Sodium (Na⁺)
Main extracellular cation that sets serum osmolality. Low values come from water excess, SIADH or diuretics; high values from water loss or hypertonic intake.
Learn MoreFourteen measured analytes that flag dangerous potassium, sodium and glucose values and show kidney and liver function at the bedside.
The Comprehensive Metabolic Panel (CMP) measures 14 analytes: glucose, calcium, sodium, potassium, chloride, total CO₂, BUN, creatinine, albumin, total protein, alkaline phosphatase (ALP), AST, ALT and total bilirubin. Anion gap, eGFR and BUN:Cr are calculated from these results and are not counted as components. The CMP is one of the most commonly ordered panels in acute care, drawn at ED triage, on ICU morning labs and before interfacility transfer.
The Basic Metabolic Panel (BMP) is the 8-analyte subset of the CMP (glucose, BUN, creatinine, sodium, potassium, chloride, CO₂, calcium). The Renal Panel adds phosphorus and albumin to the BMP. The Liver Panel is the CMP's liver subset (AST, ALT, ALP, bilirubin, albumin, total protein) plus GGT and direct bilirubin.
Main extracellular cation that sets serum osmolality. Low values come from water excess, SIADH or diuretics; high values from water loss or hypertonic intake.
Learn MoreSets resting membrane potential. Hemolysis or delayed processing can falsely raise it; ECG changes and rhythm matter more than the number alone.
Learn MoreMain extracellular anion. Interpret with sodium and CO₂: a high chloride with low CO₂ suggests a non-gap acidosis.
Learn MoreSerum bicarbonate plus dissolved CO₂. Low values indicate metabolic acidosis or compensated respiratory alkalosis; high values suggest contraction or vomiting.
Learn MoreUrea from protein catabolism. Rises with volume depletion, GI bleeding, high-protein intake and steroids as well as kidney injury; interpret with creatinine.
Learn MoreMuscle-derived marker of GFR. Rises late after kidney injury, and a normal value can mask low GFR in older adults or low muscle mass.
Learn MoreMain energy substrate and the first value to check in any altered patient. Low values need treatment before other causes are considered; high values need ketones and osmolality.
Learn MoreTotal calcium includes protein-bound fractions. Correct for albumin, or measure ionized calcium when albumin is abnormal or during transfusion or critical illness.
Learn MoreMain plasma protein that holds oncotic pressure. Low values reflect liver synthesis, malnutrition or protein loss; albumin is a slow marker, not a measure of acute liver failure.
Learn MoreAlbumin plus globulins. Low values follow malnutrition, liver disease or nephrotic losses; a high value with low albumin suggests a globulin rise.
Learn MoreAlkaline phosphatase from liver, bone and placenta. Rises in cholestasis and bone disease; a raised level in pregnancy can be normal.
Learn MoreLiver-specific aminotransferase. Rises with hepatocellular injury, hepatitis and drug or toxin injury; very high values suggest acute injury.
Learn MoreAminotransferase found in liver, heart and skeletal muscle. Raised in rhabdomyolysis and myocardial injury as well as liver injury, so interpret with ALT.
Learn MoreHemoglobin breakdown product. Fractionate (direct vs indirect) to separate hemolysis, hepatocellular injury and biliary obstruction.
Learn MoreNa⁺ − (Cl⁻ + total CO₂). Raised in high-anion-gap acidosis (lactate, ketones, uremia, toxic alcohols, salicylate); normal in non-gap acidosis.
Learn MoreEstimated GFR from creatinine, age and sex using the race-free CKD-EPI 2021 equation. Less accurate in acute kidney injury, where the value is not at steady state.
Learn MoreHelps separate prerenal azotemia (ratio above 20:1) from intrinsic kidney injury. Unreliable with GI bleeding, steroids or high-protein intake.
Learn MoreNot a CMP analyte, but often added to it. Low Mg²⁺ brings torsades and potassium that will not correct, and high levels can stop breathing.
Learn MoreNot a CMP analyte, but ordered with it. Measured osmolality, compared with the value calculated from the same draw's sodium, glucose and BUN. A gap above 10 mOsm/kg with an unexplained anion-gap acidosis: consider toxic alcohols.
Learn MoreNot a CMP analyte. The main DKA ketone, which a urine dipstick does not measure. At 3.0 mmol/L or higher with glucose ≥11.1 mmol/L or known diabetes, check venous pH and K⁺.
