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HDT 2.2 > arrhythmia and anticoagulation > Flashcards

arrhythmia and anticoagulation Flashcards

1
Q

what is the definition of arrhythmia? why do they occur?

A

when there is a change to the normal rhythm or rate of the heart

  • due to altered impulse conduction or generation
  • > changes in conduction pathway or the automaticity of pacemaker cells
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2
Q

what are the types of arrhythmias you can get?

A
  1. Bradycardia
    - <60 bpm
    - rhythm unchanged but heart rate is slow
    - caused by heart block
  2. tachycardia
    - >100 bpm
    - rhythm unchanged; can have super-ventricular where arrhythmias are above level of ventricles so within the atria
  3. AF
    - most common type
    - rapid atrial rate and disturbance of conduction pathways increases risk of thrombus formation
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3
Q

what are some complications of atrial fibrillation?

A
  • stroke

- congestive heart failure

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4
Q

what are risk factors for arrhythmia?

A
  • hypertension
  • CAD
  • valve disease
  • male
  • obesity
  • increasing age
  • lifestyle factors
  • diabetes
  • pneumonia
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5
Q

what are symptoms of AF?

A
  • breathlessness
  • light headedness
  • fatigue
  • palpitations
  • chest pain
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6
Q

how can you diagnose AF in primary care?

A

use a home BP monitor

it will detect pulse irregularity that can be caused by AF

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7
Q

what are the classifications of anti-arrhythmic drugs that are available?

A
  • Class IA - sodium channel blocker which slows Phase 0
  • Class IB - sodium channel blocker that reduces Phase 0
  • Class IC - sodium channel blocker that slows Phase 0
  • Class II - beta-adrenoreceptor blocker that blocks sympathetic activity and reduces rate and conduction
  • Class III - K+ channel blocker that delays Phase 3 and increases AP duration
  • Class iV - Ca+ channel blocker which blocks L-type calcium channels reducing rate and conduction
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8
Q

examples of Class I-IV drugs and other ones that might be used?

A 
Class I 
-> lidocaine, quinidine, propafenone, mexiletine 
Class II 
-> atenolol, esmolol, metoprolol 
Class III 
-> amiodarone, stall, dronedarone 
Class IV 
-> dilitiazem, verapamil
  • other ones are adenosine, digoxin
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9
Q

how to diagnose arrhythmia?

A

ECG
ECHO
TFTs
CXR

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10
Q

what are the types of AF you can get?

A
  1. paroxysmal; most often within 48 hours and can become a sustained form of AF
  2. persistent ; non self-terminating and longer than 7 days
  3. permanent; long standing AF and not terminated by cardioversion
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11
Q

how can you manage AF?

A
  • control the arrhythmia
  • control or treat ay underlying causes
  • can do thromboprophylaxis to prevent strokes
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12
Q

what can be offered as a first line strategy for AF?

what are the exceptions?

A 
offer rate control 
exceptions are:
-> have a reversibel AF 
-> new-onset of AF 
-> have heart failure due to AF
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13
Q

what can be offered with the rate control strategy treatment?

A

beta blocker or a rate-limiting calcium channel blocker as initial mono therapy

  • can consider digoxin monotherapy for people with non-paroxysmal AF
  • if that doesn’t work give combination with 2 of:
  • > beta blocker
  • > digoxin
  • > diltiazem
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14
Q

when should rhythm control be offered?

A
  • when symptoms continue after heart rate has been controlled
  • if rate strategy hasn’t been successful
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15
Q

what should be offered to patients with AF for over 48 hours?

A

if AF is longer than 48 hours they should be offered electrical cardioversion
- can consider giving amiodarone 4 weeks before and up to 12 months after electrical cardioversion to maintain sinus rhythm

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16
Q

what drug can be offered in long term rhythm control?

A
  • standard beta blocker as first line treatment
  • if unsuccessful then offer alternatives
  • dronedarone is recommended and is seen to be successful
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17
Q

what should not be offered for rhythm control?

A

do not offer Class Ic antiarrhythmic drugs e.g. propafenone
if patient has frequent symptoms or has induced symptoms by things like alcohol or caffeine; offer a ‘pill-in-the-pocket’ strategy and discuss with patients

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18
Q

what is the effect of amiodarone?

A

prolongs the duration of the action potential and so the refractory period

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19
Q

what is the pharmacokinetics of amiodarone?

A
  • incompletely absorbed after oral admin.
  • has a prolonged half-life of several weeks
  • clinical effects might not be achieved until months after initiation of treatment
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20
Q

what are the adverse effects of amiodarone?

A 
it can show toxic effects 
common side effects can be 
- liver toxicity 
- hyper or hypothyroidism 
- GI tolerance 
- pulmonary fibrosis 
- neuropathy
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21
Q

what are the counselling points for amiodarone?

A
  • tablet can be crushed and drank with water
  • for IV injection give continuously or intermittently over 20-120 minutes
  • protect your skin from sunlight and dont use sunbeds
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22
Q

what can rhythm abnormalities increase the risk of?

A

risk of blood clotting

23
Q

what is CHA2DS2-VASc?

A

it is a stroke risk calculator
used in decision to administer antithrombotic therapy
- male patients with score of 0 and female with 1 do not need antithrombotic therapy

24
Q

what is HAS-BLED?

A

a score to assess the risk of bleeding with patients using anticoagulants

25
Q

what is an example of a Vitamin K antagonist?

A

warfarin

26
Q

what are some anticoagulant medications that can be used in therapy?

A
  • apixaban
  • rivaroxaban
  • edoxaban
  • vitamin K antagonist
27
Q

what are some disadvantages of oral anticoagulants?

