Shaundra Jones, age 74 years, was discharged to home 3 days ago and is your first visit today. She was hospitalized for an acute MI and has received a diagnosis of left ventricular heart failure. Previously, her only diagnosed medical problem was depression, for which she had been taking sertraline (Zoloft). She says that she has had "GI bug" and diarrhea since coming home and blames "that hospital food!!"

This morning she says she has a funny feeling in her chest. "It's not at all like the heart attack - that hurt!! It's more like a bunch of butterflies in there and I feel really weak!!" You auscultate her and immediately call 911. "Send the paramedics. I think I have a torsades case here!!" you shout.

Torsades de pointes is an often fatal ventricular dysrhythmia that looks like an unorganized set of waves on the ECG. It occurs in patients with a prolonged QT interval (QT) on the ECG. Certain drugs and drug interactions can result in QT prolongation, as well as aging and electrolyte abnormalities.

Patients are at the greatest risk for torsades during the first few days of beginning a drug that prolongs the QT (Al-Khatib et al., 2003). Because patients are often sent home before QT prolongation is detected, it is important that home care clinicians understand the risks of QT prolongation and the symptoms of torsades de pointes. Immediate intervention is required to avoid sudden death.

The QT Interval

The QT interval on the ECG reflects the ability of the ventricles to depolarize and repolarize. When ion channels in the ventricular myocardium malfunction, resulting in too much sodium entering the cells or too little potassium exiting, the buildup of positive ions in the myocardial cells extends the period of ventricular repolarization. At this time QT prolongation results, which can trigger torsades de pointes.

Some people have congenital QT prolongation and are at a high risk of sudden death, even without taking medications that prolong the QT interval. However, QT prolongation is acquired in most cases. Any combination of the following increases the risk for a prolonged QT interval:

* female gender

* advanced age

* low left ventricular ejection fraction

* bradycardia

* ischemia

* hypokalemia

* hypomagnesemia

* QT-prolonging medications (block potassium movement out of cardiac cells)

* medications that inhibit drug metabolism

It is well known that initiation of antiarrhythmic drugs can prolong the QT interval and precipitate torsades de pointes, which is the reason patients are now hospitalized for 72 hours after beginning antiarrhythmic therapy (Simons et al., 1997).

Other drugs that block potassium movement out of cardiac cells also can prolong the QT interval, including:

* Antipsychotics (e.g., chlorpromazine, haloperidol, olanzapine, risperidone, thioridazine, quetiapine)

* Antidepressants (e.g., amitriptyline, desipramine, imipramine, sertraline, venlafaxine, lithium)

* Anti-infectives (e.g., erythromycin, quinolones such as levofloxacin, gatifloxacin, sparfloxacin, ofloxacin)

* Antihypertensives (e.g., isradipine, nicardipine)

* Other drugs (e.g., droperidol, salmeterol, tamoxifen)

* Drugs that inhibit the metabolism of QT-prolonging drugs are also implicated, such as anti-infectives (e.g., erythromycin, clarithromycin, telithromycin, azithromycin, ketoconazole, quinolones, pentamidine)

* GI drugs (e.g., cimetidine, omeprazole)

Patients are at the greatest risk for Torsades during the first few days of beginning a drug that prolongs the QT interval. Patients are often sent home before QT prolongation is detected, and home care clinicians should be familiar with the symptoms. Immediate intervention is required to avoid sudden death.

Drugs such as terfenadine (Seldane), cisapride (Propulsid), and grepafloxacin (Raxar) have been removed from the market because of QT prolongation and torsades de pointes resulting from drug interactions.

Shaundra Jones was an older woman with low left ventricular ejection fraction. She was taking carvedilol (Coreg), a beta-blocker usually given to patients after myocardial infarction (MI) to slow heart rate and reduce the risk of future MI. She was also taking an ACE inhibitor for her left ventricular hypertrophy and heart failure along with digoxin and furosemide.

Both digoxin and furosemide deplete potassium and magnesium. Her bout with diarrhea probably contributed to her hypokalemia and hypomagnesemia. She self-medicated her GI distress with over-the-counter cimetidine (Tagamet).

In Ms. Jones' case, her gender and advanced age put her at risk for QT prolongation. Taking a drug (sertraline) that can prolong the QT interval and her probable hypokalemia and hypomagnesemia from digoxin, furosemide, and diarrhea further increased her risk. Finally, self-medicating with a drug (cimetidine) that inhibits the metabolism of sertraline may have been the final event that triggered her torsades de pointes.

Fortunately in her case, a prompt 911 call enabled paramedics to arrive in time to prevent her death. Her potassium and magnesium levels were corrected in the hospital, and her QT interval returned to normal. She was put back on her antidepressant regimen and, because her QT interval remained normal, was discharged 72 hours later.

It is theorized that some individuals may harbor a "silent gene" that produces QT prolongation only under certain circumstances (Priori et al., 1999). Because of this, Ms. Jones was counseled to avoid over-the-counter medications and drugs of abuse that should be avoided in patients with congenital prolonged QT syndrome, including:

* cimetidine (Tagamet)

* omeprazole (Prilosec)

* ephedrine

* pseudoephedrine

* phenylephrine

* "diet pills" of any kind (many contain ephedra)

* amphetamines

* cocaine

REFERENCES