Radiofrequency ablation therapy may be suitable for M.P. However, if exercise
intolerance is her primary complaint, this might be relieved by switching M.P. to
another drug, such as verapamil.
Paroxysmal Supraventricular Tachycardia
QUESTION 1: B.J., a 32-year-old woman, presents to the emergency department (ED) complaining of
110 ms (normal, <120 ms). She has no past medical history of note.
What is the clinical presentation of PSVT, and what are the consequences of this arrhythmia?
PSVT often has a sudden onset and termination. At the time of PSVT, the heart rate
is usually 180 to 200 beats/minute. As illustrated by B.J., patients experience
palpitations and often nervousness and anxiety. In patients with a rapid ventricular
rate, dizziness, and syncope can occur, and the rhythm may degenerate to other
serious arrhythmias. Angina, HF, or shock may be precipitated by underlying severe
atherosclerosis or left ventricular dysfunction but this is not part of B.J.’s past
medical history. There is no evidence that patients with episodes of PSVT are at an
CASE 15-3, QUESTION 2: What is the arrhythmogenic mechanism of PSVT?
AV nodal reentry is the most common mechanism of paroxysmal supraventricular
arrhythmias (see Fig. 15-2). Here AV nodal impulses are blocked in one of two
directions in an antegrade fashion but when reaching the end, conducts in a retrograde
fashion setting up a circular reentrant circuit. Reciprocating tachycardias occur when
there is an accessory pathway for conduction of impulses between the atria and
ventricles, like with WPW syndrome, and PSVT results (Fig. 15-6).
be seen in a patient with Wolff–Parkinson–White syndrome.
CASE 15-3, QUESTION 3: B.J. tries the Valsalva maneuver, and her ventricular rate is reduced to 150
any drug interactions that might diminish adenosine’s effect?
Although her BP is low at 95/60 mm Hg, B.J. is maintaining an adequate perfusion
pressure, so vagal maneuvers should be attempted first. Two common vagal
techniques are pressure over the bifurcation of the internal and external carotid
arteries and the Valsalva maneuver (forcible exhalation against a closed glottis,
similar to bearing down to have a bowel movement). The increase in pressure
induced by these maneuvers is sensed by the baroreceptors, causing a reflex decrease
in sympathetic tone and an increase in vagal tone. The increase in vagal tone will
terminate in 10% to 30% of cases.
If B.J. was hemodynamically unstable or
becomes hemodynamically unstable, she should receive synchronized DC
Because most PSVT episodes involve reentry in the AV node, drugs that block the
AV node (negative dromotropic drugs) are generally effective. Adenosine, a purine
nucleoside that exerts a transient negative chronotropic and dromotropic effect on
is considered the drug of choice for the acute treatment of
PSVT because of its rapid and brief effect. An initial 6-mg IV bolus is given; if this
is unsuccessful within 2 minutes, it can be followed by one or two 12-mg IV boluses,
up to a maximum of 30 mg. Because of its short half-life (9 seconds), adenosine
should be administered as a rapid bolus (over 1–3 seconds), followed immediately
by a saline flush. Adenosine begins to be metabolized immediately after entering the
bloodstream; therefore, B.J.’s failure to respond is likely attributed to the prolonged
Theoretically, adenosine may be ineffective or higher doses may be required in
patients who are receiving theophylline because theophylline is an effective
adenosine receptor blocker. Larger
doses of other methylxanthines (caffeine, guarana) may also theoretically interact
like theophylline. Conversely, concomitant use of dipyridamole may accentuate
adenosine’s effects because dipyridamole blocks the adenosine uptake (and
CASE 15-3, QUESTION 4: B.J. is given 12 mg adenosine IV during 2 seconds, followed by a 20-mL normal
B.J. is experiencing a common side effect of adenosine. Patients receiving
adenosine should be warned that they may feel transient chest heaviness, flushing, or
a feeling of anxiety. Shortness of breath and wheezing may be observed in patients
with asthma. The denervated heart of the patient who has undergone heart transplant
is particularly sensitive to adenosine; therefore, lower doses of adenosine should be
Nondihydropyridine calcium-channel blockers, verapamil, and diltiazem, can be
used in patients with PSVT. Verapamil (5–10 mg or 0.075–0.15 mg/kg IV given over
2 minutes) achieves peak therapeutic effects in 3 to 5 minutes after dosing and can be
repeated at 10- to 15-minute intervals to a maximal dose of 20 mg if needed. The
elderly should receive the verapamil infusion over 3 minutes to minimize the risk of
adverse events. Diltiazem is given as a 0.25-mg/kg IV bolus over 2 minutes, and a
second bolus of 0.35 mg/kg can be given 15 minutes later if the effect is inadequate.
