Arrhythmias Flashcards
Arrhythmia Definition
An arrhythmia is an abnormality or disturbance in the rate or rhythm of the heartbeat leading to abnormal contraction
Sinoatrial (SA) or Sinus node
Dominant center of automaticity (dominant pacemaker) which initiates cardiac electrical impulse
Generates sinus rhythm
Paces heart at resting state of 60-100 bpm
Intranodal pathways
Conduction pathways from the SA node to the AV node
Anterior, middle, posterior
Atrioventricular (AV) node
Area of specialized tissue that conducts normal electrical impulse from atria to the ventricles
Known as the Junction box—delays SA node signal
Bundle of His
Transmits the electrical impulses from the AV node to the point of the apex of the fascicular branches (bundles of specialized muscle fibers)
AV Junction
The conducting tissues bridging the atria and ventricles are referred to as the junctional areas
Consist of AV node and Bundle of His
Between the atria and ventricles lies a fibrous AV ring that will not permit electrical stimulation
Ventricular Conduction
Left (anterior and posterior fascicles) and right bundle branches
Purkinje fibers
Membrane Potential (mV)
voltage difference across a membrane
Resting Membrane Potential (RMP)
Myocardial cells maintain a voltage difference of 60 to -90mV across the cell membranes
Inside of the cell is electrically negative (polarized) compared with the outside of the cell
RMP is generated because of difference in permeability of different ions between the inside and outside of the cell
K+ concentration is higher on ___ of the cell, while Na+ is higher on the ____ of the cell
inside
outside
K+ has a ____ effect on membrane potential because it is more permeable
greater
Threshold Potential
Membrane potential at which excitable cells undergo rapid depolarization
Threshold is typically 10-20mV above resting potential
Once threshold is reached, depolarization is spontaneous
Action Potential
Activation of cardiac cells results from movement of ions across the cell membrane, causing a transient depolarization
The action potential of the ventricular system has five phases
Phase 0
Rapid depolarization
Voltage sensitive Na+ channels open allowing Na+ to rush into the cell
Influx of Na+ caused the rapid upstroke of the action potential
Overshoot potential
Rapid depolarization more than equilibrates the electrical potential
Results in brief initial repolarization or Phase 1
Phase 1
Partial repolarization related to K+ efflux
Na+ channels are inactivated decreasing cell membrane permeability
Na+ are then refractory to further stimulation until they are reset by repolarization
Phase 2
Plateau phase
Increased influx of Ca2+ (begins during phase 0) and low efflux of K+
Phase 3
Rapid repolarization
Secondary to large K+ efflux and a reduction of Ca2+ and Na+ influx
Fast Na+ channels are resetting during this phase and may result in premature activation
Phase 4
Resting membrane potential (-80 to -90mV)
Gradual depolarization occurs because Na+ leaks inward and is balanced by a decreasing K+ efflux
Regulated by the Na+-K+-ATPase pump and Na+-Ca2+ exchanger (20% of RMP)
Threshold potenial
The juncture of phase 4 and phase 0 where rapid Na+ influx is initiated
Excitability
Ability of cardiac tissue to respond to adequate stimuli by generating an action potential followed by a mechanical contraction
Bathmotropy
The influencing of the excitability of cardiac muscle
Factors Affecting Excitability
RMP level
Threshold level
Behavior of Na+ channel
Refractory periods
Absolute refractory period (ARP)
Interval of the action potential during which no stimulus, regardless of its strength, can induce another impulse
Relative refractory period (RRP)
Interval of the action potential during which an impulse of significant magnitude may be elicited
Occurs from the end of the ARP to the time when the tissue is fully recovered
pranormal period
Period at the end of the action potential where an impulse can be generated by weaker than normal stimuli
Conductivity
The property of the cardiac muscle that allows the impulse to travel along the tissue
Dromotropy
The influencing of the conductivity of cardiac muscle
Tissue dependency
AV nodal delay
Contractility
The capacity of shortening in reaction to an appropriate membrane depolarization
