Trandate is used to treat severe high blood pressure (hypertension). Lowering high blood pressure Trandate helps prevent strokes, heart attacks and kidney problems.
Other names for this medication:
Also known as: Labetalol.
Trandate is a drug which is used for treating high blood pressure. It is related to carvedilol (Coreg). Nerves that are part of the adrenergic nervous system travel to most arteries where they release an adrenergic chemical norepinephrine. The norepinephrine attaches to receptors on the muscles of the arteries and causes the muscles to contract, narrowing the arteries, and increasing the blood pressure. Trandate blocks receptors of the adrenergic nervous system. When Trandate attaches to and blocks the receptors, the arterial muscles relax, and the arteries expand, resulting in a fall in blood pressure.
Generic name of Trandate is Labetalol.
Trandate is also known as Labetalol, Normodyne.
Brand name of Trandate is Trandate.
Take this medicine with food or milk.
If you want to achieve most effective results do not stop taking Trandate suddenly.
If you overdose Trandate and you don't feel good you should visit your doctor or health care provider immediately.
Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Trandate are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Trandate if you are allergic to Trandate components.
Be careful with Trandate if you're pregnant or you plan to have a baby, or you are a nursing mother.
Be careful with Trandate if you have a history of liver problems, heart problems, pheochromocytoma, diabetes, any allergies.
Do not take Trandate if you have a lung disease (asthma, COPD), advanced heart block, severe bradycardia, severe heart failure, post-CABG surgery.
This drug may make you dizzy for up to 3 hours after it is given. You should remain lying down during this time period in order to prevent falls.
You should get up slowly when rising from a seated or lying position.
Be very careful if you are driving machine.
Diabetic patients should be careful with Trandate.
Do not stop taking Trandate suddenly.
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Hypertension is due to disturbance of the complex interplay between numerous known and unknown mechanisms that normally control blood pressure. Antihypertensive agents may, therefore, reduce blood pressure through widely different actions and, at the same time, elicit counterregulatory responses. This is a review of the long-term hemodynamic effects at rest as well as during exercise of nine relatively new antihypertensive compounds: a beta-blocker (epanolol), an alpha-receptor blocker (doxazosin), two double-acting compounds (dilevalol and carvedilol), three calcium antagonists (amlodipine, felodipine, and diltiazem), an angiotensin-converting enzyme inhibitor (lisinopril), a serotonin antagonist (ketanserin), and low-salt diet as a nonpharmacological treatment in 171 patients with mild to moderate essential hypertension. The results in the treatment groups are compared to the hemodynamic changes seen in 28 hypertensive patients left untreated for 10 years. The patient populations of the different groups were comparable. The invasive hemodynamic technique, including intraarterial blood pressure recording and measurements of cardiac output by Cardigreen, was the same in all studies. While blood pressure remained nearly unchanged in the untreated group, all antihypertensive compounds induced significant and sustained blood pressure reduction both at rest and during exercise. The modest reduction (3-5%) in blood pressure during a low-salt diet was also statistically significant. This review shows the multiplicity of the long-term hemodynamic changes, ranging from a reduction in cardiac output to peripheral vasodilatation, during chronic antihypertensive therapy. In untreated hypertensives, the cardiac output is reduced by 1-2% per year and total peripheral resistance is increased by 2-3% per year. The review also focuses on counterregulatory responses and modify the initial reduction in blood pressure after drug treatment for hypertension. It is concluded that proper understanding of the hemodynamic effects of antihypertensive agents is useful in the selection of the right treatment for specific groups of hypertensive patients.
