The T Wave | ECG Anatomy Series

Conceptual Overview

The T wave represents ventricular repolarization - the process by which ventricular myocytes restore their resting membrane potential after depolarization. This electrical recovery phase is more heterogeneous and prolonged than depolarization, making T wave morphology exquisitely sensitive to metabolic disturbances, ischemia, and electrolyte abnormalities.

Unlike the QRS complex (which reflects rapid synchronized depolarization), the T wave represents a slower, more variable process influenced by:

Regional differences in action potential duration - epicardial cells repolarize before endocardial cells
Autonomic tone - sympathetic stimulation shortens repolarization while vagal tone prolongs it
Transmembrane ion gradients - particularly potassium, calcium, and magnesium
Myocardial perfusion and oxygenation - ischemia profoundly alters repolarization
Structural remodeling - hypertrophy and fibrosis change repolarization sequence

ECG Components showing T wave — The T wave follows the QRS complex and represents ventricular repolarization. Source: LITFL

Because repolarization normally proceeds from epicardium to endocardium (opposite to depolarization direction), the T wave is typically concordant with the QRS - meaning it points in the same direction as the dominant QRS deflection. This creates upright T waves in leads with upright QRS complexes.

Key concept: The T wave is more sensitive to pathological changes than the QRS complex because repolarization is a metabolically active process requiring ATP-dependent ion pumps. Any condition that impairs myocardial energy metabolism (ischemia, hypoxia, electrolyte disturbances) will manifest as T wave changes before QRS abnormalities appear.

Normal T Wave Characteristics

Normal T waves exhibit several consistent features that help distinguish physiologic from pathologic patterns:

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Characteristic	Normal Finding	Clinical Significance
Morphology	Asymmetric - gradual upslope with steeper downslope	Creates characteristic rounded appearance
Duration	0.10-0.25 seconds	Longer than QRS, typically 2-3 times QRS duration
Amplitude (Limb)	≤5mm	Higher amplitudes suggest abnormality
Amplitude (Precordial)	≤10mm	Increases V1→V4, then decreases
Direction	Concordant with QRS	Same polarity as dominant QRS deflection

Lead-Specific Normal Variants

Lead aVR: T wave normally inverted (QRS is also negative)
Lead V1: T wave may be inverted, flat, or slightly upright in adults
Lead III: T wave may be inverted, especially with vertical heart axis
Precordial leads: T wave amplitude increases from V1 to V4, then gradually decreases
Juvenile T wave pattern: Inverted T waves in V1-V3 can persist into early adulthood (more common in women and Black individuals)

Important distinction: T wave amplitude should be assessed in relation to QRS amplitude. A T wave that is more than 2/3 the height of the R wave may be abnormally tall, even if absolute amplitude is within normal limits. This ratio is particularly important in early ischemia detection.

Quick Hits – T Wave Essentials

Normal T waves are asymmetric with a gentle upslope and steeper downslope, typically concordant with the QRS complex
T wave inversion can indicate ischemia, strain patterns, or be a normal variant in specific leads (aVR, V1, III)
Hyperacute T waves are tall, broad, and symmetric - an early sign of acute STEMI before ST elevation develops
Tall peaked T waves suggest hyperkalemia, while flat/inverted T waves may indicate hypokalemia
Wellens syndrome shows biphasic or deeply inverted T waves in V2-V3, indicating critical LAD stenosis
T wave alternans (beat-to-beat amplitude variation) indicates electrical instability and ventricular arrhythmia risk

Tall or Peaked T Waves

Abnormally tall T waves can be physiologic or pathologic, with different morphologic characteristics helping distinguish the etiology:

Hyperacute T Waves (Early STEMI)

Morphology: Tall, broad-based, and symmetric
Timing: Earliest ECG sign of acute MI (within minutes), precedes ST elevation
Distribution: Anatomically localized to region of ischemia
Associated findings: Loss of R wave amplitude, ST segment straightening
Clinical significance: Represents acute transmural ischemia requiring immediate intervention

Hyperacute T waves in anterior STEMI — Hyperacute T waves in anterior leads - tall, broad, symmetric T waves with loss of R wave amplitude indicating acute LAD occlusion. Source: LITFL

Hyperkalemia

Morphology: Tall, narrow, peaked (tent-shaped) with narrow base
Distribution: Diffuse across all leads
Associated findings: PR prolongation, P wave flattening, QRS widening (as K+ rises)
Correlation: Severity increases with potassium level (typically >5.5-6.0 mEq/L for ECG changes)
Clinical significance: Risk of ventricular arrhythmias and cardiac arrest

Other Causes of Tall T Waves

Left ventricular hypertrophy: Tall T waves in lateral leads (I, aVL, V5-V6)
Early repolarization: Tall T waves with J-point elevation and notching
Acute pericarditis: Tall T waves in early stage before widespread ST elevation
Cerebrovascular accident: Diffuse tall T waves with prolonged QT
Athletes: Physiologic tall T waves as part of athletic heart syndrome

Distinguishing Hyperacute T Waves from Hyperkalemia:
Hyperacute T waves (ischemia): Broad-based, asymmetric, anatomically localized
Hyperkalemia: Narrow-based (tent-shaped), symmetric, diffuse distribution
Always correlate with clinical context and check potassium levels urgently if unclear.

