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

Cardiovascular complications frequently occur during status epilepticus. To determine the changes in systemic and pulmonary arterial pressure, cardi output, and left ventricular contractility during seizures, 1-week-old pigs were intubated, paralyzed, mechanicall entilated, and catheterized with a Swan-Ganz catheter. Seizures were induced with intravenous bicuculline. Early changes consisted of significant systemic and pulmonary arterial hypertension. After 2 hours of seizures, the animals developed progressive systemic hypotension and decreased cardiac output. M-mode echocardiography disclosed a decrease in left ventricular contractility. Cardiac tissue frozen in situ showed a significant increase in lactate and reductions in glucose, triglyceride, and adenosine triphosphate levels. Prolonged seizures in the neonatal pig result in cardiac dysfunction, which may play a role in the development of epileptic brain damage.
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PMID:Cardiac dysfunction during status epilepticus in the neonatal pig. 405 58

Giving a definition of analgesia in ICU needs to answer several questions: Why sedation? Which drugs can we use? How can we deal with sedation? (monitoring, continuous administration, weaning...)? Two different types of sedation must be considered: treatment-sedation (status epilepticus, tetanus, intracranial hypertension...) and comfort-sedation in anxious and/or restless and/or painful patients and in those necessitating mechanical ventilation. Analgesic consumptions vary widely with diseases and their outcome, background diseases and ICU environment. Several studies have shown that pain and analgesia are frequently neglected in ICU. The authors review the different drugs in use, with their advantages and drawbacks. A particular place is reserved to regional techniques, often underused in ICU. Indications are then fully discussed, according to several specific pathological conditions. Monitoring and weaning of sedation are also discussed at the end of the review.
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PMID:[Role of analgesia for sedation in intensive care medicine]. 776 33

We report the historical, clinical, and laboratory findings in 5 patients after crack cocaine ingestion. All patients exhibited adrenergic crisis as a result of their ingestion. Analysis of their history revealed a latency period before signs and symptoms occurred as well as a wide variation in the number of crack cocaine nuggets ingested. Signs of intoxication were hypertension, tachycardia, hyperthermia, agitation, and generalized seizure activity. Treatment included therapeutic sedation with lorazepam and adrenolysis with esmolol infusion. The majority of patients showed electrocardiographic evidence of cardiac ischemia, but not elevations in serum creatinine phosphokinase enzymes--MB fraction. One patient died of complications associated with subclinical status epilepticus. The toxicities of crack cocaine ingestion are seldom appreciated. Prompt reversal of both cardiovascular and neurological signs and symptoms with appropriate pharmacologic agents is indicated.
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PMID:Adrenergic crisis from crack cocaine ingestion: report of five cases. 759 78

Computed tomography was performed on 14 unconscious Kenyan children recovering from cerebral malaria (seven of whom had another scan 12-120 days later) to elucidate the cause of intracranial hypertension and neurological sequelae. Brain swelling, defined as a loss of cerebrospinal fluid spaces, was documented in six children, while a further two had conspicuously small ventricles only. There was severe intracranial hypertension in the two children with definite brain swelling in whom intracranial pressure was monitored. There was no evidence of acute hydrocephalus or vasogenic oedema. Four children with brain swelling also had widespread low density areas suggestive of ischaemic damage. The patterns of damage were not uniform but were consistent with a critical reduction in cerebral perfusion pressure (which was documented in the two in whom this was monitored), hypoglycaemia, or status epilepticus. All four had serious neurological sequelae. These data suggest that brain injury in cerebral malaria may be due in part to secondary systemic and intracranial factors as well as to the direct effect of intravascular sequestration.
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PMID:Brain swelling and ischaemia in Kenyans with cerebral malaria. 818 59

Typical causes of renovascular hypertension include intramural atherosclerotic lesions of the main renal arteries or their branches and fibromuscular dysplasia of the renal arterial wall with luminal narrowing. We report a patient with new-onset, accelerated hypertension (blood pressure 220/140 mm Hg, status epilepticus, retinal hemorrhages) secondary to a dissection of the anterior division of the right renal artery that was accompanied by hyperreninemia, hyperaldosteronism, and hypokalemia. At presentation in the untreated state, unstimulated plasma renin activity and the serum aldosterone level were markedly elevated. Following right nephrectomy, blood pressure levels normalized without antihypertensive therapy, and plasma renin activity, serum aldosterone and potassium levels normalized. Histologic study of the right renal artery showed an isolated dissection of the anterior branch of the vessel between the muscularis and adventitia that created marked reduction in luminal diameter and renal ischemia. There was no evidence of any other vascular abnormalities, atherosclerosis, or fibromuscular dysplasia. These findings demonstrate that an isolated dissection of a branch of the renal artery may induce profound hyperreninemia and represents a rare, reversible etiology for accelerated hypertension associated with acute encephalopathy.
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PMID:Accelerated hypertension with encephalopathy due to an isolated dissection of a renal artery branch vessel. 820 71

