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CARDIOLOGY > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

How are arrhythmias classified by their anatomical site of origin?

A

Supraventricular
- Origin = above ventricle
=> SA Node, atrial muscle, AV Node, Bundle of HIS

Ventricular

  • muscle (common)
  • fascicles of the conducting system (uncommon)
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2
Q

What arrhythmias are considered supraventricular tachycardias?

A

Atrial Fibrillation
Atrial Flutter
Ectopic atrial tachycardia

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3
Q

What arrhythmias cause a bradycardia?

A

Sinus bradycardia

Sinus pauses

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4
Q

What arrhythmias originate in the ventricles?

A
  • Ventricular ectopics
  • Ventricular Tachycardia (VT)
  • Ventricular Fibrillation (VF)
  • Asystole
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5
Q

What arrhythmias originate in the AV Node?

A
  • AVN re-entry tachycardia (AVNRT)
  • AV reciprocating or AV Re-entrant tachycardia (AVRT)
  • AV block 1st/2nd/3rd degree
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6
Q

What clinical conditions can cause arrhythmias to occur?

A
  • Abnormal anatomy (e.g. LVH/ Congenital)
  • Autonomic nervous system (symp/parasymp stimulation)
  • Metabolic (hypoxia, electrolyte imbalances e.g. K+, Ca2+, Mg2+)
  • Inflammation (viral myocarditis)
  • Drugs
  • Genetic (ion channel mutations e.g. long QT syndrome)
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7
Q

What electrophysiological mechanisms can start arrhythmias?

A

Ectopic Beats

  • beats not originating in SA Node
  • Usually from Altered Automaticity

Re-entry

  • > 1 conduction pathway
  • different speeds of conduction
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8
Q

Describe what is meant by altered automaticity

A

Ischaemic heart muscle doesn’t conduct well
=> places other than SA Node will depolarise and generate ectopic when they are not meant to

  • Can also be caused by Triggered activity
  • Afterdepolarizations reaching threshold to generate another AP
  • This can happen with digoxin OR long QT syndrome
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9
Q

What conditions can cause a re-entry circuit to be set up?

A

Structural:

  • Accessory pathway tachycardia (Wolf Parkinson White syndrome)
  • Scar from previous MI
  • Congenital heart disease

Functional:
- Conditions that slow conduction velocity
OR shorten refractory period promote functional block
=> e.g. ischaemia, drugs

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10
Q

How do ectopic beats and re-entry circuits cause a tachycardia?

A

Ectopics:

  • May cause single beats or sustained run of beats
  • If this is faster than sinus rhythm, can take over intrinsic rhythm

Re-entry
- triggered by an ectopic beat
=> self perpetuating circuit is set up

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11
Q

What are the 4 phases of a cardiac myocyte action potential (AP)?

A

Phase 0 = Depolarization, Na+ enters cell
Phase 1 = Transient Ca2+ channels open
Phase 2 = Long acting Ca+ channels open and Ca2+ enters cell. (CONTRACTION)
Phase 3 = Repolarization, K+ channels open and K+ leaves cell
Phase 4 = returns to resting membrane potential

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12
Q

Which phase of the cardiac myocyte AP is changed by abnormal physiology or pathology to cause an arrhythmia?

A

Phase 4

- change in slope gradient

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13
Q

How is phase 4 of the cardiac myocyte AP changed by abnormal physiology or pathology to cause a TACHYarrhythmia?

A

Increases phase 4 slope gradient

=> increase in HR and ectopics

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14
Q

What conditions can cause an increase in the Phase 4 slope gradient, resulting in a tachyarrhythmia?

A 
Hyperthermia
Hypoxia
Hypercapnia
Cardiac dilation
HYPOkalaemia
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15
Q

How is phase 4 of the cardiac myocyte AP changed by abnormal physiology or pathology to cause a bradycardia or Heart Block?

A

Decreases phase 4 slope gradient

=> slowed conduction (bradycardia, heart block)

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16
Q

What conditions can cause a decrease in the Phase 4 slope gradient, resulting in a bradycardia or heart block?

A

Hypothermia

HYPERkalaemia

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17
Q

What is meant by triggered activity? How does it occur?

A

In Phase 3 of the AP a small depolarization may occur
=> afterdepolarization

  • If sufficient magnitude may reach threshold and lead to a sustained train of depolarizations
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18
Q

What can cause trigger activity in patients?

A
  • digoxin toxicity

- Long QT syndrome (changes to Torsades de Pointes) - HYPOkalaemia

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19
Q

What symptoms of an arrhythmia can a patient present with?

