13.1 Acid-Base and Fluid/Electrolyte Imbalance

13.1 Acid-Base and Fluid/Electrolyte Imbalance

Quick Answer: Read a neonatal blood gas as pH first, then decide whether the primary process is respiratory (PCO2) or metabolic (HCO3 / base excess). A capillary blood gas (CBG) pH and PCO2 usually track arterial values well enough for acid-base decisions; CBG PO2 does not. Anion gap sorts high-gap acidosis (lactate, ketones, inborn error) from normal-gap bicarbonate loss. Hyponatremia is not one disease: SIADH needs water restriction, sodium wasting needs sodium and volume, and iatrogenic water excess needs less free water. Hyperkalemia with ECG change is a membrane emergency—especially in AKI and salt-wasting CAH. Extremely low-birth-weight (ELBW) infants lose water through immature skin; humidity and fluid titration prevent hypernatremic dehydration. Restrict water when the problem is overload or SIADH; replace when the problem is insensible loss, sodium wasting, or true hypovolemia.

Acid-base and fluid/electrolyte imbalance is Multisystem problem MU-1 on AACN Certification Corporation's current Neonatal CCRN Test Plan. Multisystem is 20% of the exam—the same listed weight as the entire Endocrine/Heme/GI/Renal/Integumentary cluster and twice cardiovascular. OpenExamPrep provides independent CCRN Neonatal study material covering these patient problems. It is not an AACN product and does not claim official approval. Follow your unit's gas, electrolyte, and fluid protocols at the bedside.

A blood gas is a story about ventilation, perfusion, and buffer stores, not a lab trophy. The neonate who is apneic, under-ventilated, or fighting a high dead-space circuit accumulates carbon dioxide. The neonate who is cold, hypoperfused, septic, or running anaerobic metabolism accumulates lactic acid. The neonate who has lost bicarbonate from the gut or kidney has a normal anion gap and a chloride that has risen to fill the hole. If you memorize four letters without a mechanism, you will miss the infant.

Arterial versus capillary gases

An arterial blood gas (ABG) from an umbilical arterial catheter or a peripheral arterial line is the reference for oxygenation and a clean acid-base picture. A CBG from a warmed heel is what most infants actually get.

Warm the heel. Avoid squeezing a poorly perfused foot into a falsely acidotic, hypercarbic sample. Do not “correct hypoxia” from a CBG PO2 of 35 mm Hg in a pink infant with a normal pulse oximeter. Venous gases sit lower in pH and higher in PCO2; they can still show a metabolic story if that is all you have during a code. AACN does not publish official neonatal blood-gas cutoffs. Analyzer reference ranges and unit protocols are the operational standard.

A four-step read, then compensation

1. pH. Below about 7.35 is acidemia; above about 7.45 is alkalemia.
2. Respiratory component (PCO2). High PCO2 with low pH is respiratory acidosis. Low PCO2 with high pH is respiratory alkalosis.
3. Metabolic component (HCO3 or base excess). Low HCO3 / more negative base excess with low pH is metabolic acidosis. High HCO3 with high pH is metabolic alkalosis.
4. Compensation. Lungs change PCO2 in minutes. Kidneys change HCO3 over hours to days. Acute respiratory acidosis shows a high PCO2 with a still-near-normal HCO3. Chronic respiratory acidosis (bronchopulmonary dysplasia, chronic hypoventilation) shows a high PCO2 with a high HCO3 and a pH nearer normal. Metabolic acidosis should drive a compensatory fall in PCO2 if the infant can ventilate. If PCO2 is high while HCO3 is low, you have a mixed respiratory and metabolic acidosis—common in shock plus apnea.

Do not call a compensated chronic gas “normal” just because pH is 7.38. The infant is still hypoventilating; the kidney has bought time.

Worked gas examples

Example A — under-ventilated preterm. pH 7.21, PCO2 68 mm Hg, HCO3 26 mEq/L, BE +1, CBG. Primary acute respiratory acidosis. The bicarbonate has not had time to rise. Fix ventilation: endotracheal tube position, rate, tidal volume, pneumothorax, sedation, or apnea—not a bicarbonate push.

