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Cardiovascular (Annie) > Arrhythmias 1 - Cardiac arrhythmias > Flashcards

Arrhythmias 1 - Cardiac arrhythmias Flashcards

1
Q

how are arrhythmias named?

A

1) anatomical site or chamber of origin

2) mechanism

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2
Q

what are the 2 sites of origin?

A

1) supre-ventricular (SVT)

2) ventricular

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3
Q

where does supra-ventricular refer to?

Where does ventricular origins refer to?

A

SVT
non-specific term.
= origin is ABOVETHE VENTRICLE i.e. SAN, atrial muscle, AV node or HIS origin

Ventricular
= ventricular muscle (common)
= fascicles of conducting system (uncommon)

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4
Q

what are the 2 types of supra-ventricular arrhythmias?

A

1) supra-ventricular tachycardia
- AF
- atrial flutter
- ectopic atrial tachycardia

2) bradycardia
- sinus bradycardia
- sinus pauses

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5
Q

what are types of ventricular arrhythmias?

A

1) ventricular ectopics or premature ventricular complexes
2) ventricular tachycardia
3) ventricular fibrillation
4) asystole

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6
Q

what 3 things happen in the AV node as a atrio-ventricular node arrhthymias?

A

1) AVN re-entry tachycardia
2) AV reciprocating or AV reentrant tachycardia

3) AV block
- 1st, 2nd, 3rd degree

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7
Q

what are the 6 causes arrhythmias?

A

1) abnormal anatom
2) autonomic nervous system (ANS)
3) metabolic
4) inflammation
5) drugs
6) genetic

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8
Q

what are the 3 abnormal anatomy causes of arrhythmias?

A
  • left ventricular hypertrophy
  • accessory pathways
  • congenital HD
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9
Q

what are the 2 autonomic nervous system changes that cause arrhythmias?

A

1) sympathetic stimulation: stress, exercise, hyperthyroidism
2) increased vagal tone causing bradycardia

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10
Q

what 3 metabolic changes cause arrhythmias?

A

1) hypoxia - chronic pulmonary disease, PE
2) ischaemic myocardium - acute MI, angina
3) electrolyte imbalances; K+, Ca2+, Mg2+

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11
Q

what inflammation can cause arrhythmias?

A

= viral myocarditis

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12
Q

what drugs can cause arrhythmia?

A

= direct electrop-hysiological effects of via ANS

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13
Q

what genetic changes can cause arrhythmias?

A

= mutations of genes encoding cardiac ion channels, e.g. congenital long QT syndrome

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14
Q

what are 2 electro-physiological mechanisms of arrhythmias?

A

1) ectopic beats

2) re-entry

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15
Q

what is ectopic beats?

A

= beats or rhythms that originate in places other than SA node

  • altered automaticity, e.g. iscahemia, catecholamines
  • triggered activity, e.g. digoxin, long QT syndrome
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16
Q

what is re-entry?

A

= requires more than. one conducting pathway with different speed of conduction (depolarisation) & recovery of excitability (refractoriness)

  • accessory pathway tachycardia
  • previous MI
  • congenital heart disease
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17
Q

what is the mechanism of tachycardia?

A
  • ectopic may cause single beats or a sustained run of beats, that if faster than sinus rhythm, take over the intrinsic rhythm.
  • Re-entry: triggered by an ectopic beat, resulting in a self perpetuating circuit.
  • Tachycardia may or may not be dangerous depending on how they affect the cardiac output.
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18
Q

what 2 changes to the action potential causes arrhythmia’s?

A

1) increases Phase 4 slope causing increase in heart rate, ectopics
2) decreases phase 4 causing slowed conduction (bradycardia, heart block)

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19
Q

what does an increased phase 4 cause?

A

1) hyperthermia
2) hypoxia
3) hypercapnia
4) cardiac dilation
5) hypokalaemia, prolonging depolarisation

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20
Q

what does a decreased phase 4 cause?

A

1) hypothermia

2) hyperkalaemia

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21
Q

when does triggered activity occur?

A

= in terminal phase of AP (phase 3), a small depolarisation may occur (called an after-depolarisation), and if sufficient magnitude may reach depolarisation threshold & lead to a sustained train of depolarisations

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22
Q

what does triggered activity underly?

A
  • digoxin toxicity
  • torsades de pointes in long QT syndrome
  • hypokalaemia
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23
Q

what does re-entry require?

