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Year 1: Patho/Pharm > Cardiac Dysrhythmias_ PATHO > Flashcards

Cardiac Dysrhythmias_ PATHO Flashcards

1
Q

Define
Dysrhythmia

A

Abnormal cardiac rhythm
asymptomatic to severe impact on cardiac output

2 types

  1. tachydysrhythmia
    - more common
    - heart beat is too fast
    - Rx. drug (benefit > risk, can cause dysrhythmias/death); cardioversion; ablation
  2. bradydysrhtyhmias
    - too slow
    - Rx. electrical pacemaker
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2
Q

Normal Physiology
Electrical conduction in the heart

A

SA node
- automaticity
- 60-100bpm
- cardiac pacemaker

AV node
- automaticity
- 40-60bpm
- pause conduction to allow ventricles to fill

His-Purkinje System
- automaticity
- < 40bpm
- conduction spontaneous through L/R bundle branches
- simultaneous contraction of ventricles

Myocardium
- automaticity

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3
Q

Two kinds of action potentials in the heart

A
  1. Fast action potentials
    - his-purkinje system
    - myocardial cells (atrium, ventricle)
  2. Slow action potentials
    - SA and AV node
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4
Q

Normal Physiology
Fast Action potentials
Drugs that block

A

Phase 0
Sodium channels open
- depolarization
- conduction rate through his-purkinje/myocardium
Drugs: Propafenone, lidocaine, phenytoin, procanamide (decrease conduction)

Phase 2
Calcium channels open
- depolarization
- contractility of atrium and ventricles
Drugs: beta blockers, non-dihydropyridine calcium channel blockers (decrease contractility)

Phase 3
Potassium channels open
- repolarization
- ability for another heart beat
Drugs: amiodarone (prolong refractory period, decrease HR)

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5
Q

Normal Physiology
Slow Action Potentials
Drugs that block

A

Slow action potentials
- SA node, AV node

Phase 0: Calcium channels open
- influx calcium
- depolarization
- conduction of heart
- Drugs: beta blocker, CCB non-dihydropyridines, adenosine

Phase 4: unknown channels
- depolarization to threshold
- automaticity of the heart (heart beat)
- Drugs: beta blockers, CCB non-dihydropyridines

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6
Q

Parts of the Electrocardiogram

A

P wave
- atrial contraction
- Drugs: phase 2 fast AP myocardium (CCB, beta blockers)

QRS complex
- ventricle contraction
- Drugs: phase 2 fast AP myocardium (CCB, beta blockers)

PR interval
- time from atrium contraction to ventricle contraction
- conduction through AV node
- Drug: Phase 0 slow AP (CCB and beta blocker)

QT interval
- Time for ventricular contraction to relaxation
- conduction through His-Purkinje and myocardium
- Drugs Phase 0 (lidocaine, procanamide, phenytoin, propafenone), Phase 2 (beta blocker, CCB), Phase 3 (amiodarone)

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7
Q

Two causes of Dysrhythmias

A
  1. Disturbance in automaticity (onset of new AP)
  2. Disturbance of conduction
    - AV blocks
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8
Q

Risk factors for Dysrhythmias
Automaticity

A
  • hypoxia
  • low coronary artery blood flow
  • surgery
  • inflammation
  • eletrolyte imbalances
  • myocardial infarction

Injury/ischemia/inflammation –> activation SNS –> tachydysrythmias

*automaticity can develop in any myocardial cell
- phase 4, spontaneous depolarization to threshold

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9
Q

Pathophysiology
AV blocks

A

Dysrhythmia from abnormal conduction pathway

first degree - slow conduction through AV node
- Slow AP
- Slow opening calcium channels phase 0

Second degree
- block forward flow
- re-entrant current
- self-perpetuating circuit
- ectopic beats

Third degree
- block forward and backwards flow

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10
Q

Vaughan Williams Classification
Anti-dysrhythmic drugs

A

Class I: Sodium channel blockers
- block Phase 0, fast AP (his-purkinje, atrium/ventricle myocardium)
- prevent conduction through ventricles
- lidocaine, procainamide
- phenytoin
- propafenone

Class II: beta blockers
- Block phase 2, fast AP (his-purkinje, atrium/ventricle contraction)
- decrease contractility of heart
- Block phase 0 and 4, slow AP (SA and AV node)
- decrease conduction and automaticity (heart beat)
- Drug: propranolol, acebutolol

Class III: Block potassium channels
- Block phase 4, fast AP
- prevent repolarization
- slow heart rate
- Drug: amiodarone, sotalol

Class IV: Calcium channel blockers non-dihydropyridines
- block phase 0 and 4 of slow action potentials (SA, AV node)
- decrease conduction and automaticity
- Drug: verapamil, diltiazem

Other: Digoxin

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11
Q

Con of Dysrhythmia drugs

A
  • cause new or worsen old dysrhythmias
  • increase mortality 2x
  • risk > benefit
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12
Q

Two types of dysrhythmias

A
  1. Ventricular dysrhythmia
  2. atrial dysrthyhmias (supraventricular dysrhythmia)
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13
Q

Two phases of dysrhythmia treatment

A
  1. terminate rhythm
    - cardioversion
    - electrical or pharmacological
  2. long term supression of dysrhythmia
    - drug
    - pacemaker
    - conduction pathway ablation
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14
Q

