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TEXTBOOK PRESENTATION

Patients with VT may be asymptomatic or have symptoms that range from palpitations to light-headedness, near syncope, syncope, or sudden cardiac death.

image VT occurs most commonly in patients with heart disease and should be seriously considered in patients with syncope and a history of preexisting CAD, HF, or other heart disease.

DISEASE HIGHLIGHTS

  1. Etiology and associations

    1. Ischemic heart disease

      1. Associated with CAD in 80% of cases

      2. May be secondary to acute ischemia/MI or prior scar

      3. VT and ventricular fibrillation complicates 10% of STEMIs (ST-segment elevated MI)

    2. HF

    3. Other heart diseases: HCM, valvular heart disease, infiltrative disorders

    4. Miscellaneous causes

      1. Electrolyte disorders (hypokalemia and hypomagnesemia)

      2. Hypoxia

      3. Drugs, particularly those that prolong the QT interval (eg, antiarrhythmics, antipsychotics, tricyclic antidepressants, macrolides, some fluoroquinolones, and many others)

    5. Congenital disorders

      1. Congenital heart disease

        1. Long QT syndrome

          1. The ECG of affected families demonstrates long refractory periods (long QT intervals defined as a QTc of > 450 ms in males and 460 ms in females)

          2. Affected patients are at increased risk for sudden cardiac death from a form of VT called torsades de pointes.

          3. Arrhythmias may be precipitated by emotional stress, exercise, loud abrupt noises, or during sleep.

          4. Several symptoms typically associated with vasovagal syncope are also common in the long QT syndrome: triggered by emotional stress, pain, or noise (70%); sweating (67%); nausea (29%); situational (associated with micturition, defecation, or coughing) (17%); abdominal discomfort (16%).

            image Long QT syndrome may mimic vasovagal syncope. Even patients with symptoms typical of vasovagal syncope should have an ECG performed and QTc measured.

          5. Associated with congenital neural deafness

        2. Brugada syndrome

          1. Caused by a mutation in the sodium channel gene. Affected patients are predisposed to polymorphic VT and sudden death.

          2. Suggestive baseline ECG abnormalities include a right BBB pattern with ST elevation in the right precordial leads.

  2. Prognosis

    1. VT is a potentially life-threatening arrhythmia.

    2. Predictors of mortality in patients with VT include prior cardiac arrest, LV dysfunction, post-MI, or inducible VT on EPS.

EVIDENCE-BASED DIAGNOSIS

  1. ECG criteria for VT

    1. ≥ 3 consecutive wide complex (QRS ≥ 0.12 seconds) beats (Figure 31-6) > 100 bpm constitutes a wide complex tachycardia (but not necessarily VT)

      1. 80–90% of wide complex tachycardias are due to VT

      2. However, supraventricular tachycardias also occasionally have wide QRS complexes (> 0.12 s) due to either a concomitant BBB or an accessory pathway, hyperkalemia, or drug-induced QRS changes (tricyclic antidepressants overdose and class 1a antiarrhythmics)

      3. A history of CAD or HF increases the likelihood that the wide complex tachycardia is VT.

      4. ECG criteria that increase the likelihood that the wide complex tachycardia is due to VT rather than supraventricular tachycardia with aberrancy include:

        1. Capture beats (a narrow supraventricular complex present in the midst of the wide complex tachycardia)

        2. Fusion beats (a QRS complex with a hybrid morphology between that of the normal narrow QRS complex and that of the wide complex tachycardia). ...

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