradycardia. There is no consensus as to whether mild-to-moderate hypertension in pregnancy should be treated: the risks of transient severe hypertension, antenatal hospitalisation, proteinuria at delivery and neonatal respiratory distress syndrome may be decreased by therapy, but intrauterine fetal growth may also be impaired, particularly by atenolol. Methyldopa and other beta-blockers have been used most extensively. Reporting bias and the uncertainty of outcomes as defined warrant cautious interpretation of these findings and preclude treatment recommendations.

▪ A Randomized, Double-Blind Trial of Oral Nifedipine and Intravenous Labetalol in Hypertensive Emergencies of Pregnancy

▪ A Randomized, Double-Blind Trial of Oral Nifedipine and Intravenous Labetalol in Hypertensive Emergencies of Pregnancy

Treatment of pediatric hypertension.

We conducted a MEDLINE search from January 1966-March 1999 to obtain information on clinical trials of treatment of pediatric hypertension. An article was selected for review if it described a randomized or nonrandomized study; randomized studies were given priority. Case reports were considered when studies were unavailable. Review articles were useful in identifying references. According to data we collected, hypertension is present in 1-3% of the pediatric population. Nonpharmacologic treatment may be effective initially in those with mild to moderate disease or as an adjunct to drug therapy. Drugs for treatment of chronic hypertension include calcium channel blockers, angiotensin-converting enzyme inhibitors, diuretics, and beta-blockers. Patient and drug characteristics determine therapy. Intravenous labetalol, nicardipine, and nitroprusside are effective for treating hypertensive emergencies.

A randomized, double-blind trial of oral nifedipine and intravenous labetalol in hypertensive emergencies of pregnancy

Objective: We sought to compare the efficacies of oral nifedipine and intravenous labetalol in the acute management of hypertensive emergencies of pregnancy. Study Design: We performed a randomized double-blind trial of oral nifedipine (10 mg) and intravenous labetalol (20 mg) in 50 peripartum patients with sustained systolic blood pressure of ≥170 mm Hg or diastolic blood pressure of ≥105 mm Hg. Both agents were repeated at sequentially escalating dosages every 20 minutes until a therapeutic goal of systolic blood pressure of <160 mm Hg and diastolic blood pressure of <100 mm Hg was achieved. Crossover occurred if the treatment goal was not achieved after 5 doses. Primary outcome was time to achievement of the therapeutic goal. Secondary outcome variables were agent failure, urinary output, and adverse effects. Data were analyzed by unpaired t test, Mann-Whitney U test, and analysis of variance for repeated measures. Results: The time to achieve the blood pressure goal was significantly shorter with nifedipine (mean ± SD, 25 ± 13.6 minutes) than with labetalol (43.6 ± 25.4 minutes; P = .002). No patients required crossover therapy. Urine output was significantly increased ( P < .001) at 1 hour after nifedipine dosing (99 ± 99 mL) compared with labetalol (44.8 ± 19.1 mL) and remained significantly increased at 2, 6, 12, 18, and 24 hours after initial administration. Adverse effects were infrequent. There were no differences in maternal age, gestational age, number of antepartum patients, or enrollment blood pressures between groups. Conclusions: Both oral nifedipine and intravenous labetalol are effective in the management of acute hypertensive emergencies of pregnancy; however, nifedipine controls hypertension more rapidly and is associated with a significant increase in urinary output. (Am J Obstet Gynecol 1999;181:858-61.)

Hyperperfusion syndrome after bilateral internal carotid stent-supported percutaneous transluminal angioplasty

