🩸 Blood Work & Reference Values

135 to 145 mEq/L (135 to 145 mmol/L). Widely used critical values: below 120 mEq/L and above 160 mEq/L. Confirm your facility's critical thresholds, since some labs flag at 125 and 155.

Sodium is the main cation outside the cell, so it sets serum osmolality and controls where water sits in the body. Because water follows sodium, the sodium level is really a water problem in disguise: it tells you whether the patient has too much free water diluting them or too little water concentrating them. Sodium also drives depolarization of nerve and muscle cells, which is why every symptom of an abnormal sodium is neurologic.

Hypernatremia above 145 mEq/L means the patient has more sodium than water. Causes are water loss (fever, heat exposure, watery diarrhea, hyperventilation, diabetes insipidus, osmotic diuresis from hyperglycemia), inadequate water intake in someone who cannot ask for a drink, or sodium gain from hypertonic fluids, tube feedings without free water, or excess sodium bicarbonate. Water leaves the brain cells and they shrivel, so expect thirst, dry sticky mucous membranes, flushed skin, low-grade fever, restlessness and agitation progressing to lethargy, muscle twitching, seizures, and coma. Urine is scant and concentrated unless the cause is diabetes insipidus, in which case it is copious and dilute.

Hyponatremia below 135 mEq/L usually means too much water rather than too little salt. Causes include SIADH, heart failure, cirrhosis, kidney failure, excessive hypotonic IV fluid, water intoxication or psychogenic polydipsia, adrenal insufficiency, thiazide diuretics, and true sodium loss from vomiting, nasogastric suction, diarrhea, burns, or excessive sweating replaced with plain water. Water moves into brain cells and they swell, so expect headache, confusion, personality change, lethargy, muscle cramps and weakness, nausea, hyperactive bowel sounds, and at severe levels seizures, respiratory arrest, and coma. Sort dilutional from depletional by checking fluid volume status: bounding pulse, weight gain, and edema point to dilution; poor turgor, flat neck veins, tachycardia, and orthostatic hypotension point to loss.

Get baseline neurologic status and repeat it every shift or more often, because a change in level of consciousness is the earliest and most important finding at both ends. Track daily weights on the same scale at the same time, strict intake and output, and fluid status. For hypernatremia, expect hypotonic fluid such as 0.45 percent sodium chloride or 5 percent dextrose in water and free water flushes with tube feedings; offer fluids frequently to anyone who cannot self-hydrate. For hyponatremia, expect fluid restriction first when the cause is dilutional; 3 percent sodium chloride is reserved for severe symptomatic hyponatremia and is given slowly through a pump, usually in an intensive care setting, with frequent sodium redraws. Institute seizure precautions when sodium is severely abnormal in either direction. Report a critical value immediately, document who you told and when, and reassess after the intervention.

Correct sodium slowly. Shifting serum sodium faster than roughly 8 to 12 mEq/L in 24 hours causes catastrophic brain injury, so if you see rapid infusion of hypertonic saline or a sodium that jumped sharply between draws, that is the finding you act on.

3.5 to 5.0 mEq/L (3.5 to 5.0 mmol/L). Critical values: below 2.5 mEq/L and above 6.5 mEq/L. Many facilities call any value below 3.0 or above 6.0 mEq/L.

Potassium is the main cation inside the cell and it sets the resting membrane potential, so it decides how easily excitable tissue fires. The heart is the organ that kills the patient, so every potassium result is a cardiac result. Potassium is also lost in urine, in gastric contents, and through the gut, and it moves between the cell and the serum with acid-base changes and insulin, which is why the serum number sometimes lies about total body stores.

Hyperkalemia above 5.0 mEq/L comes from kidney failure (the single most common cause), potassium-sparing diuretics, ACE inhibitors and angiotensin receptor blockers, excessive supplementation, blood transfusion of older units, and from cellular release in acidosis, crush injury, burns, tumor lysis, and rhabdomyolysis. Hemolysis of the specimen from a traumatic draw gives a false elevation. Signs: muscle weakness that starts in the legs and ascends, paresthesias, flaccid paralysis late, hyperactive bowel sounds, diarrhea and cramping, irritability, and the ECG progression of tall peaked T waves, then a flattened P wave and widened QRS, then a sine wave and cardiac arrest.

