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Clinician

Blog articles for clinicians and other medical professionals.

Understanding Peaked T Waves

March 26th, 2025

As a clinician, recognizing the significance of peaked T waves helps with the timely diagnosis and management of potentially life-threatening conditions such as hyperkalemia or acute coronary syndromes (ACS). This article provides an in-depth review of the causes, pathophysiology, diagnostic approach, and management of peaked T waves in clinical practice.

Understanding T waves on ECG

The T wave represents ventricular repolarization in the cardiac cycle. A normal T wave is asymmetrical, with a gradual upstroke and a steeper downstroke. When T waves become peaked, they appear symmetrical, tall, and narrow, often described as "tent shaped." Peaked T waves should prompt immediate evaluation for underlying causes.

Normal T wave morphology

  • Asymmetrical shape
  • Upright in leads I, II, V3–V6
  • Inverted in aVR
  • Amplitude varies by age, sex, and lead placement

Characteristics of peaked T waves

  • Tall (>5 mm in limb leads, >10 mm in precordial leads)
  • Symmetric shape
  • Narrow base
  • Most commonly seen in hyperkalemia

Causes of peaked T waves

Several clinical conditions can cause peaked T waves. The most common and critical etiology is hyperkalemia, but other causes must also be considered.

1. Hyperkalemia (most common cause)

Hyperkalemia, defined as a serum potassium level >5.5 mEq/l, is the most well-recognized cause of peaked T waves.

Mechanism

  • Elevated extracellular potassium reduces the resting membrane potential, leading to faster repolarization.
  • This accelerates T wave formation and causes them to appear as peaked.

ECG findings in hyperkalemia

  • Peaked T waves (early sign)
  • Widened QRS complex
  • Loss of P waves (moderate hyperkalemia)
  • Sine-wave pattern (severe hyperkalemia, >8.0 mmol/L), which can precede ventricular fibrillation or asystole

Clinical conditions leading to hyperkalemia

  • Renal failure (most common)
  • Medications (ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs, trimethoprim)
  • Acidosis (e.g., diabetic ketoacidosis, lactic acidosis, respiratory acidosis)
  • Cellular destruction (e.g., hemolysis, rhabdomyolysis, tumor lysis syndrome)
  • Adrenal insufficiency (Addison's disease, primary adrenal failure)
  • Excessive potassium intake (particularly in individuals with weakened kidney function)
  • Blood transfusions (due to potassium leaking from stored red blood cells)

2. Early myocardial ischemia

Peaked T waves can be seen in early acute coronary syndrome (ACS), especially in ST-elevation myocardial infarction (STEMI).

Mechanism

  • Ischemia leads to localized potassium accumulation, altering repolarization and causing peaked T waves.

ECG features

  • Peaked T waves in leads corresponding to the infarct territory.
  • It can progress to ST-segment elevation if occlusion persists.
  • Differentiation from hyperkalemia: Ischemic T waves are usually localized, whereas hyperkalemia causes diffuse peaked T waves.

3. Hyperacute T waves in STEMI

Hyperacute T waves are seen very early in an evolving STEMI before ST-segment elevation appears.

Key features

  • Localized to the affected coronary artery territory
  • Broader base compared to hyperkalemic T waves
  • May rapidly progress to ST-segment elevation

4. Left ventricular hypertrophy (LVH) and early repolarization

  • LVH can produce tall T waves, especially in lateral precordial leads.
  • Early repolarization syndrome (ERS) is an ECG finding that has been commonly observed. Recent studies indicate it might be linked to a higher risk of ventricular fibrillation and sudden cardiac death. ERS is characterized by an elevation of the J point and/or ST segment from the baseline by at least 0.1 mV in at least two adjoining leads.

5. Intracranial pathology (cerebral T waves)

  • Deeply inverted or symmetric T waves can be seen in conditions such as subarachnoid hemorrhage, stroke, or traumatic brain injury (TBI).
  • Often associated with prolonged QT interval and widespread repolarization abnormalities.

6. Pericarditis and myocarditis

  • Inflammation of the pericardium or myocardium can lead to diffuse ST elevation.
  • Often accompanied by PR depression and a "saddle-shaped" ST segment.

7. Drugs and toxins

  • Certain medications and toxins can cause peaked T waves due to effects on repolarization.
  • Examples include digitalis toxicity and lithium toxicity.
  • Cocaine and amphetamines can cause catecholamine surges that alter ECG morphology.

8. Endocrine disorders

  • Adrenal Insufficiency (Addison's disease): Adrenal insufficiency can lead to electrolyte imbalances, including hyperkalemia, which can cause peaked T waves. It can also cause prolonged PR or QT intervals, and the lack of cortisol and aldosterone from the adrenal glands leads to electrolyte imbalances and ECG changes.
  • Hypocalcemia and hypomagnesemia can alter repolarization dynamics and lead to ECG changes.

9. Pulmonary embolism

  • Pulmonary embolism (PE) may cause T wave abnormalities, typically in right-sided leads (V1–V3).
  • Often seen with sinus tachycardia, S1Q3T3 pattern, or right heart strain findings on ECG.

Diagnostic approach to peaked T waves

Step 1: Clinical assessment

  • History: Look for symptoms of weakness, palpitations, chest pain, dyspnea, altered mental status.
  • Medication review: Ask about potassium-altering drugs.
  • Past medical history: Consider renal disease, diabetes, cardiac disease, etc.

Step 2: ECG interpretation

  • Identify diffuse vs. localized peaked T waves.
  • Look for accompanying ECG changes (QRS widening, PR prolongation, ST elevation).
  • Compare with prior ECGs if available.

Step 3: Laboratory and imaging studies

  • Serum potassium (most urgent test if hyperkalemia suspected)
  • Arterial blood gas (ABG) (checks for metabolic acidosis)
  • Cardiac troponins (if ischemia suspected)
  • Renal function tests (BUN, creatinine, eGFR)
  • Thyroid function tests (if endocrine pathology suspected)
  • Toxicology screen (if drug-related causes are a concern)

Peaked T waves are an essential ECG finding that can indicate hyperkalemia, early myocardial ischemia, or other cardiac abnormalities. A systematic approach involving history, ECG interpretation, and targeted investigations allows for rapid identification and treatment. Clinicians should remain vigilant for peaked T waves as a potential harbinger of cardiac emergencies and intervene accordingly.