AF (see DM for more depth)

Question 1

what is AF

Answer 1

irregular atrial contraction, caused by chaotic
impulses; it is a supraventricular arrhythmia as the abnormality originates above the ventricles (in the atria)

Question 2

AP ECG characteristics (3)

Answer 2

absent p waves; fibrillating baseline; irregularly irregular rhythms

Question 3

what are the 4 kinds of AF

Answer 3

paroxysmal; persistent; long-standing persistent; permanent

Question 4

what is paroxysmal AF?

Answer 4

recurrent episodes (≥30 seconds in duration) that terminate spontaneously or with intervention within 7 days; usually self terminating in 48hrs

Question 5

what is persistent AF

Answer 5

AF fails to self terminate within 7 days; included AF that has been cardioverted after 7 days

Question 6

what is long-standing persistent AF

Answer 6

AF that lasts for over a year (even with treatment) - failure to revert back to sinus rhythm

Question 7

what is permanent AF

Answer 7

sinus rhythm cannot be restored or maintained and AF is
accepted final rhythm - considered long-standing if rhythm correct treatment attempted again

Question 8

presentations of AF (7)

Answer 8

asymptomatic (irregularly irregular pulse only); palpitations; dyspnoea; chest tightness; fatigue; sleeping disturbances; psychological effects

Question 9

modified EHRA symptom scale

Answer 9

1. ‘No symptoms’
   2a. ‘Mild symptoms’; normal daily activity not affected by AF symptoms
   2b. ‘Mild symptoms’; normal daily activity not affected by AF symptoms but troubled by symptoms
2. ‘Severe symptoms’; normal daily activity affected
3. ‘Disabling symptoms’; normal daily activity discontinued

Question 10

causes of AF

Answer 10

cardio - Hypertension
Ischaemic heart disease
Valvular disease (e.g. rheumatic heart disease)
Myocardial infarction
Cardiomyopathy
other - COPD, pneumonia, pulmonary embolism, hyperthyroidism, diabetes mellitus, hypokalaemia, hypomagnesaemia, hyponatraemia, thyroxine, alcohol, excessive caffeine, obesity

Question 11

what remodeling can occur due to AF? (3)

Answer 11

electrical; contractile; structural

Question 12

what is electrical remodelling (due to AF)

Answer 12

changes in electrophysiological properties as a result of atrial fibrillation - a compensatory mech to avoid intracellular Ca2+ overload; shortened atrial refractory period; increased DAD and ectopic activity; cellular Ca2+ loading; reversible

Question 13

what is contractile remodelling (due to AF)

Answer 13

a change in atria contractility; cellular Ca2+ loading; impaired contractility and increased compliance leading to atrial dilation; reversible

Question 14

what is structural remodelling (due to AF) and what are causes of it (

Answer 14

a change in the structure of the atria that can cause conduction slowing and premote re-entry, irreversible usually;
causes - LA dilation (due to increased LVED) and hypertrophy (leading to fibroblast proliferation and collagen deposition); fibrosis (due to MI etc.); dedifferentiation; apoptosis/myolysis; inflammation; oxidative stress;

Question 15

what causes AF (pathophysiology)

Answer 15

often initiated by an area of ectopic focal activity with increased automaticity; rapid activation of these foci propagate ectopic beats that create micro-re-entrant circuits throughout the atrial
muscle; no organisation of atrial electrical activity, the atrial myocytes are not able to contract simultaneously; results in blood pooling in the atria, predisposing to thrombus
formation (see DM for more in depth)

Question 16

what is an AF re-entry mechanism and how does it work

Answer 16

a propagating impulse fails to die out after normal activation of the heart and persists as a result of continuous activity around the circuit to re-excite the heart after the refractory period has ended;
1. rather than there being 2 pathways with the same conduction velocity, 2 pathways with different conduction velocities arise e.g. due to infarct, this allows for retrograde transmission of impulses from fast pathway up the slow
2. under normal circumstances a retrograde impulse will hit the refractory tissue of the slow pathway thus causing the conduction waves to be terminated and sinus rhyhm is achived
3. if there is an ectopic beat (trigger) then it may reach the fast pathway while it is still in refractory period and so it must travel down the slow pathway
4. as the impuse reached the distal end of the circuit, the fast pasth has finished repolarising and so the impulse can travel up it - RE-ENTRY
5. the conduction wave can loop around the circuit

Question 17

what does the term “AF begets AF” reffer to?

Answer 17

The longer the duration of atrial pacing, the longer the AF was maintained; it accounts for the clinical observation that recurrent episodes of paroxysmal AF often progresses to more persistent forms of AF

Question 18

what is heamodynamic stability

Answer 18

stable blood flow - stable pumping heart and good circulation of blood

Question 19

what is ectopic activity

Answer 19

an extra or a missed beat - can be normal, may be a trigger for arrythmias

Question 20

3 steps to AF management

Answer 20

rhythm control; rate control; anticoagulation

Question 21

how can rhythm be controlled acutely in AF

Answer 21

haemodynamically unstable - cardioversion;
haemodynamically stable - elective cardioversion (antigoag required if symtpms started >48hrs proior), IV admioderone (AS or HFrEF), IV vernakalant/amioderone (CAD, moderate HF), flecainide/propafenone (not structural problems)

Question 22

how can rhythm be controlled chronically in AF

Answer 22

Fleciainide (pill in pocket), amiodorone; B-blockers (sotalol), dronedarone; catheter ablation

Question 23

how should the risk of thromboembolism due to AF be reduced?

