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Apex Nursing

Chart — Lab

Metabolic Panel Interpretation Chart

BMP and CMP values organized by system — causes of abnormalities, critical thresholds, and required nursing actions for electrolytes, renal markers, glucose, liver enzymes, and proteins.

Educational use only. Reference ranges and critical thresholds vary by institution. BMP = electrolytes + BUN/Cr + glucose. CMP = BMP + liver markers + albumin + total protein. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.

Electrolytes (BMP + CMP)

TestNormalLow (↓) CausesHigh (↑) CausesCriticalNursing Action
Sodium (Na⁺)135–145 mEq/LSIADH, diuretics, HF, cirrhosis, free water excessDehydration, DI, inadequate water intake, excess Na intake< 120 or > 160 mEq/LNeurological assessment; seizure precautions; controlled correction
Potassium (K⁺)3.5–5.0 mEq/LLoop diuretics, vomiting, NG suction, alkalosis, steroidsAKI/CKD, acidosis, ACE inhibitors, cell death, hemolysis< 2.5 or > 6.5 mEq/LContinuous ECG monitoring; emergency treatment per order
Chloride (Cl⁻)98–106 mEq/LVomiting, NG suction, metabolic alkalosis, diureticsDehydration, metabolic acidosis, NS excessNot routinely established as panic valueCorrelate with Na and bicarbonate; assess for metabolic alkalosis
Bicarbonate (CO₂)22–29 mEq/LMetabolic acidosis — DKA, lactic acidosis, diarrhea, renal failureMetabolic alkalosis — vomiting, diuretics, antacid overuse< 15 or > 40 mEq/LCorrelate with ABG if abnormal; identify underlying acid-base disorder

Renal Markers (BMP + CMP)

TestNormalLow (↓) CausesHigh (↑) CausesCriticalNursing Action
BUN7–20 mg/dLLiver failure (impaired urea synthesis), malnutrition, low protein intakePre-renal (dehydration/reduced perfusion most common), AKI, CKD, GI bleeding, high protein intakeNot standard; > 100 mg/dL warrants attentionCalculate BUN:Cr ratio; assess volume status; identify bleeding source
Creatinine0.6–1.2 mg/dL (M); 0.5–1.1 mg/dL (F)Reduced muscle mass (elderly, malnutrition) — rarely significantAKI, CKD, rhabdomyolysis, nephrotoxin exposure, reduced perfusionRise of > 0.3 mg/dL from baseline = AKI definitionTrend closely; hold nephrotoxins (NSAIDs, contrast, aminoglycosides, vancomycin); assess urine output

Glucose (BMP + CMP)

TestNormalLow (↓) CausesHigh (↑) CausesCriticalNursing Action
Glucose (fasting)70–99 mg/dL (fasting); < 140 mg/dL (2h postprandial)Insulin excess, sulfonylureas, adrenal insufficiency, prolonged fasting, sepsisDiabetes, stress hyperglycemia, steroids, TPN, pancreatitis, infection< 50 mg/dL (critical low); > 500 mg/dL (critical high)< 50: D50W IV or glucagon IM IMMEDIATELY. > 500: notify provider, assess for DKA/HHS

Liver Markers (CMP only)

TestNormalLow (↓) CausesHigh (↑) CausesCriticalNursing Action
ALT7–56 units/LNot clinically significantHepatocellular injury (most specific liver enzyme) — viral hepatitis, NAFLD, drug toxicity, ischemia> 3× ULN warrants investigation; > 10× = severe hepatocellular injuryAssess for jaundice, abdominal pain, RUQ tenderness; review medications for hepatotoxins
AST10–40 units/LNot clinically significantLiver damage, MI, skeletal muscle injury, rhabdomyolysis, myositisMarkedly elevated with ALT > AST = alcoholic hepatitis patternNot liver-specific — correlate with ALT, troponin, and CK to identify source
ALP44–147 units/LHypothyroidism, pernicious anemia, zinc deficiency — rarely significantCholestatic liver disease, bile duct obstruction, bone disease, pregnancy, Paget's disease> 3× ULN with jaundice = biliary obstruction until proven otherwiseCheck GGT (elevated with liver cause); assess for jaundice, clay-colored stools, dark urine
Total Bilirubin0.2–1.2 mg/dLNot clinically significantLiver disease, hemolysis (indirect), bile duct obstruction (direct), Gilbert syndrome> 12 mg/dL = kernicterus risk in neonates; no standard adult panic value but high levels warrant urgent evaluationAssess for jaundice (visible > 2–3 mg/dL); assess urine color (dark = bilirubinuria); stool color (pale = biliary obstruction)

Proteins (CMP only)

TestNormalLow (↓) CausesHigh (↑) CausesCriticalNursing Action
Albumin3.5–5.0 g/dLMalnutrition, liver failure (impaired synthesis), nephrotic syndrome, protein-losing enteropathy, inflammationDehydration (hemoconcentration) — rarely significant< 2.0 g/dL = critical — affects drug binding, edema, wound healingApply corrected calcium formula; assess nutritional status; consider nutrition consult; assess for edema
Total Protein6.0–8.3 g/dLMalnutrition, liver failure, nephrotic syndrome, protein-losing conditionsDehydration; multiple myeloma (elevated globulin fraction)Interpret with albumin — elevated total protein with normal albumin = high globulin (may indicate MM)Calculate albumin-to-globulin ratio for further interpretation

Key Interpretation Patterns

PatternLab FindingsClinical Meaning
Pre-renal azotemiaBUN:Cr ratio > 20:1Dehydration or reduced renal perfusion — volume restore first
Hepatocellular injuryALT > AST, markedly elevated transaminasesViral hepatitis, drug toxicity, ischemic hepatitis
Alcoholic hepatitisAST:ALT ratio > 2:1 (both < 300 units/L)Classic pattern — AST rises more than ALT in alcohol-related liver injury
Cholestatic patternALP and bilirubin elevated, ALT/AST relatively normalBile duct obstruction, primary biliary cholangitis, drug-induced cholestasis
High anion gap metabolic acidosisLow bicarbonate; AG = Na − (Cl + HCO₃) > 12 mEq/LMUDPILES causes: lactic acidosis (sepsis most common), DKA, uremia, salicylates
False low calciumLow albumin with low total calciumCorrected Ca = measured Ca + (0.8 × [4 − albumin]) — may be normal once corrected

Related Resources

Standards & sources

Fact-checked Jun 21, 2026

This page is written to align with Standard laboratory reference ranges · Clinical & Laboratory Standards Institute (CLSI). It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →