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CDM 2 Exam 1 > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

Arrhythmia Definition

A

An arrhythmia is an abnormality or disturbance in the rate or rhythm of the heartbeat leading to abnormal contraction

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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

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3
Q

Intranodal pathways

A

Conduction pathways from the SA node to the AV node

Anterior, middle, posterior

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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

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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)

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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

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7
Q

Ventricular Conduction

A

Left (anterior and posterior fascicles) and right bundle branches

Purkinje fibers

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8
Q

Membrane Potential (mV)

A

voltage difference across a membrane

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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

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10
Q

K+ concentration is higher on ___ of the cell, while Na+ is higher on the ____ of the cell

A

inside

outside

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11
Q

K+ has a ____ effect on membrane potential because it is more permeable

A

greater

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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

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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

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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

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15
Q

Overshoot potential

A

Rapid depolarization more than equilibrates the electrical potential

Results in brief initial repolarization or Phase 1

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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

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17
Q

Phase 2

A

Plateau phase

Increased influx of Ca2+ (begins during phase 0) and low efflux of K+

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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

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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)

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20
Q

Threshold potenial

A

The juncture of phase 4 and phase 0 where rapid Na+ influx is initiated

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21
Q

Excitability

A

Ability of cardiac tissue to respond to adequate stimuli by generating an action potential followed by a mechanical contraction

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22
Q

Bathmotropy

A

The influencing of the excitability of cardiac muscle

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23
Q

Factors Affecting Excitability

A

RMP level
Threshold level
Behavior of Na+ channel
Refractory periods

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24
Q

Absolute refractory period (ARP)

A

Interval of the action potential during which no stimulus, regardless of its strength, can induce another impulse

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25
Q

Relative refractory period (RRP)

A

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

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26
Q

pranormal period

A

Period at the end of the action potential where an impulse can be generated by weaker than normal stimuli

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27
Q

Conductivity

A

The property of the cardiac muscle that allows the impulse to travel along the tissue

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28
Q

Dromotropy

A

The influencing of the conductivity of cardiac muscle

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29
Q

Tissue dependency

A

AV nodal delay

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30
Q

Contractility

A

The capacity of shortening in reaction to an appropriate membrane depolarization

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31
Q

Inotropy

A

The influencing of contractility

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32
Q

Automaticity

A

The ability of cardiac muscle to spontaneously depolarize in a regular constant manner

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33
Q

Chronotropy

A

The influencing of automaticity

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34
Q

Autonomic Nervous System

A

Sympathetic system

parasympathetic system

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35
Q

Sympathetic System

A

Activates cardiac B1 adrenergic receptors

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36
Q

cardiac excitatory effects of sympathetic system

A

increase rate of SA node pacing
increases rate of conduction
increases force of contraction
increases irritability of foci

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37
Q

parasympathetic system

A

activates cholinergic receptors

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38
Q

cardiac inhibitory effects of parasympathetic system

A

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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39
Q

P wave

A

Represents atrial depolarization

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40
Q

PR interval

A

Atrial depolarization plus the normal AV nodal delay

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41
Q

QRS complex

A

Represents ventricular depolarization

Atrial repolarization is occurring simultaneously and the atrial T wave is hidden by QRS complex

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42
Q

ST segment

A

Occurs after ventricular depolarization has ended and before repolarization has begun

Time for ECG silence

Initial part is termed the J point

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43
Q

T wave

A

Represents ventricular repolarization

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44
Q

QT interval

A

Represents time for depolarization and repolarization of the ventricles

Ventricular arrhythmia that can lead to sudden cardiac death

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45
Q

> _____ is risk for Torsades de Pointes

A

0.5 sec (500 msec)

46
Q

Mechanisms of Arrhythmias

A

Abnormal impulse generation

Abnormal impulse propagation

47
Q

Abnormal impulse generation

A

Alterations in Sinus node automaticity

Spontaneous (enhanced automaticity)

Triggered automaticity

  • ->Early after-depolarization (EAD)
  • ->Delayed after-depolarization (DAD)

