DW 5 dextrose in water VF ventricular Fibrillation

FIGURE 9-11. Decision algorithm for resuscitation of VF or pulseless ventricular tachycardia. (CPR, cardiopulmonary resuscitation.) defibrillation attempt should be made after every dose of drug. bEpinephrine should continue to be administered every 3 to 5 minutes throughout the remainder of the resuscitation.

Outcome Evaluation

• Monitor the patient for return of pulse and blood pressure, and for termination of VF and restoration of normal sinus rhythm.

• After successful resuscitation, monitor the patient for adverse effects of drugs administered (Table 9-7).

Torsades de Pointes

Torsades de pointes is a specific polymorphic VT that is associated with prolongation of the QT interval in the sinus beats that precede the arrhythmia.13

Epidemiology and Etiology

The incidence of torsades de pointes in the population at large is unknown. The incidence of torsades de pointes associated with specific drugs ranges from less than 1% to as high as 8% to 10%, depending on dose and plasma concentration of the drug and the presence of other risk factors for the arrhythmia.

Torsades de pointes maybe inherited or acquired. Patients with specific genetic mutations may have an inherited long QT syndrome, in which the QT interval is prolonged, and these patients are at risk for torsades de pointes. Acquired torsades de pointes may be caused by numerous drugs (Table 9-16); the list of drugs that are known to cause torsades de pointes continues to expand.


Torsades de pointes is caused by circumstances, often drugs, that lead to prolongation in the repolarization phase of the ventricular action potential (Fig. 9-2) manifested on the ECG by prolongation of the QT interval. Prolongation of ventricular repolarization occurs via inhibition of efflux of potassium through potassium channels; therefore, drugs that inhibit conductance through potassium channels may cause QT interval prolongation and torsades de pointes.

Table 9-16 Drugs That Have Been Reported to Cause Torsades de Pointes











Chlor pro nwine























1 rl methoprim-sulfa methoxa zo le




Clinical Presentation and Diagnosis of Torsades de Pointes


• As with other tachyarrhythmias, symptoms associated with torsades de pointes are dependent primarily on heart rate and arrhythmia duration, and include palpitations, dizziness, light-headedness, shortness of breath, chest pain (if underlying CAD is present), near-syncope, and syncope

• Torsades de pointes may be hemodynamically unstable if the rate is sufficiently rapid

• Like sustained monomorphic VT, torsades de pointes may result in the absence of a pulse, or may rapidly degenerate into VF, resulting in the syndrome of sudden cardiac death


• Diagnosis of torsades de pointes requires examination of the arrhythmia on ECG

• Torsades de pointes, or "twisting of the points," appears on ECG as apparent twisting of the wide QRS complexes around the isoelectric baseline

• The arrhythmia is associated with heart rates from 140 to 280 bpm

• Characteristic feature: a "long-short" initiating sequence that occurs as a result of a ventricular premature beat followed by a compensatory pause which is followed by the first beat of the torsades de pointes

• Episodes of torsades de pointes may self-terminate, with frequent recurrence

O Prolongation of ventricular repolarization likely promotes the development of early ventricular afterdepolarizations during the relative refractory period, which may provoke re-entry leading to torsades de pointes.

© Drug-induced torsades de pointes rarely occurs in patients without specific risk factors for the arrhythmia (Table 9-17). In most cases, administration of a drug known to cause torsades de pointes is unlikely to cause the arrhythmia; however, the likelihood of the arrhythmia increases markedly in patients with concomitant risk factors.

The onset of torsades de pointes associated with oral drug therapy is somewhat variable and in some cases may be delayed; often, a patient can be taking a drug known to cause torsades de pointes for months or longer without problem until another risk factor for the arrhythmia becomes present, which then may trigger the arrhythmia.

Table 9-17 Risk Factors for Drug-Induced Torsades de Pointes

QTc interval greater than 500 milliseconds

Increase in QTc interval by more than 60 milliseconds compared with the pretreatment value Female sex

Age greater than 65 years Heart failure

Electrolyte abnormalities: hypokalemia and Hypomagnesemia Bradycardia Elevated plasma concentrations of QT interval-prolonging drugs due to drug interactions or absence of dose adjustment for organ dysfunction Rapid IV infusion of torsades-inducing drugs Concomitant administration of more than one agent known to cause QT interval prolongation/torsades de pointes Possible genetic predisposition Previous history of drug-induced torsades de pointes

QTc, corrected QT interval. From Ref. 13.

In some patients, torsades de pointes may be of short duration and may terminate spontaneously. However, torsades de pointes may not terminate on its own, and if

left untreated, may degenerate into VF and result in sudden cardiac death. Several drugs, including terfenadine, astemizole, and cisapride, have been withdrawn from the U.S. market as a result of causing deaths due to torsades de pointes.

Treatment Desired Outcomes

The desired outcomes for treatment include: (a) prevention of torsades de pointes, (b) termination of torsades de pointes, (c) prevention of recurrence, and (d) prevention of sudden cardiac death.

