1. Prepare the signal. Confirm identity, indication, patient position, skin contact and electrode labels. Support relaxed limbs; reduce movement. Inspect calibration and filters before accepting machine intervals.
2. Count spaces from a palpable landmark. Find the sternal angle and second rib, then count to the fourth intercostal space for V1/V2. Locate V4 before interpolating V3. Keep V5/V6 level with V4; do not follow a rib downward.
3. Use standard limb sites. Arms and legs distal to shoulders and hips; wrists/ankles are not mandatory. Torso relocation changes the tracing and must be documented.
4. Preserve comparability. Record nonstandard sites, gain, speed and patient position. Compare like acquisitions before interpreting a new axis or voltage change.

At 25 mm/s, one small square is 40 ms; at 10 mm/mV, one small square is 0.1 mV. A displayed image may be resized: measure from its printed grid and calibration pulse, not a ruler held against a screen. Place chest electrodes against the chest wall at the anatomical landmarks; breast tissue is not a replacement landmark.

An unexpectedly negative P–QRS–T complex in I and positive aVR should trigger a cable check, especially when the prior ECG had a different orientation. An axis label from the computer cannot distinguish a biological change from a change in the measurement system.

1. Start with the P wave. Is the apparent atrial axis plausible for the rhythm? Look for coordinated polarity changes rather than an isolated negative QRS.
2. Inspect all six limb leads. With isolated RA/LA exchange, I is inverted, II/III and aVR/aVL exchange, and aVF is unchanged. These follow directly from the lead equations.
3. Inspect V1–V6. Isolated arm exchange leaves their reference unchanged. Mirror-image dextrocardia commonly gives poor or reversed progression in conventional left-sided chest leads; other causes of poor progression remain possible.
4. Trace cables to skin and repeat. Verify chest landmarks too. If dextrocardia is suspected, correlate examination/imaging and obtain an explicitly labeled adapted recording.

Baseline wander, muscle activity, loose electrodes and electrical interference can imitate rhythm or repolarization abnormalities. Look across simultaneous leads for native QRS complexes continuing through noise, and relate the pattern to movement and the observed patient. Do not use apparent clinical stability alone to dismiss a dangerous rhythm.

1. Fix acquisition first. Restore contact, relax/support limbs and inspect cables. Repeat while minimizing motion; preserve the original for comparison.
2. Read the bandwidth. The high-pass filter sets the low-frequency boundary; the low-pass filter sets the high-frequency boundary. The 50/60-Hz notch targets mains interference.
3. Choose the diagnostic question. Rhythm monitoring and diagnostic ST/QRS analysis require different fidelity. Retain a standard diagnostic recording when a stronger filter is used to make rhythm visible.
4. Document the change. Compare recordings with settings shown; an apparent improvement may be a processing effect.

A primary 45-patient experiment demonstrated artifactual ST shifts with a 0.5-Hz high-pass filter in real-time mode. This is a phase-response issue: modern validated digital filtering cannot be judged by the cutoff number alone. A 40-Hz low-pass filter can improve noise but attenuate rapid QRS detail and pacing spikes.

Original teaching schematics, not patient recordings. CC BY 4.0 or MIT. Timing and voltage are illustrative unless explicitly labeled.

1. Is the ventricular rhythm regular?

   Use a long strip and actual RR measurements. Look beyond one short sample.

2. Is atrial activity organized?

   Inspect several leads for consistent P waves, flutter activity, premature atrial beats or a rhythm marching through artifact.

3. How do atria and ventricles relate?

   A fixed relationship, variable conduction, nonconducted premature P wave or independent rhythms can explain the same pause.

Original teaching schematics, not patient recordings. CC BY 4.0 or MIT. Timing and voltage are illustrative unless explicitly labeled.

