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CARDIOLOGY > Arrhythmias > Flashcards

Arrhythmias Flashcards

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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
What can cause a sinus bradycardia?
- Physiological i.e. athlete - Drugs (B-Blocker) - Ischaemia : common in inferior STEMIs
26
What treatment is used to treat sinus bradycardia?
- Atropine (if acute, e.g. acute MI) - Pacing if haemodynamic compromise e. g. hypotension, heart failure, angina, collapse
27
A sinus tachycardia is a heart rate over what?
> 100 beats/min
28
What can cause a sinus tachycardia?
Physiological - Anxiety - Fever - Hypotension - Anaemia) Not physiological - drugs
29
How are sinus tachycardias treated?
- Treat underlying cause | - Beta Blockers
30
What symptoms do patients experience if they get atrial ectopic beats?
- Patient may be asymptomatic | - Palpitations
31
How are atrial ectopic beats treated?
- Generally no treatment - Beta blockers may help - Avoid stimulants (caffeine, cigarettes
32
What is the most common rhythm disturbance in paeds?
Regular Supraventricular Tachycardia
33
How is a regular Supraventricular Tachycardia treated?
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
What is radiofrequency catheter ablation?
- Cautery of selective cardiac tissue to prevent tachycardia - targets the re-entry circuit - catheter is inserted and fed into heart from femoral vein
35
What conditions can cause problems with conduction in the AV Node (i.e. heart block)?
- Ageing - Acute MI - Myocarditis - Cancer - Amyloid - Drugs (beta-blockers, Ca2+ channel blockers - Calcific aortic valve disease - Post-aortic valve surgery - Genetic
36
What happens in 1st degree AV Block?
- PR interval longer than normal - No specific treatment for this - make sure to rule out other pathology
37
What happens in 2nd Degree AV Block?
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
How is Mobitz Type II treated?
Patient needs a permanent pacemaker
39
What happens in 3rd Degree Heart Block?
No APs from the SA node/atria get through the AV node
40
What are the different types of pacemaker?
- Single chamber (paces RA or RV only) - Dual chamber (paces the RA and RV) => Maintains A-V synchrony
41
What can cause ventricular ectopic beats?
Structural causes: - LVH - heart failure - myocarditis Metabolic: - Ischaemic heart disease - electrolytes **May also be marker for inherited cardiac conditions**
42
How can ventricular ectopics be treated?
Beta-blockers | Ablation of focus
43
What patients usually get a ventricular tachycardia?
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
Ventricular tachycardia can cause haemodynamic compromise. TRUE/FALSE?
TRUE | - can cause large sustained reduction in arterial pressure
45
What ECG characteristics help define VT?
- 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
What is the difference between Monomorphic and Polymorphic VT?
Monomorphic - all complexes look same on ECG | Polymorphic - all complexes look different to one another
47
What is Ventricular Fibrillation?
- Chaotic ventricular electrical activity | => causes heart to lose ability to function as a pump.
48
How can VF be treated?
Defibrillation | Cardiopulmonary resuscitation
49
How can VT be treated acutely?
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
If you are unsure if an arrhythmia is VT or something else, what drug can you give to check?
Adenosine | - this can help to make a diagnosis
51
How can Long term VT be treated?
- Correct ischemia (revascularisation) - Optimise heart failure Tx - Implantable cardiovertor defbrillators (ICD) if life threatening. - VT catheter ablation.
52
What can dual chamber ICDs detect and help to treat?
- bradyarrhythmias - VT - VF
53
A wide QRS tachycardia with history of Coronary Artery Disease/ Heart Failure, is considered VT until proven otherwise. TRUE/FALSE?
TRUE
54
Anti-arrhythmic drugs are ineffective on survival. TRUE/FALSE?
TRUE | they are often used together with ICDs to reduce symptoms
55
What is AF?
- Chaotic and disorganized atrial activity - Irregular heartbeat - Most common sustained arrhythmia
56
What are the 3 classifications of AF depending on when it occurs?
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
AF can be asymptomatic. TRUE/FALSE?
TRUE | - Can be symptomatic or asymptomatic
58
The Incidence of AF increases with age. TRUE/FALSE?
TRUE
59
Describe the mechanism of the AF rhythm starting
Ectopic foci in muscle sleeves of the pulmonary veins
60
How is the AF rhythm terminated in a patient?
- Pharmacologic cardioversion (anti-arrhythmic drugs) - Electrical Cardioversion => direct current (DCCV) - Spontaneous reversion to sinus rhythm
61
What is lone or "idiopathic" AF?
- AF in the absence of heart disease - no evidence of ventricular dysfunction - Could be genetic
62
What symptoms can patients experience with AF and when are these symptoms worst?
- Palpitations - Pre-syncope (dizziness) - Syncope - Chest pain - Dyspnoea - Sweatiness - Fatigue **symptoms usually worst at onset of AF**
63
What signs of AF can be seen on an ECG?
- Atrial Rate: > 300 bpm - Rhythm: Irregularly irregular - Ventricular Rate: Variable - Absence of P waves - Presence of ‘f’ waves
64
What consequences can AF cause?
- 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
How is AF managed?
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

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