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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

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.

FIGURE 1.

Algorithm for the treatment ...

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