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A comparative study between two dopaminergic antagonists: metoclopramide and domperidone, was undertaken in nineteen (19) hypertensive patients at the Vargas Hospital, Caracas. The patients were pretreated with labetalol, 800-1,200 mg/day, orally, over a period of one week, after which they were divided into two groups: group A, a total of eleven patients were intravenously infused with dopamine hydrochloride 0.5-3 micrograms/kg/min, before and after treatment with metoclopramide (10 mg, i.v. as a bolus); group B (n = 8), was pretreated with domperidone, 20 mg b.i.d., p.o. over a period of one week and intravenously infused with dopamine hydrochloride, 0.5-3 micrograms/kg/min. In group A, dopamine induced a decrease of blood pressure from 171.9 +/- 6.35/103.6 +/- 3.12 to 152.7 +/- 7.55/93.8 +/- 2.97 mmHg (p < 0.001) without altering heart rate, and it increased plasma insulin levels from 8.29 +/- 0.70 microunits/ml to 12.09 +/- 1.83 microunits/ml (p < 0.01). Metoclopramide caused no changes of blood pressure or plasma insulin levels. However, hypotensive responses and plasma insulin rises due to dopamine were blocked by metoclopramide. In group B, domperidone also blocked dopamine-induced antihypertensive effect (from 170.0 +/- 9.23/102.8 +/- 3.80 to 160.2 +/- 9.84/95.5 +/- 2.50 mmHg) although it was less effective than metoclopramide. Domperidone also blocked dopamine-induced increase of plasma insulin levels from 9.65 +/- 4.50 microunits/ml to 11.78 microunits/ml. We conclude that a dopaminergic receptor may be involved in some cardiovascular responses and in modulating insulin secretion in man.
144 women (86 primigravid) who developed PIH after 20 weeks gestation.
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A 26 year old Gravida 1 Para 1 female 20 days post partum from a spontaneous vaginal delivery was transported from an outlying facility due to severely elevated blood pressure and transient left arm numbness and left sided facial droop. Upon arrival the patient was begun on intravenous magnesium sulfate and labetalol for a presumptive diagnosis of severe post partum preeclampsia. Her blood pressure and symptoms responded promptly. Due to her neurologic symptoms a magnetic resonance angiogram was ordered revealing 90% stenosis of her bilateral carotid and vertebral arteries.
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During the last few years, several antihypertensive drugs with multiple actions have been introduced. Most of these hybrid drugs are beta-adrenoceptor blockers with an additional vasodilator component, such as labetalol, dilevalol, carvedilol and celiprolol. A second category of antihypertensive drugs with multiple actions consists of agents which interact simultaneously with serotoninergic receptors and alpha-adrenoceptors. Urapidil, ketanserin, and a few experimental compounds related to these drugs are examples of this type of antihypertensive. They may be characterised pharmacologically as follows: (1) Ketanserin is a selective antagonist of serotonin 2 receptors with an additional much weaker alpha 1-adrenoceptor antagonistic activity. Its well documented antihypertensive activity cannot be explained by either serotonin 2-receptor blockade or alpha-adrenoceptor antagonism alone. An unknown type of interaction between serotonin 2-receptor and alpha 1-adrenoceptor blockade appears to be necessary, either in the periphery or in the CNS. (2) Urapidil is a selective alpha 1-adrenoceptor antagonist and, as such, a peripheral vasodilator. In addition, it displays central hypotensive activity, probably caused by the stimulation of serotonin 1A receptors in the CNS. This component is probably additive to the peripheral effect, and is also the background to the lack of reflex tachycardia seen with urapidil. The modes of action of both types of drugs are discussed in connection with the role of serotonin and its receptors in the cardiovascular system, both at the peripheral and the CNS levels.
In order to obtain derivatives with simultaneous alpha- and beta-adrenergic blocking activity, compounds having the phenoxypropanolaminic structure of beta-adrenergic blockers have been synthesised, as well as 1,2,4-oxadiazole moiety, which could imitate the imidazolinic nucleus characteristic of drugs acting on alpha-adrenergic receptors. The synthesised compounds have been submitted to alpha and beta receptor binding assays. Some derivatives showed an alpha-adrenoceptor binding activity higher than labetalol and similar to prazosin, but with a poor beta-adrenoceptor binding activity.
