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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.
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PMID:The management of severe pre-eclampsia and eclampsia. 83 44

Three hundred and forty-six nulliparous women with pregnancy-induced hypertension prior to term were monitored in a high-risk pregnancy unit while awaiting fetal maturity. Management included ambulation as desired, regular hospital diet without salf restriction, blood pressure measured 4 times daily, weight and urine protein determined 3 times each week, creatinine clearance determined weekly, and serial sonography to monitor fetal growth. Sedation and antihypertensive agents were not prescribed. Delivery was delayed until term unless hypertension persisted or recurred following an initial salutary response. Factors other than hypertension that contributed to the decision to effect delivery were 1) rapid weight gain, 2) decreasing creatinine clearance, 3) appearance of significant proteinuria, 4) suspected fetal growth retardation, and 5) the development of severe headache or scotomata. With this method of management the perinatal mortality rate was 9/1000. Only 5 infants developed the respiratory distress syndrome and all survived. There were 26 women who left the unit against medical advice. Severe hypertension subsequently developed in 7 of these women and 4 of their fetuses were stillborn. The perinatal mortality rate among this group of patients was 154/1000. It is concluded that the nulliparous patient with pregnancy-induced hypertension prior to term can be safely managed by hospitalization and close observation as a viable alternative to prompt delivery.
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PMID:Management of pregnancy-induced hypertension in the nullipara. 94 68

Continuous intravenous sedation is often prescribed during the intensive treatment of severe head injury. It is known that intravenous hypnotics may prevent or treat the brief intracranial hypertension episodes associated with nociceptive stimuli, like tracheal intubation. However there is yet no clear evidence in the literature showing beneficial effects of sedation in severely head-injured patients on intracranial pressure control or outcome. Sedation should be primarily administered in neurotraumatology to allow good conditions for intensive treatment, while avoiding any depressive cardiovascular action. The abrupt reversal of sedation by means of specific antagonists may induce significant elevation of both cerebral blood flow and intracranial pressure and should be avoided.
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PMID:Sedatives and antagonists in the management of severely head-injured patients. 141 44

In order to firstly evaluate the efficacy of flumazenil in reversing benzodiazepine-induced sedation because of drug overdose and secondly to register adverse events, 13 patients admitted to the intensive care unit because of drug intoxication, were given flumazenil intravenously to a maximum of 1.0 mg. Sedation state was scored on a modified Glasgow Coma Scale and arterial blood pressure, heart rate and arterial blood gases were recorded before and after flumazenil was given, and every 30 min for 2 h. Results showed that flumazenil reversed the sedation due to benzodiazepines effectively increasing the coma score significantly (P less than 0.005). We found no change in arterial blood pressure (apart from one patient), heart rate or arterial blood gases. Two patients gave further information about drug intake after flumazenil was given. Six patients became resedated, only one needed additional flumazenil. One patient developed a hypertensive crisis after flumazenil was given as a result of the unmasking of an untreated hypertension. Another patient aspirated gastric content to the trachea during resedation and needed respiratory support.
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PMID:Reversal of benzodiazepine intoxication by flumazenil. 168 59

Continuous intravenous sedation is often used during the intensive treatment of severe head injury. Hypnotic agents may prevent or treat the brief episodes of intracranial hypertension associated with nociceptive stimuli. However there is yet no clinical data in the literature showing beneficial effects of continuous sedation on intracranial pressure control or outcome in severe head injured patients. Sedation should be primarily administered to allow good conditions for intensive treatment. Benzodiazepines are sedatives with limited systemic side effects. Midazolam is very convenient because its short duration of action allows reasonable recovery time following prolonged administration. The abrupt reversal of sedation by means of specific antagonists may induce significant elevation of cerebral blood flow and intracranial pressure and should be avoided.
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PMID:[Use of benzodiazepines in neurosurgical resuscitation]. 184 99

This study documents our experience with labetalol administered by continuous intravenous infusion for severe hypertension. Infusions were performed in 14 hospitalized patients (15 infusions) with supine diastolic pressure greater than 125 mmHg or supine systolic pressure greater than 200 mmHg. Blood pressures were measured by intra-arterial recording or an Arteriosonde 1225 Doppler instrument standardized with a mercury sphygmomanometer. Patients initially received 2 mg/min continuous infusion; the infusion rate varied between 0.5 and 2.0 mg/min according to the protocol. The infusion was terminated when diastolic pressure decreased 30 mmHg or when 300 mg of the drug had been infused. Goal blood pressure was achieved in all but two infusions. Sedation was the most common adverse reaction, followed by nausea and diaphoresis. No patient required discontinuation or reduction in infusion rate secondary to side effects. We conclude that continuous intravenous infusion of labetalol offers an effective alternative to current parenteral therapy.
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PMID:Labetalol by continuous intravenous infusion in severe hypertension. 372 59

