ECG: Arrhythmias Flashcards
Explain abnormal automaticity
Two forms:
o More slowly depolarizing tissues become more dominant (under sinus node arrest)
o Automaticity occurring in cardiac tissues that normally don’t show phase 4 depolarization
• Due to injury, ischemia, metabolic disorders, drugs
On ECG: (altered automaticity)
o Gradual onset and termination of arrhythmia
o P wave of first beat of arrhythmia is typically the same as the remaining beats (if P wave is present at all)
Increase automaticity • Catecholamines • Other sympathomemetics (cocaine, phenylephrine) • Hypoxia (reflex) • Hyperthermia • Acidosis • Drugs (digoxin, etc.) • Myocardial stretch (due to chamber hypertrophy)
Decrease automaticity • Increased vagal tone • Beta blockade • Ca2+ channel blockade • Hypothermia
Triggered arrhythmias
• Triggered activity = formation of premature impulses from early (EAD) or delayed (DAD) afterdepolarizations
• Closely linked to preceding AP
• If reach stimulation threshold → trigger a premature AP → arrhythmia
Types: EADs and DADs
Early afterdepolarizations (EADs)
o Result of abnormal prolongation of AP duration in some myocytes
o Some inactivated L-type Ca2+ channels recover
o Can reopen → inward current
o Secondary depolarization phase before full repolarization
o Can result in premature ventricular beat if reach threshold
o Cardiomyocytes more prone: Purkinje fibers, M cells of mid-myocardium
o AP duration prolongation typically occurs in long QT syndrome:
1) Acquired long QT syndrome:
• Due to drug effects, electrolyte abnormalities or ischemia
• Potentially lethal side effect of some drugs
2) Congenital long QT syndrome:
• Inherited mutation in ion channel or associated protein → delayed repolarization
Delayed afterdepolarizations (DADs)
o Result of increased Ca2+ load in cytosol and SR in response to cardiac glycoside (e.g. digoxin) intoxication, ischemia, excessive catecholamines, other cardiac pathologies
o Ca2+ is taken up by SR and then transiently re-released → 2nd depolarization
o AP duration important
• Longer APs: greater SR Ca2+ influx and increased chance of DAD formation
• Shorter APs: increase size of DADs and facilitates triggered activity
Describe the characteristics necessary for reentrant arrhythmias
Reentry = circuitous propagation of electrical pulse around a non-excitable obstacle
Requires:
1) Closed loop pathway with differing conduction velocities down each limb
2) Differing refractory periods → can generate a localized unidirectional block in one limb of closed loop
3) Conduction time around pathway must be longer than the duration of the longest refractory period within the circuit to maintain an excitable gap
• Obstacle around which wavefront circulates:
A) Anatomical: scar tissue, a valve, the fossa ovalis (associated with monomorphic rhythms)
• Atrialventricular reentry
• Atrialventricular nodal reentry
• Atrial flutter
B) Functional: structurally normal but non-excitable myocardium (associated with polymorphic rhythms)
• Atrial and ventricular fibrillation
Reentry on ECG:
o Abrupt onset and termination of arrhythmia
o P wave of first beat of arrhythmia is different when compared to remaining beats (if P wave is present at all)
Identify the following arrhythmias on the ECG and describe the underlying basic mechanisms: Sinus bradycardia
o <60 bpm
o Causes:
• Intrinsic SA node disease (aging, diseases like ischemia, cardiomyopathy)
• Extrinsic factors that affect the node (medications, metabolic causes like hypothyroidism, trained athletes with increased vagal tone)
Identify the following arrhythmias on the ECG and describe the underlying basic mechanisms: Junctional rhythm
o An escape rhythm o Automaticity from AV node: 40-60 bpm ECG: • Lack of preceding P wave • Narrow QRS complex (still using His-Purkinje system)
Identify the following arrhythmias on the ECG and describe the underlying basic mechanisms: Idioventricular rhythm
o Cells in myocardium take over rhythm
o Rates: 20-40 bpm
ECG: Widened QRS complex, no preceding P wave
Atrial Premature Contractions (APCs)
Common in both healthy an diseased hearts
• Usually asymptomatic, may cause palpitations
o From automaticity or reentry in atrial tissue outside of SA node
o Can be exacerbated by sympathetic stimulation
ECG:
• Earlier than expected P wave (usually abnormal shape)
• Can get blocked APCs: if abnormal atria fires too soon → impulse encounters refractory AV node → blocked impulse
Identify the following arrhythmias on the ECG and describe the underlying basic mechanisms: Ventricular Premature Contractions (APCs)
o Often asymptomatic and benign
o In patients with heart failure or prior MI, associated with increased risk of sudden death
o Caused by ectopic ventricular focus firing an AP
ECG:
• Widened QRS complex
• Beat is not related to preceding P wave
• Can occur in repeating patterns
Identify the following arrhythmias on the ECG and describe the underlying basic mechanisms: Sinus Tachycardia
o >100 bpm
o ECG: normal P waves and QRS complexes
o Caused by increased sympathetic and/or decreased vagal tone
Identify the following arrhythmias on the ECG and describe the underlying basic mechanisms: Ectopic atrial tachycardia
o From either automaticity of an atrial focus or reentry
ECG: like sinus tachycardia but different P wave morphology
o Can be paroxysmal (limited duration) or persistant
Identify the following arrhythmias on the ECG and describe the underlying basic mechanisms: atrial flutter
o Reentrant rhythm
o Macro-reentrant circuit in wall of right atrium (cavotricuspid isthmus)
o May be paroxysmal and transient or permanent
o Clinically:
• If rate <100 bpm: asymptomatic
• If rate fast: palpitations, dyspnea, weakness
• Increased risk of atrial thromboemolism
ECG:
• Biphasic “saw-tooth” flutter waves at rate of ~300 bpm
• Flutter waves have constant amplitude, duration, and morphology
• Usually 2:1, 3:1, or 4:1 block at AV node →ventricular rates of either 150, 100, or 75 bpm
• In 2:1 block: flutter may not be apparent so need to unmask them by administering adenosine
Identify the following arrhythmias on the ECG and describe the underlying basic mechanisms: atrial fibrillation
o Reentrant rhythm
o Caused by numerous wavelets of depolarization → spread throughout the atria simultaneously → no coordinated atrial contraction
o Clinically important because can lead to hemodynamic compromise, systemic embolization, symptoms
o Often associated either right and/or left atrial enlargement = allows minimum number of reentrant circuits to sustain reentry loops
ECG:
• Absent p waves
• Presence of fine “fibrillatory” waves which vary in amplitude and morphology (low-amplitude undulations)
• Irregularly irregular ventricular responses
Identify the following arrhythmias on the ECG and describe the underlying basic mechanisms: Paroxysmal Supraventricular Tachycardias (PSVTs)
ECG: • Sudden onset and termination • Atrial rates between 140 and 250 bpm • Narrow (normal) QRS complexes o Causes: reentry involving AV node, atrium or accessory pathway between atrium and ventricles