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Although well established in treating hypertension and cardiovascular (CV) disease, clinical trial data suggest that beta-blockers (eg, atenolol) may be less effective than other antihypertensive classes in reducing stroke and CV mortality despite similar blood pressure (BP) reductions. One possible explanation is that atenolol is less effective in reducing central aortic pressure. Newer vasodilating beta-blockers may prove more effective in reducing central pressure and cardiovascular events. Carvedilol and labetalol appear to cause vasodilation through alpha(1)-receptor blockade; nebivolol induces endothelium-dependent vasodilation by stimulating nitric oxide bioactivity. Their favorable hemodynamic profile includes reduction of peripheral vascular resistance (PVR) while maintaining or improving cardiac output (CO), stroke volume, and left ventricular function, whereas nonvasodilating beta-blockers tend to raise PVR and reduce CO and left ventricular function. Compared with conventional beta-blockers, vasodilating beta-blockers have beneficial hemodynamic effects including decreased pressure wave reflection from the periphery, leading to decreases in central aortic blood pressure. Larger trials are needed to determine whether reduced central pressure will translate into improved CV outcomes compared with nonvasodilating beta-blockers.
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A 30-year-old woman, gravida 3 para 1, presented at 23 6/7 weeks of gestation with vomiting, chest pain, and severe hypertension. Investigation revealed adrenal pheochromocytoma and pseudoaneurysm at the site of a previous aortic injury. Prazosin and phenoxybenzamine achieved α-blockade with subsequent addition of labetalol for β-blockade. Concerns for aortic dissection led to endovascular aortic repair at 30 2/7 weeks of gestation. A female neonate was delivered by urgent cesarean delivery for persistent postprocedure fetal bradycardia. An adrenalectomy followed with near-immediate symptom resolution. Mother and neonate remain well.
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The high incidence of cardiovascular morbidity and mortality in hypertensive patients with left ventricular hypertrophy shows the great interest in understanding the pathophysiology of this process. Many reports suggest the role of catecholamines in generating left ventricular hypertrophy. The aim of this study is to evaluate the effect of labetalol on myocardial norepinephrine content in hypertensive subjects with left ventricular hypertrophy by using an isotopic norepinephrine marker, the 123I-meta-iodobenzylguanidine (123I-MIBG). Eight male and female hypertensive patients with left ventricular hypertrophy were investigated after a 30 day placebo period. Resting, ambulatory and effort blood pressure was measured. Echocardiographic parameters allowed measure of left ventricular mass index according to Devereux. And we considered left ventricular hypertrophy as left ventricular mass index greater than 120 g/m2. Cardiac and mediastinal radioactivity is detected 4 h after a 4 mCi i.v. injection of 123I-MIBG and MIBG myocardial uptake is definite as the cardiac/mediastinal ratio (N : 1.78 +/- 0.19). All subjects received at the beginning of the study (D0) 2 tablets of labetalol 200 mg, increased to 4 tablets if diastolic blood pressure during follow-up remained above 95 mmHg. Patients again underwent these explorations after 3 months of treatment (D90). Labetalol decreases in considerable manner MIBG myocardial uptake as it has been shown that it decreases tissular norepinephrine content in experimental studies. Therefore, MIBG myocardial uptake seems to be a reliable tool in evaluating drugs effect on cardiac sympathetic nervous system.
Searches of MEDLINE and International Pharmaceutical Abstracts through July 2011 were conducted. Search terms used included child, pediatric, hypertension, and the following drugs: captopril, enalapril, lisinopril, fosinopril, losartan, valsartan, irbesartan, candesartan, olmesartan, amlodipine, nifedipine, isradipine, felodipine, propranolol, metoprolol, labetalol, minoxidil, furosemide, spironolactone, chlorothiazide, hydrochlorothiazide, hydralazine, and prazosin. Clinical trial data were reviewed and evaluated and were limited to English-language articles.
