Lecture 11: Cardiac arrhythmias Flashcards by Lyn Hartono

What are some causes of cardiac arrhythmias?

Increased/ decreased sinus node automaticity
Escape rhythms: heart beats from a different pacemaker
Enhanced automaticity of latent pacemakers (ectopic beats/rhythms)
- E.g. junctional escape rhythm
- Premature junctional contraction
Triggered activity after depolarizations
- Could be produced by low potassium (hypokalemia) n drug toxicity
Conditional abnormalities
- Areas of the heart where beat can’t be conducted
Unidirectional block n re-entry: allows the heart to beat at enormous rates

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What is sinus tachycardia?

> 100 BPM, 100 - 180 (faster heart rate than normal)
Driven by the sinus node
CAUSE: decreased vagal/increased sympathetic tone
- Can be pathological
  - Acute hyperthyroidism
  - Heart failure
  - Hemorrhage [heart beats quicker to compensate for lack of blood]
  - Fever
  - Anemia
  - Hypovolemia
Can be seen in startles/frightened individual or during normal exercise
Never treat sinus tachycardia but treat the cause

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What is sinus bradycardia?

<60bpm
Tolerate as low as 45pm
Normally during sleep/fit athlete
CAUSE
- Blood supply to SA node interrupted following MI
- Drug induced (e.g. beta blockers, digoxin)
- Hyperkalemia, hypothyroidism, hypothermia
Treat underlying condition, stop medication

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What is sinus arrest?

Missing beats (PQRST complex) otherwise normal ECG
Sinus pause (1-2 missing beats), arrest (3 or more)
Maybe no symptoms (depends on numeber missing)
CAUSE
- Drug induced
- MI
- SA disease
- Increased vagal tone
Can cause faint [no blood supply to the brain]

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What is sick sinus syndrome?

SA node fails to excite the atria in a regular manner → slow resting heart raet
Heart rate does not increase w exercise
Can be
- Drug induced
- Intense vagal activity
- Degeneration of the pacemaker following ischemia
TREATMENT: insertion of artificial pacemaker

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What is sinus arrhythmia?

Normal phenomenon
Subtle changes in heart rate w each respiratory cycle
CAUSE: fluctuations in vagal activity
Inspiration → accelerates heart reat
Expiration → slows heart rate
Normal in children n young adults disappear w age

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What are premature ventricular contractions (PVCs)?

Ventricular ventricles are contracting separately from the normal beat
% of PVCs typically increase w age
CAUSES
- Medications that hv stimulant effect on the heart
- Caffeine
- Alcohol
- Illicit drugs
- States of heightened sympathetic activity (e.g. stress, exercise)

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What are the 2 major causes of conduction abnormalities?

Depolarization
- Injured tissue → altered balance of ionic currents → inactivation of Na n Ca channels → poor conductance → slow spread of conduction
- RESULT: less excitable (partial block) or completely inexcitable (complete conduction block)
Abnormal anatomy
- Presence of aberrant conduction pathway
- E.g. can bypass AV node which normally imposes conduction delay
- Second conduction pathway b/w atria n ventricles predispose to supraventricular arrhythmias

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What is Wolff-Parkinson-White syndrome?

Example of abnormal anatomy
- Abnormal pathway
- NORMAL
  ○ AV node
  ○ Down to ventricles
  ○ Disspitate out
- SYNDROME
  ○ Beat can come backwards into atria
  ○ Can prematurely get into the ventricles
- ECG result
  ○ Short PR interval
  ○ Wide QRS [faster accessory pathway + AV node]
- If the heart beats faster, there is a loop of activity
  Goes back into the atria to re-excite -> tachycardia [heart will stop beating much more quickly, beats persisting]

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What is first-degree block?

Long PR interval
- Beat gets to repolarize the atria -> large delay AV node
- Longer delay b/w P n QRS
- Still 1:1 relation b/w P n QRS
- Benign condition
- Many young people will show this pattern esp during sleep when there is high vagal tone
  Does not require treatment

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What is second-degree block — Mobitz Type I?

Slow increase in lengthening of PR interval
No QRS
Fails n restarts again
PR interval lengthens until AV node fails completely
Atrial rhythm is regular
Benign condition
Often no symptoms can be dizzy [not enough blood supply to tissue]

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What is bundle branch block (BBB)?

NORMAL
○ Heart beat goes down 2 bundles of His then go across ventricles to depolarize -> contraction
- Bundle branch block
  ○ Bundles fail
  ○ Only goes down one side of the heart
  ○ Will spread across the heart -> will still get contractions on the other side of the heart
  ○ Causes the QRS to widen [slow depolarization[
  Slow contraction -> loss of efficiency

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What is second-degree block — Mobitz Type II?

PR interval consistent but every Nth cycle ventricular depolarization is missing
May progress to complete heart block

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What is third degree (complete) block?

Failure of conduction b/w atria n ventricles
- Supraventricular impulses no longer trigger ventricular contraction
- Causes
  ○ Acute MI
  ○ Drug toxicity
  ○ Chronic degeneration w age
- Atria can be beating relatively normally but ventricles still beat bc they still get beat from latent pacemakers
- If no beat getting to the ventricles, they still beat but it’s not from the SA node
- Escape rhythm
  Heart rhythm initiated by lower centers when the SA fails to initiate impulses when it’s rhythmically depressed or when it’s completely blocked

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What are the symptoms of third degree (complete) block?

