Electrolyte imbalances is one of the main reasons for acquired long QT syndrome (LQTS). First will talk about the electropathophysiology of the heart very simply because this will help you to understand clearly how the electrolytes imbalances causes QT prolongation.
What Electrolyte Imbalances Cause Long QT Syndrome?
The electrolyte imbalances causing long QT syndrome are:
Hypokalemia reduces potassium levels (electrolyte imbalance) causing long QT syndrome. The proposed cellular mechanism is inhibition of the rapid delayed rectifier K+ channels, leading to excess sodium influx or a decreased potassium efflux. This excess positive ions causes an extended repolarization resulting in a prolong QTc interval.
- Excessive laxative usage
- Gastrointestinal loses – diarrhea, vomiting
- Drugs – salbutamol, insulin, amphotericin, aminoglycosides, diuretics – furosemide, thiazides
- Liver failure
- Heart failure
- Corticosteroid therapy
- Cushing’s syndrome
- Renal tubular disorders
- Prolong dietary deficiency
Reduce calcium levels (electrolyte imbalance) causes’ long QT syndrome. Low calcium levels prolong the plateau phase. This causes calcium ion channels to be open for a long time, allowing more calcium to influx to the cell, causing an extended repolarization resulting in a prolong QTc interval.
- Chronic kidney disease
- Phosphate therapy
- Hypoparathyroidism – thyroidectomy, parathyroidectomy
- Vitamin D deficiency
- Drugs – calcitonin, bisphosphonates
Reduce magnesium levels (electrolyte imbalance) makes the cell unable to retain potassium differences, intracellular and extracellular space and results in depletion of potassium inside the cell. This causes changes in the action potential and cause QTc prolongation. Hypomagnesemia also causes hypocalcemia. Both mechanisms contribute to QTc prolongation. It is shown that patients with long QT syndrome improve with magnesium therapy.
- Malabsorption, malnutrition
- Alcohol intake
- Drugs – furosemide, thiazides, digoxin, amphotericin, aminoglycosides
- Diabetic ketoacidosis
- Severe diarrhea
What is the Action Potential?
Action potential is the change in electrical potential along the membrane of a muscle cell or nerve cell by the change of electrical impulses. In the nerves this create the nerve impulse, in muscles this will contract the muscle required to produce movement.
The transmembrane potential (TMP) is the electrical potential difference (voltage) between the inside and the outside of a cell. When there is a net movement of +ve ions into a cell, the TMP becomes more +ve, and when there is a net movement of +ve ions out of a cell, TMP becomes more –ve.
Action Potential Of The Heart
Heart is also a muscle; the action potential of the heart is different from the skeletal muscles. There are 5 phases in the action potential of the heart (Phase 0-4)
Phase 0 – Depolarization
- An action potential triggered in a neighboring heart cell or pacemaker cells causes the TMP to rise from a negative charge.
- The fast Na+ channels open and Na+ influx occurs (comes inside the cell). The large Na+ current depolarize (contract) the cell. This shift in voltage is reflected by the initial spike of the action potential.
Phase 1- Depolarization
- At the beginning of this phase the fast Na+ channels close.
- Now some K+ channels open briefly and K+ efflux (goes out of the cell). This result the notch.
- The L-type (long opening) Ca2+ channels open and causes a small, steady influx of Ca2+ according to concentration gradient.
- TMP is now slightly positive.
Phase 2 – Plateau Phase
- L-type Ca2+ channels are still open and there is a constant influx of Ca2+.
- K+ leaks out of the cell according to its concentration gradient through “rapid delayed rectifier K+” and “inward rectifier K+” channels.
- These two counter currents maintains the TMP at an electrically balance plateau stage.
Phase 3 – Repolarization
- The Ca2+ channels become inactive gradually.
- Persistent efflux of K+ exceeds the Ca2+ influx. The TMP is brought back to a negative TMP and repolarization occurs. The rapid delayed rectifier K+ channels close up.
Phase 4 – Resting Phase
- The inward rectifier K+ channels remains open and bring the cell to its resting potential. Then it prepares back to another phase of depolarization.
The electrolyte imbalances causing long QT syndrome are hypokalemia, hypocalcemia and hypomagnesemia. Hypokalemia causes inhibition of the rapid delayed rectifier K+ channels, leading to excess sodium influx or a decreased potassium efflux. This excess positive ions causes an extended repolarization resulting in a prolong QTc interval. . Low calcium levels prolong the plateau phase. This causes calcium ion channels to be open for a long time, allowing more calcium to influx to the cell, causing an extended repolarization resulting in a prolong QTc interval. Hypomagnesemia causes hypokalemia and hypocalcemia which results in prolong QTc.
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