Cardiology: Cardiac Arrhythmias - Atrial flutter & AF I Flashcards
What are cardiac causes of syncope? [+]
Cardiac causes of syncope:
- Hypertrophic cardiomyopathy (HCM)
- Cardiac tampondade
- Pericardial disease
- PE
- MI
- Valvular abnormalities
- Dialted cardiomyopathy
- Aortic dissection
- Myotonic and muscular dystrophies.
- CAD
- Long QT syndrome
Cardiac syncope occurs when the source of one’s loss of consciousness stems from a problem in the heart that prevents it from supplying enough nutrients and oxygen to the brain
What is vasovagal syncope? [1]
What is it caused by? [4]
Vasovagal Syncope:
- emotional or environmental trigger (e.g. prolonged standing, fasting, dehydration) causes an activation of the PNS
- Activation of the PNS causes vasovagal reaction: bradycardia and vasodilation
- Causes a drop in BP and reduction in blood supply to brain
- Cerebral hypoperfusion and LOC
How can you differentate between cardiac and vaso-vagal syncope?
Cardiac syncope:
- preceded by exertional chest pain
- occurring during exercise or stress
- concerning cardiac history
- no prodrome
- event requiring CPR,
- abnormal physical
examination
Vasovagal syncope
- Prodromal symptoms:
- Hot or clammy
- Sweaty
- Heavy
- Dizzy or lightheaded
- Vision going blurry or dark
- Headache
What are important areas to cover in a history when someone says they’ve fainted? [4]
Precipitant/trigger:
- if situational, ask if the trigger consistently causes syncope
Warning symptoms:
- classic pre-syncopal symptoms of nausea, sweating, feeling faint
Position:
- vasovagal syncope usually happens when standing
Underlying cardiac disease?
What are key history areas for arrhythmic and structural syncope? [8]
- Palpitations
- Other cardiac symptoms (e.g. chest pain, breathlessness, oedema)
- No prodromal warning (unlike in reflex and orthostatic syncope, where there are clear pre-syncopal symptoms)
- Onset when sitting or lying down
- Onset with exercise (clarify if it is after or during exercise)
- Presence of any previous heart disease including myocardial infarctions, surgeries, and any cardiac device details (pacemakers and ICDs)
- Drug history
- Family history of sudden cardiac death
How do you manage a patient with (primary) tachycardia who is haemodynamically unstable? [+]
Assess using ABCDE
- Monitor SpO2 and give oxygen if hypoxic
- Monitor ECG and BP
- Obtain IV access
- ID and treat reversible cause (if possible)
If there are adverse features (e.g. shock, syncope, MI, HF) AND the heart is unstable:
- Deliver synchronised DC shock up to 3 times
When assessing tachycardia, if you ID that there are no adverse features, what is the next thing you are should assess? [1]
If the QRS is narrow (< 0.12s)
Describe what determines the width of the QRS complex [1]
Normal cardiac conduction uses His-purkinje system to allow R & L ventricle to depolarise within 120ms: narrow QRS complex
What does a narrow QRS complex tachycardia mean with regards to physiology? [1]
Narrow QRS complex tachycardia implies that ventricles are activated via a normal conduction system, therefore the mechansim of the tachycardia is supra ventricular.
On a normal 25 mm/sec ECG, 0.12 seconds equals [] small squares.
On a normal 25 mm/sec ECG, 0.12 seconds equals 3 small squares.
go through lectures and go through ecgs
What are the three reasons for supra-ventricular tachycardia? [4]
Atrial flutter & atrial fibrillation
AVNodal reentrant tachycardia
AV reentrant tachycardia
Describe the pathophysiology of atrial flutter [4]
Counter clockwise circuit of electrical activity goes through the right atrium due to an extra electrical pathway. Signal goes around without interruption
The signal does not usually enter the ventricles on every lap due to the long refractory period of the atrioventricular node.
