Ventricular tachycardia magnesium

Magnesium sulfate Torsades des points refractory ventricular tachycardia Magnesium sulfate 1-2.5 g/min over 10 min for a 450 kg animal max. dose 25 g for 450 kg animal... 

Magnesium sulfate may be effective in terminating refractory ventricular tachyarrhythmias, particularly polymorphic ventricular tachycardia. DigitaUs-induced arrhythmias are more likely in the presence of magnesium deficiency. Magnesium sulfate can be administered orally, intramuscularly, or, preferably, intravenously,... 

A 41-year-old woman, with liver lacerations, rib fractures, and pneumothorax after a motor vehicle accident, was given haloperidol for agitation on day 7. During the first 24 hours she received a cumulative intravenous dose of 15 mg, 70 mg on day 2, 190 mg on day 3,160 mg on days 4 and 5, and 320 mg on day 6. An hour after the first dose of 80 mg on day 7, she had ventricular extra beats followed by 5-beat and 22-beat runs of ventricular tachycardia. The rhythm strips were consistent with polymorphous ventricular tachycardia or torsade de pointes and the QTC interval was 610 ms (normally under 450 in women). She received intravenous magnesium sulfate 2 g. Concurrent medications included enoxaparin, famotidine, magnesium hydroxide, ampicillin/sulbactam, nystatin suspension, midazolam, and 0.45% saline with 20 mmol/1 of potassium chloride. She had no further dysrhythmias after haloperidol was withdrawn. Eight days after the episode of torsade de pointes she had a QTC interval of 426 ms. 

A 92-year-old woman developed sudden runs of ventricular tachycardia, a few days after she started to take cilostazol because of subacute leg ischemia. She was known to have atrial fibrillation and intraventricular conduction delay. The runs did not respond to empirical magnesium therapy but subsided shortly after withdrawal of cilostazol. 

A 65-year-old woman, who had had normal preoperative serum electrolytes and a normal QT interval with sinus rhythm, received hydroxyzine and atropine premedication followed by thiopental and vecuronium for anesthetic induction. Endotracheal intubation was difficult and precipitated atrial fibrillation, which was refractory to disopyramide 100 mg. Anesthesia was then maintained with sevoflurane 2% and nitrous oxide 50%. Ten minutes later ventricular tachycardia ensued, refractory to intravenous lidocaine, disopyramide, and magnesium. DC cardioversion resulted in a change to a supraventricular tachycardia, which then deteriorated to torsade de pointes. External cardiac massage and further DC cardioversion were initially unsuccessful, but the cardiac rhythm reverted to atrial fibrillation 10 minutes after the sevoflurane was switched off. Two weeks later she had her operation under combined epidural and general anesthesia, with no changes in cardiac rhythm. 

Two other patients had been immobilized and treated with magnesium and ritodrine for several weeks. Preoperative creatine kinase activities were 2120 IU/1 and 630 IU/1. In both cases, serum potassium increased by 2.3 mmol/1 within 2-3 minutes after suxamethonium injection (from 4.0 to 6.3 mmol/1 and from 4.9 to 7.2 mmol/1). This was accompanied by tail peaked T waves and a short period of ventricular tachycardia in one case and by tall peaked T waves and widened QRS complexes in the other. 

Ventricular tachycardia R Lidocaine infusion 20-50 (ig/min per kg or 0.25-0.5 mg/kg slow i.v. every lOmin magnesium sulfate 1-2.5g/min over 10 min for a 450 kg horse, maximum dose 25g/450kg... 

Figure 12.2 Electrocardiograms from a horse undergoing treatment for atrial fibrillation, (a, b) Base-apex (a) and modified base-apex (b) electrocardiograms after treatment with quinidine sulfate (330mg/kg). Ventricular tachycardia, (torsades de pointes) occurred after 40 h. (c) The horse was treated with five bolus doses of magnesium sulfate, together with intravenous propanoloi, which resulted in conversion to normal sinus rhythm with QRS prolongation, (d) Twenty-four hours after conversion, the electrocardiogram showed normal sinus rhythm without QRS prolongation.

Figure 12.4 Base-apex electrocardiograms from an anaesthetized horse, with endotoxemia caused by a strangulating intestinal lesion, (a) The cardiac rhythm was converted from ventricular tachycardia to the bigeminal rhythm by administration of two bolus doses of lidocaine. Although ventricular complexes (V) are preceeded by p waves (p) the p-r distance is shorter than the sinus complexes (S). (b) Magnesium sulfate administered intravenously resulted in conversion to sinus rhythm.

In addition to drugs in these classes, others may be used for certain arrhythmias. Digoxin may be used for treatment of atrial fibrillation, adrenaline for asystolic cardiac arrest, atropine for sinus bradycardia, methacholine (rarely) for supraventricular tachycardia, magnesium salts for ventricular arrhythmias, and calcium salts for ventricular arrhythmia due to hyperkalaemia. 

One of the more serious complications of magnesium deficiency is cardiac arrhythmias. Premature atrial complexes, atrial tachycardia and fibrillation, ventricular premature complexes, ventricular tachycardia, and ventricular fibrillation may be associated with magnesium deficiency. These effects maybe partly caused by the hypokalemia, renal wasting, and intracellular depletion of potassium caused by hypomagnesemia. 

Torsade de pointes polymorphous ventricular tachycardia associated with QT prolongation resulting from sotalol poisoning can be treated with isoproterenol infusion, magnesium, or overdrive pacing (see p 14). Correction of hypokalemia may also be useful. 

The physiological actions of magnesium include a direct membrane stabilizing effect by reducing early after depolcirizations and increasing the threshold stimulus required to provoke either ventricular fibrillation or ventricular tachycardia, but magnesium sulfate has not previously been used to treat persistent wide QRS complex and hemodynamic instability. 

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