Both of these calcium-channel blockers have an 85% conversion rate.
verapamil should not be used in patients with wide complex tachycardia of unknown
for radiofrequency catheter ablation therapy for PSVT?
Radiofrequency catheter ablation is frequently used as a definitive treatment for
PSVT. EP testing is used to determine the location of the reentrant tract, which then
can be ablated, thereby interrupting accessory pathways and reentrant circuits. This
treatment approach is potentially curative and is performed by an electrophysiologist.
Patients who are not candidates for ablation, or who do not wish to undergo the
procedure, can receive medications on a chronic basis. PSVT is managed with agents
that slow conduction and increase refractoriness in the AV node, thereby preventing a
rapid ventricular response. These include oral verapamil, diltiazem, β-blockers, or
digoxin. Class Ic and III agents are used occasionally to slow conduction and
increase refractoriness of the fast bypass tract to prevent triggering impulses such as
premature atrial and ventricular contractions.
B.J. has had a few episodes of PSVT in the past and may be a candidate for
ablation. Alternatively, because she responded to IV verapamil, oral SR verapamil
could be prescribed at a dosage of 240 mg/day.
Wolff–Parkinson–White Syndrome
but he stopped taking it because of side effects. What is WPW syndrome?
WPW is a preexcitation syndrome in which there is an accessory bypass tract
connecting the atria to the ventricles (Fig. 15-6). An impulse can travel down this
pathway and excite the ventricle before the expected regular impulse through the AV
node arrives. If there is antegrade conduction over the bypass tract while the patient
is in normal sinus rhythm, the ECG will demonstrate a short P-R interval (<100 ms),
a delta wave that represents a fused complex from preexcitation, and the regular QRS
complex after AV conduction. PSVT and AF occur in these patients at a higher
incidence than in the general population of the same age.
the rapid atrial impulses will be conducted directly to the ventricle through the
bypass tract, causing a rapid ventricular rate that may evolve into VF. Verapamil
(like diltiazem, β-blockers, adenosine, and amiodarone) can increase this risk by
increasing the effective refractory period of the AV node and indirectly reducing the
effective refractory period in the bypass tract.
CASE 15-4, QUESTION 2: Why did verapamil cause VF in M.B.? What therapies would be appropriate for
M.B., and what drugs should be avoided?
Because M.B. had AF, the rapid atrial impulses were conducted directly down the
bypass tract to the ventricle, causing VF.
The antiarrhythmic drugs used to chemically convert patients with AF who have
WPW, such as M.B., include procainamide, propafenone, flecainide, and
99,100 DC cardioversion is an option for more emergent conversion of AF in
patients with WPW and hemodynamic instability. Radiofrequency ablation of the
bypass tract is curative for many patients with WPW and is indicated for people who
maintain preexcitation during exercise
stress testing, a shortest preexcited RR interval <250 ms, symptoms like syncope
of palpitations, or preexisting structural heart disease. M.B. has symptoms associated
with AF in WPW and should undergo evaluation from an cardiologist to determine if
ablation is appropriate at this time.
Further therapy for M.B. may not be useful at this time. However, if he has
recurrent AF or other symptomatology associated with WPW, radiofrequency
catheter ablation could be indicated.
Various arrhythmias can result from blockage of impulse conduction. These can
occur above the ventricle, such as first-, second-, and third-degree (complete) AV
block. Others, such as right or left bundle branch block (RBBB or LBBB) and
trifascicular block, originate below the bifurcation of the His bundle. Although
conduction blocks can be classified as either supraventricular or ventricular
arrhythmias, they are discussed as a separate group because their mechanism of
arrhythmogenesis is similar and their treatment is different from other arrhythmias.