A
  • Palpitations, ”pounding heart”
  • SOB
  • Dizziness
  • Loss of consciousness (syncope)
  • Faintness “presyncope”
  • Sudden cardiac death
  • Angina, heart failure
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20
Q

What investigations can be used to try and diagnose an arrhythmia?

A
  • ECG
  • CXR
  • Echocardiogram
  • Stress ECG
  • 24 hour ECG Holter monitoring
  • Electrophysiological (EP) study (Induce arrhythmia to study mechanism)
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21
Q

How is pre-excitation found on an ECG?

A
  • delta wave shows accessory pathway is excited before SA node is firing again
  • PR interval is short and QRS is elongated by delta wave
  • ST seg. and T wave changes also present (inversion)
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22
Q

Why is an ECHO sometimes used in assessment of an arrhythmia?

A
  • To assess for structural heart disease

=> enlarged atria in AF
=> LV dilatation
=> Previous MI scar
=> Aneurysm

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23
Q

During an electrophysiological study there is also the option to treat the arrhythmia. TRUE/FALSE?

A

TRUE

- Can deliver radiofrequency ablation to extra pathway

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24
Q

Sinus Bradycardia is a heart rate below what?

A

<60 bpm

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25
Q

What can cause a sinus bradycardia?

A
  • Physiological i.e. athlete
  • Drugs (B-Blocker)
  • Ischaemia : common in inferior STEMIs
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26
Q

What treatment is used to treat sinus bradycardia?

A
  • Atropine (if acute, e.g. acute MI)
  • Pacing if haemodynamic compromise
    e. g. hypotension, heart failure, angina, collapse
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27
Q

A sinus tachycardia is a heart rate over what?

A

> 100 beats/min

28
Q

What can cause a sinus tachycardia?

A

Physiological

  • Anxiety
  • Fever
  • Hypotension
  • Anaemia)

Not physiological
- drugs

29
Q

How are sinus tachycardias treated?

A
  • Treat underlying cause

- Beta Blockers

30
Q

What symptoms do patients experience if they get atrial ectopic beats?

A
  • Patient may be asymptomatic

- Palpitations

31
Q

How are atrial ectopic beats treated?

A
  • Generally no treatment
  • Beta blockers may help
  • Avoid stimulants (caffeine, cigarettes
32
Q

What is the most common rhythm disturbance in paeds?

A

Regular Supraventricular Tachycardia

33
Q

How is a regular Supraventricular Tachycardia treated?

A

ACUTE
- Valsalva Manoeuvres, Carotid Massage
- Slow conduction in AVN
IV Adenosine or IV Verapamil

CHRONIC

  • Avoid stimulants
  • Electrophysiologic study and Radiofrequency ablation (1st Line in young, symptomatic patients)
  • Beta blockers
  • Anti-arrhythmic drugs
34
Q

What is radiofrequency catheter ablation?

A
  • Cautery of selective cardiac tissue to prevent tachycardia
  • targets the re-entry circuit
  • catheter is inserted and fed into heart from femoral vein
35
Q

What conditions can cause problems with conduction in the AV Node (i.e. heart block)?

A
  • Ageing
  • Acute MI
  • Myocarditis
  • Cancer
  • Amyloid
  • Drugs (beta-blockers, Ca2+ channel blockers
  • Calcific aortic valve disease
  • Post-aortic valve surgery
  • Genetic
36
Q

What happens in 1st degree AV Block?

A
  • PR interval longer than normal
  • No specific treatment for this
  • make sure to rule out other pathology
37
Q

What happens in 2nd Degree AV Block?

A

2 types
Mobitz I:
- lengthening of PR interval
- eventually resulting in a dropped beat

Mobitz II:

  • Pathological
  • May progress to complete heart block (3rd degree)
  • Usually 2:1, or 3:1
38
Q

How is Mobitz Type II treated?

A

Patient needs a permanent pacemaker

39
Q

What happens in 3rd Degree Heart Block?

A

No APs from the SA node/atria get through the AV node

40
Q

What are the different types of pacemaker?

A
  • Single chamber (paces RA or RV only)
  • Dual chamber (paces the RA and RV)
    => Maintains A-V synchrony
41
Q

What can cause ventricular ectopic beats?

A

Structural causes:

  • LVH
  • heart failure
  • myocarditis

Metabolic:

  • Ischaemic heart disease
  • electrolytes

May also be marker for inherited cardiac conditions

42
Q

How can ventricular ectopics be treated?

A

Beta-blockers

Ablation of focus

43
Q

What patients usually get a ventricular tachycardia?

