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PREMATURE VENTRICULAR CONTRACTION

INTRODUCTION
Background: Premature ventricular contraction (PVC) is an ectopic cardiac pacemaker located in the
ventricle. PVCs are characterized by the premature occurrence of bizarre-shaped QRS complexes,
with the QRS width usually > 120 msec. These complexes are not preceded by a P-wave and the Twave is usually large and opposite in direction to the major deflection of the QRS.
The clinical significance of PVCs is dependent on PVC frequency, complexity and hemodynamic
response.

Pathophysiology: PVCs reflect the enhanced activity of ventricular pacemaker cells. Suggested
mechanisms for PVCs are reentry, triggered activity and enhanced automaticity.
Reentry occurs when there is an ar
ea of one-way block in the Purkinje fibers and a second area of slow conduction. During ventricular
activation, the area of slow conduction activates the blocked part of the system after the remainder of
the ventricle has recovered. This results in an extra beat. Reentry can produce single ectopic beats or
can trigger paroxysmal tachycardia.
Triggered beats are felt to be due to after depolarizations triggered by the preceding action potential.
Enhanced automaticity suggests that there is an ectopic focus of pacemaker cells within the ventricle
that have a subthreshold potential for firing. The
heart's basic rhythm raises these cells to threshold, which precipitates an ectopic beat.
.
Frequency:

In the U.S.: One of the most common arrhythmias, PVCs occur in patients with and without
heart disease. In healthy, middle-aged males, more than 60% will show PVCs on routine
Holter monitoring. In patients with prior myocardial infarction (MI), more than 80% will
show evidence of PVCs on Holter.

.Mortality/Morbidity: The clinical significance of PVCs depends on the clinical context in which
they are occurring.

PVCs in young healthy patients without underlying structural heart disease are not associated
with any increased rate of mortality.

PVCs occurring in older patients, in particular those with underlying heart disease, are
clinically significant.

A PVC frequency of > 10/hour, the presence of runs of PVCs, multiple ventricular
morphologies and PVCs occurring early in the cardiac cycle (R-on-T phenomenon) are
associated with increased mortality and subsequent arrhythmic events.

Sex: Ventricular ectopy may be higher in males than in females of the same age.
Age: PVC frequency increases with age, reflecting the increased prevalence of cardiac disease in
older populations.
.

CLINICAL
History:

Patients are usually asymptomatic.

Palpitations and neck/chest discomfort can be caused by cannon a waves or by the increased
force of contraction due to postextrasystolic potentiation of contractility.

The patient may report feeling the heart has stopped after a PVC.

In patients with frequent PVCs or bigeminy, syncope can be reported due to inadequate stroke
volume or decreased cardiac output due to effectively halving the heart rate.

Long runs of PVCs can also result in hypotension.

Exercise can increase or decrease the PVC rate.

Physical:

Cannon a waves may be observed in the jugular venous pulse, if the timing of the PVC causes
an atrial contraction against a closed tricuspid valve.

Compensatory pauses following a premature beat will be detected on auscultation.

The ectopic beat may produce a diminished or absent pulse, dependent on the force of the
ventricular contraction.

Causes:

Cardiac:
o

Acute myocardial infarction/ischemia

Myocarditis

Cardiomyopathy, dilated or hypertrophic

Hypomagnesemia, hypokalemia, hypercalcemia

Mitral Valve Prolapse

Hypoxia

Medications (e.g., digoxin, sympathomimetics, tricyclic antidepressants, aminophylline,


caffeine)

Illicit substances (e.g., cocaine, amphetamines, alcohol, tobacco)

WORKUP
Lab Studies:

Serum electrolytes, in particular potassium; consider checking magnesium level, especially in


patients with low potassium.

In selected patients, a drug screen may be helpful.

For patients on medication with known pre-arrhythmic effects (e.g., digoxin or theophylline),
drug levels may be useful.

.Imaging Studies:

Electrocardiography (ECG):
o

An ECG should be obtained in patients with complex ectopy to rule out structural
heart disease.