Bradycardia
Signs of congestive heart failure (decreased CO)
- Tachypnea or respiratory distress
- Rales
- Jugular venous distention
Patients may hv signs of hypoperfusion
- Altered mental status
- Hypotension
- Lethargy
In patients w concomitant myocardial ischemia or infarction
- Signs of anxiety (e.g. agitation or unease)

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What are the potential sites of complete heart block, and what percentage of blocks occur at each site?

Complete heart block can occur at various levels: AV node, Bundle of His, and the bundle-branch Purkinje system.
Approximately 60% of blocks occur below the His bundle, around 20% at the AV node, and less than 20% at the level of the His bundle.

How does the duration of the escape QRS complex relate to the site of block and the escape rhythm pacemaker?

The duration of the escape QRS complex depends on both the site of block and the site of the escape rhythm pacemaker.
An escape rhythm from the AV node typically results in a stable heart rate of 40-60 beats per minute (BPM) and relatively normal-looking QRS complexes.
- Escape rhythms originating above the His bundle usually produce narrow QRS complexes.
However, if the block occurs below the His bundle, the QRS complex becomes wider due to problems with conduction.

What are the characteristics of escape rhythms originating below the AV node, and how do they affect patients?

Escape rhythms originate from the His bundle or Purkinje system.
Slower rate escape rhythms, usually less than 45 BPM.
Physiological effects: instability, reduced cardiac output, and blood pressure.
- HR may be unresponsive to exercise and atropine.

What is atrial flutter I?

Rapid regular atrial activity (180-350 BPM)
Many impulses reach the AV node but do not conduct to ventricles (2:1 block)
Caused by re-entry over anatomically fixed circuit
- Area of the heart that’s damaged → beat that goes around that drives increase in activity
Usually in patients w heart disease
ECG: saw-tooth appearance [continual P waves]

What is atrial flutter II?

Can be transient or permanent
If rate is <100 BPM → asymptomatic
Faster rates: palpitations, dyspnea, weakness
Risk of atrial thromboembolism [atria don’t eject blood v well → blood stays in atria → clot]
Reducing rate can make rhythm more dangerous
- Get more blood going thru ventricles → ventricles beat rapidly → won’t work either [no filling team] → ventricles will quiver
Treatment
- Electrical cardioversion
- Pacemaker
- Pharmacological therapy
- Catheter ablation

What is atrial fibrillation I?

Chaotic rhythm atrial rate (350-600 discharges per min)
Discrete P waves not discernable on ECG
Only reach some ventricles (irregular)
Ventricular rate: 150-160 BPM
CAUSE: wandering re-entrant circuits

What is atrial fibrillation II?

CAUSES
- Enlarged atria increases likelihood of occurence
- Heart failure, hypertension, CAD
- Thyrotoxicosis, alcohol
Dangerous bc
- Rapid ventricular rates reduce CO
- Blood stasis leading to thrombus/emboli
Treatment
- Anti-arrhythmic drugs
- Electrical cardioversion
- Catheter ablation
- Maze procedure

What is ventricular tachycardia (VT)? (cause, ECG, symptoms, treatment)

Sustained or non-sustained
CAUSE: heart disease, MI, heart failure
ECG: wide QRS complex [100-200 BPM]
Regular: monomorphic (same shapes) [re-entrant circuit in ventricle]
Irregular: polymorphic [delayed repolarization long QT]
Symptoms
- Syncope
- Pulmonary oedema
- Cardiac arrest
Dangerous bc can deteriorate into VF
Treatment
- Electrical cardioversion
- IV antiarrhythmic drugs

What is ventricular fibrillation (VF)? (cause, symptoms, treatment)

Life threatening
Disordered rapid stimulation of ventricles → quiver do not contract
Loss of CO (death if not quickly reversed)
CAUSE
- Heart disease
- Low K+
- Electric shock
- Some drugs
VF often initiated by episodes of ventricular tachycardia
TREATMENT
- Prompt electrical defibrillation
- IV antiarrhythmic drug to prevent recurrence
- Survivors may receive an ICD (implantable cardioverter defibrillator)
  - Similar to pacemaker but lead to ventricle is larger [allows it to deliver a larger shock to heart when necessary]

What is congenital long-QT syndromes?

- CAUSE - Mutation in heart channels usually K channels - Hereditary - Asymptomatic - ECG - Long QT [heart AP is abnormally wide → long duration [channels that repolarize hv mutation]] - Makes patients prone to ventricular arrhythmias

Why can the heart block at extremely fast rates?

- NORMAL - Cardiac beat can go around obstacle - Spread around the heart - Meet itself at X -> cancel itself out [refractory periods] - UNIDIRECTIONAL BLOCK - Only allows beat to move in one direction - Beat will go around n carry on going around the circuit - Tissue is refractory immediately after heart beat - By the time it gets to the unidirectional block, it will move around n reach an area where the tissue is still refractory -> beat will die out - Allows beat to carry on - If we slow conduction, then beat will continually go around the obstacle - Trophic focus will drive the heart → contract more quickly than normal