Arrhythmias clinical presentation

III. Clinical presentation. Within minutes to a few hours after ingestion, victims develop profound hypokalemia and skeletal muscle weakness progressing to flaccid paralysis of the limbs and respiratory muscles. Ventricular arrhythmias, hypophosphatemia, rhabdomyolysis, acute renal failure, and coagulopathy may also occur. Gastroenteritis with severe watery diarrhea, mydriasis with impaired visual accommodation, and CNS depression are sometimes present. More often, patients remain conscious even when severely Intoxicated. 

IV. Diagnosis is based on a history of exposure and the clinical presentation of mucous membrane irritation, CNS depression, arrhythmias, and hepatic necrosis. Carbon tetrachloride is radiopaque and may be visible on abdominal x-ray after acute ingestion. 

II. Toxic dose. Inhalation or ingestion of as little as 1 mg of fluoroacetate is sufficient to cause serious toxicity. Death is likely after ingestion of mote than 5 mg/kg. Clinical presentation. After a delay of minutes to several hours (in one report coma was delayed 36 hours), manifestations of diffuse cellular poisoning become apparent nausea, vomiting, diarrhea, metabolic acidosis, renal failure, agitation, confusion, seizures, coma, respiratory arrest, pulmonary edema, and ventricular arrhythmias may occur. One case series reported a high incidence of hypocalcemia and hypokalemia. 

The toxicity of ephedrine is closely related to adverse cardiovascular events, since the clinical presentation of toxicity reflects the sympathomimetic activity of these agents. The adrenergic effects can shorten cardiac refractory periods, permitting the development of reentrant cardiac arrhythmias. The worst complication related to the use of ephedrine is thrombotic stroke, presumably resulting from vasoconstriction of large cerebral arteries that in turn leads to local thrombosis [71]. Other adverse effects include hypertension, diaphoresis, hypothermia, and agitation. The best treatment in an overdose is the rapid identification of the symptoms followed by supportive management. 

Because the severity of symptoms and the absolute serum concentration are poorly correlated in some patients, institution of therapy should be dictated by the clinical scenario. All patients with hypercalcemia should be treated with aggressive rehydration normal saline at 200 to 300 mL/hour is a routine initial fluid prescription. For patients with mild hypocalcemia, hydration alone may provide adequate therapy. The moderate and severe forms of hypercalcemia are more likely to have significant manifestations and require prompt initiation of additional therapy. These patients may present with anorexia, confusion, and/or cardiac manifestations (bradycardia and arrhythmias with ECG changes). Total calcium concentrations greater than 13 mg/dL (3.25 mmol/L) are particularly worrisome, as these levels can unexpectedly precipitate acute renal failure, ventricular arrhythmias, and sudden death. 

Amiodarone may elicit life-threatening side effects in addition to presenting substantial management difh-culties associated with its use. The oral formulation of amiodarone is indicated only for the treatment of life-threatening recurrent ventricular arrhythmias (e.g., recurrent ventricular hbrillation and/or recurrent hemo-dynamicaUy unstable ventricular tachycardia) that have not responded to other potentially effective antiarrhythmic drugs or when alternative interventions could not be tolerated. Despite its efficacy as an antiarrhythmic agent, there is no evidence from clinical trials that the use of amiodarone favorably affects survival. 

Withdrawal delirium (delirium tremens), which usually appears 1 to 4 days after abstinence and peaks at about 72 to 96 hours. The mortality rate may be as high as 15% if serious complicating medical problems are also present. Clinical signs and symptoms include profound confusion, illusions, delusions, vivid hallucinations, agitation, insomnia, and autonomic hyperactivity. Death results from infection, cardiac arrhythmias, fluid and electrolyte abnormalities, or suicide (e.g., in response to hallucinations, illusions, or delusions). 

Overdose is common amongst users (up to 22% of heavy users report losing consciousness). The desired euphoria and excitement turns to acute fear, with psychotic symptoms, convulsions, hypertension, haemorrhagic storke, tachycardia, arrhythmias, hyperthermia coronary vasospasm (sufficient to present as the acute coronary syndrome with chest pain and myocardial infarction) may occur, and acute left ventricular dysfunction. Treatment is chosen according to the clinical picture (and the known mode of action), from amongst, e.g. haloperidol (rather than chlorpromazine) for mental disturbance diazepam for convulsions a vasodilator, e.g. a calcium channel blocker, for hypertension glyceryl trinitrate for myocardial ischaemia (but not a p-... 

AK is a 65-year-old white woman with asthma, HTN, arrhythmias, and a history of sulfa allergy who presents to the eye clinic for a routine eye examination. lOP = 29 mm Hg OD and 31 mm Hg OS at 8 30 A.M. Ophthalmoscopy reveals cupping of optic disc OS > OD. A diagnosis of POAG is made. Which of the following is the best initial therapy for AK ... 

This review summarizes the available morphological evidence for coronary microembolization in patients who died from coronary artery disease, most notably from sudden death. Then the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes is detailed. Finally, the review presents the available clinical evidence for coronary microembolization in patients, highlights its key features - arrhythmias, contractile dysfunction, microinfarcts and reduced coronary reserve -, compares these features to those of the experimental model and addresses its prevention by mechanical protection devices and glycoprotein Ilb/IIIa antagonism. 

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