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Yr 3 cardio > AF > Flashcards

AF Flashcards

1
Q

def AF

A

characterized by rapid, chaotic and ineffective atrial electrical conduction. Often subdivided into: ‘permanent’, ‘persistent’ and ‘paroxysmal’. 300-600bpm

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2
Q

aetiology AF

A

may be no identifiable cause (lone AF)

secondary causes lead to abnormal atrial electric pathways = AF

systemic causes - thyrotoxicosis, hypertension, pneumonia, alcohol, caffeine, post-op, hypokalemia, low Mg, haemochromatosis, sarcoid

The AV node responds intermittently to the atrial rhythm = irregular ventricular rhythm

CO drops by 10-20% as ventricles arent primed reliably

in pre-excited AF accessory pathways capable of conducting rapid rates pass erratic electrical activity from the atria to the ventricles, unfiltered by AVN

ECG - irregular, broad QRS at >200bpm

ventricles cant sustain this for long - pt is at high risk of VT and VF

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3
Q

heart causes AF

A
  • mitral valve disease
  • ischemic heart disease
  • rheumatic heart disease
  • cardiomyopathy
  • pericarditis
  • sick sinus syndrome
  • atrial myxoma
  • HF
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4
Q

lung causes AF

A

bronchial carcinoma

PE

pneumonia

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5
Q

epi AF

A

common in elderly <=9%

may be paroxysmal

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6
Q

sx af

A

often asymptomatic

palpitations/syncope

chest paun

dyspnoea

symptoms of the cause other than the AF

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7
Q

signs af

A
  • irregularly irregular pulse
  • difference in apex beat and radial pulse (apical greater than radial)
  • thyroid disease
  • valvular heart disease
  • 1st heart sound of varying intensity
  • signs of LVF
  • examine the whole pt - AF is often associated with non-cardiac disease
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8
Q

Ix AF

A

FBP

CRP see if they have an infection

thyroid check - see if hyperthyroid

troponin - in case MI

imaging - ask for echo in anyone with palpitations - see the structure of the heart, see if thrombus in L atria that can become embolic = stroke

X ray - see if lung problem

ECG

Blood

echo

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9
Q

ecg af

A

Uneven baseline (fibrillations) withabsent P waves, irregular QRS complexes. If there is asaw-tooth baseline, consider if there is atrial flutter

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10
Q

blood af

A

cardiac enzymes

TFT

lipid profile

UE

Mg, Ca (risk of digoxin toxicity increased with hypokalaemia, hypomagnesaemia or hypercalcaemia)

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11
Q

echo af

A

assess for mitral valve disease, LAD, L ventricular dysfunction, or structural abnormalities, L atrial enlargement

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12
Q

mx af

A

a-e

dont need pacemaker

irreg irreg rhythm

see if stable or not - SBP <90, chest pain, drowsy/unconscious, crackles in lungs (PE) = unstable

if unstable need to shock them - chemically or electrically

  • stable need to do rate or rhythm control
  • rate = b blocker if ejection fraction is normal. If EF is low = digoxin, if in COPD - Ca channel blocker LOOK UP NORMAL EF VALUES
  • rhythm - if had past AF
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13
Q

af rhythm control

A

If the AF is>48 h from onset, anticoagulate (at least 3–4 weeks) before attempting cardioversion.

DC cardioversion: Synchronized DC shock (2x100 J, 1x200 J).

Chemical cardioversion: Flecainide (contraindicated if there is history of ischaemic heart disease) or amiodarone.

Prophylaxis against AF: Sotalol, amiodarone or flecainide. Also consider providing ‘pill-in-the-pocket’ strategy for suitable patients.

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14
Q

af rate control

A

Chronic ‘permanent’ AF: Ventricular rate control with digoxin, verapamil and/or b-blockers. Aim for rate of 90/min.

