2.3 Fluid, Electrolyte & Acid-Base Imbalances in ESRD

Fluid, Electrolyte & Acid-Base Imbalances in ESRD

In end-stage renal disease (ESRD), total loss of functioning nephrons impairs homeostatic regulation of fluid volume, electrolyte concentrations, and systemic pH. Between intermittent hemodialysis treatments, dietary fluid, potassium, phosphate, and metabolic acids accumulate. Mastering the physiological principles of hyperkalemia, mineral disorders, and metabolic acidosis allows hemodialysis nurses to anticipate decompensation and manage emergency interventions effectively.

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Hyperkalemia: Electrophysiology & ECG Progression

Potassium is the primary intracellular cation (~3,000–4,000 mEq total). Approximately 98% resides inside cells (~140 mEq/L), maintained by the basolateral $Na^+/K^+$-ATPase pump, while 2% resides in extracellular fluid (normal: 3.5 to 5.0 mEq/L). Normal kidneys excrete 90% to 95% of daily intake. In anuric ESRD, clearance is lost, causing hyperkalemia ($K^+ > 5.0\text{ mEq/L}$).

Cellular Electrophysiology of Cardiotoxicity

Ventricular resting membrane potential ($RMP$) is determined by the transcellular potassium ratio via the Nernst equation: $E_K = -61.5 \log_{10}([K^+]_{\text{in}}/[K^+]_{\text{out}})$. Elevated extracellular potassium shifts $RMP$ to a less negative, partially depolarized state (e.g., $-90\text{ mV}$ toward $-70\text{ mV}$):

1. Fast Sodium Channel Inactivation: Causes voltage-gated inactivation of fast $Na^+$ channels ($Na_v1.5$), depressing Phase 0 upstroke velocity ($V_{\max}$) and slowing conduction through atria, AV node, and ventricles.
2. Increased extracellular potassium alters myocardial resting potential, conduction and repolarization; IKr is a rapid delayed-rectifier current, not an inward-rectifier channel.

ECG Findings and Their Limits

Hyperkalemia may produce peaked T waves, PR prolongation, loss of P waves, QRS widening or a sine-wave pattern. These changes do not occur at dependable potassium bands or in a required sequence. A normal ECG does not exclude dangerous hyperkalemia. Evaluate a critical result promptly, consider hemolysis of the specimen, repeat testing when indicated, and do not delay emergency treatment in an unstable patient while pursuing confirmation. Compare baseline conduction disease and medication effects as well as the measured potassium.

Acute Hyperkalemia Management Protocol: The Three Tiers

The three aims are cardiac protection when indicated, temporary intracellular shifting and definitive removal. In a severe emergency these measures are coordinated promptly; they are not a reason to postpone removal until every preceding drug is completed.

Tier 1: Immediate Myocardial Membrane Stabilization

• Intravenous calcium: Use the ordered emergency formulation and dose, with ECG monitoring. Gluconate and chloride are not interchangeable gram-for-gram in elemental calcium; calcium stabilizes myocardium without removing potassium.

Tier 2: Rapid Intracellular Potassium Shifting

• Insulin with glucose: Administer through the ordered hyperkalemia protocol; assess baseline glucose and continue repeated monitoring for delayed hypoglycemia, commonly at least six hours in kidney failure. Dose and glucose support are individualized.
• Nebulized albuterol: The ordered high-dose emergency regimen shifts potassium through beta-2 stimulation. Response varies, so it is adjunctive therapy rather than reliable monotherapy. Observe heart rate and symptoms and reassess measured potassium.
• Sodium bicarbonate: Not routinely recommended for acute potassium lowering. The prescriber considers acid-base status, sodium/fluid burden and the clinical situation; do not apply a universal IV-push dose or pH cutoff.

Tier 3: Definitive Total Body Potassium Removal

• Urgent hemodialysis: Removes potassium from the body. The amount and rate depend on the serum-to-dialysate gradient, flow, duration, access and redistribution. Confirm the individualized bath and ECG monitoring; do not independently select a very low-potassium bath.
• Potassium binders: Their onset, sodium load and gastrointestinal warnings differ. They do not replace urgent myocardial stabilization and definitive removal in a life-threatening emergency.

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Calcium, Phosphorus and Acid-Base Decisions

Reduced phosphate excretion and reduced calcitriol production contribute to secondary hyperparathyroidism. Interpret calcium, phosphorus and parathyroid hormone together over time. A calcium-phosphorus product is a historical teaching measure; it is not the current sole treatment target or a diagnostic test for calciphylaxis. Painful, evolving skin lesions require urgent evaluation even without a markedly elevated product. Ionized calcium is especially useful when albumin or acid-base status makes total calcium difficult to interpret.

Metabolic acidosis develops when renal acid excretion and bicarbonate regeneration fall. It may contribute to muscle catabolism, bone buffering and increased extracellular potassium. The potassium response to a pH change varies with the underlying acid, insulin status, cellular injury and renal clearance. The shortcut that every 0.1 pH fall raises potassium by 0.6 mEq/L is unreliable and must not be used to predict a safe potassium concentration or calculate treatment.

In nondialysis CKD, KDIGO 2024 advises considering treatment to prevent clinically important acidosis, giving serum bicarbonate below 18 mmol/L in adults as an example; this is not a universal dialysis prescription. During hemodialysis, the clinician individualizes dialysate buffer and follows pre- and post-treatment clinical effects. Excessive alkalinization can lower ionized calcium and potassium, increasing cramps or arrhythmia risk. Persistent low bicarbonate requires review of adequacy, nutrition, gastrointestinal loss and the delivered prescription.

For severe hyperkalemia, ordered intravenous calcium stabilizes myocardium without removing potassium. Insulin with glucose and inhaled beta agonists shift potassium temporarily; dialysis removes it. Use the emergency protocol’s formulation and dose, monitor ECG and glucose, and recognize delayed hypoglycemia in kidney failure. Glucose surveillance continues for the protocol-specified period, commonly at least six hours after insulin, rather than stopping after the first normal reading. Sodium bicarbonate is not a routine substitute for these treatments; its use depends on acidosis and clinical context. Potassium binders have formulation-specific effects and warnings and must not delay emergency stabilization or dialysis.

Sources checked 2026-10-11: KDIGO CKD and UK Kidney Association hyperkalemia guideline, July 2026 update