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ATRIAL FIBRILLATION/FLUTTER - 1B (INVESTIGATIONS (Do manual pulse…
ATRIAL FIBRILLATION/FLUTTER - 1B
DEFINITION
Classified based on pattern of episodes
:
Paroxysmal AF
Episodes lasting >30 seconds but less than 7 days
Self-terminating + recurrent
Persistent AF
Episodes >7 days
Spontaneous termination unlikely to occur after 7 days
Needs electrical/pharmacological cardioversion for termination
Permanent AF
AF that fails to terminate after cardioversion or
That is terminated but relapses within a day or
Long-standing aka
accepted permanent
AF (usually >1 year) where cardioversion not indicated or attempted
AF is an arrhythmia
Irregular, disorganised electrical activity in atria
Most common sustained cardiac arrhythmia
Irregularly irregular ventricular pulse + loss of association between cardiac apex beat + radial pulsation
PATHOPHYSIOLOGY
In most, due to cells rapidly firing impulses at junction of pulmonary veins in left atrial (LA) musculature → disorganised atrial depolarisation + ineffective atrial contractions
AVN receives more electrical impulses than it can conduct → irregular ventricular rhythm→ loss of active ventricular filling →
stagnation of blood in atria → thrombus formation + risk of embolism → increasing stroke risk
reduction in CO esp. during exercise → HF
AETIOLOGY
Most have
identifiable cause
Lone AF where no obvious cause + all investigations normal happens in small % of AF → but more common in
paroxysmal AF
Px
Most common causes of AF:
Ischaemic heart disease aka coronary heart disease e.g. MI
Hypertension
(can lead to LV hypertrophy)
Valvular heart disease
Hyperthyroidism
Other factors thought to cause/associated with AF:
Cardiac or valve conditions e.g.
HF
Rheumatic heart disease
Non-cardiac conditions e.g.
Drugs e.g. bronchodilators
Acute infection - ether resp. (e.g. chest infection) or systemic cause
Electrolyte depletion - systemic cause
Lung cancer - resp. cause
Pulmonary embolism - resp. causes
DM
Thyrotoxicosis - systemic cause
Dietary + lifestyle factors e.g.
Excessive caffeine, alcohol - systemic causes
Obesity
INVESTIGATIONS
Do manual pulse palpation for presence of irregular pulse
If irregular pulse whether symptomatic or not → ECG
If AF present:
- no P-waves
- chaotic baseline
- irregularly irregular ventricular rate (variability in R-R intervals)
Ventricular rate 160-180 bpm or ↓ esp. in asymptomatic Px
Ventricular complexes look normal unless ventricular conduction defect
If paroxysmal AF suspected + AF not detected on standard ECG →
24 hour ambulatory ECG
Thyroid function tests (TFTs)
for underlying causes of AF e.g. thyrotoxicosis
FBC
anaemia might worsen HF
sepsis?
U&E
electrolyte disturbance can worsen AF
urea is waste product metabolism excreted by kidneys in urine; ↓urea excretion = kidney disease indicator
electrolytes; abnormal serum K+ levels can worsen arrhythmias esp. if Px taking or going to take digoxin
LFTs
Coagulation screen - pre-warfarin
CXR
may indicate cardiac structural causes of AF e.g. mitral valve disease or HF
do if suspect lung pathology e.g. pneumonia, lung cancer)
Echocardiogram - transthoracic - in some
:
if considering cardioversion
if ↑risk of underlying structural (e.g. ❤ murmur) or functional (e.g. HF) heart disease that will influence management e.g. which anti-arrhythmic
CT or MRI
- if stroke/TIA suspected
COMPLICATIONS
Stroke & thromembolism incl. peripheral thromboembolism
- main complication
HF
- commonly linked with AF
HF can occur due to disorganised electrical conduction in atria → ineffective ventricular filling → pushing already compromised ventricle into failure → ↓CO further
Tachycardia-induced cardiomyopathy & critical cardiac ischaemia
Both conditions due to persistently ↑ ventricular rate in uncontrolled AF
↓ quality of life
AF → ↓exercise tolerance & impaired cognitive function
CLINICAL FEATURES
Irregular pulse with/without:
dyspnoea
palpitations
chest discomfort
syncope/dizzy
↓exercise tolerance, malaise, polyuria
potential complication of AF e.g.
