Outcome Evaluation

• Monitor the patient to determine whether the goal of ventricular rate control is met: heart rate less than 100 bpm or decrease in heart rate of 20% from the pretreatment value.

Patient Encounter, Part 3: Creating a Care Plan

Based on the information presented, create a care plan for DA S acute AF episode, and for long-term management of hisAF.

Your plan should include: (a) a statement of the drug-related needs and/or problems, (b) the goals of therapy, (c) a patient-specific detailed therapeutic plan, and (d) a plan for follow-up to determine whether the goals have been achieved and adverse effects avoided.

• Monitor ECG to assess continued presence of AF and to determine whether conversion to sinus rhythm has occurred.

• Monitor INR approximately monthly to make sure it is therapeutic (target 2.5; range 2-3).

• Monitor patients for adverse effects of specific drug therapy (Table 9-7). Monitor patients receiving warfarin for signs and symptoms of bruising or bleeding.

Paroxysmal Supraventricular Tachycardia

Paroxysmal supraventricular tachycardia (PSVT) is a term that refers to a number of arrhythmias that occur above the ventricles and that require atrial or AV nodal tissue for initiation and maintenance.34 The most common of these arrhythmias is known as AV re-entrant tachycardia, in which the arrhythmia is caused by a re-entrant circuit that involves the AV node or tissue adjacent to the AV node. Other types of PSVT include the relatively uncommon Wolff-Parkinson-White syndrome, which is caused by re-entry through an accessory extra-AV nodal pathway. For the purposes of this section, the term PSVT will refer to AV nodal re-entrant tachycardia.

Epidemiology and Etiology

While PSVT can occur in patients experiencing myocardial ischemia or infarction, it often occurs in relatively young individuals with no history of cardiac disease. The overall incidence of PSVT is unknown.


O Paroxysmal supraventricular tachycardia is caused by re-entry that includes the AV node as a part of the re-entrant circuit. Typically, electrical impulses travel forward (antegrade) down the AV node and then travel back up the AV node (retrograde) in a repetitive circuit. In some patients, the retrograde conduction pathway of the re-entrant circuit may exist in extra-AV nodal tissue adjacent to the AV node. One of these pathways usually conducts impulses rapidly, while the other usually conducts impulses slowly. Most commonly, during PSVT the impulse conducts antegrade through the slow pathway and retrograde through the faster pathway; in approximately 10% of patients, the re-entrant circuit is reversed.34

Clinical Presentation and Diagnosis of PSVT

• May occur at any age, but most commonly during the fourth and fifth decades of life34

• Occurs more commonly in females than in males; approximately two-thirds of patients that experience PSVT are women34


• Symptoms typical of tachyarrhythmias such as PSVT include palpitations, dizziness, light-headedness, shortness of breath, chest pain (if underlying CAD is present), near-syncope, and syncope. Patients commonly complain of palpitations; often the complaint is "I can feel my heart beating fast" or "I can feel my heart fluttering" or "It feels like my heart is going to beat out of my chest."

• Other symptoms are dependent on the degree to which cardiac output is diminished, which is in turn dependent on the heart rate and the degree to which stroke volume is reduced by the rapidly beating heart


• Because the symptoms of all tachyarrhythmias are dependent on heart rate and are therefore essentially the same, diagnosis depends on the presence of PSVT on the ECG, characterized by narrow QRS complexes (usually less than 0.12 seconds). P waves may or may not be visible, depending on the heart rate

• PSVT is a regular rhythm and occurs at rates ranging from 100to250bpm

Treatment Desired Outcomes

The desired outcomes for treatment are to terminate the arrhythmia, restore sinus rhythm, and prevent recurrence. Drug therapy is employed to terminate the arrhythmia and restore sinus rhythm; nonpharmacologic measures are employed to prevent recurrence.

Termination of PSVT

Hemodynamically unstable PSVT should be treated with immediate synchronized DCC, using an initial energy level of 50 J; if the DCC attempt is unsuccessful, successive cardioversion attempts maybe made at 100, 200, 300, and 360 J.14

The primary method of termination of hemodynamically stable PSVT is inhibition of impulse conduction and/or prolongation of the refractory period within the AV

node. Because PSVT is propagated via a re-entrant circuit involving the AV node, inhibition of conduction within the AV node interrupts and terminates the re-entrant circuit.

