Often asked: Can Hypocalcemia Cause Torsades?

Hypocalcemia is a common biochemical abnormality that can range in severity from asymptomatic in mild cases to life threatening crisis [1] in others. It is a very rare cause of torsades de pointes [2].

Can hypercalcemia cause torsades?

Ventricular arrhythmias, including ventricular fibrillation, have been described in patients with hypercalcaemia due to hyperparathyroidism. What does this add? Torsade de pointes can occur as a complication of hypercalcaemia in patients with multiple myeloma.

How hypocalcemia causes QT prolongation?

Hypocalcaemia is a recognised cause of QT prolongation via prolongation of the plateau phase of the cardiac action potential. This causes calcium ion channels to remain open for a longer period, allowing a late calcium inflow and the formation of early after-depolarisations.

What is the most common cause of Torsades de Pointes?

Common causes for torsades de pointes include drug-induced QT prolongation and less often diarrhea, low serum magnesium, and low serum potassium or congenital long QT syndrome. It can be seen in malnourished individuals and chronic alcoholics, due to a deficiency in potassium and/or magnesium.

What electrolyte causes Torsades de Pointes?

The electrolyte disturbances that have been reported to precipitate torsade include hypokalemia and hypomagnesemia. These disturbances cause a delay in phase III (ie, reprolongation) and form the substrate for emergence of the dysrhythmia.

How does hypocalcemia effect the heart?

THE BEST KNOWN clinical effect on the heart of hypocalcemia is prolongation of the QT interval, ie, prolongation of electrical systole. Only recently has cardiac arrhythmia been reported as a clinical manifestation of hypocalcemia.

Does hypocalcemia cause bradycardia?

In conclusion, we present mechanistic in silico and empirical in vivo data supporting the so far neglected but experimentally testable and potentially important mechanism of hypocalcemia-induced bradycardia and asystole, potentially responsible for the highly increased and so far unexplained risk of sudden cardiac

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How does hypercalcemia affect QT interval?

They found that hypercalcemia was associated with prolongation of the PR and QRS intervals (by 12 and 7 milliseconds, respectively) but shortening (by 24 milliseconds) of the QT interval. Interestingly, they found an increased incidence of J waves among patients with hypercalcemia (30% vs. 9%, P < 0.001).

Does hypocalcemia increase heart rate?

Treatment of hypocalcemia in the normotensive but moderately ill neonate has been associated with an increase in blood pressure and heart rate.

Is amiodarone contraindicated in torsades?

Do not use amiodarone, procainamide, beta-blockers, or most other antiarrhythmics. Most of these will stretch out the QT interval even further! Beta-blockers will slow down the heart rate, increasing the risk of torsades.

Why does QT prolongation cause torsades?

The long QT interval responsible for torsades de pointes can be congenital or drug-induced. QT-interval prolongation predisposes to arrhythmia by prolonging repolarization, which induces early after-depolarizations and spatial dispersion of refractoriness.

Do you defib torsades?

Pulseless torsades should be defibrillated. Intravenous magnesium is the first-line pharmacologic therapy in Torsades de Pointes. Magnesium has been shown to stabilize the cardiac membrane, though the exact mechanism is unknown. The recommended initial dose of magnesium is a slow 2 g IV push.

What drug causes torsades Depointes?

Antimicrobials. Macrolides (erythromycin, clarithromycin), fluoroquinolones, antifungals, and antimalarials have been implicated in predisposing to TdP as a result of QT prolongation.

Which electrolyte is responsible for carbohydrate metabolism?

Potassium is also important in carbohydrate metabolism and electron transport since a number of the enzymes in these metabolic pathways are potassium dependent.

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Why is magnesium given for torsades?

Magnesium is the drug of choice for suppressing early afterdepolarizations (EADs) and terminating the arrhythmia. Magnesium achieves this by decreasing the influx of calcium, thus lowering the amplitude of EADs. Magnesium can be given at 1-2 g IV initially in 30-60 seconds, which then can be repeated in 5-15 minutes.

Which electrolyte is inversely related to calcium?

Phosphorus and calcium have an inverse relationship: When the levels of one are increased, the levels of the other usually are decreased.