Clonidine (Catapres, Catapresan), guanfacine (Estulic), and methyldopa (Aldomet) are the prototypes of centrally acting antihypertensive drugs. Clonidine and guanfacine are lipophilic drugs that readily penetrate into the brain, where they stimulate alpha-adrenergic receptors in the pontomedullary region. The stimulation of these central alpha-adrenergic receptors has been shown to activate an inhibiting neuron, which causes a reduction of peripheral sympathetic tone and a subsequent fall in arterial blood pressure and heart rate. Both a centrally initiated reduction of vagus reflex activity and the activation of presynaptic alpha 2-adrenergic blocking agents in the heart may contribute to the bradycardia. Studies indicate that methyldopa also penetrates into the brain, where it is converted into alpha-methylnorepinephrine. This amine may stimulate the same central alpha-adrenergic receptors as those activated by clonidine, which will result in a hypotensive effect. Possibly, alpha-methyldopamine might also play a role. Accordingly, the modes of action of clonidine and alpha-methyldopa probably are very similar at a basic level. The central adrenergic receptors probably are located postsynaptically. Their receptor demand corresponds more closely to that of the alpha 2-subtype. Central alpha 1-adrenergic receptors might possibly play a part in the modulation of vagally induced baroreflex bradycardia. A discussion on the pharmacological basis of the side effects of the centrally acting antihypertensives has been limited to those adverse reactions that are somehow related to alpha-adrenergic receptors. Sedation, a common side effect, appears to be mediated by central alpha 2-adrenergic receptors, at least in animal models.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:The hypotensive activity and side effects of methyldopa, clonidine, and guanfacine. 609 46

The effects of 300 micrograms of oral clonidine were studied in nine patients with unilateral renal artery stenosis proved by selective renal arteriography. Blood pressure, heart rate, plasma renin activity (PRA) levels, plasma noradrenaline levels, and sedation were measured before and for eight hours after dosage. After clonidine administration, both systolic and diastolic blood pressure fell within the first hour, was maximum in the fourth hour, and remained lower than predosage levels even in the eighth hour. There was a fall in heart rate, maximum in the fourth hour. There were minimal changes in PRA levels after giving the clonidine. Plasma noradrenaline levels fell, with the maximum fall in the sixth hour. Sedation occurred within one hour of dosage and was maximum in the second hour. We conclude that in patients with unilateral renal artery stenosis clonidine causes a substantial and prolonged fall in blood pressure not accompanied by suppression of PRA levels but by a reduction in plasma noradrenaline levels. This suggests a role for central pressor mechanisms, probably linked to angiotensin II and central sympathetic activation, in the maintenance of hypertension in patients with renal artery stenosis.
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PMID:Clonidine lowers blood pressure independently of renin suppression in patients with unilateral renal artery stenosis. 633 26

Clonidine hydrochloride (Catapres), a potent antihypertensive agent, has been in clinical use since 1974 in the United States. Clonidine, an alpha-adrenergic receptor agonist, stimulates central alpha receptors in the depressor site of the vasomotor center of the medulla oblongata and hypothalamus, which diminishes efferent sympathetic tone to the heart, kidneys, and peripheral vasculature with a concomitant increase in vagal activity. Hemodynamic and renal effects include reduction in supine and erect blood pressure, heart rate, total peripheral resistance, plasma renin activity, and urinary aldosterone and catecholamine excretion, with little effect on resting cardiac output, response to exercise, and preservation of renal function. Clonidine alone produces a significant reduction in mean arterial pressure in all degrees of hypertension during acute and chronic administration, with little or no tendency toward tolerance or postural hypotension. Its antihypertensive potency is enhanced with the concomitant use of a diuretic or vasodilator, and it may be used in place of a beta blocker with equal efficacy in the diuretic plus vasodilator combination. Serious adverse effects are uncommon, with more than 93% of patients tolerating the drug well. Sedation and dry mouth, the most common adverse effects, are usually related to dose and duration and are minimized by gradually increasing the dose and by taking the major portion of the twice-daily schedule at bedtime. Clonidine may be safely given to patients with congestive heart failure, ischemic heart disease, obstructive lung disease, chronic renal insufficiency, and diabetes mellitus. Clonidine is one of the most versatile and effective agents presently available for the treatment of hypertension.
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PMID:Clonidine hydrochloride. 704 65

Computerised axial tomography requires total immobility, which must be obtained by a simple and safe technique of anaesthesia. Three anaesthesia techniques were used and analysed in 54 children aged less than 5 years: the technique of the feeding bottle, sedation with pentobarbital or diazepam and general anaesthesia with ketamine hydrochloride. The technique of the feeding bottle can be proposed in selected patients. Sedation can be also used but judiciously, not to deep. The systematic use of an depression immobilizing mattress with these two techniques gives better results. Intramuscular ketamine hydrochloride, when not contrindicate (intracranial hypertension or acute hydrocephaly), has been used always successfully.
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PMID:[Anaesthesia for computerised axial tomography in children (author's transl)]. 733 96


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