Read ECGs from calibration to clinical action, using rhythm, axis, interval and ischemia patterns with visible diagrams and complete patient cases.
A patient with chest pressure has an ECG labeled abnormal. Before naming a syndrome, decide whether the patient needs immediate resuscitation, whether the recording is trustworthy, and which finding explains the symptoms. A systematic read should produce a clinical interpretation, not a list of waveform adjectives.
An ECG pattern changes probability. A normal tracing cannot exclude acute coronary syndrome, and an isolated abnormality rarely proves one diagnosis.
Establish what the recording measures
Check the patient, recording time, symptoms, lead placement and calibration. Standard speed is 25 mm/s, making one small horizontal square 0.04 s and one large square 0.20 s. At 10 mm/mV, a 10 mm vertical deflection represents 1 mV. A recording at 50 mm/s or half-standard gain changes the arithmetic. Confirm the duration printed on a rhythm strip before using a counting shortcut. [1]
QT contains QRS; PR begins at P onset rather than at the end of P.
P represents atrial activation, QRS ventricular activation, and T ventricular recovery. Atrial recovery is usually obscured by QRS. Measure PR from P onset to QRS onset, QRS from earliest ventricular onset to its end, and QT from QRS onset to the T-wave end. A small normal septal q wave is not automatically an infarct scar; distribution, width, depth and the clinical history matter.
A usual adult PR is 120 to 200 ms. A QRS below 120 ms is conventionally called narrow for rhythm classification; complete bundle-branch block requires at least 120 ms plus appropriate morphology. A QRS of 102 ms does not establish complete LBBB. P-wave duration of at least 120 ms with notching or a broad terminal negative component in V1 supports left atrial abnormality. Tall inferior P waves, conventionally over 2.5 mm at standard gain, support right atrial abnormality. Neither pattern alone proves an enlarged chamber; imaging assesses anatomy. [2][12]
Lead misplacement and motion artifact can imitate disease. Unexpected inversion of lead I or a sudden loss of expected precordial R-wave progression should prompt an electrode check and repeat recording. Low voltage, high voltage and poor R progression require context rather than an automatic etiologic label.
Try it here · Checkpoint 1 of 3
Make your prediction before reading the choices. A first attempt is just a starting point.
Case 8
Show answer and explanations for case 8
A. Complete LBBB with an unusually short QRS (Why this does not fit)
The tracing lacks both the required complete-block duration and the characteristic lateral morphology.
B. Complete LBBB criteria are not met (Best answer)
Complete LBBB requires QRS of at least 120 ms and compatible morphology, both lacking here.
C. Complete RBBB (Why this does not fit)
No terminal right-precordial R-prime/broad lateral S pattern is described, and 102 ms is below the complete RBBB threshold.
D. Ventricular preexcitation (Why this does not fit)
A short PR and delta-wave onset would support preexcitation; neither is supplied here.
Takeaway: Verify both QRS duration and morphology before accepting a bundle-branch diagnosis.
Describe the atrial and ventricular rhythms separately
For a regular rhythm at standard speed, rate is 300 divided by large squares between R peaks, or 1500 divided by small squares. Four large squares gives 75/min. For an irregular rhythm, count QRS complexes over a verified interval and multiply by 60 divided by its duration in seconds. Twelve complexes in ten seconds estimates 72/min. This is an average, not a description of regularity.
Start with regularity, then inspect atrial activity
Pattern
Useful discriminator
Interpretation
PatternSinus rhythm
Useful discriminatorConsistent P before each QRS, usually upright in II and negative in aVR
InterpretationRate can be slow or high. Treat causes of sinus tachycardia such as fever, hypovolemia or pain.
PatternAtrial fibrillation
Useful discriminatorNo consistent discrete P waves and irregular ventricular intervals when AV conduction is intact
InterpretationAssess ventricular response, symptoms and thromboembolic risk. A PR interval cannot be assigned.
PatternAtrial flutter
Useful discriminatorOrganized repetitive atrial activity, often sawtooth in inferior leads
InterpretationTwo-to-one conduction often gives a ventricular rate near 150/min, but neither that rate nor regularity is mandatory.
PatternMultifocal atrial tachycardia
Useful discriminatorAt least three P morphologies in one lead, variable PR and irregular intervals at over 100/min
InterpretationDiscrete P waves with intervening isoelectric segments distinguish MAT from AF. Treat pulmonary illness and metabolic contributors.
PatternRegular narrow tachycardia
Useful discriminatorAbrupt episodes with P waves hidden in or near QRS
InterpretationAVNRT and orthodromic AVRT are possibilities. Rate alone cannot identify the circuit.
PatternJunctional escape
Useful discriminatorA late narrow complex after sinus failure; P may be absent or retrograde
InterpretationTiming distinguishes rescue activity from a premature ectopic complex. Retrograde P waves alone do not identify every tachycardia mechanism.
Typical AVNRT usually conducts forward through a slow nodal pathway and returns through a fast pathway. Orthodromic AVRT conducts forward through the AV node and His-Purkinje system and returns through an accessory pathway; QRS is usually narrow unless aberrancy is present. Antidromic AVRT conducts forward through the accessory pathway and usually has a wide QRS.
Vagal maneuvers and adenosine can terminate selected stable, regular narrow tachycardias that require the AV node. Transient AV block may instead reveal continuing flutter activity. Do not apply this strategy indiscriminately to irregular or polymorphic wide-complex rhythms. Wide tachycardia in a patient with prior infarction should be approached as VT until adequately characterized. AV dissociation, capture complexes and fusion complexes support VT. [3][4]
AF management has separate rate, rhythm and stroke-prevention decisions. In stable AF with rapid ventricular response and no preexcitation, beta blockers or diltiazem/verapamil can provide acute rate control, with the calcium blockers restricted to EF above 40%. Avoid IV diltiazem/verapamil in moderate or severe LV systolic dysfunction. Hemodynamic instability attributable to AF calls for immediate cardioversion.
For elective cardioversion after AF lasting at least 48 hours or an uncertain duration, the 2023 guideline recommends three weeks of therapeutic anticoagulation or imaging to exclude intracardiac thrombus beforehand. Therapeutic anticoagulation must be established before cardioversion in either pathway and continued without interruption for at least four weeks afterward. Long-term treatment depends on thromboembolic risk, not simply episode duration.
The 2023 guideline recommends warfarin over DOACs in AF with rheumatic mitral stenosis or mitral stenosis of moderate or greater severity, independently of CHA2DS2-VASc score; mechanical valves also require a vitamin K antagonist. [5]
Typical flutter circulates around the tricuspid annulus through the cavotricuspid isthmus. Catheter ablation of that isthmus is useful when flutter is symptomatic or resistant to pharmacologic rate control. Atypical flutter may use a different circuit, so an inferior-lead sawtooth pattern does not alone determine the ablation target. A premature atrial complex arrives early with an altered P wave and can conduct normally, aberrantly or fail to conduct; a premature ventricular complex arises in ventricular tissue and usually has a broad QRS. Interpret timing and atrial activity together. [3]
Read direction before naming a conduction disorder
The frontal QRS axis describes the average direction of ventricular activation. A positive net QRS points toward a lead's positive pole; a negative net complex points away. Lead I looks toward 0 degrees, aVF toward +90 degrees and II toward +60 degrees. The usual adult reference range is approximately -30 to +90 degrees. [2]
I positive, aVF positive
Axis between 0 and +90 degrees. This lies within the usual adult range.
I positive, aVF negative
Axis between -90 and 0 degrees. Inspect II. A positive II supports -30 to 0; a negative II supports left-axis deviation below -30.
I negative, aVF positive
Axis between +90 and +180 degrees. Right-axis deviation.
I negative, aVF negative
Axis between -180 and -90 degrees. Extreme axis.
A polarity map of four frontal-plane regions. Nearly isoelectric leads require more precise assessment rather than forced binary classification.
Left anterior fascicular block is supported by marked left-axis deviation with appropriate qR complexes in I/aVL and rS complexes inferiorly, usually without a fully widened QRS. Right-axis deviation has several causes, including right ventricular loading and fascicular disease. RBBB does not automatically imply right-axis deviation. Inferior infarction and body habitus can also influence axis.
Complete RBBB
QRS is at least 120 ms, with a terminal rightward deflection such as rsR' in V1/V2 and a broad terminal S in I or V6. Secondary ST-T discordance can occur in right precordial leads.
Complete LBBB
QRS is at least 120 ms, usually predominantly negative in V1, with broad or notched lateral R waves and absent normal lateral septal q waves. Secondary ST-T changes generally point opposite the main QRS direction. Width alone is insufficient for either label.
Large QRS voltages with lateral ST depression and asymmetric T inversion can support LVH with secondary repolarization abnormalities. For example, the Sokolow-Lyon criterion sums S in V1 and the larger R in V5 or V6, with a threshold of at least 35 mm at standard gain. Voltage criteria are influenced by body habitus and cannot establish ventricular mass alone. A new symptom requires assessment even when an older ECG already shows a strain pattern. [12]
Right-heart strain patterns, including rightward axis or S1Q3T3, may occur in pulmonary embolism, but they neither prove nor exclude it. Use the clinical probability and appropriate testing. Similarly, normal echocardiography cannot exclude an electrical syndrome or every early cardiomyopathy. [14][9]
Measure conduction and recovery as different problems
To classify AV block, locate P waves throughout the strip, including those hidden in T waves. Compare atrial timing, ventricular timing and PR behavior. A slow pulse alone does not tell you where conduction failed. [6]
First-degree AV delay
Every P conducts, but PR exceeds 200 ms. There are no dropped ventricular responses by definition.
Mobitz I
PR progressively lengthens before a nonconducted P, then resets shorter. Grouped ventricular complexes often make the pattern easier to see.
Mobitz II
Intermittent nonconducted P waves occur without progressive PR lengthening among conducted impulses, with a stable atrial rhythm. Exclude concealed ectopy and other mimics.
Two-to-one block
Alternate P waves fail to conduct. One conducted PR per cycle does not reveal a progressive sequence, so the strip alone cannot reliably assign Mobitz I or II.
Complete AV block
Atrial and ventricular rhythms are independent, with no consistent conduction relationship. A junctional or ventricular escape maintains a slower ventricular rhythm.
Symptomatic bradycardia with poor perfusion requires immediate support and treatment of reversible causes such as medication effects, ischemia or electrolyte disturbance. Atropine may help nodal disease, but advanced infranodal block may not respond; prepare pacing and appropriate vasoactive support. Acquired Mobitz II, high-grade block or complete AV block without a reversible or physiologic cause generally warrants permanent pacing, even without symptoms. [4][6]
QT requires a rate and a reliable T-wave end
Manually confirm the computer measurement when T waves are indistinct, U waves prominent or QRS wide. Bazett QTc equals QT divided by the square root of RR; Fridericia QTc uses the cube root. Use seconds consistently. Bazett tends to overcorrect at high rates and undercorrect at low rates. In wide QRS, consider an appropriate QRS-adjusted method or JT rather than treating all QT prolongation as delayed repolarization. [7]
Common adult screening thresholds for prolonged QTc are about 450 ms in men and 460 ms in women, with substantial context dependence. Values around or above 500 ms deserve particular attention to acquired risk, but no single number guarantees an arrhythmia. Review QT-prolonging drugs, interactions, renal function and potassium, magnesium and calcium. Prolonged QT between episodes distinguishes torsades from other polymorphic VT. [7][4]
Try it here · Checkpoint 2 of 3
Make your prediction before reading the choices. A first attempt is just a starting point.
Case 11
Show answer and explanations for case 11
A. Mobitz I is proven by the ventricular rate (Why this does not fit)
Rate alone does not reveal the mechanism or site of AV block.
B. Complete AV block is proven because some P waves do not conduct (Why this does not fit)
A fixed two-to-one relation is not equivalent to complete atrioventricular independence.
C. Two-to-one AV block is present, but Mobitz subtype is indeterminate (Best answer)
There is only one conducted PR per repeating sequence, so progressive PR behavior cannot be established.
D. Mobitz II is proven by a constant PR (Why this does not fit)
Both nodal and infranodal two-to-one block can show a constant conducted PR; further evaluation is required.
Takeaway: Use the descriptive diagnosis two-to-one block when the strip cannot reveal a Mobitz sequence.
Read ST and T changes in neighboring views of the heart. Inferior leads are II, III and aVF; lateral leads are I, aVL, V5 and V6; V1 through V4 broadly view septal and anterior regions. Coronary territories overlap. An inferior pattern often involves the RCA, but circumflex disease remains possible depending on anatomy. Reciprocal aVL depression supports inferior injury without proving a single culprit vessel. [8]
For standard STEMI criteria in the absence of LVH or LBBB, new J-point ST elevation is required in two contiguous leads, generally at least 1 mm. In V2-V3, thresholds are at least 2 mm in men aged 40 or older, 2.5 mm in younger men, and 1.5 mm in women. These thresholds support a reperfusion decision; their absence does not exclude an acute coronary occlusion. Dynamic symptoms and serial ECGs matter, and an early normal troponin cannot independently exclude MI. [8]
Look behind the anterior depression
ST depression in V1-V3 with tall R waves and upright T waves during ischemic symptoms may be the reciprocal view of posterior infarction. Record V7-V9. Posterior ST elevation of at least 0.5 mm supports this diagnosis; use at least 1 mm in men younger than 40. [17] Additional leads should clarify suspected occlusion without delaying urgent care.
Look right with inferior injury
Inferior ST elevation with hypotension, raised jugular venous pressure and relatively clear lungs raises concern for right ventricular involvement. Record right-sided leads, especially V4R, and avoid nitrates in suspected right ventricular infarction or hypotension. [16]
Early regional broad, bulky T waves can represent hyperacute ischemic changes, whereas diffuse narrow tented T waves suggest hyperkalemia. Shape is imperfect evidence in both directions, so use symptoms, serial tracings and laboratory testing. [8][11]
Recognize high-risk patterns without overclaiming their specificity
Pain-free biphasic or deeply inverted anterior T waves after anginal symptoms can indicate a Wellens pattern. Arrange urgent coronary assessment; stress testing can provoke ischemia. Upsloping precordial ST depression with tall symmetric T waves can represent a de Winter pattern. Widespread ST depression with aVR elevation suggests global subendocardial ischemia, potentially from severe coronary disease or supply-demand imbalance, rather than proving left-main occlusion. [8]
New LBBB alone is no longer an automatic STEMI equivalent. In a compatible clinical presentation, concordant ST elevation of at least 1 mm, concordant depression of at least 1 mm in V1-V3, or proportionally excessive discordant elevation raises concern. Modified Sgarbossa uses discordant ST elevation of at least 1 mm and at least 25% of the preceding S-wave depth. Apply the criteria to LBBB or ventricular pacing with clinical judgment; negative criteria do not rule out ACS. [8]
Pericarditis can cause widespread ST elevation and PR depression with pleuritic, positional pain; aVR and sometimes V1 may show reciprocal changes. The 2025 ACC guidance integrates symptoms with inflammatory markers, examination and imaging. Early repolarization may produce stable J-point notching or slurring. Neither youth nor concave ST shape establishes a benign diagnosis, and acute infarction can have concave elevation. Compare prior tracings and investigate new concerning symptoms. [10][8]
T-wave inversion is not specific to coronary disease. Secondary conduction or hypertrophy changes, right ventricular strain, stress cardiomyopathy and acute neurologic illness can also alter repolarization. New chest symptoms or neurologic findings require their own assessment; the waveform cannot identify the cause alone. [7][14]
Translate the pattern into the next clinical decision
Hyperkalemia can produce peaked T waves, P-wave loss and QRS widening, but findings do not follow a reliable concentration-based sequence. A verified severe potassium abnormality needs attention even with a normal tracing. Toxic ECG changes prompt IV calcium for membrane protection; insulin with glucose redistributes potassium, with glucose monitoring, while elimination therapy addresses excess body potassium. Bicarbonate is not routine acute treatment. [11]
Hypokalemia can flatten T waves and produce ST depression and prominent U waves. T-U fusion can falsely extend the measured QT into a QU interval. Hypocalcemia tends to prolong QT through the ST segment; hypercalcemia tends to shorten it. [18] Cold exposure with bradycardia and J-point humps suggests hypothermia-associated Osborn waves, but a J wave is not pathognomonic and does not define one exact temperature. [7][13]
A short PR with a delta wave and widened QRS indicates ventricular preexcitation. Short PR alone does not prove an accessory pathway or justify a historical Lown-Ganong-Levine label. Preexcited AF produces an irregular, very rapid rhythm with variable QRS width. Avoid AV nodal blockers, including IV amiodarone, in that setting; choose urgent cardioversion if unstable or appropriate monitored pathway-active treatment if stable. [2][5]
A coved type 1 ST pattern in V1-V2 during fever, especially with unexplained syncope, warrants Brugada assessment. Exercise-related syncope with a normal resting ECG can still indicate CPVT, particularly when bidirectional or polymorphic VT is documented under specialist supervision. Long QT with exertional, auditory or resting triggers raises a different inherited-syndrome evaluation. An ECG impression is not an automatic indication for an ICD; event history and risk guide treatment. [15][9]
No pulse with VF or polymorphic VT
Start CPR and provide unsynchronized defibrillation. Do not wait for laboratory confirmation.
Unstable organized tachycardia with a pulse
For instability caused by an organized tachyarrhythmia, use synchronized cardioversion when feasible. Sinus tachycardia caused by shock requires treatment of the underlying illness. Sustained polymorphic VT requires unsynchronized shock because reliable synchronization is not possible.
Recurrent torsades with prolonged QT
Address the culprit medication and electrolyte deficits and consider IV magnesium for recurrences associated with long QT. Routine magnesium is not recommended for polymorphic VT with a normal QT. This treatment supplements, rather than delays, shock for a sustained episode.
Stable patient with an abnormal tracing
State rate, rhythm, axis, intervals and significant ST-T findings, then identify the leading concern and the test or intervention needed to resolve it.
A. Focal atrial tachycardia with two-to-one conduction (Why this does not fit)
Focal atrial tachycardia can persist during AV block, but discrete P waves with isoelectric intervals are more typical. Continuous inferior sawtooth activity favors flutter here.
B. Atrial flutter with two-to-one AV conduction (Best answer)
The atrial rhythm continues at twice the original ventricular rate when AV conduction is interrupted.
C. AVNRT (Why this does not fit)
AVNRT can produce the initial regular narrow tachycardia, but the persistent, distinct sawtooth atrial rhythm during AV block favors atrial flutter.
D. Sinus tachycardia at 150/min (Why this does not fit)
The revealed atrial rate is 300/min and has repetitive flutter activity rather than normal sinus P waves.
Takeaway: Adenosine may expose an atrial rhythm without terminating it.
A. Possible AV node-dependent reentrant SVT; circuit undetermined (Best answer)
AVNRT and orthodromic AVRT can both produce this presentation. Response to maneuvers and additional recordings may clarify it.
B. AVNRT established by the ventricular rate of 186/min alone (Why this does not fit)
Substantial rate overlap exists between AVNRT and other regular narrow tachycardias.
C. Atrial fibrillation established by the absence of visible P waves (Why this does not fit)
AF usually produces irregular ventricular intervals when AV conduction is intact; obscured P waves alone do not establish it.
D. Sinus tachycardia established by the narrow QRS complexes (Why this does not fit)
QRS width establishes a conduction feature, not a sinus origin. Abrupt episodes and absent discernible sinus P waves retain a reentrant SVT differential.
Takeaway: Describe what the strip establishes and retain the circuit differential when surface findings overlap.
A. Atrial flutter with two-to-one conduction (Why this does not fit)
The atrial rate and independence do not fit a flutter rhythm transmitted in a fixed two-to-one ratio.
B. Complete AV block with a ventricular escape rhythm (Best answer)
Independent atrial and ventricular rhythms with a slow broad escape support complete block. Poor perfusion requires urgent support and pacing preparation.
C. Sinus bradycardia at 30/min (Why this does not fit)
The atria are firing at 88/min, so the slow ventricular rate is not explained by sinus slowing.
D. First-degree AV delay (Why this does not fit)
First-degree delay has one-to-one conduction with a consistent prolonged PR, which is absent.
Takeaway: Atrial and ventricular independence distinguishes complete AV block from a merely slow sinus rhythm.
A. Diagnose congenital long-QT syndrome from the single automated QTc value (Why this does not fit)
An acute high-rate recording and one computer value cannot establish a congenital syndrome.
B. Remeasure QT from the end of QRS to the end of the T wave (Why this does not fit)
That measures JT rather than QT and does not correct rate bias in the proposed manner.
C. Disregard QT measurements throughout the current febrile illness (Why this does not fit)
The measurement still matters, particularly with QT-prolonging drugs; it requires contextual interpretation rather than dismissal.
D. Verify QT manually; consider a correction less biased at high rates (Best answer)
Bazett often overcorrects at high rates. Confirm the measurement, apply an appropriate validated correction and reassess after the acute cause improves. Fridericia also has rate-dependent limitations; no formula independently diagnoses congenital long QT.
