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Clinical > Cardiac Arrhythmias > Flashcards

Cardiac Arrhythmias Flashcards

1
Q

How are arrhythmias named?

A

Generally named for anatomical site or chamber of origin

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2
Q

Types of arrhythmias?

A

Supraventricular - origin is above the ventricle, i.e: from the SA node, atrial muscle, AV node or of HIS origin. This is a non-specific-term and specifics are required

Ventricular - origin in the ventricle

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3
Q

Electrical separation and connections between chambers?

A

Fibrous ring is electrically inert and electrically separates the chambers

AV node is the only physiological electrical connection between atria and ventricles

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4
Q

What are ectopic beats/rhythms?

A

Beats/rhythms that originate in places other than the SA node

Ectopic focus may cause single beats or take over and pace the heart, dictating its entire rhythm - ectopic rhythms compete with normal sinus rhythm

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5
Q

When are ectopic beats/rhythms dangerous?

A

May or may not be dangerous depending on how they affect the CO

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6
Q

Types of supraventricular arrhythmias?

A

Supraventricular tachycardia:
Atrial Fibrillation
Atrial Flutter
Ectopic atrial tachycardia (area in atria fires indiscriminately)

Supraventricular bradycardia:
Sinus bradycardia (there can be issues with rhythm initiation and also block can occur somewhere)
Sinus pauses

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7
Q

Pathological reasons for AV node arrhythmias?

A

AV node re-entry

Accessory pathway, e.g: Wolff Parkinson White syndrome (WPW) is due to Bundle of Kent

AV block:
1st degree
2nd degree
3rd degree

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8
Q

Types of ventricular arrhythmias?

A

Premature Ventricular Complex (PVC) - initiated by purkinje fibres; ventricles contract first and before the atria have optimally filled the ventricles with blood (causes a transient decrease in BP)

Ventricular Tachcardia

Ventricular fibrillation

Asystole

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9
Q

Number of fascicles in the bundle of His?

A

3 fascicles:
Left bundle has 2 - anterior and posterior fascicles
Right bundle has 1

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10
Q

Clinical causes of arrhythmias?

A

Abnormal anatomy:
Left ventricular hypertrophy
Accessory pathways
Congenital heart disease

Autonomic:
Sympathetic stimulation - nervousness, exercise, CHF, hyperthyroidism
Increased vagal tone, causing bradycardia and potentially heart block

Metabolic:
Hypoxic myocardium, e.g: in COPD, PE (reduce threshold for arrhythmias)
Ischaemic myocardium, e.g: in acute MI and angina
Electrolyte imbalances, e.g: of K+, Ca2+ and Mg2+

Inflammation - viral myocarditis

Drugs, part. those that prolong the QT interval

Genetic - mutations of cardiac ion channels, e.g: the congenital long QT syndrome

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11
Q

Physiological mechanisms by which tachycardias result?

A

Altered automaticity, e.g: due to ischaemia and catecholamines

Triggered activity, e.g: digoxin use

Re-entry, e.g: accessory pathway tachycardia (WPW syndrome), previous MI

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12
Q

Symptoms of arrhythmias?

A 
Palpitations
SoB
Dizziness
Syncope
Sudden cardiac death
Worsen a pre-existing condition, e.g: angina and CHF; angina can worsen if HR increases and increases cardiac work
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13
Q

Investigations used in arrhythmia diagnosis?

A

12-lead ECG
CXR
Echocardiogram

Stress ECG to search for myocardial ischaemia and exercise-related arrhythmias

24 hour ECG holter monitoring
Event recorder
Electrophysiological study - induce arrhythmia to study it and map the pathway

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14
Q

Why is ECG used in arrhythmia investigation?

A

To assess rhythm

Signs of previous MI, e.g: pathological Q waves, pre-excitation (via accessory pathway in WPW)

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15
Q

Why is a 24 hour holter ECG used in arrhythmia investigation?

A

To assess for PAROXYSMAL arrhythmia; also, patient can press a button when they feel symptoms and these can then be linked to the underlying heart rhythm

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16
Q

Why is an echo used in arrhythmia investigation?

A

Assess for structural heart disease, e.g:
Enlarged atria in AF
Left ventricle dilatation
Previous MI scar, aneurysm- disposes to arrhythmias

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17
Q

What is the treatment and advice for ATRIAL ECTOPIC BEATS?

A

Can be asymptomatic or cause palpitations; generally, if asymptomatic, no treatment is given

β-blockers may help, by slowing down HR (target HR in for somebody on this drug is

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18
Q

What is sinus bradycardia?

A

HR of

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19
Q

Non-physiological causes of sinus bradycardia?

A

Drugs like β-blockers

Ischaemia - common in inferior STEMIs

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20
Q

Treatment for sinus bradycardia?

A

If acute, atropine, e.g: in an aMI

Pacing can be used if there is haemodynamic compromise, e.g: in hypotension, CHF, angina, collapse

21
Q

What is sinus tachycardia?

A

HR of >100 bpm and this can be physiological in anxiety, fever, hypotension, anaemia, hypoxia

22
Q

When is sinus tachycardia inappropriate?

A

Drugs and stimulants

Syndrome Inappropriate Tachycardia - most common in young females; heart rate is reset

23
Q

Acute management of supra-ventricular tachycardia?

