Renal & Electrolyte Emergencies
Acute kidney injury, CRRT, severe hyperkalemia, dysnatremias, and acid-base disorders.
Core Topics
7 topicsContinuous Renal Replacement Therapy (CRRT)
Principles of convection vs diffusion, filtration fraction, delivered effluent dosing (20–25 mL/kg/h), Regional Citrate Anticoagulation, and citrate toxicity.
Acid-Base Disorders: Comprehensive Critical Care Approach
Stepwise 6-step interpretation algorithm, compensation formulas, albumin-corrected anion gap, delta ratio, and Stewart physicochemical (SID) principles.
Metabolic Acidosis: HAGMA, NAGMA, & Bicarbonate Evidence
Differential diagnosis (GOLD MARK vs HARDCARP), toxic alcohol osmolar gaps, Urine Anion Gap, and current sodium bicarbonate evidence including BICAR-ICU and BICARICU-2.
Severe Hyperkalemia in Critical Illness
Nernst resting potential mechanics, ECG progression, the 3-step resuscitation framework (Stabilize, Shift, Eliminate), and post-dialysis rebound kinetics.
Acute Kidney Injury in Critical Care
Sepsis-AKI microcirculatory decoupling, KDIGO staging, Furosemide Stress Test (FST), urine microscopy, and the AEIOU dialysis threshold framework.
Severe Sodium Disorders: Hyponatremia & Hypernatremia
Tonicity assessment, etiologic classification, 3% hypertonic saline bolus protocols, individualized ODS-safe correction limits, DDAVP relowering, DI diagnostics, and evidence-aware hypernatremia correction.
Kidney Transplantation in the ICU
ICU care of the kidney-transplant recipient: allograft dysfunction, vascular/urologic emergencies, rejection, infection, immunosuppression toxicity and renal replacement decisions
Clinical Problems & Bedside Triage
19 guidesAcute Hypercapnia & Ventilatory Failure
Triaging rising PaCO2: distinguishing acute uncompensated acidemia from chronic compensation, identifying central vs pump vs dead-space failure, and titrating noninvasive ventilation.
Refractory Shock Despite High-Dose Vasopressors
Advanced multimodal hemodynamic rescue: second-line vasopressors (vasopressin, angiotensin II), inotropic augmentation, stress-dose steroids, metabolic correction, and mechanical circulatory support evaluation.
New Tachycardia & Tachyarrhythmias
Algorithmic triage of acute heart rates > 100–150 bpm: stability screen (immediate cardioversion if unstable), narrow vs wide QRS differentiation, Brugada VT rules, and sinus tachycardia etiology search.
New Bradycardia & Conduction Blocks
Acute bradyarrhythmia management: identifying hemodynamic instability, distinguishing sinus node arrest vs high-grade AV block, medical chronotropic support (atropine, epinephrine), and emergent pacing.
Acute Altered Mental Status & ICU Delirium
Systematic neurologic evaluation: immediate metabolic/toxic screening (glucose, hypoxia, hypercapnia), nonconvulsive status epilepticus exclusion, structural CT triage, and CAM-ICU delirium management.
New Seizure & Status Epilepticus
Time-critical stepped seizure protocol: immediate airway/oxygen/glucose check, first-line IV benzodiazepines at 5 minutes, second-line non-sedating AEDs at 10–20 minutes, and general anesthetic induction at 30 minutes for refractory status.
Rapidly Progressive Weakness / Impending Ventilatory Failure
Bedside assessment and airway decision-making in rapidly ascending or fatiguable weakness risking ventilatory pump failure.
Oliguria & Falling Urine Output
Algorithmic triage of acute oliguria (< 0.5 mL/kg/hr): urinary catheter patency check, volume responsiveness vs congestive nephropathy (VExUS Doppler), nephrotoxic drug review, and the furosemide stress test.
Acute Severe Metabolic Acidosis
Physiologic acid-base evaluation: Anion Gap and Delta-Delta calculations, Winter's formula for respiratory compensation, distinguishing ketoacidosis/lactic acidosis/toxic alcohols from non-gap acidosis, and bicarbonate therapy indications.
Severe Metabolic Alkalosis
Bedside evaluation of severe alkalemia (pH > 7.55, HCO3 > 35 mEq/L): assessing chloride responsiveness (urine chloride), diuretic-induced contraction alkalosis, nasogastric suction loss, hypokalemia, and acetazolamide/CRRT rescue.
Severe Symptomatic Hyponatremia
Treat severe neurologic symptoms with controlled 3% saline boluses, then prevent overcorrection by separating the immediate symptom target from the 24-hour safety ceiling.
