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Atrial Fibrillation and Flutter
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Arrhythmias: Supraventricular
Tachycardias, Ventricular
Tachycardias and Bradyarrhythmias
Avi Fischer*
Key Pearls
• Even nonlethal arrhythmias, such as atrial fibrillation, should be
treated by direct current (DC) cardioversion if thought to be responsible for a patient’s unstable condition.
• An electrophysiology (EP) study provides information about the presence of arrhythmias and the effectiveness of pharmacologic therapy,
and for the prediction of the future risk of sudden cardiac death.
• When deciding to implant a permanent pacemaker (PPM), it is important to ascertain that symptoms are due to the rhythm disturbance.
• During a supraventricular tachycardia (SVT), it is important to
decide whether the rhythm is regular or irregular and to attempt to
identify the presence of a P-wave as this often provides clues about
the diagnosis.
• It is important to identify whether structural heart disease is present in
the patient with ventricular tachycardia (VT), as the treatment offered
is often dictated by the presence of structural abnormalities.
247
*Mount Sinai School of Medicine, New York, NY, USA.
23
Chapter
Introduction
There are numerous mechanisms important in the genesis of atrial and
ventricular arrhythmias. It is critical for all healthcare providers to appreciate that any rhythm that is responsible for hemodynamic instability
should be treated using advanced cardiac life-support algorithms. Even
nonlethal arrhythmias, such as atrial fibrillation, should be treated by
synchronized direct current (DC) cardioversion if thought to be responsible for a patient’s unstable condition. This chapter will focus on arrhythmias commonly encountered in inpatients, concentrating on treatment
strategies.
Role of the Electrophysiology Study
Electrophysiology (EP) testing is performed to establish a mechanism for
a particular arrhythmia — either tachycardia or bradycardia. Additionally,
EP testing is often utilized to guide the treatment strategy, whether antiarrhythmic drug therapy, cardiac rhythm device implantation or ablation.
It may be performed to characterize the function of the sinus node, the
atrioventricular (AV) node and the His–Purkinje or specialized conduction
system in the heart to guide treatment for bradyarrhythmias. Furthermore,
it is used to induce tachyarrhythmias and allow for characterization, differentiation of the mechanism of the arrhythmia, and to facilitate ablation
of the substrate of the arrhythmia. With the advent of cardiac rhythm
device and catheter ablation technologies, these treatments have become
the mainstay of arrhythmia management. The procedure is performed via
a transvenous approach using venous access obtained most often via the
femoral veins. Multiple flexible, multipolar electrode catheters are positioned in specific sites within the heart, and recording and stimulation performed. The study can provide important information about the presence
of arrhythmias, evaluate the effectiveness of pharmacologic therapy of an
arrhythmia, predict the future risk of sudden cardiac death and assess the
need for an implantable cardiac rhythm device such as a pacemaker or
defibrillator.
248
A. Fischer
Bradyarrhythmias
There are a variety of conditions causing bradyarrhythmias that are transient and reversible. Reversible causes of bradycardia include the use of
drugs such as beta-blockers, calcium channel blockers and other antiarrhythmic agents, electrolyte disturbances or myocardial infarction. It is
always important to exclude any metabolic or pharmacologic contributors
prior to making the decision to implant a permanent device.
Specific clinical settings may warrant the placement of a temporary
transvenous pacemaker. Temporary pacing may be required in the setting
of acute myocardial infarction, prophylactically in the patient at risk for
developing progressive conduction disturbances, and for symptomatic
bradycardia in the patient without a reversible cause who is awaiting
placement of a permanent device. A summary of the general indications
for temporary pacing can be seen in Table 1. Once reversible causes have
been excluded, even a single episode of symptomatic bradycardia may be
enough to indicate a permanent pacemaker implant, but symptoms must
be clearly due to the rhythm disturbance.
Tachyarrhythmias
Supraventricular Arrhythmias
One of the most important methods for evaluating the mechanism of any
arrhythmia is analysis of atrial activity on the surface electrocardiogram
(ECG) and identification of the morphology of the P wave and QRS
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Arrhythmias: Supraventricular, Ventricular Tachycardias and Bradyarrhythmias
Table 1. Pacing Common Diagnoses of Regular Narrow
Complex Tachycardias
In acute myocardial infarction:
• Medically refractory sinus node or A node or AV node
dysfunction causing symptomatic bradycardia
• Mobitz II second-degree AV block with anterior infarction
• Third-degree AV block with anterior infarction
• New bifascicular block
• Alternating bundle branch block
complex. Often the inferior limb leads II, III, aVF as well as precordial
lead V1 are best for identifying P waves. Narrow complex tachycardias
are characterized by having a QRS duration of 100 ms or less. When evaluating a supraventricular tachycardia, it is also useful to identify whether
the rhythm is regular or irregular, as this often offers clues about the diagnosis. An irregularly irregular rhythm is most often indicative of atrial
fibrillation, but may also represent a multifocal atrial tachycardia.
Further dividing regular narrow complex tachycardias into those
with a short RP interval and those with a long RP interval may help in
generating a differential diagnosis and treatment plan (Table 2). The RP
interval is assessed by identifying the position of the P wave on the surface ECG and its position relative to the QRS (R wave). Short RP tachycardias have the P wave either “buried” in the QRS or present after the
QRS in the T wave such that the RP interval is shorter than the PR interval (Fig 1).
