Submodule
Signal, Leads, and Calibration
The ECG converts changing cardiac electrical vectors into calibrated lead-specific deflections and must be quality checked before interpretation.
- Depolarization and repolarization
- Lead vectors and polarity
- Paper speed and gain
- P, QRS, ST, and T sequence
Verify before measuring
Lead polarity shapes deflection
Map activation and recovery
Never read in isolation
Separate electrical from mechanical events
P waves represent atrial depolarization, QRS complexes represent ventricular depolarization, and T waves represent ventricular repolarization. The ECG does not directly show contraction, blood pressure, perfusion, or valve motion. Clinical correlation remains necessary.
Read vectors through lead polarity
A depolarization vector moving toward a positive electrode produces a positive deflection, while movement away produces a negative deflection. Limb leads view the frontal plane, and precordial leads view the horizontal plane. All leads record the same heartbeat from different angles.
Verify scale before measuring
At standard 25 mm/s speed, one small horizontal box is 0.04 second and one large box is 0.20 second. At standard 10 mm/mV gain, 10 vertical millimeters equals 1 mV. Nonstandard speed or gain changes every interval or voltage conclusion.
Protect interpretation from artifact
Motion, tremor, loose electrodes, electrical interference, and lead reversal can mimic arrhythmia, axis deviation, or infarction. Compare the tracing with the pulse, inspect simultaneous leads, correct electrodes, and repeat acquisition when quality is questionable.
Quick check
Submodule
Rate, Regularity, and Rhythm
Rhythm diagnosis begins by calculating rate, testing regularity, identifying atrial activity, and mapping every atrial event to ventricular conduction.
- Regular and irregular rate methods
- Sinus rhythm criteria
- Atrial fibrillation
- Atrial flutter and AV ratios
Use regular or irregular method
Identify patterns
Track morphology and rate
Expose block or dissociation
Calculate rate using the right method
For a regular rhythm at standard speed, divide 300 by large boxes or 1500 by small boxes between R waves. For an irregular rhythm, count QRS complexes across a known time span and scale to one minute. Report variability when one average hides clinically important pauses or bursts.
Prove sinus origin
Sinus rhythm has consistent sinus P-wave morphology, commonly upright in lead II and negative in aVR, with one P before each QRS and one QRS after each P. Regularity alone does not establish sinus origin.
Recognize atrial fibrillation carefully
Atrial fibrillation has disorganized atrial activity and an irregular ventricular response when conduction is not fixed or paced. Exclude artifact, multifocal atrial tachycardia, and frequent ectopy before assigning the diagnosis and its anticoagulation implications.
Find concealed flutter
Atrial flutter produces organized repetitive atrial activity with fixed or variable AV conduction. A regular ventricular rate near 150 beats per minute should prompt a search for 2-to-1 flutter, especially in inferior leads and V1, because one flutter wave may be hidden in the QRS or T wave.
Quick check
Submodule
Intervals, Axis, and Repolarization
PR, QRS, QTc, frontal axis, and waveform morphology turn timing and direction into clinically useful localization and medication-safety information.
- PR interval
- QRS duration
- QT and correction formulas
- Frontal QRS axis
Measure onset to onset
Wide means altered activation
Correct and interpret by context
Use limb-lead polarity
Measure PR from onset to onset
Measure from the beginning of the P wave to the beginning of the QRS. The interval includes atrial, AV nodal, His, and proximal bundle conduction. Assess duration and beat-to-beat behavior because progressive prolongation, fixed prolongation, and AV dissociation mean different things.
Use QRS width to frame activation
A wide QRS indicates altered ventricular activation from ventricular origin, bundle-branch block, pacing, preexcitation, hyperkalemia, or sodium-channel blockade. Width does not determine the cause by itself, so morphology and clinical context remain essential.
Correct QT with humility
Measure QT to the end of the T wave in a clear lead and correct for heart rate. Bazett can overcorrect at faster rates and undercorrect at slower rates, while other formulas have different properties. Wide QRS and U waves complicate interpretation. Review the raw tracing when drug safety depends on QTc.
Estimate frontal axis from limb leads
Use QRS polarity in leads I and aVF as a rapid quadrant screen, then use lead II when needed to separate normal from leftward axis. Check for limb-lead reversal before attributing an unusual axis to conduction, infarction, or chamber disease.
Quick check
Submodule
Conduction Blocks and Ventricular Activation
AV block and bundle-branch block are recognized through atrial and ventricular relationships, interval behavior, QRS morphology, escape reliability, symptoms, and reversible causes.
