Acid–Base Disorders, Electrolytes & Renal Replacement

ABPN Neurocritical Care Study Guide Exam

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1 Chapter 1: Neurologic Examination & Coma Assessment in the ICU

Current Examination, Blueprint & Preparation Neurologic Examination in Critically Ill Patients Coma Evaluation & Consciousness Alterations Delirium & Toxic-Metabolic Encephalopathy in the ICU

2 Chapter 2: Cerebral Physiology & Intracranial Dynamics

Cerebral Blood Flow, Metabolism & Autoregulation Intracranial Pressure & Compliance Cerebral Edema & Herniation Syndromes

3 Chapter 3: Intracranial Hypertension & Cerebral Perfusion Management

Tiered ICP Management Protocols Hyperosmolar Therapy & Fluid Management Advanced & Refractory ICP Interventions

4 Chapter 4: Airway, Mechanical Ventilation & Pulmonary ICU Management

Emergency Airway Management & Neuro-Intubation Mechanical Ventilation Strategies in Acute Brain Injury Tracheostomy & Ventilator Weaning in Neurocritical Care Pulmonary Complications in the Neuro-ICU Obstructive Lung Disease, Pulmonary Hypertension & Bronchoscopy

5 Chapter 5: Hemodynamics, Shock & Cardiovascular Management

Hemodynamic Monitoring & Blood Pressure Targets Vasoactive Agents: Inotropes, Vasopressors & Antihypertensives Cardiac Complications of Brain Injury

6 Chapter 6: Neuropharmacology, Analgesia & Sedation

ICU Sedation & Analgesia Neuromuscular Blockade & Monitoring Propofol Infusion Syndrome & Drug Toxicities Antiseizure Drug Pharmacology in the ICU

7 Bleeding, Thrombosis & Hematologic Emergencies

Warfarin & Heparin Reversal Direct Oral Anticoagulant (DOAC) Reversal Antiplatelet Management & Platelet Dysfunction Venous Thromboembolism Prophylaxis & Management Transfusion, Coagulopathy, TMA & Cellular-Therapy Neurotoxicity

8 Chapter 8: Systemic ICU Care, Fluids, Electrolytes & Endocrine

Hyponatremia & Osmoregulation: SIADH vs Cerebral Salt Wasting Diabetes Insipidus, Hypernatremia & Endocrine Crises Critical Care Prophylaxis, Nutrition & Infection Prevention

9 Systemic Trauma & Environmental Injury

Polytrauma, Chest Injury & Abdominal Hemorrhage Burns, Electrical Injury & Hanging

10 Cardiac Emergencies & Mechanical Support

IABP, Ventricular Devices & ECMO Acute Coronary, Valvular, Rhythm & Aortic Emergencies

11 Kidney Injury, Acid–Base & Renal Replacement

Acute Kidney Injury & Renal Drug Clearance Acid–Base Disorders, Electrolytes & Renal Replacement

12 Systemic Infection & Endocrine Emergencies

Sepsis, Endocarditis & Antimicrobial Principles Thyroid, Adrenal & Dysglycemic Emergencies

13 Gastrointestinal & Hepatic Emergencies

Acute Abdomen, GI Bleeding & Abdominal Compartment Syndrome Acute Liver Failure, Cirrhosis & Hepatic Drug Effects

14 Chapter 9: Neuroimaging in the Neuro-ICU

Non-Contrast CT & CT Angiography CT Perfusion & Advanced Perfusion Imaging Magnetic Resonance Imaging in Critical Illness

15 Chapter 10: Electrophysiology & Neuromonitoring

Continuous EEG & ACNS Standardized Critical Care Terminology Invasive Neuromonitoring: ICP & External Ventricular Drains Multimodal Monitoring: PbtO2, Microdialysis & Transcranial Doppler

16 Angiography, Electrodiagnosis & CSF Analysis

Conventional Angiography & Cranial–Spinal Shunts EMG, Nerve Conduction & Acute Muscle Disease CSF Analysis: Infection, Inflammation & Hemorrhage

17 Chapter 11: Bedside Procedures, Ultrasound & Death by Neurologic Criteria

Critical Care Procedural Skills Critical Care Ultrasound & Echocardiography Determination of Death by Neurologic Criteria