Severe Hypernatremia & Water Deficit
Bedside evaluation of severe hypernatremia: free-water deficit, ongoing losses, central vs nephrogenic diabetes insipidus, volume resuscitation, and individualized monitored sodium correction.
Severe Hyperkalemia & Cardiac Membrane Instability
Time-critical hyperkalemia protocol (K+ > 6.5 mEq/L or ECG changes): immediate membrane stabilization with IV Calcium, intracellular shifting with Insulin/Dextrose and beta-agonists, and definitive potassium elimination.
Persistent Fever Despite Broad-Spectrum Antibiotics
Evaluating unresolved fever after 48–72 hours of antimicrobial therapy: undrained closed-space infection, resistant/fungal pathogens, catheter infections, C. difficile, drug fever, and ICU thrombosis.
Immunocompromised Patient with Fever + Organ Failure
Bedside diagnostic framing and emergency management of acute fever, sepsis, respiratory failure, or oncologic emergency in an immunocompromised host.
Acute Bleeding & Falling Hemoglobin
Bedside triage of acute blood loss: active hemorrhage vs occult bleeding vs hemodilution, context-specific RBC thresholds, protocolized massive-hemorrhage resuscitation, targeted component therapy, and anticoagulant reversal.
New Thrombocytopenia & Coagulopathy in the ICU
Differential diagnosis of acute platelet drops and clotting derangements: 4Ts-based HIT assessment, dynamic disease-specific DIC scoring, recognition of thrombotic microangiopathy/TTP, and targeted replacement or anticoagulant therapy.
Rising Airway Pressure + Oliguria + Distended Abdomen
Recognize pressure-mediated multiorgan failure and move from measurement to decompression.
Polyuria with Rising Sodium / Suspected AVP Deficiency
High urine output with hypernatremia: distinguish AVP deficiency from osmotic diuresis, restore circulation first when depleted, replace free water, and use desmopressin with close sodium/urine monitoring.
Physiology Modules & Waveforms
20 conceptsFiltration
The filtration barrier — capillary endothelium, glomerular basement membrane, and podocyte foot processes — restricts passage based on molecular size and, for negatively charged molecules like albumin, electrical charge. Net filtration pressure is the balance of glomerular capillary hydrostatic pressure (favoring filtration) against Bowman's space hydrostatic pressure and plasma oncotic pressure (opposing it). Injury to any layer of the barrier — from inflammation, immune complex deposition, or direct toxin/ischemic injury — can allow protein or blood cells to leak into the filtrate, producing proteinuria or hematuria.
Glomerular Filtration Rate
Filtration pressure is set by the balance of hydrostatic and oncotic pressures across the glomerular capillary, and is actively regulated by the relative tone of the afferent and efferent arterioles — dilating the afferent or constricting the efferent arteriole raises filtration pressure, and vice versa. This autoregulation keeps GFR relatively stable across a range of systemic blood pressures, but it depends on intact renal perfusion and intact prostaglandin- and angiotensin-mediated arteriolar tone — which is exactly what NSAIDs and ACE inhibitors/ARBs interfere with, respectively.
Tubular Function
Each tubular segment has a distinct job: the proximal tubule reabsorbs the bulk of filtered sodium, water, glucose, and bicarbonate; the loop of Henle establishes the medullary concentration gradient that allows urine to be concentrated; the distal tubule and collecting duct perform fine-tuning of sodium, potassium, and water balance under hormonal control (aldosterone, ADH). Because the tubules are metabolically active and oxygen-hungry — especially the proximal tubule and thick ascending limb — they're highly vulnerable to ischemia, which is why prolonged hypoperfusion (prerenal azotemia, if sustained) progresses to acute tubular necrosis, the most common intrinsic cause of AKI in the ICU.
Sodium Handling
The proximal tubule reabsorbs the largest share of filtered sodium, with progressively finer regulation downstream — the thick ascending limb, distal tubule, and collecting duct, the last under the control of aldosterone, which is released in response to volume depletion sensed by the renin-angiotensin-aldosterone system. Because sodium is the primary determinant of extracellular fluid volume, sodium handling and volume status are functionally the same axis: a kidney that senses low effective circulating volume (true hypovolemia, or a low-output/vasodilated state that mimics it) avidly retains sodium, producing a low urine sodium even when total body sodium is already normal or high.