Open the rotating QRS-axis lab: six leads, one vector →

1. No pulse? Activate the cardiac-arrest pathway: CPR and defibrillation for VF/pulseless VT.
2. Pulse, with instability caused by the tachycardia? Hypotension/shock, altered mental status, ischemic discomfort or acute heart failure → prompt synchronized cardioversion for monomorphic WCT. Sedate if feasible without delaying treatment.
3. Sustained polymorphic VT? Immediate unsynchronized shock; variable QRS complexes do not offer a reliable synchronization target.
4. Stable regular monomorphic WCT? Monitor, defibrillator ready, IV access, 12-lead ECG and expert help. Investigate VT, SVT with aberrancy, pre-excitation and pacing; check toxic/metabolic causes.

Record response without overinterpreting it: some idiopathic VTs terminate with adenosine, so termination alone does not prove SVT. Failure to terminate is also not a stand-alone VT test. A slower VT can occur below the familiar 150/min treatment-algorithm heuristic.

1. No RS complex in any of V1–V6? Yes → algorithm classifies VT. An RS requires an R followed by an S; QS and qR do not qualify. If at least one RS exists, continue.
2. Longest RS interval >100 ms in any precordial lead? Measure from R onset to the deepest S point in each measurable RS; use the longest. Yes → VT. Exactly 100 ms does not satisfy “>100.”
3. A–V dissociation? Demonstrate atrial and ventricular independence; true capture/fusion beats can expose it. Yes → VT. No visible P waves means “not demonstrated,” not proof of A–V association.
4. VT morphology in both the V1/V2 region and V6? Use the pattern-specific criteria below. Yes → VT. All four steps negative → original algorithm labels SVT with aberrancy; clinical uncertainty may remain.

Original schematics; not patient tracings. Time and voltage are illustrative unless a measurement is labeled.

The original 554-tachycardia study reported excellent performance; independent validation was less favorable. “Algorithm favors SVT” does not authorize unsafe SVT treatment when the clinical prior remains strongly ventricular.

Original schematics; not patient tracings. Time and voltage are illustrative unless a measurement is labeled.

Compare the right-precordial and lateral leads together. Measure R and S amplitudes from the same baseline; “R:S <1” means positive peak height smaller than negative depth, not a duration ratio. A deep q followed by R is a qR, not an rS.

Marriott/Sandler studied RBBB-type ectopic morphology; Wellens tested tachycardias against His-bundle recordings; Kindwall developed the LBBB criteria. These are morphology observations, not interchangeable point systems. QRS width and axis add context, but do not replace the lead-specific analysis or establish a mechanism alone.

1. Initial R in aVR? An initial dominant R, including R or Rs configuration, is a positive VT criterion. Distinguish it from a small r in rS, or a terminal R after an initial q. If absent, continue.
2. Initial r or q wider than 40 ms? Measure the initial wave’s duration, from its onset to return to baseline. Yes → VT; exactly 40 ms does not satisfy “>40.”
3. Notch on the initial downstroke of a predominantly negative QRS? Yes → VT. A late terminal notch or arbitrary baseline noise is not this finding.
4. Initial/terminal 40-ms excursion ratio vᵢ/vₜ ≤1? Yes → VT. A reliably measured ratio >1 yields the original algorithm’s SVT classification. See the next measurement plate.

Original schematics; not patient tracings. Time and voltage are illustrative unless a measurement is labeled.

Each step is evaluated only if preceding steps are negative. Initial positive forces and slow early activation favor a ventricular origin because ordinary supraventricular conduction usually activates ventricles rapidly through the specialized conduction system.

Small-amplitude aVR, noisy onset/offset, prior scar and pre-excitation limit interpretation. The original aVR study included 483 WCTs from 313 patients; subsequent independent testing did not reproduce uniformly high diagnostic performance. One lead simplifies acquisition, not uncertainty.

Original schematics; not patient tracings. Time and voltage are illustrative unless a measurement is labeled.

