Premature Ventricular Contractions

Description

Premature ventricular contractions (PVCs) describe a discordant ventricular contraction that is caused by an ectopic ventricular pacemaker focus. PVCs are also referred to as ventricular premature beats (VPBs) and ventricular extrasystoles.
Although PVCs can be a common, non-pathologic occurrence, the new onset or an increased frequency in the perioperative period should alert the anaesthetist to the possibility of ominous underlying pathology:
- Hypoxia
- Hypercarbia
- Acidosis
- Myocardial ischemia

Epidemiology

Incidence

True incidence is hard to ascertain secondary to most being asymptomatic at onset and over time.
Increases primarily with age.
Predilection toward males, and African Americans (vs. Caucasians).

Prevalence

Numbers vary greatly with the length of the monitoring period; longer periods result in a much higher detection rate (e.g., single EKG versus 2 minute EKG versus 24-hour Holter monitoring).
PVCs are detected in at least 50% of young men and women (on 24-hour Holter monitoring) (1,2).
Elderly patients in one study had a nearly 30% incidence of >30 PVCs/hr (Lown classification 2) (3).

Morbidity

Palpitations causing distress, or uncommonly, pre-syncopal or syncopal episodes.
Related to underlying condition.
Bigeminy, over time, can lead to cardiomyopathy irrespective of other disease processes (4).

Mortality

Related to the underlying condition or progression to more malignant arrhythmias.
Increased mortality has been associated with:
- Increased frequency/number
- Multiform waves
- Runs of PVCs (couplets, NSVT)
- Complex arrhythmias during exercise, and particularly after exercise (5).

Etiology/Risk Factors

Perioperative
- Normal variant
- Hypoxemia
- Hypercarbia/acidosis
- Myocardial ischemia/infarction
- Pulmonary embolism
- Electrolyte imbalance: Hypokalemia, hypomagnesemia, and hypercalcemia (can result from intraoperative furosemide, mannitol, and IV contrast dye)
- Any high-catecholamine state
- Medications: Epinephrine, norepinephrine, dopamine, digoxin, tricyclic antidepressants, aminophylline, other anti-arrhythmic agents (flecainide, etc.)
- Bradycardia
- Anxiety
- Localized irritation/mechanical factors: Central venous line introducer wire or catheter, pulmonary artery catheter, surgical tools or hands in the operative field (particularly in open heart surgery as well as in thoracic surgery, Nuss procedures, etc.)
Chronic conditions: Hypertension, left ventricular hypertrophy, prior myocardial infarction, cardiomyopathy, and valvular heart disease
Provocative events: Exercise, smoking/nicotine exposure, caffeine and chocolate ingestion

Physiology/Pathophysiology

Three mechanisms in general:
- Enhanced automaticity: Electrolyte disturbances and elevated-catecholamine states can affect the membrane resting potential/automaticity of ventricular pacemakers
- Triggered activation: Ischemia, digoxin
- Re-entrant phenomenon: Ischemic pathways or old infarcts can delay normal impulse conduction and cause delayed firing that is "off-cycle" or "out-of-sync."
May originate from one focus or multiple foci within one or both ventricles (i.e., outside the SA–AV-nodal or His–Purkinje systems)
Hemodynamic concerns:
- Can cause hemodynamic instability; the lack of an atrial kick during ventricular diastole can decrease the stroke volume and cardiac output (particularly with bigeminy or frequent PVCs).
- Although commonly benign in nature, may signify a more sinister underlying disorder.
- May progress to malignant dysrhythmias in certain conditions (6).

Prevantative Measures

In the operating room, avoid hypoxemia, hypercarbia/acidosis, hypotension or tachycardia (myocardial ischemia), and other above-mentioned causes.
- Chronic beta-blocker therapy may be appropriate in certain settings (i.e., symptomatic, post-MI arrhythmias, etc.) (7).
Outpatient setting: Avoid caffeine, nicotine, alcohol, and chocolate, as well as herbals and diet pills containing stimulants (pseudoephedrine, etc.).

