Download Cardiac Arrhythmias

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

Protection of the body by white blood cells, antibodies,

Regulation of body temperature, fluid pH,
throughout the body and removal of metabolic wastes
(carbon dioxide, nitrogenous wastes).
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.
and water content of cells.
Pulmonary & Systemic Circulation
Cardiac Function
In order to maintain sufficient cardiac output, the
heart needs:

Normal LV function
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Normal structure
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Chamber size/function
Competent valves
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Normal coronary arteries
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Lung function
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Viable muscle w/ normal contractility
Cardiac output—volume of blood pumped by the
heart/minute
Adequate myocardial blood
supply
Adequate blood volume
Oxygen availability
Normal pressures
Properly functioning conduction system
Cardiac Action Potential

Cardiac Muscle Automaticity

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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
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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

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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

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Normal impulse begins in Sinoatrial (SA)
node—Pacemaker
Bundle
of His
Spreads through internodal pathways to SA Node
Atrioventricular (AV) node, where the
impulse is delayed slightly to
allow atria to complete contraction
and fill ventricles
AV Node
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
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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

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Usually results in
ventricular depolarization
Can occur in the:
 Atria
 AV Junction
 Ventricles
PAC’s/PJC’s
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A premature impulse generated by an ectopic focus somewhere in the
atria/ AV nodal region prior to the next expected sinus impulse
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The premature impulse usually causes atrial depolarization and normal
ventricular depolarization
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PAC—Premature Atrial Contraction
PJC—Premature Junctional Contraction
Does not impact cardiac output
Benign Finding
PVC’s
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Premature impulses generated by an
ectopic focus in the ventricle
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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
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Hormonal Imbalances
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Thyroid disorders
Electrolyte Imbalance
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K+, Mg
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Prolonged QT
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Hypoxia
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Medications
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Repolarization changes
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Drug-induced prolonged QT
Altered conduction
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Velocity of conduction
Changes in action potential
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Stress, Exercise
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Caffeine, ETOH, Nicotine
PVC’s
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Significance of PVC’s is related to:
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Frequency
Characteristics
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Unifocal vs. Multifocal
Bigeminy, Trigeminy
Sequential PVC’s
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Occurring w/ exercise
Ventricular Tachycardia
Underlying cause
Presence of symptoms
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Couplets, Triplets
SOB/DOE
Angina
Dizziness/Syncope
Effect on cardiac output
Type & severity of associated
structural heart disease
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CAD
Valve disease
Cardiomyopathy
PVC’s—Complications
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Ventricular Tachycardia (VT)
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A rapid rhythm that originates
in the ventricles
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Non-sustained VT
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Heart rate >120 bpm
Lasts <30 sec
Sustained VT—lasts >30 sec
Ventricular Fibrillation
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Sudden Death
Treatment of PVC’s
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Treatment of underlying cause
Elimination of triggers
Electrolyte replacement
Pharmacological Agents
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Beta Blockers
Calcium Channel Blockers
Anti-arrhythmics
Radiofrequency Catheter Ablation
Implantable Cardioverter-Defibrillators
Atrial Fibrillation (AF)
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“Irregularly irregular” rhythm
The regular sinus node impulses are
overwhelmed by the rapid and
random impulses discharged by multiple
irritable foci in the atria
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Sinus Rhythm
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
Atrial Fibrillation
Atrial Flutter
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The atrial impulses travel in a circular
course, setting up regular, rapid flutter
waves w/o any isoelectric baseline
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Sawtooth Pattern
Atrial Flutter
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 Fibrillation
Important Terms:
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Controlled AF—Ventricular rate <100bpm
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Rapid AF—Uncontrolled—ventricular rate >100bpm
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Paroxysmal AF—Episodes that terminate w/in 7 days
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Chronic AF—Persistent AF
Causes of AF
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Hemodynamic stress
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Increased intra-atrial
pressure
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Ventricular ischemia leads
to increased atrial pressure
and AF
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Myocarditis/pericarditis
Viral/bacterial infections
Pulmonary embolism
Pneumonia
Lung cancer
COPD
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Alcohol and drug use
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Endocrine disorders
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Inflammation
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Non-cardiovascular respiratory
disorders
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Mitral & tricuspid valve
disease
LV dysfunction
Pulmonary hypertension
Atrial ischemia
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Hyperthyroidism
Pheochromocytoma
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Genetic factors
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Idiopathic—”Lone” AF
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Advancing age
Complications of AF
Congestive Heart Failure
Embolic Stroke
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Pooled blood in atrium tends to
clot
Thrombus breaks away and
travels to blood vessels in brain
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Loss of atrial kick reduces blood
volume in ventricle
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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:
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Cause
Persistence
Ventricular rate
Presence of symptoms
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Impact on cardiac output
Presence and severity of associated cardiac disease
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SOB/DOE, angina, fatigue, dizziness/syncope
CAD
Cardiomyopathy
Valve disease
Thrombus Risk
Complications
AF—Treatment
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Goals of Treatment
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Restore sinus rhythm, if possible
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Pharmacological agents
Cardioversion
Radiofrequency Ablation
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Beta blockers
Calcium channel blockers
digoxin
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Anticoagulants
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MAZE Procedure
Control ventricular rate
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Pulmonary vein
AV Nodal ablation
Maintain adequate cardiac output
Reduce thrombus risk
Pulmonary Vein Ablation
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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
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Cardiac perforation
Cardiac tamponade
Pericardial effusion
Pulmonary vein stenosis (6%)
AV Nodal Ablation w/ Pacemaker
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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
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Surgical compartmentalization of the atria
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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
Atrial Fib
PVC’s
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Cause, if known
Characteristics of PVC’s
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Presence of cardiac disease
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CAD
Valve Disease
Cardiomyopathy
Results of cardiac w/u
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Frequency
Complexity
History of VT
Presence during/after exercise
Stress imaging study
Echocardiogram
Cardiac catheterization
EPS
Associated symptoms
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Chest pain
SOB/Dyspnea
Heart failure
Dizziness/Syncope
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Underling cause, if known
Presence of cardiac disease
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Rate control
Results of cardiac w/u
History of stroke
Use of anticoagulants
Symptoms
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CAD
Valve Disease
Cardiomyopathy
CHF
Angina
SOB/Dyspnea
Presence of complications from
treatment
ETOH use