H.T.’s rhythm strip initially revealed a diagnosis of LBBB. Bundle branch block
occurs when the electrical impulse cannot be conducted along the left or right
fascicle of the His-Purkinje system (see Fig. 15-1). In H.T., the impulse travels down
the right bundle normally, and the right ventricle contracts at the normal time. The left
bundle is blocked, and, therefore, the left side is depolarized from an impulse
conducted from the right ventricle. This impulse must travel through atypical
conduction tissues (with slower conduction), and hence the left side depolarizes
later. This is revealed on the ECG by a widened QRS complex. Bundle branch
blocks, particularly in the left fascicle, are associated with coronary artery disease,
systemic hypertension, aortic valve stenosis, and cardiomyopathy.
do not lead to clinical cardiac dysfunction on their own. Because H.T. has LBBB, he
can develop complete heart block (third-degree block) if for any reason his right
First-degree AV block usually is asymptomatic. The ECG will show P waves with
a prolonged P-R interval (normal, <200 ms), but each P wave is followed by a
normal QRS complex. First-degree AV block is a common finding in patients taking
digoxin, verapamil, or other drugs that slow AV conduction.
Second-degree heart block consists of two types. Mobitz type I (Wenckebach) is
characterized by progressive lengthening of the P-R interval with each beat until an
impulse is not conducted; the cycle then starts over again. Mobitz type II (Fig. 15-8)
impulse conduction is blocked in a fixed, regular pattern (e.g., 3:1 block, in which
for every three P waves, only one is conducted). A major difference is that Mobitz
type I can be drug induced or exacerbated by negative dromotropic drugs but not
Third-degree heart block (complete heart block) occurs when none of the impulses
from the SA node are conducted to the ventricles. During third-degree block, the
ventricle must develop its own pacemaker (escape rhythm), which may be too slow
to provide adequate cardiac output, causing the patient to become symptomatic. A
mechanical pacemaker is needed for treatment of third-degree AV block. AV blocks
can be caused by drugs (β-blockers, calcium-channel blockers, digoxin), acute MI,
amyloidosis, and congenital abnormalities.
CASE 15-5, QUESTION 2: How should H.T.’s heart block be treated?
H.T. is experiencing a Wenckebach rhythm, which often is transient after an
inferior wall MI. As long as he is hemodynamically stable, he should be monitored
closely. If his heart rate and BP drop, atropine 0.5 mg IV bolus (maximum 2 mg) or a
temporary pacemaker can increase the heart rate. If the hemodynamic compromise
persists, a permanent pacemaker must be inserted to initiate the impulse to control the
complex is not conducted and then the cycle repeats.
usually are defined as VT, which can be nonsustained or sustained. Ventricular
flutter, VF, and TdP are other serious forms of ventricular arrhythmias. The
presentation, etiology, treatment, and ion channels associated with TdP are discussed
Nonsustained ventricular tachycardia (NSVT) (Fig. 15-10) commonly is defined
as three or more consecutive PVCs lasting less than 30 seconds and terminating
spontaneously. Sustained VT (SuVT) is defined as consecutive PVCs lasting more
than 30 seconds, with a rate usually in the range of 150 to 200 beats/minute. P waves
are lost in the QRS complex and are indiscernible. SuVT (Fig. 15-11) is a serious
development because it can degenerate into VF. Ventricular flutter is characterized
by sustained, rapid, regular ventricular beats (normal, >250 beats/minute) and
usually degenerates into VF. VF (see Fig. 15-12) is characterized by irregular,
disorganized, rapid beats with no identifiable P waves or QRS complexes. It is
thought to be triggered by multiple reentrant wavelets in the ventricle. There is no
effective cardiac output in patients with VF.
Neonatology Pathophysiology & Management of the Newborn. 6th ed. Philadelphia: Lippincott Williams &
Figure 15-11 Sustained ventricular tachycardia.
Figure 15-12 Ventricular fibrillation.
Common factors that cause ventricular arrhythmias are ischemia, the presence of
organic heart disease, exercise, metabolic or electrolyte imbalance (e.g., acidosis,
hypokalemia or hyperkalemia, hypomagnesemia), or drugs (digitalis,
sympathomimetic amines, antiarrhythmic drugs). It is essential to identify and remove
any treatable cause (e.g., metabolic or electrolyte imbalance and proarrhythmic
drugs) before initiating antiarrhythmic drug therapy.
