“ECG triad” in chronic kidney disease

Q1. Which ECG change in CKD is caused by hyperkalemia?
A. Tall, peaked T waves
B. QT prolongation
C. LVH pattern
D. ST depression
Hyperkalemia → tall, tented T waves = earliest sign.
Q2. Prolonged QT interval in CKD is usually due to?
A. Hyperkalemia
B. Hypocalcemia
C. LVH
D. Hypermagnesemia
CKD → ↓ Vitamin D activation & phosphate retention → hypocalcemia → QT prolongation.
Q3. LVH pattern in CKD is mainly due to?
A. Hypocalcemia
B. Hyperkalemia
C. Hypertension & volume overload
D. Metabolic acidosis
Chronic HTN + volume overload in CKD → LVH pattern on ECG.
Q4. The ECG triad strongly suggestive of chronic renal failure includes?
A. RBBB, ST elevation, U waves
B. Tall T waves, prolonged QT, LVH
C. Delta waves, short PR, QRS widening
D. ST depression, LV strain, PVCs
ECG triad in CRF: hyperkalemia (tall T), hypocalcemia (prolonged QT), LVH.
Q5. Hyperkalemia in CKD produces which sequence of ECG changes?
A. Short PR → delta wave → narrow QRS
B. Flat T → U wave → bradycardia
C. Tall T → wide QRS → sine wave → asystole
D. QT prolongation → torsades
Hyperkalemia progression: tall T → PR prolong → QRS widening → sine wave → arrest.
Q6. Hypocalcemia in CKD mainly affects?
A. PR interval
B. QRS duration
C. QT interval (prolongation)
D. ST segment elevation
Low calcium prolongs repolarization → QT prolongation.
Q7. CKD patients often show LVH on ECG because?
A. Electrolyte imbalance only
B. Anemia alone
C. Coronary artery disease
D. Hypertension and fluid overload
HTN + volume expansion → LV pressure overload → LVH.
Q8. Which electrolyte imbalance in CKD is most arrhythmogenic?
A. Hyperkalemia
B. Hypocalcemia
C. Hypomagnesemia
D. Hyponatremia
Hyperkalemia → conduction block, arrhythmias, cardiac arrest.
Q9. The earliest ECG change in hyperkalemia is?
A. QT prolongation
B. PR prolongation
C. Tall, peaked T waves
D. Wide QRS
Tall, tented T = first sign of ↑K⁺.
Q10. CKD patients with prolonged QT are predisposed to?
A. AV block
B. Bradycardia
C. Torsades de pointes
D. WPW syndrome
Prolonged QT → risk of torsades de pointes.
Q11. In CKD, hyperkalemia widens QRS because?
A. Increases calcium influx
B. Stimulates sodium channels
C. Depresses conduction velocity
D. Enhances repolarization
↑K⁺ → reduced resting potential → slowed depolarization → wide QRS.
Q12. Which is NOT part of the CRF ECG triad?
A. Tall T waves
B. LVH
C. QT prolongation
D. Delta waves
Delta wave is WPW, not CRF triad.
Q13. Hypocalcemia in CKD leads to QT prolongation mainly by?
A. Delayed ventricular repolarization
B. Early depolarization
C. Faster conduction
D. Short PR interval
↓Ca²⁺ prolongs phase 2 → delayed repolarization → QT prolongation.
Q14. What mechanism causes LVH in CKD patients?
A. Hypocalcemia-induced conduction delay
B. Pressure overload due to hypertension
C. Hyperkalemia-induced conduction block
D. Coronary ischemia
HTN + volume overload → concentric LV hypertrophy.
Q15. In severe hyperkalemia, the ECG may show?
A. Tall P waves
B. Prolonged QT
C. Sine wave pattern
D. Delta wave
Sine wave → pre-terminal sign in severe hyperkalemia.
Q16. Why is QT interval prolonged in hypocalcemia but shortened in hypercalcemia?
A. Early depolarization vs delayed depolarization
B. Sodium channel activation differences
C. Alteration of plateau phase duration
D. Change in resting membrane potential
↓Ca²⁺ → longer plateau phase → prolonged QT; ↑Ca²⁺ → shorter plateau → short QT.
Q17. Which ECG change is reversible after dialysis in CKD?
A. LVH pattern
B. Hyperkalemia-induced T waves
C. QT prolongation from hypocalcemia
D. Fibrotic conduction blocks
Dialysis removes potassium → tall T waves normalize.
Q18. In CRF, arrhythmias are most commonly precipitated by?
A. Hypoglycemia
B. Anemia
C. Hypothermia
D. Electrolyte disturbances
Hyperkalemia, hypocalcemia, Mg²⁺ shifts → arrhythmias.
Q19. Tall, tented T waves are most likely seen in?
A. Hyperkalemia of CKD
B. Hypocalcemia of CKD
C. Hypermagnesemia
D. Acute ischemia only
Tented T = hallmark of ↑K⁺ in CRF.
Q20. The ECG triad in chronic renal failure helps primarily in?
A. Differentiating ischemia
B. Diagnosing congenital syndromes
C. Predicting sudden cardiac arrest only
D. Recognizing CKD-related electrolyte & structural effects
Triad = Tall T (↑K⁺), Prolonged QT (↓Ca²⁺), LVH (HTN/overload).