Diagnosis ⬆ ⬇

Intraoperatively

Primarily an EKG diagnosis: Level 1A (7)
- Premature ventricular depolarization
- No P wave (as seen with a premature atrial depolarization/contraction)
- Irregular, wide-complex QRS
- Compensatory pause takes place prior to the next normal beat.
- R–R interval of surrounding beats is usually constant
- If multifocal, it will show various QRS morphologies.
Pulse oximeter or arterial line waveform can be observed to rule out electrical artifact, patient movement, or movement around the patient. If it is "real" one would see an irregularly placed pulsation/beat with a smaller waveform (amplitude).
Initial diagnostic tests
- 12-lead EKG would be helpful if new-onset ischemia is suspected
- Arterial blood gas to check for acidosis, hypoxia, hypercarbia
- Electrolyte studies
- Initial cardiac enzymes if ischemia is suspected
Other diagnostic tests:
- CXR if a central venous line or retained wire is suspected
- Digoxin level (if applicable)
- Urine drug screen
- Echocardiogram

Awake or outpatient setting:

History
- Many are asymptomatic
- Can be associated with palpitations (from the augmented beat after the PVC) or a "pause" in the heartbeat from non-sustained ventricular tachycardia (NSVT) or ventricular tachycardia (VT)
- Previous presyncopal or syncopal episodes from bigeminy or progression to NSVT/VT
- Presence on the preoperative EKG; however, it is more likely to be detected on intraoperative EKG (longer duration of monitoring than preoperative 10-second EKG)
Diagnostic tests
- 24-hour Holter monitoring: Level 1A (7)
- Cardiac stress testing
- Coronary angiography
- Electrophysiologic testing
Lown classification system: (8)
- 0 = No PVCs
- I = <30 PVCs/hr
- II = 30 PVCs/hr
- III = Multiform PVCs
- IVa = Couplets (normal beat followed by two PVCs sequentially)
- IVb = Ventricular tachycardia (3 PVCs sequentially)

Differential Diagnosis

EKG artifact from motion (patient or other people touching the patient)
EKG artifact from electrocautery or ESWL
Premature atrial contractions
Sinus pauses
Second-degree type I or II heart block
Third-degree heart block

Treatment ⬆ ⬇

Management involves concurrent correction or treatment of the underlying cause as well as ensuring hemodynamic stability.
- Stable: If new-onset, investigate for ominous causes. If absent, remain vigilant to possibly detect any secondary causes.
- Unstable: Consider stopping the surgical interventions (pneumoperitoneum, pericardial manipulation, etc.), and/or finishing/canceling the case. Consider implementing the BLS/ACLS algorithms (i.e., defibrillation for pulseless VT, etc.).
Treat secondary causes as appropriate:
- Electrolyte replacement
- Ventilator changes for respiratory acidosis
- Central venous line manipulation if it is in too deep.
- Optimizing myocardial oxygen supply and demand if acute coronary syndrome or ischemia may be present.
Symptomatic treatment: Suppression of PVCs in the perioperative period with lidocaine or metoprolol may aid with hemodynamic stability. However, there are no studies on this particular scenario and, thus, it should not delay the above-mentioned therapies.

Follow-Up ⬆ ⬇

If a history of pre-syncope or syncope is uncovered preoperatively, one may consider cardiology evaluation prior to elective procedures.
If new onset occurs intraoperatively, a cardiology consult, telemetry monitoring, and/or further diagnostic tests may be warranted depending on the history and situation.
Patients with malignant arrhythmias or frequent PVCs may benefit from ablation therapy (7).

References ⬆ ⬇

Brodsky M , Wu D , Denes P , et al. Arrhythmias documented by 24-hour continuous electrocardiographic monitoring in 50 male medical students without apparent heart disease. Am J Cardiol. 1977;39:390–395.
Sobotka PA , Mayer JH , Bauernfeind RA , et al. Arrhythmias documented by 24-hour continuous ambulatory electrocardiographic monitoring in young women without apparent heart disease. Am Heart J. 1981;101:753–759.
Glaser SP , Clark PJ , Appelbaum HJ. Occurrence of frequent complex arrhythmias detected by ambulatory monitoring. Chest. 1979;75:565–568.
Chugh SS , Shen WK , Luria DM , et al. First evidence of premature ventricular complex-induced cardiomyopathy: A potentially reversible cause of heart failure. J Cardiovasc Electrophysiol. 2000;11(3):328–329.
Dewey FE , Kapoor JR , Williams RS , et al. Ventricular arrhythmias during clinical testing and prognosis. Arch Intern Med. 2008;168:225–234.
Dalal D , Nasir K , Bomma C , et al. Arrhythmogenic right ventricular dysplasia: A United States experience. Circulation. 2005;112:3823–3832.
Zipes DP , Camm AJ , Borggrefe M , et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task force and the European Society of Cardiology Committee for Practice Guidelines. Circulation. 2006;114:e385–e484.
Lown B , Wolf M. Approaches to sudden death from coronary heart disease. Circulation. 1971;44:130–142.

section name header

Basics ⬇

Incidence

Prevalence

Morbidity

Mortality

Diagnosis ⬆ ⬇

Treatment ⬆ ⬇

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