Nursing: Lab Values & Vital Signs

Normal: 136-145 mEq/L. Hyponatremia (<136): causes — SIADH, water intoxication, diuretics, heart failure, vomiting/diarrhea. Symptoms: confusion, headache, nausea, seizures (severe <120). Correct slowly (<8-12 mEq/L per 24 hrs — rapid correction → osmotic demyelination syndrome/central pontine myelinolysis). Hypernatremia (>145): causes — dehydration, diabetes insipidus, excessive sodium intake. Symptoms: thirst, dry mucous membranes, restlessness, seizures. Correct slowly (reduce no more than 10-12 mEq/L per 24 hrs — rapid correction → cerebral edema).

Normal: 3.5-5.0 mEq/L. Hypokalemia (<3.5): causes — diuretics (loop, thiazide), vomiting, diarrhea, alkalosis. Symptoms: muscle weakness, leg cramps, fatigue, decreased bowel sounds, shallow respirations. ECG: flattened T waves, ST depression, U waves, prolonged QT. Increases digoxin toxicity risk. Hyperkalemia (>5.0): causes — renal failure, ACE inhibitors, K+-sparing diuretics, acidosis, tissue destruction (burns, crush injury). Symptoms: muscle weakness, paresthesias, bradycardia, cardiac arrest. ECG: tall peaked T waves, widened QRS, prolonged PR, sine wave → Vfib. CRITICAL VALUE: >6.0 mEq/L. Treatment: calcium gluconate (cardiac membrane stabilizer — first), insulin + D50 (shifts K+ into cells), sodium bicarb, kayexalate/patiromer (GI elimination), albuterol nebulizer, dialysis.

Normal: 98-106 mEq/L. Follows sodium — usually changes in same direction. Hypochloremia (<98): causes — vomiting, NG suctioning (loss of HCl), metabolic alkalosis, diuretics, SIADH. Hyperchloremia (>106): causes — dehydration, renal tubular acidosis, excessive NS infusion, metabolic acidosis (non-anion gap). Chloride helps maintain acid-base balance and electrical neutrality. Assess in context of sodium and bicarbonate levels.

Normal: 22-26 mEq/L (venous CO2 on BMP represents bicarbonate). HCO3 is a BASE — regulated by kidneys. Low HCO3 (<22) = metabolic acidosis (DKA, lactic acidosis, renal failure, severe diarrhea). High HCO3 (>26) = metabolic alkalosis (vomiting, NG suction, excessive antacids, hypokalemia). Kidneys compensate for respiratory disorders by retaining or excreting HCO3 (takes 24-48 hrs). On ABG: HCO3 22-26 mEq/L. If metabolic acidosis: calculate anion gap = Na - (Cl + HCO3); normal 8-12. Elevated anion gap = MUDPILES causes.

Normal: 10-20 mg/dL. Measures urea — end product of protein metabolism cleared by kidneys. Elevated (azotemia): prerenal (dehydration, heart failure, shock, GI bleeding, high protein diet), renal (kidney disease, nephrotoxic drugs), postrenal (obstruction). Decreased: liver failure (can't produce urea), malnutrition, overhydration. BUN/Creatinine ratio: normally 10:1 to 20:1. Elevated ratio (>20:1): suggests prerenal cause (dehydration, GI bleed). Normal ratio with both elevated: intrinsic renal disease. Always interpret BUN with creatinine. Affected by protein intake, hydration status, GI bleeding.

Normal: 0.7-1.3 mg/dL (male), 0.6-1.1 mg/dL (female). Byproduct of muscle metabolism — reflects GFR more accurately than BUN because it is NOT affected by protein intake, hydration, or GI bleeding. Elevated creatinine = decreased kidney function. Even small increases are significant (doubling = 50% loss of renal function). eGFR calculated from creatinine, age, sex, race: normal >90 mL/min. CKD staging: Stage 1: eGFR >90 + kidney damage, Stage 2: 60-89, Stage 3a: 45-59, Stage 3b: 30-44, Stage 4: 15-29, Stage 5 (ESRD): <15. Notify provider for acute rise in creatinine (acute kidney injury).

Fasting: 70-100 mg/dL. Random: 70-140 mg/dL. Pre-diabetes (fasting): 100-125 mg/dL. Diabetes diagnosis: fasting ≥126 mg/dL (two occasions) or random ≥200 with symptoms or A1C ≥65%. Hypoglycemia: <70 mg/dL — shakiness, diaphoresis, confusion, tachycardia, irritability, pallor. Severe <54 mg/dL. Treatment: Rule of 15 — 15g fast-acting carbs (4 oz juice, glucose tabs), recheck in 15 min. If unconscious: glucagon 1 mg IM/SubQ or D50 25 mL IV push. Hyperglycemia: DKA >250-300 with ketosis (Type 1), HHS >600 with severe dehydration (Type 2). Critical values: <40 or >500 mg/dL — notify provider immediately.

