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Year 3 Medicine Block > CARDIO: Arrythmias > Flashcards

CARDIO: Arrythmias Flashcards

1
Q

What is absolute bradycardia?

A

HR is <40bpm

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2
Q

What is relative bradycardia?

A

Where HR is inappropriately slow for the haemodynamic state of the patient.

Oxford clinical handbook definition of bradycardia = <60bpm

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3
Q

Signs that may indicate haemodynamic instability?

A 
Systolic BP < 90mmHg 
HR <40 
Poor perfusion 
Poor urine output 
Ventricular arrhythmias that need suppression 
Heart failure
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4
Q

How can bradycardia be classified?

A

Based on the pacemaker that is faulty:

  • sinus node e.g. sinus bradycardia
  • AV node
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5
Q

List some causes of bradycardia

A

Physiological:
- athletes

Cardiac:

  • degenerative changes/fibrosis of conduction pathways in elderly
  • post-MI (especially inferior MI (leads II, III, aVF)
  • sick sinus syndrome
  • iatrogenic —> ablation, surgery
  • aortic valve disease e.g. infective endocarditis (rheumatic fever)
  • myocarditis, cardiomyopathy, sarcoidosis, SLE

Non-cardiac origin:

  • vasovagal
  • endocrine = hypothyroidism, adrenal insufficiency
  • metabolic = hyperkalaemia, hypoxia
  • other = hypothermia, raised ICP (Cushing’s triad - bradycardia, hypertension and irregular breathing), pericarditis, haemochromatosis,

Drug induced:

  • Beta blockers
  • amiodarone
  • verapamil
  • diltiazem
  • digoxin
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6
Q

Main management for pt with symptomatic sinus node disease (e.g. a sinus bradycardia)?

A

Pacemaker is indicated

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7
Q

What are categories of sinus node dysfunction?

A

Sinus bradycardia
Sick sinus syndrome
Sinus arrest
Part of vasovagal syncope

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8
Q

How are AV node bradycardias classified?

A

According to the degree of nodal dysfunction:

  • First degree AV block
  • Second degree AV block Mobitz Type I aka Wenckebach
  • Second degree AV block Mobitz Type II
  • Complete/Third degree AV block
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9
Q

How is First degree AV block characterised?

A

PR interval >0.2s

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10
Q

Pt has bradycardia. What rate limiting drug should you check pt is on and why?

A

Digoxin. Why? Digoxin toxicity - can worsen conduction abnormalities and worsen heart block

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11
Q

How is Second degree AV block: Wenckebach/Mobitz Type I characterised?

A

Lengthening of PR interval. Followed by failure of atrial impulse to conduct to the ventricles.

i.e. QRS is dropped after progressive lengthening of PR interval.

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12
Q

Who is more likely to have Second degree AV block: Wenckebach/Mobitz Type I?

A
  • Young fit patients with a high vagal tone

- Patients after inferior MI

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13
Q

How is Second degree AV block: Mobitz Type II characterised?

A

Constant PR interval followed by sudden failure of a p wave to be conducted to the ventricles.

i.e. PR length constant, then drop of QRS. 2 p waves for every QRS

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14
Q

How is complete heart block/ Third degree AV block characterised?

A

No conduction from atria to the ventricles. No relationship between p waves and QRS complexes

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15
Q

What does complete/ third degree heart block look like on ECG?

A

Rate is slow. Broad complex QRS escape rhythm seen, with no linkage of p waves and QRS - they are both independent.
Sometimes can look intermittent - see trifascicular or bifascicular block (RBBB, with or without prolonged PR interval) and alternating LBBB and RBBB.

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16
Q

Where can complete/third degree block occur?

A

Either:

  • above AV node at the HIS region
  • beneath AV node
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17
Q

Causes of complete/third degree AV block?

A

Anti-arrhythmic drugs - especially digoxin toxicity!!
Post- inferior STEMI (will resolve in hrs-days)
Anterior MI
Severe hyperkalaemia

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18
Q

How to treat severe hyperkalaemia causing. complete/third degree AV heart block?

A
  • IV calcium gluconate/calcium chloride 30ml of 10% solution over 3-5 mins: to stabilise the myocardium
  • insulin/dextrose infusion: short-term shift in potassium from ECF to ICF
  • other treatments such as nebulised salbutamol may be given to temporarily lower the serum potassium
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19
Q

How to treat a haemodynamically unstable patient with complete/third degree AV heart block?

A

Atropine - 500micrograme to 3 mg.

Isoprenaline - at rate of 5micrograms/minute

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20
Q

Main management for complete/ third degree AV heart block?

A

Urgent permanent pacemaker. Within 24hrs unless they are likely to have a recovery of conduction (e.g post inferior STEMI)

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21
Q

Types of tachycardic arrhythmias?

A

Atrial fibrillation
Supraventricular tachycardia = in atria
Ventricular tachycardia

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22
Q

Presentation of AFib?

A 
Asymptomatic 
Breathlessness 
Palpatations
Syncope/dizziness 
Chest discomfort 
Stroke or TIA
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23
Q

Complications of AFib?

A

Cardioembolic stroke
Cardiac instability
Death

Increase in healthcare costs

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24
Q

How to diagnose A fib?

A

Presence of symptoms - palpitations, dizziness/syncope, breathlessness, chest discomfort, stroke, TIA
ECG used to confirm if an irregular pulse is due to A fib.

25
Q

What to do before treating suspected AFib just from clinical picture?

A

Do an ECG to confirm.

Why? Irregular pulse may be due to other reasons

26
Q

Pt has intermittent AFib. What is next step in investigation?

A

Short term cardiac monitoring with 24hr cardiac monitor

27
Q

Disadvantage of 24hr cardiac monitor to identify arrhythmia?