Regular Narrow Complex Tachycardia with a Short RP Interval
There are three main tachycardia types that manifest as regular, narrow and
with a short RP interval (RP < PR interval). These tachycardias include
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A. Fischer
Table 2. Indications for Temporary Pacing
In the absence of myocardial infarction:
• Medically refractory symptomatic bradycardia,
sinus node dysfunction, second- or third-degree AV block
• Third-degree AV block with wide QRS escape rhythm, ventricular
rate < 50 bpm or signs of hypoperfusion
Prophylactic
• New AV block or bundle branch block with acute endocarditis
(especially aortic valve)
• Perioperatively in patient with history of syncope and with
bifascicular block
• To allow treatment with drugs that worsen bradycardias
typical AV-nodal re-entrant tachycardia, AV re-entrant tachycardia and an
atrial tachycardia with a first degree AV block where the P wave occurs late
in the QRS complex or within the T wave.
AV-nodal re-entrant tachycardia
AV-nodal re-entrant tachycardia (AVNRT) is a common arrhythmia occurring in young, healthy individuals with no structural heart disease. It is
more common in females, and patients often describe abrupt onset and
offset of palpitations and tachycardia. Mechanistically, there are two pathways of AV nodal conduction present (slow and fast), and the typical form
consists of anterograde conduction over the slow pathway and retrograde
conduction over the fast pathway. As retrograde conduction of the impulse
back to the atria is rapid, the P wave either is not visible because it occurs
simultaneously with the QRS or is seen in the terminal portion of the QRS
(Fig. 2). Acutely, vagal maneuvers, adenosine or AV-nodal blockers such
as calcium channel or beta-blockers are effective therapies for termination
of the arrhythmia. For long-term management, AV-nodal blockers are
most effective and can be used either on a daily or “as needed” basis when
tachycardia occurs. Other antiarrhythmics can be used either alone or in
conjunction with AV-nodal blocking agents. Catheter ablation of the slow
AV-nodal pathway is curative in 95% of patients, but a complete AV block
can complicate slow pathway ablation in 0.5%–1% of patients.
1
251
Arrhythmias: Supraventricular, Ventricular Tachycardias and Bradyarrhythmias
Fig. 1. Measurement of the RP and PR intervals on the surface electrocardiogram.
Black lines indicate the P wave and the R wave used to measure these intervals.
RP PR
AV re-entrant tachycardia
AV re-entrant tachycardia (AVRT) involves an accessory atrioventricular
connection or pathway such as that seen in the Wolff–Parkinson–White
(WPW) syndrome. Patients with WPW have the characteristic “delta
wave” seen on the surface ECG, associated with a short PR interval of less
than 120 ms, a slurred upstroke of the QRS indicating pre-excitation (delta
wave), a broad QRS and secondary ST and T wave changes (Fig. 3). In
patients with WPW, the most common arrhythmia is AVRT that utilizes
the AV node for antegrade conduction and the accessory pathway for retrograde conduction. As with AVNRT, this tachycardia often has abrupt
onset and offset and is characterized by a short RP interval. The presence
of alternation in the amplitude of the QRS complexes (QRS alternans) on
the surface ECG during tachycardia points to AVRT as the mechanism,
but this finding is not limited to AVRT. The location of the accessory pathway is along the lateral mitral valve annulus in approximately 50% of
cases, in the posteroseptum in 25%, along the lateral tricuspid valve annulus in 25% and in the anteroseptum in 2%.
2
Acutely, vagal maneuvers,
252
A. Fischer
Fig. 2. Twelve-lead electrocardiogram of a narrow complex tachycardia with P waves
seen in the terminal portion of the QRS complex. The arrow in the magnified trace of lead
V1 identifies a clearer image of the P wave.
V1
adenosine or AV-nodal blockers such as calcium channel or beta-blockers
are effective therapies for termination. Chronically, AV-nodal blockers are
most effective and can be used either on a daily or “as needed” basis when
tachycardia occurs. Catheter ablation of the accessory pathway is curative
in 95% of patients and an AV block is uncommon except when ablating
anteroseptal pathways as these are located close to the AV node.
2
Atrial tachycardia
In contrast to AVNRT and AVRT, the mechanism of atrial tachycardia
(AT) is most often not re-entrant and patients are often older and may have
structural heart disease. As a result of increased automaticity, an impulse
arises from an ectopic focus in either the right or left atrium. Often the
tachycardia is incessant in nature and, depending on the rate of the AT, can
occur with 1:1 AV conduction. Bursts of nonsustained tachycardia can
often occur and P wave morphology can often be seen most clearly in the
initiating beat (Fig. 4).
The morphology of the P wave on the surface ECG is often helpful in
predicting the location of the ectopic focus. In particular, inverted P waves
in limb leads I and aVL suggest the presence of a left atrial focus. Acutely,
adenosine will terminate 10%–15% of ATs and AV-nodal blockers are
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Arrhythmias: Supraventricular, Ventricular Tachycardias and Bradyarrhythmias
Fig. 3. Twelve-lead electrocardiogram from a patient with Wolff–Parkinson–White.
Note the short PR interval, the slurred upstroke of the initial portion of the QRS complex
and the nonspecific T wave changes.