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Gen Med Unit 7a: Cardio 2 > Cardiac Arrhythmias > Flashcards

Cardiac Arrhythmias Flashcards

1
Q

Arrhythmias classifications are based on:

A 
1. Pathophysiology
A. Disorders of impulse formation or automaticity
B. Abnormalities of conduction
C. Re-entry activity
2. Origin
A. Supraventricular
B> Ventricular
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2
Q

What are the metabolic disturbances that cause arrhythmias?

A
  1. Electrolyte abnormalities
  2. Hormonal imbalance
  3. Hypoxia
  4. Drug side effects
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3
Q

What are the structural heart disturbances that cause arrhythmias?

A
  1. Myocardial ischemia (CAD)
  2. Healing after cardiac surgery
  3. Valve disorders
  4. Cardiomyopathies
  5. Hypertensive cardiomegaly
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4
Q

What are the clinical presentations of arrhythmias?

A
  1. Presentation variable depending on effects on CO
  2. Asymptomatic
  3. Symptomatic & hemodynamically stable
  4. Symptomatic & hemodynamically unstable
  5. Fatal
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5
Q

What are the potential sxs of arrhythmias?

A
  1. None
  2. Palpitations
    A. Skipped heartbeats
    B. Fluttering
    C. “Flip-flops
  3. Pounding in the chest
  4. Dizziness or feeling lightheaded
  5. Syncope or near syncope
  6. SOB
  7. Chest discomfort
  8. Weakness or fatigue
  9. Cardiac arrest
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6
Q

What are the atrial arrhythmias?

A
  1. Premature atrial contractions
  2. Supraventricular tachycardia
  3. Atrial fibrillation
  4. Atrial fluttter
  5. Accessory pathway tachycardia
  6. Multifocal atrialtachycardia
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7
Q

What are the Sinus node arrhythmias?

A
  1. Sinus bradycardia

2. Sinus tachycardia

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8
Q

What are the junctional arrhythmias?

A

Junctional rhythm

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9
Q

What are the ventricular arrhythmias?

A
  1. Premature ventricular contractions
  2. Ventricular tachycardia
  3. Ventricular fibrillation
  4. Long QT
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10
Q

Define bradyarrhythmias

A
  1. Slow heart rhythm usually caused by disease in the heart’s conduction system
    A. Sinus node dysfunction
    B. Heart block
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11
Q

What are the dx studies for arrhyhtmias?

A
  1. EKG monitoring
  2. Heart rate and rhythm monitoring
    A. Holter monitor
    B. King of Hearts monitor
    C. Implantable EKG loop monitor
  3. Electrophysiology testing
  4. Stress testing
  5. Echo
  6. Autonomic testing
    A. Tilt table test
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12
Q

What is an electrophysiology study (EPS)?

A
  1. Special heart catheterization that evaluates heart’s electrical system
  2. Catheters inserted into heart to record the electrical activity
  3. Arrhythmia can be safely reproduced & terminated
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13
Q

What are the general tx measures for arrhythmias?

A
  1. Lifestyle changes
  2. Antiarrhythmic drugs
  3. Electrical cardioversion
  4. Catheter ablation
  5. Permanent pacemaker
  6. Implantable cardioverter-defibrillator (ICD)
  7. Surgery
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14
Q

What are the goals of arryhthmia tx?

A
  1. Eliminate symptoms
  2. Prevent imminent death & hemodynamic collapse due to a life-threatening arrhythmia
  3. Reduce possible risks other than the direct effects of the arrhythmia
    A. Stroke in A. Fib
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15
Q

What are the class 1a antiarrhythmic drugs moa? What is an example?

A 
1. Na & K channel blockers
A. Depress depolarization
B. ↓ Excitogenicity
C. Stabilize cell membrane
D. Prolong repolarization
-K blockade
  1. Quinidine
  2. Procainamide
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16
Q

When are the class 1a antiarrhythmic drugs indicated?

A

Supraventricular & ventricular arrhythmias

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17
Q

What are the class 1b antiarrhythmic drugs moa? What is an example?

A
  1. Na & K channel blockers
    A. Shorten repolarization
    B. Suppresses arrhythmias from abnormal automaticity
  2. Lidocaine
  3. Mexiletine
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18
Q

When are the class 1b antiarrhythmic drugs indicated?

A
  1. V Tach

A. Med of choice for V Tach asst w/ischemia

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19
Q

What are the class 1c antiarrhythmic drugs moa? What is an example?

A
  1. Na channel blockers
    A. Slow conduction
    B. Prevents re-entry
    C. Safety is an issue with these drugs
  2. Flecainide (Tambocor)
    A. Most potent Na channel blocker
  3. Propafenone (Rhythmol)
  4. Moricizone
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20
Q

When are the class 1c antiarrhythmic drugs indicated?