Inotropy
The influencing of contractility
Automaticity
The ability of cardiac muscle to spontaneously depolarize in a regular constant manner
Chronotropy
The influencing of automaticity
Autonomic Nervous System
Sympathetic system
parasympathetic system
Sympathetic System
Activates cardiac B1 adrenergic receptors
cardiac excitatory effects of sympathetic system
increase rate of SA node pacing
increases rate of conduction
increases force of contraction
increases irritability of foci
parasympathetic system
activates cholinergic receptors
cardiac inhibitory effects of parasympathetic system
decreases rate of SA node pacing
decreases rate of conduction
decreases force of contraction
decreases irritability of atrial and junctional foci
P wave
Represents atrial depolarization
PR interval
Atrial depolarization plus the normal AV nodal delay
QRS complex
Represents ventricular depolarization
Atrial repolarization is occurring simultaneously and the atrial T wave is hidden by QRS complex
ST segment
Occurs after ventricular depolarization has ended and before repolarization has begun
Time for ECG silence
Initial part is termed the J point
T wave
Represents ventricular repolarization
QT interval
Represents time for depolarization and repolarization of the ventricles
Ventricular arrhythmia that can lead to sudden cardiac death
> _____ is risk for Torsades de Pointes
0.5 sec (500 msec)
Mechanisms of Arrhythmias
Abnormal impulse generation
Abnormal impulse propagation
Abnormal impulse generation
Alterations in Sinus node automaticity
Spontaneous (enhanced automaticity)
Triggered automaticity
- ->Early after-depolarization (EAD)
- ->Delayed after-depolarization (DAD)
Abnormal automaticity
Abnormal impulse propagation
Conduction block
Reentry
Bypass tracts
Increase Sinus node automaticity
mainly governed by sympathetic system
Decreased Sinus node automaticity
mainly governed by parasympathetic system
Ectopic Focus
The whole heart will be driven more rapidly by the abnormal pacemaker
Spontaneous (Automaticity)
Increased slope of phase 4 depolarization that causes a heightened automaticity of tissues and competition with the SA node for dominance of cardiac rhythm
Spontaneous (Automaticity) causes
Autonomic control (catecholamines) Digoxin Metabolic (↓O2, ↑CO2, ↑acidity, ↑temperature) Ischemia (leading cause) Hypokalemia Hypercalcemia Fiber stretch (cardiac dilatation)
Tiggered Automaticity
Early after-depolarization
Delayed after-depolarization (DAD)
Early after-depolarization
Implicated as a cause of Torsades de pointes
Delayed after-depolarization (DAD)
May be precipitated by digoxin toxicity or excess catecholamine release
Conduction Block
Occurs when a propagating impulse passes a region of the heart that is unexcitable
Reentry
Concept that involves indefinite propagation of the cardiac impulse and continued activation of previously refractory tissue
Reentry requirements
Two pathways for impulse conduction
A area of unidirectional block (prolonged refractoriness) in one of the pathways
Slow conduction in the other pathway
things affecting reentry
Timing (conduction velocity)
Refractoriness (absolute refractory period)
Changes in autonomic control
Bypass Tracts
Bypass tracts are additional accessory pathways for the conduction of the SA node action potential
Some people have additional pathways between the atrium and ventricles
The most common pathway is called the bundle of Kent
Shorter PR interval and wide QRS complex
Common Causes of Arrhythmias:
Normal physiology
Idiopathic
Genetic mutations
Common Causes of Arrhythmias:
Cardiac Disorders
Congenital abnormality Cardiomyopathy Heart failure Valvular heart disease Coronary artery or ischemic heart disease Rheumatic heart disease
Common Causes of Arrhythmias:
Pulmonary Disorders
Pulmonary hypertension
Chronic lung disease
Common Causes of Arrhythmias:
Disturbances of the autonomic system
Illicit drug use Alcohol intoxication Thyrotoxicosis Pheochromocytoma Neurologic abnormalities Medications
Common Causes of Arrhythmias:
Electrolyte Abnormalities
K+
Mg2+
Ca2+
Common Causes of Arrhythmias:
Medications
Antiarrhythmics Digoxin Pseudoephedrine Appetite suppressants Herbals
Most common types of Arrhythmias
Origin
Rate
Bradyarrhythmia
HR = <60 bpm
Tachyarrhythmia