Learn MoreNot a CMP analyte. A pancreatic enzyme, not a liver test. Above 3 times the ULN with typical pain or imaging supports acute pancreatitis, and a normal value does not rule it out.
Learn MoreNot a CMP analyte. Rises with skeletal muscle injury, including rhabdomyolysis; not a cardiac-specific marker. Check potassium, creatinine and urine myoglobin when it is rising.
Learn More| Test | Adult Normal (conventional) | SI Units | Critical Low | Critical High | Notes |
|---|---|---|---|---|---|
| Sodium | 135–145 mEq/L | 135–145 mmol/L | <120 | >160 | Serum osmolality-linked |
| Potassium | 3.5–5.0 mEq/L | 3.5–5.0 mmol/L | <2.5 | ≥6.5 | Hemolysis-prone |
| Chloride | 96–106 mEq/L | 96–106 mmol/L | — | — | Interpret with Na⁺ and CO₂ |
| Total CO₂ | 22–29 mEq/L | 22–29 mmol/L | <10 | >40 | Arterial HCO₃⁻ is 22–26 |
| BUN | 8–23 mg/dL | 2.9–8.2 mmol/L (urea) | — | — | Age- and protein-dependent |
| Creatinine | M 0.7–1.3 | F 0.6–1.1 mg/dL | M 62–115 | F 53–97 µmol/L | — | — | Sex-specific; lab-dependent |
| Glucose | 70–99 mg/dL (fasting) | 3.9–5.5 mmol/L | <40 | >450 | Fasting interval |
| Total Calcium | 8.5–10.5 mg/dL | 2.12–2.62 mmol/L | <6.0 | >13.0 | Albumin-dependent |
| Albumin | 3.5–5.0 g/dL | 35–50 g/L | — | — | Slow marker |
| Total Protein | 6.0–8.3 g/dL | 60–83 g/L | — | — | Albumin + globulin |
| ALP | 30–120 U/L | 30–120 U/L | — | — | Pregnancy and bone raise it |
| ALT | 10–40 U/L | 10–40 U/L | — | — | ACG healthy ULN 33 M | 25 F |
| AST | 10–30 U/L | 10–30 U/L | — | — | Also muscle and heart |
| Total Bilirubin | 0.3–1.2 mg/dL | 5–21 µmol/L | — | — | Fractionate if raised |
Each pattern below is a combination of CMP results. Check it against the clinical picture, then run the next test listed.
| Pattern | Key Findings | Common Causes | Next Step |
|---|---|---|---|
| Prerenal AKI | Creatinine up, BUN:Cr above 20:1, low urine sodium | Volume loss, low perfusion, NSAIDs, ACE inhibitor or ARB | Volume status, urine studies, fluid challenge |
| Intrinsic AKI | Creatinine up, BUN:Cr near 10–15:1, muddy casts | Ischemic or toxic tubular injury, sepsis, contrast | Urinalysis, urine sodium, nephrology if persistent |
| High-anion-gap acidosis | Anion gap above 12 with low CO₂ | Lactate, ketones (DKA, starvation), uremia, toxic alcohols, salicylate | Lactate, beta-hydroxybutyrate, osmolar gap, toxicology |
| Normal-anion-gap acidosis | Normal gap, high chloride, low CO₂ | Diarrhea, renal tubular acidosis, saline-heavy fluids | Urine anion gap, stool or urine electrolytes |
| Hypovolemic hyponatremia | Low Na⁺, low serum osmolality, low urine sodium | Diuretics, GI losses, third-spacing | Volume exam, urine sodium and osmolality |
| SIADH | Low Na⁺ and osmolality, urine osmolality inappropriately high, normal volume | Medications, CNS disease, pulmonary disease, malignancy | Exclude hypothyroidism and adrenal insufficiency first |
| Hypercalcemia | Corrected Ca above 10.5 mg/dL, often with low phosphorus | Hyperparathyroidism, malignancy, thiazides, vitamin D excess | Ionized calcium, PTH, medication review |
| Cholestatic pattern | ALP and bilirubin up, ALT near normal, R-factor below 2 | Biliary obstruction, drug-induced cholestasis, infiltrative liver disease | Liver ultrasound, GGT, refer to the liver panel |
| Analyte | Changes After | Peak or Nadir | Repeat Interval | Monitoring Target |