A
  1. Life threatening V Tach

2. Refractory SVT

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21
Q

What are the class II antiarrhythmic drugs moa? What is an example?

A 
1. Beta blockers
A. Depress automaticity
B. Slow AV conduction
C. ↓ HR & contractility
2. Metoprolol (Toprol XL/Corgard)
A. Beta 1 selective
3. Esmilol (Breviblock)
A. Beta 1 selective
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22
Q

When are the class II antiarrhythmic drugs indicated?

A
  1. A Fib
  2. A Flutter
  3. SVT
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23
Q

What are the class III antiarrhythmic drugs moa? What is an example?

A 
1. Anti-arrhythmics
A. Block  K  channels 
B. Prolongs action potential & refractory period
C. Slows HR
2. Amiodarone (Cordarone)
A. Class I, II, III & IV actions
3. Sotalol (Betapace)
A. Blocks K channels and beta receptors
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24
Q

When are the class III antiarrhythmic drugs indicated?

A
  1. Life threatening ventricular arrhythmias

2. Supraventricular arrhythmias

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25
Q

What are the class IV antiarrhythmic drugs moa? What is an example?

A 
1. CCB’s
A. Slows conduction through AV node
B. Provides vasodilation
2. Verapamil (Calan)
3. Diltiazem (Cardizem)
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26
Q

When are the class IV antiarrhythmic drugs indicated?

A
  1. A fib

2. A flutter

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27
Q

What is the moa of digoxin?

A
  1. Inhibits Na, K, ATPase
    A. Slows AV conduction
    B. ↑ Refractory period
  2. ↑ Intracellular Ca  ↑ contractility
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28
Q

What is the indication for digoxin?

A

Controls ventricular response rate in A Fib & A Flutter

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29
Q

What is the moa of adenosine?

A
  1. Opens K channels
  2. Inhibits Ca influx in SA and AV nodes
  3. Slows AV conduction
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30
Q

What is the indication for adenosine?

A

SVT

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31
Q

What are the general characteristics of sinus brady?

A
  1. Heart rate < 60 bpm
  2. Normal in well conditioned hearts
  3. May represent SA node pathology
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32
Q

What are the physiologic effects of sinus brady?

A
  1. Dizziness
  2. Weakness
  3. Confusion
  4. Hypotension
  5. Syncope
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33
Q

When is pacemaker required in sinus brady?

A

Temporary or permanent pacemaker may be required if sx’s correlate with bradycardia

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34
Q

Define sinus tachy?

A

Heart rate > 100 bpm

35
Q

What may sinus tachy be asst with?

A
  1. Fever
  2. Exercise
  3. Pain
  4. Emotion
  5. Shock
  6. Thyrotoxicosis
  7. Anemia
  8. Heart failure
  9. Response to drugs
36
Q

What are the general characteristics of a PAC?

A
  1. Frequently seen in normal hearts
  2. Usually asymptomatic
  3. Can occur before development of A Fib
37
Q

What is the pathophys of PACs?

A
  1. Ectopic atrial foci fire before sinus node impulse

2. Contour of P wave differs from sinus P wave

38
Q

Define Supraventricular tachycardia

A

Narrow QRS complex (< 120 msec) reflects rapid activation of the ventricles via the normal His-Purkinje system (arrhythmia originates above or w/in the His bundle)

39
Q

Where can SVT’s originate from?

A

Site of origin may be in the SA node, atria, AV node, His bundle, or combination of these sites

40
Q

When can SVTs produce a widened QRS?

A
  1. SVT can produce a widened QRS (≥ 120 msec) if either pre-existing or rate-related abnormalities are w/in the His-Purkinje system
    A. SVT with aberrancy
    B. Conduction occurs over an accessory pathway
41
Q

What are the general characteristics of SVT?

A
  1. Most common cause of palpitations in pts w/normal hearts
  2. Women > men
  3. More common in young adults
  4. Generally well tolerated and rarely life threatening
42
Q

What are some known triggers for SVT?

A

Caffeine, exertion, alcohol, abrupt D/C of beta blockers, amphetamines

43
Q

What are the rhythm strip characteristics for SVT?

A
  1. Regular rhythm
  2. Rate > 160 bpm
    A. Rarely exceeds 250 bpm
  3. P waves regular
  4. P waves precede each QRS but are difficult to differentiate from preceding T wave
  5. If the rhythm starts and stops suddenly, it is called paroxysmal SVT (PSVT)
44
Q

What are the two types of SVT?

A
  1. Anatomical re-entry circuit involving Bundle of Kent (AVRT)
  2. Functional re-entry circuit (AVNRT)
45
Q

What is the most common cause of narrow QRS complex tachycardia?