1. Set landmarks. Identify QRS onset and offset using the simultaneous augmented leads (aVR, aVL, aVF), as in the original study; then mark onset +40 ms and offset −40 ms on the aVR complex being measured. At 25 mm/s each window is one small square; at 50 mm/s, two.
2. Measure excursion, not area. vᵢ is the absolute vertical excursion during the first window; vₜ is the corresponding excursion during the last. Use one voltage scale. These are proxies for activation velocity, not directly measured tissue conduction speeds.
3. Respect changes of direction. For a genuinely biphasic window, account for its component vertical excursions rather than allowing positive and negative components to cancel. Do not trace noise fluctuations as real deflections.
4. Compare. vᵢ/vₜ ≤1 favors VT in the 2008 algorithm; >1 favors SVT. Apply this only after the first three aVR criteria are negative.

Early Purkinje recruitment can make VT’s initial forces rapid. Conversely, scar or drug-related slowing can make SVT’s initial forces slow. A mathematically clean ratio does not remove those biological exceptions.

Original schematics; not patient tracings. Time and voltage are illustrative unless a measurement is labeled.

Pava: lead II RWPT ≥50 ms

Measure from QRS onset to the first change in direction of the initial deflection: an R peak, S nadir, or genuine early notch. It is not necessarily the tallest R, and it is not total QRS duration. At 25 mm/s, 50 ms is 1.25 small squares. The original 218-ECG EPS-confirmed study reported LR+ 34.8; the independent 2012 comparison found much weaker performance (sensitivity 60%, specificity 82.7%). A negative result cannot safely rule out VT.

VT score: count the published findings

The range is 0–8. In the original 786-WCT study, ≥3 points had 99.6% specificity. A threshold ≥4 had 100% observed specificity, but only about one third of VTs reached it. Those are cohort findings, not guaranteed certainty. High specificity does not imply high sensitivity. Low scores do not exclude VT.

Original educational arithmetic pathway. An assumed prior and one external whole-algorithm LR are used, not a validated patient calculator.

For one diagnostic test: prior odds = p/(1−p); posterior odds = prior odds × LR; posterior probability = odds/(1+odds). The external 2012 Brugada sensitivity 0.890 and specificity 0.592 imply LR− = (1−0.890)/0.592 ≈0.186. At an assumed 90% prior, a negative classification still leaves about 63% probability; at 50% prior, about 16%.

Name provenance: Swanick/LaCamera/Marriott (1972) concerns right-ventricular ectopic morphology, not a Bayesian WCT classifier.

A · Compare both clocks

PauseReplay

B · Repeated shape is not mechanism

Left: original conceptual timing diagram, CC BY 4.0 or MIT. Right: Rocuronium Bromide, Wikimedia Commons · CC0 1.0. Unchanged PNG rendering of the source vector. Teaching illustration, not a patient recording.

What independent validation changes

In the 260-WCT head-to-head study, reference diagnoses came from EPS (216), device electrograms (38) and serial ECGs (6). Brugada accuracy was 77.5%; RWPT-II accuracy 68.8%. These data argue against treating derivation accuracy as universal or averaging algorithm outputs into a new diagnosis.

Report example: “Regular monomorphic WCT. VT favored by prolonged precordial RS interval; atrial activity indeterminate. Baseline tracing unavailable. Manage as uncertain/likely ventricular WCT pending expert assessment.” Separate what was measured from what was inferred.

1. Choose and document. Inspect all leads; use one with a clear terminal T, often II or V5/V6. Record lead, speed, gain, beat selection and endpoint method. Follow the same method on serial ECGs.
2. Mark QRS onset. Start at the beginning of ventricular depolarization, including an initial Q if present, rather than the R peak.
3. Mark terminal T. Threshold measurement follows T to the baseline. The tangent method extends the steepest terminal downslope to the isoelectric baseline. In a negative T, use the terminal return toward baseline. A second component of a genuinely biphasic/notched T belongs to T; a separate U does not.
4. Check another lead. T–U fusion, low amplitude and noise can make the endpoint indeterminate. Do not silently measure QU or invent precision: compare leads and obtain expert review if the decision hinges on it.