Spirit of Recovery D. Monthei Nelson (Milwaukee, Wisconsin) Background: Parish nurses integrate mmd, body and as they work with people in the context of their homes and communities, (neighborhood, friends, family, church, agencies), as well as the hospital, nursing home and rehabilitation settings; and they do this over a prolonged length of time. Understanding the Spirit's role in healing the stroke victim is the focus of this paper. Methods: Work with three individuals, their families, caregivers and faith communities over the past 2 1/2 years, as well as a detailed questionnaire resulted in this anecdotal paper. Pm~r is Good Medicine, Larry Dossey, 1996, and Wellness Practitioner, Carolyn Chambers Clark, 1996, were helpful resources. Results: This paper recognizes the spirit as a make or break element to recovery and long term wellness in the stroke patient. Conclusions: Strength of (faith, hope, attitude, soul, will) holds the key to recovery and continuing wellness of the stroke victim. Health care professionals, families, friends, and faith communities who know this and build support and strengthening of this into their caring will enhance their effectiveness and the wellness of those they love immeasurably. 275 Stroke Outcomes in an African-American Population L. Simon, D. Lockridge (Louisville, Kentucky) Background: We reviewed records of all African-American patients diagnosed with stroke over a one year period. Methods: Admissions (n=100) in 1998 were reviewed to identify a primary care physician, health insurance, prophylactic medication prior to admission, length of stay and discharge disposition. Results: Thirty three patients (33%) had no primary care physician. Of this group, twenty five (76%) had Medicare coverage. Average length of stay was 7.8 days (7.2 days for total stroke population). Average length of stay for patients with no health insurance (n=7) was 9.5 days. Twenty patients (20%) took medication for stroke prevention. Thirty five patients (35%) want to in-patient rehabilitation, twenty eight (28%) to extended care, sixteen (16%) to home, fourteen (14%) to home health, and seven (7%) expired. 40% of the total stroke population was discharged home and 17% discharged to an extended care facility. Conclusions: The impact of stroke on African-Americans is more devastating in terms of impaired functional ability requiring extended periods of rehabilitation. Access to healthcare and identification and modification of stroke dsk factors are key elements in reducing stroke incidence and improving outcomes in this population. Hyperperfusion Syndrome after Bilateral Internal Carotid Stent-supported Percutaneous Transluminal Angioplasty G.S. Silva, E.L.V. Costa (Fortaleza-CE-Brazii), A.M. Forteza (Miami-FL) Background The cerebral hyperperfusion syndrome is a well-described complication following carotid endarterectomy for severe carotid stenosis. It has been rarely described following carotid artery stent-supported percutaneous transluminal angioplasty (PTA). Case Report We report the case of a 73-year-old patient who developed left hemiparesis, hemineglect, confusion and seizures after bilateral PTA for high-grade symptomatic internal carotid stenosis. A brain computed tomographic scan showed edematous sulci over the right cerebral hemisphere raising the differential diagnosis of early ischemia versus cerebral hyperperfusion. The patient responded favorably to therapy with intravenous labetalol with considerable improvement of mental status, regaining normal speech and motor function. Single photon emission computerized tomographie scan 8 days after the procedure showed increased perfusion over the right cerebral hemisphere. Conclusion The cerebral hyperperfusion syndrome has to be considered in the differential diagnosis o f complications related to carotid artery stent-supported percutaneous transluminal angioplasty. Pre-Hospital Provider Stoke Knowledge Base Assessment John Bruns, Jr., MD Denise Nassisi, MD Kevin Baumlin, MD Andy Jagoda, MD Objectives: To assess the stroke knowledge base ofprehospital providers (PHPs); to determine their management and transport practices. Methods: An electronic survey administered to 14 emergency medical technicians (EMTs) and 48 paramedics (EMT-Ps) during a stroke symposium. A computer driven interactive system allowed 100% audience participation to prelecture questions. Results: 31% of EMTs and 18% of EMT-Ps reported they are uncomfortable performing a neurologic exam. 42% of EMTs and 17% of EMT-Ps were unaware of the 3 hour thrombolytic therapeutic window. 65% of PHPs transport stroke patients with lights & sirens or pre-notify the receiving hospital. 45% of PHPs failed to recognize blindness or dizziness as possible stroke symptoms. 43% of paramedics did not know the indications for glucose administration in stroke patients with altered mental status. Given a BP of200/110 in a stroke patient, 33% of EMT-Ps were uncertain of management, and 20% would have given a detrimental therapy. Conclusions: Deficits exist in PHPs performance of a neurologie exam and recognition of stroke. Appropriate transport practices and therapeutic interventions varies among PHPs. Enhanced education for PHPs on stroke recognition and management is needed in this new era of stroke management.

Pharmacologic reduction of mean arterial pressure does not adversely affect regional cerebral blood flow and intracranial pressure in experimental intracerebral hemorrhage.

