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LF266: Blood and Circulation > Lecture 11: Cardiac arrhythmias > Flashcards

Lecture 11: Cardiac arrhythmias Flashcards

1
Q

What are some causes of cardiac arrhythmias?

A
  • 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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2
Q

What is sinus tachycardia?

A
  • > 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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3
Q

What is sinus bradycardia?

A
  • <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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4
Q

What is sinus arrest?

A
  • 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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5
Q

What is sick sinus syndrome?

A
  • 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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6
Q

What is sinus arrhythmia?

A
  • 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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7
Q

What are premature ventricular contractions (PVCs)?

A
  • 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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8
Q

What are the 2 major causes of conduction abnormalities?

A
  • 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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9
Q

What is Wolff-Parkinson-White syndrome?

A
  • 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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10
Q

What is first-degree block?

A
  • 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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11
Q

What is second-degree block — Mobitz Type I?

A
  • 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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12
Q

What is bundle branch block (BBB)?

A
  • 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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13
Q

What is second-degree block — Mobitz Type II?

A
  • PR interval consistent but every Nth cycle ventricular depolarization is missing
  • May progress to complete heart block
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14
Q

What is third degree (complete) block?

A
  • 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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15
Q

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

A
  • 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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16
Q

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

A

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.

17
Q

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

A
  • 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.
18
Q

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

A
  • 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.
19
Q

What is atrial flutter I?

A
  • 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]
20
Q

What is atrial flutter II?

A
  • 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
21
Q

What is atrial fibrillation I?

A
  • 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
22
Q

What is atrial fibrillation II?

A
  • 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
23
Q

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

A
  • 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
24
Q

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

A
  • 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]
25
Q

What is congenital long-QT syndromes?

A
  • 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
26
Q

Why can the heart block at extremely fast rates?

A
  • 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

LF266: Blood and Circulation (12 decks)

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