Arrhythmias: Supraventricular tachycardias Flashcards

1
Q

Categorise the types of Supraventricular tachycardia

A

Sinus tachycardia Paroxysmal SVTs: AVNRT and AVRT Atrial tachyarrythmias: -Atrial fibrillation -Atrial flutter -Atrial tachycardia -Atrial ectopic beats

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2
Q

Categorise the types of Ventricular tachycardia

A

Life-threatening: -Sustained ventricular tachycardia -Ventricular fibrillation -Torsades de pointes Normal heart ventricular tachycardia Non-sustained ventricular tachycardia Ventricular ectopic beats

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3
Q

Define supraventricular and ventricular tachycardias

A

Supraventricular tachycardias arise from atrium or AV junction. Conduction via the His-Purkinje system produces a narrow QRS (<120ms). Ventricular tachycardias arise from the ventricles.

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4
Q

Define inappropriate sinus tachycardia

A

A persistent increase in resting heart rate unrelated to, or out of proportion with, the level of physical or emotional stress.

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5
Q

Outline the aetiology of sinus tachycardia

A

Generally a secondary phenomenon: Acute: Exercise, emotion, pain, fever, infection, PE etc. Chronic: Pregnancy, anaemia, hyperthyroid, catecholamine excess. Inappropriate sinus tachycardis is extremely rare. Can be due to enhanced automaticity, or abnormal autonomic regulation of the heart.

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6
Q

What are paroxysmal SVTs?

A

Tachycardias that occur at the AV junction, including AV nodal re-entrant tachycardia (AVNRT) and AV re-entrant tachycardia (AVRT). These are often seen in young patients with little or no structural heart disease. Commonly presents between ages 12-30.

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7
Q

Explain AVNRT

A

AVNRT is the commonest cause of palpitations in patients with normal heart structure. Mechanism: re-entrant circuit around the AVN, typically ‘slow-fast’ AVNRT.

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8
Q

What ECG changes are seen in AVNRT?

A

Tachycardia (usually 140-240 bpm) Regular R-R interval Absent P wave (if simultaneous atrial and ventricular activation), or Inverted P wave immediately before/after QRS Narrow QRS complexes

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9
Q

Explain AVRT

A

Formation of a re-entrant pathway comprising of the AV node, the His bundle, the ventricle, and an accessory pathways between ventricle and atria. This is a macro re-entry circuit activated sequentially.

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10
Q

What ECG changes are seen in AVRT?

A

Tachycardia (usually 200-300bpm) Regular R-R interval Orthodromic: Narrow QRS complex, P wave visible between QRS and T wave Antidromic: Wide QRS complex

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11
Q

Define Wolff-Parkinson-White syndrome

A

A congenital condition featuring: -Bundle of Kent -Symptomatic episodes of tachyarrhythmia/palpitations

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12
Q

What ECG changes are seen in Wolff-Parkinson-White syndrome in sinus rhythm?

A

Delta wave Narrow QRS complex elongation >110ms Short PR interval <120ms

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13
Q

How can Wolff-Parkinson-White syndrome present?

A

AVRT: 200-300bpm -Orthodromic: Narrow QRS complex, P wave visible between QRS and T wave -Antidromic (5%): Wide QRS complex AF: risk of VF in WPW -Palpitations, SoB, chest pain, syncope, stroke/TIA Sudden cardiac death (rare)

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14
Q

Outline the definitive treatment of Wolff-Parkinson-White syndrome

A

Asymptomatic: Monitor for symptoms Minimally symptomatic: Ablation of bundle of Kent Symptomatic: Ablation of bundle of Kent

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15
Q

Describe the clinical features of paroxysmal SVTs

A

Regular rapid palpitations: Sudden onset and offset May be terminated by Valsalva manoeuvre May include: anxiety, dizziness, dyspnoea, neck pulsation, central chest pain, fatigue Polyuria due to ANP release, esp in AVNRT and AF Syncope (10-15%)

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16
Q

Describe the acute management of paroxysmal SVTs

A

SVT + haemodynamic instability -> DC cardioversion SVT + haemodynamic stablility: 1. Valsalva manoeuvre or carotid sinus massage 2. IV adenosine: initially 6mg, then 2x12mg if needed -Verapamil, metoprolol, or diltiazem if adenosine contraindicated e.g. Asthma 3. DC cardioversion *slightly differs if known WPW syndrome

17
Q

What is the mechanism of action of adenosine

A

Adenosine causes very short complete heart block, which can interrupt re-entrant pathways in the AV node, and restore normal sinus rhythm in paroxysmal SVTs.

18
Q

List 3 side effects of adenosine

A

Bronchospasm Flushing Chest pain Heaviness of limbs Sense of impending doom*: important advise this will only be for a brief time

19
Q

Name 2 contraindications of non-dihydropyridine CCBs and Beta-blockers in the treatment of paroxysmal SVTs

A

AVN blockers: Verapamil, diltiazem, and beta-blockers should not be given: -After Beta-blocker, or -Broad-QRS complex tachycardias

20
Q

Describe the Valsalva manoeuvre

A

Should be undertaken in supine position Forceful exhalation against a closed airway Avoid deep inspiration prior to straining

21
Q

Name 5 causes of atrial tachyarrhythmias

A

Increasing age MI Hypertension Obesity Diabetes mellitus Hypertrophic cardiomyopathy Heart failure Valvular heart disease Myocarditis/pericarditis Cardiothoracic surgery Chest infections Hyperthyroidism Electrolyte imbalances

22
Q

Define atrial flutter

A

Organised atrial rhythm with an atrial rate typically between 300-350 bpm. These can occur around the tricuspid annulus, fibrosis, or pulmonary veins (LA).

23
Q

How is ventricular rate determined in atrial flutter?

A

Ventricular rate is determined by the AV conduction ratio. 2:1 block (commonest): 150 bpm 1:1 block: 300 bpm - associated with severe haemodynamic instability and progression to VF 3:1 block: 100 bpm 4:1 block: 75 bpm - seen when receiving treatment, or underlying heart disease

24
Q

What is 1:1 atrial flutter associated with?

A

Severe haemodynamic instability Progression to VF

25
Q

What ECG changes are seen with typical atrial flutter?

A

Sawtooth pattern: best seen in II, III, aVF Narrow QRS complex, Broad QRS in 1:1 flutter Regular R-R interval P waves present

26
Q

How is atrial flutter managed?

A

Similar to atrial fibrillation Symptomatic acute paroxysmal flutter: DC cardioversion Ablation has greater success rate than in AF

27
Q

What monitoring is required whilst taking amiodarone?

A

Prior to treatment: TFTs: risk of thyroid dysfunction LFTs: raised serum transaminase, risk of cirrhosis U&Es: hypokalaemia can cause arrhythmias CXR: risk of pulmonary fibrosis Every 6 months: TFTs LFTs

28
Q

Describe the treatment of SVT episodes in known WPW

A

SVT + haemodynamic instability -> DC cardioversion SVT + haemodynamic stablility: 1. Valsalva manoeuvre or carotid sinus massage 2. Flecainide: blocks accessory pathway conduction 3. DC cardioversion

29
Q

What SVT drugs should be avoided in known WPW?

A

Adenosine: small risk of precipitating pre-excited AF Digoxin: promotes accessory pathway conduction