Takeaway: Rate correction is a model, so inspect its limitations before making a syndrome diagnosis.
A. Reciprocal change in aVR excludes pericarditis (Why this does not fit)
aVR may show reciprocal ST and PR changes in pericarditis.
B. Concave ST shape alone rules out infarction (Why this does not fit)
ST shape is not sufficiently specific to exclude acute coronary disease.
C. The ECG proves a large pericardial effusion (Why this does not fit)
Electrical inflammation patterns do not quantify pericardial fluid; imaging assesses effusion.
D. Acute pericardial inflammation is likely and should be assessed with examination, inflammatory markers and imaging (Best answer)
The symptom pattern and diffuse ST/PR changes support pericarditis; an integrated assessment evaluates associated myocardial involvement and complications.
Takeaway: Pericarditis is a clinical and imaging diagnosis supported by ECG findings, not established by ST shape alone.
A. IV insulin with glucose (Why this does not fit)
Insulin is appropriate for redistribution, but it does not provide the immediate membrane protection specifically requested here.
B. Nebulized salbutamol (Why this does not fit)
A beta-2 agonist can supplement intracellular redistribution. It is not a substitute for calcium when toxic ECG changes require membrane stabilization.
C. IV calcium (Best answer)
Calcium provides membrane stabilization. Potassium redistribution and elimination must be arranged separately.
D. Urgent hemodialysis (Why this does not fit)
Dialysis can provide definitive potassium elimination in kidney failure, but IV calcium supplies immediate membrane protection while dialysis is arranged.
Takeaway: Treat toxic hyperkalemic ECG changes promptly while addressing the potassium excess.
A. A PR below 120 ms proves an accessory pathway in every patient (Why this does not fit)
Enhanced AV conduction and other mechanisms can shorten PR without manifest accessory-pathway activation.
B. The absent delta wave confirms a historical Lown-Ganong-Levine pathway (Why this does not fit)
That historical label does not identify a single proven anatomic mechanism.
C. A normal QRS excludes every possible supraventricular tachycardia mechanism (Why this does not fit)
Concealed pathways and AVNRT can exist without a delta wave at rest.
D. Short PR alone does not establish ventricular preexcitation (Best answer)
Manifest preexcitation requires additional evidence such as a delta wave and altered ventricular activation. History and further evaluation determine significance.
Takeaway: Do not turn one short interval into an unproven accessory-pathway diagnosis.
A. One week of therapeutic anticoagulation before cardioversion without thrombus imaging, then four weeks afterward (Why this does not fit)
Without imaging to exclude thrombus, one week is shorter than the recommended three-week preparation for AF of uncertain duration.
B. Thrombus-excluding imaging followed by cardioversion, starting anticoagulation only after the procedure (Why this does not fit)
Imaging does not replace the need to establish therapeutic anticoagulation before cardioversion and continue it afterward.
C. Three weeks of therapeutic anticoagulation beforehand, discontinued once sinus rhythm is restored (Why this does not fit)
Anticoagulation should continue without interruption for at least four weeks afterward; successful conversion does not eliminate the immediate embolic risk.
D. Three weeks of therapeutic anticoagulation or imaging to exclude thrombus, with therapeutic anticoagulation established before cardioversion and continued for at least four weeks afterward (Best answer)
For AF of uncertain duration, either preparation pathway requires therapeutic anticoagulation before cardioversion and uninterrupted continuation afterward. Assess longer-term treatment separately.
Takeaway: Plan embolic protection before and after elective cardioversion; assess longer-term anticoagulation separately.
Concealed long-QT disease can have a normal resting QT, but exercise-induced bidirectional VT is more characteristic of CPVT.
B. Catecholaminergic polymorphic ventricular tachycardia (Best answer)
Adrenergic provocation with bidirectional VT and a usually normal resting ECG is characteristic of CPVT.
C. Arrhythmogenic right ventricular cardiomyopathy (Why this does not fit)
Early disease can evade echocardiography, but this stress-provoked bidirectional pattern with normal resting studies more strongly supports CPVT.
D. Brugada syndrome (Why this does not fit)
Brugada events more often occur at rest or during fever, with a characteristic right-precordial ECG pattern, rather than this exercise-provoked bidirectional rhythm.
Takeaway: Exercise-related symptoms may reveal inherited disease that is invisible on a resting tracing.