Total calcium: 9.0-10.5 mg/dL. Ionized calcium: 4.5-5.6 mg/dL (more accurate — not affected by albumin). Hypocalcemia (<9.0): causes — hypoparathyroidism, vitamin D deficiency, chronic kidney disease, acute pancreatitis, massive blood transfusion (citrate binds Ca). Symptoms: numbness/tingling (perioral, fingers), muscle cramps, tetany, Chvostek sign (facial twitching with tap), Trousseau sign (carpopedal spasm with BP cuff), laryngospasm, seizures, prolonged QT → cardiac arrest. Hypercalcemia (>10.5): causes — hyperparathyroidism (#1), malignancy, immobility, thiazide diuretics. Symptoms: 'bones, stones, groans, moans' — bone pain, kidney stones, abdominal pain/constipation, confusion/lethargy. ECG: shortened QT. Treatment: IV NS hydration, loop diuretics (furosemide — promotes Ca excretion), calcitonin, bisphosphonates. Correct calcium for low albumin: add 0.8 mg/dL for every 1 g/dL albumin below 4.

Normal: 1.5-2.5 mEq/L (or 1.8-2.4 mg/dL). Hypomagnesemia (<1.5): causes — alcoholism, malnutrition, diarrhea, PPIs (long-term), diuretics, DKA. Symptoms mirror hypocalcemia: tremors, hyperreflexia, tetany, seizures, cardiac arrhythmias (torsades de pointes), Chvostek/Trousseau positive. KEY: must correct Mg before K+ will correct (refractory hypokalemia). Hypermagnesemia (>2.5): causes — renal failure, excessive Mg administration (antacids, laxatives, Mg sulfate infusion). Symptoms: decreased DTRs (first sign), lethargy, hypotension, respiratory depression, cardiac arrest. Antidote: calcium gluconate. Monitor in patients on mag sulfate drip (preeclampsia).

Normal: 2.5-4.5 mg/dL (adult), 4.0-7.0 mg/dL (children — higher due to growth). Inverse relationship with calcium — when one rises, the other falls. Hypophosphatemia (<2.5): causes — refeeding syndrome (most dangerous), alcoholism, DKA treatment (insulin drives phosphorus into cells), antacids (bind phosphorus). Symptoms: muscle weakness, respiratory failure, confusion, rhabdomyolysis, impaired WBC function. Hyperphosphatemia (>4.5): causes — renal failure (#1), hypoparathyroidism, tumor lysis syndrome, excessive intake. Causes reciprocal hypocalcemia → tetany, calcification of soft tissues. Treatment: phosphate binders (calcium carbonate, sevelamer) with meals, dietary restriction, dialysis.

Normal WBC: 4,500-11,000/mm³ (4.5-11.0 × 10⁹/L). Leukocytosis (>11,000): infection, inflammation, stress response, corticosteroids, leukemia. Leukopenia (<4,500): bone marrow suppression (chemo), viral infections, autoimmune disorders, overwhelming sepsis. Differential (mnemonic: Never Let Monkeys Eat Bananas): Neutrophils 55-70% (bacterial infection, first responders — 'left shift' = increased bands/immature neutrophils, indicates acute infection), Lymphocytes 20-40% (viral infection, chronic infection, immune response), Monocytes 2-8% (chronic inflammation), Eosinophils 1-4% (allergies, parasitic infections), Basophils 0.5-1% (allergic reactions, inflammation). Neutropenia: ANC <1500 — infection risk. ANC <500: severe — institute neutropenic precautions (private room, no fresh flowers/fruits, hand hygiene, avoid crowds, no rectal temps).

RBC: Male 4.7-6.1 million/mm³, Female 4.2-5.4 million/mm³. Hemoglobin (carries O2): Male 14-18 g/dL, Female 12-16 g/dL. Hematocrit (% of blood that is RBCs): Male 42-52%, Female 37-47%. Hgb roughly = Hct ÷ 3. Decreased (anemia): blood loss, iron deficiency, chronic disease, B12/folate deficiency, bone marrow failure. Symptoms: fatigue, pallor, tachycardia, dyspnea, dizziness. Transfuse when Hgb <7 g/dL (stable patients) or <8 g/dL (cardiac disease); also transfuse if symptomatic at higher levels — each unit raises Hgb ~1 g/dL. Increased (polycythemia): dehydration (relative), polycythemia vera, chronic hypoxia (COPD, high altitude), smoking. Risk: thrombosis. Critical values: Hgb <7 or >20 g/dL — notify provider.

