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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:
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.
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.
The ectopic beat may produce a diminished or absent pulse, dependent on the force of the
ventricular contraction.
Causes:
Cardiac:
o
Myocarditis
Hypoxia
WORKUP
Lab Studies:
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.
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.
PVCs are usually described in terms of the Lown grading system for premature beats.
The higher the grade, the more serious the ectopy.
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.
The most important role for Holter monitoring is risk stratification of patients with a
recent myocardial infarction or known left ventricular dysfunction.
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.
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.
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).
Acute Ischemia/Infarction:
o
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.
Beta-blockers have proven efficacy in the setting of acute myocardial infarction and
are safe to use.
Drug Name
Pediatric Dose
Contraindications
Interactions
Pregnancy
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
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
Contraindications
Pregnancy
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
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
Precautions
Drug Name
Adult Dose
Pediatric Dose
Contraindications
Interactions
Pregnancy
Precautions
Drug Name
Pediatric Dose
Contraindications
Interactions
Pregnancy
Precautions
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.
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
Contraindications
Interactions
MAO inhibitors may increase metoprolol levels, and thus its toxicity
or pharmacologic effects.
Pregnancy
Precautions
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
Contraindications
Interactions
Pregnancy
A - Safe in pregnancy
Precautions
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
Adult Dose
80-160 mg tid
Pediatric Dose
Contraindications
Interactions
Pregnancy
Precautions
.
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
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.
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.
BIBLIOGRAPHY
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Hammill SC , Trusty JM, Wood DL: Influence of ventricular function and presence or
absence of coronary artery disease on results of electrophysiologic testing for asymptomatic
nonsustained ventricular tachycardia. Am J Cardiol 1990; 65: 722-728.
Hargarten K, Chapman PD, Stueven HA: Prehospital prophylactic lidocaine does not
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