Cathy Percival, RN, FALU, FLMI VP, Medical Director

AIG Life and Retirement Company

Cardiac Arrhythmias

The Cardiovascular System

Three primary functions Transport of oxygen, nutrients, and hormones to cells

throughout the body and removal of metabolic wastes (carbon dioxide, nitrogenous wastes).

Protection of the body by white blood cells, antibodies, and complement proteins that circulate in the blood and defend the body against foreign microbes and toxins. Clotting mechanisms are also present that protect the body from blood loss after injuries.

Regulation of body temperature, fluid pH, and water content of cells.

Pulmonary & Systemic Circulation

Cardiac Function

In order to maintain sufficient cardiac output, the heart needs: Normal LV function

Viable muscle w/ normal contractility Cardiac output—volume of blood pumped by the

heart/minute Normal structure

Chamber size/function Competent valves

Adequate myocardial blood supply

Normal coronary arteries Adequate blood volume Oxygen availability

Lung function Normal pressures Properly functioning conduction system

Cardiac Action Potential

Cardiac Muscle Automaticity Unique ability of cardiac muscle cells to depolarize

spontaneously w/o external stimulation from nervous system

The electrical stimulation required is provided by the heart’s own conduction system

Electrical impulses cause changes in extracellular and intracellular concentrations of sodium (Na+), potassium (K+), and calcium (Ca++) ions

The movement of ions alters cellular polarity (charge) and generates energy that results in depolarization of myocardial cells Depolarization—myocardial stimulation due to change in polarity of cell

from negative to positive Repolarization—return of myocardial cell to resting state and negative

charge

Conduction System

An independently functioning system of specialized cells responsible for initiating and transmitting electrical impulses in an organized manner, causing excitation and depolarization of cardiac muscle cells

Time-ordered stimulation of the

myocardium allows efficient contraction of all 4 chambers of the heart Maximizes cardiac output

Conduction Pathway

Normal impulse begins in Sinoatrial (SA) node—Pacemaker

Spreads through internodal pathways to Atrioventricular (AV) node, where the impulse is delayed slightly to allow atria to complete contraction and fill ventricles

Impulse then travels to Bundle of His, then enters both Right and Left Bundle Branches

The impulse is then carried through Purkinje fibers to ventricular myocardial tissue

SA Node

AV Node

Bundle

of His

Left Bundle

Branches

Right

Bundle Branch Purkinje Fibers

P Wave

PR Interval

QRS Complex

T Wave

Action Potential & Impulse Conduction

The EKG

Records the voltage generated by depolarization of the different regions of the heart in sequence and through time

Cardiac Cycle

Cardiac Cycle—Systole

Cardiac Cycle—Diastole

Cardiac Cycle

Arrhythmia

Term applied to any abnormality in impulse generation or conduction: Location of impulse generation

Rate of impulse generation

Conduction of impulse

The significance of an arrhythmia ultimately depends on it’s impact on cardiac output

Premature Beats

An ectopic area (focus) outside the normal sinus mechanism generates an impulse prior to the next expected impulse Usually results in

ventricular depolarization

Can occur in the:

Atria

AV Junction

Ventricles

PAC’s/PJC’s

A premature impulse generated by an ectopic focus somewhere in the atria/ AV nodal region prior to the next expected sinus impulse PAC—Premature Atrial Contraction PJC—Premature Junctional Contraction

The premature impulse usually causes atrial depolarization and normal ventricular depolarization Does not impact cardiac output

Benign Finding

PVC’s

Premature impulses generated by an ectopic focus in the ventricle PVC—Premature Ventricular Contraction

The premature impulse results in ventricular depolarization

Because ventricular depolarization occurs before adequate filling of the chamber, stroke volume for that contraction is significantly reduced

PVC’s—Cardiac Causes

Coronary Artery Disease Ischemia/Injury

Valve Disease

PVC’s—Cardiac Causes

Cardiomyopathy

Dilated Cardiomyopathy

Hypertrophic Cardiomyopathy

PVC’s—Hereditary Ion Channel Disorders

Prolonged QT Syndrome Brugada Syndrome

PVC’s—Cardiac Causes

Accessory Pathway Disorders

Wolff-Parkinson-White Syndrome Lown-Ganong-Levine Syndrome

PVC’s—Other Causes

Hormonal Imbalances Thyroid disorders

Electrolyte Imbalance

K+, Mg Prolonged QT

Hypoxia

Medications Repolarization changes

Drug-induced prolonged QT Altered conduction

Velocity of conduction Changes in action potential

Stress, Exercise

Caffeine, ETOH, Nicotine

PVC’s

Significance of PVC’s is related to: Frequency Characteristics

Unifocal vs. Multifocal Bigeminy, Trigeminy Sequential PVC’s

Couplets, Triplets Occurring w/ exercise Ventricular Tachycardia

Underlying cause Presence of symptoms

SOB/DOE Angina Dizziness/Syncope

Effect on cardiac output Type & severity of associated

structural heart disease CAD Valve disease Cardiomyopathy

PVC’s—Complications

Ventricular Tachycardia (VT) A rapid rhythm that originates

in the ventricles Heart rate >120 bpm

Non-sustained VT Lasts <30 sec

Sustained VT—lasts >30 sec

Ventricular Fibrillation Sudden Death

Treatment of PVC’s

Treatment of underlying cause Elimination of triggers Electrolyte replacement Pharmacological Agents