Normal: 150,000-400,000/mm³. Thrombocytopenia (<150,000): causes — HIT, ITP, TTP, DIC, chemo, aplastic anemia, liver disease. Bleeding risk increases as count drops: <50,000 — bleeding with procedures; <20,000 — spontaneous bleeding risk; <10,000 — spontaneous hemorrhage risk (transfuse platelets). Signs: petechiae, purpura, ecchymoses, bleeding gums, epistaxis, melena, hematuria. Nursing: fall prevention, soft toothbrush, no razors (electric only), avoid IM injections, no rectal temps, hold pressure on puncture sites, avoid aspirin/NSAIDs. Thrombocytosis (>400,000): reactive (infection, iron deficiency, post-splenectomy) or primary (myeloproliferative disorder). Risk: thrombosis.

PT (Prothrombin Time): 11-13.5 seconds. Measures extrinsic pathway (factors I, II, V, VII, X). INR (International Normalized Ratio): standardized PT ratio. Normal INR: 0.8-1.1. Therapeutic INR for warfarin: 2.0-3.0 (DVT, PE, afib); 2.5-3.5 (mechanical heart valve). INR >4.0: high bleeding risk. INR >5.0: hold warfarin, consider vitamin K. PT/INR monitors WARFARIN therapy. Elevated PT/INR: liver disease (liver makes clotting factors), DIC, vitamin K deficiency, warfarin therapy. Nursing: consistent vitamin K intake while on warfarin, monitor for bleeding (gums, bruising, dark stools, hematuria), avoid interactions (cranberry, alcohol, many drugs).

Normal aPTT: 25-35 seconds (varies by lab). Measures intrinsic pathway (factors I, II, V, VIII, IX, X, XI, XII). Monitors HEPARIN (unfractionated) therapy. Therapeutic aPTT: 1.5-2.5× control (typically 46-70 seconds). Elevated aPTT: heparin therapy, hemophilia (factor VIII or IX deficiency), DIC, liver disease, von Willebrand disease. If aPTT >100 seconds: high bleeding risk — hold heparin, notify provider. Antidote: protamine sulfate. Draw aPTT 6 hours after dose change and adjust per protocol. Do NOT use aPTT to monitor LMWH (enoxaparin) — use anti-Xa level if monitoring needed.

Normal: 200-400 mg/dL. Fibrinogen (Factor I) is converted to fibrin for clot formation. Decreased (<200): DIC (consumed in widespread clotting), severe liver disease, massive transfusion (dilution), fibrinolytic therapy. DIC: fibrinogen critically low + elevated D-dimer + elevated PT/aPTT + low platelets + microangiopathic hemolytic anemia (schistocytes). Increased (>400): acute inflammation (acute phase reactant), infection, pregnancy, malignancy. Treatment of low fibrinogen: cryoprecipitate (rich in fibrinogen, factor VIII, vWF). Critical value: <100 mg/dL — significant hemorrhage risk.

ALT (Alanine Aminotransferase): 7-56 U/L. More specific to liver. AST (Aspartate Aminotransferase): 10-40 U/L. Found in liver, heart, muscle, kidneys. Elevated: hepatitis (viral, alcoholic, drug-induced), cirrhosis, liver cancer, cholestasis. AST also elevated in MI, rhabdomyolysis, muscle injury. AST:ALT ratio >2:1 suggests alcoholic liver disease. Drug-induced hepatotoxicity: acetaminophen (#1 cause), statins, isoniazid, valproic acid — monitor LFTs. Markedly elevated (>1000): acute hepatitis, acetaminophen toxicity, ischemic hepatitis. Mild elevation (2-3× normal): fatty liver, chronic hepatitis, medications.

Total bilirubin: 0.1-1.2 mg/dL. Direct (conjugated): 0-0.3 mg/dL — elevated in obstructive jaundice (gallstones, pancreatic head tumor, biliary stricture). Indirect (unconjugated): 0.2-0.8 mg/dL — elevated in hemolytic conditions (sickle cell, transfusion reaction, hemolytic disease of newborn), impaired conjugation (Gilbert syndrome, neonatal jaundice). Clinical significance: jaundice visible when total bilirubin >2.5-3.0 mg/dL (skin, sclera). Assess jaundice in natural light. Neonates: pathologic if total bilirubin >12-15 mg/dL (term) or appearing within first 24 hours. Kernicterus risk with very high levels (>25-30 mg/dL). Dark urine (tea-colored) with elevated direct bilirubin; clay-colored stools with obstructive jaundice.

Normal: 3.5-5.0 g/dL. Major plasma protein produced by liver — maintains oncotic pressure, transports drugs, reflects nutritional status. Decreased (<3.5): malnutrition (takes 2-3 weeks to reflect dietary changes — prealbumin is more sensitive for acute changes), liver disease (cirrhosis — can't produce albumin), nephrotic syndrome (lost in urine), burns, inflammatory states. Consequences: peripheral edema, ascites, impaired wound healing. Affects drug binding: low albumin → higher free drug levels (increased effect/toxicity) — important for phenytoin, warfarin. Critically low: <2.0 g/dL. Prealbumin (transthyretin): 15-36 mg/dL — better indicator of recent nutritional status (half-life 2-3 days vs albumin 20 days).

