Arrhythmia and AF Flashcards

1
Q

When is external cardiac pacing used in patients with symptomatic Bradycardia?

A

When Atropine fails to increase the patient’s heart rate

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2
Q

What are some adverse signs associated with symptomatic Bradycardia?

A

Shock, syncope, myocardial ischaemia, heart failure

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3
Q

What is Bradycardia defined as?

A

< 60 bpm

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4
Q

What do the QRS complexes appear like in VT and SVT?

A
VT = Broad complexes
SVT = Narrow complexes
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5
Q

What is Tachycardia defined as?

A

> 100 bpm

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6
Q

A patient with broad complex tachycardia is unstable, what is the first line treatment option?

A

Cardioversion

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7
Q

A patient with broad complex tachycardia is stable, what is the first line treatment option?

A

Amiodarone, then Lidocaine, then Procaindamide

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8
Q

A patient with narrow complex tachycardia is unstable, what is the first line treatment option?

A

Cardioversion

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9
Q

A patient with narrow complex tachycardia is stable, what is the first line treatment option?

A

Valsalva manoeuvre, if this fails, then Adenosine 6mg, if this fails then Adenosine 12 mg

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10
Q

What are the three ECG changes associated with Atrial Fibrillation?

A
  • Absent p waves
  • Presence of fibrillatory waves
  • Irregularly irregular QRS complexes
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11
Q

What is the best way to diagnose Paroxysmal AF?

A

Holter monitoring

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12
Q

Strokes from AF commonly form where?

A

In left atria appendage

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13
Q

Patients with AF have a _ fold increased risk of stroke

A

Five-fold risk

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14
Q

What is the HASBLED tool used for?

A

To assess the 1-year risk of major bleeding in AF patients taking anticoagulants

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15
Q

Discuss the points of HASBLED screening tool? How many points is for each component?

A
H - Hypertension (1)
A - Abnormal renal / liver function (1/2)
S - Stroke (1)
B - Bleeding (1)
L - Labile INR (1)
E - Elderly >65 (1)
D - Alcohol / drugs (1/2)

Maximum score is 9. >3 is a high risk of bleeding

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16
Q

What is the CHADSVASc tool used for?

A

Used to assess risk of stroke in AF patients

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17
Q

Discuss the points of CHADSVSc screening tool. How many is for each component?

A
C - Congestive Heart Failure (1)
H - Hypertension (1)
A - Age 65-74, >75 (1/2)
D - Diabetes (1)
S - Stroke / TIA (2)
V - Vascular Disease i.e. MI (1)
S - Sex i.e. Female (1)

If >2, Offer coagulation

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18
Q

What is Paroxysmal, Persistent and Permanent AF?

A
Paroxysmal = < 7 days long
Persistent = > 7 days, not self-terminating
Permanent = > 7 days, resistant to therapy
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19
Q

If a male patient and a female patient had a CHADSVASc score of 1, how does this guide treatment options?

A

Males - Consider anticoagulation

Females - Do not consider until score is 2

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20
Q

Why are patients cardioverted if symptoms are less than 48 hours, and if longer, why must they be anticoagulated?

A

When switching from AF to sinus rhythm, this is the most likely point at which a thrombus can cause a stroke. Symptoms must therefore be present <48 hours or patients must be anti-coagulated for a long period of time

21
Q

What is the first-line treatment for symptomatic Bradycardia with adverse signs?

A

Atropine 500 mcg IV, up to 6 administrations every 3-5mins to a maximum of 3mg

22
Q

What is the definition of 1st degree heart block?

A

Fixed PR internal >0.2s

23
Q

What is the definition of 2nd degree, Mobitz Type 1 (Wenklebach) heart block?

A

Progressively prolonged PR interval, with a dropped QRS complex

24
Q

What is the definition of 2nd degree, Mobitz Type 2 heart block?

A

Fixed PR internal, with a dropped QRS complex

25
Q

What is the definition of 3rd degree heart block?

A

When p waves and QRS complex are unrelated

26
Q

Where is the conduction pathology in patients with Type 1 heart block?

A

Between the SAN and AVN (in the atria)

27
Q

Where is the conduction pathology in patients with Type 2 Mobitz Type 1 heart block?

A

Occurs in the AVN

28
Q

Where is the conduction pathology in patients with Type 2 Mobitz Type 2 heart block?

A

After the AVN, at the level of the bundle of His

29
Q

Where is the conduction pathology in patients with Type 3 heart block?

