Tachyarrhythmias

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A wide complex rhythm suggests an aberrancy in the normal conduction system and is usually the result of one of the following:
- A preexisting or rate-related abnormality within the normal conduction system (e.g., bundle branch block).
- An accessory pathway (e.g., Wolff–Parkinson–White syndrome [WPW]).

Table 21.1. Classification of common tachyarrhythmias

Presentation

Classic presentation

Ironically, the “classic presentation” mostly consists of nonspecific symptoms. Patients may complain of palpitations, chest pain, lightheadedness, dyspnea, or nonspecific weakness.
Further evaluation will reveal a rapid heart rate on physical examination or on the electrocardiogram (ECG).

Critical presentation

Patients with unstable tachyarrhythmias present with signs and symptoms of hypoperfusion and hemodynamic compromise while still maintaining a palpable pulse:
- Hypotension
- Altered mentation
- Ischemic chest pain
- Pulmonary edema.
Patients who do not have a palpable pulse are deemed to be in cardiac arrest and are treated according to Advanced Cardiovascular Life Support (ACLS) guidelines.

Diagnosis and evaluation

Primary evaluation consists of performing an ECG with a rhythm strip.
Once tachyarrhythmia is confirmed, consideration should be given to whether the arrhythmia has an underlying noncardiac etiology such as a toxic ingestion or a metabolic disturbance.
- Clinical history is useful and important. Attention should be paid to the patient’s medical history and potential use of QT-prolonging medications.
- A chest radiograph and basic blood work may be helpful in identifying a metabolic or infectious etiology of the arrhythmia.
The type of arrhythmia can be determined on the basis of the ECG:
- Sinus tachycardia:
  - Narrow-complex tachycardia.
  - Regular rate greater than 100 bpm.
  - Rates >160 bpm are not typically attributable to sinus tachycardia.
  - Each P wave is associated with a QRS complex.
  - There is a fixed P-R interval.
Supraventricular tachycardia (SVT):
- Narrow-complex tachycardia.
- Regular rate between 140 and 250 bpm.
- P waves may be present but difficult to see due to the rate.
- The most common cause of SVT is atrioventricular nodal reentrant tachycardia (AVNRT).
- SVT may also present as a wide-complex tachycardia if it is associated with a rate-related or preexisting bundle branch block. This is often referred to as “SVT with aberrant conduction” and may mimic VT.
Atrial fibrillation:
- Atrial fibrillation is the most common cardiac arrhythmia.
- Usually narrow complex, but can present with a wide QRS in the presence of underlying disease of the conduction system.
- Irregularly irregular rhythm with absent P waves and atrial rates varying from 400 to 700 bpm.
- Ventricular response is usually 120–180 bpm.
- Irregularly irregular rate distinguishes AF from other arrhythmias, even when the complex is wide.
Atrial flutter:
- On a spectrum of sinus node dysfunction with atrial fibrillation.
- Usually narrow complex.
- Presents with a classic “sawtooth” pattern of P waves.
- The atrial rate ranges between 250 and 350 bpm.
- Atrial flutter is associated with varying degrees of AV block and can present as a regular or regularly irregular rhythm.
- Most often, the atrial rate is regular at 300 bpm with a 2:1 block, producing a regular ventricular rate of 150 bpm.
Multifocal atrial tachycardia:
- Irregularly irregular tachyarrhythmia.
- Diagnosed by the presence of at least three different P wave morphologies with varying P-R intervals.
- MAT is almost always seen in the elderly and those with pulmonary disease. It is also associated with hypomagnesemia, hypokalemia, and coronary artery disease.
Ventricular tachycardia:
- Wide complex regular tachyarrhythmia.
- Ventricular rate is greater than 120 bpm.
- VT can be monomorphic or polymorphic:
  - Monomorphic VT usually presents with rates between 120 and 300 bpm.
  - Polymorphic VT usually has rates >200 bpm.
  - Torsades de pointes is a polymorphic VT with a prolonged QT. On the ECG, the QRS complex appears to be twisting around an axis. It is a subtype, not a synonym, of polymorphic VT.
All wide-complex regular tachycardias are potentially life threatening and should be considered VT until proven otherwise.
Ventricular fibrillation:
- Wide complex irregular tachyarrhythmia.
- Always associated with unstable or pulseless patient.

Critical management

In patients with tachyarrhythmias, critical management actions include
- Assessment of overall stability with ABCs
- ECG and continuous telemetry
- Intravenous access
- Placement of pacer/defibrillation pads on the patient in anticipation of potential deterioration
Definitive therapy will vary depending on the underlying rhythm.
Commonly used medications as well as their dosage are presented in Table 21.2.
- Sinus tachycardia
  - The primary goal with a patient in sinus tachycardia (ST) is to treat the underlying condition rather than the tachycardia itself.
  - The primary indication for rate control in ST is during acute myocardial infarction, where tachycardia is associated with worse outcomes. Nodal agents, particularly beta-blockers, are useful in this setting.
- Paroxysmal supraventricular tachycardia
  - Generally unrelated to an underlying cause.
  - Rhythm control is the primary intervention.
  - Vagal maneuvers can be attempted prior to pharmacological therapy.
  - Adenosine is the medication of choice as it is both diagnostic and therapeutic.
    - Adenosine is metabolized quickly by nonspecific esterases in the plasma and therefore should be pushed quickly via the intravenous access closest to the heart.
- If adenosine fails, consider synchronized cardioversion or rate control with agents that slow conduction through the AV node.
- Atrial fibrillation and atrial flutter
  - These rhythms are modulated by sinus automaticity and, like sinus tachycardia, can be driven by underlying etiologies.
  - Rate control is the primary treatment modality
    - Nodal blockers and digoxin are reasonable options.
    - Amiodarone is an appropriate alternative.
    - Of note, rapid atrial fibrillation with a wide QRS complex suggestive of WPW should not be treated with AV nodal blocking agents. In this setting, procainamide or synchronized cardioversion should be used.
Multifocal atrial tachycardia
- Initial therapy for MAT should be aimed at treating the underlying cause such as hypomagnesemia, hypokalemia, pulmonary, or cardiac disease.
- Pharmacological therapy is indicated if the arrhythmia is causing significant symptoms such as ischemia, hypoxia, heart failure, or shock.
- Nodal blockers can be used, though their efficacy is limited.
Ventricular tachycardia
- In stable patients with monomorphic VT, procainamide or amiodarone can be used.
- Polymorphic VT is often caused by myocardial ischemia. Diagnosis and treatment of potential myocardial infarction should be pursued.
- Treatment of torsades de pointes is aimed at decreasing the QT interval.
  - Intravenous magnesium sulfate is the first-line treatment.
  - Overdrive pacing also shortens the QT interval and can be used if magnesium therapy is ineffective. It can be achieved by transcutaneous pacing or with pharmacological agents such as isoproterenol.
- Ventricular fibrillation:
  - VF is an unstable rhythm that should be primarily managed by defibrillation.
  - ACLS should be initiated promptly in all patients exhibiting this rhythm.