Cardiac dysrhythmias intravenous

Diazoxide is a potassium channel opener with a rapid antihypertensive action after intravenous administration. Diazoxide causes hyperglycaemia which may underlie side-effects such as nausea and vomiting, cardiac dysrhythmia and ketosis. Diazoxide was used occasionally in the management of hypertensive emergencies, but it is now largely abandoned for this indication. Diazoxide is an alternative for glucagons in patients with hypogycaemia. 

Diazepam produces less sedation in cigarette smokers, and higher (not lower, as stated in SEDA-20) doses may be required for the same sedative or anxiolytic effect. Owing in part to its continued widespread use, several unusual adverse effects of diazepam continue to be reported. These include cases of urinary retention and compartment syndrome, which are not explicable by its pharmacology. On the other hand, accumulation of diazepam and attendant complications of obtundation and respiratory depression may be understood in terms of its long half-life, particularly in elderly people and medically ill patients. Caution about the intravenous use of diazepam comes from a study that showed cardiac dysrhythmias (mainly ventricular extra beats) in a quarter of oral surgery patients midazolam and lorazepam were much safer (1). 

Roelofse JA, van der Bijl P. Cardiac dysrhythmias associated with intravenous lorazepam, diazepam, and midazolam during oral surgery. J Oral Maxillofac Surg 1994 52(3) 247-50. 

Cardiovascular effects include tachycardia, hypertension, and increased cardiac irritability large intravenous doses can cause cardiac failure. Cardiac dysrhythmias have been ascribed to a direct toxic effect of cocaine and a secondary sensitization of ventricular tissue to catecholamines (17), along with slowed cardiac conduction secondary to local anesthetic effects. Myocardial infarction has increased as a complication of cocaine abuse (7,8). Dilated cardiomyopathies, with subsequent recurrent myocardial infarction, have been associated with long-term use of cocaine, raising the possibility of chronic effects on the heart (18). Many victims have evidence of pre-existing fixed coronary artery disease precipitated by cocaine (SEDA-9, 35) (19-21). However, myocardial infarction has been noted even in young intranasal users with no evidence of coronary disease (22), defined by autopsy or angiography (23,24). If applied to mucous membranes, cocaine causes local vasoconstriction, and, with chronic use, necrosis. 

Adenosine is contraindicated in patients with aberrant conduction pathways, because it can cause cardiac dysrhythmias. Supraventricular dysrhythmias occurred in three children with Wolff-Parkinson-White syndrome who were given intravenous adenosine (22). 

There have been reports of cardiac dysrhythmias in patients given either an intravenous infusion of adenosine or a single bolus dose. 

Ajmaline and its derivatives, prajmalium bitartrate (rINN A-propylajmaline), lorajmine (rINN chloroacetylajma-line), detajmium bitartrate (rINN), and diethylaminohy-droxypropylajmaline, are Rauwolfia alkaloids. Their use is restricted by serious adverse effects, such as neutropenia and cardiac dysrhythmias, which have been reviewed (1). Other adverse effects include dizziness, headache, and a sensation of warmth after intravenous injection. 

A few studies have also reported the effects and adverse effects of intravenous amiodarone in patients with atrial fibrillation. Of 67 patients with atrial fibrillation, of whom 33 received amiodarone and 34 received placebo, conversion to sinus rhythm occurred in 16 of the patients who received amiodarone and in none of those who received placebo (242). In five patients the systolic blood pressure fell significantly during the first trial of intravenous drug administration. There were no cardiac dysrhythmias. Thrombophlebitis occurred in 12 patients who received amiodarone. 

Cardiac dysrhythmias induced by anticonvulsants are rare and occur mainly in patients other than those known to be at high risk of sudden death (14). Phenytoin has been rarely associated with bradydysrhythmias, almost exclusively after intravenous dosing, and some of these have been fatal. Hypotension can also complicate intravenous phenytoin. Carbamazepine can depress cardiac conduction, mostly in elderly or otherwise predisposed patients. Third-degree atrioventricular block occurred in one patient with pre-existing right bnndle branch block treated with topiramate, but a cause-and-effect relation was uncertain (SEDA-21, 76). 

Hyperkalemia carries a poor prognosis and is usually an indication for antidigoxin antibody. The suggestion that intravenous calcium should be used to treat the hjrper-kalemia that can occur in digitalis intoxication (173) has been challenged, on the grounds that it can increase the risk of cardiac dysrhythmias in such cases (174). 

In an FDA database analysis, 346 cases of cardiac dysrhythmias associated with erythromycin were identified. There was a preponderance of women, as there was among those with life-threatening ventricular dysrhythmias and deaths after intravenous erythromycin lactobionate. A sex difference in cardiac repolarization response to erythromycin is a potential contributing factor, since in an in vitro experiment on rabbit hearts, erythromycin caused significantly greater QT prolongation in female than in male hearts (7). 

Most parenteral iron is administered intramuscularly, but intravenous injections have enjoyed a wave of popularity for no very good medical reason it seems particularly likely to precipitate acute allergic or anaphylactic reactions in sensitive individuals, sometimes involving cardiac dysrhythmias, hypotension, circulatory collapse, and pulmonary edema. 

