1/58. acebutolol-induced ventricular tachycardia reversed with sodium bicarbonate.BACKGROUND: acebutolol is a unique beta blocker that possesses cardioselectivity, partial agonist activity, and membrane stabilizing activity. sodium bicarbonate is used to reverse the cardiotoxic effects of other drugs with membrane stabilizing activity. There have been no reported cases of acebutolol-induced ventricular dysrhythmias treated successfully with bolus sodium bicarbonate. CASE PRESENTATION: A 48-year-old man ingested approximately 6.4 g of acebutolol with ethanol (blood ethanol 61 mmol/L). There were no other coingestants identified. One hour after presentation, the patient had a cardiac arrest with the monitor showing ventricular tachycardia. sodium bicarbonate 50 mEq intravenous push converted the patient to sinus rhythm and the blood pressure improved to 129/90 mm Hg. CONCLUSION: This case demonstrates a temporal relationship between bolus sodium bicarbonate administration and the termination of acebutolol-induced ventricular tachycardia.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
2/58. neuroleptic malignant syndrome due to promethazine.A 42-year-old man came to our emergency room hyperthermic (oral temperature, 42.4 degrees C), diaphoretic, and delirious. Other findings included labile blood pressure, sinus tachycardia (heart rate, 138/min), tachypnea (respiratory rate 34/min), muscle rigidity, and incontinence. Two days earlier, he had gone to a local clinic with complaints of abdominal pain, nausea, and vomiting. promethazine was prescribed, and this was the patient's only medication on admission. Laboratory studies showed leukocytosis, hypernatremia, metabolic acidosis, elevated creatinine phosphokinase level, elevated transaminase levels, azotemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and myoglobulinuria. The clinical and laboratory findings were characteristic of the neuroleptic malignant syndrome, with promethazine as the offending agent.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
3/58. Interaction of genetic predisposition and environmental factors in the pathogenesis of idiopathic orthostatic intolerance.BACKGROUND: The hemodynamic and autonomic abnormalities in idiopathic orthostatic intolerance (IOI) have been studied extensively. However, the mechanisms underlying these abnormalities are not understood. If genetic predisposition were important in the pathogenesis of IOI, monozygotic twins of patients with IOI should have similar hemodynamic and autonomic abnormalities. methods: We studied two patients with IOI and their identical twins. Both siblings in the first twin pair had orthostatic symptoms, significant orthostatic tachycardia, increased plasma norepinephrine levels with standing, and a greater than normal decrease in systolic blood pressure with trimethaphan infusion. RESULTS: Both siblings had a normal response of plasma renin activity to upright posture. In the second twin pair, only one sibling had symptoms of orthostatic intolerance, an orthostatic tachycardia, and raised plasma catecholamines with standing. The affected sibling had inappropriately low plasma renin activity with standing and was 8-fold more sensitive to the pressor effect of phenylephrine than the unaffected sibling. CONCLUSIONS: We conclude that in some patients, IOI seems to be strongly influenced by genetic factors. In others, however, IOI may be mainly caused by nongenetic factors. These findings suggest that IOI is heterogenous, and that both genetic and environmental factors contribute individually or collectively to create the IOI phenotype.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
4/58. Severe gamma-hydroxybutyrate withdrawal: a case report and literature review.We report a case of gamma-hydroxybutyrate (GHB) withdrawal resulting in severe agitation, mental status changes, elevated blood pressure, and tachycardia hours after stopping chronic use of GHB. The patient admitted to substantial GHB abuse on a daily basis for 2.5 years. Previous attempts at cessation reportedly resulted in diaphoresis, tremors, and agitation. The patient's symptoms, negative polypharmacy history, and negative urine and blood toxicological analysis for alcohol, benzodiazepines, sedative-hypnotics, or other substances suggested the diagnosis of GHB withdrawal. Later analysis of a patient drug sample confirmed the presence of GHB. The patient required 507 mg of lorazepam and 120 mg of diazepam over 90 h to control agitation. This is one of the few reported cases of GHB withdrawal and one of the most severe. Given the increasing use of GHB, more cases of severe GHB withdrawal should be anticipated.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