Normal: <0.04 ng/mL (conventional assay); high-sensitivity troponin: <14 ng/L (varies by assay). Troponin I and T: cardiac-specific biomarkers — most sensitive and specific for myocardial injury. Timing: rises 3-6 hours after MI onset, peaks 12-24 hours, remains elevated 7-14 days (troponin I) or 10-14 days (troponin T). Serial measurements: draw at presentation, 3-6 hrs, optionally at 6-12 hrs. Rising pattern confirms acute MI. Other causes of elevated troponin (not MI): PE, myocarditis, heart failure exacerbation, renal failure, sepsis, cardioversion. Always interpret in clinical context. High-sensitivity troponin can detect very small amounts — improves early rule-out. Critical value: any elevation above 99th percentile of normal reference.

BNP: <100 pg/mL (normal). NT-proBNP: <300 pg/mL for rule-out of acute HF. Released from ventricles in response to volume overload and increased wall stress. BNP >100 pg/mL: suggests heart failure. BNP >400 pg/mL: high likelihood of HF. Used to: differentiate cardiac from pulmonary dyspnea, monitor HF treatment effectiveness (should decrease with effective treatment), and guide prognosis (higher BNP = worse prognosis). Falsely low in obesity. Falsely elevated in renal failure, atrial fibrillation, PE, advanced age. Track trends over time rather than single values.

Normal CK-MB: <5% of total CK (or <25 IU/L). CK-MB is the cardiac-specific fraction of creatine kinase. Rises 4-8 hours after MI, peaks 12-24 hours, returns to normal in 48-72 hours. Clinical use: largely replaced by troponin for MI diagnosis but still useful for: detecting reinfarction (returns to normal faster than troponin — a second rise indicates new event), timing of MI, and perioperative MI detection. Total CK: 30-170 U/L (male), 25-150 U/L (female). Also elevated in rhabdomyolysis (CK >5× normal, often >10,000), muscle trauma, strenuous exercise.

TSH: 0.5-4.0 mIU/L (most sensitive screening test — interpret FIRST). Free T4: 0.8-1.8 ng/dL. Free T3: 2.3-4.2 pg/mL. Hypothyroidism: TSH HIGH, T3/T4 LOW (thyroid underproducing → pituitary increases TSH). Symptoms: fatigue, weight gain, cold intolerance, constipation, bradycardia, dry skin, depression, myxedema. Treatment: levothyroxine. Hyperthyroidism: TSH LOW, T3/T4 HIGH (thyroid overproducing → pituitary suppresses TSH). Symptoms: weight loss, heat intolerance, tachycardia/afib, tremor, diarrhea, exophthalmos (Graves disease), anxiety. Treatment: methimazole (PTU in first trimester or thyroid storm), radioactive iodine, surgery. Thyroid storm: extreme hyperthyroidism — fever >104°F, tachycardia, delirium — emergency.

Normal: <5.7%. Pre-diabetes: 5.7-6.4%. Diabetes diagnosis: ≥6.5%. Reflects average blood glucose over past 2-3 months (lifespan of RBC). Target for most diabetics: <7.0% (ADA recommendation). Elderly/comorbid patients: may accept <8.0% (avoid hypoglycemia). Estimated average glucose (eAG): A1C 6% ≈ 126 mg/dL, 7% ≈ 154 mg/dL, 8% ≈ 183 mg/dL, 9% ≈ 212 mg/dL, 10% ≈ 240 mg/dL (formula: eAG = 28.7 × A1C - 46.7). Conditions affecting accuracy: hemolytic anemia, chronic bleeding, transfusions, sickle cell disease — may falsely lower A1C. Iron deficiency anemia may falsely elevate A1C. Test every 3-6 months in diabetic patients.

Total cholesterol: <200 mg/dL (desirable), 200-239 (borderline high), ≥240 (high). LDL ('bad' cholesterol): <100 mg/dL (optimal), <70 mg/dL (high-risk/CAD patients on statin therapy). HDL ('good' cholesterol): >40 mg/dL (male), >50 mg/dL (female) — higher is better (≥60 is protective). Triglycerides: <150 mg/dL (normal), 150-199 (borderline), 200-499 (high), ≥500 (very high — pancreatitis risk). Fasting: 9-12 hours for accurate triglycerides/LDL. Non-HDL cholesterol = Total - HDL (secondary target). Statins: first-line for LDL lowering — monitor LFTs, CK (rhabdomyolysis risk), teach: take at bedtime (some statins), avoid grapefruit (some statins), report muscle pain.

pH: 7.35-7.45. PaCO2: 35-45 mmHg (respiratory component — acid). PaO2: 80-100 mmHg (oxygenation — not acid-base). HCO3: 22-26 mEq/L (metabolic component — base). SaO2: >95%. Base excess/deficit: -2 to +2 mEq/L (negative = base deficit = metabolic acidosis; positive = base excess = metabolic alkalosis). Quick interpretation: pH and PaCO2 move in OPPOSITE directions = respiratory cause. pH and HCO3 move in SAME direction = metabolic cause. Compensation: the unaffected system moves to normalize pH. Full compensation = normal pH. The system that moved FIRST (and is more abnormal) is the primary disorder.