Inverted T Waves

T wave inversion is one of the most common ECG abnormalities and can represent a spectrum from benign normal variants to life-threatening ischemia:

Ischemic T Wave Inversion

Morphology: Deep, symmetric inversion (often >5mm)
Timing: Develops hours to days after acute MI (evolutionary change)
Distribution: Anatomically localized to territory of affected vessel
Wellens syndrome: Biphasic or deeply inverted T waves in V2-V3 indicating critical LAD stenosis
Clinical significance: May indicate non-STEMI, evolving MI, or critical stenosis requiring intervention

Wellens syndrome Type A - biphasic T waves in V2-V3 indicating critical proximal LAD stenosis. High risk of extensive anterior MI if not intervened. Source: LITFL

Wellens syndrome Type B - deeply inverted T waves in V2-V4, also indicating critical LAD disease. Source: LITFL

Strain Patterns

Left ventricular strain: Asymmetric T wave inversion with ST depression in lateral leads (I, aVL, V5-V6)
Right ventricular strain: T wave inversion in right precordial leads (V1-V4) with acute PE or RV pressure overload
Morphology: Asymmetric with gradual downslope and rapid upslope (opposite of normal)

Right ventricular strain pattern in acute pulmonary embolism - T wave inversion in V1-V4 with S1Q3T3 pattern. Source: LITFL

Cerebral T Waves

Morphology: Deep, symmetric inversion with prolonged QT interval
Cause: Subarachnoid hemorrhage, intracerebral hemorrhage, ischemic stroke
Mechanism: Catecholamine surge causing myocardial injury (neurogenic stunned myocardium)
Distribution: Often diffuse, particularly in precordial leads

Other Causes of T Wave Inversion

Bundle branch blocks: Secondary T wave inversion in leads with predominant S wave (appropriate discordance)
Hypertrophic cardiomyopathy: Deep T wave inversion in lateral and/or inferior leads
Takotsubo cardiomyopathy: Diffuse T wave inversion with QT prolongation
Pericarditis (late stage): T wave inversion after ST segments normalize
Persistent juvenile pattern: Benign T wave inversion in V1-V3 in young adults
Digoxin effect: Downsloping ST depression with asymmetric T wave inversion (Salvador Dali sign)

Wellens Syndrome Recognition: This is a high-risk acute coronary syndrome pattern:
• History of recent chest pain (now resolved)
• Minimal or no cardiac enzyme elevation
• Biphasic or deeply inverted T waves in V2-V3
• Preserved R wave progression
• No significant ST elevation or Q waves
Action: Requires urgent cardiology consultation and angiography - 75% will develop extensive anterior MI within weeks if not treated.

Special T Wave Patterns

T Wave Alternans

Beat-to-beat variation in T wave amplitude, axis, or morphology:

Microvolt alternans: Requires special equipment to detect, predicts ventricular arrhythmia risk
Macroscopic alternans: Visible on standard ECG, indicates severe electrical instability
Causes: Acute ischemia, long QT syndrome, severe electrolyte disturbance, pericardial effusion
Clinical significance: High risk for ventricular tachycardia/fibrillation - requires immediate intervention

Biphasic T waves in ischemia - initial upward deflection followed by downward deflection indicating myocardial ischemia. Source: LITFL

Other Special Patterns

Bifid (Notched) T Waves: T wave with two peaks or a notch - causes include hypokalemia, LVH, ischemia, hypothermia
Camelback T Waves: Biphasic T wave morphology - seen in Wellens syndrome, HCM, juvenile pattern, digoxin effect
Tall T Waves in Athletes: Part of athletic heart syndrome - symmetric and gradual (not hyperacute), no ischemic symptoms

Systematic Interpretation Approach

Use this structured approach to systematically evaluate T wave abnormalities:

1. Assess T Wave Direction

Upright: Normal in most leads (except aVR)
Inverted: Identify distribution (localized vs. diffuse) and morphology (symmetric vs. asymmetric)
Biphasic: Consider Wellens syndrome if in V2-V3 with chest pain history
Flat: Think electrolytes (hypokalemia) or nonspecific abnormality

2. Evaluate T Wave Amplitude

Tall/Peaked: Measure amplitude and assess morphology (broad vs. narrow base)
If broad-based and localized: Consider hyperacute T waves of STEMI
If narrow-based and diffuse: Check potassium for hyperkalemia
Low amplitude: Assess for hypokalemia, hypothyroidism, pericardial effusion

3. Determine Distribution Pattern

Anterior (V1-V4): LAD territory, RV strain, PE
Lateral (I, aVL, V5-V6): Circumflex territory, LV strain/hypertrophy
Inferior (II, III, aVF): RCA or LCx territory
Diffuse/Global: Think metabolic (electrolytes), CNS event, myocarditis, PE, Takotsubo

