Tachycardia, Paroxysmal Supraventricular

SOURCE

Source: Sanoski CA, Bauman JL. The arrhythmias. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146057036. Accessed March 28, 2017.

DEFINITION

• Paroxysmal supraventricular tachycardia (PSVT) is rapid heart rhythm originating above ventricles that occurs episodically.

ETIOLOGY

• May occur in healthy individuals.

• Premature atrial or ventricular ectopic beats.

• Hyperthyroidism.

• Stimulant use (including caffeine)

• Previous myocardial infarction, mitral valve prolapse, rheumatic heart disease, pericarditis, pneumonia, chronic lung disease, alcohol intoxication.

• Digoxin toxicity.

PATHOPHYSIOLOGY

• PSVT arising by reentrant mechanisms includes arrhythmias caused by atrioventricular (AV) nodal reentry, AV reentry incorporating an anomalous AV pathway, sinoatrial (SA) nodal reentry, and intra-atrial reentry.

RISK FACTORS

• See Etiology.

CLINICAL PRESENTATION

SIGNS AND SYMPTOMS

• Many patients asymptomatic or have only occasional minor palpitations or irregular pulse.

• Patients may experience:

  • Intermittent episodes of rapid heart rate/palpitations.

  • Choking or pressure sensation.

  • Dizziness.

  • Lightheadedness.

  • Shortness of breath.

  • Syncope.

  • Symptoms of heart failure.

  • Anginal chest pain.

• Symptoms may be severe and even life threatening in some patients.

• Heart rate ranges from 140 to 240 beats/min and is regular.

DIAGNOSIS

MEANS OF CONFIRMATION AND DIAGNOSIS

• Electrocardiogram (ECG) shows regular rhythm with rate between 140 and 240 beats/min.

LABORATORY TESTS

• May be performed if underlying causes suspected (eg, hyperthyroidism, digoxin toxicity).

DIFFERENTIAL DIAGNOSIS

• Atrial tachycardia, flutter, or fibrillation.

• Atrioventricular nodal reentrant tachycardia (AVNRT)

• Sinus node dysfunction.

• Ventricular tachycardia or fibrillation

DESIRED OUTCOMES

• Identify and correct underlying causes.

• Terminate acute episodes and resolve symptoms.

• Prevent recurrences.

• Avoid complications from therapy.

TREATMENT: NONPHARMACOLOGIC THERAPY

• For mild to moderate symptoms, measures that increase vagal tone to AV node (unilateral carotid sinus massage, Valsalva maneuver, ice water facial immersion, or induced retching) used initially.

• For severe symptoms (ie, syncope, near syncope, angina, or severe heart failure), synchronized direct current cardioversion (DCC) treatment of choice.

TREATMENT: PHARMACOLOGIC THERAPY

• Used for mild to moderate symptoms if nondrug measures fail.

• Drug selection based on symptom severity and QRS complex (Figure 1).

  • Directly or indirectly increase vagal tone to AV node, with digoxin.

  • Depress conduction through slow, calcium-dependent tissue:

    • Adenosine.

    • β-blockers.

    • Nondihydropyridine calcium channel blockers.

  • Depress conduction through fast, sodium-dependent tissue.

    • Quinidine.

    • Procainamide.

    • Disopyramide.

    • Flecainide.

• Adenosine is a drug of first choice because its short duration of action will not cause prolonged hemodynamic compromise in patients with wide QRS complexes who actually have ventricular tachycardia rather than PSVT.