|---|---|---|---|---|
| Potassium | Insulin, beta-agonist or binder treatment | Early effect, then rebound | 1, 2, 4, 6 and 24 hr after treatment (UKKA 2026 guideline) | K⁺ below 6.0 mEq/L and no ECG change |
| Glucose | Insulin infusion or insulin-glucose bolus | Falls within 1 hr; late hypoglycemia possible | Before the dose, then at 30, 60, 90, 120, 180, 240, 300 and 360 min (at least 6 hr; UKKA 2026 guideline). Extend beyond 6 hr after repeat doses or in high-risk patients (see Pitfall) | Glucose above 70 mg/dL |
| Sodium | Hypertonic saline bolus | Rise within 1 hr of a bolus | After each bolus; every 2–4 hr while infusing | Rise limited to 8–12 mEq/L per 24 hr by ODS risk (see Critical Findings) |
| Creatinine | Kidney injury | Rises over 24–48 hr | Every 24 hr until stable | Stable or falling creatinine |
| Ionized calcium | IV calcium or massive transfusion | Effect within minutes, lasts 30–60 min | After each dose and with each blood gas during transfusion | Ionized calcium within the lab range |
Recognize: peaked T waves, PR prolongation, lost P waves, QRS widening, bradycardia or sine wave. When the ECG changes are present, treat now. Don't wait for a repeat level.
Note: Outside arrest, IV sodium bicarbonate is not routine for acute hyperkalemia (UKKA 2026 guideline). Calcium does not lower K⁺ at all. It protects the heart muscle while the K⁺ is being shifted. In cardiac arrest from suspected hyperkalemia (2025 AHA Guidelines for CPR and ECC, Part 10, Electrolyte Abnormalities: Hyperkalemia): For IV calcium (calcium chloride 10 mL, 1 g IV/IO push), the class is 2b (LOE C-LD), and IV sodium bicarbonate and IV insulin with glucose are also class 2b (LOE C-EO), since their effectiveness is still poorly established. In arrest without a suspected hyperkalemic cause, routine calcium is not recommended (2025 AHA Part 9, COR 3: No Benefit). Bicarbonate runs at 50 mEq IV/IO, repeated every 5–10 min guided by blood gas (US label; UKKA 2026 suggests, 2C). Inhaled beta-2 agonists sit at class 3: No Benefit. For adults in arrest, AHA Table 3 gives regular insulin 10 units IV over 15–30 min with D50 50 g. Differs from UKKA 2026 and ERC: They give 25 g, plus D10 50 mL/hr if glucose is under 126 mg/dL. AHA 2025 Table 3 gives 50 g. In hyperkalemic arrest, AHA rates insulin-glucose COR 2b, with effectiveness not well established. Some US protocols give 5 units or 0.1 units/kg instead. A pooled analysis of 10 retrospective studies found less hypoglycemia with lower doses, and the K⁺ fall did not differ (see References). A later study found that 10 units lowered K⁺ more (0.9 vs 0.63 mmol/L, see References). UKKA 2026 says more study is needed before 5 units can be recommended. The glucose rules above come with the 10 units this site uses.
Recognize: Think hypotonic hyponatremia with neurologic symptoms. Acute or chronic, treat now. If a sample is quick to draw, check the sodium and serum osmolality. Don't hold treatment for the result.
Recognize: Watch for sweating, confusion, seizure or unresponsiveness. Check glucose first in every altered patient, before you consider any other cause.
Recognize: carpopedal spasm, laryngospasm, seizure, QT prolongation. Check both ionized calcium and magnesium.
Recognize: total Ca above 13 mg/dL (critical high) with confusion, vomiting or polyuria; or pH below 7.20 with low CO₂.