Hypokalemia below 3.5 mEq/L comes from loop and thiazide diuretics, vomiting, nasogastric suction, diarrhea, laxative abuse, corticosteroids, poor intake, alkalosis, and insulin therapy driving potassium into cells. Signs mirror hyperkalemia in the sense that both cause weakness, but hypokalemia slows down smooth muscle: weakness and leg cramps, hypoactive or absent bowel sounds, abdominal distention and paralytic ileus, constipation, nausea, shallow respirations from weak respiratory muscles, weak thready pulse, hypotension, lethargy, and ECG changes of flattened or inverted T waves, ST depression, and a prominent U wave. Low potassium markedly increases digoxin toxicity risk.

Never push potassium IV. It is always diluted and always infused with a pump, and a standard peripheral rate limit is 10 mEq/hour with 20 mEq/hour used only with continuous cardiac monitoring and central access per policy. Confirm urine output of at least 30 mL/hour before giving potassium, because a patient who cannot make urine cannot excrete it. Assess the IV site frequently, since potassium is a vesicant and burns. For hyperkalemia, expect calcium gluconate to stabilize the myocardium (it does not lower potassium), insulin with dextrose and sometimes a beta agonist to shift potassium into cells, and sodium polystyrene sulfonate, patiromer, or dialysis to actually remove it. Put the patient on a cardiac monitor for any critical potassium and teach dietary sources: bananas, oranges, potatoes, tomatoes, avocado, spinach, and salt substitutes, which are potassium chloride and are a hidden cause of hyperkalemia.

Potassium given by IV push is fatal. If an order says IV push potassium chloride, do not give it and clarify the order. On the assessment side, any potassium below 3.5 or above 5.0 mEq/L means you get an ECG or cardiac monitor going.

Approximately 30 to 40 seconds, with the exact interval set by the individual laboratory's reagent, so always read the range printed on the report. Therapeutic anticoagulation with continuous unfractionated heparin is 1.5 to 2.5 times the control value, commonly about 60 to 80 seconds. A value greater than roughly 70 seconds in a patient not intentionally anticoagulated, or greater than 100 seconds in any patient, is generally treated as critical.

The aPTT measures the intrinsic and common coagulation pathways, and it is the test used to monitor continuous intravenous unfractionated heparin. It is also drawn to work up unexplained bleeding, hemophilia, von Willebrand disease, disseminated intravascular coagulation, and liver disease. Low molecular weight heparin such as enoxaparin does not require aPTT monitoring, and that distinction is heavily tested.

A prolonged aPTT means the blood is taking too long to clot: heparin effect, clotting factor deficiency such as hemophilia, liver disease, vitamin K deficiency, disseminated intravascular coagulation, or a circulating inhibitor. Expect bleeding gums, epistaxis, bruising, petechiae, hematuria, blood in stool or emesis, prolonged bleeding at puncture sites, and in a serious bleed, tachycardia, hypotension, and a falling hemoglobin. New headache, unequal pupils, or altered mentation in an anticoagulated patient means intracranial bleeding until proven otherwise.

A shortened or subtherapeutic aPTT in a heparinized patient means the dose is inadequate and the patient is at risk of extending the clot, of a new pulmonary embolus, or of stroke. A short aPTT on its own can also reflect early disseminated intravascular coagulation or an acute-phase hypercoagulable state. Assess for signs of new or extending thrombosis: unilateral calf swelling, warmth and pain, sudden dyspnea and pleuritic chest pain, or new neurologic deficit.

Draw the sample from an extremity opposite the heparin infusion, or the result will be falsely and dangerously high. Timing depends on protocol; with continuous infusions, expect a redraw about 6 hours after a rate change and then daily once stable. Hold pressure on venipuncture sites for at least 5 minutes. Institute bleeding precautions: electric razor, soft toothbrush, no rectal temperatures or suppositories, no intramuscular injections when avoidable, fall prevention. Know that the antidote for heparin is protamine sulfate and that it should be immediately available. Check platelets serially, because heparin-induced thrombocytopenia presents as a platelet drop of 50 percent or more with new clotting, not bleeding.

aPTT monitors unfractionated heparin, and heparin is reversed with protamine sulfate. If the aPTT exceeds the therapeutic window or the patient shows active bleeding, stop the infusion first and then notify the provider.

PT approximately 11 to 12.5 seconds, again laboratory dependent. INR is approximately 0.8 to 1.2 in a person not taking an anticoagulant. Therapeutic INR on warfarin is 2.0 to 3.0 for atrial fibrillation, venous thromboembolism, and most indications, and 2.5 to 3.5 for a mechanical mitral valve. An INR above 5 is widely treated as critical because bleeding risk climbs steeply.

The PT measures the extrinsic and common pathways and is the test used to monitor warfarin. Because PT reagents differ between laboratories, the INR was created to standardize the result so a patient's value means the same thing anywhere. PT and INR are also sensitive markers of hepatic synthetic function and of vitamin K deficiency, since the liver makes factors II, VII, IX, and X and needs vitamin K to do it.

A prolonged PT or elevated INR means excessive anticoagulation or impaired clotting factor production: too much warfarin, drug interactions (antibiotics, amiodarone, many others), acute alcohol intake, liver disease, biliary obstruction, vitamin K deficiency, or disseminated intravascular coagulation. Expect the full bleeding picture: bruising, gum and nose bleeding, hematuria, melena, heavy menses, prolonged oozing, and with severe elevation, spontaneous internal or intracranial hemorrhage.

A subtherapeutic INR in a patient on warfarin means insufficient anticoagulation and continued clot risk, and it is commonly caused by missed doses or a sudden increase in dietary vitamin K such as a new habit of large green salads. Watch for the thrombotic complication the drug was prescribed to prevent: stroke in atrial fibrillation, deep vein thrombosis or pulmonary embolism, or valve thrombosis.

Teach consistency, not avoidance, with vitamin K foods such as spinach, kale, broccoli, Brussels sprouts, and cabbage; the goal is a steady daily intake so the dose can be matched to it. Warn about interacting drugs, including over-the-counter aspirin and NSAIDs and herbal products such as ginkgo and garlic, and stress no alcohol binges. The antidote for warfarin is vitamin K (phytonadione); serious bleeding is treated with prothrombin complex concentrate or fresh frozen plasma. Reinforce that the patient must attend scheduled INR draws, carry medical identification, and report black stools, red or brown urine, or unexplained bruising. Direct oral anticoagulants such as apixaban and rivaroxaban do not use INR monitoring.

PT and INR monitor warfarin, and warfarin is reversed with vitamin K. Hold the dose and notify the provider for an INR above the therapeutic range or any active bleeding.

150,000 to 400,000/mm3 (150 to 400 x 10 to the 9th per liter). Bleeding risk rises meaningfully below 50,000/mm3, and spontaneous bleeding including intracranial hemorrhage becomes a real threat below 20,000/mm3. A count below 20,000/mm3 or above about 1,000,000/mm3 is typically flagged critical.

Platelets create the initial plug that stops bleeding, so the count is your direct measure of primary hemostasis. It is checked before invasive procedures and surgery, during chemotherapy and radiation, in liver disease, in suspected disseminated intravascular coagulation, and serially in any patient receiving heparin.

Thrombocytosis above 400,000/mm3 can be reactive after splenectomy, infection, inflammation, iron deficiency, or malignancy, or it can reflect a primary bone marrow disorder such as essential thrombocythemia. The danger is clotting rather than bleeding: deep vein thrombosis, stroke, myocardial infarction, and in very high counts, paradoxical bleeding because the platelets are dysfunctional. Assess for unilateral limb swelling and pain, chest pain, dyspnea, and neurologic change.

