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Ch. 1 - Cardiology > Atrial Fibrillation & Flutter > Flashcards

Atrial Fibrillation & Flutter Flashcards

1
Q

Is A.Fib a type of SVT or is it grouped with Atrial flutter?

A

Both A.Fib and flutter are types of SVT as they both originate over the purkinje-His bundle

Just for information:
Atrial dilatation for example due to Mitral stenosis or congestive HF as well as cardiac ischaemia (MI CAD) are causes of atrial fibrillation. Atrial dilatation affects its electric circuitry => causing Atrial remodeling => re-entry circuits

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2
Q

The management plan for A.fib is typically composed of 3 components: Rate control, rhythm control, and anticoagulation. In what scenario is one of the 3 components not pursued?

A

When there is permanent A.fib (prolonged >1 year + decision made to no longer pursue rhythm control), Rhythm control is stopped

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3
Q

What are the 4 types of A.fib?

A

Paroxysmal A.fib <7 days
Persistent A.fib >7 days
Long standing persistent >1 year
Permanent A.fib >1year + decision made to no longer pursue rhythm control

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4
Q

What % of those with paroxysmal A.fib will develop Persistent A.fib?

A

25%

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5
Q

Define Atrial fibrillation

A

Irregularly irregular arrhythmia characterised by rapid and irregular depolarisation of the cardiac atria
To bypass the last part, you can state the ECG findings of A.fib

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6
Q

List all the causes of atrial fibrillation

A

CCCHASE = 2 cardiac CHASE noncardiac

Cardiac causes: CC
C1: LA enlargement due to mitral stenosis or congestive HF
C2: Ischaemia => Previous MI/CAD

Non-cardiac causes:
Catecholamines: Epinephrine/NE released during sepsis, post-op, phaeochromocytoma, thyrotoxicosis/hyperthyroidism

Hypoxia: PE, pneumonia, COPD

Alcohol binge (Holiday heart syndrome) => Hypokalaemia + Hypomagnesia

Sympathomimetics: Cocaine, MDMA

Electrolytes: Hypokalameia/hyperkalaemia, Hypomagnesia

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7
Q

How would the cardiac causes of Atrial fibrillation lead to an arrhythmia?
honours => not in book

A

Atrial dilatation for example due to Mitral stenosis or congestive HF as well as cardiac ischaemia (MI CAD) are causes of atrial fibrillation. Atrial dilatation affects its electric circuitry => causing Atrial remodeling => re-entry circuits

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8
Q

What are the typical symptoms you would like to elicit in a hx of A.fib.
There is also extra information about what to ask in a hx if you wanna have a go at it too

A

Any arrhythmia:
Palpitations
Syncope/pre-syncope
SOB/Dyspnoea
Chest pain
Fatigue
! feeling of rapid neck pulsation !
+ Sxs of HF (+orthopnoea, PND, weight gain, swelling,)
+ Sx of Thromboembolic (neurological deficit for stroke, Abdo pain for mesenteric ischaemia, Leg pain for critical limb ischaemia and DVT, chest pain for PE)

Extra
+ RF of CAD (previous MI, surgery,
+ Thyroid, alcohol use…. Must ask about all RF

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9
Q

You are asked to perform an cardiac examination on a patient with atrial fibrillation. What findings are you looking for?

A

Dont forget heart failure (kinda all the findings lol)
Vitals: maybe tachypneic
General inspection: Typically asymptomatic, maybe SOB
Closer Inspection: Peripheral cyanosis, peripheral oedema, raised JVP
Palpation: Peripheral/sacral oedema, parasternal heave
Percussion: Pulmonary oedema is hyporesonant
Auscultation: Mitral stenosis (cause), tricuspid regurg for HF

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10
Q

List the RFs of Atrial fibrillation

A

From the causes:
Modifiable:
Smoking
Alcohol
HTN
Glycaemic control (or diabetes)
Hyperthyroidism

Non-modifiable:
Male
Age
Hx of CAD/MI
Family hx
Diabetes (or glycemic control)
!Rheumatic heart disease

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11
Q

What leads are best for assessing the P waves?

