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p. 305

ATRIAL FIBRILLATION (AF)/FLUTTER

Chest palpitations, light-headedness, and reduced exercise tolerance are

the most common symptoms of AF, but stroke is among the severe

complications. The goals of therapy are to control the ventricular rate

and reduce the risk of stroke.

Case 15-1 (Questions 1, 2)

Digoxin, β-blockers, and nondihydropyridine calcium-channel blockers

are appropriate rate-controlling medications. Digoxin is usually

adjunctive therapy. Antiarrhythmic drugs are recommended in patients

with symptoms but not needed in asymptomatic patients (no symptoms

other than palpitations).

Case 15-1 (Questions 3–7)

Before converting AF to sinus rhythm, assurance of a lack of clot is

important but not required if someone is unconscious or

hemodynamically unstable. People with a CHA2DS2

-VASc score of 2

or greater should receive chronic anticoagulant therapy with warfarin,

dabigatran, rivaroxaban, edoxaban, or apixaban. Those with a score of 0

do not require antithrombotic therapy, and those with a score of 1 can

receive no therapy, aspirin, or anticoagulant therapy based on patient

and clinician preference.

Case 15-1 (Questions 8, 13)

Antiarrhythmic drugs convert patients out of AF 50% of the time,

whereas electricalshock is successful 90% of the time. To maintain

sinus rhythm after conversion, class Ib agents cannot be used, class Ic

agents cannot be used in patients with structural heart disease (left

ventricular hypertrophy, myocardial infarction, or heart failure), and

class Ia and III agents can increase the risk of torsades de pointes.

Propafenone, sotalol, dronedarone, dofetilide, and amiodarone are

commonly used antiarrhythmic agents for AF.

Case 15-1 (Questions 9–12)

Atrial flutter is less common than AF, but similar rate control and

antiarrhythmic strategies can be tried. Radiofrequency ablation can be

used to terminate atrial flutter.

Case 15-2 (Question 1)

PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT)

PSVT is caused by reentry within the atrioventricular (AV) node.

Palpitations and hypotension can occur. The Valsalva maneuver,

Case 15-3 (Questions 1–6)

adenosine, or nondihydropyridine calcium-channel blockers can be used

to treat the arrhythmia.

In Wolff–Parkinson–White syndrome patients with PSVT, the use of

AV nodal blocking agents such as β-blockers, nondihydropyridine

calcium-channel blockers, and digoxin can increase the risk of cardiac

arrest. Ablation can destroy the bypass tract and cure the patient.

Case 15-4 (Questions 1, 2)

ATRIOVENTRICULAR (AV) BLOCK

β-Blockers, digoxin, and nondihydropyridine calcium-channel blockers

should be withheld in patients with type 1 second- or third-degree AV

block. Atropine can be used to treat this disorder.

Case 15-5 (Questions 1, 2)

VENTRICULAR ARRHYTHMIAS

In patients with premature ventricular complexes (PVCs) and

myocardial infarction,

β-blockers are the treatment of choice. Catheter ablation is

recommended for those with ventricular compromise due to high PVC

burden.

Case 15-6 (Questions 1, 2)

p. 306

p. 307

Patients with myocardial infarction and nonsustained ventricular

tachycardia (VT) should receive β-blockers and need to be evaluated to

determine whether they should receive an implantable cardioverterdefibrillator (ICD).

Case 15-6 (Question 1)

Patients with sustained VT should be treated with intravenous

antiarrhythmic agents unless they are hemodynamically unstable, in

which case they should be electrically converted. To prevent death from

arrhythmia recurrence, ICDs are superior to antiarrhythmic drugs, but to

decrease the occurrence of painfulshocks, both strategies may be used

simultaneously.

Case 15-7 (Questions 1–3)

TORSADES DE POINTES (TDP)

TdP occurs secondary to antiarrhythmic and nonantiarrhythmic

medications that prolong the QTc interval. Class Ia and III

antiarrhythmic agents, antipsychotic agents, citalopram,

fluoroquinolones, macrolides, azole antifungals, and methadone can

prolong the QTc interval. Magnesium is the treatment of choice for

hemodynamically stable TdP with electrical cardioversion reserved for

the hemodynamically unstable.

Case 15-8 (Questions 1–4)

CARDIAC ARREST

Cardiac arrest should be treated with 2-minute cycles of aggressive

cardiopulmonary resuscitation, electricalshock for VT or ventricular

fibrillation (VF), epinephrine or vasopressin, and amiodarone for

refractory VT or VF according to the Advanced Cardiac Life Support

Case 15-9 (Questions 1–4),

Case 15-10 (Question 1),

Case 15-11 (Questions 1–3)

guidelines from the American Heart Association.

Adequate circulation depends on continuous, well-coordinated electrical activity

within the heart. This chapter reviews and discusses cardiac electrophysiology,

arrhythmogenesis, common arrhythmias, and antiarrhythmic treatment.

ELECTROPHYSIOLOGY

Understanding Electrophysiology

CELLULAR ELECTROPHYSIOLOGY

An electrical potential exists across the cell membrane, and the electrical potential

changes in a cyclic manner that is related to the flux of K+

, Na

+

, and Ca

2+

ions across

the cell membrane.

1

If the change in the membrane potential is plotted against time in

a given cycle of a His-Purkinje fiber, a typical action potential results (Fig. 15-1).

The action potential can be described in five phases.

1 Phase 0 is related to

ventricular depolarization resulting from sodium entry into the cell through fast

sodium channels. On a surface electrocardiogram (ECG), phase 0 is represented by

the QRS complex. Phase 1 is the overshoot phase in which calcium enters the cell

and contraction occurs. During phase 2, the plateau phase, inward depolarizing

currents through slow sodium and calcium channels are counterbalanced by outward

repolarizing potassium currents. Phase 3 constitutes repolarization, which on the

ECG is represented by the T wave. During phase 4, sodium moves out of the cell and

potassium moves into the cell via an active pumping mechanism. During this phase,

the action potential remains flat in some cells (e.g., ventricular muscle) and does not

change until it receives an impulse from above. In other cells (e.g., sinoatrial [SA]

node), the cell slowly depolarizes until it reaches the threshold potential and again

spontaneously depolarizes (phase 0). The shape of the action potential depends on

the location of the cell (see Fig. 15-1). In both the SA and atrioventricular (AV)

nodes, the cells are more dependent on calcium influx than sodium influx, resulting in

a less negative resting membrane potential, a slow rise of phase 0, and the capability

of spontaneous (automatic) phase 4 depolarization (Fig. 15-1).