AF (see DM for more depth) Flashcards
what is AF
irregular atrial contraction, caused by chaotic
impulses; it is a supraventricular arrhythmia as the abnormality originates above the ventricles (in the atria)
AP ECG characteristics (3)
absent p waves; fibrillating baseline; irregularly irregular rhythms
what are the 4 kinds of AF
paroxysmal; persistent; long-standing persistent; permanent
what is paroxysmal AF?
recurrent episodes (≥30 seconds in duration) that terminate spontaneously or with intervention within 7 days; usually self terminating in 48hrs
what is persistent AF
AF fails to self terminate within 7 days; included AF that has been cardioverted after 7 days
what is long-standing persistent AF
AF that lasts for over a year (even with treatment) - failure to revert back to sinus rhythm
what is permanent AF
sinus rhythm cannot be restored or maintained and AF is
accepted final rhythm - considered long-standing if rhythm correct treatment attempted again
presentations of AF (7)
asymptomatic (irregularly irregular pulse only); palpitations; dyspnoea; chest tightness; fatigue; sleeping disturbances; psychological effects
modified EHRA symptom scale
- ‘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 - ‘Severe symptoms’; normal daily activity affected
- ‘Disabling symptoms’; normal daily activity discontinued
causes of AF
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
what remodeling can occur due to AF? (3)
electrical; contractile; structural
what is electrical remodelling (due to AF)
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
what is contractile remodelling (due to AF)
a change in atria contractility; cellular Ca2+ loading; impaired contractility and increased compliance leading to atrial dilation; reversible
what is structural remodelling (due to AF) and what are causes of it (
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;
what causes AF (pathophysiology)
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)
what is an AF re-entry mechanism and how does it work
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
what does the term “AF begets AF” reffer to?
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
what is heamodynamic stability
stable blood flow - stable pumping heart and good circulation of blood
what is ectopic activity
an extra or a missed beat - can be normal, may be a trigger for arrythmias
3 steps to AF management
rhythm control; rate control; anticoagulation
how can rhythm be controlled acutely in AF
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)
how can rhythm be controlled chronically in AF
Fleciainide (pill in pocket), amiodorone; B-blockers (sotalol), dronedarone; catheter ablation
how should the risk of thromboembolism due to AF be reduced?
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
who is catheter ablation recommended for
pts with symptomatic paroxysmal AF who still have symptoms despite antiarrhythmic drugs; younger pts and athletes; sometimes done with permanent AF
what can cause AF in atheletes?
LA stretch, not well understood
what area is targeted when treating AF with ablation
pulmonary vein foci - it is responsible for initiating AF; isolation of the foci is a cornerstone of ablation
acute rate control for AF
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
what is CHA2DS2-VASc scoring (not criteria)
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
CHA2DS2-VASc scoring criteria
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)
how to assess bleeding risk
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
chronic rate control for AF
LVEF <40% - Bblocker or digoxin, consider low dose combination therapy;
VEF >40% - Bblocker (first line) or digoxin/veramapil/diltiazem, consider combination therapy as appropriate
when can DOACs not be given and what can be given instead to anticoagulate
mechanical heart valves, mitral stenosis; VitK antagonists (warfarin) can be given instead
what is the pace and ablate strategy
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
when is pace and ablate indicated
in pts where the rate is unable to be controlled pharmacologically; intractable symptoms (palpitations); deterioration in LV function; suboptimal biventricular pacing
modifiable risk factors for bleeding (7)
HTN; liable INR; medications predisposing (e.g. edoxaban, aspirin); excess alcohol; anaemia; impaired renal/liver function; reduced platelet count
non-modifiable risk factor (7)
age; history of major bleeding; previous stroke; renal transplant/dialysis; liver disease; malignancy; genetic factors
when is anticoagulation recommended
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)
when should left atrial appendage occlusion be considered
in patients with a CHADS2-VASc score >2 but contraindications to anticoagulations
what is the risk associated with the left atrial appendage in AF
thrombi tend to form here which can then embolise
focal mechanism of AF
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
link between sleep apnea and AF
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
digoxin toxicity signs