Beta Blockers Calcium Channel Blockers Anti-arrhythmics

Radiofrequency Catheter Ablation Implantable Cardioverter-Defibrillators

Atrial Fibrillation (AF)

“Irregularly irregular” rhythm The regular sinus node impulses are

overwhelmed by the rapid and random impulses discharged by multiple irritable foci in the atria No atrial contraction occurs Loss of “atrial kick”

Atrial rate 300-600 impulses/minute Depolarization of the ventricles is random and

irregular Ventricular rate depends on the number

of atrial impulses that get through the AV node

Sinus Rhythm

Atrial Fibrillation

Atrial Flutter

The atrial impulses travel in a circular course, setting up regular, rapid flutter waves w/o any isoelectric baseline Sawtooth Pattern

The Atrial rate is very rapid300-400 impulses/minute

The ventricular rate may be regular or irregular and slower, depending upon conduction ratio of impulses to the ventricles

Atrial Flutter

Atrial Fibrillation

Important Terms: Controlled AF—Ventricular rate <100bpm

Rapid AF—Uncontrolled—ventricular rate >100bpm

Paroxysmal AF—Episodes that terminate w/in 7 days

Chronic AF—Persistent AF

Causes of AF

Hemodynamic stress Increased intra-atrial

pressure Mitral & tricuspid valve

disease LV dysfunction Pulmonary hypertension

Atrial ischemia Ventricular ischemia leads

to increased atrial pressure and AF

Inflammation Myocarditis/pericarditis Viral/bacterial infections

Non-cardiovascular respiratory disorders

Pulmonary embolism Pneumonia Lung cancer COPD

Alcohol and drug use

Endocrine disorders

Hyperthyroidism Pheochromocytoma

Genetic factors

Idiopathic—”Lone” AF

Advancing age

Complications of AF Embolic Stroke

Pooled blood in atrium tends to clot

Thrombus breaks away and travels to blood vessels in brain

Congestive Heart Failure Loss of atrial kick reduces blood

volume in ventricle LV must work harder to maintain

cardiac output

Increased blood volume in left atrium increases pressure/volume in lungs

Atrial Fibrillation

Significance of AF is related to: Cause

Persistence

Ventricular rate

Presence of symptoms SOB/DOE, angina, fatigue, dizziness/syncope

Impact on cardiac output

Presence and severity of associated cardiac disease CAD

Cardiomyopathy

Valve disease

Thrombus Risk

Complications

AF—Treatment

Goals of Treatment Restore sinus rhythm, if possible

Pharmacological agents Cardioversion Radiofrequency Ablation

Pulmonary vein AV Nodal ablation

MAZE Procedure

Control ventricular rate Beta blockers Calcium channel blockers digoxin

Maintain adequate cardiac output Reduce thrombus risk

Anticoagulants

Pulmonary Vein Ablation

Isolation and ablation of pulmonary vein, along w/ left atrial ablation to eliminate AF

Success rate 60-80% over 1-2 years of f/u

Complications Cardiac perforation Cardiac tamponade Pericardial effusion Pulmonary vein stenosis (6%)

AV Nodal Ablation w/ Pacemaker

Catheter ablation of the AV junction permanently interrupts conduction from the atria to the ventricles

Results in AV block, requiring permanent pacemaker

AF may still be present, but pacemaker governs ventricular response

Stroke risk from underlying AF persists, so patient requires anticoagulation

Cox-Maze Procedure

Surgical compartmentalization of the atria Open heart procedure

Series of small endocardial incisions in Rt and Lt Atria

Isolate pulmonary veins and interrupt potential reentrant pathways to disrupt AF

Arrhythmias—UW Considerations

Underling cause, if known Presence of cardiac disease

CAD Valve Disease Cardiomyopathy

Rate control Results of cardiac w/u History of stroke Use of anticoagulants Symptoms

CHF Angina SOB/Dyspnea

Presence of complications from treatment

ETOH use

Cause, if known Characteristics of PVC’s

Frequency Complexity History of VT Presence during/after exercise

Presence of cardiac disease CAD Valve Disease Cardiomyopathy

Results of cardiac w/u Stress imaging study Echocardiogram Cardiac catheterization EPS

Associated symptoms Chest pain SOB/Dyspnea Heart failure Dizziness/Syncope

PVC’s Atrial Fib