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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
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