For stable sinus rhythm, use several representative beats. In AF, do not cherry-pick a single short or long cycle: a multiple-beat average better matched subsequent sinus-rhythm measurements in a comparative study. No universal AF measurement/correction method is established; document the averaging approach and residual uncertainty.

Use RR in seconds. QT may remain in milliseconds, giving QTc in milliseconds. State the method; a machine’s “QTc” without its formula is incomplete information.

1. Measure first. Verify the endpoint and QRS width before interpreting a computed QTc.
2. Choose for the question. A congenital-LQTS diagnostic score uses its specified correction; do not quietly replace it with another formula. Drug-specific initiation protocols may likewise prescribe a method.
3. Compare consistently. Use the same lead, method and correction longitudinally. Reassess after a stable rate when feasible.

In a large observational study, Fridericia reduced rate dependence relative to Bazett in recordings without conduction defects or ventricular pacing. This supports deliberate formula choice, not switching formulas until a desired threshold is crossed.

A bundle-branch block lengthens ventricular activation and therefore QT. A conventional narrow-QRS QTc cutoff cannot simply identify how much of that increase is abnormal recovery. Report rhythm, QRS width, raw QT, rate and the chosen adjustment.

1. Establish the context. Compare a prior narrow-QRS ECG when available. New conduction disease also needs its own explanation.
2. Inspect repolarization separately. AHA/ACCF/HRS guidance favors JT assessment in conduction delay. State exactly how any rate correction is performed: “JTc” may mean a rate-corrected JT or QTc minus QRS, which are not algebraically identical.
3. If using an LBBB estimate, name it. The simplified Bogossian approach is QTm = measured QT − 0.50 × QRS. Subtract half of the full LBBB QRS duration before heart-rate correction, not half of only the excess above 120 ms.

No universal JTc threshold is supplied here. A borderline estimate with syncope, T–U distortion or ventricular ectopy needs expert interpretation rather than a second decimal place.

1. Recognize the substrate. QT prolongation plus reduced repolarization reserve: QT-active drugs or interacting drugs, low potassium/magnesium, bradycardia/pauses, and impaired drug clearance.
2. Recognize the trigger. A premature beat may be followed by a long pause; the next beat develops exaggerated T–U prolongation. A subsequent early ventricular beat can initiate polymorphic VT: the classic short–long–short sequence.
3. Escalate the warning. QTc >500 ms or an increase ≥60 ms after an at-risk drug warrants prompt review, especially with post-pause distortion, alternans, couplets or nonsustained polymorphic VT. These are warning thresholds, not a claim that every prolonged QT causes torsades.
4. Act on the setting. Stop the culprit when appropriate, review interactions and clearance, correct electrolytes and provide monitored care with immediate defibrillation available. Recurrent pause-dependent episodes may require rate support under specialist direction.

Drug decisions also depend on the agent and clinical benefit: follow its specific monitoring protocol. Rate acceleration with drugs is not a generic maneuver for congenital LQTS; obtain expert help. A prior “normal” ECG does not eliminate an acquired multi-hit risk.

1. Exclude an acquired explanation. Recheck QT manually and review drugs, electrolytes, bradycardia and conduction delay. A reversible cause and an inherited predisposition can coexist.
2. Apply the stated criteria. ESC 2022 supports diagnosis with QTc ≥480 ms on repeated 12-lead ECGs or a modified diagnostic score >3; a pathogenic mutation establishes diagnosis regardless of QT duration. In arrhythmic syncope or cardiac arrest, QTc ≥460 ms raises a stronger diagnostic concern.
3. Escalate appropriately. Use inherited-arrhythmia assessment and genetic counseling, including family evaluation. A variant of uncertain significance is not interchangeable with a pathogenic variant.

Modified score: key weights

A low or borderline resting QTc does not exclude concealed familial LQTS. Conversely, a borderline machine value without corroborating evidence is not sufficient to attach a lifelong inherited diagnosis.

Original schematics; not patient tracings or calibrated waveforms · CC BY 4.0.