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15
Q

af stroke risk prevention

A

low risk pts managed with aspirin

high risk warfarin

  • previous thromboembolic event,
  • >75yrs with HTN, dm or vascular disease
  • clinical evidence of valve disease, HF or impaired l ventricular function
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16
Q

mx acute af

A

if showing adverse signs (shock, myocardial ischemia - chest pain/ECG changes), syncope, HF

  • ABCDE
  • senior input
  • DC cardioversion (synchronized shock, start at 120–150J) ± amiodarone if unsuccessful
  • dont delay treatment to start anti-coagulation

if stable and started <48hr ago

  • rate/rhythm control
  • start heparin in case cardioversion is delayed

if stable and >48hrs or unclear time of onset

  • rate control eg with bisoprolol or diltiazem
  • If rhythm control is chosen, the patient must be anticoagulated for >3wks first.

correct electrolyte imbalance (K, Mg, Ca), treat associated illnesses, and consider anti-coagulation

17
Q

chronic af mx

A

main goals are rate control and anti-coag

rate control is at least as good as rhythm, but rhythm may be appropriate if

  • symptomatic/CCF
  • younger
  • presenting for 1st time with lone AF
  • AF from corrected precipitant

anticoag

18
Q

rate control - chronic af

A

B blcoker or rate limiting CCB 1st choice

if fails, add digoxin, then consider amiodarone

Digoxin as monotherapy in chronic AF is only acceptable in sedentary patients.

do not give B-blockers with verapamil.

Aim for heart rate <90bpm at rest and 200 minus age (yrs) bpm on exertion. Avoid getting fi xated on a target heart rate.

19
Q

rhythm control chronic af

A

elective DC cardioversion

  • echo 1st to check for intracardiac thrombi
  • If there is increased risk of cardioversion failure (past failure, or past recurrence) give amiodarone for 4wks before the procedure and 12 months after

elective pharmacological cardioversion

  • flecainide is 1st choice (CI if structural heart disease, eg scar tissue from MI: use IV amiodarone instead)
  • In refractory cases, AVN ablation with pacing, pulmonary vein ablation, or the maze procedure may be considered.
20
Q

paroxysmal af mx

A

Pill in the pocket’ (eg sotalol or flecainide PRN) may be tried if: infrequent AF, BP >100mmHg systolic, no past LV dysfunction.

Anticoagulate

Consider ablation if symptomatic or frequent episodes

21
Q

anticaog acute af

A

heparin until full risk assessment for emboli made

trans-oesophageal-guided cardioversion is an option if urgent cardioversion is required (ie cant wait for the 3weeks of anticoag if AF >48hrs ago)

Use a DOAC (eg apixaban) or warfarin (target INR2–3) if high risk of emboli (past ischaemic stroke, TIA, or emboli; >75yrs with high BP, DM; coronary or peripheral arterial disease; evidence of valve disease or low LV function/CCF—only do echo if unsure).

no anticoagulation if stable sinus rhythm has been restored, no risk factors for emboli, andAF recurrence unlikely (ie no failed cardioversions, no structural heart disease, no previous recurrences, no sustained AF for >1yr)

22
Q

anticoag chronic af

A

Chronic AF may be paroxysmal (terminates in <7d but may recur), persistent (lasts >7d), or permanent (long-term, continuous AF, sinus rhythm not achievable despite treatment).

the need for anticoagulation should be assessed using the CHA2DS2-VASc score to assess embolic stroke risk - consider anti-coag if score men >0, women >1

and balancing this against the risks of anticoagulation to the patient, assessed with the HAS-BLED score.

Long-term anticoagulation should be with a DOAC or warfarin.

23
Q

a flutter mx

A

similar to AF - rate and rhythm control and anticoag

DC cardioversion preferred to pharmacological - start with 70-120J

IV amiodarone may be needed if rate control is proving difficult.

Recurrence rates are high so radiofrequency ablation is often recommended for long-term management.

24
Q

complications af

A

Thromboembolism (e.g. embolic stroke 4% risk per year, increase risk with left atrial enlargement or left ventricular dysfunction).

Worsens any existing heart failure.

25
Q

px af

A

Chronic AF in a diseased heart does not usually return to sinus rhythm.

Yr 3 cardio (38 decks)

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