A

Anywhere after the AVN

30
Q

Long QT syndrome is believed to be caused by dysfunction of which channels?

A

L-type Calcium channels

31
Q

What are the two treatments for Long QT syndrome?

A

Beta blockers

Implantable cardioverter defibrillators

32
Q

What medications can cause Long QT syndrome?

A

Class Ia anti-arrhythmics
Class III anti-arrhythmics: Sotalol, Amiodarone
TCAs, SSRIs (Citalopram)
Methadone, Chloroquine, Erythromycin, Haloperidol, Ondansetron

33
Q

What are five causes of Atrial Fibrillation?

A
SMITH mnemonic
S - Sepsis
M - Mitral valve pathology (stenosis, regurgitation)
I - Ischaemic Heart Disease
T - Thyrotoxicosis
H - Hypertension
34
Q

In patients with Atrial Fibrillation, how do you decide between rate and rhythm control?

A

Choose rate control UNLESS:

  • Patient has first event of AF
  • There is a clear reversible cause
  • They have HF caused by AF
  • They are symptomatic

Chose rate control especially:

  • When they are above 65 years old
  • Have Ischaemic Heart Disease
35
Q

What are the medication options of rate control when managing patients with Atrial Fibrillation?

A
  1. Beta blockers (Contraindicated with asthmatics)
  2. CCBs i.e. Diltiazem or Verapamil
  3. Digoxin - only those with heart failure
36
Q

Outline the two ways patients can be treated by rhythm control if they have Atrial Fibrillation?

A
  1. Pharmacological cardioversion
  2. Electrical cardioversion

Can be immediate, or delayed

37
Q
  1. How do you decide whether to rhythm control someone immediately or delayed?
  2. What other treatments must be provided alongside delayed cardioversion?
  3. How might you pharmacologically cardiovert a patient with Atrial Fibrillation?
A
    • If hemodynamically unstable, then IMMEDIATE CARDIOVERSION
  • If symptoms less than 48 hours, then iMMEDIATE CARDIOVERSION
  • If symptoms greater than 48 hours and hemodynamically stable, then DELAYED CARDIOVERSION
    2. If having delayed cardioversion, must be anticoagulated for at least 3 weeks prior and 4 weeks after, OR can have a TOE to exclude a L atrial appendage, heparinised and cardioverted immediately
    3. Amiodarone if structural heart disease, Flecainide or Amiodarone if no structural heart disease
38
Q

What are the two basic principles of management of a patient with Atrial Fibrillation?

A
  1. Rate vs rhythm control

2. Anticoagulation

39
Q
  1. What tool is used to assess whether an AF patient needs to be anticoagulated?
  2. What medications are used for anticoagulation?
  3. When do patients with AF + stroke start anticoagulation?
A
  1. CHA2DS2VS
  2. Warfarin or DOACs
  3. 2 weeks after stroke
40
Q

Amiodarone:

  1. What class anti-arrhythmic agent is it?
  2. What is the mechanism of action?
  3. What is the half life?
  4. Why must it be given by a central vein?
  5. What syndrome can cause it?
  6. Is it a P450 Inhibitor or inducer?
  7. What are some adverse effects?
  8. What is the initial and later monitoring of Amiodarone?
A
  1. Class III, some Class I action
  2. Potassium channel blocker
  3. Long half life, 20-100 days
  4. Causes thrombophlebitis
  5. Long QT syndrome
  6. P450 Inhibitor
  7. Hypo/hyperthyroidism, grey appearance, corneal deposits, pulmonary fibrosis, liver fibrosis thrombophlebitis, bradycardia, long QT
  8. Initially: CXR, U&E, LFTs, TFTs, later TFTs and LFTs every 6 months
41
Q
  1. What is Atrial Flutter?
  2. What is the main ECG finding?
  3. What is the underlying atrial rate?
  4. If the ventricular rate in AFlutter is 2:1, what is the rate?
  5. What is the management of Atrial Flutter?
A
  1. A type of supraventricular tachycardia, characterised by rapid atrial depolarisation
  2. Sawtooth baseline
  3. 300 bpm
  4. 150 bpm
  5. Similar to AFib, however medications are less effective and cardioversion is more effective. Radiofrequency ablation of tricuspid valve isthmus is curative
42
Q

ADAM-STOKES ATTACK

  1. What is it?
A
  1. Periodic fainting spell, with intermittent complete heart block. Causes loss of spontaneous circulation and poor flow to brain
43
Q