Evaluation of Life-Threatening Ventricular
An episode of life-threatening ventricular arrhythmia (i.e., SuVT, TdP, VF) carries a
significant risk of morbidity and mortality. Adequate documentation of the arrhythmia
and its suppression by either drugs or a mechanical device are essential. Patients
suspected of having, or documented to have, symptoms of a life-threatening
arrhythmia (e.g., syncope, out-of-hospital cardiac arrest) should be admitted to the
hospital and evaluated. At present, the European Heart Rhythm Association
(EHRA)/Heart Rhythm Society (HRS)/Asia Pacific Heart Rhythm Society (APHRS)
practice guidelines provided a class IIa recommendation for standard testing with a
12-lead ECG in all patients undergoing evaluation for ventricular arrhythmias, along
with echocardiography (detects structural heart disease). Contrast-enhanced magnetic
resonance imaging (MRI) may provide additional guidance in the management of
certain forms of structural heart disease, such as dilated cardiomyopathy,
hypertrophic cardiomyopathy, sarcoidosis, amyloidosis, and arrhythmogenic right
103 Ambulatory monitoring and EP studies are two
additional approaches used to evaluate the arrhythmia and the effectiveness of
The frequency of suspected ventricular arrhythmias determines the ambulatory
monitoring device indicated for patients.
104,105 For more frequent occurrences (once
daily) of arrhythmias, Holter monitoring during a 24- to 48-hour period represents
the first-line ambulatory monitoring device. The patient wears a portable ECG
monitoring device in a purse-like carrier, and electrodes connected to the monitor are
taped to the patient’s chest. The ECG is played back in the laboratory, correlating the
presence of arrhythmias with a written patient activity and symptom log. In contrast,
30-day ambulatory event recorders are selected for patients presenting with
arrhythmias that occur less frequently.
104,105 The event recorder (or loop recorder) is
worn constantly for 30 days and stores and saves data upon activation by the patient.
Whenever a patient experiences symptoms, a switch on the recorder is depressed,
resulting in storage of a record of the patient’s heart rhythm at the time of the event. A
telephone can transfer event recorder data for analysis. On rare occasions,
cardiologists will order mobile outpatient cardiac telemetry, which is the outpatient
equivalent of continuous inpatient cardiac telemetry.
device can be worn for up to 6 weeks, and offers the advantage of real-time
automatic detection. However, because of its high cost, many third-party payers deny
coverage for patients, thereby limiting more widespread use.
EP studies represent another approach to evaluating ventricular arrhythmias,
especially in patients with sporadic ventricular arrhythmias that may be missed by
103 EP testing serves as a diagnostic tool for evaluating drug
effects, assessing the inducibility of VT, determining the risks of recurrent VT or
sudden cardiac death (SCD), guiding ablation, and assessing the need for an
implantable cardioverter-defibrillator (ICD).
Premature Ventricular Contractions
Auscultation of the heart reveals an S3
gallop. Her electrolytes include potassium (K) 3.8 mEq/L, and
magnesium (Mg) 1.2 mEq/L Otherwise, her examination is within normal limits. Two days later, an
was ordered. Should A.S.’s multiple PVCs be treated with a class I antiarrhythmic drug?
Occasional PVCs are a benign, natural occurrence, even in a healthy heart, and are
not an indication for drug therapy. Similarly, asymptomatic simple forms of PVCs,
even in patients with other cardiac disease, usually do not need treatment. However,
the presence of frequent PVCs may be associated with ischemia with impaired left
103 Of note, it is also possible that PVCs may emerge as a result
of an underlying cardiomyopathy, thereby making it difficult to prospectively
determine which of these sequences apply to a given patient.
Because PVCs are a risk factor for SCD, the National Institutes of Health launched
the Cardiac Arrhythmia Suppression Trial (CAST)
suppression in survivors of MI. The CAST was a prospective, randomized, placebo-
controlled trial that evaluated three antiarrhythmic agents: flecainide, encainide, and
moricizine (all class Ic agents). The choice of these drugs was based on results of a
pilot study of 1,498 patients that showed adequate suppression of arrhythmia (PVCs)
in the target population. Ten months after initiation of the study, CAST was
discontinued because of excess total mortality and cardiac arrests in patients
receiving flecainide and encainide. Total mortality in the flecainide and encainide
groups was 8.3% compared with 3.5% in the placebo group.