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The era of cross-sectional "snapshot" clinical epidemiology studies in consultation-liaison psychiatry, while still important, do not in themselves yield the critical outcome information needed to document both the clinical efficacy and cost-efficacy of timely psychiatric treatment of patients with concurrent medical-psychiatric illness. As consultation-liaison psychiatry has been plagued by problems regarding reimbursement for clinical services rendered and has only a few systematic outcome studies as yet documenting the effectiveness of treatment interventions, more prospective studies are desperately needed to confirm the value of our efforts. The era of proselytizing the virtues of consultation-liaison psychiatry is over, and as with every other area of psychiatric therapy, governmental policy makers and third party payors are appropriately demanding to see "proof" that our treatments are both clinically- and cost-effective. As may be seen from this brief overview of our research demonstrating the potential reversibility of disabling cognitive dysfunction in depressed medical-psychiatric patients and the efficacy of labetalol in decreasing cardiovascular complications from ECT in high risk medical patients, positive reports from clinical investigations that are strategically planned and implemented on specific populations form strong arguments for the clinical and probable cost efficacy of both consultation-liaison psychiatry and medical-psychiatric units.
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Evaluate the ease of use and tolerability of labetalol (L) and nicardipine (N) for hypertension management in patients with acute stroke.
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The noradrenergic system may mediate some of the acute physiological effects of nicotine and nicotine withdrawal symptoms. This study examined the effects of labetalol, an alpha- and beta-adrenergic receptor blocker, on acute physiological and subjective effects of intravenous nicotine and on tobacco withdrawal symptoms. Five female and four male smokers participated in a double-blind, placebo-controlled, crossover study. Following overnight abstinence from smoking, subjects were treated orally with a single 100- or 200-mg dose of labetalol or placebo in each of three experimental sessions. Two hours after the medication treatment, subjects received an intravenous injection of 15 microg/kg nicotine. The nicotine-induced increases in heart rate were attenuated with the high dose of labetalol. No treatment effects were found for systolic or diastolic blood pressure changes. For the subjective effects of nicotine, treatment with both high and low doses of labetalol enhanced the ratings of "head rush" and "drug strength." The attenuation of tobacco withdrawal symptoms following intravenous nicotine administration was significantly greater with high-dose labetalol treatment, compared with placebo. These results support the proposed role of adrenergic receptors in nicotine withdrawal symptoms. The utility of adrenergic blockers, in combination with nicotine replacement therapies, for smoking cessation needs to be examined further in controlled clinical trials.
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The antihypertensive effect of oral labetalol and propranolol were evaluated in 65 black and 75 white patients with mild to moderate hypertension (standing diastolic blood pressure (StDBP) of 90-115 mmHg) in a double-blind multicenter clinical trial. Following a 4-week placebo phase, labetalol (n = 70) or propranolol (n = 70) was randomly assigned. During a 5-week titration phase, labetalol could be increased from 100 mg BID to 600 mg BID to achieve a StDBP of less than 90 mmHg and a decrement of greater than or equal to 10 mmHg. Propranolol could be titrated from 40 to 240 mg BID. A 3-month maintenance phase was followed by an optional 8-month maintenance phase. Hydrochlorothiazide (HCTZ) could be added at any time during the maintenance phase. Supine and standing blood pressures were measured at each visit. Statistical analysis revealed significant (ANOVA, p less than 0.05) treatment by race effects. Therefore, the treatment groups were stratified retrospectively by race. This study demonstrated that labetalol is equally effective in white and black patients, whereas, propranolol is significantly (p less than 0.05) more effective in white than in black patients. Moreover, labetalol is significantly more effective than propranolol in lowering the standing systolic/diastolic blood pressure of black patients (p less than 0.02/p less than 0.001). These blood-pressure effects were accompanied by a significantly greater (p less than 0.04) reduction in heart rate with propranolol. Furthermore, significantly more (p less than 0.05) black patients treated with propranolol compared to those treated with labetalol required the addition of a diuretic for control of their blood pressure.