This will be useful not only in evaluating the ejection fraction, which is important
prognostically, but any valvular disease and evidence of hypertrophy.

An ECG is essential to the diagnosis and work-up of PVCs.

Instances in which the ECG can be very helpful in determining the cause of
ventricular ectopy include: acute ischemia/infarction (ST segment, T-wave changes),
electrolyte abnormalities (hyperacute T-waves, QT prolongation drug effects (QRS
widening and QT prolongation) or hypertrophy.

Electrocardiographic findings in PVCs may include any of the following:


a. They are premature in relation to the next expected beat of the basic rhythm.
b. The pause following the premature beat is usually a fully compensatory pause.
c. The R-R interval surrounding the premature beat is equal to double the basic R-R
interval, showing that the ectopic beat did not reset the sinus node.

PVCs may appear in a pattern of bigeminy, trigeminy or quadrigeminy, which


describe a pattern of PVCs occuring every other, every third or every fourth beat,
respectively.

PVCs with identical morphology on a tracing are called monomorphic or unifocal. If


the PVCs demonstrate two or more different morphologies, they are referred to as
multiform, pleomorphic or polymorphic.

PVCs are usually described in terms of the Lown grading system for premature beats.
The higher the grade, the more serious the ectopy.

Grade 0 = No premature beats


Grade 1 = Occasional (< 30 per hour)
Grade 2 = Frequent (> 30 per hour)
Grade 3 = Multiform
Grade 4 = Repetitive (A = Couplets, B = Salvos of = or > 3)
Grade 5 = R-on-T

Other Tests:

Holter 24-hour monitors are useful in quantifying and characterizing ventricular ectopy.
o

Holters have also been used to determine treatment efficacy in patents with frequent
or complex PVCs.

Suppression of ectopy on Holter monitoring is not always predictive of survival.

The most important role for Holter monitoring is risk stratification of patients with a
recent myocardial infarction or known left ventricular dysfunction.

Signal Averaged ECG (SAECG):


o

SAECGs may have a future role in identifying patients at risk for complex ventricular
ectopy and NSVT.

SAECGs may have a role in identifying patients with complex ectopy who may
benefit from EPS.

.Procedures:

Exercise Stress Testing (EST) is best used complementary to Holter monitoring. In patients
with complex ectopy, EST can unmask nonsustained ventricular tachycardia triggered by
increased catecholamines or myocardial ischemia.

The role of electrophysiologic studies (EPS) in complex ventricular ectopy is an area of both
intense research and debate. A joint AHA/ACC statement suggested the following:

There is no indication for routine EPS in low-risk patients after MI. Low risk refers to
simple ectopy, good LV function and low CHF class.

It is indicated in high-risk patients with complex ectopy.

EPS is felt to be beneficial in those patients with sustained ventricular tachycardia


greater than 24 hours after an MI.

TREATMENT
Prehospital Care:

Telemetry

IV access

Oxygen

Lidocaine should be used for patients with complex ectopy and hemodynamic instability. It is
not indicated routinely for chest pain.

Emergency Department Care:

Whether or not to treat PVCs in the emergency or outpatient settings depends on the clinical
scenario. In the absence of cardiac disease, isolated, asymptomatic ventricular ectopy
regardless of configuration or frequency, requires no treatment. With cardiac disease, certain
toxicities and electrolyte imbalances, treatment may be required. Telemetry, IV access,
oxygen and a twelve lead ECG should be established.

Hypoxia: Treat the underlying cause and provide oxygen and the ABCs.

Drug Toxicity: Specific therapy indicated for certain toxicities. Examples include digoxin
(Fab antibodies), tricyclics (bicarbonate) and aminophylline (gastrointestinal decontamination
and, possibly, hemodialysis).

Correct electrolyte imbalances, particularly those of magnesium, calcium and potassium.

Acute Ischemia/Infarction:
o

Early diagnosis and treatment of acute infarction/ischemia is the cornerstone of


therapy.