group, which was reported separately in CAST II, 16 of 660 patients in the drug
group died compared with 3 of 668 patients in the placebo group in the initial 2
weeks. Subsequent long-term follow-up did not show a difference between
patients enrolled in CAST were asymptomatic and at low risk for the development of
arrhythmias, they were at greater risk for drug toxicity (relative to benefit). Although
many issues have been raised concerning CAST, one conclusion is that patients with
a recent MI and the presence of asymptomatic PVCs should not be treated with
encainide, flecainide, or moricizine. Whether other class I antiarrhythmic agents will
produce similar results is unknown. Thus, the decision to avoid using a class I
antiarrhythmic medication to treat A.S.’s PVCs was a sound one. The proarrhythmic
effects of the drug may outweigh the potential danger of PVCs at this time.
(>10,000/24 hours) or in patients without structural disease who continue to
103 Despite the limited efficacy of this class of drugs with regard
to PVC elimination (10%–15% achieve >90% PVC suppression), β-blockers
represent the mainstay of medical suppression of PVCs. Blockade of β1
decreases automaticity in response to reduced intracellular cyclic adenosine
In addition, β-blockers exert negative chronotropic effects,
lowering the resting sinus rate, along with slowing AV nodal conduction.
It is estimated that SCD accounts for 50% of all deaths among MI patients.
pooled analysis from 31 clinical trials evaluating β-blockers in MI, a 20% to 25%
reduction in the risks of death and reinfarction during an average of 2 years of
109 The beneficial effects of β-blockers on mortality were
primarily attributed to a decrease in SCD, usually caused by arrhythmias such as
110 Similarly, a meta-analysis of 28 randomized trials demonstrated that IV
followed by oral β-blocker therapy resulted in a 15% to 20% decrease in the relative
risks of reinfarction and cardiac arrest during the first 7 days of hospitalization for
The COMMIT/CCS2 (Clopidogrel and Metoprolol in Myocardial Infarction
Trial/Second Chinese Cardiac Study) collaborative group assessed the effect of IV
metoprolol (up to three 5-mg doses in the first 15 minutes) followed by oral
metoprolol (200 mg/day in divided doses, then 200 mg once daily) or placebo on
cardiovascular outcomes in 45,852 acute MI patients.
did not result in significant reductions in the rate of achieving the coprimary study
outcomes, but five fewer episodes of VF for every 1,000 patients occurred during
therapy with metoprolol (odds ratio [OR], 0.83; 95% confidence interval [CI], 0.75–
0.93; p = 0.001). However, metoprolol-treated patients experienced 11 more
episodes of cardiogenic shock for every 1,000 patients during the treatment period
(OR, 1.30; 95% CI, 1.19–1.41; p < 0.00001).
The American College of Cardiology Foundation/American Heart Association
Task Force group recommended the routine use of oral β-blocker therapy during the
first 24 hours for patients who do not have contraindications (see Chapter 13, Acute
Coronary Syndrome) to prevent the early occurrence of VF. Furthermore, the task
113 Hence, in A.S. a β-blocker is an important first-line agent to
In high-risk patients with MI who are not candidates for β-blockade, alternative
antiarrhythmic therapy with amiodarone can be considered.
class III antiarrhythmic agent, but also has antiadrenergic, class I, and class IV
activity. However, given that cumulative exposure to this drug can result in damage
to multiple organs, caution should be exercised before using it for PVC
103,105 An evaluation of amiodarone in post-MI patients with frequent
PVCs (≥10/hour) or at least one run of VT was conducted in the Canadian
Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT).
amiodarone significantly reduced the incidence of VF or arrhythmic death by 48.5%
Similarly, the European Myocardial Infarct Amiodarone Trial (EMIAT), evaluated
MI survivors with a reduced ejection fraction (<40%).
reduced arrhythmic deaths by 35% compared with placebo, but this did not
demonstrate any difference in mortality (13.86% with amiodarone vs. 13.72% with
placebo). This suggests that amiodarone should not be used in all patients with a
reduced ejection fraction after an MI, but that it could benefit patients in whom
antiarrhythmic therapy is indicated. Hence, if A.S. reports problematic symptoms
associated with the PVCs or develops additional risk factors for arrhythmia while on
β-blockade, the first-line treatment option, antiarrhythmic therapy with amiodarone,
can be given without an increased risk of overall mortality.