Potassium Handling
Distal potassium secretion depends on adequate distal sodium delivery and flow (which drives the electrochemical gradient for potassium secretion) and on aldosterone, which upregulates the sodium channels and pumps that make secretion possible. AKI disrupts this in two ways at once: reduced GFR means less filtrate and less distal flow, and tubular injury directly impairs the secretory machinery — which is why potassium excretion falls sharply in AKI even before GFR has dropped to zero, making hyperkalemia one of the earliest and most dangerous consequences of acute kidney injury.
Renal Acid-Base Regulation
Unlike the rapid, minutes-scale respiratory compensation for acid-base disturbances, renal compensation is slow — it takes one to several days to fully develop, because it depends on adjusting the rate of new bicarbonate generation and ammonium excretion rather than simply changing a rate of breathing. This is why an acute respiratory acidosis or alkalosis shows a smaller compensatory change in bicarbonate than the same disturbance present for several days (acute versus chronic compensation), and why renal failure (via impaired acid excretion) produces a metabolic acidosis of its own even without a primary respiratory problem.
Henderson-Hasselbalch Equation
Because pH depends on the ratio of HCO3 to PaCO2 rather than either value alone, the same pH can arise from many different combinations of the two — which is precisely why a blood gas can't be interpreted from pH alone. This ratio-based relationship is also why compensation works: a primary change in one component (metabolic or respiratory) can be partly offset by a directionally appropriate change in the other, moving pH back toward — but not all the way to — normal.
Anion Gap
Plasma must remain electrically neutral, so the total concentration of cations always equals the total concentration of anions — the 'gap' only exists because routine labs don't measure every ion. A rising anion gap during a metabolic acidosis means an unmeasured anion (lactate, ketoacids, or a toxic metabolite) is accumulating and displacing bicarbonate as it's consumed in buffering. A normal-anion-gap acidosis, by contrast, means bicarbonate is being lost directly and replaced by chloride, keeping the calculated gap unchanged.
Delta Gap
In a pure HAGMA, each unmeasured acid anion that accumulates consumes roughly one bicarbonate in buffering, so the rise in anion gap and the fall in bicarbonate should track together, producing a delta ratio near 1 (clinically, roughly 1–2). A ratio well below this range means bicarbonate has fallen more than the anion gap rose — some of the bicarbonate loss is unaccounted for by the gap acidosis alone, implying a concurrent normal-anion-gap process. A ratio well above this range means bicarbonate is higher than the gap would predict, implying a concurrent metabolic alkalosis is also present and partially offsetting the acidosis.
Osmolar Gap
The calculated osmolality only accounts for sodium, glucose, and urea — the routinely measured osmotically active solutes. Any other osmotically active substance present in significant concentration (most importantly the toxic alcohols: methanol, ethylene glycol, and isopropyl alcohol, as well as ethanol itself) raises the measured osmolality without being reflected in the calculation, producing a gap. Because these alcohols are metabolized over time into their toxic acid metabolites, the osmolar gap is often most elevated early, before a high anion gap has fully developed — the two findings can appear at different points in the same poisoning.
Acid-Base Compensation
Respiratory compensation is fast (minutes to hours) because it only requires a change in minute ventilation; renal compensation is slow (one to several days) because it requires actually changing rates of bicarbonate reabsorption and generation. Compensation is never complete — it moves pH back toward normal but does not fully normalize it — and each type of primary disturbance has a predictable, quantifiable compensatory response (e.g. Winter's formula for a metabolic acidosis), which is what allows a clinician to check whether the observed compensation is appropriate or whether a second, independent disturbance is also present.
Winter's Formula
A falling bicarbonate normally triggers a proportional increase in ventilation (via central and peripheral chemoreceptors sensing the resulting acidemia), lowering PaCO2 and partially restoring the HCO3/PaCO2 ratio toward normal. Winter's formula captures the empirically observed slope of this response. If the measured PaCO2 falls within the predicted range, compensation is appropriate and only one primary process is likely present; if it falls outside that range, a second, independent respiratory disorder must also be present.
Mixed Acid-Base Disorders
Because compensation and a second primary disorder can move pH, PaCO2, and bicarbonate in similar directions, a mixed disorder can't reliably be detected from pH alone — it requires systematically checking whether the observed PaCO2 matches the expected compensation (via Winter's formula or an equivalent rule) and, for a high-anion-gap acidosis, whether the delta gap suggests an additional process. Critically ill patients very commonly have more than one acid-base process at once — for example, a septic patient can simultaneously have a lactic acidosis (metabolic acidosis), a compensatory or sepsis-driven tachypnea (respiratory alkalosis), and diuretic use (metabolic alkalosis) — so mixed disorders should be actively sought, not assumed to be the exception.
