Potassium ventricular tachycardia

The serum potassium concentration was 2.6 mmol/1. Catecholaminergic polymorphous ventricular tachycardia was later diagnosed. 

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 She had no further dysrhythmias after haloperidol was withdrawn.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. 

In contrast, amiodarone and sotalol are effective in most supraventricular and ventricular tachycardias. Amiodarone displays electrophysiologic characteristics consistent with each type of antiarrhythmic drug, ft is a sodium channel blocker with relatively fast on-off kinetics, has nonselec-tive j8-blocking actions, blocks potassium channels, and has slight calcium antagonist activity. The impressive effectiveness and low proarrhythmic potential of amiodarone have challenged the notion that selective ion channel blockade is preferable. Sotalol is a potent inhibitor of outward... 

SOTALOL DIURETICS-CARBONIC ANHYDRASE INHIBITORS, LOOP DIURETICS, THIAZIDES t risk of ventricular arrhythmias, particularly torsades de pointes ventricular tachycardia, caused by sotalol Hypokalaemia, a side-effect of these diuretics, predisposes to arrhythmias during sotalol therapy Normalize potassium levels before starting sotalol in patients already taking these diuretics. When starting these diuretics in patients already taking sotalol, monitor potassium levels eveiy 4-6 weeks until stable... 

Reductions in the outward potassium ion flow prolong QT, a harbinger of Torsade de Pointes (TdP), and ventricular fibrillation (VF). Sodium channel blockers delay the entry of sodium ions, widening the QRS complex. In extreme cases, asystole ensues. A subsidiary event may be ventricular tachycardia degenerating into VF. 

A 28-year-old man with severe hjrpertension and end-stage renal disease was given two intravenous doses of labetalol 20 mg 1 hour apart for malignant hypertension. The serum potassium concentration before treatment was 6.2 mmol/1, but 8 hours after labetalol it rose to 9.9 mmol/1 and he developed left bundle branch block, ventricular tachycardia, and hjrpotension. He was given intravenous calcium gluconate, sodium bicarbonate, and lidocaine and reverted to sinus rhythm. The potassium... 

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. 

Procainamide, proprietary name Pronestyl, is used for therapy of PVCs, ventricular tachycardia, atrial fibrillation, and paroxysmal atrial tachycardia. Its mechanism of action is similar to that of quinidine in that it increases the threshold membrane potential by blocking potassium outflow, reducing excitability and contraction velocity in Purkinje s fibers and ventricular muscle. 

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. 

Arrhythmias are observed during the ischemic phase as well as at reperfusion in most of the animal models. In the first 2-10 min of ischemia, a burst of irregular ventricular tachycardia occurs but evolution to ventricular flbrillation is rare. These arrhythmias are mainly of a reentry nature. A second phase of arrhythmias is evident after 20-30 min of ischemia. The percentage of animals that show this delayed phase of arrhythmias is small and the evolution to ventricular flbrillation is more frequent and the animals can die. This phase is associated with a massive release of catecholamines, changes in calcium overload and an increase in extracellular potassium, reviewed by Carmeliet.55... 

Arrhythmias occur within a few seconds after reperfusion, following ischemic periods of 10-30 min long. They start by a spontaneous stimulus in the reperfused zone and change afterward in a re-entry multiple wavelet type of ventricular tachycardia (VT) or ventricular fibrillation (VF). Extremely short action potential, short refractory period and slow conduction are the main contributing factors. Increased hyperpolarization and elevated intracellular calcium that act negatively on gap conductance impair conduction. Unidirectional conduction is favored by the marked heterogeneity in extracellular potassium, action potential and refractory period. The extra stimulus is initiated in the reperfused zone, probably by early (EAD) and late (DAD) afterdepolirizations. 

Stable Strontium. Cardiovascular effects of strontium have been investigated by intravenous infusion studies in dogs. Infusions of strontium (as chloride or gluconate) averaging 172 mg strontium/kg under conditions of lowered potassium induced accelerated ventricular escape beats, ventricular tachycardia, or atrial fibrillation (Foster et al. 1977). High levels of strontium also induced oscillatory potentials and... 

Adenosine is a potent vasodilator that is produced endogenously. It mediates an outward flow of potassium from adenosine-sensitive potassium channels, stabilizing cardiac membranes. This results in a decrease in the duration of the atrial action potential, as well as negative chronotropic and inotropic actions. In addition, by stabilizing excitable tissue in the AV node, the drug effectively inhibits the conversion of paroxysmal atrial tachycardia to ventricular tachycardia, which could lead to fibrillation. 

Antiarrhythmic drugs that block potassium channels, such as sotalol and quinidine, can cause the polymorphic ventricular tachycardia known as torsades de pointes (see Chapter 34). The abnormal repolarization that leads to polymorphic ventricular tachycardia is potentiated by hypokalemia, and diuretics that produce potassium loss increase the risk of this drug-induced arrhythmia. 

All cardiac glycosides preparations have the potential to cause toxicity. Because the minimal toxic dose of the glycosides is only two- to threefold the therapeutic dose, intoxication is quite common. In mild to moderate toxicity, the common symptoms are anorexia, nausea and vomiting, muscular weakness, bradycardia, and ventricular premature contractions. The nausea is a result of excitation of the chemoreceptor trigger zone in the medulla. In severe toxicity, the common symptoms are blurred vision, disorientation, diarrhea, ventricular tachycardia, and AV block, which may progress into ventricular fibrillation. It generally is accepted that the toxicity of the cardiac glycosides results from inhibition of the Na /K -ATPase pump, which results in increased intracellular levels of Ca ". Hypokalemia (decreased potassium), which can be induced by coadministration of... 

APD, action potential duration ARVD/C, arrhythmogenic right ventricular dysplasia/cardiomyopathy CM, cardiomyocyte CPVT, catecholaminergic polymorphic ventricular tachycardia DAD, delayed after depolarizations DCM, dilated cardiomyopathy EAD, early after depolarization HCM, hypertrophic cardiomyopathy 1 rectifier potassium current 1, sodium current MEA, multielectrode array TNNT2, troponin T type 2. 

An 82-year-old man developed ventricular tachycardia and torsade de pointes after he took garenoxacin for pneumonia. He had hypokalemia (2.3 mmol/1) due to licorice and had also taken disopyramide, bicalutamide, and silodosin. After withdrawal of all drugs and the administration of spironolactone and oral potassium supplements, the hypokalemia and dysrhythmias resolved. 

Propafenone, l- 2-[2-hydroxy-3-(propylamino)propoxy]phenyl -3-phenylpropan-l-one, is a conunonly used sodium and potassium channel blocker for the treatment of ventricular tachycardia and atrial fibrillation [15]. Propafenone hydrochloride is a class IC antiarrhy tmic agent that shows structural similarity and activity related to p-adrenoly tic agents. The drug is efficacious in suppressing supraventricular and ventricular rhythm disorders [15] (Figure 14.12). 

---