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Arrhythmias Flashcards

1
Q

What causes an arrhythmia?

A

interruption of the sinus impulse or the sequence of conduction through the heart

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2
Q

What are the 3 kinds of arrhythmias?

A

Arrhythmias can be benign, asymptomatic, or life-threatening

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3
Q

What is the conduction pathway?

A
  1. Sinoatrial node
  2. Atroventricular node
  3. Bundle of His
    Bundle branch, fascicle, ventricle
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4
Q

Which cells have intrinsic automaticity?

A

Cells that normally have this ability are in the cardiac specialized conduction system:
–Sinoatrial (SA) node
–Atrioventricular (AV) node
–His-Purkinje system (pacemaker cells)
If automatic rate is higher than SA node rate, then ectopic beats/rhythm results

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5
Q

What are the myocyte action potentials?

A
  1. Na+ in - straight line up (+)
  2. K+ and Cl- out - small dip
  3. Ca2+ in and K+ out - plateau
  4. K+ out - full depolarization
  5. K+ - plateau
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6
Q

What is normal sinus rhythm?

A

Implies normal sequence of conduction, originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system.
EKG Characteristics:
Rate 60-100 bpm
Regular rhythm
Each QRS complex is preceded by a P wave and vice versa
P wave is upright in lead II & downgoing in lead aVR

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7
Q

What are the phases of pacemaker action potential?

A

Phase 0: Ca2+ in
Phase 3: K+ out
Phase 4: Na+ and Ca2+ in

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8
Q

What does beta-adrenergic stimulation do?

A

steeper Phase 4 slope, shifts action potential threshold more negatively (more open Ca++)

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9
Q

What does parasympathetic stimulation do?

A

vagus nerve decreases open If (Na+), causing flatter Phase 4 slope; shifts action potential threshold voltage more positively (less open Ca++)

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10
Q

What is triggered activity and how does it differ from automaticity?

A

Under certain conditions (such as prolonged repolarization), one abnormally depolarized action potential can trigger subsequent depolarizations (called afterdepolarizations).; Differs from automaticity because afterdepolarizations are not spontaneous but instead require a prior action potential to stimulate (hence the term “triggered” activity).; If afterdepolarizations reach threshold voltage, can result in ectopic beats or tachyarrhythmias.

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11
Q

What are early afterdepolarizations?

A

Augmentation in inward Ca++ (if during Phase 2) or Na+ channels (if during Phase 3). Usually occur in the setting of prolonged repolarization, causing depolarization if reaches membrane threshold.

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12
Q

What are examples of early afterdepolarizations?

A

Long QT syndrome, Torsades des Pointes

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13
Q

What are delayed afterdepolarizations?

A

Augmentation in a Ca++ channels in Phase 4, causing depolarization

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14
Q

What are examples of delayed afterdepolarizations?

A

Clinical scenario: digoxin toxicity (secondary to elevated intracellular Ca++ that is released from cells) or catecholamine stimulation.
Arrhythmia: bidirectional/ idiopathic VT

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15
Q

What is a conduction block?

A

Occurs when impulse reaches electrically unexcitable area; Block could be transient vs. permanent, bidirectional vs. unidirectional; Complete conduction block can lead to bradyarrhythmias

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16
Q

What can cause altered impulse conduction?

A

Ischemia, fibrosis, drugs

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17
Q

What promotes re-entrant arrhythmias?

A

Decreased conduction velocity: Partially depolarized tissue with inactivated sodium channels- myocardial ischemia, Scarring, disruption of architecture- chronic MI, Remodeling/redistribution of connexins- cardiomyopathies; Heterogenous refractoriness: Myocardial ischemia/infarction, Inflammation, Cardiomyopathies, Electrolyte abnormalities/drugs

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18
Q

What kinds of acquired structural heart disease promote arrhythmias?

A 
A.Acute myocardial infarction
B.Chronic ischemic heart disease
C.Hypertensive heart disease
D.Dilated non-ischemic cardiomyopathy
E.Infiltrative cardiomyopathy
F.Cardiac sarcoidoses
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19
Q

What kinds of congenital structural heart disease promote arrhythmias?

A

A.Hypertrophic cardiomyopathies
B.Congenital dilated cardiomyopathies
C.Arrhythmogenic right ventricular dysplasia
D.Anomalous coronary arteries

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20
Q

How do long and short QT syndrome affect arrhythmias?

A

potassium or sodium channelopathies resulting in abnormal repolarization and propensity to polymorphic VT (Torsades des Pointes)

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21
Q

What is sinus tachycardia? What causes it?

A

Occurs when sinus rhythm increases above 100 bpm; Caused by fever, hyperthyroidism, volume depletion, anxiety, sepsis, etc

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22
Q

What is Premature Atrial Complex?