A

= more than one conduction pathway, with different speeds of condition (depolarisation) & recovery of excitability (refractoriness)

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24
Q

re-entry

A

1) structural abnormalities
- accessory pathways
- scar from MI
- congenital heart disease

2) functional
- conditions that depress conduction velocity or shorten refractory period promote functional block

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25
Q

what are 7 symptoms of arrhythmias?

A

1) palpitations, pounding heart
2) shortness of breath
3) dizziness
4) loss of consciousness, syncope
5) faintness, pre-syncope
6) sudden cardiac death
7) angina, heart failure

26
Q

what investigations can be done to investigate arrhythmias?

A

1) 12 lead ECG
2) Chest X-ray
3) echocardiogram
4) stress ECG
5) 24 hour ECG holter monitoring

6) event recorder
= capture the arrythmia

7) electro-physiological (EP( study

27
Q

what are you looking for in the a normal ECG and stress ECG?

A

Normal ECG

1) rhythm
2) previous MI (q wave)
3) pre-excitation (wolf Parkinson white syndrome)

Stress ECG

1) myocardial ischaemia
2) exercise induced arrhythmia

28
Q

what does a 24hour holder CG assess for?

A

1) paroxysmal arrhythmias

2) linking symptoms to underlying heart rhythm

29
Q

what does an echocardiograph assess?

what does an electro-physiological study do?

A

1) assess for structural heart disease
e.g.
= enlarged atria in AF
= LV dilation
= previous MI scar
= aneurysm

triggers clinical arrhythmias so you can study its mechanism and pathway

30
Q

what is normal sinus arrhythmia?

A

IT IS NORMAL/healthy
= where there are VARIATIONS IN HEART RATE due to reflex changes in vagal tone during resp cycle

  • inspiration reduces vagal tone, increasing heart rate
31
Q

what is sinus bradycardia?

who often gets sinus bradycardia?

what can cause your heart rate to be low and get sinus rhythm?

A

= slower heart rate < 60BPM

Who gets it
= athletes

Causes
= drugs, beta blockers
= ischaemia: common in inferior STEMIs

32
Q

how would you treat sinus bradycardia?

A

1) atropine (if acute, e.g. MI)

2) pacing if haemodynamic compromise: hypotension, CHF, angina, collapse.

33
Q

what is sinus tachycardia?

who often gets sinus tachycardia?

What can cause it?

A

= faster heart rate > 100BPM

Who gets it; 
= anxiety
= fever
= hypotension 
= anaemia

Causes
= inappropriate use of drugs

34
Q

how would you treat sinus tachycardia?

A

1) treat underlying cause

2) B-adrenergic blockers

35
Q

what are symptoms of atrial ectopic beats?

A

1) asymptomatic

2) palpitations

36
Q

how would you treat it?

A
  • generally no treatment

= B-adrenergic blockers may help
= avoid stimulants (caffeine, cigarettes)

37
Q

what can regular supra-ventricular tachycardia be due to?

A

1) AV nodal re-entrant tachycardia (AVNRT)
2) AV reciprocating tachycardia/AV re-entrant tachycardia (via an accessory pathway) (AVRT)
3) ectopic atrial tachycardia (EAT)

38
Q

how would you acutely manage supra-ventricular tachycardia?

A

ACUTELY manage;
1) increases vagal tone
= valsalva
= carotid massage

2) slow conduction in AVN
- IV adenosine
- IV verapamil

39
Q

how would you chronically manage supra-ventricular tachycardia?

A

CHRONIC management;

1) avoid stimulants
2) electro-physiologic study & radiogrequency ablation
3) beta blockers
4) anti-arrhythmic drugs

40
Q

what is radio-frequency catheter ablation?

A

= selective cautery of cardiac tissue to prevent tachycardia, targeting either an autonomic focus or part of re-entry circuit

41
Q

what does radio-frequency catheter ablation involve?

A
  • ECG catheters placed in heart via femoral veins
  • intra-cardiac ECG reordered during sinus rhythm, tachycardia and during pacing manoeuvres to find location & mechanism of tachycardia
  • catheter placed over focus/pathway & tip heated to high
42
Q

what are the causes of AVN conduction disease (heart block?)

A

1) Ageing process
2) Acute MI
3) Myocarditis
4) Infiltrative disease
= Amyloid
5) Drugs
= B-adrenergic blockers
= Calcium channel blockers
6) Calcific aortic valve disease
7) Post-aortic valve surgery
8) Genetic
= Lenegre’s disease, myotonic dystrophy

43
Q

what would you find on an ECG in a 1st degree AV heart block?

A
  • not really block, conduction following each P wave takes longer
  • PR interval longer than normal
44
Q

how would you treat 1st degree AV block?

