Potassium ventricular fibrillation

Proarrhythmia refers to development of a significant new arrhythmia (such as VT, ventricular fibrillation [VF], or TdP) or worsening of an existing arrhythmia. Proarrhythmia results from the same mechanisms that cause other arrhythmias or from an alteration in the underlying substrate due to the antiarrhythmic agent. TdP is a rapid form of polymorphic VT associated with evidence of delayed ventricular repolarization due to blockade of potassium conductance. TdP may be hereditary or acquired. Acquired forms are associated with many clinical conditions and drugs, especially type la and type III IKr blockers. 

Subcutaneous administration of -hexanc at 143 mg/kg/day for 30 days has been reported to decrease the threshold for ventricular fibrillation in perfused hearts from male Wistar rats (Khedun et al. 1996). Myocardial magnesium and potassium levels were reduced in treated rats. When these levels were corrected by supplementation, the ventricular fibrillation potential was still reduced. Histological alterations (disordered myocardial Z-bands) were also observed in exposed rats. 

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. 

Cyanide primarily blocks oxidative phosphorylation and ATP production. Every heart beat uses up to 2% of the energy available to the cell. Arsenic primarily causes long QT (LQT) interval on the ECG, by blocking the fast potassium current, an action that is a precursor to ventricular fibrillation. 

The most important complication of overdosage of digitalis in all age groups is disturbance of cardiac conduction, but in addition any dysrhythmia can occur. Death can result from asystole or ventricular fibrillation. Hyperkalemia is common, and the higher the plasma potassium concentration the poorer the prognosis (157). 

Quigley PJ, Maurer BJ. Ventricular fibrillation during coronary angiography association with potassium-containing glyceryl trinitrate. Am J Cardiol 1985 56(1) 191. 

III Potassium channel blocking Amiodarone Bretylium Resistant ventricular fibrillation... 

Ingestion of toxic doses of barium affects the muscles, especially the heart. Barium has a digitalis-type effect on the heart. Ventricular fibrillation and slowed pulse rate are noted. This may be related to barium s tendency to displace potassium the resulting potassium deficiency causes muscle weakness. 

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 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. 

Estrogens induced cardioprotection seems to involve the ERa receptor. In fact, hearts from estrogens receptor-alpha knock out mice were sensitive to ischemia and reperfusion injury". Furthermore, estrogens receptor modulators which lack some of the estrogens side effects are shown to be cardioprotective raloxifene limited infarct size and incidence of ventricular fibrillation in an in vivo canine model of coronary occlusion and reperfusion. This effect was attenuated by the inhibition of NO synthase (NOS) or calcium activated potassium channels and completely abolished by both blocking NOS and Ca2+-activated K+ channels. Ischemia and reperfusion induced p38 MAPK activation was also attenuated in raloxifene treated hearts.12... 

Higham PD, Adams PC, Murray A, Campbell RW. Plasma potassium, serum magnesium and ventricular fibrillation A prospective smdy. Q J Med 1993 86 609-617. 

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... 

Hyperkalemia (serum potassium > 5 mEq/L) produces muscle weakness and interferes with normal cardiac conduction. Peaked T waves and prolonged PR Intervals are the earliest signs of cardiotoxicity. Critical hyperkalemia produces widened QRS inten/als, AV block, ventricular fibrillation, and cardiac arrest (see Figure 1-5). 

A 63-year-old woman with a non-ischemic dilated cardiomyopathy possibly caused by alcohol had paroxysmal atrial fibrillation for which she took sotalol 80 mg bd. She took oseltamivir 75 mg bd for presumed influenza and after 4 days developed ventricular fibrillation. Sinus rhythm was restored with multiple shocks and intravenous magnesium. The serum potassium was normal at 4.1 mmol/1. Electrocardiography showed a QT, interval of 521 ms. The QT interval gradually shortened after withdrawal of both sotalol and oseltamivir. 

In surgical practice, hyperventilation occurs if a very ill patient on life support including mechanical ventilation is inadvertently overventilated. The dangers of severe alkalosis caused by hyperventilation are related to the associated potassium depletion, the mechanism of which is described in Chapter 3. This hypokalaemia (low concentration of potassium in the blood) results in ventricular arrhythmia and death due to ventricular fibrillation. 

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