Arrhythmias Flashcards
(111 cards)
1
Q
Arrhythmia Definition
A
An arrhythmia is an abnormality or disturbance in the rate or rhythm of the heartbeat leading to abnormal contraction
2
Q
Sinoatrial (SA) or Sinus node
A
Dominant center of automaticity (dominant pacemaker) which initiates cardiac electrical impulse
Generates sinus rhythm
Paces heart at resting state of 60-100 bpm
3
Q
Intranodal pathways
A
Conduction pathways from the SA node to the AV node
Anterior, middle, posterior
4
Q
Atrioventricular (AV) node
A
Area of specialized tissue that conducts normal electrical impulse from atria to the ventricles
Known as the Junction box—delays SA node signal
5
Q
Bundle of His
A
Transmits the electrical impulses from the AV node to the point of the apex of the fascicular branches (bundles of specialized muscle fibers)
6
Q
AV Junction
A
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
7
Q
Ventricular Conduction
A
Left (anterior and posterior fascicles) and right bundle branches
Purkinje fibers
8
Q
Membrane Potential (mV)
A
voltage difference across a membrane
9
Q
Resting Membrane Potential (RMP)
A
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
10
Q
K+ concentration is higher on ___ of the cell, while Na+ is higher on the ____ of the cell
A
inside
outside
11
Q
K+ has a ____ effect on membrane potential because it is more permeable
A
greater
12
Q
Threshold Potential
A
Membrane potential at which excitable cells undergo rapid depolarization
Threshold is typically 10-20mV above resting potential
Once threshold is reached, depolarization is spontaneous
13
Q
Action Potential
A
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
14
Q
Phase 0
A
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
15
Q
Overshoot potential
A
Rapid depolarization more than equilibrates the electrical potential
Results in brief initial repolarization or Phase 1
16
Q
Phase 1
A
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
17
Q
Phase 2
A
Plateau phase
Increased influx of Ca2+ (begins during phase 0) and low efflux of K+
18
Q
Phase 3
A
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
19
Q
Phase 4
A
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)
20
Q
Threshold potenial
A
The juncture of phase 4 and phase 0 where rapid Na+ influx is initiated
21
Q
Excitability
A
Ability of cardiac tissue to respond to adequate stimuli by generating an action potential followed by a mechanical contraction
22
Q
Bathmotropy
A
The influencing of the excitability of cardiac muscle
23
Q
Factors Affecting Excitability
A
RMP level
Threshold level
Behavior of Na+ channel
Refractory periods
24
Q
Absolute refractory period (ARP)
A
Interval of the action potential during which no stimulus, regardless of its strength, can induce another impulse
25
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
26
pranormal period
Period at the end of the action potential where an impulse can be generated by weaker than normal stimuli
27
Conductivity
The property of the cardiac muscle that allows the impulse to travel along the tissue
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Dromotropy
The influencing of the conductivity of cardiac muscle
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Tissue dependency
AV nodal delay
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Contractility
The capacity of shortening in reaction to an appropriate membrane depolarization
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Inotropy
The influencing of contractility
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Automaticity
The ability of cardiac muscle to spontaneously depolarize in a regular constant manner
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Chronotropy
The influencing of automaticity
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Autonomic Nervous System
Sympathetic system
| parasympathetic system
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Sympathetic System
Activates cardiac B1 adrenergic receptors
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cardiac excitatory effects of sympathetic system
increase rate of SA node pacing
increases rate of conduction
increases force of contraction
increases irritability of foci
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parasympathetic system
activates cholinergic receptors
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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
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P wave
Represents atrial depolarization
40
PR interval
Atrial depolarization plus the normal AV nodal delay
41
QRS complex
Represents ventricular depolarization
Atrial repolarization is occurring simultaneously and the atrial T wave is hidden by QRS complex
42
ST segment
Occurs after ventricular depolarization has ended and before repolarization has begun
Time for ECG silence
Initial part is termed the J point
43
T wave
Represents ventricular repolarization
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QT interval
Represents time for depolarization and repolarization of the ventricles
Ventricular arrhythmia that can lead to sudden cardiac death
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> _____ is risk for Torsades de Pointes
0.5 sec (500 msec)
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Mechanisms of Arrhythmias
Abnormal impulse generation
| Abnormal impulse propagation
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Abnormal impulse generation
Alterations in Sinus node automaticity
Spontaneous (enhanced automaticity)
Triggered automaticity
- ->Early after-depolarization (EAD)
- ->Delayed after-depolarization (DAD)
Abnormal automaticity
48
Abnormal impulse propagation
Conduction block
Reentry
Bypass tracts
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Increase Sinus node automaticity
mainly governed by sympathetic system
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Decreased Sinus node automaticity
mainly governed by parasympathetic system
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Ectopic Focus
The whole heart will be driven more rapidly by the abnormal pacemaker
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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
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Spontaneous (Automaticity) causes
```
Autonomic control (catecholamines)
Digoxin