A

Most patients have significant heart disease

  • Coronary artery disease
  • previous MI

Rare causes:

  • Cardiomyopathy
  • Inherited/ Familial arrhythmia syndromes
    e. g. Long QT, Brugada syndrome
44
Q

Ventricular tachycardia can cause haemodynamic compromise. TRUE/FALSE?

A

TRUE

- can cause large sustained reduction in arterial pressure

45
Q

What ECG characteristics help define VT?

A
  • QRS complexes = rapid, wide, distorted
  • T waves = large with deflections opposite QRS complexes.
  • Ventricular rhythm = usually regular.
  • P waves = usually not visible.
  • PR interval NOT measurable.
46
Q

What is the difference between Monomorphic and Polymorphic VT?

A

Monomorphic - all complexes look same on ECG

Polymorphic - all complexes look different to one another

47
Q

What is Ventricular Fibrillation?

A
  • Chaotic ventricular electrical activity

=> causes heart to lose ability to function as a pump.

48
Q

How can VF be treated?

A

Defibrillation

Cardiopulmonary resuscitation

49
Q

How can VT be treated acutely?

A

ACUTE

  • Direct current cardioversion if unstable.
  • If stable: pharmacologic cardioversion with anti-arrhythmic drugs

Correct triggers; Look for causes

  • Electrolytes
  • Ischaemia
  • Hypoxia
  • Pro-arrhythmic medications (eg drugs that prolong the QT interval eg. sotalol)
50
Q

If you are unsure if an arrhythmia is VT or something else, what drug can you give to check?

A

Adenosine

- this can help to make a diagnosis

51
Q

How can Long term VT be treated?

A
  • Correct ischemia (revascularisation)
  • Optimise heart failure Tx
  • Implantable cardiovertor defbrillators (ICD) if life threatening.
  • VT catheter ablation.
52
Q

What can dual chamber ICDs detect and help to treat?

A
  • bradyarrhythmias
  • VT
  • VF
53
Q

A wide QRS tachycardia with history of Coronary Artery Disease/ Heart Failure, is considered VT until proven otherwise. TRUE/FALSE?

54
Q

Anti-arrhythmic drugs are ineffective on survival. TRUE/FALSE?

A

TRUE

they are often used together with ICDs to reduce symptoms

55
Q

What is AF?

A
  • Chaotic and disorganized atrial activity
  • Irregular heartbeat
  • Most common sustained arrhythmia
56
Q

What are the 3 classifications of AF depending on when it occurs?

A

Paroxysmal

  • paroxysmal (@night) and lasts <48hrs
  • recurrent

Persistent

  • episode of AF lasting >48 hours
  • can still be cardioverted to sinus rhythm
  • unlikely to spontaneously revert

Permanent (chronic)
- Inability of pharmacologic or non-pharmacologic methods to restore sinus rhythm

57
Q

AF can be asymptomatic. TRUE/FALSE?

A

TRUE

- Can be symptomatic or asymptomatic

58
Q

The Incidence of AF increases with age. TRUE/FALSE?

59
Q

Describe the mechanism of the AF rhythm starting

A

Ectopic foci in muscle sleeves of the pulmonary veins

60
Q

How is the AF rhythm terminated in a patient?

A
  • Pharmacologic cardioversion (anti-arrhythmic drugs)
  • Electrical Cardioversion => direct current (DCCV)
  • Spontaneous reversion to sinus rhythm
61
Q

What is lone or “idiopathic” AF?

A
  • AF in the absence of heart disease
  • no evidence of ventricular dysfunction
  • Could be genetic
62
Q

What symptoms can patients experience with AF and when are these symptoms worst?

A
  • Palpitations
  • Pre-syncope (dizziness)
  • Syncope
  • Chest pain
  • Dyspnoea
  • Sweatiness
  • Fatigue

symptoms usually worst at onset of AF

63
Q

What signs of AF can be seen on an ECG?

A
  • Atrial Rate: > 300 bpm
  • Rhythm: Irregularly irregular
  • Ventricular Rate: Variable
  • Absence of P waves
  • Presence of ‘f’ waves
64
Q

What consequences can AF cause?

A
  • decreased filling time (reduced diastole)
    => reduced cardiac output
    => congestive heart failure

Ventricular rates < 60 bpm suggest AV conduction disease (e.g. heart block)
=> May require permanent pacing

65
Q

How is AF managed?

A

Rhythm control => Objective : Maintain Sinus Rhythm
OR
Rate control
Objective: Accept AF but control ventricular rate

Anti-coagulation for both approaches if high risk for thromboembolism

CARDIOLOGY (14 decks)

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