A

V1 + inferior leads (II, III, aVF)

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12
Q

What ECG findings are consistent with A.fib

A

Irregularly irregular
Tachycardia
No P waves (instead, fibrillating waves in leads V1, II, III, aVF
Narrow QRS <80ms or 0.08s

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13
Q

What investigations will you perform for A.fib? always with justification

A

As for any arrhythmia: except ECG
Bedside:
ECG/!Holter monitor: Looking for tachycardic, irregularly, irregular, absent P waves/fibrillating waves narrow QRS <80ms + screen for previous MI, BBB, or LV hypertrophy
Urine dipstick (sepsis)
Urinalysis (evidence of CKD to guide management between DOAC and Warfarin) + Toxicology (sympathetomimetics)

Bloods:
FBC - Anaemia, infection, low platelets if DIC, infection, sepsis)
CRP - raised in infl. + inf.
U&E - Hypomagnesia + hyper/hypokalaemia + medications
TFTs - hyperthyroidism
Troponin + CKMB (ischaemia as a cause or result of arrhythmia)
BNP - HF in severe arrhythmia
HbA1c and Lipid profile (RFs)

Imaging:
CXR - sx of HF (ABCDE)
ECHO - TTE - atrial/ventricular size (LA enlargement/LV hypertrophy), RV systolic pressure, valvular involvement, pericardial disease - TOE - LA (appendage) thrombus, Rule out vegetations in IE

Procedure: Exercise stress test - helps identify ischaemia

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14
Q

In the management of A.fib, what is meant by recent onset A.fib

A

A.fib sx <48 hours

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15
Q

How would you determine if A.fib is valvular or not?

A

TOE ECHO

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16
Q

How is long term anticoagulation in A.fib decided on?

A

CHADs VASC

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17
Q

Run me through the CHADs VASc score

A
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18
Q

The management plan for A.fib is typically composed of 3 components: Rate control, rhythm control, and anticoagulation.

How would you choose which anticoagulant to give in recent onset vs not? Go through it all

A

If recent onset A.fib <48 hours -> Unfractionated heparin before cardioversion

Chronic
DOAC in all cases except CKD, valvular A.fib or prosthetic valve

2 strategies:
Conventional: 3 weeks DOAC before cardioversion, 4 weeks after, then based off of CHADS VASc

TOE strategy: TOE performed for LA (appendage) thrombus

If no LAA thrombus -> immediate unfractionated heparin before cardioversion (so we dont wait for a thrombus to pop up)

If LAA thrombus -> DOAC/warfarin for 3 weeks -> Check again. If gone, immediate heparin and cardioversion (likke before). If still present, Long term anticoagulation based off of CHADS VASc

19
Q

The management plan for A.fib is typically composed of 3 components: Rate control, rhythm control, and anticoagulation.

How will you manage rate control acutely?

A

acute => A.fib sx <48 hours => recent onset A.fib

If no other disease, HTN, or HFpEF: Beta blocker -> CCB -> Amiodarone

If LV dysfunction/HF: Beta blocker (metoprolol not bisop) -> Digoxin-> Amiodarone

If COPD: CCB (non-dihydro like the rest)

20
Q

What medication regime is required alongside DC cardioversion in any case? be very specific (not doses tho)

A

Anticoagulation with Unfractionated heparin in the acute case
DOAC 3 weeks before and 4 weeks after
Warfarin 3 weeks before and 4 weeks after if CKD or valvular A.fib

+

Sedation with Midazolam or Propafol
Anaglesia with Morphine or Fentanyl

+/- Amiodarone as an adjunct up to 1 year post-cardioversion

21
Q

In the management of A.fib, what are the indications for DC cardioversion

A

1) Haemodynamically unstable patient
2) Recent onset A.fib <48 hours
3) Anticoagulation for 3 weeks prior + TOE shows no signs of thrombus

22
Q

Why can cardioversion just be done acutely without the need to perform an ECHO, or 3 weeks of anticoagulation ahead of time etc…

A

in recent onset A.fib, there is not enough time for a thrombus to form and hence the risk of VTE is relatively small

23
Q

A patient presents to you and is not haemodynamically stable. The consultant asks you to prepare them for DC cardioversion. You know that you need to give them an anticoagulant. What anticoagulant are you giving them? when are you giving it?

A

Unfractionated heparin immediately before

24
Q

The pill in the pocket approach is given to patients with A.fib for rate control. What medications would be given in this case?

The pill in the pocket approach requires evidence of no structural heart disease. How will you know?

