Dysrhythmia

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). 

Cardiac arrhythmias or dysrhythmias are disturbances of the normal regular rhythm which may be caused by an abnormality in the site of impulse generation, its rate or regularity, or its propagation or conduction (1,2). The more commonly encountered cardiac arrhythmias are... 

The amide local anaesthetic lidocaine may also be used as an antianhythmic for ventricular tachycardia and exra-systoles after injection into the blood circulation. Drugs with high lipid solubility such as bupivacaine cannot be used for these purposes because their prolonged binding to the channel may induce dysrhythmias or asystolic heart failure [3]. Systemically applied lidocaine has also been used successfully in some cases of neuropathic pain syndromes [4]. Here, electrical activity in the peripheral nervous system is reduced by used-dependent but incomplete sodium channel blockade. 

With regard to epinephrines potential adverse cardiac effects, it is important to remember that in anaphylaxis, the heart is a target organ. Mast cells located between myocardial fibers, in perivascular tissue, and in the arterial intima are activated through IgE and other mechanisms to release chemical mediators of inflammation, including histamine, leukotriene C4, and prostaglandin D2. Coronary artery spasm, myocardial injury, and cardiac dysrhythmias have been documented in some patients before epinephrine has been injected for treatment of anaphylaxis, as well as in patients with anaphylaxis who have not been treated with epinephrine [11, 12]. 

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. 

Propofol infusion syndrome has been described and may result in severe metabolic acidosis, cardiac dysrhythmias, cardiovascular collapse, rhabdomyolysis, and death. The risk may be increased with concomitant catecholamine infusions or when the dose exceeds... 

Continuous cardiovascular and hemodynamic monitoring should be used for significant pH disturbances, as the most serious sequelae of acid-base disorders include electrolyte abnormalities, cardiac dysrhythmias, and systemic hypotension. 

Sympathetic (sympatholytic) Heart Sinus node Atrioventricular (AV node) Slowing Increased refractory period Bradycardia Dysrhythmias, conduction block... 

Warner MA, Harper JV (1985) Cardiac dysrhythmias associated with chemical peeling with phenol. Anesthesiology 62 366-7... 

Consider tracheal intubation in cases of respiratory compromise. Treat patients who have bronchospasm with aerosolized bronchodilators. Use these and all catecholamines with caution because of the enhanced risk of cardiac dysrhythmias after exposure to some chemicals. When bronchodilators are needed, the lowest effective dose should be given and cardiac rhythm should be monitored. After decontamination, patients who are comatose,... 

Cardiac failure (dysrhythmias, arrest, cardiogenic shock)... 

Lorazepam is currently considered the BZ of choice. It takes longer to reach peak brain levels than diazepam but has a longer duration of action (12 to 24 hours). Patients chronically on BZs may require larger doses. The administration rate of diazepam and lorazepam should not exceed 5 and 2 mg/min, respectively, because the propylene glycol in the vehicle can cause dysrhythmia and hypotension. 

Prolonged Q-T interval syndromes and dysrhythmias (potassium channel variants HERG, KvLQTl,KCNE2 late-opening sodium channels, with specific blockers)... 

Convulsions Convulsions and Tremors Transient, self-sustaining electrical dysrhythmias which have a tendency to recur. Convulsions are generally associated with a finite period of unconsciousness and have a muscular involvement manifested as disorganized limb movements. 

Cavero, I., Mestre, M., Guillon, J.M. and Crumb, W. (2000) Drugs that prolong QT interval as an unwanted effect assessing their likelihood of inducing hazardous cardiac dysrhythmias. Expert Opinion on Pharmacotherapy, 1, 947-973. 

Grabowski CT. 1983b. The electrocardiogram of fetal and newborn rats and dysrhythmias induced by toxic exposure. In Abnormal functional development of the heart, lungs and kidneys Approches to functional teratology. New York, NY Alan R Liss, Inc., 185-206. 

Note that the x axis is logarithmic to allow a wide range of frequencies to be shown. The y axis is the current threshold at which adverse physiological events (dysrhythmias etc.) may occur. The highest risk of an adverse event occurs at current frequencies of around 50 Hz, which is the UK mains frequency. At diathermy frequencies, the threshold for an adverse event is massively raised. 

Cardiovascular Effects. In a recent report on the clinical treatment of phenol poisoning, Langford et al. (1998) provide a summary of a case report in which a woman accidentally consumed an ounce of 89% phenol which had been mistakenly been given to her in preparation for an in-office procedure. Her immediate reaction upon consuming the phenol was to clutch her throat and collapse, and within 30 minutes she was comatose and had gone into respiratory arrest. Treatment was initiated with an endotracheal intubation. Ventilation with a bag and mask led to the detection of a lamp oil odor. Within an hour she developed ventricular tachycardia which responded to cardioversion however, she subsequently developed (in the first 24 hours) supraventricular and ventricular dysrhythmias, metabolic acidosis, and experienced a grand mal seizure. After a 15-day hospital stay, she was completely recovered with no evidence of impaired motility or compromised gastrointestinal or cardiovascular systems. 

Morrison JE, Matthews D, Washington R, et al. 1991. Phenol motor point blocks in children Plasma concentrations and cardiac dysrhythmias. Anesthesiology 75 359-362. 

Associations have also been made between areca and cardiovascular disease, diabetes, and asthma (Winstock et al. in press). Areca may affect cardiovascular disease by increasing homocysteine concentrations and/or through areca copper concentrations and interaction with the lysyl oxidase enzyme (Trivedy et al. 1999). Areca chewing has been associated with cardiac dysrhythmias in a few cases and a case of myocardial infarction was temporally associated with areca use (Hung and Deng 1998 Chiang etal. 1998). 

Wilton LV, Heeley El, Pickering RM, et al. Comparative study of mortahty rates and cardiac dysrhythmias in post-marketing surveillance studies of sertindole and two other atypical antipsychotic drugs, risperidone and olanzapine. J Psychophar-macol 2001 15 120-6. 

In humans, early symptoms of intoxication may include headache, dizziness, nausea, vomiting, malaise, and myoclonic jerks of the limbs clonic and tonic convulsions and sometimes coma follow and may occur without the premonitory symptoms. A suicidal person who ingested 25.6mg/kg developed convulsions within 20 minutes that persisted recurrently until large amounts of barbiturates had been administered. Hematuria and azotemia occurred the day after ingestion and continued for 18 days. Liver function studies were within normal limits except for an elevated icterus index an electroencephalogram revealed generalized cerebral dysrhythmia, which returned to normal after 5 months. ... 

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