The routine use of lidocaine and other type I anti-arrhythmic agents in the setting of
acute myocardial infarction is no longer recommended due to toxicity.

This includes patients with ectopy in the immediate period after receiving
thrombolytic agents, in which complex ectopy is frequently seen.

Only in the setting of symptomatic, complex ectopy is lidocaine likely to benefit a


patient having an infarction.

Beta-blockers have proven efficacy in the setting of acute myocardial infarction and
are safe to use.

.Consultations: Cardiology involvement may be indicated if the patient is refractory to standard


therapy.
MEDICATION
Therapy for complex ventricular ectopy depends on the setting and the underlying cause. In drug
toxicity, specific therapies are available. With electrolyte imbalances, correction of abnormalities is
therapeutic. Lidocaine is the DOC in the setting of complex ectopy in the peri-MI period if the patient
is symptomatic, yet there is no firm evidence to support this practice.
Drug Category: Anti-arrhythmics - These agents alter the electrophysiologic mechanisms responsible
for premature ventricular contractions (PVCs).

Drug Name

Lidocaine - It is a class IB agent that stabilizes cell membranes and


blunt phase 0 of the action potential. Furthermore, it shortens
repolarization. The net effect is to decrease firing of the ectopic foci
and allow a normal rhythm to reassert itself.

Administer a bolus of 1-1.5 mg/kg IV and repeat, as necessary, using


1.5 mg/kg boluses q3-5 min to a total of 3 mg/kg. Follow with a
continuous IV infusion of 2 mg/min after return of perfusion.
Adult Dose

In the event that a continuous IV infusion is not started, additional


boluses of 0.5 mg/kg should be administered q10 min to maintain the
medication's effect.
If endotracheal administration is done, the dose used should be 2-2.5
times the IV dose.

Pediatric Dose

The endotracheal, intraosseous, and IV loading dose for children is 1


mg/kg and, if necessary, may repeat twice at q 10-15 min. Following
the loading dose, start a continuous IV infusion of 20-50 mcg/kg/min.

All fibrinolytics are contraindicated in the following situations:

Contraindications

Lidocaine is contraindicated for patients with documented


hypersensitivity to amide-type local anesthetics. Its use should be
avoided in patients with Adams-Stokes syndrome and Wolf-Parkinson
white syndrome. It should also be avoided in patients with severe
sinoatrial, atrioventricular (AV) or intraventricular block, if an
artificial pacemaker is not in place.

Interactions

Pregnancy

When taken concomitantly with cimetidine or beta-blockers, lidocaine


plasma concentrations can reach toxic levels. In addition, when the
drug is taken with procainamide and tocainide, the combination may
result in additive cardiodepressant action. Lidocaine may also
increase the effects of succinylcholine.

B - Usually safe but benefits must outweigh the risks.

Do not use a drug solution that contains preservatives. Exercise


caution also when the drug is administered to patients with heart
failure, hepatic disease, hypoxia, hypovolemia or shock, respiratorydepression, and bradycardia.
Precautions

The elderly may also be at increased risk for CNS and cardiac side
effects due to increased half-life or decreased clearance of the drug.
High plasma concentrations can cause seizures, heart block, and AV
conduction abnormalities. In addition, the use of lidocaine has been
associated with malignant hyperthermic crisis.

Drug Name

Adult Dose

Procainamide - It is a Class I-A antiarrhythmic used for PVCs. It


increases the refractory period of the atria and ventricles. Myocardiac
excitability is reduced by an increase in the threshold for excitation
and inhibition of ectopic pacemaker activity.

