QT Abnormalities and Electrolyte Disturbances
The QT Interval
The QT interval represents ventricular depolarization and repolarization (phase 0-3 of the action potential, Fig. 8.1). The length of the QT interval is dependent on heart rate. Typically, the QT interval lengthens when the heart rate slows and shortens when the heart rate increases. The QTc measurement corrects for heart rate. To calculate the QTc, look for the lead displaying the longest discernible QT length and plug this length into the Bazett formula (Fig. 8.2). The QT interval is measured from the beginning of the QRS complex to the end of the T wave.
 FIGURE 8.1 Relationship between action potential and QTc interval. The upper normal limit differs between men and women. |
Causes of Prolonged QT Interval
Neurologic
Subarachnoid Hemorrhage
Autonomic Neuropathy
Stroke
Metabolic
Hypokalemia
Hypocalcemia
Genetic
Congenital Prolonged QT Syndrome
 FIGURE 8.2 ECG representation of Bazett formula components. |
Pharmacologic
There are numerous drugs that have been associated with prolonging the QT interval, most often by blocking the potassium rectifier channel (IKr). They fall under the following general categories:
Antipsychotics
Haloperidol, chlorpromazine, and thioridazine
Antidepressants
Fluoxetine, paroxetine, and tricyclic antidepressants
Antiarrhythmics
Sotalol, amiodarone, quinidine, procainamide, disopyramide, and flecainide
Antibiotics/Antifungals/Antimalarials
Macrolides and azoles
Antihistamines
Loratadine
Antimigraine Drugs
Sumatriptan
Methadone1
A more complete list of QT-prolonging drugs can be found at www.torsades.org or www.qtdrugs.org.
Congenital Long QT Syndrome
Congenital QT syndrome is a potentially fatal autosomal dominant genetic disorder caused by a mutation in any of several cardiac ion channels involved in ventricular repolarization. Patients with this syndrome are at increased risk of torsades de pointes (TdP) and present with syncope or sudden cardiac death.
Mutations and Channels
Several syndromes (and hundreds of mutations in 12 susceptibility genes) have been identified. Many patients with congenital long QT have not been linked to any of these genotypes. There is a wide range in QTc length within genotypes and families. Two named syndromes have been described.
TABLE 8.1 Different Long QT Syndromes | |||||||||||||||||||||||||||||||||||||||||||||||||
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 FIGURE 8.3 Sites where long QT mutations prolong the action potential. The action potential also represents the myocardial cell membrane. |
ECG Features
QT Prolongation
Despite QT prolongation being characteristic of these mutations, the QT interval may be borderline or normal at any given point in time.
QT Dispersion
There is greater lead-to-lead variability in QT lengths in patients with congenital prolonged QT syndrome. This may reflect regional variation in ventricular repolarization times that increases the risk for re-entry.2
Treatment
The standard treatment is beta-blocker therapy. Competitive sports are contraindicated. High-risk patients may be selected for ICD placement. Pacemaker therapy may be recommended for patients with bradycardia-associated QT prolongation or those who have failed medical therapy. For asymptomatic patients with no history of syncope, no family history of sudden cardiac death, and who have never demonstrated QTc > 500 msec, therapy may not be indicated.
Hypocalcemia
ST Segment Lengthening
When the level of extracellular calcium is low, less calcium enters the myocardial cell during phase 2 of the action potential, and phase 2 becomes prolonged. This phase of the action potential corresponds to the ST segment on the ECG. QT prolongation from hypocalcemia results from prolongation of the ST segment.
Prolonged QT Interval
Heart block and ventricular dysrhythmias are rare.
Hypercalcemia
ST Segment Shortening
Hypercalcemia shortens the duration of phase 2 of the action potential. This typically occurs with serum calcium levels greater than 13 mg/dL. The corresponding ST segment is shortened, accounting for the shortened QT interval.
Shortened QT Interval
ST Elevation
ST elevation occurs in patients with significant hypercalcemia, and these changes may be mistaken for acute myocardial infarction (MI).3 It is possible that ST elevation reflects an ST segment that is shortened enough to make the upright T wave appear joined to the QRS wave. These elevations disappear with correction of the serum calcium level (Fig. 8.5D).
AV Block
At extremely high calcium levels (greater than 15 mg/dL), varying degrees of AV block may progress to complete heart block.
 FIGURE 8.4 A. Action potential affected by hypocalcemia. B. Corresponding change in ECG appearance. C. ECG appearance in hypercalcemia. D. ST elevation in setting of hypercalcemia. |
Hyperkalemia
While the serum level of potassium cannot predict the appearance of an ECG in a single individual and vice versa, the ECG changes associated with hyperkalemia progress in a typical fashion.
 FIGURE 8.5 ECG appearance of different stages of hyperkalemia. A. Peaked T wave. B. QRS widening and PR prolongation. C. Sine wave. |
Mimics
ST elevation (often in leads V1 and V2) can accompany hyperkalemia leading to mistaking this electrolyte disturbance for an ST elevation MI. ST elevation improves with treatment.5 Sinus tachycardia with sine wave morphology from severe hyperkalemia can be mistaken for ventricular tachycardia.
ECG Changes Can Be Masked by:
Other Electrolyte Abnormalities
Concomitant electrolyte disturbances can mask the ECG changes typical of hyperkalemia.
Chronic Renal Failure
In some patients, particularly in those with chronic renal failure, ECG changes may be absent, even in moderate to severe hyperkalemia.
Arrhythmia and Conduction Block
Severe hyperkalemia can produce bradycardia and AV block. Marked bradycardia with wide QRS complexes should make one suspect severe hyperkalemia. This rhythm can degenerate into asystole or ventricular fibrillation.
Hypokalemia
ECG Features
T-Wave Flattening
In hypokalemia, the amplitude of the T wave decreases.
ST Depression and T-Wave Inversion
These changes may mimic subendocardial ischemia.
U Waves
As hypokalemia becomes more severe, U waves become more prominent, and their amplitude exceeds that of the T wave. U waves can best be seen in leads V2-V4. With even more severe hypokalemia, the prominent U waves combine with the T waves (Fig. 8.6C,D).
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