If A.S. had nonsustained runs of VT instead of just PVCs, β-blockade would
remain the first-line treatment option and amiodarone could similarly be considered
if β-blockers are unsuccessful but in this scenario, A.S. would need to be assessed by
a cardiologist to see if she would meet the criteria for receiving an ICD.
The EHRA/HRS/APHRS panel members recommend catheter ablation for patients
with reversible left ventricular dysfunction associated with high PVC burden
(>10,000/24 hours), who have failed, did not tolerate, or declined medical
103 The most commonly employed technique involves activation mapping,
where electrophysiologists maneuver catheters to target the precise PVC origin in the
heart, which is subsequently ablated.
104,105 Catheter ablation is not without risk, but
has been shown to abolish PVCs in 74% to 100% of patients in numerous
Sustained Monomorphic Ventricular Tachycardia
(LVEF) of 35%.How should she be treated?
The majority of patients with SuVT have structural heart disease, and therefore
require ICD placement with optimal programming. In addition to ICD placement,
patients with SuVT and ischemic structural disease usually receive adjunctive
therapy with antiarrhythmic drugs or undergo catheter ablation if they experience
incessant SuVT. Patients with nonischemic structural disease may receive adjunctive
therapy with an antiarrhythmic drug, but are less likely to undergo catheter ablation,
unless they experience recurrent VT while receiving medications.
The acute treatment of patients with SuVT depends on their hemodynamic stability
If unstable, patients should receive DC cardioversion
synchronized to the QRS on the surface ECG. If the patient is conscious, but
experiencing marked hypotension or excessive symptoms from SuVT, a short-acting
benzodiazepine (e.g., midazolam) should be administered before undergoing
To date, antiarrhythmic monotherapy has not been shown to improve mortality in
patients with non-acute SuVT and structural heart disease.
In the OPTIC study, amiodarone was superior to β-blocker monotherapy in
lowering the frequency of recurrent appropriate ICD therapy (shocks) during 1-year
follow-up of patients receiving
120 The OPTIC (Optimal Pharmacological Therapy in
Cardioverter Defibrillator Patients) study enrolled 412 patients with St. Jude’s
Medical dual-chamber ICDs; LVEF <40% who had inducible VT or VF or prior;
history of SuVT, VF, or cardiac arrest; or syncope of unknown cause with VF or VT.
The effect of amiodarone plus β-blocker (metoprolol, carvedilol, or bisoprolol)
compared with sotalol or β-blocker alone on the primary end point, first occurrence
of any shock delivered by the ICD, was assessed for a median of 359 days. One-year
shock rates were 10.3%, 24.3%, and 38.5%, respectively, in amiodarone/β-blocker–
treated patients, in sotalol-treated patients, and in β-blocker–treated patients. Patients
receiving amiodarone combined with β-blocker had significantly lower risk of shock
compared with patients receiving β-blocker monotherapy and sotalol monotherapy.
Of note, adverse effects such as pulmonary toxicity, thyroid effects, and symptomatic
bradycardia contributed to an 18.2% discontinuation rate for amiodarone at 1 year.
However, longer term studies assessing the safety and efficacy of amiodarone for
secondary prophylaxis, showed higher rates of VT recurrence and major adverse
effects, compared with placebo.
combination of mexiletine and amiodarone, have shown reductions in recurrences of
The 2010 AHA guidelines for cardiopulmonary resuscitation (CPR) and
emergency cardiovascular care addressed the potential efficacy of IV antiarrhythmic
drugs in stable VT patients. A class IIa rating for the use of IV procainamide was
recommended by the AHA guidelines, with amiodarone (class IIb) and sotalol (class
IIb) representing alternative choices of antiarrhythmic therapy for wide complex
IV amiodarone should be administered as a 150-mg dose for
10 minutes, followed by a 6-hour infusion at a rate of 1 mg/minute, and finally a 0.5-
mg/minute infusion for 18 hours. For recurrent or resistant arrhythmias, supplemental
infusions of 150 mg can be repeated every 10 minutes, up to a maximal total daily IV
dose of 2.25 g. Commonly seen adverse effects associated with IV amiodarone
include hypotension and bradycardia, which can be prevented by slowing the drug
125 Per AHA 2010 recommendations, patients with monomorphic VT
who receive IV sotalol should receive a 100-mg (1.5 mg/kg) dose infused for 5
IV sotalol is approximately dose-equivalent to the oral formulation,
because an IV dose of 75 mg equals an 80-mg oral dose.