To determine the effect of mean arterial pressure (MAP) reduction on regional cerebral blood flow and intracranial pressure (ICP) in intracerebral hemorrhage. We tested the hypothesis that there is ischemia in the perihematoma region after intracerebral hemorrhage, which can be exacerbated by a pharmacologic reduction of MAP. Prospective, controlled, laboratory trial. Animal research laboratory. Eighteen mongrel dogs, weighing 15 to 25 kg. We introduced intracerebral hemorrhage in 12 anesthetized dogs by autologous blood injection under arterial pressure in the deep white matter adjacent to the left caudate region. We measured serial regional cerebral blood flow using radiolabeled microspheres in animals with two different volumes of injected blood (2.8 mL [Group A, n = 6] and 4.4 mL [Group B, n = 6]) and compared them with control animals (n = 6). Intravenous labetalol was administered 90 mins after administration of hematoma, while maintaining cerebral perfusion pressure >65 mm Hg. Regional cerebral blood flow measurements were repeated 10 and 30 mins after labetalol administration. MAP and ICP were monitored continuously using intra-arterial and cisterna magna catheters, respectively. Compared with control animals, significant elevation in ICP was observed in Groups A and B and elevation in MAP was observed in Group B at 45 mins after injection of blood. These hemodynamic alterations were not accompanied by any significant differences in regional cerebral blood flow in any group. Administration of labetalol resulted in a decrease in MAP (mm Hg+/-SEM) in Groups A (119.0+/-9.2 to 103.0+/-9.1) and B (124.5+/-7.4 to 100.5+/-4.8) and controls (103.5+/-4.3 to 85.0+/-8.0). No differences were observed in regional cerebral blood flow after MAP reduction in both Groups A and B compared with controls in regions around or distant to the hematoma. There were no changes in ICP in Groups A and B both at 10 and 30 mins after reduction in MAP compared with pretreatment values. In our model, pharmacologic reduction of MAP within the normal autoregulatory limits of cerebral perfusion pressure, 90 mins after onset, had no adverse effect on ICP and regional cerebral blood flow in regions around or distant to the hematoma. These results support the controlled use of antihypertensive treatment in intracerebral hemorrhage in the initial time period.

Acute Hypertension Promotes Hemorrhagic Transformation in a Rabbit Embolic Stroke Model: Effect of Labetalol

We examined the relationship between acute hypertension following cerebral embolization and subsequent hemorrhagic transformation (HT) in a rabbit embolic stroke model. We have shown previously that the likelihood and severity of hemorrhage were significantly correlated with the magnitude of an acute hypertensive response to embolization. It was not clear, however, whether hypertension actually caused hemorrhage or was merely a marker of more severe stroke. In the current studies, we attempted to clarify the relationship between acute hypertension and HT by either pharmacologically inducing or attenuating the brief hypertensive response to embolization in rabbits. Under halothane anesthesia, two catheters were implanted in the right carotid arteries of male New Zealand white rabbits, one oriented toward the heart and one toward the brain. The animals were allowed to awaken and were embolized using blood clot emboli injected into the middle cerebral artery. Blood pressure was monitored via the second carotid catheter. In the first experiment, hypertension was induced with angiotensin II, administered at the time of embolization or 1 h later. In the second experiment, we attempted to attenuate the hypertensive response using intravenous labetalol. The animals were sacrificed 18 h after embolization and the brains evaluated for hemorrhage. In the first experiment, administration of angiotensin II immediately after embolization did not increase the hypertensive response to embolization further than that spontaneously occurring, and no angiotensin II-related HT was observed. In contrast, an additional angiotensin-II-induced hypertensive episode 1 h after embolization significantly increased the number of 5-mm serial brain sections displaying HT, from 3.0 ± .3 (mean±SE) in Controls to 5.4 ± .8 in treated animals. In the second experiment, administration of labetalol (15 mg/kg) significantly reduced the number of brain sections with visible HT, from 3.2 ± .5 in controls to 1.6 ± .4 in treated animals. Acute hypertension during the first hour after cerebral embolization promotes HT in this rabbit embolic stroke model. Labetalol prevents blood pressure elevation and reduces the extent of HT in the same model.

Hypertensive crisis in children.