A
  • P wave from another atrial focus
  • Occurs earlier in cycle
  • Different morphology of p wave
  • Benign, common cause of perceived irregular rhythm
  • Can cause symptoms such as: skipped beats, palpitations
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23
Q

What is Atrioventricular Nodal Tachycardia?

A

reentrant loop - a little conduction block down one limb, but come around on second pass - two pathways (“fast” and “slow”); Usually symptomatic with abrupt onset/offset of regular palpitations; causes simultaneous atrial and ventricular activation

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24
Q

What is Atrioventricular Reentry Tachycardia?

A

Accessory Pathway or Bypass Tract - not going through normal electrical conducting fibers - going
through ventricles on cell-to-cell basis (this is slower than
going through electrically insulated conduction tissue)

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25
What is seen on EKG when Atrioventricular Reentry Tachycardia occurs?
Delta wave (slurring of QRS), Shortened PR, Widened QRS
26
What is Wolff-Parkinson-White Syndrome?
Atrioventricular Reentry Tachycardia
27
What is Focal Atrial Tachycardia?
single site of origin a tach
28
What is Multifocal Atrial Tachycardia?
multiple (3+) sites of origin
29
What is atrial fibrillation?
SVT marked by rapid (350+ bpm), irregular and disorganized atrial activity (i.e., no discrete p-waves!); Ventricular rate is irregular; most common sustained arrhythmia seen in clinical practice
30
What causes a fib?
``` Altered atrial anatomy/physiology •Fibrosis (age or myopathy-related) •Inflammation – e.g., pericarditis •Enlarged atrial size – e.g., concomitant valvular disease –Altered atrial refractoriness (i.e, shorter) •Hyperthyroidism •Alcohol, stimulants •Vagal tone ```
31
What is atrial flutter?
Macroreentrant circuit, usually originating in right atrium and revolving around the tricuspid valve (approximately 300 bpm).
32
What is a junctional rhythm?
Characterized by lack of p-waves; Due to increased automaticity of AV node junction over Sinus node; Junctional Rhythm is typically 40-60 bpm (automatic rhythm of AV node)
33
What are common etiologies of junctional rhythm?
* Digoxin toxicity * Beta-agonists, e.g. isoproterenol * Myocardial ischemia * Myocarditis * Cardiac surgery * Anything that decreases sinus node automaticity: e.g., beta-blockers
34
Which supraventricular tachycardias have irregular ventricular rates?
- Multifocal Atrial Tachycardia - Atrial Fibrillation - Atrial Flutter/variable AV Block - Atrial Tachycardia/variable AV Block
35
Which supraventricular tachycardias have regular ventricular rates and p waves?
- Sinus Tachycardia - Atrial Tachycardia - Atrial Flutter - some AVNRT/AVRT
36
Which supraventricular tachycardias have regular ventricular rates and no p waves?
- Junctional Tachycardia | - AVNRT
37
What is Premature Ventricular Complex?
bizarre widened beat that occurs before it should; Extremely common throughout the population, both with and without heart disease; Usually asymptomatic, except rarely dizziness or fatigue in patients that have frequent PVCs and significant LV dysfunction
38
What is non-sustained ventricular tachycardia?
3 or more consecutive ventricular beats with rate 100+ bpm, lasting less than 30 seconds
39
What is sustained ventricular tachycardia?
consecutive ventricular beats with rate 100+ bpm, lasting more than 30 seconds
40
What are Torsades des Pointes?
Polymorphic VT in the setting of long QT interval
41
What is Ventricular Fibrillation?
Chaotic, disorganized ventricular rhythm; like a fib in that the ventricles are being depolarized in a totally chaotic manner, but unlike a fib, this is a lethal state if it is perpetuated b/c the ventricles can't sustain CO @ 300 bpm
42
What are causes of sinus bradycardia?
* Normal aging * 15-25% Acute MI, esp. affecting inferior wall- often resolves * Hypothyroidism, infiltrative diseases (sarcoid, amyloid) * Hypothermia, hypokalemia * Collagen vascular diseases * Situational: micturation, coughing * Drugs: beta-blockers, digitalis, calcium channel blockers, amiodarone, lithium
43
What is 1st Degree AV block?
PR interval 200+ms; If accompanied by wide QRS, refer to cardiology secondary to risk of progression to higher-degree block (ventricle may also be diseased); Otherwise, benign if asymptomatic
44
What is 2nd Degree AV Block Mobitz type I (Wenckebach)?
Progressive PR prolongation, with eventual non-conduction of a p wave; Usually asymptomatic; Can be caused by drugs that slow conduction (beta blockers, calcium channel blockers, digoxin); Can be corrected if reversible cause- e.g., avoid meds that block conduction; Can cause angina, syncope (esp. in elderly), leading to requiring a Pacemaker
45
What is 2nd degree block Type II (Mobitz 2)?