Abnormal automaticity

48
Q

Abnormal impulse propagation

A

Conduction block
Reentry
Bypass tracts

49
Q

Increase Sinus node automaticity

A

mainly governed by sympathetic system

50
Q

Decreased Sinus node automaticity

A

mainly governed by parasympathetic system

51
Q

Ectopic Focus

A

The whole heart will be driven more rapidly by the abnormal pacemaker

52
Q

Spontaneous (Automaticity)

A

Increased slope of phase 4 depolarization that causes a heightened automaticity of tissues and competition with the SA node for dominance of cardiac rhythm

53
Q

Spontaneous (Automaticity) causes

A 
Autonomic control (catecholamines)
Digoxin
Metabolic (↓O2, ↑CO2, ↑acidity, ↑temperature)
Ischemia (leading cause)
Hypokalemia
Hypercalcemia
Fiber stretch (cardiac dilatation)
54
Q

Tiggered Automaticity

A

Early after-depolarization

Delayed after-depolarization (DAD)

55
Q

Early after-depolarization

A

Implicated as a cause of Torsades de pointes

56
Q

Delayed after-depolarization (DAD)

A

May be precipitated by digoxin toxicity or excess catecholamine release

57
Q

Conduction Block

A

Occurs when a propagating impulse passes a region of the heart that is unexcitable

58
Q

Reentry

A

Concept that involves indefinite propagation of the cardiac impulse and continued activation of previously refractory tissue

59
Q

Reentry requirements

A

Two pathways for impulse conduction

A area of unidirectional block (prolonged refractoriness) in one of the pathways

Slow conduction in the other pathway

60
Q

things affecting reentry

A

Timing (conduction velocity)

Refractoriness (absolute refractory period)

Changes in autonomic control

61
Q

Bypass Tracts

A

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

62
Q

Common Causes of Arrhythmias:

Normal physiology

A

Idiopathic

Genetic mutations

63
Q

Common Causes of Arrhythmias:

Cardiac Disorders

A 
Congenital abnormality
Cardiomyopathy
Heart failure
Valvular heart disease
Coronary artery or ischemic heart disease
Rheumatic heart disease
64
Q

Common Causes of Arrhythmias:

Pulmonary Disorders

A

Pulmonary hypertension

Chronic lung disease

65
Q

Common Causes of Arrhythmias:

Disturbances of the autonomic system

A 
Illicit drug use
Alcohol intoxication
Thyrotoxicosis
Pheochromocytoma
Neurologic abnormalities
Medications
66
Q

Common Causes of Arrhythmias:

Electrolyte Abnormalities

A

K+
Mg2+
Ca2+

67
Q

Common Causes of Arrhythmias:

Medications

A 
Antiarrhythmics
Digoxin
Pseudoephedrine
Appetite suppressants
Herbals
68
Q

Most common types of Arrhythmias

A

Origin

Rate

69
Q

Bradyarrhythmia

A

HR = <60 bpm

70
Q

Tachyarrhythmia

A

HR > 100 bpm

71
Q

Supraventricular Arrhythmias

A

Originate above bundle of His

Characterized by abnormal P waves but normal QRS and QTc intervals

72
Q

Supraventricular Arrhythmias Examples

A

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
Q

Ventricular Arrhythmias

A

Originate below the bundle of His

Characterized by abnormal QRS and QTc interval but normal P waves

74
Q

Most serious ventricular arrhythmias

A

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
Q

Nodal and Junctional Arrhythmias

A

Originates in AV nodal or junctional area typically as a result of less rate of impulse formation from SA node

76
Q

Nodal and Junctional Arrhythmias examples

A

Premature junctional contraction
Junctional tachycardia
AV nodal reentrant tachycardia
AV reentrant tachycardia

77
Q

Heart Block

A

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
Q

<60 bpm

Bradyarrhythmias

A 
Sinus bradycardia
 Heart block
1st degree AV block
 2nd degree AV block
 3rd degree AV block
79
Q