Children presenting with hypertension should be considered for emergency treatment when there is evidence of end-organ toxicity. Complications of extreme hypertension may be very serious, even life threatening, with the potential for life-long sequelae. Of greatest significance is damage to the central nervous system. Treatment of hypertensive emergencies should be directed toward the lowering of blood pressure enough to reduce toxicity, but not at a rate likely to cause hypoperfusion of vital organs. This blood pressure reduction should, in general, be carefully controlled in an intensive care unit, with attention to central nervous system, cardiac, and renal function. Intravenous agents are preferable under these circumstances, due to greater ease in modulating blood pressure. In the absence of specific contraindications, a continuous infusion of nicardipine or sodium nitroprusside is preferable. Intravenous labetalol by bolus injection, followed by continuous infusion, also may be used. Oral agents should be reserved for circumstances in which symptoms of end-organ toxicity are mild or absent. Since general pediatricians have limited experience with the treatment of hypertensive emergencies, consultation with physicians experienced in treating hypertensive emergencies is suggested when possible.

Effect of Preinduction Intravenous Labetalol on Cardiovascular Responses to Tracheal Intubation

Effect of Preinduction Intravenous Labetalol on Cardiovascular Responses to Tracheal Intubation

Influence of labetalol on cocaine-induced coronary vasoconstriction in humans

purpose: Although labetalol is sometimes given to patients with cocaine-associated chest pain, its influence on cocaine-induced coronary vasoconstriction is unknown. patients and methods: In 15 patients (7 men, 8 women, aged 40 to 79 years) undergoing catheterization for chest pain, heart rate, mean arterial pressure, and coronary arterial area (by computer-assisted quantitative angiography) were measured (1) at baseline, (2) 15 minutes after intranasal cocaine, 2 mg/kg, then (3) 5 minutes after intravenous saline (n = 6) or labetalol, 0.25 mg/kg (n = 9). results: Of 40 coronary arterial segments analyzed, cocaine induced a 13% ± 10% (mean ± standard deviation) decrease in coronary arterial area in 32. Subsequently, no variable changed after saline administration. Although labetalol reduced mean arterial pressure (117 ± 14 mm Hg after cocaine, 110 ± 11 mm Hg after labetalol; p < 0.05), it induced no change in the coronary arterial area (3.47 ± 1.37 mm 2 after cocaine, 3.37 ± 1.32 mm 2 after labetalol; p = NS). conclusion: Labetalol reverses the cocaine-induced rise in mean arterial pressure, but does not alleviate cocaine-induced coronary vasoconstriction.

Malignant ventricular arrhythmias in eclampsia: A comparison of labetalol with dihydralazine

Our aim was to assess the impact of beta-adrenergic blockade during the peripartum period on the previously observed high incidence of ventricular arrhythmias in eclamptic parturients. An open, randomized comparison of intravenous labetalol versus dihydralazine was conducted in 40 eclamptic subjects in the peripartum period. Cardiac rhythm was assessed by blinded analysis of a 24-hour Holter record by means of the Lown classification of arrhythmias. There was a significantly higher incidence of serious ventricular arrhythmias in patients receiving dihydralazine (81%) than in those receiving labetalol (17%, p < 0.0001). Patients receiving labetalol showed a significant decrease in mean heart rate (p < 0.0001), whereas patients receiving dihydralazine showed a significant increase (p < 0.0001). The introduction of beta-adrenergic blockade into peripartum hypertensive management of eclampsia significantly reduced the incidence of dangerous ventricular arrhythmias. Myocardial oxygen supply/demand ratio may be improved by beta-blockade.

Cerebral Blood Flow Measurements During Blood Pressure Control with Intravenous Labetalol Following Craniotomy