These are group associations from genotype–phenotype studies. There is substantial overlap and variation across leads, rate and serial ECGs. Morphology can direct scrutiny and family evaluation; it cannot establish a genotype or choose a genotype-specific treatment on its own. Normal-looking T waves do not exclude a pathogenic variant.

Use recovery deliberately

1. Specify the test. Obtain supervised exercise and recovery recordings when appropriate to the inherited-arrhythmia evaluation.
2. Keep the clock. QTc ≥480 ms at the fourth minute of recovery adds one diagnostic-score point; it is not interchangeable with a peak-exercise or immediate-recovery value.
3. Keep the population in mind. The exercise-algorithm derivation/validation study evaluated relatives of LQTS probands, not indiscriminate low-risk population screening.

Original schematics; not patient tracings or calibrated waveforms · CC BY 4.0.

1. Name what is present. Describe type 1 pattern, lead and electrode position. A simple rSr′ or right bundle-branch block label does not capture the diagnostic ST–T contour.
2. Look for a mimic. Evaluate ischemia, electrolyte disorders and other reversible or structural explanations. Resolution after correction alone does not settle whether underlying susceptibility exists.
3. Separate pattern from syndrome. A spontaneous type 1 pattern after exclusion of other heart disease has different diagnostic weight from an induced pattern. Drug-induced type 1 alone is less specific and requires supporting clinical/family/genetic evidence under contemporary guidance.

Risk assessment depends on documented ventricular arrhythmia, probable arrhythmic syncope, spontaneous versus induced pattern and the broader evaluation. The drawing is a contour lesson, not a calibrated diagnostic tracing.

1. Acquire a valid baseline. Accidental superior placement on a supposedly standard ECG creates ambiguity. Keep standard leads and intentional high-right recordings distinguishable.
2. Record the circumstance. Document fever, relevant drugs, electrolytes and symptoms. The phenotype can be intermittent; compare serial recordings.
3. Treat fever promptly. Fever can unmask the pattern and increase arrhythmic risk in susceptible people. Syncope, ventricular arrhythmia or high-risk presentation needs urgent assessment rather than waiting for an outpatient repeat.
4. Use drug challenge selectively. Sodium-channel blocker testing belongs in an experienced, monitored setting with resuscitation capability and a predefined protocol. It can produce conduction slowing and ventricular arrhythmia, and a positive test has imperfect specificity.

Review possible Brugada-provoking drugs with a reliable, current specialist resource; do not use this chapter as a drug list. A fever- or drug-associated pattern should be reported with its trigger and expert interpretation. “It disappeared” describes a dynamic phenotype; it does not by itself prove a harmless phenocopy or establish an inherited syndrome.

This published case pairs an initial ECG during fever with a repeat after fever resolved. The authors described a type 1-like pattern in V1 on the first recording. These are original clinical images, not generated or redrawn signals.

Overview only: open each unchanged image to inspect the right-precordial contour and calibration at full resolution.

1. Find V1 before comparing. The two figures use different lead layouts and recording rates; follow the labels instead of assuming the same panel position.
2. Compare contour. Examine the terminal QRS, elevated ST segment and subsequent T, not just the height of one peak.
3. Read the clinical provenance. The report’s first subject had no reported syncope or relevant family history, no observed arrhythmia during admission, and resolution of the pattern after fever treatment. Follow-up including genetic testing was planned.
4. Keep the limit. Planned testing is not a confirmed genetic result. This paired example demonstrates dynamic expression; it does not prove that all fever-associated patterns are benign or that this individual had genetically confirmed inherited Brugada syndrome.

1. Check gain. The authentic example in the next case uses 5 mm/mV: double measured millimeters to compare with standard-gain thresholds, or calculate in mV directly.
2. Measure named deflections. Sum amplitudes relative to the local baseline, not total peak-to-peak QRS height.
3. Look beyond voltage. Lateral downsloping ST depression with asymmetric T inversion can be secondary to altered activation/repolarization. Report the pattern and compare prior tracings.
4. Correlate anatomy. Echocardiography assesses mass, geometry and competing disease when clinically indicated.