Hyperkalemia: Membrane Excitability, Shifting, and Elimination
The cardiac resting membrane potential (Em) is determined primarily by the Nernst equilibrium for potassium: Em = -61.5 × log([K+]in / [K+]out). As extracellular potassium rises, the ratio [K+]in / [K+]out decreases, making the resting membrane potential less negative (e.g., from -90 mV toward -70 mV). This resting depolarization partially inactivates fast voltage-gated sodium channels (Nav1.5), slowing phase 0 depolarization velocity (dV/dt) and prolonging intraventricular conduction (peaked T waves → PR prolongation → QRS widening → sine wave → VF/asystole). Management requires a three-pillar physiological strategy: 1. Stabilize: IV Calcium raises the cardiac threshold potential, restoring the normal safety margin between resting and threshold potentials without lowering serum K+. 2. Shift: Regular Insulin + Dextrose, Beta-2 agonists (Albuterol), and Sodium Bicarbonate activate the Na+/K+ ATPase, rapidly pumping potassium into cells for 2–4 hours. 3. Eliminate: Loop diuretics, potassium binders (Patiromer, ZS-9), or Hemodialysis remove potassium from the body permanently.
Diabetic Ketoacidosis: Insulin Deficiency, Ketogenesis, and Potassium Paradox
Insulin deficiency combined with high glucagon uninhibits hormone-sensitive lipase in adipose tissue, releasing massive quantities of free fatty acids (FFAs) into the circulation. In hepatocytes, carnitine palmitoyltransferase-1 (CPT-1) channels FFAs into mitochondrial beta-oxidation, producing acetoacetate and beta-hydroxybutyrate. These ketoacids dissociate into hydrogen ions and ketoacid anions, consuming serum bicarbonate and creating a severe High Anion Gap Metabolic Acidosis (HAGMA). Concurrently, severe hyperglycemia exceeds the renal tubular absorptive threshold (180 mg/dL), driving profound osmotic diuresis with massive urinary loss of water, sodium, potassium, and magnesium. The Potassium Paradox: Acidosis, insulinopenia, and hyperosmolarity shift potassium OUT of cells into the bloodstream, making initial serum potassium appear normal or high despite catastrophic total-body potassium deficits (300–600 mEq). Starting insulin drives potassium rapidly back into cells, causing lethal hypokalemia unless potassium is repleted concurrently.
Loop Diuretics: NKCC2 Blockade, Electrolyte Wasting, and Alkalosis
The thick ascending limb reabsorbs 25% of the filtered sodium and chloride load via the apical NKCC2 cotransporter. Reabsorption of these ions without water generates the hypertonic medullary interstitium required for downstream collecting duct water reabsorption via ADH-mediated aquaporins. Loop diuretics bind the chloride-binding site of NKCC2, blocking solute reabsorption. This increases distal delivery of sodium, chloride, and fluid to the distal tubule and collecting duct. In the cortical collecting duct, increased sodium delivery stimulates the epithelial sodium channel (ENaC), driving electrical-gradient secretion of potassium (kaliuresis) and hydrogen ions (H+ ATPase), producing hypokalemic, hypochloremic metabolic alkalosis (contraction alkalosis). NKCC2 blockade also collapses the lumen-positive transepithelial potential, inhibiting paracellular reabsorption of divalent cations (magnesium and calcium).
Primary Acid-Base Disorders: 4 Pathologies & Compensatory Limits
The body utilizes chemical buffers (bicarbonate, hemoglobin, intracellular proteins), respiratory minute ventilation adjustment (acting within minutes to hours), and renal tubular proton secretion/bicarbonate reabsorption (acting over 2–5 days) to defend physiological pH (7.35–7.45). Compensatory rules: 1. Metabolic Acidosis: For every 1 mEq/L fall in HCO3-, PaCO2 drops by ~1.2 mmHg (Winter's Formula: Expected PaCO2 = 1.5 × [HCO3-] + 8 ± 2). 2. Metabolic Alkalosis: For every 1 mEq/L rise in HCO3-, PaCO2 rises by ~0.7 mmHg (Expected PaCO2 = 0.7 × [HCO3-] + 21 ± 2). 3. Acute Respiratory Acidosis: For every 10 mmHg rise in PaCO2, HCO3- rises by 1 mEq/L (cellular buffering). Chronic: HCO3- rises by 3.5–4 mEq/L (renal retention). 4. Acute Respiratory Alkalosis: For every 10 mmHg fall in PaCO2, HCO3- falls by 2 mEq/L. Chronic: HCO3- falls by 4–5 mEq/L.