diluting sotalol in 100 to 250 mL of 5% dextrose, normal saline, or lactated Ringer’s
solution, and administering the drug using a volumetric infusion pump for a 5-hour
period. Common adverse effects associated with sotalol include bradycardia and
hypotension. The propensity of this agent to induce TdP is covered later in this
chapter. The mean elimination half-life of sotalol is 12 hours. Because it is cleared
by the kidneys, its clearance is reduced and its half-life prolonged in patients with
renal dysfunction. Consequently, patients receiving sotalol should receive continuous
BP, heart rate, and ECG monitoring. Patients who experience excessive QT
prolongation while on sotalol should receive lower doses or the drug should be
Implantable Cardiac Defibrillators (ICDs)
CASE 15-7, QUESTION 2: On hospital day 2, S.L. experiences a run of VT lasting about 2 minutes. The
Transvenous ICDs are devices implanted under the skin with wires or patches that
are advanced or attached so they are in direct contact with the ventricular
myocardium. The ICD is composed of a pulse generator, sensing and pacing
electrodes, and defibrillation coils. The pulse generator consists of a
microprocessor, a memory component capable of storing ECG data, a high-voltage
capacitor, and a battery. The microprocessor controls the analysis of cardiac rhythm
and delivery of therapy. An electrode is usually placed at the endocardium of the
right ventricular apex, but in some rare cases, it is surgically placed on the
epicardium. Patients with dual-chamber ICDs have a second electrode placed in the
right atrial appendage. Biventricular ICDs have an additional electrode placed
surgically on the epicardium of the left ventricle, or more commonly, placed
transcutaneously in a branch off of the coronary sinus. Defibrillation coils are
positioned on the right ventricular electrode at the level of the right ventricle and the
superior vena cava. In most ICD systems, biphasic defibrillation current flows from
the distal defibrillation coil to the pulse generator and to the proximal defibrillation
Since 2012, numerous advancements in ICD technology have occurred: (a)
development of longer-lasting batteries (up to 12 years for Boston Scientific
models); (b) emergence of quadripolar leads to optimize therapeutic efficacy through
improved device programming; (c) development of subcutaneous ICDs (s-ICDs); and
(d) development of MRI-safe ICDs (available in Europe).
(model SQ-RX 1010, Cameron Health, Inc., San Clemente, California) consists of a
subcutaneous pulse generator and a single subcutaneous electrode, comprised of
sensing and defibrillating components.
129 The pulse generator is usually placed in the
subcutaneous pocket created over the fifth intercostal space between the mid and
anterior axillary lines. Placement of the subcutaneous lead is parallel to the left side
of the sternum, with its upper pole situated at the level of the sternal notch and the
lower electrode positioned beneath the level of the xiphoid process. Some of the
advantages of using the s-ICD system include elimination of potential adverse events
associated with venous access, minimal physical stress on leads associated with
cardiac motion, and relative ease of device extraction. However, unlike transvenous
ICDs, the currently marketed s-ICD has a larger pulse generator, along with having
less data on long-term performance. Furthermore, the current s-ICD does not provide
antitachycardia pacing for VT.
129 Multiple clinical trials have proved the superiority
of ICD treatment over antiarrhythmic therapy for the secondary prevention of SCD.
On the basis of evidence from numerous clinical trials of primary and secondary
prevention of SCD, the American College of Cardiology/American Heart
Association/Heart Rhythm Society 2012 guidelines for device-based therapy of
cardiac rhythm abnormalities assigned a class Ia rating for ICD implantation in seven
groups of patients. ICD therapy is indicated for (a) survivors of cardiac arrest caused
by VF or hemodynamically unstable sustained VT (level of evidence [LOE] A); (b)
patients with LVEF equal to or less than 35% caused by a prior MI who are at least
40 days after the event and are in NYHA functional class II or III (LOE A); (c)
patients with LVEF equal to or less than 30% caused by prior MI who are at least 40
days after the event and are in NYHA functional class I (LOE A); (d) patients
experiencing spontaneous SuVT in conjunction with structural heart disease,
regardless of hemodynamic stability (LOE B); (e) hemodynamically compromised
patients with electrophysiology study–induced SuVT or VF associated with syncope
of undetermined origin; (f) patients with LVEF less than or equal to 35% associated
with nonischemic dilated cardiomyopathy and are in NYHA functional class II or III
(LOE B); and (g) patients with LVEF less than or equal to 40% in conjunction with
NSVT secondary to prior myocardial infarction, who experience SuVT or inducible
Although ICDs have been shown to improve survival in select patient populations,
the benefit may be offset by diminished quality
of life associated with painful shocks, increased mortality compared with ICD
patients who do not require shocks, and incomplete protection from the occurrence of
SCD (5% of patients fail to respond).