Color: pale yellow to amber. Clarity: clear. Specific gravity: 1.005-1.030 (higher = concentrated/dehydrated, lower = dilute/overhydrated, diabetes insipidus). pH: 4.5-8.0 (average 6.0). Protein: negative (positive = kidney damage, preeclampsia, nephrotic syndrome). Glucose: negative (positive = DM with glucose >180 mg/dL — renal threshold). Ketones: negative (positive = DKA, starvation, low-carb diet). Blood: negative (positive = UTI, kidney stones, glomerulonephritis, menstruation). Nitrites: negative (positive suggests bacterial infection — gram-negative bacteria convert nitrates to nitrites). Leukocyte esterase: negative (positive = WBCs in urine, infection). WBC: 0-5/HPF. RBC: 0-3/HPF. Casts: none (RBC casts = glomerulonephritis, WBC casts = pyelonephritis, waxy casts = chronic renal failure). Bacteria: none.

Potassium: <2.5 or >6.0 mEq/L (cardiac arrest risk). Sodium: <120 or >160 mEq/L (seizures, neurological damage). Glucose: <40 or >500 mg/dL. Calcium: <6.0 or >13.0 mg/dL. Magnesium: <1.0 or >4.7 mEq/L. Hemoglobin: <7.0 or >20 g/dL. Platelets: <50,000 or >1,000,000/mm³. WBC: <2,000 or >30,000/mm³. INR: >5.0. aPTT: >100 seconds. Troponin: any elevation above normal. pH: <7.20 or >7.60. PaCO2: <20 or >60 mmHg. PaO2: <40 mmHg. Lactate: >4.0 mmol/L. Positive blood cultures. Nursing responsibility: read back results, document time of notification, name of provider notified, and any orders received. Follow institution's critical value reporting policy — typically notify within 30-60 minutes.

Normal: <500 ng/mL (or <0.5 mcg/mL FEU). D-dimer is a fibrin degradation product — elevated when clots are being broken down. Clinical use: HIGH negative predictive value — if normal, effectively RULES OUT DVT/PE (in low-to-moderate pretest probability). If elevated: NOT diagnostic — requires further imaging (CT-PA for PE, duplex ultrasound for DVT). Also elevated in: DIC, post-surgery, trauma, pregnancy, malignancy, infection, liver disease, advanced age. Not useful for monitoring anticoagulation therapy. Best used as a rule-out test, not a rule-in test.

Normal: 0.5-2.0 mmol/L. Elevated lactate indicates tissue hypoperfusion/anaerobic metabolism. Causes: sepsis/septic shock, cardiogenic shock, hypovolemia, severe hypoxia, liver failure (decreased clearance), medications (metformin, epinephrine), seizures, strenuous exercise. In sepsis: lactate >2 mmol/L indicates tissue hypoperfusion. Lactate >4 mmol/L: high mortality risk — triggers aggressive resuscitation (SEP-1 bundle). Sepsis bundle: measure lactate, blood cultures before antibiotics, broad-spectrum antibiotics within 1 hour, IV crystalloid 30 mL/kg for hypotension or lactate ≥4, vasopressors if hypotensive after fluids. Serial lactate measurements: target lactate clearance ≥10% over first 6 hours indicates response to treatment.

Normal: 15-45 mcg/dL (varies by lab). Ammonia is produced from protein metabolism and cleared by the liver (converted to urea). Elevated: hepatic encephalopathy (liver cannot clear ammonia → crosses blood-brain barrier), Reye syndrome, urea cycle disorders, GI bleeding (blood = protein → ammonia in gut). Symptoms of hepatic encephalopathy: confusion, asterixis (flapping tremor), altered LOC → coma. Treatment: lactulose (osmotic laxative — promotes ammonia excretion in stool, goal: 2-3 soft stools/day), rifaximin (gut antibiotic — reduces ammonia-producing bacteria), protein restriction (mild/short-term only — moderate protein intake preferred). Specimen handling: collect on ice, send immediately to lab. Do NOT use tourniquet or have patient clench fist (falsely elevates).

Normal: 3.5-7.2 mg/dL (male), 2.6-6.0 mg/dL (female). End product of purine metabolism. Elevated (hyperuricemia): gout (#1 association — crystal deposition in joints, especially great toe/first MTP), tumor lysis syndrome (massive cell destruction releases purines), renal calculi (uric acid stones), chronic kidney disease, thiazide diuretics, high-purine diet (red meat, organ meats, shellfish, beer). Treatment: acute gout — NSAIDs (indomethacin), colchicine, corticosteroids. Prophylaxis: allopurinol or febuxostat (xanthine oxidase inhibitors — decrease uric acid production). Tumor lysis syndrome prevention: rasburicase (recombinant urate oxidase), IV hydration, allopurinol. Teach: avoid high-purine foods, adequate hydration, limit alcohol.