A

Acute management:
Vagal manoeuvres and carotid massage (never do this in elderly people with cerebro-vascular disease) increase vagal tone

IV adenosine (drug of choice - slows AV node conduction)

IV verapamil (rate-limiting CCB - slows down AV node conduction)

24
Q

Chronic management of supra-ventricular tachycardia?

A

Avoid stimulants

Radiofrequency ablation is preffered

Anti-arrhythmic drugs (class II or IV)

25
Q

What is ablation?

A

Selective CAUTERY (burning) of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit

26
Q

Radiofrequency ablation procedure?

A

Catheters placed in heart via femoral veins; catheter is placed over focus/pathway and the tip is heated

An intracardiac ECG is recorded during sinus rhythm, tachycardia and during pacing manoeuvres

27
Q

Causes of AV node conduction disease?

A 
Ageing process
Acute MI
Myocarditis
Infiltrative disease, e.g: amyloid
Drugs, e.g: β-blockers, CCB

Calcific aortic valve disease - close to AV node and so it can be involved

Post-aortic valve surgery

Genetic: Lenegre’s disease, myotonic dystrophy

28
Q

What is 1st degree AV block?

A

Not really a block; PR INTERVAL IS PROLONGED (> 2 secs)

29
Q

Treatment for 1st degree AV block?

A

Treatment: none

Long-term follow up recommended, as more advanced block may develop over time

30
Q

What is 2nd degree AV block?

A

Intermittent block at the AV node, so sometimes there are dropped beats

31
Q

Types of 2nd degree AV block?

A

Mobitz type I - progressive lengthening of PR interval that eventually results in a dropped beat; usually vagal in origin

Mobitz type II - pathological and can progress to complete heart block

32
Q

Naming of Mobitz type II heart block?

A

Usually 2:1 or 3:1 but can be variable, e.g: if 3 APs are produced but only one gets through (3:1)

33
Q

Treatment of Mobitz type II heart block?

A

Permanent pacemaker is indicated

34
Q

What is 3rd degree AV block?

A

Complete heart block - no APs from the SA node/atria get through the AV node

Requires ventricular pacing

35
Q

Types of pacemakers and when they are used?

A

Single chamber (paces right atrium OR right ventricle only):
Atrial pacemakers - used in isolated SA node disease when the AV node is normal
Ventricular pacemakers - used in AF with a slow ventricular rate

Dual chamber (paces the right atrium AND right ventricle):
Maintains AV synchrony to preserve atrial kick
Used for AV node disease
36
Q

Brief rule about pacemaker entry into heart?

A

Go into RIGHT SIDE of heart, not the left side (arterial risk of bleeding and thrombosis)

37
Q

How do pacemakers affect the CO?

A

Cause contraction from bottom to top of heart (normally, contraction goes from top to bottom); this can decrease CO

38
Q

What is and caution with broad complex tachycardia?

A

Wide QRS complex and patient is tachycardic

Assume that all broad complex tachycardia are VENTRICULAR, UNTIL PROVEN OTHERWISE - in VT, there is a large, sustained reduction in arterial pressure

39
Q

Outcome of Ventricular Tachycardia?

A

Life-threatening but may be haemodynamically stable

40
Q

Causes of VT?

A

Most patients have significant heart disease:
CAD
Previous MI

Rarer causes:
Cardiomyopathy
Inherited/familial arrhythmia syndrome, e.g: Long QT

41
Q

Differentiating stable and unstable VT?

A

No chest pain, hypotension, CHF, altered conscious level

42
Q

ECG characteristics of VT?

A

QRS complexes are rapid, wide and distorted

T waves are large with deflections opposite the QRS complexes

Ventricular rhythm is usually regular

P waves are not usually visible

PR interval is not measurable

AV dissociation may be present

VA conduction may or may not be present

43
Q

Types of VT?

A

Monomorphic VT - same pattern and QRS distance; look for ischaemia/scarring

Polymorphic VT - different QRS complexes, e.g: Torsades de pointe causes of which include hypokalaemia, hypomagnesaemia

44
Q

Treatment of acute VT?

A

If unstable - DC cardioversion (converts to normal rhythm)

If stable - consider pharmacologic cardioversion with anti-arrhythmic drugs

If unsure if this is VT or something else, use adenosine to differentiate

Correct triggers

45
Q

What is ventricular fibrillation?

A

Chaotic, ventricular electrical activity causing the heart to lose ability to function as a pump - LIFE THREATENING

46
Q

Treatment of ventricular fibrillation?

A

Defibrillation (only “treatment”)

CPR

47
Q

Management of VT?

A

Look for causes, e.g: electrolytes, ischaemia, hypoxia, medications (prolong QT interval, e.g: sotalol, arythromycin, quinidine)

If it does not respond to Mg, it is not torsades

Implantable Cardiovertor Defibrillators (ICD) if life-threatening - pacemaker + defibrillator

Optimise CHF therapies

48
Q

Functions of ICDs in atrium and ventricle?

A 
Ventricle:
VT prevention
Anti-tachycardia pacing
Cardioversion
Defibrillation

Atrium and ventricle:
Bradycardia sensing
Bradycardia pacing

Clinical (54 decks)

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