Cerebral blood flow measurements using a thermal diffusion technique were made in conjunction with an extensive cardiovascular evaluation, during and after administration of intravenous labetalol given for blood pressure control in craniotomy patients. Eighteen patients, ages 30-65 years, ASAII and III, scheduled for elective craniotomy, became hypertensive during emergence and recovery from a pentothal/fentanyl/vecuronium/N2O/isoflurane general anesthesia. Labetalol was administered in a stepwise manner every 10 minutes during an average period of 1 h. After this titration period, an 8-h maintenance period followed. During titration and maintenance periods, comprehensive systemic hemodynamic parameters were collected through intra-arterial and flow-directed pulmonary artery catheters. Cerebral cortical blood flow (CBF) was continuously recorded using a thermal diffusion cortical blood flow probe (Saber System). Data were analyzed using variance F tests to evaluate changes from baseline over time. Labetalol controlled postoperative hypertension in all cases with a total dose range of 0.4-6.8 mg/kg. During titration, statistically significant decreases in blood pressure were obtained, accompanied by a small decrease in systemic vascular resistance (SVR) and slight increase in cardiac index (CI). Heart rate decreased in a manner directly proportional to the dose of labetalol administered. In the maintenance period, further decreases in blood pressure and heart rate were observed, with significant decreases in central venous pressure, pulmonary capillary wedge pressure, and SVR and an increase in CI. All values remained within normal ranges and no adverse effects were observed. CBF decreased slightly during the study period, although not significantly (from 67 +/- 8 to 57 +/- 7 ml 100 g min). Blood pressure control achieved with labetalol in postoperative neurosurgical patients seems to be the result of mild alpha-adrenoceptor blocking effects (i.e., reduced SVR) and beta-adrenoceptor blocking effects (i.e., reduced heart rate) at higher doses. The 6-8 h duration of effect of labetalol was enough to control postoperative hypertension in all patients with no additional therapy. Compared with alternative drugs available for blood pressure control in similar clinical conditions, labetalol appears to be reliable, safe, and effective, by providing a lasting effect with no evidence of rebound hypertension, increased CBF, or cardiac dysfunction.

Maternal and fetal haemodynamics in hypertensive pregnancies during maternal treatment with intravenous hydralazine or labetalol

BJOG: An International Journal of Obstetrics & GynaecologyVolume 98, Issue 11 p. 1186-1187 Maternal and fetal haemodynamics in hypertensive pregnancies during maternal treatment with intravenous hydralazine or labetalol Fiona M. Fairlie, Fiona M. Fairlie Department of Obstetrics and Gynaecology Royal Infirmary Queen Elizabeth Building 10 Alexander Parade Glasgow G31 2ERSearch for more papers by this authorJames J. Walker, James J. Walker Department of Obstetrics and Gynaecology Royal Infirmary Queen Elizabeth Building 10 Alexander Parade Glasgow G31 2ERSearch for more papers by this author Fiona M. Fairlie, Fiona M. Fairlie Department of Obstetrics and Gynaecology Royal Infirmary Queen Elizabeth Building 10 Alexander Parade Glasgow G31 2ERSearch for more papers by this authorJames J. Walker, James J. Walker Department of Obstetrics and Gynaecology Royal Infirmary Queen Elizabeth Building 10 Alexander Parade Glasgow G31 2ERSearch for more papers by this author First published: November 1991 https://doi.org/10.1111/j.1471-0528.1991.tb15381.xRead the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume98, Issue11November 1991Pages 1186-1187 RelatedInformation

Maternal and fetal haemodynamics in hypertensive pregnancies during maternal treatment with intravenous hydralazine or labetalol

Intravenous treatment with 10 mg of hydralazine or 100 mg of labetalol was randomly allocated to 30 hypertensive pregnant women. Umbilical artery flow velocity waveforms were recorded using a pulsed Doppler duplex scanner (ATL Mk V) and umbilical artery pulsatility index (PI) and fetal heart rate (FHR) were derived from these recordings. Maternal blood pressure decreased significantly after both drugs. Maternal pulse rate increased after hydralazine but did not change significantly after labetalol. FHR did not change significantly after hydralazine but decreased after labetalol. PI decreased after hydralazine and increased after labetalol--most fetuses showed little change but a few in each group showed large changes in PI, as did two of five additional patients studied. We attributed the decrease in PI in some fetuses after hydralazine to vasodilation, and the increase in PI in some fetuses after labetalol to vasoconstriction in the fetoplacental circulation, suggesting that fetal beta-blockade may occur after maternal treatment with labetalol.