Normal: 15-36 mg/dL. Half-life: 2-3 days (vs albumin's 20 days) — reflects recent nutritional changes more rapidly. Better indicator of acute nutritional status and response to nutritional intervention. Mild depletion: 10-15 mg/dL. Moderate: 5-10 mg/dL. Severe: <5 mg/dL. Decreased in: malnutrition, liver disease, inflammation (negative acute phase reactant — decreases with infection/inflammation, which limits its accuracy during acute illness). Use serial measurements to track nutritional improvement. Monitor in patients on TPN, post-surgical patients, critically ill patients. CRP can be measured alongside prealbumin — if CRP is elevated, low prealbumin may reflect inflammation rather than malnutrition.

Temperature: 97.8-99.1°F (36.5-37.3°C). Oral is standard; rectal is most accurate (+1°F above oral); axillary is least accurate (-1°F below oral); tympanic approximates core. Fever: >100.4°F (38°C). Heart Rate: 60-100 bpm. Bradycardia <60, Tachycardia >100. Respiratory Rate: 12-20 breaths/min. Bradypnea <12, Tachypnea >20. Blood Pressure: <120/80 (normal). Pulse Oximetry: 95-100% (normal). <90% = respiratory failure. Orthostatic hypotension: SBP drop ≥20 mmHg or DBP drop ≥10 mmHg or HR increase ≥20 bpm within 3 min of standing — indicates hypovolemia. Always assess VS together — changes in one may explain others.

Children are NOT small adults — their physiology changes with growth. HR decreases with age: newborns rely on HR for cardiac output (cannot increase stroke volume well). RR decreases with age: smaller lungs require faster rate. BP increases with age: blood volume and vascular resistance increase. KEY PRINCIPLE: tachycardia is the FIRST sign of distress/shock in children. Hypotension is a LATE sign (indicates decompensated shock — 25% blood loss). Weight-based calculations: fluid bolus 20 mL/kg NS, maintenance fluids by 4-2-1 rule (4 mL/kg/hr for first 10 kg + 2 mL/kg/hr for next 10 kg + 1 mL/kg/hr for each kg above 20). Always weigh in kilograms for medication dosing.

ESR (Erythrocyte Sedimentation Rate): Male <15 mm/hr (age <50) or <20 mm/hr (>50). Female <20 mm/hr (<50) or <30 mm/hr (>50). CRP (C-Reactive Protein): <1.0 mg/dL (or <10 mg/L). Both are nonspecific markers of inflammation — elevated in infection, autoimmune disease, malignancy, tissue injury. ESR: slow to rise (24-48 hrs) and slow to normalize. CRP: rises within 6-8 hrs and normalizes faster — better for monitoring acute changes. Uses: monitor disease activity (rheumatoid arthritis, SLE, IBD, temporal arteritis — ESR often >100 mm/hr in temporal arteritis), response to treatment, detect infection. hs-CRP (high sensitivity): <1.0 mg/L low CV risk, 1.0-3.0 moderate, >3.0 high — used for cardiovascular risk assessment.

Serum iron: 60-170 mcg/dL. TIBC (Total Iron Binding Capacity): 250-370 mcg/dL. Transferrin saturation: 20-50%. Ferritin: Male 12-300 ng/mL, Female 10-150 ng/mL. Iron deficiency anemia pattern: LOW serum iron, HIGH TIBC (body makes more transferrin trying to capture scarce iron), LOW ferritin (depleted iron stores), LOW transferrin saturation. Microcytic, hypochromic RBCs on smear. Ferritin is the best single test for iron deficiency (first to decrease). However, ferritin is also an acute phase reactant — can be falsely elevated in inflammation/infection even with true iron deficiency. Anemia of chronic disease: LOW iron, LOW TIBC, NORMAL or HIGH ferritin. Treatment: oral iron (ferrous sulfate — take on empty stomach with vitamin C for absorption, expect dark stools), IV iron (iron dextran — test dose required, anaphylaxis risk).

Uncompensated: pH abnormal, one system abnormal, other system normal. Partially compensated: pH still abnormal, BOTH systems abnormal (compensating system moving to correct pH). Fully compensated: pH NORMAL (7.35-7.45), BOTH systems abnormal. To identify primary disorder when fully compensated: look at which side of 7.40 the pH falls — acidotic side (7.35-7.40) → primary acidosis; alkalotic side (7.40-7.45) → primary alkalosis. Example: pH 7.32, PaCO2 55, HCO3 30. pH acidotic, PaCO2 high (respiratory acidosis), HCO3 high (metabolic alkalosis — compensation). Primary: respiratory acidosis with partial metabolic compensation (pH still abnormal). Clinical: likely COPD with chronic CO2 retention.