stroke
transient ischaemic attack
HF
Absence of irregular pulse makes AF unlikely
but
still presence of it isn't reliable indicator of AF either
Suspect paroxysmal AF if symptoms episodic last <48 hours
DDx
Atrial flutter
saw-tooth pattern of regular atrial activation on ECG
AF can alternate with atrial flutter
atrial flutter may develop into AF
atrial flutter might happen during treatment of AF with ani-arrhythmic drugs
Sinus tachycardia
sinus rhythm with >100bpm
Supraventricular tachycardia e.g.
atrial tachycardia, atrioventricular nodal re-entry tachycardia
MANAGEMENT
SUMMARY of MANAGEMENT FOR FIRST/ONSET NEW + PAROXYSMAL AF - NICE:
Admit/refer if severe symptoms
rapid pulse >150bpm
hypotension
syncope, dizzy
ongoing chest pain
increasing dyspnoea
Admit/refer if severe complications
stroke
TIA
acute HF
ID + manage underlying causes
Treat arrhythmia
rate control (BB or CCB)
refer for rhythm control/cardioversion
assess stroke risk using CHA2DS2VASc
assess if anticoagulation appropriate i.e. if stroke risk high + use HAS-BLED for bleeding risk
follow up
advice/info on AF etc. + support groups
TREATMENT DETAILS
NICE TREATMENT - FOR FIRST/NEW PRESENTATION OF AF:
RATE
control treatment - most Px →
BB (LOL)
or
rate-limiting
CCB (verapamil/diltiazem)
Whether BB or CCB depends on CI (❌), e.g. BB ❌ in asthma vs. CCB ❌ in co-existing HF
❌ sotalol - don't prescribe in GP for
RATE
control (can be life-threatening) - only specialists can prescribe for
RHYTHM
control
Digoxin monotherapy
for
non-paroxysmal sedentary Px
Follow up
to assess tolerance + review symptom control, HR, BP
Refer to cardiologist
for
RHYTHM
control (CARDIOVERSION)
for:
New onset AF
AF with
reversible cause
e.g. chest infection
If have
HF
mostly caused/worsened by AF
If have
atrial flutter
+ restoring sinus rhythm is possible
Rhythm control used by specialists:
Electrical cardioversion → if persisted for >48 hours
Pharmacological cardioversion → e.g. sotalol or amiodarone
Anticoagulate Px (warfaring/NOAC) BEFORE cardioversion
as risk of embolism leading to stroke is highest the moment Px switches from AF to sinus rhythm in cardioversion - as thrombus formed in fibrillating atrium can suddenly be pushed out when sinus rhythm restored
at least 3 weeks before and some time after cardioversion
NB: If AF Px presenting acutely with
non-life threatening haemodynamic instability
:
Rate control or rhythm control - depends time of onset of AF
NICE thromboprophylaxis treatment for new/all AF incl. paroxysmal AF
:
anticoagulants
Assess
stroke risk
→
CHA2DS2VASc
score
2 or above
→ anticoagulation therapy
C
- Congestive HF/LV dysfunction (HTN with ↓ ejection fraction =
1
H
- HTN (resting BP >140/90mmHg) or current HTN meds =
1
A
- Age >= 75yo =
2
D
- DM (fasting plasma glucose >=7.0 mmol/L) or insulin/DM meds =
1
S
- Stroke/TIA/thromboembolism =
2
V
- Vascular disease (prior MI, peripheral artery disease, aortic plaque) =
1
A
- Age 65-75 yo =
1
S
- Sex category - female =
1
↓risk of stroke are females ( with score 1) and males (score 0) on CHADSVAS score - don't offer anticoagulation to these ↓risk Px
Warfarin (vitamin K-antagonist) or NOACs
NOACs: non-reversible effect, ££, but less monitoring
ends in "-XABAN" or "-TRAN")
Warfarin: regular blood tests to monitor coagulation control but reversible + cheaper
ANTI-PLATELET therapy instead
for stroke prevention if anticoagulation❌→ give
aspirin + clopidogrel
❌ don't prescribe aspirin or clopidogrel monotherapy/alone
Assess
bleeding risk
→
HAS-BLED
- to ID Px ↑risk of bleeding who can benefit from ↑vigilance to ↓risk of bleeding by managing modifiable risk factors for bleeding
H
- HTN =
1
A
- Abnormal liver function, renal function; alcohol (harmful consumption) =
1
S
- Stroke =
1
B
- Bleeding Hx of predisposition =
1
L
- Labile INR (international normalised ratios) =
1
E
- Elderly (>65yo) =
1
D
- Drugs (anti-platelets or NSAIDs) =
1