A Comparison of Labetalol and Nitroprusside for Inducing Hypotension During Major Surgery

The hemodynamic and intrapulmonary shunt effects of intravenous labetalol and nitroprusside were compared during induced hypotension for major spinal surgery. A randomized, double-blind protocol was used in which 20 patients, ASA physical status I or II, received either nitroprusside infusion (n = 10) or labetalol bolus injections of 10 mg every 10 min (n = 10) until mean arterial blood pressure was reduced to 55-60 mm Hg. Pulmonary artery pressures were measured and mixed venous samples obtained via a pulmonary artery catheter. Nitroprusside increased heart rate significantly more than labetalol during the period of hypotension. When compared with prehypotension baseline values, nitroprusside increased heart rate significantly with a concomitant significant decrease in systemic vascular resistance. Cardiac output increased significantly 60 min after hypotension was achieved in patients treated with nitroprusside. Systemic vascular resistance decreased significantly below baseline levels in patients treated with labetalol but without changes in cardiac output, heart rate, or mean pulmonary artery pressure. There was a 122% increase in intrapulmonary shunt with nitroprusside administration, compared with an 11% increase with labetalol. Labetalol was effective for inducing hypotension and was not associated with an increase in heart rate, intrapulmonary shunt, or cardiac output as seen with nitroprusside.

Labetalol for the control of elevated blood pressure following coronary artery bypass grafting

In a multicenter study, the efficacy and safety of intravenous (IV) labetalol for the control of elevated blood pressure were studied in the intensive care unit (ICU) in 65 patients within 4 hours following coronary artery bypass grafting (CABG). Patients with pre-existing ventricular dysfunction, bradycardia, bronchospastic disease, or postoperative complications were excluded. All patients were monitored with a thermodilution pulmonary artery catheter. Entry criteria were a systolic blood pressure (SBP) greater than 140 mm Hg or diastolic blood pressure (DBP) greater than 90 mm Hg for at least five minutes. Intravenous labetalol was loaded incrementally (5, 10, 20, and 40 mg at 10-minute intervals) to a maximum cumulative dose of 75 mg, until either SBP decreased 10% or DBP decreased 10% and was less than 90 mm Hg. Responders were entered into a 6-hour maintenance period, and received 5 to 40 mg of IV labetalol every 10 minutes as needed for blood pressure control. Hemodynamic data and temperature were recorded at baseline, just before each dose of labetalol during the loading period, and at the end of the maintenance period. Alternative therapy was given in the case of nonresponse or adverse events. Intravenous labetalol successfully controlled post-CABG hypertension in 55 of 65 patients (85%); of these, 46 responded to 35 mg or less. Although 28 patients required no further labetalol in the maintenance period, in the others dosage varied from 5 to 400 mg. Reductions in SBP and DBP were associated with moderate reductions in pulse pressure (SBP-DBP) and heart rate (HR). Cardiac index decreased by 18.5%, with a 12.5% decrease in stroke index and 8.1 % decrease in HR. Systemic vascular resistance did not increase significantly. Four patients (6%) developed hypotension related to IV labetalol. There was one death due to perioperative myocardial infarction, which was unrelated to labetalol use. The mechanism of action of IV labetalol in controlling hypertension after CABG surgery seems to be moderate negative inotropy and chronotropy. Its α-blocking effects seem to be important in preventing reflex vasoconstriction. This is directly opposite to the primary vasodilator effect found when IV labetalol is used to control nonsurgical hypertension. Because of these actions, labetalol should be avoided or used with caution in patients with preoperative and postoperative cardiac dysfunction. In patients with normal left ventricular function, IV labetalol appears to be a safe, effective agent in controlling post-CABG hypertension, with the added potential benefit of enhanced myocardial oxygen balance.

Intravenous labetalol for the treatment of hypertension after carotid endarterectomy