Pharmacologicand Nonpharmacologic Therapy

© In patients with risk factors for torsades de pointes, drugs with the potential to cause QT interval prolongation and torsades de pointes should be avoided or used with extreme caution, and diligent QT interval monitoring should be performed.

Management of drug-induced torsades de pointes includes discontinuation of the potentially causative agent. Patients with hemodynamically unstable torsades de pointes should undergo immediate synchronized DCC. In patients with hemodynamically stable torsades de pointes, electrolyte abnormalities such as hypokalemia and hypomagnesemia should be corrected. Hemodynamically stable torsades de pointes is often treated with IV magnesium, irrespective of whether the patient is hypomag-nesemic; magnesium has been shown to terminate torsades de pointes in normomag-nesemic patients. Magnesium may be administered IV in doses of 1 to 2 g, diluted in 50 to 100 mL 5% dextrose in water (D5W), administered over 5 to 10 minutes; doses maybe repeated to a total of 12 g.

Alternatively, a continuous magnesium infusion may be initiated after the first bolus, at a rate of 0.5 to 1 g/h. Alternative treatments include: transvenous insertion of a temporary pacemaker for overdrive pacing, which shortens the QT interval and may terminate torsades de pointes and reduce the risk of recurrence; IV isoproterenol 2 to 10 mcg/min, to increase the heart rate and shorten the QT interval; IV lidocaine, which may shorten the duration of ventricular repolarization; or IV phenytoin, which may also shorten the duration of ventricular repolarization, administered at a dose of 10 to 15 mg/kg infused at a rate of 25 to 50 mg/min.

Patient Care and Monitoring

1. Perform a thorough medication history to determine whether the patient is receiving any prescription or nonprescription drugs that may cause or contribute to the development of an arrhythmia.

2. Evaluate the patient for the presence of drug-induced diseases, drug allergies, and drug interactions.

3. Determine and monitor the patient's serum electrolyte concentrations to determine the presence or absence of hypokalemia, hyperkalemia, hypomagnesemia, or hy-permagnesemia.

4. Consider the patient's heart rate, blood pressure, and symptoms to determine whether he or she is hemodynamically stable or unstable.

5. Monitor the patient's 12-lead ECG or single rhythm strips to determine if an arrhythmia is present and to identify the specific arrhythmia, and evaluate and monitor the patient's symptoms.

6. Develop drug therapy treatment plans for management of the specific arrhythmia that the patient is experiencing: sinus bradycardia, AV nodal blockade, AF, PSVT, VPDs, VT (including torsades de pointes), or VF.

7. Develop specific drug therapy monitoring plans for the treatment plan implemented. Monitoring includes assessment of symptoms, ECG, adverse effects of drugs, and potential drug interactions.

8. In those receiving warfarin for AF, determine whether the patient's INR is therapeutic.

9. Provide information regarding safe and effective warfarin therapy:

• Notify appropriate clinicians in the event of severe bruising, blood in urine or stool, or frequent nosebleeds.

• Avoid radical changes in diet.

• Do not take nonprescription medications or herbal/alternative/complementary medicines without notifying your physician, pharmacist, and/or health care team members.

10. Stress the importance of adherence to the therapeutic regimen.

11. Provide patient education regarding disease state and drug therapy.

Outcome Evaluation

• Monitor vital signs (heart rate and blood pressure).

• Monitor the ECG to determine the QTc interval (maintain less than 450 milliseconds) and for the presence of torsades de pointes.

• Monitor serum potassium and magnesium concentrations.

• Monitor for symptoms of tachycardia.

Abbreviations Introduced in This Chapter


Atrial fibrillation


Ad cno si ne t riph<?sphat ase






Coronary arLerv disease


Card i ac A rrhy t h m ia Suppre ss U>n 1 riaI


Calcium channel blocker


Card iopul mo n a ry nesu sc i tat io n


Direct current cardioversion


5% Dextrose in water


Emergency department


Heart failure


I nip 1 a n t able e a rd iover tcr- de fib rill ato r


International Normalized Ratio






Left ventricular


Left ventricular ejection fraction


Left ventricular hypertrophy


Mvoc a rd ia ] in fare t io n j


Sod iu m


New York Hcari Association


Paroxysmal sup raven LricuJar tachycardia


Partial thromboplastin time


P remafcu re ven l ric u ] ar con \ rae t io n


Corrected QT Interval


RR interval


Si no atria J


I ransesbphagca 1 ec hoca rd iogra m


Transient ischemic attack


Ventricular pre mal urc bea!


Ven t ríe u la r pre in at u rc co n 1 rat t ion


Vent r ic u lar premat u re depol a r iz at ion


Ventricular fibril Jal ion


Vent r ic u lar l AChyc a I'd i a

Self-assessment questions and answers are available at ht-tp://www. mhpharmacotherapy. com/pp.html.


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