Use continued IV infusion rates of 30 mg/min until either the


arrhythmia is suppressed, the patient becomes hypotensive, the QRS
widens 50% above baseline, or a maximum dose of 17 mg/kg is
administered.
Once arrhythmia is suppressed, may infuse at a continuous rate of 1-4
mg/min

Pediatric Dose
Safety and efficacy in children have not been established. However,
the following doses have been suggested.
po: 15 to 50 mg/kg/d divided q3-6h
Do not exceed 4 g/d
IM: 20 to 30 mg/kg/d divided q4-6h

Do not exceed 4 g/d


IV: 3-6 mg/kg/dose infused over 5 min
The maintenance dose is 20 to 80 mcg/kg/min administered as a
continuous infusion.
Do not exceed 100 mg/dose or 2 g/d

Contraindications

Do not administer to patients diagnosed with complete heart block or


second or third degree heart block if a pacemaker is not in place.
Avoid also in patients with torsade de pointes. Do not use in patients
with documented hypersensitivity to procainamide or related drugs or
patients diagnosed with systemic lupus erythematosus.

Increased levels of procainamide metabolite NAPA can be expected in


patients taking cimetidine, amiodarone, trimethoprim, ranitidine, betablockers, and quinidine.
Interactions

Pregnancy

Procainamide may also increase the effect of skeletal muscle


relaxants, quinidine and lidocaine and neuromuscular blockers.
Ofloxacin inhibits the tubular secretion of procainamide and may
increase peak plasma concentrations and bioavailability. In addition,
when the drug is taken concurrently with sparfloxacin, it may increase
the risk of cardiotoxicity.
C - Safety for use during pregnancy has not been established.

The long-term use of this drug leads to the development of a positive


antinuclear antibody test in 50% of the patients. This may result in
lupus erythematosus-like syndrome in about 20% to 30% of the
patients.
Precautions

Fatal blood dyscrasias have also been reported with therapeutic doses.
The plasma concentration of procainamide and its active metabolite,
NAPA , may also be increased in renal failure.
High or toxic concentrations may induce AV block or abnormal
automaticity. Use caution in patients with complete AV block, digitalis
intoxication, organic heart disease, renal disease, and hepatic
insufficiency.

Drug Name

Bretylium - It is a class III anti-arrhythmic agent used in the treatment


of PVCs and it should be avoided as an initial treatment because of its

side effects and initial catecholamine-releasing properties.


Its use is limited to PVCs that are refractory to class I antiarrhythmics. It increases the fibrillation threshold, and causes a
refractory period by decreasing potassium conductance.
Administer an IV dose of 5 mg/kg (undiluted) over 1 min. If PVCs
persist, administer 10 mg/kg (undiluted) over 1 min
Adult Dose

If necessary, repeat q15-30 min


Do not exceed 30-35 mg/kg
The maintenance dose, when the treatment has become effective, is 1
to 2 mg/min
Safety and efficacy in children have not been established. It has been
administered to a limited number of pediatric patients, but such use
has been inadequate to define proper dosage and limitations.
Nonetheless, the following doses have been suggested.

Pediatric Dose
10 mg/kg over 1 min and repeat, as necessary, q15 min
Do not exceed 30 mg/kg
The maintenance dose is 5 to 10 mg/kg/dose q6h
Do not administer to patients with complete heart block or second or
third degree heart block if a pacemaker is not in place. Avoid also in
patients with torsade de pointes.
Contraindications
Do not use in patients with documented hypersensitivity to
procainamide or related drugs, or patients diagnosed with systemic
lupus erythematosus. It should also be avoided in digitalis-induced
arrhythmias.

Interactions

Increased toxicity has been reported when this drug is taken with
pressor catecholamines, and digitalis. In addition, the risk of
cardiotoxicity, when taken concurrently with sparfloxacin may
increase.

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Hypotension is associated with the use of this drug, especially in


patients with a fixed cardiac output (e.g., aortic stenosis). Use caution
in patients with renal insufficiency, severe pulmonary hypertension,

and aortic stenosis.


The drug has a prolonged half-life in the elderly and thus, when renal
clearance is 10-50 ml/min, administer 25% to 50% of the dose. Rapid
IV injection may also result in transient hypertension, nausea and
vomiting. Limit the injection to 5 ml (undiluted) at each site.
Drug Category: Beta-Blockers - This category of drugs has the potential to suppress ventricular
ectopy due to ischemia or excess catecholamines. In the setting of myocardial ischemia beta-blockers
have antiarrhythmic properties and reduce myocardial oxygen demand, secondary to elevations in
heart rate and inotropy.