Extrinsic pathway: triggered by tissue factor (tissue damage) → factor VII → activates factor X. Monitored by PT/INR. Warfarin affects extrinsic pathway. Mnemonic: PT = ProThrombin time = Warfarin (P and W don't touch — remember by exclusion vs aPTT). Intrinsic pathway: triggered by contact activation (factor XII) → factors XI, IX, VIII → activates factor X. Monitored by aPTT. Heparin affects intrinsic pathway. Mnemonic: aPTT = heParin (both have P). Common pathway: factor X → prothrombin → thrombin → fibrinogen → fibrin clot. Both PT and aPTT affected by common pathway issues (factor X, V, prothrombin, fibrinogen). DIC affects all pathways: elevated PT, aPTT, D-dimer; decreased fibrinogen and platelets.

Heart Rate: 120-160 bpm (may be 100 during sleep, up to 180 with crying). Respiratory Rate: 30-60 breaths/min. Periodic breathing is normal (pauses <20 sec); apnea = pause >20 sec or any pause with bradycardia/cyanosis. Temperature: 97.7-99.5°F (36.5-37.5°C) axillary. Blood Pressure: 60-80/40-50 mmHg (term newborn). SpO2: pre-ductal (right hand) ≥95%, post-ductal (left hand or foot) ≥95%, difference <3% (screening for critical congenital heart disease). Weight: average term 2,500-4,000g (5.5-8.8 lbs). Normal weight loss: up to 7-10% in first 3-5 days; regain birth weight by 10-14 days.

Heart Rate: 100-160 bpm (decreases as infant grows). Respiratory Rate: 24-40 breaths/min. Temperature: 97.7-99.5°F (36.5-37.5°C). Blood Pressure: approximately 80-100/50-65 mmHg (increases with age). Key assessment: anterior fontanelle (soft spot) — bulging = increased ICP (meningitis, hydrocephalus), sunken = dehydration. Closes by 12-18 months. Posterior fontanelle closes by 2-3 months. Weight milestones: doubles birth weight by 5-6 months, triples by 12 months. Head circumference: most important growth parameter in first year (brain growth). Measure at every well visit.

Heart Rate: 80-130 bpm (1-3 years), 80-120 bpm (3-5 years). Respiratory Rate: 20-30 breaths/min. Blood Pressure: approximately 90-105/55-70 mmHg. Hypertension in children: >95th percentile for age/height/sex on 3+ separate occasions. Temperature: same as adult norms. Key considerations: toddlers cannot localize pain well — may present with irritability, decreased activity, poor feeding. Use age-appropriate pain scales (FLACC for preverbal). Growth: weight quadruples birth weight by 2.5 years. Height at age 2 is approximately half adult height.

School-age HR: 70-110 bpm. Adolescent HR: 60-100 bpm (approaching adult). School-age RR: 18-25 breaths/min. Adolescent RR: 12-20 breaths/min (adult range). School-age BP: approximately 100-120/60-75 mmHg. Adolescent BP: approaching adult norms (<120/80). Screen for hypertension annually starting at age 3. Adolescent-specific: screen for scoliosis, eating disorders, depression, substance use. Tanner staging for pubertal development. BMI screening: >85th percentile = overweight, >95th percentile = obese.

Timing: fasting (before meals), 2-hour postprandial, before bedtime, at 3 AM (Somogyi effect vs dawn phenomenon). Technique: wash hands with warm water (no alcohol — can affect reading), use side of fingertip (less painful, better blood flow), rotate puncture sites, do not squeeze excessively (dilutes with tissue fluid). Target ranges: pre-meal 80-130 mg/dL, peak postprandial <180 mg/dL (ADA). Continuous glucose monitoring (CGM): measures interstitial glucose every 5 minutes, 5-15 minute lag behind blood glucose, useful for trend identification. Time in range (TIR): goal >70% of time between 70-180 mg/dL. Somogyi effect: nocturnal hypoglycemia → rebound morning hyperglycemia (treatment: reduce evening insulin or add bedtime snack). Dawn phenomenon: early morning growth hormone/cortisol surge → hyperglycemia (treatment: adjust basal insulin timing).

Normal: <120/80 mmHg. Elevated: SBP 120-129 AND DBP <80. Stage 1 Hypertension: SBP 130-139 OR DBP 80-89. Stage 2 Hypertension: SBP ≥140 OR DBP ≥90. Hypertensive Crisis: SBP >180 AND/OR DBP >120 — assess for target organ damage (headache, visual changes, chest pain, dyspnea, neurological deficits). Hypertensive urgency: severely elevated without organ damage — reduce BP gradually over 24-48 hours. Hypertensive emergency: with organ damage — IV medications (nitroprusside, labetalol, nicardipine), reduce MAP by no more than 25% in first hour (too rapid = stroke, MI, renal failure). Proper BP measurement: rest 5 min, empty bladder, supported arm at heart level, appropriate cuff size (bladder 80% of arm circumference).