Transient receptor potential vanilloid 1 (TRPV1) is involved in sensory nerve nociceptive signaling. Recently, it has been discovered that TRPV1 receptors also regulate basal body temperature in multiple species from mice to humans. In the present study, we investigated whether TRPV1 modulates basal sympathetic nervous system (SNS) activity. C57BL6/J wild-type (WT) mice and TRPV1 knockout (KO) mice were implanted with radiotelemetry probes for measurement of core body temperature. AMG9810 (50 mg/kg) or vehicle (2% DMSO/5% Tween 80/10 ml/kg saline) was injected intraperitoneally. Adrenoceptor antagonists or vehicle (5 ml/kg saline) was injected subcutaneously. In WT mice, the TRPV1 antagonist, AMG9810, caused significant hyperthermia, associated with increased noradrenaline concentrations in brown adipose tissue. The hyperthermia was significantly attenuated by the β-adrenoceptor antagonist propranolol, the mixed α-/β-adrenoceptor antagonist labetalol, and the α1-adrenoceptor antagonist prazosin. TRPV1 KO mice have a normal basal body temperature, indicative of developmental compensation. d-Amphetamine (potent sympathomimetic) caused hyperthermia in WT mice, which was reduced in TRPV1 KO mice, suggesting a decreased sympathetic drive in KOs. This study provides new evidence that TRPV1 controls thermoregulation upstream of the SNS, providing a potential therapeutic target for sympathetic hyperactivity thermoregulatory disorders.
Hemodynamic data were analyzed from 25 courses of intravenous pulse labetalol therapy for postoperative hypertension in 12 patients after major vascular surgeries. The hemodynamic determinations were obtained an average of 15 minutes after a therapeutic total dose of 10-120 mg of labetalol (mean, 37.5 mg). The mean arterial pressure (MAP) decreased an average of 27 mmHg or 20% after intravenous labetalol. This normalization of the postoperative hypertension was associated with a 19% increase in cardiac output (CO) and cardiac index (CI) (CO mean increase of 0.58 L/min and CI increase of 0.31 L/min/m2). Commensurate with this decrease in MAP and increase in CO was an average decrease in systemic vascular resistance (SVR) of 625 dyne/sec/cm-5 or 25%. The pulmonary vascular resistance decreased 15 dyne/sec/cm-5 or 4%. The heart rate decreased 9 beats per minute or 10% and the left ventricular stroke work improved by 9% or 1.6 g/m2/beat while the right ventricular stroke work increased by 33% or 2.8 g/m2/beat. The hemodynamic responses to intravenous labetalol in these patients were all beneficial, and there were no adverse effects secondary to the pulse doses of labetalol. Labetalol appears to be safe and efficacious for the treatment of postoperative hypertension in patients undergoing major vascular surgery.
The management of chronic arterial hypertension during pregnancy and postpartum requires first to estimate the risk of the pregnancy, linked with the severity of hypertension, with cardiac and renal involvement, with its cause as well as with the background (obesity, diabetes, possible history of placental vascular pathology). On a very practical approach, antihypertensive drug has to be started or increased if systolic pressure reaches or exceeds 160 mmHg or if diastolic pressure reaches or exceeds 105 mmHg. Below this level, there are no evidence-based medicine data, but it seems reasonable to treat if pressure increases over 150/100 mmHg (140/90 mmHg in case of ambulatory monitoring). Excessive pressure figures control must be avoided as much as insufficient ones: in practice, it is necessary to decrease the treatment dose if figures are below 130/80 mmHg. Three antihypertensive drugs are consensually recommended today: alphametyldopa, calcium-channel blockers and labetalol. Monotherapy is most often sufficient; if needed, two of these drugs can easily be associated, and even three if necessary. Converting enzyme inhibitors and angiotensin receptor II antagonists should not be prescribed to pregnant women. Betablockers and diuretics are not recommended. Whatever is the antihypertensive drug used, it is necessary to detect the signs of bad placenta blood circulation with uterine Doppler ultrasound and regular controls of fetal growth, and to check for appearance of proteinuria, defining then over-imposed pre-eclampsia needing immediate admission to the maternity. After delivery, lacatation suppresion with bromocriptin should not be prescribed.