18 Chapter 12: Acute Ischemic Stroke & Reperfusion Therapies

Acute Ischemic Stroke Management & Thrombolysis Endovascular Thrombectomy & Large Vessel Occlusion Malignant Hemispheric & Cerebellar Infarction

19 Chapter 13: Spontaneous Intracerebral Hemorrhage & Intraventricular Hemorrhage

Acute Intraparenchymal Hemorrhage Management Intraventricular Hemorrhage & Hydrocephalus Surgical Evacuation & Minimally Invasive Surgery in ICH

20 Chapter 14: Aneurysmal Subarachnoid Hemorrhage & Delayed Cerebral Ischemia

Aneurysmal Subarachnoid Hemorrhage: Acute Resuscitation & Securing Delayed Cerebral Ischemia & Cerebral Vasospasm Non-Aneurysmal Subarachnoid Hemorrhage & Vascular Malformations

21 Venous, Spinal & Traumatic Vascular Disease

Cerebral Venous Thrombosis & Spinal Cord Infarction Traumatic Dissection, Carotid–Cavernous Fistula & Penetrating Injury

22 Chapter 15: Traumatic Brain & Spinal Cord Injury

Severe Traumatic Brain Injury & Contusions Acute Traumatic Spinal Cord Injury & Neurogenic Shock Spine Trauma, Fractures & Cord Syndromes

23 Chapter 16: Status Epilepticus, Seizures & Neuromuscular Emergencies

Status Epilepticus: Convulsive & Non-Convulsive Refractory & Super-Refractory Status Epilepticus Acute Neuromuscular Respiratory Failure

24 Chapter 17: Post-Cardiac Arrest Care, CNS Infections & Encephalitis

Targeted Temperature Management & Post-Cardiac Arrest Care Post-Cardiac Arrest Neuroprognostication Acute CNS Infections, Encephalitis & Inflammatory Emergencies

25 Neuroinflammation & Neurooncology

Fulminant Demyelination & Autoimmune Encephalitis Brain, Spinal & Leptomeningeal Cancer Emergencies

26 Pregnancy, Transplantation & Pediatric Care

Pregnancy, Postpartum & Post-Transplant Neurologic Care Pediatric Neurocritical Care

27 Chapter 18: Neurosurgical & Perioperative Emergencies

Postoperative Neurosurgical Complications Device Complications: EVDs, Shunts & ICP Monitors Cerebral Hyperperfusion Syndrome & Post-Interventional Emergencies

28 Chapter 19: Ethics, Palliative Care & Organ Donation in the Neuro-ICU

Communication, Surrogate Decision-Making & Conflict Resolution Neuroprognostication Ethics, Withdrawal of Life Support & Palliative Care Organ Donation & Management of the Deceased Donor

Acid–Base Disorders, Electrolytes & Renal Replacement

Key Takeaways Explain This Topic AI

Anion gap equals sodium minus chloride minus bicarbonate; low albumin can conceal an increased gap.

For metabolic acidosis, expected PaCO2 is approximately 1.5 times bicarbonate plus 8, with a range of about 2 mm Hg.

Hyperkalemic ECG changes require immediate membrane stabilization and potassium-lowering treatment.

KDIGO suggests CRRT rather than intermittent treatment in AKI with acute brain injury or increased ICP.

Last updated: October 2026

Read the Gas and Chemistry Together

A blood gas provides pH and a respiratory component; serum chemistry adds bicarbonate, electrolytes, kidney function, and context. Determine whether the predominant process is metabolic or respiratory, then assess whether the compensatory response is appropriate. Compensation does not normally overcorrect the pH past normal. A near-normal pH can conceal two severe opposing processes, such as lactic acidosis plus respiratory alkalosis in sepsis.

For a metabolic acidosis , calculate the anion gap using sodium minus chloride minus bicarbonate. Potassium is conventionally omitted in this formulation. Reference ranges depend on the laboratory. Albumin contributes substantially to the normal gap; low albumin can hide unmeasured anions, so consider an albumin-adjusted interpretation. An increased gap prompts evaluation for lactate, ketones, renal retention of acids, and selected toxins. Hyperchloremic acidosis can follow large chloride loads, gastrointestinal bicarbonate loss, or renal tubular processes.

