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TCA 9 - HF > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

What causes arrhythmia?

A
  • Abnormal pacemaker/triggered activity

* Re-entry

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2
Q

What is AF?

A

Contraction of atria is uncoordinated, rapid and irregular.
This disorganised electrical activity in the atria also leads to irregular conduction of electrical impulses to the ventricles.

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3
Q

How does the risk of stroke increase with AF?

A
  • Blood collects in atria and forms blood clots

- Clots can become emboli and travel to the brain and block cerebral arteries causing ischaemic stroke

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4
Q

How does AF present?

A
  • Palpitations
  • Chest discomfort
  • SOB
  • Syncope
  • Symptoms of associated conditions (stoke, sepsis or thyrotoxicosis)
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5
Q

What does AF look like on an ECG?

A
  • Narrow QRS complex Tachycardia
  • Irregularly irregular rhythm
  • Absence of P-waves
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6
Q

What are the causes of AF?

A 
Mrs SMITH
•	S - Sepsis
•	M - Mitral valve pathology 
•	Ischaemic heart disease (IHD)
•	T - Thyrotoxicosis
•	H - HTN
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7
Q

What is the treatment for AF?

A
  • Rate OR rhythm control

* Anticoagulation to prevent stroke

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8
Q

What would you NOT give rate control treatment for AF?

A
  • There is a reversible cause of AF
  • Their AF is new onset (48hrs)
  • Their AF is causing HF
  • They remain symptomatic despite being effectively rate controlled
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9
Q

What are the drug options for rate control of AF?

A
  1. Beta blocker -> atenolol 50-100mg o.d.
    Remember atenolol is not licensed in HF, but rate control is not given in AF with HF
  2. CCB -> diltiazem
  3. Digoxin
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10
Q

What is the mechanism of action of digoxin

A

Reversibly inhibits Na-K ATPase, causing an increase in intracellular Na+ and Ca2+ inside the myocardial cells, increasing contractility of the heart.
ncreases vagal afferents to the heart which reduces SAN firing, decreasing the HR.

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11
Q

If rate control monotherapy for AF does not work, what would you do?

A

Combine 2 of:

  • Beta blocker -> atenolol 50-100mg o.d.
  • CCB -> diltiazem
  • Digoxin
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12
Q

When would you give rhythm control for HF?

A
  • There is a reversible cause of their AF
  • Their AF of new onset (<48hrs)
  • Their AF is causing HF
  • They remain symptomatic despite being effectively rate controlled
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13
Q

Why can you not give rate control to a patient who has had AF>48 hrs?

A

The risk of clots forming is greater is the patient had had AF for >48hrs.

  • If a normal sinus rhythm was restored through rhythm control, the clots could become dislodged and would increase the risk of embolic stroke.
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14
Q

What would you give for rhythm control?

A 
Cardioversion:
- Defibrillation
- Drugs:
      Flecainide
      Amiodarone

Long-term

  1. Beta-blockers
  2. Dronedarone
  3. Amiodarone
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15
Q

What is the CHA2DS2-VASc score?

A 
Assesses whether patient with AF should be started on anticoagulation.
Score:
•	0 = no anticoagulation
•	1 = consider anticoagulation
•	>1 = offer anticoagulation
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16
Q

What does the CHA2DS2-VASc score look at?

A
  • C - Congestive HF
  • H - HTN
  • A2 – Age >75 (scores 2)
  • D - Diabetes
  • S2 – Stroke or TIA previous (scores 2)
  • V –Vascular disease
  • A – Age 65-74
  • S – Sex (female)
17
Q

Which anticoagulants can you give for AF?

A
  • Warfarin
  • Apixaban
  • Dabigatran
  • Rivaroxaban

DO NOT GIVE ASPIRIN

18
Q

When would you give a NOAC?

A
  • > 75yrs
  • Prior stroke or TIA
  • HTN
  • DM
19
Q

When would you give dabigatran?

A
  • Previous systemic embolism
  • LVEF <40%
  • > 65yrs + DM, CAD or HTN
20
Q

How do you assess a patient’s major risk of bleeding whilst on anticoagulation?

A

HAS BLED

  • H – HTN
  • A – Abnormal renal and liver function
  • S – Stroke
  • B – Bleeding
  • L – Labile INRs (whilst on warfarin)
  • E – Elderly
  • D – Drugs or alcohol
21
Q

What is paroxysmal AF?

A

AF comes and goes in episodes, usually not lasting >48hrs.

22
Q

How is paroxysmal AF treated?

A

“pill in the pocket” approach -> flecainide

23
Q

What is the mechanism of action of amiodarone?

A

Class III antiarrhythmic -> Blocks the K+ rectifier currents that are responsible for repolarisation of the heart to slow down nerve activity and relax an overactive heart.

24
Q

What is the mechanism of action of flecainide?

A

Blocks the Ca2+ channel to slow the upstroke of the cardiac action potential

25
Q

What is the mechanism of action of dronedarone?

A

Inhibits rapid Na+ currents, antagonises alpha and beta receptors, block K+ outward current and blocks Ca2+ inward currents

26
Q

What do you do if a patient’s INR >8 and they are having a major bleed?

A
  • Stop Warfarin
  • IV Vit K 5mg
  • Give prothrombin complex concentrate or FFP
27
Q

What do you do if a patient’s INR >8 and they are having a minor bleed?

A
  • Stop warfarin
  • IV Vit K 1-3mg
  • If INR has not gotten to target level in 24 hours, give Vit K again
  • Give warfarin when INR <5
28
Q

What do you do if a patient’s INR >8 and they are not bleeding?

A
  • Stop warfarin
  • Oral Vit K 1-5mg
  • If INR has not gotten to target level in 24 hours, give Vit K again
  • Give warfarin when INR <5
29
Q

What do you do if a patient’s INR is between 5-8 and they are bleeding?

A
  • Stop warfarin
  • IV Vit K 1-3mg
  • Give warfarin when INR <5
30
Q

What do you do if a patient’s INR is between 5-8 and they are not bleeding?

A
  • Stop next 1/2 doses of warfarin

- Reduce subsequent maintenance dose

31
Q

What is the target INR for AF and VTE?

A

2.5

32
Q

What are the side effects of warfarin?

A
  • Haemorrhage
  • Teratogenic (safe in breastfeeding)
  • Purple toes
  • Skin necrosis
33
Q

What may potentiate the effects of warfarin?

A
  • Liver disease
  • P450 enzyme inhibitors (ciprofloxacin, amiodarone, fluconazole)
  • Cranberry juice
  • NSAIDs

TCA 9 - HF (5 decks)

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