A
  1. Reentry is the most common cause of narrow QRS complex tachycardia
  2. Increased automaticity and triggered activity occur less frequently
46
Q

What is AV re-entrant tachycardia?

A
  1. Includes Wolff Parkinson White Syndrome (WPW)
    A. Also called pre-excitation syndrome
  2. Accessory path predisposes pt to develop re-entry tachycardia
47
Q

What are the rhythm strip characteristics for AV Re-entrant tachy?

A
  1. Produces short PR interval (0.10 sec
48
Q

What are the sxs of Anatomical re-entry tachy (AVRT)/WPW?

A
  1. Palpitations
  2. Lightheadedness
  3. SOB
  4. Syncope
49
Q

How is WPW treated medically?

A
  1. Pharmacologic
    A. Adenosine IV – acute treatment
    B. Verapamil IV – acute treatment
    C. CCB or beta blockers – chronic treatment
50
Q

How is WPW treated surgically?

A
  1. Catheter ablation
    A. Procedure of choice
    C. Definitive treatment
51
Q

What is the pathophys of AVNRT?

A
  1. Abnormal AV node conduction
  2. Two paths of conduction:
    A. Slow Path with short refractory period
    B. Fast Path with long refractory period
  3. During sinus rhythm, electrical impulses travel down both paths simultaneously
  4. Impulse traveling down fast path enters distal end of slow path -> cancels each impulse out
  5. If PAC arrives while fast path is still refractory, the electrical impulse is directed solely down slow path
  6. By the time impulse reaches end of slow path, fast path is no longer refractory
    A. Impulse passes retrogradely up the fast path
    B. Creates circus movement where impulse continually cycles around 2 paths
52
Q

What are the clinical manifestations of AVNRT/PSVT?

A
  1. Palpitations, anxiety, uncomfortable
  2. Exercise tolerance low with very high rates
  3. May become unstable tachycardia
53
Q

What are the EKG findings for AVNRT?

A
  1. Tachycardia 140-250 bpm
  2. Regular rhythm
  3. Narrow complex tachycardia (QRS < 120 ms) unless pre-existing BBB or accessory path
  4. P waves may be buried in the QRS complex, visible after the QRS complex, or very rarely visible before the QRS complex
54
Q

What is the acute treatment for SVT via mechanical measures?

A 
1. Stimulate vagus nerve, delay AV conduction and block re-entry mechanism
A. Valsalva maneuver
B. Coughing
C. Breath holding
D. Unilateral carotid sinus massage
-Do not do if pt has carotid bruits
-Massage one carotid at a time
55
Q

What is the acute treatment for SVT via pharmacologic measures?

A
  1. Adenosine 6 mg fast IVP (1-2 secs)
    A. If no response after 1-2 minutes, 12 mg IVP
    B. Adenosine blocks conduction through AV node
  2. IV verapamil
    A. 2.5 mg IVP q 1-3 mins for max dose 20 mg
    B. Blocks conduction through AV node
  3. Prevention
    A. CCB (verapamil/Calan)
    B. B Blocker (metoprolol/Toprol XL)
56
Q

When is cardioversion indicated for SVT?

A

Pt hemodynamically unstable

Contraindications to adenosine or verapamil

57
Q

Define synchronized electrical cardioversion

A
  1. Synchronized DC discharge with the R or S wave of the QRS complex
  2. Interrupts self-perpetuating circuit and restores a sinus rhythm
58
Q

What are the EKG findings for A flutter?

A
  1. Atrial rates 250-350 bpm, usually with transmission of every 2nd, 3rd, or 4th impulse through AV node
  2. Regular heart rhythm with ventricular rate of 100-150 bpm
  3. “Sawtooth” appearance on EKG
59
Q

Which pts may have A flutter?

A

Occurs most often in pts with COPD

Also seen with CHF, CAD, ASD

60
Q

What is the pathophys of A flutter?

A

Re-entry tachycardia

61
Q

What are the sxs of A flutter?

A
  1. Acute onset palpitations
  2. Fatigue
  3. SOB
62
Q

What is the acute treatment for A Flutter?

A
  1. Class III anti-arrhythmic
    A. Ibultilide: Conversion rates 50-70% within 60-90 mins of infusion
  2. Anticoagulation
    A. If rhythm change > 48 hrs since onset
  3. DC Cardioversion: Conversion rates 90%
    A. Anticoagulation NOT necessary if episode < 48 hrs duration
63
Q

What is the chronic treatment for A Flutter?

A
  1. Rate control is difficult
    A. Amiodarone & dofetilide are drugs of choice
  2. Anticoagulation
  3. Catheter ablation
    A. Preferred treatment for recurrent a flutter with typical re-entry circuit
64
Q

What are the general characteristics of Atrial fibrillation?

