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My MRCP > Arrhythmia > Flashcards

Arrhythmia Flashcards

1
Q

Cardiac causes [6]

A

Ischemic heart disease
Structural changes
Cardiomyopathy
Pericarditis
Myocarditis
Aberrant conduction pathways (WPW syndrome)

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2
Q

Non cardiac causes [5]

A

Electrolyte imbalance
Metabolic - hypoxia/acidosis/thyroid
Caffeine, Smoking, Alcohol
Pneumonia, phaeochromocytoma
Drugs

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3
Q

Drugs that cause arrhythmia [5]

A

Levodopa
Digoxin
Beta 2 agonists (asthma drugs)
Tricyclic antidepressants
Doxorubicin

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4
Q

Presentation [7]

A

Palpitations
Dyspnoea
Chest pain
Fatigue
syncope/presyncope
Pulmonary oedema
Can be asymptomatic

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5
Q

Initial mx of arrhythmias [6]

A

ABCDE
Oxygen
Gain IV access
12 lead ECG
Correct metabolic abnormalities
Classify patient as stable or unstable

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6
Q

What is a sinus arrhythmia? [3]

Management?

A

Normal conduction at faster frequency
HR increases inspiration
Decreases expiration

No Rx needed

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7
Q

Causes of sinus arrhythmia [7]

A

Infection, fever
dehydration, hypovolaemia
pain / exercise
drugs, salbutamol
adrenaline
PE
hypothyroid
MI

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8
Q

Categorisation of tachyarrhythmias

A

Supraventricular - narrow complex
Ventricular - broad complex
Sinus tachycardia

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9
Q

Features suggesting VT rather than SVT with aberrant conduction

A

AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms

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10
Q

What is a narrow complex tachycardia and why? [4]

A

> 100BPM
QRS <120
Short P wave
Ventricles depolarised via normal pathway so QRS normal

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11
Q

Types of regular narrow complex tachycardias [5]

A

Regular
* Sinus tachycardia
* Atrial tachycardia (unifocal)
* Atrial flutter
* AV re-entry tachycardia (WPW pattern)
* AV nodal re-entrant tachycardia (AVNRT)

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12
Q

Multifocal atrial tachycardia

Definition? Demographic it is more common in

A

Multifocal atrial tachycardia (MAT) may be defined as a irregular cardiac rhythm caused by at least three different sites in the atria, which may be demonstrated by morphologically distinctive P waves. It is more common in elderly patients with chronic lung disease, for example COPD

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13
Q

How is multifocal atrial tachycardia managed?

A

correction of hypoxia and electrolyte disturbances
rate-limiting calcium channel blockers are often used first-line
cardioversion and digoxin are not useful in the management of MAT

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14
Q

What is WPW [2]

ECG [2]

A

AV re-entrant tachycardia - another pathway through atrial and ventricle not AV node
Complications: AF, VF
ECG:
- short PR interval
- wide QRS complexes with a slurred upstroke - ‘delta wave’

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15
Q

What causes irregular narrow complex [3]

A

Irregular NCT
* AF
* Atrial flutter with irregular block
* Multifocal atrial tachycardia

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16
Q

What is associated with WPW [4]

A

HOCM
Mitral valve prolapse
Ebstein
Thyrotoxicosis

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17
Q

APs can be left-sided or right-sided, and ECG features will vary depending on this:

Describe ECG features in Type A vs Type B

A

Left-sided AP: produces a positive delta wave in all precordial leads, with R/S > 1 in V1. Sometimes referred to as a type A WPW pattern
Right-sided AP: produces a negative delta wave in leads V1 and V2. Sometimes referred to as a type B WPW pattern

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18
Q

Localisation of the aberrant accessory pathway in AVRT

A

The closer the accesory pathway is to the sinoatrial node or site of atrial ectopy, the greater the degree of pre-excitation.

Pathway originating from right free wall
* shortened PR interval
* broader QRS

Pathway originating from left free wall
* more normal ECG

19
Q

Orthodromic vs Antidromic AVRT

A

Orthodromic
* Atrial ectopic beat is propagated in usual anterograde fashion, then retrograde conduction occurs along aberrant accessory pathway.

Antidromic
* If ventricular ectopic is propagated in a retrograde fashion via myocardial cells not usual conduction system, this results in a boarder QRS - this may resemble VT.

20
Q

Management of AVRT and AVNRT are similar

A

AVNRT
* Paroxysmal AVNRT - transient AV node blockade using verapamil, BB, verapamil. These induce block along slow pathway.
* Infrequent symptoms but clear onset, prescribe PRN flecainide.
* Definitive mx includes catheter ablation of the slow pathway.

21
Q

Pathophysiology in AVNRT

A

AV NODAL re-entry
* Congenital abnormality where AVN has dual physiology - fast and slow circuits.
* Premature atrial complex occurs when fast pathway is in refractory mode > so the electricity is conducted on slow pathway. Once the electricity goes along two pathways this creates a re-entry circuit.

Remember the major difference in AVRT vs AVNRT is
AVRT = WPW and is caused by a congenital ‘aberrant’ accessory pathway connecting atria and ventricles, NOT through the AV node.

22
Q

In narrow complex tachycardias, what can you use instead of adenosine if contraindicated?