4. Assess Morphology

Symmetric inversion: Ischemia or cerebral T waves
Asymmetric inversion: Strain pattern (LVH, RVH), bundle branch blocks
Hyperacute morphology: Broad-based, tall, symmetric - acute STEMI
Peaked morphology: Narrow-based, tent-shaped - hyperkalemia

5. Compare to Previous ECGs

New T wave inversion: Much more concerning than chronic changes
Pseudonormalization: Previously inverted T waves now upright may indicate acute ischemia
Evolutionary changes: Progressive T wave inversion after STEMI is expected

Key Decision Points:

Immediate cardiology consultation if:
• New T wave inversions in contiguous leads with chest pain
• Wellens pattern (biphasic or deeply inverted T waves in V2-V3)
• Hyperacute T waves with ischemic symptoms
• De Winter pattern (upsloping ST depression + tall T waves)
• T wave alternans (risk of ventricular arrhythmias)

Check electrolytes urgently if:
• Peaked T waves (hyperkalemia screening)
• Flat T waves + prominent U waves (hypokalemia)
• New T wave changes in dialysis patients or with renal failure

Clinical Pearls

Serial ECGs are crucial: Evolutionary T wave changes (hyperacute → upright → inverted → pseudonormalization) help distinguish acute from old MI
T wave/QRS ratio: T wave amplitude >2/3 of R wave height suggests hyperacute changes or hyperkalemia
Lead specificity matters: T wave inversion in aVR is always normal; in V1-V3 may be normal variant; in V2-V4 raises concern for LAD disease
Pseudonormalization: Previously inverted ischemic T waves becoming upright during acute ischemia - represents reinjury, not improvement
De Winter T waves: Tall, symmetric T waves in precordial leads with upsloping ST depression at J-point - STEMI equivalent requiring emergent intervention
Concordance rule: In bundle branch blocks, T waves should be discordant (opposite direction) to QRS; concordant T waves suggest superimposed ischemia
Memory T waves: Transient T wave inversion after tachycardia resolution, ventricular pacing, or WPW - benign but can mimic ischemia
Global T wave inversion: If present in most leads (except aVR), think: PE, myocarditis, Takotsubo, or CNS event

Critical Recognition - De Winter T Waves:
Pattern: Upsloping ST depression (≥1mm at J-point) + tall, prominent symmetric T waves in precordial leads
Significance: STEMI equivalent pattern (2% of LAD occlusions) requiring immediate cath lab activation
Key point: These are NOT normal tall T waves - the upsloping ST depression is the critical distinguishing feature

References

Farkas, Josh MD. (2015). Table of Contents - EMCrit Project. EMCrit Project. https://emcrit.org/ibcc/toc/
Khan, M. G. (2007). Rapid ECG Interpretation. Humana.
Sigg, D. C., Iaizzo, P. A., Xiao, Y.-F., Bin He, & Springerlink (Online Service). (2010). Cardiac Electrophysiology Methods and Models. Springer Us.
Wang, K. (2012). Atlas of Electrocardiography. JP Medical Ltd.
ECG Library • LITFL • ECG Library Basics. (2018). Life in the Fast Lane • LITFL • Medical Blog. https://litfl.com/ecg-library/

Flattened or Low-Amplitude T Waves

T wave flattening is a nonspecific finding that can indicate various metabolic, ischemic, or structural abnormalities:

Common Causes

Hypokalemia: T wave flattening is often the earliest ECG sign, progressing to inversion with prominent U waves
Ischemia: Subendocardial ischemia can produce flat or minimally inverted T waves (non-STEMI pattern)
Hypothyroidism: Diffuse low-voltage T waves with bradycardia
Pericardial effusion: Low voltage QRS and T waves (electrical alternans if large effusion with tamponade)
Cardiomyopathy: Diffuse T wave flattening in dilated or restrictive cardiomyopathy
Normal variant: Can be normal in older adults or with increased chest wall thickness

Hypokalemia with flattened T waves — Hypokalemia - global T wave flattening with prominent U waves visible in anterior leads (V2 and V3). Source: LITFL

Clinical significance: While T wave flattening is nonspecific, the combination of flat T waves + prominent U waves + QT prolongation strongly suggests hypokalemia and increases risk of Torsades de Pointes. Check potassium urgently and consider ECG monitoring.

Electrolyte Abnormalities

Electrolyte disturbances profoundly affect ventricular repolarization, with characteristic T wave patterns:

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Electrolyte	T Wave Pattern	Additional Findings
Hyperkalemia	Tall, narrow, peaked (tent-shaped)	PR prolongation, P wave flattening, QRS widening
Hypokalemia	Flattened/inverted with prominent U waves	QT prolongation, ST depression
Hypercalcemia	Normal/tall T waves	Short QT interval, no ST segment
Hypocalcemia	Normal T wave amplitude	Prolonged QT (prolonged ST segment)
Hypomagnesemia	Similar to hypokalemia	Often coexists with hypokalemia

Severe hypokalemia - prominent U waves merging with T waves creating "camel hump" appearance. Source: LITFL