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HDT 2.2 COPY > Antiarrhythmia and Anticoagulation > Flashcards

Antiarrhythmia and Anticoagulation Flashcards

1
Q

What is the normal heart rate?

A

60-100bpm

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2
Q

What is arrhythmias?

A

any change in the normal rate or rhythm of the heart

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3
Q

How do arrhythmias occur?

A
  • altered impulse generation eg change in automaticity (ability to generate electrical impulses spontaneously leading to depolarisation) of the pacemaker cells in SA node
  • altered impulse conduction eg complete or partial block of conduction pathways within the myocardium
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4
Q

What are the three types of arrhythmias?

A
  • bradycardia
  • tachycardia
  • atrial flutter or atrial fibrillation
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5
Q

Describe bradycardia.

A
  • heart rate <60bpm
  • if HR slow byt rhythm unchanged = sinus bradycardia
  • may also be caused by heart block
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6
Q

Describe tachycardia.

A
  • heart rate > 100bpm
  • if HR increases by rhythm unchanged = sinus tachycardia
  • supra ventricular tachycardia = arrhythmias that arise above the level of the ventricles
  • ventricular tachycardia = arise within the ventricles themselves
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7
Q

Describe atrial flutter and atrial fibrillation.

A
  • atrial flutter occurs less frequently
  • atrial fibrillation is the most common type of arrhythmias
  • rapid atrial rate and disturbance of conduction pathways in atrial flutter increases the risk of localised thrombus formation and secondary embolic events (thrombotic stroke)

atrial fibrillation = atria beat irregularly

atrial flutter = atria beat regularly, but faster than usual

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8
Q

What are risk factors of atrial fibrillation?

A
  • hypertension
  • coronary artery disease
  • diabetes
  • heart failure
  • valve disease
  • alcohol
  • male
  • increasing age
  • obesity
  • acute MI
  • stress
  • caffiene
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9
Q

What are complications of AF?

A
  • stroke
  • congestive heart failure
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10
Q

What are symptoms of AF?

A
  • breathlessness
  • light-headedness
  • fatigue
  • palpitations - describes heart as racing, pounding or thumping in chest
  • chest pain
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11
Q

How is AF diagnosed in primary care?

A
  • WatchBP Home A device is an oscillometric blood pressure monitor
  • it records blood pressure and automatically detects pulse irregularity caused by symptomatic or asymptomatic AF
  • device should be considered for use in people with suspected hypertension and those being screened or monitored for hypertension
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12
Q

What do anti-arrhythmic agents block?

A

initial fast sodium inward current that causes depolarisation

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13
Q

What are the classifications of antiarrhtymic medications?

A
  • IA - Na channel blocker - slows depolarisation
  • IB - Na channel blocker - small reduction depolarisation
  • IC - Na channel blocker - markedly slows depolarisation
  • II - beta-adrenoreceptor blocker - blocks sympathetic activity; reduces rate and conduction
  • III - K channel blocker - delays repolarisation and increases AP duration and effective refractory period
  • IV - Ca channel blocker - blocked L-type Calcium channels; most effective at SA and AV nodes; reduce rate and conduction
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14
Q

Give examples of class I, class II, class III, class IV drugs and others

A
  • I lidocaine, quinadine
  • II atenolol, metoprolol
  • III amiodarone
  • IV - diltiazem, verapamil
  • others adenosine, digoxin
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15
Q

How do you diagnose AF?

A
  • ECG - may need 24 hour tape to rule out paroxysmal AF
  • ECHO (electrocardiogram of the heart)
  • TFTs thyroid function tests as hypertention can lead to AF
  • chest x ray (may indicate cardiac structural causes of AF, such as mitral valve disease or HF)
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16
Q

What are the different types of AF?

A
  • paroxysmal: spontaneous termination within 7 days and most often within 48 hours. may degenerate into a sustained form of AF
  • persistent: not self-terminating; lasting longer than 7 days or prior cardioversion. Persistent AF may degenerate into permanent AF
  • permanent: long standing AF (over a year) that is not terminated by cardioversion, when cardioversion is not pursued or has relapsed following termination - needs management

reversion of permanent AF to normal sinus rhythm is possible, particularly when AF is caused by an underlying disease which is successfully treated or where a specialist procedure is formed modifying the electrophysiological properties of the heart

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17
Q

What is the management of AF?

A
  • control of the arrhythmia (by rhythm or rate control)
  • thromboprophylaxis to prevent strokes
  • treat any underlying cause
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18
Q

What is first line treatment for people with atrial fibrillation?

A

rate control, except in people

  • who’s atrial fibrillation has a reversible cause
  • who have heart failure thought to be primarily caused by AF
  • with new onset atrial fibrillation

rhythm control would be more suitable

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19
Q

What are the rate control guidelines?

A
  • either a STANDARD BETA BLOCKER eg atenolol bisoprolol or RATE LIMITING CALCIUM CHANNEL BLOCKER eg diltiazem verapamil
  • consider digoxin monotherapy for people with non-paroxysmal atrial fibrillation only if they are sedentary (do no or little exercise)
  • if monotherpy doesnt work and if symptoms are due to poor ventricular rate control, consider combination therapy with any 2 of:
    • a beta blocker
    • diltiazem
    • digoxin
20
Q

What is rhythm control guidelines?

