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SOURCE

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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.

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DEFINITION

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

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ETIOLOGY

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  • 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.

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PATHOPHYSIOLOGY

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  • 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.

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RISK FACTORS

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  • See Etiology.

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CLINICAL PRESENTATION

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SIGNS AND SYMPTOMS
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  • 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.

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DIAGNOSIS

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MEANS OF CONFIRMATION AND DIAGNOSIS
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  • Electrocardiogram (ECG) shows regular rhythm with rate between 140 and 240 beats/min.

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

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DIFFERENTIAL DIAGNOSIS
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DESIRED OUTCOMES

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  • Identify and correct underlying causes.

  • Terminate acute episodes and resolve symptoms.

  • Prevent recurrences.

  • Avoid complications from therapy.

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TREATMENT: NONPHARMACOLOGIC THERAPY

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  • 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.

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TREATMENT: PHARMACOLOGIC THERAPY

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  • 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.

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FIGURE 1.

Algorithm for the treatment ...

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