Metabolic (↓O2, ↑CO2, ↑acidity, ↑temperature)
Ischemia (leading cause)
Hypokalemia
Hypercalcemia
Fiber stretch (cardiac dilatation)
```
54
Tiggered Automaticity
Early after-depolarization
| Delayed after-depolarization (DAD)
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Early after-depolarization
Implicated as a cause of Torsades de pointes
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Delayed after-depolarization (DAD)
May be precipitated by digoxin toxicity or excess catecholamine release
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Conduction Block
Occurs when a propagating impulse passes a region of the heart that is unexcitable
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Reentry
Concept that involves indefinite propagation of the cardiac impulse and continued activation of previously refractory tissue
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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
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things affecting reentry
Timing (conduction velocity)
Refractoriness (absolute refractory period)
Changes in autonomic control
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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
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Common Causes of Arrhythmias:
| Normal physiology
Idiopathic
| Genetic mutations
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Common Causes of Arrhythmias:
| Cardiac Disorders
```
Congenital abnormality
Cardiomyopathy
Heart failure
Valvular heart disease
Coronary artery or ischemic heart disease
Rheumatic heart disease
```
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Common Causes of Arrhythmias:
| Pulmonary Disorders
Pulmonary hypertension
| Chronic lung disease
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Common Causes of Arrhythmias:
| Disturbances of the autonomic system
```
Illicit drug use
Alcohol intoxication
Thyrotoxicosis
Pheochromocytoma
Neurologic abnormalities
Medications
```
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Common Causes of Arrhythmias:
| Electrolyte Abnormalities
K+
Mg2+
Ca2+
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Common Causes of Arrhythmias:
| Medications
```
Antiarrhythmics
Digoxin
Pseudoephedrine
Appetite suppressants
Herbals
```
68
Most common types of Arrhythmias
Origin
Rate
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Bradyarrhythmia
HR = <60 bpm
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Tachyarrhythmia
HR > 100 bpm
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Supraventricular Arrhythmias
Originate above bundle of His
Characterized by abnormal P waves but normal QRS and QTc intervals
72
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
73
Ventricular Arrhythmias
Originate below the bundle of His
| Characterized by abnormal QRS and QTc interval but normal P waves
74
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
75
Nodal and Junctional Arrhythmias
Originates in AV nodal or junctional area typically as a result of less rate of impulse formation from SA node
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Nodal and Junctional Arrhythmias examples
Premature junctional contraction
Junctional tachycardia
AV nodal reentrant tachycardia
AV reentrant tachycardia
77
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)
```
78
<60 bpm
| Bradyarrhythmias
```
Sinus bradycardia
Heart block
1st degree AV block
2nd degree AV block
3rd degree AV block
```
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>100 bpm
| Tachyarrhythmias
```
Sinus tachycardia
Supraventricular
A-fib
A-flutter
PSVT
Ventricular
PVCs
V-tach
V-fib
TdP
```
80
Normal Sinus Rhythm
HR = 60-100 beats/min
1 P wave for every QRS interval
1 atrial contraction for every ventricular contraction
81
Sinus Bradycardia
Increased vagal tone
Drugs: ß-blockers, non-DHP CCB’s, digoxin
Usually asymptomatic
82
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
83
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
84
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
85
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
86
Asystole (Ventricular Standstill)
```
HR - absent
Rhythm - absent
P wave - absent or present
PR interval - N/A
QRS - Absent
```
87
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
88
Atrial Flutter
HR - A: 220-430 bpm
V:<300 bpm
Rhythm-regular
P wave -sawtoothed appearance
PR interval - N/A
QRS -
89
Atrial Fibrillation
HR: A -350-650 bpm
V: slow to rapid
Rhythm -irregular
P wave - Fibrillatory
PR interval-N/A
QRS -
90
Paroxysmal Supraventricular Tachycardia (PSVT)
Atrioventricular nodal reentrant tachycardia (AVNRT)
Atrioventricular reentrant tachycardia (AVRT)
Wolff-Parkinson-White (WPW) Syndrome
91
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
92
AVRT
Depends on the presence of an anomalous or accessory, extranodal pathway that bypasses the normal AV conduction pathway
93
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
94
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
95
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
96
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
```
97
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)
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Clinical Manifestations
```
Asymptomatic
Palpitations (heart pounding)
Shortness of breath (dyspnea)
Fatigue
Lightheadedness
Anxiety
Chest pain (angina)
Loss of consciousness (syncope)
```
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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
100
Goals of antiarrhythmic therapy
To restore normal rhythm and conduction
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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
102
Vaughan-Williams Classification
```
Class I
IA
IB
IC
Class II
Class III
Class IV
```
103
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
104
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
105
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
106
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
107
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
108
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
109
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
```
110
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
111
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
