Arrhythmias: Supraventricular tachycardias Flashcards
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&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