Prior to initiation of drug therapy for termination of hemodynamically stable PSVT, some simple nonpharmacologic methods known as vagal maneuvers may be attempted.35 Vagal maneuvers stimulate the activity of the parasympathetic nervous system, which inhibits AV nodal conduction, facilitating termination of the arrhythmia. Perhaps the simplest vagal maneuver is cough, which stimulates the vagus nerve. Instructing the patient to cough two or three times may successfully terminate the PSVT. Another vagal maneuver that may be attempted is carotid sinus massage;

one of the carotid sinuses, located in the neck in the vicinity of the carotid arteries,

may be gently massaged, stimulating vagal activity. Carotid sinus massage should not be performed in patients with a history of stroke or transient ischemic attack, or in those in whom carotid bruits may be heard on auscultation. The Valsalva maneuver,

during which patients bear down against a closed glottis, may also be attempted.

If vagal maneuvers are unsuccessful, IV drug therapy should be initiated.34 Drugs that may be used for termination of hemodynamically stable PSVT are presented in Table 9-12. A decision strategy for pharmacologic termination of hemodynamically stable PSVT is presented in Figure 9-9.35 Adenosine is the drug of choice for pharmacologic termination of PSVT and is successful in 90% to 95% of patients. Adenosine is associated with adverse effects (Table 9-7) including flushing, sinus bradycardia or AV nodal blockade, and bronchospasm in susceptible patients. In addition, adenosine may cause chest pain that mimics the discomfort of myocardial ischemia, but which is not actually associated with ischemia. The half-life of aden-osine is approximately 10 seconds, due to deamination in the blood; therefore, in the vast majority of patients, adverse effects are of short duration.

If adenosine therapy is unsuccessful for termination of PSVT, subsequent choices of therapy depend on whether the patient has heart failure and/or a depressed left ventricular ejection fraction (LVEF).

Nonpharmacologic Therapy: Prevention of Recurrence

In the past, prevention of recurrence of PSVT was attempted using long-term oral therapy with drugs such as verapamil or digoxin. Unfortunately, oral therapy with these drugs was associated with relatively limited success. Currently, the treatment of choice for long-term prevention of recurrence of PSVT is radiofrequency catheter abla tion. During this procedure, a catheter is introduced transvenously and directed to the right atrium under fluoroscopic guidance. The catheter is advanced to the AV node, and radiofrequency energy is delivered to ablate, or destroy, one of the pathways of the re-entrant circuit. This procedure usually achieves a complete cure of PSVT and is associated with a relatively low risk of complications, and therefore obviates the need for long-term antiarrhythmic drug therapy in this population.

Table 9-12 Drugs for Termination of PSVT




Drug Inlrr.ictiom


AV nodal Ifthifciiiori

e^Wiifi^ 1-? mifuJt«, Ii mg 1V rapid bolus, IF no response in 1 -? mlfuji^ 1? irig IV i,i|ih1 holm

ri^ii.viiiiv? irtr. tjiri. response to adenosine l)i|:y imkiIi- .Ki<T'iH..ili". I = --.|:- ■.■ io adenosine


Dirtier AV nudjl inhibits

1. OJ075-0.1S mg/kg- IVover 1 3 minute

Inhibili d'jMKi" elimination

?. lirK*(".l<iy. in .icfilliitiiiSI mi^/

ky nuyüi' jJuMiiMrd 30 ffllnulB Ijlt-r

[Ji«vr AV inhihiifai

2. If necessary, Ü.3i mg/kg Mover i minutes aliet first do«

J. Maüwawra iriluiion: i-lS rn^/n

Inhibit dimlnMtoh cf c^ctoponne


1, Vjgsl Kimuliilicxi

&?5 mg IV every 1 liuuiv up to 15 mg

AiniuJjnurH: jnd veupaniil [inTitiic

1. rsreci AV nodal inhibmon

¡Spavin Hun narlon)

ß Blockes

Dircit AV nodal inhibrlon

Esmolol SCO maykg IVover 1 minute then SO-iOO

nvigAa/rnin tonfinuojs infiiüori Itcpfincikil mq/kg IV WL'Ißuiökjl 2.5-S mg IV > >3 itos«



5-? mg/k] IVove* 30-iOininuiei rhen 12-1 JSg

Inhibrts ehminaitoo of digcmnand

Calcium channel block«

[Mr JJ hours W infusion


AVr atrioventricular: PSVT paroxysmal supraventrculaf lachycardia.

AVr atrioventricular: PSVT paroxysmal supraventrculaf lachycardia.

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