A
  • requires blood tests
  • antidote available
  • needs thorough patient counselling
28
Q

what can warfarin be used for?

A
  1. pulmonary embolism
  2. deep vein thrombosis
  3. AF
  4. mechanical heart valves
29
Q

what is the INR ?

A

it is a index of blood coagulability
International Normalised Ratio
a normal value of INR would be 1

30
Q

how would you initiate warfarin?

A
  • anticoagulant therapy like warfarin will change INR to 2-4
  • so for AF, PE and DVT you should aim for INR to be 2-3
  • must determine the base-line prothrombin time
    for patients who need treatment rapidly they should get 5-10mg on first day and dosage then depends on INR and prothrombin time
    should be given with heparin for at least five days and until INR is constant at 2.0 for at least two days
    for patients who dont need treatment can give a loading dose over about 3-4 weeks
    daily maintenance dosage is usually 3-9mg
31
Q

what are NOACS?

A

they are non-vitamin K Antagonist oral anticoagulants

  • can inhibit direct thrombin or inhibit activated factor Xa
    e. g. rivaroxaban, edoxaban, apixaban

do not need INR monitoring

32
Q

what is factor Xa?

A

it is a blood clotting factor that cleaves prothrombin to produce thrombin for the coagulation cascade

33
Q

what is seen to be a good alternative to warfarin?

A

NOACS
they prevent strokes and systemic embolism in AF patients
as effective as warfarin but reduced risks

34
Q

who should anticoagulation be offered to?

A

patients with a CHA2DS2-VASc score of 2 or above

  • take bleeding risk into account
  • dont offer aspirin monotherapy solely for stroke prevention
  • patients taking VK antagonist and have stable AF should continue with current medication and regular discussions should be had about their medication treatment
35
Q

what is Fondaparinux?

A

synthetic pentasaccharide that inhibits factor X

  • used in prophylaxis of VTE and treatment of DVT and PE
  • used in acute management of MI
36
Q

what are LMWH? what monitoring is needed for it?

A

low molecular weight heparins

  • contain smaller polysaccharide chains
  • have an anticoagulant effect by inactivating factor Xa
  • longer half life
  • excreted renally so should look at renal impairment risk
  • dont need to monitor APTT
37
Q

what is UFH?

A

‘conventional heparin’

  • large molecules
  • immediate anticoagulant properties
  • prevents fibrin production
  • given IV or SC
  • has a shorter half life so safer for risk of renal impairment
38
Q

how can you reverse anticoagulant effects?

A

use idarucizumab

used in emergency surgery or urgent procedures

39
Q

of an ECG graph, what is occurring at P, R and T?

A

P is when atrial depolarisation occurs
R is when ventricular depolarisation occurs
T is when ventricular repolarisation occurs

40
Q

what is an ECG?

A
  • measures heart electrical conduction system
  • detected by electrodes attached to surface of the skin
  • picks up electrical impulses from polarisation and depolarisation of cardiac tissues
  • current is transformed into waveforms
41
Q

why record an ECG?

A

allows us to see sequence of electrical events in cardiac cells

  • powerful diagnostic tool to look at:
  • > rhythm disturbances
  • > conduction disturbances
  • > MI
42
Q

what are the ECG leads?

A 
- bipolar limb leads 
there are four limb leads 
- attached to two arms and legs 
red = right arm 
yellow = left arm 
green = left leg 
black = right leg

each lead has three separate bipolar leads

43
Q

what is the AVF lead?

A

it uses the left foot electrode as positive and both arms as the negative

44
Q

what is the AVR and AVL lead?

A

AVR lead; the right arm electrode is positive and remaining two electrodes are negative (left foot and hand)
AVL lead; the left arm electrode is positive and the other two are negative (right arm and left foot)

45
Q

how is the ‘frontal’ plane of the patients chest?

A

you have six leads; AVR, AVL, AVF, I, II, III
they intersecting and lie in a flat frontal plane of the patients chest
they all record form a different angle and viewpoint to provide different views of the cardiac activity ; more accurate

46
Q

what kind of electrode do the leads require?

A

a positive electrode

47
Q

where are right and left chest leads placed?

A

right chest leads are placed on right ventricle and left leads on left ventricle

48
Q

what is the upward deflection on the ECG due to?

A

the depolarisation wave moving towards the positive electrode

49
Q

what is the heart axis normal value? where does it usually point?

A

it is usually between -30 and +90 degrees

it usually points in the direction of the average electrical vector of all depolarising heart cells

50
Q

what does a positive QRS complex mean in terms of the heart axis?

A

it means that the heart axis is going in that leads direction
QRS should be positive in lead I and II for a normal heart axis

51
Q

what does ECG paper usually look like

A

vertically it is one large box ; represents 0.5mV
horizontally you have on small box; 0.04 secs
one large box is 0.2 secs

there are markers for every 3 seconds present

52
Q

how would you do rhythm analysis?

A
  1. calculate the rate; count number of complete R to R waves in 6 sec strip then x10
  2. determine the regularity
  3. assess P waves; are there waves? do they look like the same and occur regularly?
  4. find the PR interval; should be 3-5 boxes (0.12-0.20 secs)
  5. find the QRS duration; normal is 0.04-0.12 seconds so 1-3 small boxes
53
Q

what is the PR interval?

A

it is atrial depolarisation + delay in the AV junction (bundle of His/AV node)

54
Q

why is there a delay in the AV node?

A

to allow the atria to contract before the ventricles contract

HDT 2.2 (10 decks)

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