5/58. orthostatic intolerance and tachycardia associated with norepinephrine-transporter deficiency.BACKGROUND: orthostatic intolerance is a syndrome characterized by lightheadedness, fatigue, altered mentation, and syncope and associated with postural tachycardia and plasma norepinephrine concentrations that are disproportionately high in relation to sympathetic outflow. We tested the hypothesis that impaired functioning of the norepinephrine transporter contributes to the pathophysiologic mechanism of orthostatic intolerance. methods: In a patient with orthostatic intolerance and her relatives, we measured postural blood pressure, heart rate, plasma catecholamines, and systemic norepinephrine spillover and clearance, and we sequenced the norepinephrine-transporter gene and evaluated its function. RESULTS: The patient had a high mean plasma norepinephrine concentration while standing, as compared with the mean ( /-SD) concentration in normal subjects (923 vs. 439 /-129 pg per milliliter [5.46 vs. 2.59 /-0.76 nmol per liter]), reduced systemic norepinephrine clearance (1.56 vs. 2.42 /-0.71 liters per minute), impairment in the increase in the plasma norepinephrine concentration after the administration of tyramine (12 vs. 56 /-63 pg per milliliter [0.07 vs. 0.33 /-0.37 pmol per liter]), and a disproportionate increase in the concentration of plasma norepinephrine relative to that of dihydroxyphenylglycol. Analysis of the norepinephrine-transporter gene revealed that the proband was heterozygous for a mutation in exon 9 (encoding a change from guanine to cytosine at position 237) that resulted in more than a 98 percent loss of function as compared with that of the wild-type gene. Impairment of synaptic norepinephrine clearance may result in a syndrome characterized by excessive sympathetic activation in response to physiologic stimuli. The mutant allele in the proband's family segregated with the postural heart rate and abnormal plasma catecholamine homeostasis. CONCLUSIONS: Genetic or acquired deficits in norepinephrine inactivation may underlie hyperadrenergic states that lead to orthostatic intolerance.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
6/58. Hormonal and cardiovascular reflex assessment in a female patient with pure autonomic failure.We report the case of a 72-year-old female with pure autonomic failure, a rare entity, whose diagnosis of autonomic dysfunction was determined with a series of complementary tests. For approximately 2 years, the patient has been experiencing dizziness and a tendency to fall, a significant weight loss, generalized weakness, dysphagia, intestinal constipation, blurred vision, dry mouth, and changes in her voice. She underwent clinical assessment and laboratory tests (biochemical tests, chest X-ray, digestive endoscopy, colonoscopy, chest computed tomography, abdomen and pelvis computed tomography, abdominal ultrasound, and ambulatory blood pressure monitoring). Measurements of catecholamine and plasmatic renin activity were performed at rest and after physical exercise. Finally the patient underwent physiological and pharmacological autonomic tests that better diagnosed dysautonomia.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
7/58. Endogenous circulating sympatholytic factor in orthostatic intolerance.Sympathotonic orthostatic hypotension (SOH) is an idiopathic syndrome characterized by tachycardia, hypotension, elevated plasma norepinephrine, and symptoms of orthostatic intolerance provoked by assumption of an upright posture. We studied a woman with severe progressive SOH with blood pressure unresponsive to the pressor effects of alpha(1)-adrenergic receptor (AR) agonists. We tested the hypothesis that a circulating factor in this patient interferes with vascular adrenergic neurotransmission. Preincubation of porcine pulmonary artery vessel rings with patient plasma produced a dose-dependent inhibition of vasoconstriction to phenylephrine in vitro, abolished vasoconstriction to direct electrical stimulation, and had no effect on nonadrenergic vasoconstrictive stimuli (endothelin-1), PGF-2alpha (or KCl). Preincubation of vessels with control plasma was devoid of