Example B — cold, hypotensive ELBW. pH 7.18, PCO2 32 mm Hg, HCO3 11 mEq/L, BE −16, lactate 8 mmol/L. High-anion-gap metabolic acidosis with respiratory compensation (the PCO2 has fallen). Warm, fill, treat shock and sepsis, and look at perfusion. Sodium bicarbonate is not first-line if the problem is oxygen delivery; it can worsen intracellular acidosis and add a sodium load.

Example C — mixed disaster. pH 7.10, PCO2 70 mm Hg, HCO3 12 mEq/L, BE −18. Both systems are failing: the infant is not ventilating and is producing or losing acid. Airway plus circulation, not a single-lever answer.

Example D — chronic lung disease. pH 7.37, PCO2 62 mm Hg, HCO3 35 mEq/L. Compensated chronic respiratory acidosis. Do not “normalize” PCO2 to 40 mm Hg in a moment; acute hypocarbia on that background drops cerebral blood flow (chapter 11).

Example E — overventilation. pH 7.52, PCO2 26 mm Hg, HCO3 21 mEq/L. Acute respiratory alkalosis. Turn the ventilator down. Hypocarbia is a white-matter and cerebral-blood-flow problem in preterm infants.

Anion gap, conceptually

Anion gap ≈ Na+ − (Cl− + HCO3−). Unmeasured anions (albumin, phosphate, sulfate, organic acids) make a normal gap, often discussed near 8–12 mEq/L on older assays and somewhat higher on some modern analyzers. AACN does not publish an official gap cutoff. Know the concept:

• High gap: lactic acidosis (shock, NEC gut ischemia, hypoxia), ketoacidosis, many inborn errors (organic acidemias—chapter 6), toxins, severe renal failure with retained anions.
• Normal gap (hyperchloremic): bicarbonate loss from diarrhea or a high-output ostomy, renal tubular acidosis, or dilution with chloride-rich fluid.

Worked numbers: Na 138, Cl 100, HCO3 10 → gap 28, high-gap story. Na 138, Cl 118, HCO3 12 → gap 8, hyperchloremic bicarbonate loss. Do not chase a gap while the infant is coding. Do use it once you have a metabolic acidosis and need a branch point.

Chapter 6 already taught that urea-cycle disease can show hyperammonemia with little acidosis, while organic acidemias add anion-gap acidosis. Bring that branch to MU-1 items: a high-gap gas plus encephalopathy after a well interval is a metabolic-team call, not only “give bicarb.”

Sodium: three hyponatremia mechanisms

Serum sodium is a water story as much as a salt story. Typical operational range is about 135–145 mEq/L; units differ. The exam cares whether you restrict, replace, or stop hypotonic fluid.

Hypernatremia in the ELBW infant is often a free-water deficit from transepidermal water loss, not a salt overdose. The skin is the leak. Raising incubator humidity, using a humidified circuit, and matching fluid intake to weight and sodium trends treat the cause. Adding more sodium into an already concentrating infant can worsen hypernatremia if the real deficit is water.

A 900 g infant whose sodium climbs from 142 to 158 mEq/L over 24 hours while weight falls is drying out. A 900 g infant whose sodium falls from 140 to 126 mEq/L while weight rises on 160 mL/kg/day of hypotonic fluid is waterlogged. Same ion, opposite fluids. Chapter 9 owns congenital renal disease and AKI definitions; this section owns the fluid and electrolyte moves those kidneys force.

