QRS interval prolongation caused

Adverse/Toxic Antacid, laxative None significant. Systemic May produce prolonged PR interval, widening of QRS intervals may cause loss of deep tendon reflexes, heart block, respiratory paralysis, and cardiac arrest. Antidote 10-20 ml 10% calcium gluconate (5-10 mEq of calcium)... 

A. Assessment. Examples of drugs and toxins causing QRS interval prolongation are listed in Table 1-5. 

Cardiac effects Acute, usually reversible, EGG changes (PR and QTc prolongation QRS widening) caused by dolasetron have been observed. Dolasetron appears to prolong depolarization and, to a lesser extent, repolarization time. The magnitude and frequency of the EGG changes increased with dose. These EGG interval prolongations usually returned to baseline within 6 to 8 hours but in some patients were present at 24-hour follow up. 

Flecainide increases the PR, QRS, and to a lesser extent, QTc intervals. The rate of ventricular repolarization is not affected, and the QT interval prolongation is caused by the increase in the QRS duration. 

Overdose may increase QRS duration, prolong QT interval, cause conduction disturbances, reduce myocardial contractility, and cause hypotension. 

Cibenzoline prolongs the PR interval, the QRS interval, and the QT interval (4—7). It also prolongs the AH and HV intervals (5,8) and shortens the sinus cycle length (5-8). Because of these effects it can cause dysrhythmias (4,6,7,9). 

Overdoses of tricyclic antidepressants can cause arrhythmias, such as prolonged QRS intervals and ventricular dysrhythmias, coma, respiratory depression, and seizures and are treated with symptomatic care and intravenous sodium bicarbonate. 

Doses of chloroquine used for oral therapy of the acute malarial attack may cause GI upset, headache, visual disturbances, and urticaria. Pruritus also occurs, most commonly among dark-skinned persons. Prolonged medication with suppressive doses occasionally causes side effects such as headache, blurring of vision, diplopia, confusion, convulsions, lichenoid skin eruptions, bleaching of hair, widening of the QRS interval, and T-wave abnormalities. These complications usually disappear soon rffter the drug is withheld. Rare instances of hemolysis and blood dyscrasias have been reported. Chloroquine may cause discoloration of nail beds and mucous membranes. 

B. Severe intoxication may cause coma, seizures, and respiratory arrest. The ECG may show QTc interval prolongation and occasionally QRS prolongation (particularly with thioridazine [Mellaril]). Hypothennia or hyperthennia may occur. Clozapine can cause a prolong confusional state and rarely cardiac toxicity. 

A. Ataxia, nystagmus, ophthalmoplegia, movement disorders (dyskinesia, dystonia), mydriasis, and sinus tachycardia are common with mild to moderate overdose. With more serious intoxication, myoclonus, seizures (including status epilepticus), hyperthermia, coma, and respiratory arrest may occur. Atrioventricular (AV) block and bradycardia have been reported, particularly in the elderly. Based on Its structure similarity to tricyclic antidepressants, carbamazepine may cause QRS and QT interval prolongation and myocardial depression however, in case reports of overdose, QRS widening rarely exceeds 100-120 msec and Is usually transient. 

B. Severe chloroquine overdose may cause convulsions, coma, shock, and respiratory or cardiac arrest. Quinidine-like cardiotoxicity may be seen, including sinoatrial arrest, depressed myocardial contractility, QRS or QT interval prolongation, heart block, and ventricular arrhythmias. Severe hypokalemia sometimes occurs and may contribute to arrhythmias. 

A. Cardiotoxic effects of the type la agents include sinus bradycardia sinus node arrest or asystole PR, QRS, or QT interval prolongation sinus tachycardia (caused by anticholinergic effects) polymorphous ventricular tachycardia (torsade de pointes) and depressed myocardial contractility, which, along with alpha-adrenergic or ganglionic blockade, may result in hypotension and occasionally pulmonary edema. 

B. Severe intoxication may cause ataxia, obtundation, convulsions, coma, and respiratory arrest. With massive intoxication, quinidine-like cardiotoxicity (hypotension, QRS and QT interval prolongation, AV block, and ventricular arrhythmias) may be fatal. 

C. Cardiotoxicity with impaired ventricular depolarization (as evidenced by a prolonged QRS interval) caused by tricyclic antidepressants, type la or type Ic antiarrhythmics, and other membrane-depressant dmgs (see Table 11-7, p 88). Note Not effective for dysrhythmias associated with abnormal repolarization (prolonged QT interval and torsade de pointes). 

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