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Fundamentals of ECG, Part 3 Making the most of the ECG: the clinical interpretation of individual ECGs MCQs
Fundamentals of ECG · MBBS / Medicine · 23 practice questions
- ECG localisation of infarct territory
- P wave abnormalities
- Cardiac hypertrophy - ECG patterns
- Pacemaker mode identification from ECG
- Serial ECG evolution after STEMI
- Rhythm and conduction interpretation
- Sick sinus syndrome and pacing indications
- Pulmonary embolism - ECG diagnostic utility
1. A 78-year-old woman undergoes ambulatory ECG monitoring for recurrent dizzy spells. The recording shows sinus rhythm at 38 bpm, an atrial extrasystole with an abnormal P wave, and then a 3.5-second pause before the next sinus beat resumes. She takes no rate-limiting medications. Which of the following is the most appropriate next step in management?
- AGive intravenous atropine and observe
- BStart an oral anticoagulant and reassess in one month
- CStart a beta-blocker to control the atrial extrasystoles
- DArrange permanent pacemaker implantation
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D. Arrange permanent pacemaker implantation The tracing shows sinus bradycardia with a prolonged pause corresponding to symptomatic sick sinus syndrome; since there is no effective medical treatment for symptomatic bradycardia, permanent pacing is the appropriate management. A beta-blocker would worsen the bradycardia. Atropine is a temporising measure for acute bradyarrhythmia, not definitive management of chronic symptomatic sinus node disease. Anticoagulation does not address the underlying conduction problem causing her symptoms.
2. A 65-year-old man presents with an acute anterior ST elevation myocardial infarction. On day 1 he develops complete heart block with a ventricular rate of 38 bpm and hypotension. Which of the following best explains why temporary pacing is more likely to be required in this patient than in a patient with inferior STEMI who develops the same rhythm?
- AAnterior STEMI more frequently causes reperfusion arrhythmias requiring cardioversion
- BAnterior STEMI causes heart block via increased vagal tone, which resolves spontaneously
- CComplete heart block in anterior STEMI usually reflects a large area of damaged myocardium rather than a transient conduction disturbance
- DComplete heart block in inferior STEMI is always asymptomatic and never requires treatment
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C. Complete heart block in anterior STEMI usually reflects a large area of damaged myocardium rather than a transient conduction disturbance The source states that complete block complicating anterior STEMI usually reflects a large amount of damaged myocardium, making temporary pacing more often necessary, whereas complete heart block in inferior STEMI is usually temporary and does not need pacing unless there is haemodynamic compromise from bradycardia. Inferior STEMI heart block can still require pacing if haemodynamically significant, so it is not 'never' needed. Vagally-mediated block is a feature of inferior, not anterior, infarction. Reperfusion arrhythmias are not the mechanism described for anterior STEMI heart block in the source.
3. A 55-year-old sedentary office worker has an ECG at a routine screening visit showing a regular sinus rhythm at 80 bpm with a constant PR interval of 336 ms in every beat; QRS, ST segments, and T waves are otherwise normal apart from loss of the R wave in one anterior lead suggesting an old infarction. He denies any symptoms and is not an athlete. How should this PR interval finding be interpreted?
- AIt is within the accepted upper limit of normal for a middle-aged, non-athletic adult
- BDespite the patient's asymptomatic status, this degree of PR prolongation likely reflects underlying conducting tissue disease
- CIt is a normal variant frequently seen in healthy non-athletic adults and requires no further evaluation
- DIt reflects Mobitz 1 (Wenckebach) second degree block, common and benign in this age group
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B. Despite the patient's asymptomatic status, this degree of PR prolongation likely reflects underlying conducting tissue disease A PR interval of 336 ms far exceeds even the extended range occasionally seen in healthy athletes (up to about 220 ms) and, per the passage, PR prolongation to this extent is probably evidence of disease of the conducting tissue even in an asymptomatic person. It is not a benign normal variant, as those are only slightly above 200 ms and typically seen in athletes. Wenckebach is a form of second degree block with progressively lengthening PR intervals before a dropped beat, not a fixed markedly prolonged PR interval as seen here. Describing it as within normal limits ignores that normal upper limits are around 200 ms (with rare benign exceptions only slightly above 220 ms).
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