Cardiac Arrhythmias Cathy Percival, RN, FALU, FLMI VP, Medical Director AIG Life and Retirement Company
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 AV Node SA Node Bundle of His Left Bundle Branches 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 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 Hypertrophic Cardiomyopathy Dilated 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 Atrial Flutter The ventricular rate may be regular or irregular and slower, depending upon conduction ratio of impulses to the ventricles
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 PVC s 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 Atrial Fib 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