Drug Name

Metoprolol - It is a selective beta 1 -adrenergic receptor blocker. It


decreases the automaticity of contractions.

Adult Dose

3 IV bolus injections of 5 mg each q 2 min

Pediatric Dose

Safety and efficacy in children have not been established.

Contraindications

Avoid use in patients with documented hypersensitivity to this drug or


related products and those diagnosed with uncompensated congestive
heart failure, cardiogenic shock, bradycardia, and A-V conduction
abnormalities.

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts,


cholestyramine, and rifampin may decrease its bioavailability and
plasma levels, possibly resulting in a decreased pharmacologic effect.
Conversely, loop diuretics, MAO inhibitors, haloperidol, and
hydralazine may increase metoprolol levels and thus its toxicity or
pharmacologic effects.

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Beta-adrenergic blockade may blunt the signs and symptoms of acute


hypoglycemia. In addition, beta-adrenergic blockers may mask
clinical signs (eg, tachycardia) of developing or continuing
hyperthyroidism. Abrupt withdrawal may exacerbate symptoms of
hyperthyroidism, including thyroid storm. Monitor the patient closely
and withdraw the drug slowly.

During IV administration, carefully monitor blood pressure, heart


rate, and ECG.

Drug Name

Esmolol - It is an excellent drug for use in patients at risk for


experiencing complications from beta-blockade. This is particularly
true in patients with mild-moderate LV dysfunction, reactive airway
disease, and peripheral vascular disease. The short half-life of 8 min
allows for titration to desired effect, and the ability to stop quickly if
needed.

Initially administer a loading dose infusion of 500 mcg/kg/min for 1


min followed by a 4 min maintenance infusion of 50 mcg/kg/min.
Repeat the loading dose and follow with a maintenance infusion of
100 mcg/kg/min if an adequate therapeutic effect is not observed
within 5 min.
Adult Dose

Continue the titration procedure, repeating the loading infusion and


increasing the maintenance infusion by increments of 50 mcg/kg/min
(for 4 min).
As the desired heart rate or a therapeutic end-point (eg, lowered blood
pressure) is approached, omit the loading infusion and reduce the
incremental dose in maintenance infusion from 50 mcg/kg/min to 25
mcg/kg/min or lower. Also, if desired, increase the interval between
the titration steps from 5 to 10 min.

Pediatric Dose

Safety and efficacy in children have not been established.


The suggested dose is 100-500 mcg/kg administered over 1 min

Contraindications

Avoid use in patients with documented hypersensitivity to this drug or


related products and in those diagnosed with cardiogenic shock,
congestive heart failure, bradycardia, and A-V conduction
abnormalities.

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts,


cholestyramine, and rifampin may decrease its bioavailability and
plasma levels, possibly resulting in a decreased pharmacologic effect.
Conversely, loop diuretics, haloperidol, hydralazine, and MAO
inhibitors may increase metoprolol levels and thus its toxicity or
pharmacologic effects.

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Beta-adrenergic blockade may blunt the signs and symptoms of acute


hypoglycemia. In addition, beta-adrenergic blockers may mask the
clinical signs (eg, tachycardia) of developing or continuing
hyperthyroidism. Abrupt withdrawal may exacerbate symptoms of
hyperthyroidism, including thyroid storm.

Drug Name

Propranolol - It is a class II anti-arrhythmic nonselective betaadrenergic receptor blocker. It has membrane-stabilizing activity and
decreases the automaticity of contractions.

Administer 1-3 mg under careful monitoring and do not exceed 1


mg/min to avoid lowering blood pressure and causing a cardiac
standstill.
Adult Dose

Allow time for the drug to reach the site of action, particularly when
slow circulation is present. If necessary, give a second dose after 2
min. Thereafter, do not give additional drug in less than 4h.
Do not give additional propranolol after the desired alteration if the
desired rate and/or rhythm are achieved. Transfer to oral therapy as
soon as possible. The usual dose-range is 10-30 mg tid-qid.