A

Class 1c antiarrhythmetics (slow ass/dissociation)
=> Flecainide or Propafenone

ECHO

25
Q

The management plan for A.fib is typically composed of 3 components: Rate control, rhythm control, and anticoagulation.

How will you manage Rhythm control acutely?

A

acute => A.fib sx <48 hours
=> emergency => ABCDE call for help
First check if the patient is haemodynamically stable
If not -> Immediate unfractionated heparin -> Cardioversion

If haemodynamically stable, the patient and physician will decide if they would prefer electrical or pharmacological management.

For electrical it is an elective cardioversion but needs 3 weeks DOAC/Warfarin

For pharmacological: Based on evidence of structural heart disease from ECHO:

If none: Pill in pocket Class Ic (Flecainide, Propafenone) -> IV Ic, or III (Ibutilide, Vernakalant) -> IV amiodarone (class III)

If moderate structural heart disease: IV class III (Ibutilide, Vernakalant) -> IV amiodarone

If severe -> IV amiodarone

Notice how each just removes the initial step

26
Q

The management plan for A.fib is typically composed of 3 components: Rate control, rhythm control, and anticoagulation.

How would you manage rate control in a chronic setting such as OPD?

A

Beta blocker -> CCB if contra indicated
As always non-dihydro CCB

27
Q

The management plan for A.fib is typically composed of 3 components: Rate control, rhythm control, and anticoagulation.

How would you manage rhythm control chronically?

A

You dont, once it has been over 12 months, rhythm control is ceased and focus becomes on anticoagulation

28
Q

In a refractory case where all else has failed in the long term management of A.fib. What surgical options remain?

A

Radiofrequency ablation
Maze procedure

(not in the acute setting)

29
Q

What is a Maze procedure?

A

Incisions or ablations in the atria forming a maze to disrupt abnormal electrical activity that may cause A.fib

Note: Mini-Maze also exists where radiofrequency or cryoablation is used hence bypassing the need for open heart surgery

30
Q

A patient is on their way by ambulance complaining of palpitations that started 15 hours ago and hasnt stopped/. Paramedics say the ECG is showing tachycardia, no P waves, fibrillation waves, and a narrow QRS. What your full management approach?

A

acute => A.fib sx <48 hours => recent onset A.fib

Rate control:
If no other disease, HTN, or HFpEF: Beta blocker -> CCB -> Amiodarone

If LV dysfunction/HF: Beta blocker (metoprolol not bisop) -> Digoxin-> Amiodarone

If COPD: CCB (non-dihydro like the rest)

Rhythm control:
First check if the patient is haemodynamically stable
If not -> Immediate unfractionated heparin -> Cardioversion

If haemodynamically stable, the patient and physician will decide if they would prefer electrical or pharmacological management.

For electrical it is an elective cardioversion but needs 3 weeks DOAC/Warfarin

For pharmacological: Based on evidence of structural heart disease from ECHO:

If none: Pill in pocket Class Ic (Flecainide, Propafenone) -> IV Ic, or III (Ibutilide, Vernakalant) -> IV amiodarone (class III)

If moderate structural heart disease: IV class III (Ibutilide, Vernakalant) -> IV amiodarone

If severe -> IV amiodarone

Anticoagulation:
In the acute setting it is just unfractionated heparin prior to cardioversion if present

31
Q

A patient presents to the OPD after being referred by her GP complaining of palpitations for the past year and an ECG showing tachycardia, no P waves, fibrillation waves, and a narrow QRS. Records show that she has been admitted after 3 episodes of syncope due to this yet has not resolved. What will you prescribe to this patient

A

This is a chronic case with permanent A.fib that hasnt resolved on previous admissions where it can be assumed cardioversion was administered or given. In simple terms, acute is <48 hrs and chronic is >48 hours yet in a discussion know that the following treatment is given once the decision has been made to stop rhythm control. If there is still rhythm control indicated then treat as acute elective route (based on structural heart disease on ECHO)

Lifestyle:
Referral to dietician for weight loss, reduced cholesterol and salt intake for HTN
Smoking cessation: Quit.ie, Patient education, NRT, Varenicline and Bupropion
Reduce alcohol intake to 14U, education, patient support groups (AA), Disulfiram, Acamprosate
Physiotherapy for exercise and rehabilitation
Strict BP and glycaemic contro

Rate control:
Beta blocker -> CCB if contra indicated
As always non-dihydro CCB

Anticoagulation:
DOAC in all cases except CKD, valvular A.fib or prosthetic valve