The case is reported of a 45-year-old woman who was being treated for chronic back and right leg pain with intrathecal morphine administered via a subcutaneous continuous-infusion device. She received an accidental 450-mg bolus injection of morphine intrathecally and developed hypertension, status epilepticus, intracerebral hemorrhage, and respiratory failure. Treatment with continuous intravenous naloxone infusion, lumbar catheter drainage of cerebrospinal fluid, and control of hypertension and status epilepticus resulted in an excellent outcome with return to neurological baseline. Care providers who refill pump reservoirs with morphine must be knowledgeable about these devices and the life-threatening consequences associated with errors in refilling them. This case describes the complications and successful treatment of high-dose intrathecal morphine overdose.
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PMID:Treatment of high-dose intrathecal morphine overdose. Case report. 781 22

Generalized seizures can induce both hypertension and hyperglycemia which may aggravate preexisting cerebral or medical conditions in patients. In vivo fluorescent imaging of regional cortical blood flow and brain intracellular pH (pHi) was performed in fasted New Zealand rabbits (n = 35) in which either mean arterial blood pressure (MABP) or serum glucose was the covaried factor during pentylenetetrazole induced status epilepticus under 1.5% inspired halothane. Baseline brain pHi and regional cortical blood flow were 7.02 +/- 0.02 and 51.1 +/- 1.7 ml/100 g/min, respectively. Following seizure induction, MABP increased to 105 mm Hg and brain pHi fell to 6.79 +/- 0.03 within 15 min and remained at this level for 1 h (P < 0.001). With normalization of MABP during ongoing seizures, there was no worsening in brain pHi despite a significant decrease in regional cortical blood flow. Hyperglycemia decreased pHi to 6.71 +/- 0.02 compared to 6.84 +/- 0.04 in normoglycemic animals (P < 0.001). Using pHi as a cerebral metabolic index, these data suggest that normalization of MABP does not increase metabolic injury while hyperglycemia does significantly worsen brain acidosis. Therefore, administration of glucose to patients with status epilepticus should be avoided unless there is documented hypoglycemia.
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PMID:Effect of arterial blood pressure and serum glucose on brain intracellular pH, cerebral and cortical blood flow during status epilepticus in the white New Zealand rabbit. 845 50

Generalized convulsive status epilepticus (GCSE) is accompanied by a marked increase in plasma catecholamines. This produces a number of changes in general systemic physiology including hypertension, tachycardia, cardiac arrhythmias, hyperglycemia, acidosis, and hyperpyrexia. If SE is stopped quickly, these changes are self-correcting and do not produce an increased risk of neuropathology. However, if seizures continue, many of the early physiologic changes reverse, and late status epilepticus is marked by hypotension, hypoglycemia, pulmonary edema and a continued acidosis and elevation of body temperature. Prevention of serious hypoglycemia, maintenance of adequate systemic blood pressure to provide adequate cerebral perfusion, and normalizing the body temperature will minimize or prevent neuropathologic sequelae to SE of extended duration.
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PMID:Systemic effects of generalized convulsive status epilepticus. 846 91

The pathogenesis of neurogenic pulmonary edema has been debated for many years. Whether cardiogenic mechanisms and increased pulmonary vascular pressures are primary or even necessary for the production of pulmonary edema has been argued. We used postictal pulmonary edema to study this problem in a sheep model of neurogenic pulmonary edema with bicucullin-induced status epilepticus. Seizure-induced increases in pulmonary vascular pressures were averted with a reservoir system to maintain left atrial pressure (LAP) and pulmonary artery pressure (PAP) at preseizure levels. No increase in lung lymph flow occurred during seizures, in contrast to the doubling of lung lymph flow that occurred during seizures when ictal pulmonary vascular hypertension was not blocked. These data support a primary role of pulmonary vascular pressure increases in the production of neurogenic pulmonary edema.
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PMID:Postictal pulmonary edema requires pulmonary vascular pressure increases. 861 70

An 11-year-old girl developed signs of intracranial hypertension after status epilepticus with convulsive movements of her right upper limb. Computerized tomography revealed left hemispheric hypodensity with mass effect, attributed to vasogenic edema. Intracranial hypertension was controlled under intracranial pressure monitoring and clinical status slowly improved. The patient was aphasic and right hemiplegic when she recovered consciousness but she remarkably recovered from her neurological deficits during the following two years despite neuroradiological evolution demonstrating extensive destruction of the left cortex and white matter. Two positron emission tomography (PET) scans were performed respectively six weeks and eight months after status epilepticus, and both demonstrated profound left hemispheric hypometabolism except in the lenticular nucleus and a restricted area of motor/premotor cortex. On the other hand, glucose metabolism in the right hemisphere was heterogeneously increased on the second PET when compared with the first PET. We concluded that, in this case, clinical recovery might have implicated functional reorganization arising from the intact hemisphere.
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PMID:[Cerebral lesions following convulsive partial status epilepticus. Clinical, neuroradiologic and PET study of a case]. 919 Mar 70


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