ECG & arrhythmias flashcards
28 high-yield MRCP Part 1 cards from the Intellect Medicos Cardiology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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A patient with Wolff–Parkinson–White syndrome develops an irregular broad-complex tachycardia (pre-excited atrial fibrillation). Which group of drugs must be avoided?
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AV node-blocking drugs: adenosine, verapamil, diltiazem, beta-blockers and digoxin.
Why? Blocking the AV node pushes more atrial impulses down the accessory pathway. The ventricular rate can then rise further and degenerate into ventricular fibrillation.
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A 66-year-old with a previous anterior MI has palpitations. BP 128/80 mmHg, alert, no chest pain or breathlessness. ECG: regular broad-complex tachycardia at 170/min. What rhythm should you assume until proven otherwise?
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Ventricular tachycardia (VT).
Why? In someone with structural heart disease, a regular broad-complex tachycardia is far more often VT than SVT with aberrant conduction. Treating SVT as VT is safe; treating VT as SVT can be fatal.
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First-line drug treatment for torsades de pointes is intravenous ______.
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magnesium sulfate
Why? Torsades is polymorphic VT associated with a long QT interval. Magnesium suppresses the early after-depolarisations that trigger it, even when the serum magnesium is normal.
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In stable narrow-complex SVT, what are the IV adenosine bolus doses if the first fails?
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6 mg, then 12 mg, then 18 mg, as rapid IV boluses.
Why? Adenosine has a half-life of seconds, so it must be pushed fast through a large vein with a flush to reach the AV node in an effective concentration.
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Atrial flutter with 2:1 block typically produces a ventricular rate of about what?
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About 150 beats per minute.
Why? The atrial rate in flutter is around 300/min. With every second impulse blocked at the AV node, the ventricles beat at about 150/min.
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What is the first-line definitive treatment for typical atrial flutter?
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Catheter ablation of the cavotricuspid isthmus.
Why? Typical flutter is a macro-re-entry circuit in the right atrium that passes through the cavotricuspid isthmus. Ablating that narrow isthmus breaks the circuit; success is over 90%.
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A 74-year-old with an exacerbation of COPD is hypoxic. ECG: irregularly irregular rhythm at 120/min with at least three different P-wave morphologies. What is the rhythm?
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Multifocal atrial tachycardia (MAT).
Why? Several ectopic atrial foci fire, each producing its own P-wave shape. MAT is usually driven by systemic illness — hypoxia, electrolyte disturbance or catecholamine excess — rather than primary heart disease.
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For AF of more than 48 hours, how long should anticoagulation be given before elective electrical cardioversion?
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At least 3 weeks (or exclude left atrial thrombus with transoesophageal echo).
Why? Thrombus may already have formed in the left atrial appendage. Restoring organised atrial contraction can dislodge it, so the patient must be protected first.
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Why is flecainide avoided for rhythm control in a patient with ischaemic or structural heart disease?
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It can provoke dangerous ventricular arrhythmias (pro-arrhythmia) in a scarred or structurally abnormal heart.
Why? Flecainide is a class Ic sodium channel blocker that slows conduction. In ischaemic myocardium this promotes re-entry and increased mortality. Amiodarone is the choice when there is structural heart disease.
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In a patient with AF and moderate–severe mitral stenosis, which anticoagulant is used?
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Warfarin. DOACs are not recommended in this group.
Why? The DOAC trials excluded significant (mostly rheumatic) mitral stenosis, where thromboembolic risk is very high. Warfarin is also used with mechanical valves.
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For a man with AF, at what CHA₂DS₂-VASc score does NICE say to consider, and to offer, anticoagulation?
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Consider at a score of 1; offer at 2 or more (in women, offer at 2 or more).
Why? Female sex scores one point but does not by itself increase risk. A score of 0 in men or 1 in women means no anticoagulation.
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In a cardiac arrest with a shockable rhythm (VF or pulseless VT), when is amiodarone 300 mg IV first given?
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After the 3rd shock (with adrenaline 1 mg).
Why? Early shocks are the priority. If VF persists after three shocks, adrenaline and amiodarone 300 mg are given; amiodarone 150 mg can follow after the 5th shock.
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Peri-arrest bradycardia with adverse features: what is the first drug and its dose?
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Atropine 500 micrograms IV, repeated every 3–5 minutes to a maximum of 3 mg.
Why? Atropine blocks muscarinic receptors, removing vagal slowing of the SA and AV nodes.
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What are the earliest ECG changes of hyperkalaemia?
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Tall, narrow, tented T waves.
Why? As potassium rises further: flattened/absent P waves, PR prolongation, QRS widening, then a sine-wave pattern and VF/asystole.
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What is the characteristic ECG wave of hypothermia?
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The Osborn (J) wave — a positive hump at the junction of QRS and ST segment.
Why? Other features: bradycardia, long PR/QT and arrhythmias (AF, VF, asystole). Defibrillation may be ineffective below 30°C.
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What does the ECG "reverse tick" (Salvador Dalí moustache) ST depression indicate?