Voltage criteria are insensitive and depend on age, body habitus, sex, ancestry and lead placement. Thin or athletic people can have large voltages; obesity or emphysema can attenuate them. Bundle block, pacing and scar complicate standard criteria. “Strain” is a conventional ECG description, not a measurement of myocardial deformation. A broad/notched P in II or prominent terminal negative P component in V1 suggests left atrial abnormality; tall inferior P waves suggest right atrial abnormality. Confirm chamber size by imaging rather than equating electrical criteria with enlargement.

1. Validate the recording. Recheck V1 placement, QRS duration and comparison ECG.
2. Describe the components. Axis, R/S distribution, conduction and ST–T findings are separate observations.
3. Use the time course. Chronic pulmonary or congenital disease differs from sudden dyspnea, syncope or hypoxemia.
4. Use the clinical pathway. Assess PE probability and obtain indicated testing; imaging evaluates RV structure/function.

In a community population without clinical cardiovascular disease, the MESA-RV study found ECG criteria unsuitable for screening mild RVH. Performance in selected congenital or pulmonary-hypertension populations cannot be transplanted to an incidental ECG. The source-annotated RVH record in the next case is a comparison exercise, not proof that every voltage criterion must be present.

Crochetage describes notching near the ascent or apex of the R wave in inferior leads II, III and aVF. Its classic association is secundum atrial septal defect. Do not use the term interchangeably with terminal R′ in V1 or with every fragmented QRS pattern.

1. Confirm the notch is real. Look for reproducibility across beats and at diagnostic bandwidth; noise and processing can create or erase fine detail.
2. Check all inferior leads. Note whether the feature occurs in one, two or all three; distribution mattered in the original study.
3. Assemble the context. Consider accompanying rightward axis, incomplete RBBB and clinical evidence of right-sided volume loading, without treating any as proof.
4. Resolve anatomy. Echocardiography evaluates septal anatomy and right-heart size; further shunt assessment follows the clinical question.

Heller and colleagues compared 1,560 people across several structural diagnoses and controls. Crochetage occurred in 73.1% of the secundum-ASD group, but also in other groups. Presence in all three inferior leads was more specific in that study. These selected-population results are not a universal screening probability.

Conventional low-voltage thresholds are QRS peak-to-peak amplitudes ≤5 mm in every limb lead or ≤10 mm in every precordial lead at 10 mm/mV. State which distribution is involved; one small lead does not meet a global criterion. First exclude reduced gain, poor contact and acquisition differences.

1. Verify the amplitude. Use the calibration pulse and all relevant leads; compare a prior recording at the same gain.
2. Consider attenuation. Body habitus, emphysema, effusions and other extracardiac factors may reduce the measured signal.
3. Compare imaging. Increased wall thickness with unexpectedly low or modest voltage raises suspicion for amyloidosis, especially with conduction disease or a pseudoinfarction pattern.
4. Follow the disease pathway. Integrate echocardiography/CMR, phenotype and appropriate amyloid testing rather than typing the disease from ECG.

Normal or high QRS voltage does not exclude cardiac amyloidosis; the classic voltage–thickness mismatch is absent in many affected patients. Low voltage also cannot distinguish AL from ATTR. A positive bone-tracer scan should not be interpreted as ATTR without the required monoclonal-protein assessment.

1. Establish timing. Identify atrial activity, stimulus markers, native QRS complexes and their relationships. Digital display artifacts are not always true pacing stimuli.
2. Assess capture. A stimulus should produce the expected atrial or ventricular response when tissue is excitable. Compare morphology across multiple beats.
3. Recognize mixed activation. Fusion combines paced and intrinsic activation; pseudofusion is a pacing stimulus that does not contribute materially to an already activated QRS.
4. Use the device record. New pauses, symptoms or changing paced morphology require clinical assessment and interrogation, not a diagnosis from one printed strip alone.