A
  1. Most common chronic arrhythmia
  2. Incidence increases with age
  3. Called “holiday heart”
    a. Excessive alcohol around holidays or alcohol withdrawal can precipitate A fib
65
Q

What is the most serious consequence of a fib?

A
  1. thrombus formation
    A. Due to stasis in atria, esp left atrial appendage
    B. Can result in emboli –>stroke
66
Q

What are the risk factors for A fib?

A 
1. HTN
A. #1 Risk factor
2. COPD
3. Thyrotoxicosis
4. Ischemic heart disease
5. Mitral stenosis
6. Binge alcohol drinking
A. “Holiday heart”
67
Q

How is Acute A fib defined?

A

New onset lasting < 48 hrs

68
Q

How is paroxysmal A fib defined?

A

Recurrent, < 48 hrs, converts spontaneously to NSR

69
Q

How is persistent A fib defined?

A

> 1 week, requires treatment to convert

70
Q

How is permanent A fib defined?

A

Cannot be converted

71
Q

What are the clinical manifestations of A fib?

A
  1. Rapid vent response: DOE, SOB, acute pulm edema
  2. Loss of atrial kick: decreased CO and coronary perfusion
  3. Palpitations
  4. Can be asymptomatic
72
Q

What are the EKG findings for a fib?

A
  1. Atrial and ventricular rhythms irregularly irregular
  2. Atrial rate 350-600 bpm
  3. QRS complexes of uniform configuration & duration
  4. PR interval indiscernible
  5. No P waves
73
Q

What are the Dx studies and results for a FIb?

A
  1. Trop, CK-MB: Rule out MI
  2. BNP: Rule out HF
  3. Electrolytes
    A. Hyper/hypokalemia
    B. Hypomagnesemia
  4. FT4, TSH: Rule out hyperthyroidism
  5. EKG
    A. A fib: Controlled ventricular response or Rapid ventricular response
  6. ECHO
    A. Assess for valvular abnormalities
    B. Assess for hypokinesis of ventricular wall
    -Indicates myocardial ischemia/infarction
74
Q

How is Newly diagnosed A fib patient who is hemodynamically unstable managed?

A
  1. Hospitalization & immediate treatment required
  2. Direct cardioversion
  3. Class III anti-arrhythmic (amiodarone)
75
Q

What are the sxs of Newly diagnosed A fib patient who is hemodynamically unstable?

A

Rapid Vent response, angina, CHF

76
Q

How is direct cardioversion done?

A
  1. Attempt to convert rhythm to NSR
  2. Initial shock 100-200 joules
  3. If no response, 360 joules
  4. If no response, IV ibutilide
77
Q

How is Newly diagnosed A fib patient who is hemodynamically stable managed?

A
  1. Rate control & anticoagulation
    A. Target ventricular rate 50-100 bpm
  2. If co-existing MI or ischemia, beta blockers are preferred agents
    A. Metoprolol (Toprol or Lopressor)
  3. If co-existing HTN or if beta blockers contraindicated, CCB are preferred
    A. Diltiazem (Cardizem) or verapamil (Calan)
  4. Other agents:
    A. Amiodarone (Class I, II,II, IV anti-arrhythmic)
    B. Digoxin – indicated in pts with CHF
78
Q

When is a TEE recommended in A fib?

A

If duration of A fib > 48 hrs, if rate control unsuccessful or if cardioversion is considered

79
Q

If no atrial thrombus is present, how is an A Fib pt managed?

A

DC cardioversion followed by anticoagulation for minimum 4 weeks

80
Q

If an atrial thrombus is present, how is an A Fib pt managed?

A

4 week anticoagulation recommended prior to cardioversion

81
Q

What is the chronic treatment for A Fib?

A
  1. Anticoagulation
    A. Warfarin: INR target 2.0 - 3.0
  2. Rate Control
    A. Amiodarone: Adverse SE: thyroid disease, pulmonary fibrosis
82
Q

What is AV junctional rhythm asst with?

A

Asst with myocarditis, CAD, digoxin toxicity, beta blockers, as well as normal hearts

83
Q

When is an AV junction present?

A

AV junction may assume pacemaker activity for heart if SA node fails or if AV block exists

84
Q

What are the EKG findings for junctional rhythms?

A
  1. Rate ≈ 40-60 bpm
  2. Accelerated junctional rhythm (60-100 bpm) → rate of an AV junctional pacemaker exceeds that of the sinus node
  3. Junctional tach (>100 bpm)
  4. Regular heart rhythm w/out P waves

Gen Med Unit 7a: Cardio 2 (8 decks)

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