Check Respiratory Compensation

Winter's formula estimates the expected PaCO2 in a metabolic acidosis: 1.5 multiplied by serum bicarbonate, plus 8, with an approximate range of plus or minus 2 mm Hg. If bicarbonate is 12 mEq/L, expected PaCO2 is 26 mm Hg, approximately 24–28. A measured PaCO2 of 40 indicates an additional respiratory acidosis rather than adequate compensation. The same measured CO2 that seems normal in another patient can therefore represent severe ventilatory failure here.

This matters during intubation. A patient with profound metabolic acidosis may maintain pH through very high spontaneous minute ventilation. Apnea or a much lower ventilator minute ventilation can produce abrupt acidemia and cardiovascular collapse. Prepare a ventilation and hemodynamic plan before induction when possible. In concomitant brain injury, monitor the conflict between compensatory hypocapnia and cerebral perfusion instead of blindly applying a single CO2 target without acknowledging the acid–base disorder.

Electrolyte Emergencies

Disorder Neurologic or systemic risk Initial clinical priorities

Hyperkalemia Conduction failure and cardiac arrest ECG assessment; IV calcium for membrane stabilization when indicated; intracellular shift and definitive potassium removal

Severe hypokalemia Weakness, arrhythmia, rhabdomyolysis Controlled replacement, magnesium assessment, cardiac monitoring

• Hypomagnesemia Arrhythmia and seizures Replace magnesium and investigate ongoing losses
• Hypocalcemia Tetany, seizures, prolonged QT Assess ionized calcium and treat symptomatic severe deficiency

Severe hypophosphatemia Respiratory muscle weakness and impaired energy metabolism Replacement with renal-function and electrolyte monitoring

Calcium stabilizes the myocardium in hyperkalemia but does not remove potassium. Insulin with appropriate glucose shifts potassium intracellularly and requires glucose monitoring; inhaled beta-agonists can be adjunctive. Persistent or recurrent hyperkalemia may require renal replacement. Assess exogenous potassium, acidosis, renal failure, tissue breakdown, and medications. A reassuring initial ECG does not exclude dangerous hyperkalemia.

Differentiate a total calcium change due to albumin from an ionized calcium abnormality. Acid–base shifts influence protein binding, so ionized calcium is especially useful in critical illness and major transfusion. Replace phosphate or magnesium carefully in renal dysfunction because the same treatment that corrects deficiency can accumulate when clearance falls.

When Renal Replacement Is Needed

Consider urgent treatment for refractory electrolyte abnormalities, severe acid–base derangement, clinically important fluid overload, selected poisonings, or uremic complications. Evaluate the overall trajectory and treatable cause rather than waiting for a universal BUN or creatinine threshold. The modality, rate, anticoagulation, and fluid-removal goals must match the patient's physiology.

Intermittent hemodialysis can lower solute concentrations rapidly and cause hypotension. Both reduced MAP and osmotic brain water shifts can compromise an injured brain. Continuous renal replacement therapy (CRRT) generally allows slower fluid and solute changes and is suggested by KDIGO for AKI with acute brain injury, increased ICP, or generalized cerebral edema. This preference does not make CRRT risk-free; close monitoring remains necessary.

If the neurocritical care team has prescribed hypernatremia for a specific indication, ordinary replacement or dialysate sodium can reduce the serum concentration unexpectedly. Coordinate the prescription and monitor the rate of change. Account for citrate and calcium when regional citrate anticoagulation is used; accumulation and electrolyte abnormalities require specialist interpretation, particularly in severe shock or impaired metabolism. Circuit interruption also changes fluid balance and medication clearance.

Avoid the Osmotic and Medication Traps

Dialysis disequilibrium reflects rapid osmotic change with potential cerebral edema and neurologic deterioration. Risk assessment and a gradual initial prescription are especially important with marked azotemia or intracranial disease. If consciousness worsens during therapy, evaluate systemic pressure, oxygenation, glucose, sodium, seizures, and structural causes rather than assuming every event is disequilibrium.

Renal replacement removes some antibiotics and antiseizure drugs, sometimes requiring different maintenance doses or supplementary doses. Changes in effluent rate, residual renal function, and downtime matter. A free drug concentration may help when protein binding is altered. Document the modality and prescription in the medication plan so that a renal dose adjustment does not inadvertently become undertreatment after CRRT begins.

Source checked October 17, 2026: KDIGO AKI guideline, renal replacement recommendations .