Lactate Kinetics & Cellular Dysoxia in Shock
Type A Hyperlactatemia is caused by tissue hypoperfusion and anaerobic metabolism. In the absence of oxygen, mitochondrial pyruvate dehydrogenase (PDH) is inhibited and NADH accumulates, shifting pyruvate to lactate via lactate dehydrogenase (LDH) with an elevated lactate-to-pyruvate ratio (>20:1). Type B Hyperlactatemia occurs with preserved tissue oxygenation: - Type B1: Underlying disease (liver failure, malignancy, thiamine deficiency). - Type B2: Drugs and toxins (epinephrine, linezolid, metformin, beta-2 agonists via Na+/K+-ATPase stimulation). - Type B3: Inborn errors of metabolism. In sepsis, endogenous and exogenous adrenergic stimulation accelerates aerobic glycolysis via beta-2 receptors faster than PDH can process pyruvate, generating lactate despite adequate tissue PO2.
Osmoregulation, ADH & Free Water Balance
Hypothalamic osmoreceptors detect changes in tonicity as small as 1%. When Posm exceeds 285 mOsm/kg, pituitary ADH release triggers insertion of aquaporin-2 water channels into collecting duct apical membranes, concentrating urine (Uosm > 600–800 mOsm/kg) and conserving free water. Non-osmotic stimuli (arterial baroreceptor unloading from hypovolemia, heart failure, cirrhosis, sepsis, pain, nausea, and stress) override osmotic inhibition. In these states, ADH is secreted even when serum osmolality is low, resulting in impaired free water excretion and dilutional hyponatremia if hypotonic fluids are administered.
Central DI vs Osmotic Diuresis Differentiation
In Central Diabetes Insipidus (e.g. post-transsphenoidal pituitary surgery, severe TBI, brain death), absolute deficiency of pituitary ADH prevents aquaporin-2 insertion in the collecting duct. The kidney cannot concentrate urine: urine is maximally dilute (Uosm < 100–200 mOsm/kg, specific gravity < 1.005), leading to rapid hypernatremic dehydration if free water is not replaced. In Osmotic Diuresis (e.g. DKA/HHS with glycosuria, post-mannitol administration, or urea excretion during post-AKI recovery), unreabsorbed high-concentration luminal solutes create an osmotic gradient that drags water and electrolytes along the tubule. Urine osmolality is isotonic or moderately concentrated (Uosm > 300 mOsm/kg), and total daily solute excretion is markedly elevated.
Clinical Reasoning Cases
14 casesSevere Hyperkalemia with Cardiac Toxicity
Membrane stabilization, intracellular shifting, monitoring, and definitive potassium removal
Severe Diabetic Ketoacidosis Resuscitation
Fluid resuscitation, potassium kinetics, insulin therapy, and safe transition
Hypertensive Emergency with Target-Organ Injury
Controlled BP reduction in hypertensive encephalopathy with phenotype-specific exceptions
Severe Symptomatic Hyponatremia with Seizures
Emergency hypertonic saline, close sodium monitoring, and prevention/rescue of overcorrection
Triple Mixed Acid-Base Disorder in Sepsis & Cirrhosis
High-anion-gap metabolic acidosis with concurrent respiratory and metabolic alkalosis
Severe Metabolic Alkalosis After Massive Transfusion
Mechanism-based management of severe alkalemia, electrolyte abnormalities, and volume overload
Acetaminophen-Associated Acute Liver Failure
Late NAC, early transplant evaluation, hyperammonemia, and cerebral-edema prevention
Immune Thrombotic Thrombocytopenic Purpura
Immediate recognition, ADAMTS13 testing, plasma exchange, and caplacizumab-based therapy
Toxic Alcohol Ingestion
Recognition and emergency treatment of suspected methanol or ethylene glycol poisoning
Central Diabetes Insipidus / Arginine Vasopressin Deficiency
Post-operative water-balance emergency after pituitary surgery
Abdominal Compartment Syndrome
Standardized IAP measurement and stepwise decompression of overt ACS
Severe AKI: Renal Replacement Therapy Decision
When to start kidney replacement therapy and how to select modality/dose
Severe Metabolic Acidosis & Peri-Intubation Collapse
Physiologically difficult airway management when compensatory ventilation is life-sustaining
Acute Liver Failure with Cerebral-Edema Risk
Hyperammonemia, osmotherapy, CRRT, and neuroprotection during transplant evaluation