Thrombocytopenia comes from decreased production (bone marrow suppression from chemotherapy, radiation, leukemia, aplastic anemia, alcohol, B12 or folate deficiency), increased destruction (immune thrombocytopenia, heparin-induced thrombocytopenia, disseminated intravascular coagulation, sepsis), or sequestration in an enlarged spleen from cirrhosis. Signs are petechiae, purpura, ecchymoses, gum and nose bleeding, prolonged bleeding from punctures, hematuria, melena, heavy menses, and with severe drops, headache and altered mental status from intracranial bleeding.

Implement bleeding precautions when the count falls: electric razor only, soft toothbrush or oral swabs, no flossing if the count is very low, no rectal temperatures, enemas, or suppositories, avoid intramuscular injections and invasive procedures, hold pressure 5 to 10 minutes after any needle stick, avoid aspirin and NSAIDs, prevent constipation with stool softeners so the patient does not strain, and pad the environment and prevent falls. Assess urine, stool, emesis, and sputum for blood, and check neurologic status. Anticipate platelet transfusion at very low counts or with active bleeding. If the patient is on heparin and the platelet count falls by half or more, suspect heparin-induced thrombocytopenia, stop all heparin including flushes, and notify the provider.

Below 50,000/mm3, expect bleeding with trauma and procedures; below 20,000/mm3, expect spontaneous bleeding and treat a new headache or change in level of consciousness as intracranial hemorrhage.

Hemoglobin: approximately 14 to 18 g/dL in adult males and 12 to 16 g/dL in adult females. Hematocrit: approximately 42 to 52 percent in adult males and 37 to 47 percent in adult females. Hematocrit normally runs about three times the hemoglobin. A hemoglobin below roughly 7 g/dL or a hematocrit below about 20 percent is commonly a critical value.

Hemoglobin is the protein that carries oxygen, and hematocrit is the percentage of blood volume made up of red cells. Together they tell you the patient's oxygen-carrying capacity and, indirectly, their fluid status. They are drawn to evaluate anemia, to quantify blood loss, to follow chronic kidney disease and chemotherapy, and to decide whether transfusion is needed.

Elevated values occur with dehydration and hemoconcentration (the most common cause on a medical unit), chronic hypoxia from COPD or living at altitude, heavy smoking, and polycythemia vera. Thick, sluggish blood raises clotting risk. Expect ruddy or flushed complexion, headache, dizziness, visual changes, hypertension, itching after a hot shower in polycythemia vera, and risk of stroke, myocardial infarction, and venous thrombosis. In dehydration, the number falls back to baseline once fluid is replaced, so evaluate it alongside intake and output, weight, and mucous membranes.

Low values mean anemia or acute blood loss: iron, B12, or folate deficiency, chronic kidney disease with low erythropoietin, bone marrow failure, hemolysis, gastrointestinal bleeding, trauma, surgery, or heavy menses. Fluid overload also dilutes the values. Signs are fatigue, pallor of skin, conjunctivae, and nail beds, tachycardia, tachypnea and dyspnea on exertion, dizziness, cold intolerance, headache, and in severe or rapid loss, hypotension, chest pain, and altered mental status. Remember that in acute hemorrhage the hemoglobin and hematocrit do not fall right away, because whole blood is lost and it takes hours of fluid shift or fluid resuscitation for the drop to appear.

Assess for the functional consequence, not just the number: activity tolerance, dyspnea, chest pain, dizziness on standing, and mental status. Cluster care and space activities to conserve oxygen. Institute fall precautions and have the patient rise slowly. Monitor for occult bleeding by checking stools, emesis, drains, dressings, and abdominal girth. Teach dietary iron with a vitamin C source to improve absorption, and warn that oral iron turns stool dark green or black and causes constipation. If transfusion is ordered, verify with two nurses per policy, use normal saline only as the compatible fluid, start slowly and stay with the patient for the first 15 minutes, and monitor vital signs for a reaction. Expect roughly a 1 g/dL rise in hemoglobin per unit of packed red cells.

In an acute bleed, trend the vital signs, not the hemoglobin. Rising heart rate and falling blood pressure precede the hemoglobin drop, so a normal hemoglobin never rules out active hemorrhage.