2 strategies:
Conventional: 3 weeks DOAC before cardioversion, 4 weeks after, then based off of CHADS VASc

TOE strategy: TOE performed for LA (appendage) thrombus

If no LAA thrombus -> immediate unfractionated heparin before cardioversion (so we dont wait for a thrombus to pop up)

If LAA thrombus -> DOAC/warfarin for 3 weeks -> Check again. If gone, immediate heparin and cardioversion (likke before). If still present, Long term anticoagulation based off of CHADS VASc

Surgical:
Radiofrequency ablation
Maze procedure

32
Q

A patient is on their way by ambulance complaining of palpitations that started 15 hours ago and hasnt stopped/. Paramedics say the ECG is showing tachycardia, no P waves, fibrillation waves, and a wide QRS >120ms. Why might they have a wide QRS?

A

Just like in SVT that would indicate there is also a BBB or WPW.

Recall range of QRS is 80-100 but some sources say 60-120

33
Q

What are the complications of Atrial Fibrillation?

A

1) Thromboembolic: Stroke/TIA, mesenteric ischaemia, critical limb ischaemia, PE…
2) HF
3) Dilated cardiomyopathy
4) Bradycardia and hypotension (meds)
5) Death

34
Q

What is Virchow’s Triad?

A

Virchows triad:
3 primary factors cause thrombus formation
1) Endothelial injury
2) stasis of blood flow
3) hypercoagulability

35
Q

What is the typical rate of atrial depolarisation in Atrial flutter

A

around 300 (240-340)

36
Q

If atrial fibrillation is irregularly irregular, what is Atrial flutter?

A

Regularly irregular

37
Q

The etiology of Atrial flutter is similar to A.fib but what is interesting to note is that atrial flutter is very uncommon in a structurally normal heart. Define Atrial Flutter

A

Arrhythmia characterised by rapid, !!!regular atrial depolarisations at about 300bpm and a regular ventricular rate due to X:1 conduction

38
Q

You are asked to perform an ECG on a patient with palpitations. What findings would be consistent with with atrial flutter

A

Atrial rate about 300 in a sawtooth pattern
P waves absent
Narrow complex <0.8
X:1 conduction across AV node

39
Q

Atrial flutter is often described as X:1 sawtooth pattern. What are the most common values for X

A

Even>Odd
=> 2:1, 4:1, 3:1, 5:1

40
Q

What is the sawtooth pattern actually?

A

Flutter waves (get it?)
Its the same thing as in atrial fibrillation, p waves are replaced with fibrillation waves

41
Q

When performing an ECG for any arrhythmia, you are typically looking for the specific findings related to common diagnoses such as A.fib and atrial flutter, or something like SVT or VT. What are some other things to look for that are relevant in any arrhythmia? (give the specific ECG findings for each think you’re looking to screen for)

A

Previous MI: Pathological Q waves in the affected leads indicates necrotic tissue

LV hypertrophy:
Prolonged P waves in I
Tall R waves in II
Left axis deviation

Bundle Branch Block: WILLIAM MARROW in V1 and V6 (explains widened QRS in arrhythmias)

42
Q

The investigations for Atrial flutter are the same as that for A.fib except the specific ECG findings. What is the full management algorithm for Atrial flutter?

A

Same principles as A.fib

Rate control: Beta blocker (Class II) -> Non-dihydro CCB (IV)

Anticoagulation: same principle as A.fib. DOAC in all cases except CKD, valvular A.fib or prosthetic valve

!!Anticoagulation must be started 3 weeks prior to rhythm control
+ TOE to rule out LA (appendage) thrombus

Rhythm control:
Due to the high rate of recurrence in A.flutter, it is preferrable to perform surgical tx first
1) Radiofrequency catheter ablation
2) Class III - Amiodarone, Sotalol
3) Class Ic - Flecainide/Propafenone

43
Q

A good question to ask to patients who are obese and CVD history is whether they use a CPAP at night. What factors lead to the formation of a thrombus in cardiovascular disease?

A

Thrombus => based on Virchow’s Triad
1) Endothelial injury (post-MI)
2) Stasis (Wall motion abnormality post-MI)/Turbulent flow (A.Fib)
3) +/- Hypercoagulability (whether genetic or medication induced or from RF of CVD)

Ch. 1 - Cardiology (13 decks)

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