Saxappeal1

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Bump, I'd like to know too.
 

Phloston

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Anyone know the mechanism??
Bump, I'd like to know too.
This is all UpToDate has to say:

(btw a good point to be aware of here is that hypoMg causes hypoCa [high-yield] but also causes hypoK; most students remember this point about Ca but not K)

"
OTHER CAUSES OF TdP

Hypokalemia, hypomagnesemia, and hypocalcemia — Hypokalemia and hypomagnesemia can predispose to TdP. These disorders can occur together since hypomagnesemia directly causes hypokalemia. Hypocalcemia, alone or induced by hypomagnesemia, is a less common cause [78-80]. (See "Clinical manifestations of magnesium depletion", section on 'Hypokalemia' and "Clinical manifestations of magnesium depletion", section on 'Calcium metabolism'.)

The risk for developing TdP in the presence of hypokalemia and/or hypomagnesemia is greatest in patients taking antiarrhythmic drugs [35,42,81-83]. This was illustrated in a report of 32 such patients [82]. Serum drug concentrations were in the therapeutic range in 22 of 26 patients in whom they were measured. However, 20 patients had, either alone or in combination, baseline prolongation of the QT interval, hypokalemia, or hypomagnesemia. In another series of 92 patients with drug-induced LQTS, 27 percent had hypokalemia or hypomagnesemia [35]. Similar findings were noted in a report of 24 patients with quinidine-induced LQTS: the serum quinidine concentration was well within the therapeutic range in one-half of patients and the serum potassium concentration was below 4.0 meq/L in 13 [42].

As noted above, virtually all of the drugs that produce LQTS act by blocking the IKr current mediated by the potassium channel encoded by the KCNH2 gene [12-25,28]. The increase in risk with hypokalemia may be related to enhanced drug blockade of IKr [14]. The risk of hypokalemia itself may also be related to decreased IKr activity.

Further support for the importance of hypomagnesemia is the beneficial effect of magnesium administration in the acute therapy of TdP. (See 'Management' below.)

"

Then the part about 'see management below' is:

"

Intravenous magnesium sulfate is first-line therapy, being highly effective for both the treatment and prevention of recurrence of long QT-related ventricular ectopic beats or TdP [5,6,95]. The benefit occurs without shortening of the QT interval and is seen even in patients with normal serum magnesium concentrations at baseline.

The standard regimen for an adult consists of a 2 gram intravenous bolus of magnesium sulfate (4 mL of 50% solution [ie, 500 mg/mL] mixed with D5W to a total volume of 10 mL or more) [95,96]. The rate of magnesium infusion depends on the clinical situation. In patients with pulseless cardiac arrest, infusion occurs over one to two minutes; in patients without cardiac arrest, infusion should occur over 15 minutes as rapid magnesium infusion may be associated with hypotension and asystole. Some patients also receive a continuous infusion at a rate of 3 to 20 mg/min. The bolus dose in children is 25 to 50 mg/kg; there are no published data on intravenous maintenance dosing in children.

"
 

Saxappeal1

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I know this may seem like a stupid question Phloston, but why does hypomagnesemia cause hypok?
 

Phloston

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I know this may seem like a stupid question Phloston, but why does hypomagnesemia cause hypok?
Magnesium apparently plays an inhibitory role on renal potassium secretion by deactivating ROMK channels. Mg below basal levels relieves this inhibition. So in short, low magnesium promotes renal potassium wasting.
 
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ftp902

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Thank you for the response @Phloston!
Btw, how does hypomagnesemia exactly cause hypocalcemia?
I looked it up and it seems like hypomagnesmia causes less synthesis/secretion of PTH --> less reabsorption of Ca in the DCT.
Is this the only mechanism?

Also how does hypocalcemia exactly cause TdP?

Thank you so much!
 

Phloston

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OnePunchBiopsy

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Hypomagnesemia leads to hypokalemia which leads to prolonged QT.

For Step 2 CK and on the wards, you always correct Mg before correcting for K.