Total cholesterol desirable below 200 mg/dL. LDL cholesterol optimal below 100 mg/dL, and below 70 mg/dL for patients at very high cardiovascular risk. HDL cholesterol desirable above 40 mg/dL in men and above 50 mg/dL in women, with above 60 mg/dL considered protective. Triglycerides normal below 150 mg/dL, with levels above 500 mg/dL carrying pancreatitis risk.

The lipid panel estimates atherosclerotic cardiovascular risk. LDL delivers cholesterol to the arterial wall and drives plaque formation, so it is the primary treatment target. HDL carries cholesterol back to the liver, so higher is better. Triglycerides rise with poorly controlled diabetes, obesity, alcohol, and high refined carbohydrate intake, and very high levels inflame the pancreas.

High total cholesterol, high LDL, or high triglycerides mean accelerated atherosclerosis and increased risk of coronary artery disease, myocardial infarction, stroke, and peripheral arterial disease. Contributors are diet high in saturated and trans fat, sedentary lifestyle, obesity, uncontrolled diabetes, hypothyroidism, nephrotic syndrome, alcohol, and familial hyperlipidemia. Hyperlipidemia itself is silent; the findings you see are the consequences, such as angina, claudication, carotid bruit, or xanthomas and corneal arcus in familial disease.

A low HDL, generally under 40 mg/dL, is an independent cardiac risk factor and is associated with sedentary living, smoking, obesity, and type 2 diabetes. Very low total cholesterol and LDL are uncommon and can reflect malnutrition, malabsorption, hyperthyroidism, liver failure, or critical illness, so evaluate nutritional status rather than treating the number as good news.

Teach fasting requirements clearly when a full panel with calculated LDL is ordered: nothing but water for 9 to 12 hours, and no alcohol for 24 hours. Many panels are now drawn nonfasting, so verify the order. Counsel on reducing saturated fat and eliminating trans fat, increasing soluble fiber, oats, and fatty fish, weight reduction, smoking cessation, and at least 150 minutes per week of moderate aerobic activity. For statins, teach evening dosing for the shorter-acting agents, and instruct the patient to report unexplained muscle pain, tenderness, or weakness and dark urine, which suggest rhabdomyolysis, and to have liver enzymes monitored. Avoid grapefruit juice with several statins. Warn that niacin causes flushing that aspirin taken beforehand can blunt, and that bile acid sequestrants interfere with absorption of other drugs.

LDL is the target you treat and HDL is the one you want high. New muscle pain with dark urine in a patient on a statin is rhabdomyolysis, and the drug is held and the provider notified.

70 to 99 mg/dL after at least 8 hours without caloric intake. 100 to 125 mg/dL indicates impaired fasting glucose (prediabetes). 126 mg/dL or higher on two separate occasions is diagnostic of diabetes mellitus. Values below about 50 mg/dL and above about 400 mg/dL are typically critical.

Fasting glucose shows how well the body maintains euglycemia without the confounding effect of a recent meal, so it is used to screen for and diagnose diabetes, to evaluate hypoglycemia, and to monitor patients on insulin, oral agents, corticosteroids, or parenteral nutrition.

Hyperglycemia results from diabetes, illness or infection, surgery and stress, corticosteroids, thiazides, parenteral nutrition, pancreatitis, Cushing syndrome, and missed or insufficient diabetes medication. Classic signs are the three polys: polyuria, polydipsia, and polyphagia, plus fatigue, blurred vision, weight loss in type 1, slow wound healing, and recurrent infections. Severe hyperglycemia progresses to diabetic ketoacidosis with Kussmaul respirations, fruity acetone breath, abdominal pain, and dehydration, or to hyperosmolar hyperglycemic state with profound dehydration and altered mental status but without significant ketosis.

Hypoglycemia below 70 mg/dL is most often caused by too much insulin or sulfonylurea, a skipped or delayed meal, unusual exercise, alcohol, or improving renal function that slows insulin clearance. Early signs are adrenergic: shakiness, sweating, palpitations, tachycardia, anxiety, and hunger. As glucose falls further, neuroglycopenic signs appear: confusion, slurred speech, blurred vision, irritability, headache, seizure, and coma. Beta blockers mask the adrenergic warning signs, so a patient on a beta blocker may go straight to confusion, and that is a favorite exam point.