Potassium: hyperkalemia as an emergency

Neonatal potassium often runs a bit higher than adult values in the first days. A non-hemolyzed value above about 6.5–7 mEq/L, especially with ECG change, is a crisis conversation. Confirm the sample is not hemolyzed from a squeezed heel. True hyperkalemia clusters in:

• Acute kidney injury (oliguria, rising creatinine)
• Salt-wasting CAH (hyponatremia + hyperkalemia + shock)
• Acidosis shifting K+ out of cells
• Cell lysis, massive transfusion, or potassium in parenteral nutrition running too fast

ECG: peaked T waves, flattened P waves, wide QRS, bradycardia, sine-wave ventricular arrhythmia. Stabilize the membrane with intravenous calcium (usually 10% calcium gluconate, slow, on a monitor) when there are ECG changes, then shift potassium inward with insulin plus glucose, nebulized albuterol, and bicarbonate if acidotic per protocol, then remove potassium with diuretics if urine is flowing, cation-exchange resin (use cautiously—intestinal injury is a historical concern), or dialysis/CRRT (chapter 16). Do not treat a hemolyzed 7.8 with calcium while the repeat plasma is 4.9. Do not treat a true 8.2 with “recheck in the morning.”

Hypokalemia follows diuretics, gastric losses, and alkalosis. Replace potassium carefully; peripheral concentrated potassium is a vesicant.

Calcium overlap

Early hypocalcemia (first 24–48 hours) in preterm infants, infants of diabetic mothers, and asphyxia is taught in chapter 6. MU-1 items still mix calcium with acid-base because acidosis increases ionized calcium slightly and bicarbonate therapy can drop ionized calcium. Citrate in blood products binds calcium. Jitteriness is glucose, calcium, and magnesium until you measure all three. Refractory hypocalcemia needs magnesium. IDM-specific hypocalcemia is applied again in section 13.4.

ELBW insensible losses

Insensible water loss (IWL) is water you never bag: skin plus respiratory tract. In an ELBW infant, transepidermal water loss (TEWL) can dwarf urine in the first 48–72 hours if humidity is low. Immature stratum corneum, a huge surface-area-to-mass ratio, radiant warmers without humidity, phototherapy, and tachypnea all increase IWL. Older, dry, open-warmer practice could lose several milliliters per kilogram per hour through skin alone. Modern humidified incubators (often targeting high relative humidity, commonly discussed near 70–80% in the first days for the most immature infants) cut that leak dramatically. Chapter 9 covers TEWL as skin integrity; here the electrolyte consequence is hypernatremia, concentrating of remaining ions, and weight collapse.

Typical starting fluid ranges (unit- and humidity-dependent, not AACN constants):

Phototherapy, fever, tachypnea, and an ostomy add replacement. A patent ductus, evolving BPD, or postoperative SIADH subtract free water.

Restriction versus replacement

Restrict when water is the toxin: SIADH, pulmonary edema, hemodynamically significant PDA with overload, hyponatremia with weight gain, and some postoperative states. Restriction means less free water, not less sodium in a wasting infant.

Replace when water or salt is leaving: high IWL, phototherapy, fever, diarrhea, ostomy, nasogastric losses, sodium wasting, and true hypovolemic shock. Measure outputs and weigh the infant. A large early weight drop in an ELBW infant is not a rounding error.

Worked scenario: a 24-week, 620 g infant in 40% humidity on a radiant warmer has sodium 154 mEq/L at 18 hours, down 8% from birth weight, urine 1 mL/kg/h. This is under-replaced IWL, not SIADH. Raise humidity, increase free water, and stop chasing “fluid restriction for all preterms.” Contrast: a 39-week infant 24 hours after asphyxia has sodium 128 mEq/L, weight up 6%, concentrated urine. That is an SIADH-pattern; restriction plus treating the brain injury is the fluid move.

Exam traps: treating CBG PO2 as PaO2; giving bicarbonate for isolated respiratory acidosis; restricting fluids in sodium wasting or CAH; flooding SIADH; ignoring hemolyzed potassium; inventing an AACN official milliliter-per-kilogram number; and forgetting that Multisystem is 20% of this exam. Practice application is at /practice/ccrn-neonatal. Adult acid-base at /study-guides/ccrn uses the same ABG logic with adult PaO2 targets—do not import those oxygenation numbers into the NICU.