Conventional RV pacing often resembles LBBB, but pacing site, conduction-system capture, biventricular pacing and fusion can produce other morphologies. A relatively narrow QRS does not exclude pacing. Bipolar pacing spikes may be very small or filtered out; absence of a printed spike is not proof of absent output.

CRT may deliberately exploit fusion with intrinsic conduction. Therefore an intermediate QRS shape is not automatically malfunction. Conversely, a pacing spike that falls in refractory tissue does not demonstrate successful capture simply because a QRS is nearby. Verify the interval and morphology.

LVAD electromagnetic interference can obscure P waves, QRS boundaries and the baseline. Evaluate the patient and circulation immediately if unstable; neither apparent artifact nor a weak/absent palpable pulse establishes the rhythm in continuous-flow support.

1. Improve contact first. Prepare skin, replace loose electrodes, support cables and reduce motion. Verify standard lead placement before comparing morphology.
2. Compare simultaneously. Look for organized complexes in less affected leads and examine prior/device recordings. Record the LVAD model and prescribed speed as context.
3. Preserve the diagnostic tracing. A documented 40-Hz low-pass view may clarify rhythm; retain the standard-bandwidth ECG for QRS/ST–T assessment. Targeted bandstop filtering needs appropriate technical support.
4. Escalate uncertainty. Involve the VAD/electrophysiology team if rhythm or device behavior remains unclear. Never change pump speed for ECG acquisition.

In a nine-patient study, HeartMate 3 at 5700 rpm produced a dominant 95-Hz artifact; model-specific spectra included additional peaks. Legacy HeartWare examples showed a dominant component near twice the rotational frequency. These observations explain interference; they are not validated noninvasive pump diagnostics.

A 2024 electrode-placement study abstract found no alternative configuration that consistently reduced noise. Do not promise that a particular limb site, side of the body or manufacturer-specific arrangement will solve interference. If nonstandard placement is necessary, label it and avoid direct voltage/axis comparison with standard ECGs.

1. Find the J point and compare with baseline.

   Check gain and QRS morphology, then inspect contiguous leads. New ST elevation in two contiguous leads supports a STEMI pattern when appropriate clinical context and exclusions are met.

2. Apply the correct thresholds.

   Usually ≥1 mm; in V2–V3, ≥2 mm in men ≥40 years, ≥2.5 mm in younger men, and ≥1.5 mm in women. These standard thresholds assume no confounding LVH or bundle-branch block.

3. Act on the entire presentation.

   Persistent ischemic symptoms, shock, dynamic changes or an occlusion-equivalent pattern warrant urgent expert assessment even without classic thresholds.

Original teaching schematics, not patient recordings. CC BY 4.0 or MIT. Timing and voltage are illustrative unless explicitly labeled.

The original Sgarbossa rule scores concordant elevation 5 points, concordant V1–V3 depression 3, and discordant elevation ≥5 mm 2; a total ≥3 is positive. Do not mix the original score with the modified proportional rule.

Original teaching schematics, not patient recordings. CC BY 4.0 or MIT. Timing and voltage are illustrative unless explicitly labeled.

1. Identify a coherent pattern.

   A short PR, delta wave and widened QRS support manifest ventricular pre-excitation. Fusion can make the pattern subtle; compare multiple leads and prior ECGs.

2. Recognize the dangerous rhythm.

   A very fast, irregular wide-complex rhythm with changing QRS appearance may represent pre-excited AF. AV-nodal blocking drugs can be harmful; use urgent rhythm-specific management.

3. Keep localization in its own validated framework.

   Initial delta-wave polarity, lead placement and the intended study population matter. A concealed pathway with no antegrade pre-excitation cannot be localized by a delta-wave algorithm.

Sources and image reuse

Each chapter links its primary studies or professional guidance. Original schematics are educational abstractions; real ECGs retain case or dataset provenance, licenses and stated transformations. The axis, QT and Bayesian tools teach their stated models; they do not establish a patient diagnosis.