Get 2:1 ratio of atrial to ventricular contractions. Usually causes atrial rate to be usually around 300 beats per minute; and the ventricles to be 150 bpm
There can be 3:1 or 4:1 or variable conduction ratios
Explain the different clinical features of atrial flutter [5]
Haemodynamic Manifestations:
- Loss of co-ordinated atrial contractions causes reduced ventricular filling and reduced CO
- Causes dyspnea; fatigue; lightheadedness; syncope
Palpitations
Chest pain
- Due to increased myocardial oxygen demand secondary to rapid ventricular rates or decreased diastolic filling time causing subendocardial ischaemia
Heart Failure Symptoms
- May get tachycardia induced cardiomyopathy
- Orthopnea; paroxysmal nocturnal dyspnea, and peripheral oedema
Thromboembolic Complications:
- predisposes patients to thrombus formation
How do you investigate for atrial flutter? [1]
ECG: Flutter waves (saw toothed morphology) with atrial rate 250/300 bpm
Describe the first line treatment algorithm for a patient with acute atrial flutter who is haemodynamically stable? [3]
What is the long term anticoagulation used? [2]
Primary option: Use an atrioventricular nodal blocking drug for rate control:
Beta blocker:
- Bisoprolol or others
OR
Non-dihydropyridine calcium-channel blockers:
- Verapamil
- Diltiazem
Secondary options:
- Digoxin
may convert atrial flutter to atrial fibrillation, which can be easier to manage.
CONSIDER:
Initial anticoagulation:
- heparin
or
- enoxaparin
Long term anticoagulation:
- 1st: apixaban or ther DOAC
- 2nd: warfarin
BMJ BP
Describe the second [1] and third line [2] treatment algorithm for a patient with acute atrial flutter who is haemodynamically stable?
2nd line:
- elective electrical cardioversion
3rd line: pharmacological cardioversion
- flecainide
OR
- amiodarone
Describe the treament regime for chronic / recurrent atrial flutter [5]
1st line:
- Catheter ablation
- Long term anticoagulation strategy (see previos)
2nd lines:
- Long term rate control
- Long term anticoagulation therapy
- Long-term anti-arrhythmic therapy
Describe the pathophysiology of atrial fibrillation [3]
- Myocytes in the atria contract largely independently of each other and in an unsynchronised pattern, leading to the macroscopic appearance of ‘fibrillation’
- This disrupts the electrical activity of the atria, with multiple groups of myocytes depolarising independently of the SAN and each other
- This results in an irregularly irregular ventricular contraction.
Permenant AF
An elderly patient with a history of atrial fibrillation presents with a sudden painless loss of vision in one eye. Fundoscopy reveals a ‘cherry red’ spot on a pale retina is a stereotypical history of:
occlusion of central retinal artery
What is the cause of the cherry red spot? [1]
It is most frequently caused by emboli obstructing the retinal artery (e.g. stroke). Occasionally, it can be caused by vasculitis (e.g. giant cell arteritis).
Classical appearance is of a “cherry-red spot”. This occurs due to the intact reflex of the fovea standing out against a pale, ischaemic retina.
No anticoagulation:
CHA2DS2-VASc of 1 (female)
CHA2DS2-VASc of 0
First time atrial fibrillation
What change in JVP wave is associated with AF? [1]
Absent a wave
‘a’ wave = atrial contraction
Mesenteric ischaemia
According to NICE guidelines, what is the target international normalized ratio (INR) range for patients on warfarin therapy for atrial fibrillation?
A. 1.0-2.0
B. 2.0-3.0
C. 3.0-4.0
D. 4.0-5.0
According to NICE guidelines, what is the target international normalized ratio (INR) range for patients on warfarin therapy for atrial fibrillation?
A. 1.0-2.0
B. 2.0-3.0
C. 3.0-4.0
D. 4.0-5.0
According to NICE, what is the recommended anticoagulant therapy for patients with non-valvular atrial fibrillation and a CHA2DS2-VASc score of 2 or more?
A. Aspirin
B. Warfarin
C. Dabigatran
D. Clopidogrel
According to NICE, what is the recommended anticoagulant therapy for patients with non-valvular atrial fibrillation and a CHA2DS2-VASc score of 2 or more?
A. Aspirin
B. Warfarin
C. Dabigatran
D. Clopidogrel