Hypertension after carotid endarterectomy has a variable incidence ranging up to 56%. Blood pressure (BP) control is essential due to possible increased risk of morbidity from neurologic deficits or cardiovascular complications. This study evaluated intravenous labetalol for control of hypertension after carotid endarterectomy. Sixty ASA II-IV patients were studied; 20 developed BP high enough for treatment with labetalol. The anesthetic technique was standardized. Labetalol was administered at the conclusion of surgery as a 20-mg bolus over two minutes followed by 40 mg every 10 minutes until the desired BP was achieved (BP less than or equal to 10% above average preoperative BP or less than 150 mmHg, systolic) or 300 mg had been given. The mean total dose of labetalol was 42.0 +/- 33.0 mg (mean +/- SD) and mean time to reach the desired BP was 16.2 +/- 21.4 minutes. Systolic, diastolic, mean arterial pressure and heart rate significantly decreased after labetalol treatment and remained so for the remainder of the 180-minute study period. There was no hypotension, bradycardia, evidence of myocardial ischemia or central nervous system dysfunction present with labetalol treatment. Blood samples were obtained for determination of plasma renin activity, epinephrine, and norepinephrine in 10 patients who developed hypertension and received labetalol, and 10 patients who did not develop hypertension. In the patients developing hypertension, there was a significant elevation in epinephrine just before treatment, that decreased by 30 minutes after treatment. Norepinephrine levels became significantly elevated five minutes after labetalol treatment in the group with hypertension and remained elevated for 120 minutes. Concomitantly, there was a significantly lower plasma renin activity seen in this group.(ABSTRACT TRUNCATED AT 250 WORDS)

Effectiveness and hemodynamic mechanism of action of blood pressure lowering by intravenous labetalol in patients with a critical increase in blood pressure

Labetalol (L) was intravenously given to ten patients with an acute elevation of arterial blood pressure above to 200 to 100 mmHg. Blood pressure was controlled in 9 of 10 patients (less than or equal to 170/100 mmHg) with 50 mg in 4, 100 mg in 4 and 200 mg L in 1 patient. In 9 responders, systolic pressure decreased from 207 +/- 20 to 161 +/- 9, diastolic pressure from 107 +/- 11 to 90 +/- 8, and mean pressure from 140 +/- 11 to 113 +/- 5 mmHg, and all pressures remained at these levels during a 25 min control period. Heart rate decreased significantly from 87 +/- 20 to 69 +/- 11 per min and cardiac index from 3.2 +/- 0.8 to 2.6 +/- 0.61/min x m2. Stroke volume index remained unchanged. Total peripheral resistance and pulmonary artery occlusion pressure were not significantly altered but tended to increase, resulting in a small shift to the right of the ventricular function curve. Pulmonary vascular resistance increased significantly from 236 +/- 108 to 314 +/- 132 dyn x sec x cm-5 and mixed venous oxygen saturation decreased from 70 +/- 5 to 65 +/- 8%. Peripheral resistance was considerably higher and cardiac index lower in patients with a heart rate below 70/min. We conclude that L effectively lowers the arterial blood pressure in hypertensive crisis, but the substance should not be used in patients with heart rates below 70/min, as in this case the beta-blocking effect may supervene resulting in a high-resistance low-output state.

Labetalol to Control Blood Pressure After Cerebrovascular Surgery

Fifteen patients who had undergone neurovascular surgery for arteriovenous malformations or cerebrovascular aneurysms and had intracranial pressure (ICP) monitors were studied. The patients had been treated initially with sodium nitroprusside to maintain their arterial BP in a prescribed range, but, because of excessive nitroprusside dose requirements, they were considered either to have refractory BP or to be at risk for thiocyanate toxicity. Intravenous labetalol therapy was started either by frequent bolus pulse therapy every 1 to 2 h or by continuous infusion therapy. The degree of desired arterial BP control and the effects on ICP and cerebral perfusion pressure (CPP) were assessed and compared with the results during nitroprusside therapy. The degree of arterial BP control with labetalol was assessed to be good; 11 patients were weaned off nitroprusside and the remaining four patients had a substantial reduction in their nitroprusside requirements, needing an average of only 1.5 micrograms/kg.min of nitroprusside to control their BP compared with average requirements of 10 micrograms/kg.min of nitroprusside before labetalol therapy. Labetalol therapy improved CPP in six patients and ICP in five patients, with no significant change in cerebral pressure in the remainder. Overall, the CPP in the 15 patients improved from 63 +/- 15 (SD) mm Hg with nitroprusside to 65 +/- 10 mm Hg with labetalol therapy and the ICP decreased from 11.3 +/- 6.1 mm Hg with nitroprusside to 8.6 +/- 3.1 mm Hg with labetalol therapy (p less than .05 by Wilcoxon matched pairs).(ABSTRACT TRUNCATED AT 250 WORDS)