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Digoxin effect.
Why? Digoxin produces scooped ST depression and a short QT at therapeutic levels. It does not by itself mean toxicity; toxicity causes arrhythmias such as AV block.
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Hypercalcaemia ______ and hypocalcaemia ______ the QT interval.
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shortens; prolongs
Why? Calcium entry governs the plateau (phase 2) of the action potential. More extracellular calcium shortens the plateau; less prolongs it.
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What does NICE recommend as initial rate-control monotherapy in atrial fibrillation?
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A standard beta-blocker (not sotalol) or a rate-limiting calcium channel blocker (diltiazem or verapamil).
Why? Both slow AV node conduction. Choose by comorbidity — rate-limiting CCBs are avoided in HFrEF. Digoxin is added if one drug is not enough.
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Name two groups of AF patients in whom NICE prefers rhythm control over rate control first-line.
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Any two of: AF with a reversible cause; heart failure thought to be caused by AF; new-onset AF; atrial flutter suitable for ablation; rhythm control judged more suitable.
Why? For everyone else, rate control is first-line because it is as good as rhythm control for outcomes and avoids antiarrhythmic toxicity.
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For stable AF of under 48 hours, pharmacological cardioversion uses ______ if there is no structural heart disease, or amiodarone if there is.
Show answer
flecainide
Why? NICE offers a choice of flecainide or amiodarone when there is no structural or ischaemic heart disease, and amiodarone only when there is. Flecainide is pro-arrhythmic in structurally abnormal hearts. Do not use magnesium or a calcium channel blocker for pharmacological cardioversion.
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For stable AF of under 48 hours, pharmacological cardioversion uses flecainide if there is no structural heart disease, or ______ if there is.
Show answer
amiodarone
Why? NICE offers a choice of flecainide or amiodarone when there is no structural or ischaemic heart disease, and amiodarone only when there is. Flecainide is pro-arrhythmic in structurally abnormal hearts. Do not use magnesium or a calcium channel blocker for pharmacological cardioversion.
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Catheter ablation for atrial fibrillation electrically isolates which structures?
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The pulmonary veins, from the left atrium (pulmonary vein isolation).
Why? Most AF triggers fire from muscle sleeves in the pulmonary veins. NICE suggests radiofrequency point-by-point ablation first, with cryoballoon or laser balloon ablation if that is unsuitable, when drugs fail or are not tolerated.
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Which antiarrhythmic is second-line (per the notes) for maintaining sinus rhythm after cardioversion of AF, and must be avoided in heart failure?
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Dronedarone.
Why? It is related to amiodarone but has no iodine. It increased mortality in people with heart failure or LV systolic dysfunction and in permanent AF, so it is contraindicated there.
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Which class of anticoagulant is first-line for stroke prevention in non-valvular atrial fibrillation?
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A direct oral anticoagulant (DOAC): apixaban, dabigatran, edoxaban or rivaroxaban.
Why? DOACs are at least as effective as warfarin, cause less intracranial bleeding and need no INR monitoring.
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Which drug is used for a "pill-in-the-pocket" strategy in infrequent paroxysmal AF without structural heart disease?
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Flecainide, taken orally at the start of an episode.
Why? NICE allows it for people with infrequent symptomatic paroxysms, no LV dysfunction, valve or ischaemic heart disease, systolic BP above 100 mmHg and resting heart rate above 70, who can use it reliably.
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What is the first-line treatment for a haemodynamically stable regular narrow-complex SVT?
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Vagal manoeuvres — the modified Valsalva manoeuvre is the most effective.
Why? Raising vagal tone slows AV node conduction and can break the re-entry circuit. If they fail, give IV adenosine; unstable patients go straight to synchronised DC cardioversion.
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Current RCUK algorithm: what is the first-line treatment of a STABLE regular broad-complex tachycardia treated as VT?
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Synchronised DC cardioversion under sedation or anaesthesia. If that risk is too high: IV procainamide, or amiodarone if procainamide is unavailable.
Why? Cardioversion is more reliably effective than drugs. Amiodarone is given as 300 mg IV over 10–60 minutes, then 900 mg over 24 hours.
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Tachyarrhythmia with a pulse and life-threatening features: what is given if up to three synchronised shocks fail?
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IV amiodarone 300 mg over 10–20 minutes (or procainamide 10–15 mg/kg over 20 minutes), then repeat the synchronised shock.
Why? Life-threatening features (shock, syncope, myocardial ischaemia, severe heart failure) mean electricity comes first. The drug makes further shocks more likely to work.
More Cardiology topics
- Physiology & haemodynamics
- Heart sounds, pulses & murmurs
- Valvular heart disease
- Inherited & sudden cardiac death syndromes
- Ischaemic heart disease
- Heart failure & cardiomyopathies
- Pericardial disease
- Endocarditis & rheumatic fever
- Congenital heart disease
- Hypertension, aorta & emboli
- Cardiovascular pharmacology
- Lipids & statins