BRUGADA SYNDROME

  1. What is it?
  2. What is the inheritance pattern?
  3. What ethnicity is it more common in?
  4. What are the ECG findings?
  5. What is the investigation?
  6. What is the management?
A
  1. An inherited cardiovascular disease of sudden cardiac death
  2. Autosomal dominant
  3. More common in Asians
  4. Partial RBBB, ST elevation and negative T wave in V1-3
  5. Ajmaline or Flecainide - ECG changes become more apparent
  6. Implantable cardioverter defibrillator
44
Q

LONG QT SYNDROME

  1. What drugs cause Long QT Syndrome?
  2. What are other causes of Long QT Syndrome?
  3. What is a complication of Long QT Syndrome?
  4. How do you manage Long QT Syndrome?
A
  1. Amiodarone, Sotalol, TCAs i.e. Citalopram, Escitalopram, Methadone, Chloroquine, Erythromycin, Haloperidol, Ondansteron
  2. Hypocalcaemia, hypomagnesemia, hypokalaemia, hypothermia, acute MI, SAH
  3. Torsades de Pointes
  4. Avoid offending drug, beta-blockers and in severe cases an implantable cardioverter
45
Q

TORSADES DE POINTES

  1. What is the management of Torsades de Pointes?
A
  1. Magnesium Sulphate
46
Q

WOLFF-PARKINSON WHITE

  1. What is it?
  2. What are the ECG features?
  3. What is the definitive management?
  4. What are other forms of management?
A
  1. A congenital accessory conduction pathway between the atria and the ventricle
  2. Widened QRS complexes with a slurred upstroke “delta wave”, short PR interval. Can also get LAD and RAD
  3. Radiofrequency ablation of pathway
  4. Sotalol
47
Q

HOCM

  1. What is HOCM?
  2. What is the inheritance pattern?
  3. What type of heart failure does it cause?
  4. What murmur is associated with HOCM?
  5. What makes the HOCM murmur quieter?
  6. What makes the HOCM murmur louder?
  7. What are findings on the Echo? MR SAM ASH
  8. What are findings on ECG?
  9. What is the management of HOCM?
A
  1. The most common cause of sudden cardiac death
  2. Autosomal dominant
  3. Diastolic dysfunction
  4. Ejection systolic, crescendo-decrescendo murmur
  5. Squatting, handgrip manoeuver
  6. Standing up, valsalva
  7. Mitral regurgitation, Systolic anterior motion (of mitral valve) and asymmetric hypertrophy
  8. LVH
  9. ABCDE (Amiodarone, Beta blockers, cardioverter defibrillator, dual chamber pacemaker and endocarditis prophylaxis
48
Q

SUPRAVENTRICULAR TACHYCARDIA

  1. What is SVT also known as?
  2. How is it defined on an ECG?
  3. If a patient has SVT and adverse signs, how do you treat?
  4. If a patient has SVT and no adverse signs, how do you treat?
  5. What is the half-life of adenosine?
  6. What are SEs to warn patients of for adenosine?
  7. Adenosine is contraindicated in which patients? What is an alternative?
  8. How should Adenosine be given?
A
  1. Narrow Complex Tachycardia
  2. ECG rate >100 bpm, with a QRS <0.12s (3 small squares)
  3. DC Cardioversion
  4. Vagal manoeuvres, followed by Adenosine 6mg, Adenosine 12mg, Adenosine 12mg
  5. 10 seconds
  6. Flushing
  7. Asthmatics, give Verapamil instead
  8. Via a wide-bore cannula due to short half-life
49
Q

BROAD COMPLEX TACHYCARDIA

  1. How is BCT defined on an ECG?
  2. If a patient has BCT and adverse signs, how do you treat?
  3. What electrolyte abnormalities can cause Broad Complex Tachycardia?
  4. If a patient has BCT and no adverse signs, how do you treat?
  5. How is this medication administered?
  6. What are other options?
  7. What medication is absolutely contraindicated in Broad Complex Tachycadia?
  8. If a patient has Pulseless VT or VF, how do you initially manage them?
A
  1. ECG rate >100 bpm, with a QRS >0.12s (3 small squares)
  2. DC Cardioversion
  3. Hypokalaemia, hypocalcaemia, hypomagnesemia
  4. 300mg Amiodarone IV
  5. Via a central line
  6. Procainamide, Lignocaine
  7. Verapamil
  8. 1 shock + 2mins of CPR, or if witnessed and monitored already, then 3 shocks. Only after 3 shocks can you give 1mg adrenaline and 300mg Amiodarone