Normal PR intervals with sudden failure of a p wave to conduct; Usually below AV node and accompanied by BBB or fascicular block; Often causes pre/syncope; exercise worsens symptoms; Treat with pacemaker
46
What is 3rd Degree AV Block?
Complete AV dissociation with atrial rate faster than ventricular rate; Will often be symptomatic- dizziness, syncope, angina, heart failure
47
What are the 3 strategies of antiarrhythmic agents?
1.Decrease automaticity - Decrease Phase 4 slope 2.Change conduction velocity - Decrease Phase 0 slope (and Phase 4) 3.Change refractory period - Prolong Phase 2 & Phase 3
48
Which drugs slow automaticity?
Beta and calcium blockers
49
Which drugs change refractoriness or conduction velocity?
Potassium and sodium blockers
50
What is the Vaughan Williams Classification?
``` •Class I: sodium channel blockers –Inhibit depolarization/slow conduction velocity •Class II: beta-blockers –Slow sinus node and AV node •Class III: potassium channel blockers –Prolong repolarization •Class IV: calcium-channel blockers –Slow SA node (some) and AV node (more) ```
51
What do Class I drugs do?
Sodium Channel Blockers - Decrease slope of Phase 4 - Decrease slope of Phase 0 - IA & IC prolong repolarization and IB shortens repolarization
52
What are the 3 kinds of Class I drugs?
IA: moderate decrease in slope IB: mild decrease IC: marked decrease
53
What are Class IA drugs?
Class IA agents: quinidine, procainamide, disopyramide –Increase action potential duration – watch QT –Caution in renal dysfunction
54
When are Class IA drugs used?
SVTs, AF, VT; Use has declined because of more effective/less proarrhythmic meds
55
What are Class IB drugs?
Class IB agents: lidocaine (IV), mexiletine (oral), phenytoin (rarely used) –Use-dependent: better effect at faster heart rates secondary to affinity for open Na channels •Little effect on atrial tissue: atrial cells have a shorter action potential duration; less time for drug to bind to activated Na channels. Large effect on diseased/ischemic ventricular tissue –Reduce action potential duration (block Na channels that persist through phase 2) •Do not increase QT, so can be used for afterdepolarizations (e.g., digoxin-induced VT and torsades de pointes/long QT) –Caution in hepatic dysfunction
56
When are Class IB drugs used?
VT (doesn't work well in atrial cells)
57
What are Class IC drugs?
Type IC agents: flecainide, propafenone –Slower kinetics, affinity for activated sodium channel –Most potent sodium blocking effect, and therefore largest effect on ECG (even at rest secondary to slower kinetics): watch for widening of the QRS
58
When are Class IC drugs used?
AF, refractory SVTs; dangerous to use in patients with structural heart disease
59
What is the dangerous side effect of Class IC drugs?
Pro-arrhythmic!!!!! •Increased mortality in patients with structural heart disease (e.g., post-myocardial infarction) •Can slow atrial flutter rates and cause 1:1 AV conduction – use with AV node blockers
60
What are Class II drugs?
Beta-adrenergic Blockers; Class II agents: metoprolol, propranolol, esmolol, etc… Class II mechanisms: block cardiac beta-1 adrenergic receptors –Slow sinus rate –Prolong A-V node conduction and refractoriness –Inhibit automaticity –Block effect of catecholamines
61
When are Class II drugs used?
–Useful for SVTs and VT (esp. exercise- or emotionally-induced) –Controls ventricular rate in AF/FL –Mortality benefit in MI and CHF patients
62
What are Class III drugs?
Class III: Potassium Channel Blockers Class III agents: amiodarone, sotalol, dofetilide, ibutilide (IV), dronedarone Class III mechanisms: block cardiac potassium channels (phase 3) –Prolong refractoriness/QT –Amiodarone also: Decreases conduction velocity (phase 0) and automaticity (phase 4)
63
When are Class III drugs used?
Atrial fibrillation, VT
64
What are the dangerous side effects of Class III drugs?
Long QT/Torsades, Reverse-use dependence (Greater drug effect at slower heart rate, causing more tissue refractoriness/long QT/Torsades at slower heart rates); May be better at preventing arrhythmias than stopping them
65
What is Amiodarone?
Features of all 4 Vaughan Williams classes; Most effective drug for preventing recurrent AF and for VT/VF – particularly in cardiomyopathy patients, where other drugs can be more proarrhythmic; adverse events are in basically every organ system
66
What are Class IV drugs?
Class IV agents: diltiazem and verapamil Class IV mechanism: block L-type calcium channels (Phase 4 & 0) –Clinical effects •Prolonged AV node conduction and refractoriness •Sinus node slowing (mild) •Reduce automaticity (mild) •Use-dependent properties
67
When are Class IV drugs used?
Rate control for AF/AFL, treatment of SVT

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