Recognize: hypokalemia with arrhythmia, weakness or paralysis; hypernatremia with confusion, seizure or altered consciousness. Treat per local protocol and medical direction.
| Device / Method | Analytes | Specimen | Limitations |
|---|---|---|---|
| i-STAT CHEM8+ | Na⁺, K⁺, Cl⁻, iCa, glucose, BUN, creatinine, TCO₂ | Whole blood, heparinized | No liver tests; eGFR reporting depends on analyzer configuration; cartridge temperature and storage limits |
| i-STAT CG8+ or blood-gas cartridge | Electrolytes, iCa, glucose, lactate, Hct | Whole blood, heparinized | Used for arterial or venous samples; follow the cartridge insert |
| Glucometer | Glucose only | Capillary blood | Unreliable in shock or hypoperfusion; interference from maltose, icodextrin and high-dose vitamin C |
Several analytes have age-specific reference intervals in children. The age-band tables are not on this page, so use the laboratory's pediatric table. The weight-based doses are listed below (see weight-based dosing and pediatric vital signs).
| Indication | Pediatric Dose | Max / Repeat | Notes |
|---|---|---|---|
| Hyperkalemia with ECG changes | Calcium chloride 10%: 20 mg/kg (0.2 mL/kg of 10%) IV/IO slowly; push in arrest | Max 1 g per dose; repeat if ECG toxicity persists | Equivalent calcium gluconate 60 mg/kg (0.6 mL/kg of 10%), max 3 g. Per-kg dose not verified in a primary source |
| Hyperkalemia (insulin) | Regular insulin 0.1 units/kg IV with dextrose 0.5 g/kg | Max 10 units per dose | Cardiac arrest dosing per 2025 AHA Guidelines for CPR and ECC, Part 10 (Table 3): regular insulin 0.1 units/kg IV over 15–30 min with D10W 5 mL/kg; maximum 10 units for severe hyperkalemia. Outside arrest, per pediatric protocol with glucose checks as adult |
| Hypoglycemia | Dextrose 0.5–1 g/kg IV/IO (D10 5–10 mL/kg preferred) | Max 25 g per dose; reassess after each dose | D10 preferred at every age |
| Severe symptomatic hyponatremia | 3% NaCl 2 mL/kg IV over 10 min | Max 100 mL per dose; recheck Na⁺ | High-alert; never free-flow |
| Symptomatic hypocalcemia | Calcium chloride 10%: protocol range 10–20 mg/kg IV slowly | Max 1 g per dose | Per-kg range not verified in a primary source; check a pediatric formulary |
Pregnancy changes the picture. Dilution lowers hemoglobin and sodium. A respiratory alkalosis is normal here, with PaCO₂ around 28–32 mmHg and HCO₃⁻ around 18–21 mEq/L. The placenta pushes ALP up. Creatinine above 0.8 mg/dL is abnormal. A pregnant patient with headache, hypertension or right-upper-quadrant pain needs ALT, AST and platelets checked. Think HELLP syndrome or preeclampsia. Treat hyperkalemia and hypoglycemia in pregnancy as you would in non-pregnant adults.
A normal creatinine can hide a markedly reduced GFR when muscle mass is low. Use eGFR, and cystatin C where the lab offers it (2021 race-free CKD-EPI creatinine-cystatin equation). In this group, the usual causes of hyperkalemia, hyponatremia and AKI are volume depletion and polypharmacy (diuretics, ACE inhibitors, ARBs, potassium-sparing drugs).
Read K⁺ and HCO₃⁻ against the dialysis schedule. The pre-dialysis sample is the reference. RAAS inhibitors, mineralocorticoid antagonists and tissue breakdown all push hyperkalemia risk up. Dialysis patients with severe hyperkalemia need urgent dialysis. IV calcium should still go in for ECG changes while dialysis is being arranged (UKKA 2026 guideline). Low albumin and fluid overload both change the calcium and sodium readings.
| Interferent | Effect on Results | Prevention |
|---|---|---|
| Hemolysis | Falsely high K⁺, AST, LDH, phosphorus | Avoid fist clenching and prolonged tourniquet; repeat on a clean draw |
| Drawing above an IV line | Dilution: low values for sodium, glucose and protein; high K⁺ if K⁺ is in the fluid | Draw from the opposite arm or stop infusion and flush per protocol |
| EDTA contamination | Falsely high K⁺, low calcium and ALP | Correct order of draw; do not pour between tubes |
| Delayed processing | Low glucose, high K⁺ and phosphorus | Process promptly or separate serum from cells |
| Lipemia or icterus | Analyzer interference, especially for some enzymes and bilirubin | Check the lab's hemolysis, lipemia and icterus indices |
| Biotin | Interferes with streptavidin-biotin immunoassays (for example, some troponin and TSH assays); routine CMP chemistries are generally unaffected | Ask about supplements; hold biotin 2–3 days before the draw if the lab advises |