Cardiac Dysrhythmias_ PATHO Flashcards
Define
Dysrhythmia
Abnormal cardiac rhythm
asymptomatic to severe impact on cardiac output
2 types
- tachydysrhythmia
- more common
- heart beat is too fast
- Rx. drug (benefit > risk, can cause dysrhythmias/death); cardioversion; ablation - bradydysrhtyhmias
- too slow
- Rx. electrical pacemaker
Normal Physiology
Electrical conduction in the heart
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
Two kinds of action potentials in the heart
- Fast action potentials
- his-purkinje system
- myocardial cells (atrium, ventricle) - Slow action potentials
- SA and AV node
Normal Physiology
Fast Action potentials
Drugs that block
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)
Normal Physiology
Slow Action Potentials
Drugs that block
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
Parts of the Electrocardiogram
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)
Two causes of Dysrhythmias
- Disturbance in automaticity (onset of new AP)
- Disturbance of conduction
- AV blocks
Risk factors for Dysrhythmias
Automaticity
- 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
Pathophysiology
AV blocks
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
Vaughan Williams Classification
Anti-dysrhythmic drugs
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
Con of Dysrhythmia drugs
- cause new or worsen old dysrhythmias
- increase mortality 2x
- risk > benefit
Two types of dysrhythmias
- Ventricular dysrhythmia
- atrial dysrthyhmias (supraventricular dysrhythmia)
Two phases of dysrhythmia treatment
- terminate rhythm
- cardioversion
- electrical or pharmacological - long term supression of dysrhythmia
- drug
- pacemaker
- conduction pathway ablation
Atrial Fibrillation
Description
- 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
Atrial fibrillation
Treatment Pathways
- No treatment
- asymptomatic - 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 - Cardioversion
- Ventricle influenced –> cardiac output influenced and symptomatic
- Drug: Phase 4, potassium channel blockers (slow automaticity, fast AP); amiodarone / Sotalol - Long Term Treatment
- Slow atrial conduction and automaticity (Slow AP, AV node)
- Drugs: non-dihydropyridine CCB + beta blockers
Atrial Fibrillation
Defintion, prevalence
Uncoordinated electrical activity of the atrium
ectopic firing
irregular ventricular rate
no atrial kick
most common dysrhythmia
1% population
Atrial fibrillation
Etiology
- cardiac
- non-cardiac
- anything that results in injury/inflammation and cardiac remodelling of the atrium
- change electrical automaticity
- shorten phase 4 refractory period - change in conduction pathways
- re-entrant, AV blocks (second degree)
Trigger (Ectopic focus) and Substrate Theory
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
Multiple wavelet theory
AF
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
Paroxysmal AF
AF spontaneously terminates < 7 days
usually < 2 days
Recurrent AF
> 2 episodes
Persistent AF
> 7 days
< 1 year
requires cardioversion or ablation for treatment
Lonstanding persistent AF
> 1 year
persuing 1. conversion 2. prevention recurrence
Permanent AF / Chronic AF
> 1 year
stopping attempts to restore regular rhythm
Lone AF
individuals < 65 years
no history cardiovascular disease
Atrial Fibrillation
Clinical Manifestations
- Asymptomatic
- Ectopic beats transverse AV node influence ventricle
- irregular rhythm
- palpitations
- decreased CO: dizziness, weakness, SOB, fatigue
Diagnosis
Atrial fibrillation
- ECG
- fibrillatory baseline waves
- no P wave
- irregular QRS complex rhythm - Holter monitor
- Transthoracic echocardiogram
- structural remodelling of the heart
Blood Tests
Atrial fibrillation
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)
Clinical Management and Treatment
Atrial fibrillation
Treatment indicated if
- symptomatic
- hemodynamically unstable
- sustained
- Cardioversion
- > 48 hours AF, 3 weeks DOAC
- < 48 hours, heparin / DOAC
- electro-cardioversion OR drug cardio-version (class III - sotalol, amiodarone) - Rate control
- beta blocker / non-dihydropyridine calcium channel blocker (phase 0 and 4, slow AP; phase 2 fast AP)
- AV ablation and pacemaker - Rhythm control
- persistent AF (< 1 year) only
- *increase mortality, new arrhythmias, worsening old arrhythmias
- Drugs: amiodarone, sotalol propafenone - Clot control
- DOAC
Precipitating Causes
Atrial fibrillation
Anything that causes injury/inflammation/remodelling cardiac
Ectopic foci/SNS activation
- Cardiac
- cardiac structural, functional, electrical - Metabolic
- hypoxemia, electrolyte imbalances, acute reactant proteins - endocrine diseases
- thyroid, pregnancy, diabetes, obesity - medicaitons
- anti-arrhythmic drugs
- sympatheticomimetics
- NSAIDS, corticosteroids - MI, HTN, BG - Hyperadrenergic states
- hyperthyroidism
- OSA
- pheochromocytoma
- post-operations