Answer 23

Vit K anatagonists (e.g.warfarin): Mainstay for many yrs, Regular INR checks;
DOACs: Direct Xa inhibitors (e.g. apixaban,
rivaroxaban) & direct thrombin inhibitors (e.g. Dabigatran),No monitoring req

Question 24

who is catheter ablation recommended for

Answer 24

pts with symptomatic paroxysmal AF who still have symptoms despite antiarrhythmic drugs; younger pts and athletes; sometimes done with permanent AF

Question 25

what can cause AF in atheletes?

Answer 25

LA stretch, not well understood

Question 26

what area is targeted when treating AF with ablation

Answer 26

pulmonary vein foci - it is responsible for initiating AF; isolation of the foci is a cornerstone of ablation

Question 27

acute rate control for AF

Answer 27

aim: HR below 110bpm but avoid bradycardia
LVEF<40/ signs of congestive heart failure - smallest dose of B-blockers, then digoxin, consider anti-coag need and echo;
LVEF >40% - Bblocker/veramapil/diltiazem, then digoxin, consider anti-coag need and echo
caution due to negative ionotropy

Question 28

what is CHA2DS2-VASc scoring (not criteria)

Answer 28

Risk startification tool to assess embolic event risk in pt w AF; Result of score → guide need for anticoagulation, 1st line: DOAC, 2nd line:
Warfarin - must also assess BLEEDING RISK

Question 29

CHA2DS2-VASc scoring criteria

Answer 29

C - congestive heart failure
H- hypertension
A2 - age (>75)
D - diabetes melluitis
S2 - stroke/TIA/thromboembolism prior
V- vascular disease
A- age (65-74yr)
Sc - sex (female, additive not alone)

Question 30

how to assess bleeding risk

Answer 30

H - Hypertension
A - Abnormal Renal/Liver Function
S - Stroke
B - Bleeding History or Predisposition
L- Labile INR
E - Elderly
D - Drugs/Alcohol Concomitantly
ORBIT score may be used now

Question 31

chronic rate control for AF

Answer 31

LVEF <40% - Bblocker or digoxin, consider low dose combination therapy;
VEF >40% - Bblocker (first line) or digoxin/veramapil/diltiazem, consider combination therapy as appropriate

Question 32

when can DOACs not be given and what can be given instead to anticoagulate

Answer 32

mechanical heart valves, mitral stenosis; VitK antagonists (warfarin) can be given instead

Question 33

what is the pace and ablate strategy

Answer 33

ablation of the AVN and insertion of a pacemaker; Following AV node ablation,
the atria continue to fibrillate, but none of the rapid electrical activity in the atria reaches the
ventricles, so they will typically beat slowly and in a regular rhythm; a pacemaker is used to ensure that they beat at an appropriate speed, both at rest and during physical activity

Question 34

when is pace and ablate indicated

Answer 34

in pts where the rate is unable to be controlled pharmacologically; intractable symptoms (palpitations); deterioration in LV function; suboptimal biventricular pacing

Question 35

modifiable risk factors for bleeding (7)

Answer 35

HTN; liable INR; medications predisposing (e.g. edoxaban, aspirin); excess alcohol; anaemia; impaired renal/liver function; reduced platelet count

Question 36

non-modifiable risk factor (7)

Answer 36

age; history of major bleeding; previous stroke; renal transplant/dialysis; liver disease; malignancy; genetic factors

Question 37

when is anticoagulation recommended

Answer 37

men: all AF patients with CHADS2-VASc >2
women: all AF patients with CHADS2-VASc >3
mitral stenosis/mech heart valves: recommended in all pts (vit K antagonist)

Question 38

when should left atrial appendage occlusion be considered

Answer 38

in patients with a CHADS2-VASc score >2 but contraindications to anticoagulations

Question 39

what is the risk associated with the left atrial appendage in AF

Answer 39

thrombi tend to form here which can then embolise

Question 40

focal mechanism of AF

Answer 40

spontaneous depolarization due to cellular perturbations (delayed afterdepolarization, early afterdepolarization, and enhanced cellular automaticity); ectopic fringe is caused by Ca2 + spontaneous release within the cell; triggers inward currents leading to depolarization or the excessive prolongation of the action potential resulting in early afterdepolarization

Question 41

link between sleep apnea and AF

Answer 41

untreated sleep apnea can cause conditions like hypertension, stroke, and diabetes; sleep apnea can trigger arrhythmias during sleep - chemical changes occur whenever a person is startled awake by lack of oxygen

Question 42

digoxin toxicity signs