HR > 100 bpm
Supraventricular Arrhythmias
Originate above bundle of His
Characterized by abnormal P waves but normal QRS and QTc intervals
Supraventricular Arrhythmias Examples
Premature atrial contraction (atrial extrasystoles)
Atrial fibrillation (A-fib)
Atrial flutter
Paroxsymal supraventricular tachycardia (PSVT)
Wolff-Parkinson-White syndrome (WPW) (pre-excitation syndrome)
Sick sinus syndrome (SSS)
Sinus bradycardia or tachycardia
Ventricular Arrhythmias
Originate below the bundle of His
Characterized by abnormal QRS and QTc interval but normal P waves
Most serious ventricular arrhythmias
Premature ventricular contractions (PVCs) (VPBs) (ventricular extrasystoles)
Ventricular tachycardia (V-tach)
Ventricular fibrillation (V-fib)
Incompatible with life
Torsades de pointes (TdP) (www.qtdrugs.org)
Associated with QTc >500msec
Nodal and Junctional Arrhythmias
Originates in AV nodal or junctional area typically as a result of less rate of impulse formation from SA node
Nodal and Junctional Arrhythmias examples
Premature junctional contraction
Junctional tachycardia
AV nodal reentrant tachycardia
AV reentrant tachycardia
Heart Block
Characterized by a disruption of impulses through the AV node
First degree AV block Second degree AV block Type I or Mobitz type I or Wenckebach Type II or Mobitz type II Third degree AV block (complete heart block)
<60 bpm
Bradyarrhythmias
Sinus bradycardia Heart block 1st degree AV block 2nd degree AV block 3rd degree AV block
> 100 bpm
Tachyarrhythmias
Sinus tachycardia Supraventricular A-fib A-flutter PSVT Ventricular PVCs V-tach V-fib TdP
Normal Sinus Rhythm
HR = 60-100 beats/min
1 P wave for every QRS interval
1 atrial contraction for every ventricular contraction
Sinus Bradycardia
Increased vagal tone
Drugs: ß-blockers, non-DHP CCB’s, digoxin
Usually asymptomatic
1st degree AV block
Increased vagal tone, medications that depress conduction through AV node, cardiac disease
Benign, asymptomatic that does not require treatment
Prolonged PR interval
2nd degree AV block Type I (Wenckebach)
Increased vagal tone, medications that depress conduction through AV node, inferior wall MI
Benign, asymptomatic that does not require treatment
increasingly prolonged PR interval
2nd degree AV block Type II (Mobitz II)
Atrial impulses are randomly blocked from reaching the ventricles which leads to dropped QRS complexes
Increased vagal tone, medications that depress conduction through AV node, inferior wall MI
Benign, asymptomatic that does not require treatment
3rd degree AV block (Complete Heart Block)
MI, drug toxicity, and chronic degeneration of the conduction pathways
Lightheadedness and syncope.
A pacemaker is almost always necessary
no PR interval
Asystole (Ventricular Standstill)
HR - absent Rhythm - absent P wave - absent or present PR interval - N/A QRS - Absent
Sinus Tachycardia
Increase sympathetic tone is most common.
Drugs, hypoxemia, hypovolemia, fever, stress, response to pain
Asymptomatic or noticeable palpitations and usually requires no treatment
Atrial Flutter
HR - A: 220-430 bpm
V:<300 bpm
Rhythm-regular
P wave -sawtoothed appearance
PR interval - N/A
QRS -
Atrial Fibrillation
HR: A -350-650 bpm
V: slow to rapid
Rhythm -irregular
P wave - Fibrillatory
PR interval-N/A
QRS -
Paroxysmal Supraventricular Tachycardia (PSVT)
Atrioventricular nodal reentrant tachycardia (AVNRT)
Atrioventricular reentrant tachycardia (AVRT)
Wolff-Parkinson-White (WPW) Syndrome
AVNRT
Narrow complex tachycardia
150-250 bpm
Reentry through dual AV nodal pathways. Most common type of PSVT. Can occur in any age group.
Palpitations, dizziness, SOB, chest pain, fatigue, syncope, diaphoresis, nausea
Unstable: adenosine, direct current cardioversion
Stable: ß-blockers, non-DHP CCBs, ablation
AVRT
Depends on the presence of an anomalous or accessory, extranodal pathway that bypasses the normal AV conduction pathway
Wolff-Parkinson-White (WPW) Syndrome
“Preexcitation syndrome”
AV conduction occurs through the bypass tract known as “the bundle of Kent” resulting in earlier activation “preexcitation” of the ventricles than if the impulse had traveled through the AV node
avoid BB, non-DHP CCBs or digoxin
Ventricular Tachycardia (V-tach)
Wide QRS complex with sawtooth appearance and rates 100-200 bpm.