Pediatric Dose

IV use in children is not recommended. However, an unlabeled dose


of 0.01-0.1 mg/kg/dose to a maximum of 1 mg/dose, by slow push has
been used for arrhythmias. Transfer to oral therapy as soon as
possible.
The usual pediatric dosage range is 2-4 mg/kg/d divided bid (ie, 1 to 2
mg/kg twice daily).

Contraindications

Interactions

Avoid use in patients with documented hypersensitivity to this drug or


related products and those diagnosed with uncompensated congestive
heart failure, cardiogenic shock, bradycardia, and A-V conduction
abnormalities.

Aluminum salts, NSAIDs, penicillins, barbiturates, calcium salts,


cholestyramine, and rifampin may decrease its bioavailability, and
plasma levels, possibly resulting in a decreased pharmacologic
effects. Conversely, loop diuretics, haloperidol, hydralazine, and

MAO inhibitors may increase metoprolol levels, and thus its toxicity
or pharmacologic effects.

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Beta-adrenergic blockade may suppress the signs and symptoms of


acute hypoglycemia. In addition, beta-adrenergic blockers may mask
the clinical signs (eg, tachycardia) of developing or continuing
hyperthyroidism. The abrupt withdrawal of this medication may
exacerbate symptoms of hyperthyroidism, including thyroid storm.

Drug Category: Electrolytes - These agents are considered to be therapeutic alternatives for refractory
PVCs. Patients with persistent or recurrent PVCs following antiarrhythmic administration, should be
assessed for underlying electrolyte abnormalities as a cause for their refractory dysrhythmia.
Hypomagnesemia is associated with the onset of PVCs.

Drug Name

Adult Dose

Morphine sulfate - It acts as an anti-arrhythmic agent and diminishes


the frequency of PVCs, particularly when it is secondary to acute
ischemia.

Administer 1- 2 g diluted in 100 ml of D5W over a period of 1-2 min


for refractory VF and known or suspected hypomagnesemia (Mg +2
less than 1.4 mEq/L).
Do not exceed a dose of 30-40 g/d, or a rate of infusion for
maintenance of 1-2 g/h

Contraindications

Avoid use in patients with documented hypersensitivity to magnesium


and in those diagnosed with heart block, Addison's disease,
myocardial damage, or severe hepatitis.

Interactions

Concurrent use with nifedipine may cause hypotension and


neuromuscular blockade. Magnesium may also increase the
neuromuscular blockade seen with aminoglycosides and other agents
causing neuromuscular antagonism. In addition, it may increase the
CNS effects of CNS depressants. Magnesium also increases the
toxicity of CNS depressants, betamethasone, and cardiotoxicity of
ritodrine.

Pregnancy

A - Safe in pregnancy

Precautions

Magnesium may alter cardiac conduction leading to heart block in


digitalized patients. Respiratory rate, deep tendon reflex, and renal
function should be monitored when this electrolyte is administered
parenterally. Use caution when administering the magnesium dose
since it may produce significant hypertension or asystole.

Drug Category: Calcium channel blockers - In specialized automatic and conducting cells in the heart,
calcium is involved in the generation of the action potential. The calcium channel blockers share the
ability to inhibit movement of calcium ions across the cell membrane. This effect can depress both
impulse formation (automaticity) and conduction velocity.

Drug Name

Verapamil - It can diminish PVCs associated with perfusion therapy


and decrease the risk of ventricular fibrillation and ventricular
tachycardia. By interrupting reentry at the AV node, verapamil can
restore normal sinus rhythm in patients with paroxysmal
supraventricular tachycardias (PSVT).

Adult Dose

80-160 mg tid

Pediatric Dose

Safety and efficacy in children have not been established.