these effects. SOH plasma inhibited the binding of an alpha(1)-selective antagonist radioligand ([(125)I]HEAT) to membrane fractions derived from porcine pulmonary artery vessel rings, rat liver, and cell lines selectively overexpressing human ARs of the alpha(1B) subtype but not other AR subtypes (alpha(1A) and alpha(1D)). We conclude that a factor in SOH plasma can selectively and irreversibly inhibit adrenergic ligand binding to alpha(1B) ARs. We propose that this factor contributes to a novel pathogenesis for SOH in this patient. This patient's syndrome represents a new disease entity, and her plasma may provide a unique tool for probing the selective functions of alpha(1)-ARs.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
8/58. Sustained accelerated idioventricular rhythm.A 73-year-old white man became easily fatigued and hypotensive six weeks after a documented acute inferior myocardial infarction. Continuous ECG monitoring showed a sustained tachycardia with a right bundle branch block pattern. A His bundle electrogram showed no His deflection prior to ventricular activation. The patient was successfully treated with intravenous procaine amide resulting in reversion to sinus rhythm, loss of symptoms, and return of blood pressure to normal levels. The unique aspects of this case and therapeutic considerations in the management of this problem are discussed.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
9/58. Cerebrovascular and cardiovascular responses associated with orthostatic intolerance and tachycardia.Idiopathic orthostatic intolerance syndrome is characterized by postural symptoms of cerebral hypoperfusion without arterial hypotension. Abnormal baroreceptor responses with deranged cerebral autoregulation leading to cerebral vasoconstriction have been proposed as a causative mechanism. The authors report the cerebrovascular and cardiovascular responses in a patient who recovered from orthostatic intolerance and tachycardia. Changes in the orthostatic responses of mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and transcranial Doppler middle cerebral artery (MCA) mean blood flow velocity (Vmean) were assessed at admission and again 6 months after recovery. Normal cardiovascular responses to forced breathing and to standing indicated intact overall baroreflex integrity with normal baroreflex sensitivity (10.2 msec.mm Hg(-1)). After the patient stood for 8 minutes, presyncopal symptoms developed, with unchanged MAP but increased HR ( 41 beats/min) and reduced stroke volume (SV) (-69%), CO (-50%), and MCA Vmean (-46%; 57 to 31 cm. s(-1)). After a reconditioning program and recovery, the patient was reexamined. The supine MCA Vmean was larger (79 cm. s(-1)), as were MAP (76 versus 70 mm Hg) and CO ( 15%). The orthostatic HR increase was smaller ( 5 beats/min), as was the reduction in SV (-44%) and CO (-30%), with an increase in MAP to 93 mm Hg. The orthostatic reduction in MCA Vmean was smaller (-13 versus -26 cm.s(-1)) and standing cerebrovascular resistance decreased (1.41 versus 2.39 mm Hg.cm. s(-1)). In this patient who had intact baroreflex control and no postural decrease in blood pressure, the reduction in MCA Vmean, concomitant with a large decrease in CO, seemed reversible. The result suggests that a symptomatic reduction in cerebrovascular conductance during standing is to be interpreted as being an adaptive response to a critically limited systemic blood flow, rather than to derangement of cerebral autoregulation.- - - - - - - - - - ranking = 2keywords = pressure (Clic here for more details about this article) |
10/58. Postural tachycardia syndrome in a 28-year-old Japanese woman.Postural tachycardia syndrome is defined as the development of orthostatic symptoms without orthostatic hypotension. We report a 28-year-old female patient with postural tachycardia syndrome who exhibited palpitation, low-grade fever and weight loss. Evaluation of autonomic nervous system functions showed that cardiovagal function was normal. sweat response to acetylcholine was decreased. Excessive blood pressure elevation was seen in phase IV of the valsalva maneuver. Pathophysiologic factors in this case were considered to be alpha adrenergic denervation and beta adrenergic hyperresponsiveness. It is important that this syndrome be widely recognized and properly diagnosed.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
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