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High-quality evidence for pharmacological treatment of cocaine cardiovascular toxicity is limited but can guide acute management of associated tachycardia, dysrhythmia, hypertension, and coronary vasospasm. Future randomized prospective trials are needed to evaluate new agents and further define optimal treatment of cocaine-toxic patients.
A 66-year-old hypertensive woman presented with epigastric and scapular pain on the basis of type 3 aortic dissection. Appropriate therapy with a combined alpha-adrenergic and beta-adrenergic antagonist agent prevented further ongoing dissection and amelioration of symptoms. On day 5, an episode of coronary vasospasm occurred presumably due to beta-blockade with unopposed alpha-adrenergic activity.
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Single doses of labetalol (200 mg i.v. over 5 min, 200 and 400 mg orally) were given to five healthy men on three different occasions. Plasma levels were followed for up to 25 h and blood pressure for 5 h. The elimination half-life was 1.6 to 8.5 h for the first 8 h. The oral bioavailability ranged from 4 to 23%. All doses induced a significant fall in systolic blood pressure at 2 h, the peak effect occurring at 30--120 (mean 63-72) min. After intravenous administration the peak supine blood-pressure fall was significant for both systolic and diastolic blood pressure and occurred 16 min after administration.
This randomized clinical trial shows that labetalol and hydralazine fulfill the criteria required for an antihypertensive drug to treat severe hypertension in pregnancy.
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The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration's (FDA's) Med Watch program (800-FDA-1088). If you have reported an interesting, preventable ADR to Med Watch, please consider sharing the account with our readers. Write to Dr. Mancano at ISMP, 200 Lakeside Drive, Suite 200, Horsham, PA 19044 (phone: 215-707-4936; e-mail: firstname.lastname@example.org). Your report will be published anonymously unless otherwise requested. This feature is provided by the Institute for Safe Medication Practices (ISMP) in cooperation with the FDA's Med Watch program and Temple University School of Pharmacy. ISMP is an FDA Med Watch partner.
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1 Cerebral blood flow (CBF) was measured by the 133xenon inhalation method in 33 newly-diagnosed hypertensive patients prior to commencing therapy. 2 Blood pressure was treated by using a varying sequence of four different drugs, namely labetalol, metoprolol, oxprenolol and sotalol, each of which is a beta-adrenergic receptor blocking agent, but with differing additional properties. 3 CBF measurements were repeated when blood pressure was controlled. No significant change in CBF was found with any of the four drugs, in contrast to the fall which has been reported when drugs of this type are administered acutely.
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1 The effects of labetalol, bethanidine and combined treatment with both drugs were compared in a within-patient randomized cross-over study in mild essential hypertension. Attention was directed to whether or not labetalol and bethanidine differed in their pattern of effect on arterial BP and whether evidence of synergism was apparent. 2 At the doses used labetalol significantly lowered systolic and diastolic BPs and heart rate lying, sitting, standing and after exercise. The dose of bethanidine used did not affect heart rate significantly while lowering systolic and diastolic BPs only after exercise and less clearly on standing. Combined treatment lowered BPs on standing and after exercise and heart rate after exercise. 3 The type and frequency of side-effects were similar with bethanidine and labetalol but were much less with combined treatment. 4 No evidence of synergism was observed.