A
  • consider pharmacological and/or electrical rhythm control
  • for people whose symptoms continue after heart rate has been controlled or if rate control has been unsuccessful
21
Q

What is cardioversion?

A
  • for people who have had AF for over 48 hours, offer electrical (rather than pharmacological) cardioversion
  • consider amiodarone therapy starting 4 weeks before and continuing for up to 12 months after to maintain sinus rhythm
22
Q

What are the drug treatment options for long term rhythm control?

A
  1. standard beta blocker unless contraindicated
  2. assess suitability of alternative drugs for rhythm control, taking comorbidities into account
  3. dronedarone after successful cardioversion in people with paroxysmal or persistent AF
23
Q

What should you not give to someone with known ischaemic or structural heart disease?

A

class 1c antiarrhythmic drugs such as flecainide or propafenone

24
Q

What is recommended for someone with infrequent paroxysms and few symptoms or when symptoms are induced by known precipitants?

A

no drug treatment strategy

25
Q

How does amiodarone act on the heart?

A
  • contains iodine
  • related structurally to thyroxine
  • shows class I, II, III and IV actions
  • prolongation of AP duration and refractory period
26
Q

What is unusual about amiodarones half life?

A
  • several weeks
  • distributes extensively in adipose tissue
  • full clinical effects may not be achieved until months after initiation of treatment
27
Q

What are amiodarones adverse effects?

A
  • interstitial pulmonary fibrosis
  • GIT intolerance
  • hyper/hypothyroidism
  • livertoxicity
  • photosensitivity - wear hats and apply sunscreen
28
Q

What are non drug treatments for AF?

A
  • ablation (pulmonary vein)
  • ablate and pace (AV node ablation)
  • atrial defibrillators
  • maze procedure
  • removal of left atrial appendage
29
Q

How do you calculate risk of stroke in people with AF?

A

CHADSVASc score

people at low risk (males 0 females 1) do not need antithrombotic therapy

30
Q

How can you calculate bleeding risk in people who are starting or have started anticoagulation?

A

HAS-BLED score

31
Q

What does the SAMe-TT2R2 score helps?

A

aids decision making between a non-VKA oral anticoagulant (NOAC) and a vitmain K antagonist

32
Q

What drugs are for anticoagulant therapy?

A
  • apixaban
  • dabigatran etexilate
  • rivaroxaban
  • edoxaban
  • or a witamin k antagonist (warfarin)
33
Q

How do you initiate warfarin?

A
  • differs depending on indication
  • can be used in pulmonary embolism, deep vein thrombosis, AF, mechanical heart valves
  • need to rule out contraindications eg active bleeding
  • baseline INR is taken
34
Q

What is INR?

A

international normalised ratio

index of blood coagulability - normal INR = 1

35
Q

What does anticoagulant therapy adjust INR to?

A

to 2-4 - takes 2-4 times longer to clot

36
Q

What is target INR for AF, DVT, PE and mechanic heart valves?

A

AF, DVT, PE = 2-3

heart valce = 2.5 - 3.5

37
Q

What are doses for warfarin?

A

base line prothrombin time should be determined but intial dose should not be delayed while waiting for result

  • usually 5-10mg on first day (lower for elderly)
  • subsequent doses depend on INR
  • heparin should be given first day, continued for at least 5 days and until the patients INR is at least 2 for 2 consecutive days
  • daily maintenance is usually 3-9mg (taken at same time each day)

for patients who dont require rapid anticoagulation, a lower loading dose can be used over 3-4 weeks

38
Q

What is recommended as alternatives to warfarin?

A
  • NOACS in the prevention of stroke and systemic embolismin patients with AF
  • as effective as warfarin
39
Q

What is offered to people with a CHAD-VASc score of 2 or above?

A
  • anticoagulation, take bleeding risk into account
  • do not offer aspirin monotherapy to people with AF
40
Q

How can you reverse anticoagulant effects and when would you do this?

A
  • idarucizumab (PRAXBIND)
  • used for rapid reversal of dabigatran in the case of emergency surgery or urgent procedures or in life threatening or uncontrolled bleeding
41
Q

How do you initiate NOACs?

A
  • decision after a discussion between clinician and patient regarding risks vs benefits compared with warfarin
  • SE: GIT bleeding
42
Q

What does unfractioned heparin do?

A
  • prevents production of fibrin from fibrinogen
  • inhibition of production of activated clotting factors
  • given IV or subcutaneously
  • major adverse effect: haemorrhage
  • safer in renal impairment due to shorter half life than LMWH
43
Q

Discuss LWMH.

A
  • anticoagulant effect by inactivating factor Xa
  • eg dalteparin, enoxaparin and tinzaparin
  • longer and more predictable half life than UFH
  • mainly renal excretion so care in renal impairment
  • smaller risk of heparin induced thrombocytopenia, potential SE of heparin
44
Q

Discuss the use of fondaparinux

A
  • inhibits activated factor X
  • used in prophylaxis of VTE and treatment of DVT and PE
  • used in acute management of MI
45
Q
A

HDT 2.2 COPY (18 decks)

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