The adverse effects of high-dose intravenous melphalan have been reviewed (2). Two patients who received less than 100 mg/m recovered from marrow aplasia within 3 weeks without major complications. A third patient died 6 days after injection of 290 mg/m, probably because of a cardiac dysrhythmia before complete marrow failure had become established. After intravenous administration of more than 125 mg/m, gastrointestinal adverse effects, such as hemorrhagic diarrhea, or bowel perforation, can occur. These, together with reduced ADH secretion and electrolyte disturbances are the predominant clinical problems and the reasons for early death before the occurrence of infectious or bleeding complications from prolonged marrow aplasia. 

Olprinone is an inhibitor of phosphodiesterase type III, and has a positive inotropic effect. It is given intravenously and is mostly eliminated by the kidneys. Its pharmacological effects have been reviewed (1). Its major adverse effects are cardiac dysrhythmias and thrombocytopenia, the latter with a reported incidence of 0.43%. 

In a prospective randomized, double-blind, placebo-controlled study in 100 patients scheduled for elective orthopedic surgery and presenting with pruritus induced by epidural or intrathecal morphine, intravenous ondansetron 8 mg was effective in 70% of cases and placebo in 30% (23). Ondansetron was well tolerated, did not change the degree of analgesia, and was not associated with adverse effects usually associated with ondansetron, such as headache, abdominal pain, and cardiac dysrhythmias. 

For acute anaphylaxis, immediate treatment is essential, with adrenaline followed by intravenous histamine Hi receptor antagonists, glucocorticoids, fluids, and electrolytes. In view of the frequency of cardiac dysrhythmias and conduction disturbances in patients with anaphylactic shock, they should immediately be monitored (198,199). 

Intravenous phenytoin can cause cardiac dysrhythmias, hypotension, and potentially fatal cardiovascular collapse, especially if the highest recommended infusion rate (50 mg/minute or 1 mg/kg/minute in children) is exceeded. One case of hypersensitivity myocarditis was probably initiated by phenytoin, although carbamazepine may have contributed (SED-13,142) (3). 

A 75-year-old woman received ropivacaine 160 mg intravenously through an epidural catheter (10). After completion of the injection, she suddenly became unresponsive and had a generalized tonic-clonic convulsion accompanied by a sinus tachycardia of 120/minute but no other cardiac dysrhythmias. 

Sulmazole commonly causes adverse gastrointestinal effects dose-related anorexia, nausea, and vomiting have been reported in about 50% of patients given an intravenous infusion (1,2) and also after single oral doses (3). Cardiac dysrhythmias, mostly ventricular, have been reported occasionally with sulmazole (4). Other reported adverse effects in small numbers of patients include headache (1), temporary visual disturbances (2,5), discoloration of the urine (attributed to a metabolite) (2,6), and a small reduction in platelet count (1). 

Quinine rarely causes cardiovascular complications unless target plasma concentrations are exceeded. QTc prolongation is mild and does not appear to be affected by concurrent mefloquine treatment. However, severe hypotension is predictable when quinine is administered too rapidly intravenously. Acute overdosage also may cause serious and even fatal cardiac dysrhythmias. Quinidine is even more cardiotoxic than quinine. Cardiac monitoring of patients on intravenous quinidine is advisable where possible. 

C. Hypotension, bradycardia, syncope, and cardiac dysrhythmias caused by rapid intravenous administration. 

Cardiotoxicity and nephrotoxicity have occurred in patients having phenol chemical peels [328,338]. In a study of 181 patients undergoing a phenol chemical peel with no more than 3 mL applied, 12 developed cardiac dysrhythmias [338]. These dysrhythmias consisted of a few ventricular extrasystoles in 9 patients, bigeminy in 1 patient, and polytropic extrasystoles in 2 patients. In 4 of these 12 patients, the dysrhythmia was self-limited (resolved spontaneously) and in the other 8 patients treatment with 100 mg of intravenous lidocaine controlled the dysrhythmias. No patients developed hanodynamic instability [338]. 

In a retrospective analysis of 36 patients who received intravenous levetiracetam for refractory status epilepticus [209 ] a median dose of 3000 mg/day (range 1000-9000) was used as a loading bolus or by continuous pump infusion. Status epilepticus was terminated in 69% of patients. None had cardiac dysrhythmias or significantly reduced blood pressure, or required an increase in the dose of catecholamines. Two patients had nausea and vomiting during levetiracetam loading, leading to aspiration pneumonia in one. 

Phenytoin and valproate Phenytoin ( = 25) by infusion and intravenous valproate ( = 49) have been compared in status epilepticus or acute repetitive seizures in 74 patients [241 ]. There were no adverse effects with valproate but three patients who received phenytoin had adverse effects cardiac dysrhythmias, vertigo, and hyponatremia). 

In a comparison of intravenous valproate n = 49) and phenytoin infusion n = 25) in 74 patients with status epilepticus or acute repetitive seizures, the two drugs were equally effective but there were adverse effects in none of those given valproate and in three of those who were given phenytoin (cardiac dysrhythmia, vertigo, and hyponatremia) [241 ]. 

Ajmaline occasionally causes cardiac dysrh5dhmias (SEDA-17, 219). Of 1995 patients who were given ajmaline 1 mg/kg intravenously during an electrophysiological study, 63 developed a supraventricular tachydysrhythmia (atrial flutter, fibrillation, or tachycardia), and seven an atrioventricular re-entrant tachycardia (2). Those most at risk were older patients, those with underlying cardiac disease, and those with a history of dysrhythmias or sinus node dysfunction. 

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