Endotracheal intubation following anesthesia induction frequently produces hypertension and tachycardia. This study evaluated the efficacy of preinduction IV labetalol for attenuating the hemodynamic responses to intubation following thiopental and succinylcholine induction of anesthesia. Two hours after diazepam (10 mg by mouth), 60 patients were randomized in a double-blind manner and received IV saline or labetalol at doses of 0.25, 0.5, 0.75, or 1 mg/kg in a parallel design study. Five minutes later, thiopental (4 mg/kg) and succinylcholine (1 mg/kg) were administered, and the trachea was intubated in 2 minutes. Nitrous oxide (70%) anesthesia was maintained for 10 minutes. Hemodynamic parameters were grouped and analyzed for significance (p less than 0.05) by two-way repeated measures analysis of variance and t-test with Bonferroni adjustments. Baseline group demographics and hemodynamics were comparable. All doses of labetalol significantly attenuated the rate-pressure product increase immediately postintubation versus placebo. There was a dose-dependent attenuation of the increases in heart rate and the systolic, diastolic, and mean blood pressures versus placebo following intubation. IV labetalol at doses up to 0.75 mg/kg offers an effective pharmacologic means of attenuating preoperative hemodynamic responses to endotracheal intubation.
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We report the specifics of 12 cases of severe hypertension after the intraoperative use of topical phenylephrine, submucosal epinephrine, or both. Ten of these 12 patients also developed severe pulmonary edema. Seven of the twelve were treated with beta blockers; 3 of whom suffered cardiac arrest. We propose a common mechanism: the vasoconstrictors caused systemic hypertension, increased left ventricular afterload, decreased left ventricular compliance, and decreased cardiac output. In those patients treated with beta blockers, decreased contractility and inability to increase heart rate further compromised cardiopulmonary function.
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Although definitions of severe hypertension vary, thresholds of >or=160-170 mm Hg systolic and/or >or=110 mm Hg diastolic are in most common usage. A recent focus has been placed on systolic hypertension given the increased pulse pressure in these women. In pregnancy, there is a general consensus that severe hypertension should be treated. Among woman with pre-eclampsia, attention must be paid to other end organ dysfunction, as blood pressure (BP) management is but one aspect of care. The urgency of antihypertensive therapy will depend primarily on the absolute level of BP. However, most clinicians will also consider both the rate of BP rise and the presence of maternal symptoms. Most commonly, severe hypertension is treated with parenteral labetalol or hydralazine, or oral nifedipine (capsules or PA tablet). Other options will depend on local availability. MgSO(4) should not be relied on as an antihypertensive.
The hemodynamic effects of intravenous labetalol (a combined alpha- and beta-blocking agent) were studied in 11 patients during early post-open heart surgery hypertension. With a mean dosage of 15 mg, labetalol reduced both systemic arterial pressures and the heart rate by an average of 21 percent (p < .001). The patients failed to compensate for the decline in pressure and pulse rate by elevation of their stroke volume, and even the cardiac index (CI) was severely depressed (from 2.30 to 1.67 L/min/m2, ie, 27 percent; p < .001). Neither left ventricular filling pressure nor vascular resistance was affected by labetalol early after open heart surgery. In four patients, 3 mg of glucagon after administration of labetalol elevated pulmonary arterial pressures and increased the CI by 16 percent. Two patients were observed on the preoperative day, and their response to labetalol was similar to that described in earlier studies: during blood pressure decline, CI was slightly augmented, and the systemic vascular resistance was greatly reduced (26 percent). The results indicate that after open heart surgery, patients are highly sensitive to the beta-blocking effects of labetalol, and although labetalol can greatly reduce myocardial oxygen consumption, it cannot be recommended for the treatment of post-open heart surgery hypertension.
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Five patients with malignant arterial hypertension and terminal (3) or advanced (2) renal failure were treated with the alpha-beta blocker labetalol and the angiotensin-converting enzyme inhibitor captopril. Labetalol alone or in combination with other antihypertensive agents had been ineffective in two cases and captopril alone in one; yet hypertension was rapidly controlled when the two drugs were given together. The return of blood pressure to normal levels brought about regression of digitalis-resistant cardiac failure in 2 patients and slight improvement of renal function in 2 other patients. The captopril-labetalol combination probably has a synergistic effect, and although its mechanism remains obscure this effect may be used to treat patients with severe or malignant arterial hypertension.
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