Contraindications

Avoid use in patients with documented hypersensitivity to this drug or


related products and in those diagnosed with severe CHF, sick sinus
syndrome or second- or third-degree AV block, and hypotension (less
than 90 mm Hg systolic).

Interactions

Serum verapamil levels may be decreased by hydantoins. Loss of


clinical effectiveness of oral verapamil may occur. The IV route may
bypass this interaction.

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Several cases of hepatocellular injury have been associated with


verapamil use. This medication may increase the activity of
transaminases with and without concomitant elevations in alkaline
phosphatase and bilirubin. Elevations have been transient and may

disappear with continued verapamil treatment. Monitor liver function,


periodically, in patients treated with this medication.

.
FOLLOW-UP
Prognosis:

In asymptomatic patients without underlying heart disease, the long-term prognosis is similar
to that of the general population. Asymptomatic patients with ejection fractions greater than
40% demonstrate an approximately 3.5% incidence of sustained ventricular tachycardia or
cardiac arrest. Thus, in patients with absence of heart disease on noninvasive work-up,
reassurance is appropriate.

In the setting of acute coronary ischemia/infarction, patients with simple PVCs rarely
progress to malignant arrhythmias. However, persistent complex ectopy after a myocardial
infarction is associated with increased risk of sudden death and may be an indication for EPS.

Patients with underlying chronic structural heart disease (e.g., cardiomyopathy, infarction, and
valvular disease) and complex ectopy (or > 10 PVCs/hour) have a significantly increased
mortality.
o

There is also a poor understanding of the role of anti-arrhythmic therapy in the


months post myocardial infarction. The Cardiac Arrhythmia Suppression Trial
(CAST) studied patients with ventricular ectopy post MI, to see if anti-arrhythmic
therapy improved survival. Despite suppression of ectopy on Holter monitoring,
patients treated with encainide, flecainide or moricizine actually had higher rates of
sudden death and all-cause mortality. Recent studies have suggested a role for
amiodarone in this patient population, and have demonstrated significant reductions
in post-MI ventricular arrhythmias and death.

Left ventricular function has a much stronger association with increased mortality
than do PVCs. PVCs are felt by many to reflect the severity of heart disease, rather
than having a precipitating role in arrhythmogenesis as was once thought.
EPS has a primary role in risk stratification of patients with frequent or complex
PVCs. Patients with PVCs that are noninducible (i.e., unable to trigger ventricular
tachycardia during stimulation) have a low risk of sudden death.

MISCELLANEOUS

Special Concerns:

Pediatrics:
o

PVCs are less common in children than in adults but do occur in normal children.

About 20% of healthy boys, age 10-13, show PVCs on routine Holter.

PVCs in healthy newborns generally resolve by the twelfth week and usually require
no treatment once the presence of a normal heart is confirmed.

This is probably related to developmental factors associated with the autonomic


nervous system.

In older children, PVCs are often related to transient or exogenous factors including
mild viral myocarditis, excessive caffeine or sympathomimetic drugs (cold or asthma
medications). They usually resolve without treatment.

When complex ectopy is seen in pregnancy, or immediately after, obtain an ECG for possible
peripartum cardiomyopathy.

Patients with presentations that indicate an ischemic basis for their PVCs (e.g., chest pain,
dyspnea, and syncope) or are hemodynamically unstable, should be closely monitored while
in the ED and admitted to an appropriate monitored setting.

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Hargarten K, Chapman PD, Stueven HA: Prehospital prophylactic lidocaine does not
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Kennedy HA, Whitlock JA, Sprague MK: Long term follow-up of asymptomatic healthy
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Lown B, Wolf M: Approaches to sudden death from coronary heart disease. Circulation 1071;
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Maggioni AP, Zuanetti G, Franzoni MG: Prevalence and prognostic significance of


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Rehnqvist N, Olsson G, Erhardt L: Metoprolol in acute myocardial infarction reduces


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Teo KK, Yusef S, Furberg CD: Effects of prophylactic antiarrhythmic drug therapy in acute
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