In recent years, investigators have
examined various approaches to reducing the frequency of ICD shocks.
Antiarrhythmic medications and prophylactic catheter ablation have been shown to
reduce the incidence of ICD firing.
120,131,132 The EHRA/HRS/APHRS taskforce group
assigned a class IIa rating for the strategies of programming ICDs to a delayed VT
detection interval and a high VF detection rate in patients requiring primary
Defibrillation threshold is classified as the minimum amount of energy needed to
result in successful defibrillation of the heart and restoration of normal sinus
It is important for clinicians to be aware that antiarrhythmic agents have
been associated with increases (amiodarone) or reductions (dofetilide) in ventricular
Clearly, S.L. should have an ICD implanted. It is her best chance for prolonging
long-term survival. Depending on the number of times the machine discharges per
month and the patient’s response, adjunctive antiarrhythmic drugs or prophylactic
ablation may be needed, along with optimizing ICD programming.
is to be treated with amiodarone, how should it be initiated and monitored?
Amiodarone exhibits properties of classes I, II, III, and IV antiarrhythmic agents.
Although it has class II effects on the heart, amiodarone is virtually devoid of
antiadrenergic effects outside the heart and is not contraindicated in patients with
asthma. The antiadrenergic effects arise from inhibition of adenylate cyclase, the
enzyme that catalyzes production of the second-messenger product cyclic adenosine
monophosphate. Amiodarone can also cause a reduction in β1
Because of the extremely long half-life of amiodarone, loading doses are used to
accelerate the onset of drug effect. The OPTIC trial used a loading dose of oral
amiodarone 400 mg, given twice daily for 2 weeks, followed by a daily dose of 400
mg for the next 4 weeks, and a daily maintenance dose of 200 mg thereafter.
Although a concentration–effect relationship is hard to determine for amiodarone,
levels greater than 2.5 mg/L are associated with an increased incidence of adverse
Amiodarone has many serious adverse effects involving a variety of organ
systems, the most serious and life-threatening of which is pulmonary toxicity.
Amiodarone-induced pulmonary toxicity (AIPT) has been shown to account for 11%
of the sum total of all reported adverse events associated with this agent.
presents as an acute process or a chronic condition that develops several months
after starting amiodarone therapy. The pathophysiologic mechanism for AIPT has not
maladaptive immune response; (c) increased tumor necrosis factor-α activity; and (d)
angiotensin-mediated apoptotic effects of amiodarone on alveolar epithelial cells. It
has been suggested that higher doses of amiodarone, older age, and preexisting
pulmonary disease may predispose patients to developing AIPT. However, AIPT has
been shown to occur after patients received low doses of amiodarone (200 mg/day).
Manifestations of chronic AIPT include cough, dyspnea, impaired diffusion capacity
of carbon monoxide, infiltrates on chest radiograph, weight loss, and fever. In
contrast, patients presenting with acute AIPT experience rapid decline in respiratory
function, potentially culminating in the development of acute respiratory distress
syndrome (ARDS) with alveolar opacities. Given the prolonged half-life of
amiodarone, symptom resolution will be a slow process for patients with AIPT.
Patients presenting with marked radiographic opacities and hypoxemia may need to
receive prednisone 40 to 60 mg daily for several months. Mortality rates for patients
with AIPT have been shown to approach 10%, with higher mortality rates seen in
patients requiring hospitalization (20%–30%) or who develop ARDS (50%).
A baseline chest radiograph and pulmonary function tests (diffusion capacity in
particular) are recommended by the manufacturer.
140 The chest radiograph should be
repeated at 3- to 6-month intervals, and patients should be specifically questioned
about pulmonary symptoms because early detection can decrease the extent of lung
Comments
Post a Comment
اكتب تعليق حول الموضوع