A

= NONE

  • rule out other pathology
  • long term follow up
45
Q

what is 2nd degree AV block?

A

= intermittent block at AVN (dropped beats).

- each beat gets longer until you drop a beat, then it goes normal again (a cycle)

46
Q

what are the 2 types of 2nd degree AV block and what do they each mean?

A

1) mobitz I
= progressive lengthening of the PR interval, eventually resulting in a dropped beat.
- Usually vagal in origin

2) mobitz II
= Pathological, may progress to complete heart block (3rd degree HB)
- Usually 2:1, or 3:1, but may be variable
- Permanent pacemaker indicated

47
Q

how do you treat 2nd degree, Mobitz II, AV block?

A

= ventricular pacing

48
Q

what is 3rd degree AV block?

A

= complete heart block

- no action potential from SA node/atria getting through AV node

49
Q

what are 2 types of pacemakers and where do they run?

A

1) single chamber
= paces the right atria or right ventricle ONLY

2) dual chamber (paces RA & RV)
= maintains AV synchrony (preserves atrial kick)
= used for AVN disease

50
Q

what are the causes of ventricular ectopics?

How do you treat ventricular ectopics?

A

1) structural causes
- LVH
- heart failure
- myocarditis

2) metabolic
- ischaemic heart dsiease
- electrolytes

  • Beta-blockers
  • ablation of focus
51
Q

what are ventricular tachycardias (VT)?

What would an ECG of ventricular tachycardia show?

A

= life threatening but may be haemo-dynamically stable

= widen QRS complex with a fast heart rate

52
Q

what do most patients with VTs have?

A

most patients have significant heart disease;

  • coronary artery disease
  • previous MI
53
Q

what is a rarer cause of Its?

A
  • cardiomyopathy
    = inherited/familial arrhythmia syndromes
    = long QTs, brigade syndrome
54
Q

in people with ventricular tachycardia with haemodynamic compromise, describe the arterial pressure?

A

= large, sustained reduction of arterial pressure

55
Q

what ECG changes characterise a monomorphic VT?

A

1) The QRS complexes are rapid, wide, and distorted.
2) The T waves are large with deflections opposite the QRS complexes.
3) The ventricular rhythm is usually regular.
4) P waves are usually not visible.
5) The PR interval is not measurable.
6) A-V dissociation may be present.
7) V-A conduction may or may not be present.

56
Q

what changes characterise a polymorphic VT?

A

1) The QRS complexes are rapid, wide, and distorted.
2) The T waves are large with deflections opposite the QRS complexes.
3) The ventricular rhythm is usually regular.
4) P waves are usually not visible.
5) The PR interval is not measurable.
6) A-V dissociation may be present.
7) V-A conduction may or may not be present.

57
Q

what is ventricular fibrillation?

how would you treat it?

What would ventricular fibrillation look like on an ECG?

A

= chaotic ventricular electrical activity causing heart to lose ability to function as a pump

Treatment;
= defibrillator
= cardio-pulmonary resuscitation

  • rate is unmeasurable
  • highly irregular rhythm
  • P wave is absent
  • PR interval is unmeasurable
  • No QRS complex
58
Q

what is VT acute treatment if unstable or stable or unsure?

A

UNSTABLE
= Direct current cardioversion (DCCV) .

STABLE
= consider pharmacologic cardioversion with AAD, in meantime prepare for DCCV.

UNSURE
= if VT or something else, consider adenosine to make a diagnosis

4) Correct triggers; Look for causes
Electrolytes
Ischaemia
Hypoxia 
Pro-arrhythmic medications (eg drugs that prolong the QT interval eg., sotalol).
59
Q

what is long term treatment for VT?

A

1) Correct ischemia (revascularisation)
2) Optimise CHF therapies.
3) Anti-arrhythmic drugs
4) Implantable cardiovertor defbrillators (ICD) if life threatening.
5) VT catheter ablation.

60
Q

what is Ventricular tachycardia /ventricualr fibrillation pearls?

A

1) A wide QRS tachycardia with history of CAD/HF = VT until proven otherwise.
2) Most ventricular arrhythmias occur in the setting of structural heart disease (CHF, CAD).
3) Anti-arrhythmic drugs are ineffective on survival, but are often used together with ICDs to reduce symptoms.
4) Optimal management of the underlying condition e.g. CHF, CAD are important

5) Remember primary electrical disease
VT/VF in structurally normal hearts may be genetic
implications for family members

Cardiovascular (Annie) (36 decks)

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