Arrhythmias: Supraventricular tachycardias Flashcards Preview

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Flashcards in Arrhythmias: Supraventricular tachycardias Deck (29)
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Categorise the types of Supraventricular tachycardia

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


Categorise the types of Ventricular tachycardia

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


Define supraventricular and ventricular tachycardias

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.


Define inappropriate sinus tachycardia

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


Outline the aetiology of sinus tachycardia

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.


What are paroxysmal SVTs?

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.


Explain AVNRT

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


What ECG changes are seen in AVNRT?

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


Explain AVRT

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.


What ECG changes are seen in AVRT?

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


Define Wolff-Parkinson-White syndrome

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


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

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


How can Wolff-Parkinson-White syndrome present?

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)


Outline the definitive treatment of Wolff-Parkinson-White syndrome

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


Describe the clinical features of paroxysmal SVTs

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%)


Describe the acute management of paroxysmal SVTs

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


What is the mechanism of action of adenosine

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.


List 3 side effects of adenosine

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


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

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


Describe the Valsalva manoeuvre

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


Name 5 causes of atrial tachyarrhythmias

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


Define atrial flutter

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


How is ventricular rate determined in atrial flutter?

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


What is 1:1 atrial flutter associated with?

Severe haemodynamic instability Progression to VF


What ECG changes are seen with typical atrial flutter?

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


How is atrial flutter managed?

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


What monitoring is required whilst taking amiodarone?

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


Describe the treatment of SVT episodes in known WPW

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


What SVT drugs should be avoided in known WPW?

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