Atrial activity may be dissociated from ventricular activity so P waves may not be present
Reentry circuit in ventricles (usually caused by scare tissue from an MI)
Non-sustained, sustained, pulseless (monomorphic or polymorphic)
Most frequently encountered life-threatening arrhythmia
May degenerate to V-fib and death
ACLS, DCC, antiarrhythmics
Torsades de Pointes
Polymorphic V-tach preceded by marked QT prolongation
Polymorphic QRS complexes change in amplitude and cycle length which gives the appearance of oscillations around the baseline (looks like a party streamer)
QTc interval is usually ≥ 500 msec
Torsades de Pointes causes
Triggered EAD Congenital (Long QT Syndrome) Electrolyte disturbances (Hypo Mg2+, Hypo K+) Drugs: antiarrhythmics (Class IA, IC, III—amiodarone may be protective) Typical antipsychotics (haloperidol) Atypical antipsychotics (mainly ziprasidone) Azole antifungals Macrolide antibiotics Methadone Quinolones (mainly moxifloxacin) Tricyclic antidepressants Chloroquine Pentamidine Ranolazine
Ventricular Fibrillation (V-fib)
Primary cause of sudden cardiac death (SCD)
Not compatible with life
Usually occurs without forewarning
Causes: Multiple ectopic ventricular foci
Often preceded by V-tach and associated with cardiac disease
Treatment: BLS/ACLS protocol (CPR, defibrillation, epinephrine, vasopressin, amiodarone)
Clinical Manifestations
Asymptomatic Palpitations (heart pounding) Shortness of breath (dyspnea) Fatigue Lightheadedness Anxiety Chest pain (angina) Loss of consciousness (syncope)
Complications
Tachycardia-induced CARDIOMYOPATHY and heart failure
Valvular heart disease
Cardioembolic embolism
Blood clot that results from stasis of blood that may lead to stroke (A-fib)
Cardiac arrest [Sudden cardiac death (SCD)]
Asystole, V-tach, V-fib, TdP
Goals of antiarrhythmic therapy
To restore normal rhythm and conduction
Antiarrhythmics drugs are used to:
Decrease or increase conduction velocity
Alter the excitability of cardiac cells by changing the duration of the effective refractory period
Suppress abnormal automaticity
Vaughan-Williams Classification
Class I IA IB IC Class II Class III Class IV
Class IA (Moderate Na+ blockers – fast fibers)
Decreases conduction velocity
Increases refractory period
Decreases automaticity
Useful for supraventricular and ventricular dysrhythmias
Prolongs QT
Agents: Quinidine, Procainamide, Disopyramide
Class IB (Weak Na+ blockers – fast fibers)
No effect on conduction velocity
Decreases refractory period
Decreases automaticity
More effect on fast HR (little or no effect on slow HR)
Used for ventricular dysrhythmias only
Agents: Lidocaine, Mexilitine, Phenytoin
Class IC (Strong Na+ blockers – fast fibers)
Profoundly decreases conduction velocity
No significant effect on refractory period
Decreases automaticity
Effective in both supraventricular and ventricular dysrhythmias
Prolongs QT (flecainide)
Do not use in pts w/cardiovascular disease secondary to proarrhythmia and mortality
Agents: Flecainide, Propafenone
Class II (SA/AV nodal tissue)
Blocks catecholamines
Decreases conduction velocity
Increases refractory period (nodal tissue)
Decreases automaticity
Useful in slowing ventricular response to supraventricular tachycardias (e.g., A-fib)
Agents: ß-Blockers
Class III(K+ blockers – fast fibers)
Does not effect conduction velocity (except amiodarone and dronedarone)
Profound increase in the refractory period
No effect of automaticity (except amiodarone, dronedarone and sotalol)
Useful in both supraventricular and ventricular dysrhythmias
Prolongs QT (rare with amiodarone)
Agents: Amiodarone, Dofetilide, Dronedarone, Ibutilide, Sotalol
Class IV (SA/AV nodal tissue)
Blocks Ca2+ channels
Decreases conduction velocity
Increases refractory period (nodal tissue)
Decreases automaticity
Useful in slowing ventricular response to supraventricular tachycardias (e.g., A-fib)
Agents: Diltiazem, Verapamil
Antiarrhythmics and Mortality
Class I agents
Several studies (CAST I and II) have shown and increase in mortality in patients with CAD (MI) or CHF Avoid in patients for short or long-term use Okay in patients without CAD or CHF
Antiarrhythmics and Mortality
Class III
No increase in mortality in any patient population (Amiodarone/Dofetilide)
Amiodarone may have mortality benefit
Class of choice for patients with CAD or CHF
Avoid Sotalol and Dronedarone in patients with CHF
Antiarrhythmics and Mortality
Class III
No increase in mortality in any patient population (Amiodarone/Dofetilide)
Amiodarone may have mortality benefit
Class of choice for patients with CAD or CHF
Avoid Sotalol and Dronedarone in patients with CHF