Verify the patient actually fasted; coffee with cream, gum, and smoking invalidate the result. For hypoglycemia in a conscious patient who can swallow, follow the rule of 15: give 15 grams of fast-acting carbohydrate such as 4 ounces of juice or regular soda, 3 to 4 glucose tablets, or a tablespoon of honey, recheck in 15 minutes, and repeat until the glucose is above 70 mg/dL, then follow with a protein and carbohydrate snack if the next meal is more than an hour away. If the patient is unconscious or cannot swallow, give nothing by mouth: administer intramuscular or subcutaneous glucagon, or intravenous 50 percent dextrose if there is IV access, then recheck and protect the airway. For hyperglycemia, expect IV fluids, insulin, and close potassium monitoring, since insulin drives potassium into the cell and can precipitate hypokalemia. Teach sick day rules: never omit insulin during illness, check glucose every 3 to 4 hours, check ketones, and maintain fluid intake.

Treat hypoglycemia before hyperglycemia. A low glucose can kill in minutes, and an unconscious hypoglycemic patient gets glucagon or IV dextrose, never oral carbohydrate.

Normal below 5.7 percent. Prediabetes 5.7 to 6.4 percent. Diabetes 6.5 percent or higher. The general treatment goal for most nonpregnant adults with diabetes is below 7 percent, with a less strict goal such as below 8 percent for older adults or those with limited life expectancy or hypoglycemia unawareness.

Glucose attaches irreversibly to hemoglobin, so the percentage of glycosylated hemoglobin reflects average blood glucose over the preceding 2 to 3 months, the life span of the red cell. This makes it the measure of long-term control, immune to the good breakfast a patient ate before clinic. It is drawn at diagnosis and then generally every 3 months until stable, then twice yearly.

An elevated HbA1c means sustained hyperglycemia over months from nonadherence, an inadequate regimen, weight gain, illness, or corticosteroid use. It predicts microvascular and macrovascular complications: retinopathy, nephropathy, peripheral and autonomic neuropathy, coronary artery disease, stroke, and peripheral arterial disease with poor wound healing and amputation risk. Falsely high results occur with iron deficiency anemia, B12 deficiency, and uremia.

A low or unexpectedly normal HbA1c in a treated diabetic can mean excellent control, but it can also mean frequent unrecognized hypoglycemia averaging down the result, so pair it with the patient's glucose logs or continuous monitor data. It is falsely low in any condition that shortens red cell survival: hemolytic anemia, recent significant blood loss, recent transfusion, pregnancy, sickle cell disease and other hemoglobinopathies, and chronic kidney disease with erythropoietin therapy. In those patients the HbA1c is unreliable and fructosamine or continuous glucose monitoring is used instead.

No fasting is required and the test can be drawn at any time of day; teaching that point prevents a lot of unnecessary patient anxiety. Use the result as a teaching tool rather than a judgment: review technique for glucose monitoring and insulin administration, site rotation, meal timing and carbohydrate counting, activity, foot care with daily inspection and no barefoot walking, annual dilated eye exams, and monitoring of urine albumin and kidney function. Reinforce that a good fingerstick this morning does not mean control is good, and that the HbA1c catches the pattern the meter misses.

HbA1c reports the average glucose over about 3 months and requires no fasting. An HbA1c of 6.5 percent or higher supports the diagnosis of diabetes, and below 7 percent is the usual target for most adults being treated.

Blood urea nitrogen (BUN) 10 to 20 mg/dL. Serum creatinine approximately 0.6 to 1.2 mg/dL in men and 0.5 to 1.1 mg/dL in women, with the value depending heavily on muscle mass. BUN to creatinine ratio roughly 10:1 to 20:1. Estimated glomerular filtration rate (eGFR) greater than 60 mL/min/1.73 m2 is considered normal; below 60 for 3 months or more defines chronic kidney disease, and below 15 is kidney failure. Urine specific gravity 1.005 to 1.030.