- First-degree and Mobitz I
- Mobitz II and complete block
- Right bundle-branch block
- Left bundle-branch block
Distinguish Wenckebach from fixed PR
Higher progression risk
Assess concordant clinical context
Treat unstable bradycardia
Differentiate delayed from dropped conduction
First-degree AV block has prolonged PR with complete 1-to-1 conduction. Mobitz I usually shows progressive PR prolongation before a dropped QRS. Medication, ischemic, electrolyte, vagal, and structural causes need review in both patterns.
Recognize high-risk block
Mobitz II has intermittently nonconducted P waves without progressive PR prolongation and often reflects infranodal disease. Complete heart block has AV dissociation and an escape rhythm. Symptoms, perfusion, QRS width, escape reliability, and cause determine urgency, but pacing preparation should not be delayed in instability.
Read right bundle activation
RBBB widens the QRS and produces characteristic terminal rightward forces in V1 and broad terminal S waves in lateral leads. Compare with prior ECG and interpret within pulmonary, ischemic, structural, and rate-related contexts.
Respect secondary changes in LBBB
LBBB reverses the normal left ventricular activation sequence and produces secondary ST-T discordance. Acute coronary occlusion assessment uses symptoms, serial ECGs, biomarkers, imaging, and validated concordance patterns. LBBB alone is neither proof nor exclusion of infarction.
Quick check
Submodule
Ischemia, Electrolytes, and Medication Effects
ST, T, QRS, and QT abnormalities emerge from ischemia, infarction, pericardial disease, conduction, electrolytes, drug exposure, toxins, and normal variation.
- ST elevation and reciprocal change
- ST depression and T-wave inversion
- Potassium and magnesium patterns
- QT-active and sodium-channel drugs
Seek a territorial pattern
One tracing is not the diagnosis
Treat dangerous physiology
Connect target to waveform
Treat acute occlusion as time sensitive
ST elevation in contiguous leads with supportive symptoms, morphology, and reciprocal change can identify acute coronary occlusion before troponin rises. Obtain posterior or right-sided leads when the territory is concealed and use emergency pathways without waiting for biomarker confirmation when the pattern is diagnostic.
Keep the ST-T differential open
ST depression and T-wave inversion can reflect ischemia, reciprocal change, ventricular strain, bundle-branch block, pacing, electrolytes, medication effects, or baseline variation. Distribution, dynamic change, symmetry, symptoms, and QRS context refine meaning.
Recognize dangerous electrolyte physiology
Hyperkalemia can progress through peaked T waves, conduction slowing, P-wave loss, QRS widening, and arrest, but severe values may lack classic ECG changes. Hypokalemia can flatten T waves, depress ST segments, create U waves, and increase ectopy. Hypomagnesemia amplifies torsades risk.
Connect medication targets to waveforms
QT-active drugs delay repolarization, while sodium-channel blockade can widen QRS and alter axis. Risk rises with concentration, interactions, organ dysfunction, bradycardia, electrolyte depletion, and multiple active agents. Treat the exposure and physiology, not only the printed interval.
Quick check
Submodule
Emergency Interpretation Workflow
A fixed interpretation sequence supports accuracy, but pulse, perfusion, and symptoms determine when electrical treatment or stabilization must precede detailed classification.
- Instability assessment
- Wide-complex tachycardia
- Symptomatic bradycardia
- Repeat ECG and cause correction
Identify instability
Check quality and calibration
Use a fixed sequence
Repeat after intervention
Start with the patient
Check pulse, airway, oxygenation, blood pressure, mental status, ischemic discomfort, shock, and acute heart failure. Decide whether the rhythm is causing instability or reflecting another unstable illness such as sepsis, hypoxia, hemorrhage, or toxicity.
Treat unstable tachycardia electrically
When a tachyarrhythmia with a pulse causes hypotension, altered mental status, shock, ischemic chest discomfort, or acute heart failure, prompt synchronized cardioversion is indicated. Polymorphic VT cannot be synchronized reliably and requires unsynchronized shock.
Approach wide-complex tachycardia cautiously
Wide-complex tachycardia can be ventricular or supraventricular with aberrancy or preexcitation, and can arise from pacing, hyperkalemia, or sodium-channel blockade. When uncertainty remains, avoid therapies that can destabilize ventricular tachycardia and treat the most dangerous plausible diagnosis.
Support unstable bradycardia and reverse causes
Symptomatic bradycardia requires perfusion support, atropine when appropriate, and pacing or adrenergic support when instability persists. Treat ischemia, hypoxia, temperature disturbance, electrolytes, and medication or toxin causes concurrently. Repeat the tracing after meaningful intervention.
Quick check
Module test
Check the connections.
Each attempt draws 10 questions from the complete 108 question bank.
Each attempt draws a fresh set and rearranges the answer choices.
References
Current clinical foundation.
Lecture material was synthesized with the following contemporary guidance. Verify local policy and current guidance before applying clinical information.