Atrial Fibrillation
Description

A
  • multiple ectopic foci in the atrium (fast AP)
  • chaotic, rapid, unable to count
  • most common sustained dysrhythmia
  • symptomatic only when ventricle influenced (faint, dizziness)

ECG findings
- irregular rhythm
- chaotic waves
- regular rate

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15
Q

Atrial fibrillation
Treatment Pathways

A
  1. No treatment
    - asymptomatic
  2. Anti-coagulation therapy
    - clots form in atrium (stagnant blood)
    - 1. Warfarin
    - 2. DOAC (direct oral anticoagulants - Anti-Xa)
    - 3. ASA + clopidogrel
    - *2-3 weeks before cardioversion
  3. Cardioversion
    - Ventricle influenced –> cardiac output influenced and symptomatic
    - Drug: Phase 4, potassium channel blockers (slow automaticity, fast AP); amiodarone / Sotalol
  4. Long Term Treatment
    - Slow atrial conduction and automaticity (Slow AP, AV node)
    - Drugs: non-dihydropyridine CCB + beta blockers
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16
Q

Atrial Fibrillation
Defintion, prevalence

A

Uncoordinated electrical activity of the atrium
ectopic firing
irregular ventricular rate
no atrial kick

most common dysrhythmia

1% population

17
Q

Atrial fibrillation
Etiology

A
  1. cardiac
  2. non-cardiac
  • anything that results in injury/inflammation and cardiac remodelling of the atrium
  1. change electrical automaticity
    - shorten phase 4 refractory period
  2. change in conduction pathways
    - re-entrant, AV blocks (second degree)
18
Q

Trigger (Ectopic focus) and Substrate Theory

A

Ectopic focus
- trigger that initiates AF
- automatic focus theory (occur in the automaticity cells)
- ex. superior vena cava, pulmonary veins, coronary sinus etc.

Susceptible substrate
- abnormality in cardiac function/structure from conditions that cause cardiac injury/inflammation/remodeling:
Examples:
- HTN
- MI
- obesity, smoking, alcohol, type II DM, thyroid
- HF

AF stresses the heart
- leads to calcification, fibrosis, scaring
- persistent AF –> longstanding AF

19
Q

Multiple wavelet theory
AF

A

Re-entrant theory
- ectopic foci in automaticity cells generate AF trigger
- conduction pathway alteration (AV block) results in re-entrant currents
- multiple wavefronts
- stresses the heart leading to re-modeling

20
Q

Paroxysmal AF

A

AF spontaneously terminates < 7 days
usually < 2 days

21
Q

Recurrent AF

A

> 2 episodes

22
Q

Persistent AF

A

> 7 days
< 1 year
requires cardioversion or ablation for treatment

23
Q

Lonstanding persistent AF

A

> 1 year
persuing 1. conversion 2. prevention recurrence

24
Q

Permanent AF / Chronic AF

A

> 1 year
stopping attempts to restore regular rhythm

25
Q

Lone AF

A

individuals < 65 years
no history cardiovascular disease

26
Q

Atrial Fibrillation
Clinical Manifestations

A
  • Asymptomatic
  • Ectopic beats transverse AV node influence ventricle
  • irregular rhythm
  • palpitations
  • decreased CO: dizziness, weakness, SOB, fatigue
27
Q

Diagnosis
Atrial fibrillation

A
  1. ECG
    - fibrillatory baseline waves
    - no P wave
    - irregular QRS complex rhythm
  2. Holter monitor
  3. Transthoracic echocardiogram
    - structural remodelling of the heart
28
Q

Blood Tests
Atrial fibrillation

A

Etiology
1. cardiac
2. non cardiac

  • Electrolytes
  • lipid pannel
  • FBG and A1C pannel
  • coagulation profile
  • renal and liver function
  • TSH, free T3, free T4
  • BNP and ANP (elevated with atrial fibrillation and HF)
29
Q

Clinical Management and Treatment
Atrial fibrillation

A

Treatment indicated if
- symptomatic
- hemodynamically unstable
- sustained

  1. Cardioversion
    - > 48 hours AF, 3 weeks DOAC
    - < 48 hours, heparin / DOAC
    - electro-cardioversion OR drug cardio-version (class III - sotalol, amiodarone)
  2. Rate control
    - beta blocker / non-dihydropyridine calcium channel blocker (phase 0 and 4, slow AP; phase 2 fast AP)
    - AV ablation and pacemaker
  3. Rhythm control
    - persistent AF (< 1 year) only
    - *increase mortality, new arrhythmias, worsening old arrhythmias
    - Drugs: amiodarone, sotalol propafenone
  4. Clot control
    - DOAC
30
Q

Precipitating Causes
Atrial fibrillation

A

Anything that causes injury/inflammation/remodelling cardiac
Ectopic foci/SNS activation

  1. Cardiac
    - cardiac structural, functional, electrical
  2. Metabolic
    - hypoxemia, electrolyte imbalances, acute reactant proteins
  3. endocrine diseases
    - thyroid, pregnancy, diabetes, obesity
  4. medicaitons
    - anti-arrhythmic drugs
    - sympatheticomimetics
    - NSAIDS, corticosteroids - MI, HTN, BG
  5. Hyperadrenergic states
    - hyperthyroidism
    - OSA
    - pheochromocytoma
    - post-operations

Year 1: Patho/Pharm (39 decks)

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