These tests tell you how well the kidney is filtering. Creatinine is a waste product of muscle metabolism excreted almost entirely by glomerular filtration and is not affected by diet or hydration, so it is the more specific kidney marker. BUN reflects protein metabolism and is influenced by hydration, protein intake, gastrointestinal bleeding, steroids, and liver function, so it is sensitive but not specific. eGFR, calculated from creatinine with age and sex, is the best single estimate of overall kidney function and is the number used to stage chronic kidney disease and adjust drug doses.

A high BUN and creatinine with a low eGFR indicate impaired filtration from acute kidney injury or chronic kidney disease, obstruction, nephrotoxic drugs such as aminoglycosides, vancomycin, NSAIDs, and IV contrast, or reduced renal perfusion. A BUN that is elevated out of proportion to creatinine, a ratio above 20:1, points to a prerenal cause such as dehydration, heart failure, shock, or upper gastrointestinal bleeding rather than intrinsic kidney damage. Signs of uremia include decreasing urine output, edema, hypertension, fatigue, nausea and vomiting, metallic taste, pruritus, muscle cramps, confusion, and in severe cases pericardial friction rub and asterixis. Expect hyperkalemia, metabolic acidosis, hyperphosphatemia, hypocalcemia, and anemia to travel with it.

A low BUN suggests overhydration, malnutrition with low protein intake, or severe liver disease that cannot make urea. A low creatinine reflects reduced muscle mass in older adults, malnourished patients, and amputees, and this matters enormously: an older thin patient can have significant kidney impairment with a creatinine that still reads normal, so use eGFR rather than creatinine alone when dosing drugs in that population.

Track intake and output and report urine output below 30 mL/hour or 0.5 mL/kg/hour. Weigh daily on the same scale, since 1 kg of weight equals about 1 liter of fluid. Monitor blood pressure, edema, lung sounds, and neurologic status, and check electrolytes with each renal panel. Review the medication list for nephrotoxins and for renally cleared drugs that need dose reduction, and hold metformin around iodinated contrast per policy. Ensure adequate hydration before and after contrast studies. For chronic kidney disease, teach restriction of sodium, potassium, phosphorus, and often protein and fluid, and teach protection of a fistula or graft: no blood pressure cuffs, venipuncture, or IVs in that arm, and check for a thrill and bruit every shift.

Creatinine and eGFR are the true measure of kidney function. Check them and the urine output before giving any nephrotoxic drug, IV contrast, or renally excreted medication.

5,000 to 10,000/mm3 (5 to 10 x 10 to the 9th per liter). Differential: neutrophils 55 to 70 percent, lymphocytes 20 to 40 percent, monocytes 2 to 8 percent, eosinophils 1 to 4 percent, basophils 0.5 to 1 percent. Absolute neutrophil count below 1,000/mm3 means neutropenia and below 500/mm3 means severe neutropenia with high infection risk. Counts below about 2,000/mm3 or above about 30,000/mm3 are commonly critical.

The WBC count is the body's infection and inflammation gauge, and the differential tells you what kind of problem it is. Neutrophils rise with acute bacterial infection, lymphocytes with viral infection, eosinophils with allergy and parasites. The count is followed closely in patients on chemotherapy, corticosteroids, or immunosuppressants, and before and after surgery.

Leukocytosis above 10,000/mm3 occurs with bacterial infection, inflammation, tissue necrosis such as myocardial infarction or burns, stress, corticosteroids, and leukemia. A left shift, meaning an increase in immature band neutrophils, signals that the marrow is dumping cells to meet an overwhelming acute bacterial demand. Expect fever, chills, malaise, tachycardia, localized redness, warmth, swelling, and purulent drainage. Very high counts in leukemia bring bleeding and anemia along with them, because the marrow is crowded out.

Leukopenia below 5,000/mm3 results from chemotherapy and radiation, bone marrow disorders, overwhelming sepsis that consumes cells, autoimmune disease, HIV, and drugs including clozapine and some antithyroid and anticonvulsant agents. The danger is that the immunocompromised patient cannot mount the usual response, so classic signs of infection are blunted or absent: there may be no redness, no swelling, and no purulence. A low-grade fever or a subtle change such as new confusion or fatigue may be the only clue, and in a neutropenic patient a single temperature of 38 degrees Celsius (100.4 degrees Fahrenheit) is an emergency.