A

Symptoms need to be very frequent to diagnose an arrhythmia - this is a short time period - delivers low yield results.

28
Q

What are the different types of prolonged cardiac monitors?

A

Prolonged Holter monitor

Implantable loop recorder

29
Q

When/ In what circumstances is an echocardiogram carried out for AFib ?

A
  1. Suspected structural heart disease - from symptoms, murmer or signs of HF
  2. When considering cardioversion to control rhythm
  3. When a baseline is needed to inform long term management
30
Q

How to manage AFib?

A
  1. Anticoagulation to prevent stroke
  2. Rate control
  3. Rhythm control
31
Q

Scoring tool to assess whether pt with AFib needs anticoagulation? State and explain

A 
CHA2DS2-VASc
Congestive heart failure 
Hypertension 
Age >75 = 2, 65-74 = 1
Diabetes
Stroke or Tia = 2
Vascular disease 
Sex category (female)

Higher score = higher risk of stroke or embolism.

  • Score of 2+ = significant risk. Offer anticoagulant.
  • Score of 1 in men = intermediate risk, consider anticoagulant
  • Score of 0 = low risk, not offered anticoagulant
32
Q

Scoring tool to assess risk of major bleeding when on anticoagulation?

A

ORBIT is now used.

HAS-BLED 
Hypertension 
Abnormal renal and liver function - 1 point for each  
Stroke 
Bleeding 
Labile INRs (poor INR control while on warfarin)
Elderly (65 + )
Drugs or alcohol - 1 point each
33
Q

Anticoagulant options for AFib?

A

DOACs - apixaban, rivaroxaban, edoxaban, dabigatran

34
Q

How does the mechanism of action of dabigatran differ to other DOACs?

A

Apixaban, rivaroxaban, edoxaban = inhibit factor Xa directly so prevent conversion of prothrombin —> thrombin.

Dabigatraan = direct thrombin inhibitor so prevents conversation of fibrinogen —> fibrin

35
Q

Benefit of DOAC compared to warfarin?

A

Less monitoring (INR monitoring)
No restrictions on food or alcohol
Lower rates of bleeding to warfarin
Better reduction in stroke

36
Q

How are DOACs excreted and why is this important?

A

Via kidney. Need to monitor renal function yearly

37
Q

Other management options available for AFib, other than anticoagulants?

A

Rate control
Electrical cardioversion
Drug therapy

38
Q

Pathophysiology of supraventricular tachycardia (SVT)?

A

AV nodal re-entry tachycardia (a re-entry within the AV node)
OR
Atrio-ventricular re-entry tachycardia (an anatomical re-entry)

Both of these depend on AV nodal conduction

39
Q

First line treatment of supra ventricular tachycardia in haemodynamically stable patients?

A

Vagal manoeuvres

e. g. breath holding, valsalva manoeuvre
e. g. carotid massage (younger patients)

These slow down conduction in AV node so can interrupt re-entrant circuit

40
Q

What should you do before attempting carotid massage for treating supra ventricular tachycardia?

A

Auscultate for bruits before carotid massage manoeuvre

Why? Risk of stroke from emboli

41
Q

Short term management options for SVT if vagal manoeuvres do not help?

A

IV adenosine

CCBs

42
Q

Route of administration and dose of adenosine for SVT?

A

IV - rapid bolus Followed by saline flush immediately.
Administered via three way stopcock.
Give 6mg stat followed by 12mg if unsuccessful. Repeat 12mg if unsuccessful after first 12mg dose.
In antecubital fossa

43
Q

Describe half life of adenosine?

A

Very short half life

44
Q

Why is it important that dose of adenosine is given IV and in antecubital fossa via large bore cannula?

A

Needs to reach heart quickly to minimise cellular uptake en route - so need large bore cannula and entry to be as proximal as possible.

45
Q

ADRs of adenosine given for SVT?

A

Chest discomfort
Transient hypotension
Flushing

46
Q

Contraindication for adenosine use in SVT management?

A

Pts with significant reversible airway disease e.g asthma or COPD - as can cause bronchospasm

47
Q

Safety precautions to have in place before administering adenosine to a pt?

A

Crash trolley next to pt - as possibility of bradyarrhythmia or tachyarrhythmia

48
Q

ECG findings of SVT?

A

A narrow-complex tachycardias with a QRS interval of 100 ms or less

49
Q

When is verapamil contraindicated for SVT control?

A

Pts on B-blockers

Pts with LV dysfunction

50
Q

If adenosine and verapamil are ineffective/contraindicated for SVT, what can be done for SVT?

A

Electrical cardioversion under GA or sedation

51
Q

Second line drugs for SVT?

A

IV flecainide can be used if they don’t have PMH of MI
Sotalol
Amiodarone

52
Q

ECG findings of VT?

A

Regular broad QRS

53
Q

Management for sustained VT in haemodynamically compromised pts?

A
  • oxygen
  • IV access
  • exclude reversible factors - e.g. PA catheter in RV, hypokalaemia, hypomagnesia
  • synchronised DC shock - up to 3 attempts
  • if unsuccessful = Amiodarone 300 mg IV over 10–20 min. Repeat synchronised DC shock
54
Q

Pharmacological options for VT?

A

B-blockers
Amiodarone
Lidocaine

55
Q

Maximum dose of lidocaine that can be given in 1hr?

A

200-300mg

56
Q

Reversal agent for Apixaban?

A

Adanexanet alfa

57
Q

Reversal agent for Dabigatran?

A

Idarucizumab

58
Q

Reversal agent for Rivoraxban?

A

Adanexanet alfa

Year 3 Medicine Block (56 decks)

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