> 100 bpm

Tachyarrhythmias

A 
Sinus tachycardia
 Supraventricular
 A-fib
 A-flutter
 PSVT
 Ventricular
PVCs
V-tach
V-fib
TdP
80
Q

Normal Sinus Rhythm

A

HR = 60-100 beats/min
1 P wave for every QRS interval
1 atrial contraction for every ventricular contraction

81
Q

Sinus Bradycardia

A

Increased vagal tone
Drugs: ß-blockers, non-DHP CCB’s, digoxin

Usually asymptomatic

82
Q

1st degree AV block

A

Increased vagal tone, medications that depress conduction through AV node, cardiac disease

Benign, asymptomatic that does not require treatment

Prolonged PR interval

83
Q

2nd degree AV block Type I (Wenckebach)

A

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
Q

2nd degree AV block Type II (Mobitz II)

A

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
Q

3rd degree AV block (Complete Heart Block)

A

MI, drug toxicity, and chronic degeneration of the conduction pathways

Lightheadedness and syncope.
A pacemaker is almost always necessary

no PR interval

86
Q

Asystole (Ventricular Standstill)

A 
HR - absent 
Rhythm - absent
P wave - absent or present 
PR interval - N/A
QRS - Absent
87
Q

Sinus Tachycardia

A

Increase sympathetic tone is most common.
Drugs, hypoxemia, hypovolemia, fever, stress, response to pain

Asymptomatic or noticeable palpitations and usually requires no treatment

88
Q

Atrial Flutter

A

HR - A: 220-430 bpm
V:<300 bpm

Rhythm-regular

P wave -sawtoothed appearance

PR interval - N/A

QRS -

89
Q

Atrial Fibrillation

A

HR: A -350-650 bpm
V: slow to rapid

Rhythm -irregular

P wave - Fibrillatory

PR interval-N/A

QRS -

90
Q

Paroxysmal Supraventricular Tachycardia (PSVT)

A

Atrioventricular nodal reentrant tachycardia (AVNRT)

Atrioventricular reentrant tachycardia (AVRT)
Wolff-Parkinson-White (WPW) Syndrome

91
Q

AVNRT

A

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
Q

AVRT

A

Depends on the presence of an anomalous or accessory, extranodal pathway that bypasses the normal AV conduction pathway

93
Q

Wolff-Parkinson-White (WPW) Syndrome

A

“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
Q

Ventricular Tachycardia (V-tach)

A

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
Q

Torsades de Pointes

A

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
Q

Torsades de Pointes causes

A 
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
Q

Ventricular Fibrillation (V-fib)

A

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)

98
Q

Clinical Manifestations

A 
Asymptomatic
Palpitations (heart pounding)
Shortness of breath (dyspnea)
Fatigue
Lightheadedness
Anxiety
Chest pain (angina)
Loss of consciousness (syncope)
99
Q

Complications

A

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
Q

Goals of antiarrhythmic therapy

A

To restore normal rhythm and conduction

101
Q

Antiarrhythmics drugs are used to:

A

Decrease or increase conduction velocity
Alter the excitability of cardiac cells by changing the duration of the effective refractory period
Suppress abnormal automaticity

102
Q

Vaughan-Williams Classification

A 
Class I
IA
IB
IC
Class II
Class III
Class IV
103
Q

Class IA (Moderate Na+ blockers – fast fibers)

A

Decreases conduction velocity
Increases refractory period
Decreases automaticity

Useful for supraventricular and ventricular dysrhythmias
Prolongs QT
Agents: Quinidine, Procainamide, Disopyramide

104
Q

Class IB (Weak Na+ blockers – fast fibers)

A

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
Q

Class IC (Strong Na+ blockers – fast fibers)

A

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
Q

Class II (SA/AV nodal tissue)

A

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
Q

Class III(K+ blockers – fast fibers)

A

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
Q

Class IV (SA/AV nodal tissue)

A

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
Q

Antiarrhythmics and Mortality

Class I agents

A 
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
Q

Antiarrhythmics and Mortality

Class III

A

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
Q

Antiarrhythmics and Mortality

Class III

A

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

CDM 2 Exam 1 (3 decks)

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