A

Adenosine is contraindicated in asthma
Another option is to use verapamil which slows AV nodal conduction

23
Q

Management of supraventricular tachycardias

A

Acute management
1. vagal manoeuvres:
Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
carotid sinus massage
2. intravenous adenosine
rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
3. electrical cardioversion

Prevention of episodes
* beta-blockers
* radio-frequency ablation

24
Q

What is the Valsalva manoeuvre [5]

A 
Forced expiration against closed glottis
Increases intrathoracic pressure
Reduced venous return due to increased atrial pressure
Reduced preload 
Reduced CO
25
Q

Atrial flutter [4]

A
  • characterised by a succession of rapid atrial depolarisation waves.
  • ECG: sawtooth appearance
  • as the underlying atrial rate is often around 300/min
  • the ventricular or heart rate is dependent on the degree of AV block.
    For example if there is 2:1 block the ventricular rate will be 150/min
26
Q

Atrial flutter management [2]

A
  • cardioversion

- radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

27
Q

Atrial fibrillation pathophysiology [3]

Types [3]

A
  1. SA node isn’t firing properly = disorganised signal
  2. Other sites as well as SA node initiate conduction
  3. CO drops as ventricles not primed reliably leading to HF / increased risk of stroke
    Paroxysmal - <7 days and self terminate
    Persistent
    Permanent - resistant to Rx
28
Q

What are cardiac causes of AF: valvular [1] and non-valvular [9]

A

Valvular = MS / prosthetic heart valve issue

Non-valvular
* Ischaemia = most common UK
* Rheumatic = common world wide
* HF
* Hypertension
* IHD
* Cardiomyopathy
* Myocarditis
* Endocarditis
* Surgery

29
Q

What are non-cardiac causes [8]

A 
Sepsis
PE, Bleed 
Pneumonia
Hyperthyroid
Alcohol, Caffiene, Drugs
Post op
Metabolic: Low K / Mg / Ca, Acidosis
30
Q

Most common causes of AF (SMITH)

A

SMITH
Sepsis
Mitral valve - S or R
IHD
Thyrotoxicosis
Hypertension

31
Q

Aetiology Bradycardia

split into extrinsic or intrinsic

A

Intrinsic
* Idiopathic degeneration - ageing
* Infiltrative disease - sarcoidosis, amyloidosis
* Infectious - endocarditis
* Autoimmune - SLE, RA, scleroderma
* Trauma - valve replacement
Extrinsic
* Increased vagal tone from Vasovagal syncope ir exercise training
* Electrolyte imbalancce - hypo/hyperkaelemia, hyponatremia
* Metabolic - hypothyroidism, hypothermia
* Neurological - raised ICP

32
Q

What is the complication in WPW and management principles

A

Patient has AF
1:1 conduction > VF > SCD
So this affects clinical management because blocking AV node will encourage conduction along aberrant pathway.

PRN flecainide can be an option in infrequent episodes with no LV dysfunction, no IHD.

Definitive treatment
Catheter ablation

33
Q

Management of peri-arrest bradycardia

A

◆ IV atropine ± isoprenaline if symptomatic.
◆ Treat reversible causes (e.g. metabolic abnormality or stop offending drug).
◆ Consider pacemaker insertion.

34
Q

Indications for pacing [7]

A
  • Sinus node disease
  • Acquired AV Block
  • Congenital AV block
  • Neurocardiogenic syncope
  • Overdrive pacing for atrial tachyarrhythmias
  • Left ventricular outflow tract obstruction in HOCM
    *–Right ventricular apical pacing with short AV delay reduces LVOT gradient and symptoms in a subset of HOCM patients
  • Acquired long QT syndrome e.g., amiodarone overdose
35
Q

What is considered persistent or permanent atrial fibrillation

A

persistent (>7 days, but ‘cardiovertable’) or permanent (>7 days + NSR not
possible).

36
Q

Annual stroke risk

CHA2DS2VASC score

A

Remember that if a CHA2DS2-VASc score suggests no need for anticoagulation it is important to ensure a transthoracic echocardiogram has been done to exclude valvular heart disease, which in combination with AF is an absolute indication for anticoagulation.
Same risk for paroxysmal vs persistent

Apixaban 5mg BD lifelong

37
Q

May be used in conjunction with the CHA₂DS₂-Vasc Score to risk stratify patients for clinically significant bleeding to help guide decisions on anticoagulation in patients with atrial fibrillation.
ORBIT score

A
  • Age >74 +1
  • Bleeding history - any history of GI bleed, intracranial bleeding/ haemorrhagic stroke +2
  • GFR<60 +1
  • Treatment with antiplatelet agents
38
Q

Management of atrial fibrillation, what factors do you have to consider?

A
  • Age: elderly > rate control. Young symptomatic patients, consider rhythm control
  • If young patient and adverse featurse > DC cardioversion
  • Onset of symptoms >48h: delay cardioversion until they have been maintained on therapeutic anticoagulation for a minimum of 3 weeks (if considered for long term rhythm control). If elderly then just rate control
39
Q

What is sinus arrest? [2]

Management [2]

A

SA node fails to generate an impulse
No pulse

Mx:
CPR pathway
Adrenaline

40
Q

Palpitations

24 hour ECG or event recorder electrocardiogram?

A

Those who have episodes less than 24 hours apart should have a 24-hour ambulatory electrocardiogram. In patients who experience episodes more than 24 hours apart, an event recorder electrocardiogram would be the most suitable investigation of choice.

41
Q

Long QT syndromes

an inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death.

A

Long QT1 - usually associated with exertional syncope, often swimming
Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli
Long QT3 - events often occur at night or at rest

42
Q

2 Congenital causes of Long QT

A

Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
Romano-Ward syndrome (no deafness)

43
Q

Drugs that cause long QT

A

amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
methadone
chloroquine
terfenadine
erythromycin
haloperidol
ondanestron

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