Normal SpO2: 95-100%. Mild hypoxemia: 91-94%. Moderate hypoxemia: 86-90%. Severe hypoxemia: <85%. Factors causing FALSE readings: motion artifact, poor perfusion (shock, hypothermia, vasoconstriction), dark nail polish (especially blue, black, green — remove or use earlobe/forehead sensor), carbon monoxide poisoning (SpO2 reads falsely HIGH because CO-Hgb absorbs light similarly to O2-Hgb — get ABG with co-oximetry), methemoglobinemia (reads ~85% regardless of true saturation), anemia (SpO2 may be normal despite inadequate O2 delivery — check Hgb), ambient light interference. PaO2 vs SpO2: PaO2 80-100 mmHg = SpO2 95-100%. PaO2 60 mmHg = SpO2 ~90% (critical point on oxyhemoglobin dissociation curve — below this, saturation drops rapidly).

Routes and accuracy: Rectal = most accurate core temp (contraindicated in neutropenia, rectal surgery, neonates in some facilities). Oral = standard in adults (wait 15-30 min after eating/drinking). Tympanic = reflects core temp, quick, but technique-dependent. Temporal artery = noninvasive, reasonable accuracy. Axillary = least accurate, used when other routes contraindicated. Conversions: F = (C × 9/5) + 32; C = (F - 32) × 5/9. Fever: >100.4°F (38°C). Hyperthermia vs fever: fever = hypothalamic setpoint elevated (infection, inflammation); hyperthermia = body overwhelmed/setpoint normal (heat stroke, malignant hyperthermia). Malignant hyperthermia: genetic reaction to succinylcholine/volatile anesthetics — treat with dantrolene. Hypothermia: <95°F (35°C) — mild 90-95°F, moderate 82-90°F, severe <82°F. Rewarm gradually.

Numeric Rating Scale (NRS): 0-10, for adults and children >7 years who can self-report. Wong-Baker FACES: ages 3-7+, patient points to face matching pain level. FLACC Scale: ages 2 months to 7 years or nonverbal — Face, Legs, Activity, Cry, Consolability (0-2 each, total 0-10). CPOT (Critical Care Pain Observation Tool): for intubated/unconscious patients — facial expression, body movements, muscle tension, ventilator compliance. PAINAD: for dementia patients — breathing, vocalization, facial expression, body language, consolability. Assessment: use consistent scale, assess before and after interventions (30 min post-IV, 60 min post-PO), document location, quality, onset, duration, aggravating/alleviating factors. WHO pain ladder: Step 1 non-opioid (acetaminophen, NSAIDs), Step 2 weak opioid, Step 3 strong opioid.

Normal adult urine output: 0.5-1.0 mL/kg/hr (approximately 30-60 mL/hr or 1,500-2,000 mL/day). Oliguria: <400 mL/day or <0.5 mL/kg/hr (may indicate AKI, dehydration, shock). Anuria: <100 mL/day (renal failure, obstruction). Polyuria: >3,000 mL/day (diabetes insipidus, DM, diuretics, psychogenic polydipsia). Intake includes: oral fluids, IV fluids, tube feeding, IV medications/flushes, blood products, irrigation fluid retained. Output includes: urine, emesis, wound drainage (chest tube, JP, Hemovac), NG suction, stool (especially diarrhea), estimated blood loss. Normal insensible loss: ~500-1,000 mL/day (lungs, skin) — increases with fever, tachypnea, burns. Pediatric urine output: infant 2 mL/kg/hr, child 1 mL/kg/hr, adolescent 0.5 mL/kg/hr. Wet diapers: minimum 6-8/day for adequate hydration in infants.

Dehydration signs: thirst, dry mucous membranes, decreased skin turgor (tenting), sunken eyes/fontanelle (infants), tachycardia, hypotension, orthostatic changes, oliguria, concentrated urine (high specific gravity >1.030), elevated BUN/creatinine ratio (>20:1), weight loss (1 L fluid = 1 kg = 2.2 lbs). Mild: 3-5% weight loss, Moderate: 6-9%, Severe: >10%. Fluid overload signs: edema (peripheral, periorbital, sacral in bedridden patients), weight gain, distended neck veins (JVD), crackles/rales in lungs, dyspnea, S3 heart sound, bounding pulse, elevated BP, decreased BUN/Hct (hemodilution), low urine specific gravity. Treatment: dehydration — isotonic IV fluids (0.9% NS or LR), oral rehydration. Fluid overload — fluid restriction, diuretics (furosemide), sodium restriction, elevate HOB, monitor daily weights (same time, same scale, same clothing). I&O monitoring essential for both.