ECG triad strongly suggestive of chronic renal failure (CRF/CKD) refers to the classic features seen due to hyperkalemia, hypocalcemia, and uremic effects.

👉 The accepted ECG triad of CRF is:

  1. Tall, tented (peaked) T waves – from hyperkalemia
  2. Prolonged QT interval – from hypocalcemia
  3. Left ventricular hypertrophy (LVH) pattern – from long-standing hypertension (common in CKD)

🔑 Mnemonic:
“T-Q-L” = T waves (tented), QT prolongation, LVH → CKD triad


mechanism behind the ECG triad in Chronic Renal Failure (CRF/CKD):


1. Tall, tented T waves (Hyperkalemia)

  • CKD → ↓ renal excretion of potassium → hyperkalemia
  • Hyperkalemia → faster repolarization of ventricles → tall, narrow, peaked T waves
  • As K⁺ rises further → QRS widening, P wave flattening, sine-wave pattern → risk of ventricular fibrillation / asystole

2. Prolonged QT interval (Hypocalcemia)

  • CKD → ↓ renal activation of Vitamin D (1,25-dihydroxycholecalciferol) + phosphate retention → hypocalcemia
  • Hypocalcemia → prolongs ventricular depolarization & repolarization → QT interval prolongation
  • Risk of Torsades de Pointes / ventricular arrhythmia

3. Left Ventricular Hypertrophy (LVH pattern)

  • CKD patients often have chronic hypertension + volume overload + anemia
  • These factors → pressure + volume overload on LV
  • Over time → LV hypertrophy seen on ECG (tall R waves in left precordial leads, deep S waves in right precordial leads, left axis deviation)
  • Contributes to heart failure & arrhythmias

📌 Summary:

  • Hyperkalemia → Peaked T waves
  • Hypocalcemia → Prolonged QT
  • Hypertension/overload → LVH
    = The ECG triad strongly suggestive of chronic renal failure

ECG FindingUnderlying CauseMechanism
Tall, tented T wavesHyperkalemia (↓ renal K⁺ excretion)↑ Extracellular K⁺ → rapid ventricular repolarization → tall, peaked T waves (earliest hyperkalemia change)
Prolonged QT intervalHypocalcemia (↓ Vitamin D activation, phosphate retention)↓ Serum Ca²⁺ → delayed ventricular depolarization & repolarization → QT prolongation
Left Ventricular Hypertrophy (LVH) patternChronic Hypertension, volume overload, anemia in CKDPressure & volume overload on LV → myocardial hypertrophy → ECG shows LVH (tall R in V5–V6, deep S in V1–V2, left axis deviation)

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