For neutropenia, implement protective precautions: meticulous hand hygiene by everyone entering, private room, no fresh flowers or standing water, no raw or undercooked foods, screen visitors for illness, no live vaccines, avoid rectal temperatures, suppositories, enemas, and indwelling catheters when possible, and provide scrupulous oral and perineal hygiene. Assess every possible portal of entry every shift: mouth, IV sites, perineum, skin folds, and lungs. Take a temperature at least every 4 hours in a neutropenic patient and report fever immediately, because blood cultures and broad-spectrum antibiotics must be started within about an hour. Teach patients on colony-stimulating factors that bone pain is an expected effect. For leukocytosis, obtain cultures before the first antibiotic dose, monitor for sepsis with the trend of heart rate, respiratory rate, blood pressure, temperature, and mental status, and remember that a falling blood pressure with a rising lactate is late.

Fever in a neutropenic patient is a medical emergency, not a wait-and-see finding. Neutropenic patients may show no other sign of infection, so a single temperature of 100.4 degrees Fahrenheit or higher gets cultures and antibiotics immediately.

There is no single universal set of normals. Each laboratory establishes its own reference interval from its own instruments, reagents, and local population, so the authoritative range is the one printed beside the result on that patient's report.

A reference interval is defined statistically as the range containing the central 95 percent of results from a healthy reference population, which means about 5 percent of perfectly healthy people fall outside it by definition, and running a twenty-test panel on a healthy person will usually flag something. Understanding this keeps you from chasing a trivially abnormal number and, more importantly, from ignoring a value that is technically in range but wrong for that patient. Reference intervals also shift by age, sex, pregnancy, altitude, and sometimes by whether the specimen is serum or plasma.

Read the result with the laboratory's own range next to it. Identify the units and make sure you are comparing like to like, since the same analyte reports differently in conventional and international units, for example hemoglobin in g/dL versus g/L and glucose in mg/dL versus mmol/L. Compare the value to the patient's own previous results, because the trend is often more meaningful than a single point. Ask whether the specimen conditions were right: was the patient fasting, was the drug level a peak or a trough, was the sample drawn above an infusing IV, was it hemolyzed. Then interpret the number in the context of the patient in front of you: assessment findings, medications, diagnosis, and age. Finally, recognize which values are critical and require immediate provider notification regardless of context.

Comparing a value to a memorized range from a different source rather than the reported range leads to false alarms and false reassurance. Ignoring units causes tenfold errors. Treating a single number as truth rather than checking the trend or requesting a redraw misses both specimen error and real deterioration. Assuming that a normal value rules out a problem is a serious error, since hemoglobin is normal in early hemorrhage and creatinine is normal in a low-muscle-mass patient with real kidney impairment. Conversely, treating any flagged value as an emergency wastes clinical attention that belongs elsewhere.

For a critical value, the laboratory will call you directly. Write the value down, read it back to the caller for verification, notify the provider immediately, document the value, the time, the name of the person you notified, and the response, then carry out orders and reassess. Before you call, gather what the provider will ask for: current vital signs, relevant assessment findings, recent related labs, intake and output, and the medication list. If the result does not fit the patient at all, say a potassium of 7.0 mEq/L in a comfortable patient with a normal ECG, suspect a specimen problem such as hemolysis and request a redraw while still treating the patient as though the value could be real until it is disproven.

Treat the patient, not the number, but never sit on a critical value. Verify it, report it immediately by read-back, and document exactly whom you notified and when.

Not a numeric value. The standard is correct patient identification with two identifiers, correct tube in the correct order of draw, correct labeling at the bedside in the patient's presence, and correct handling and transport.

Most laboratory errors happen before the specimen ever reaches the analyzer. A mislabeled tube can lead to a fatal transfusion reaction or a wrong medication dose; a hemolyzed tube gives a falsely high potassium that triggers unnecessary and risky treatment; a sample drawn above an IV is diluted and meaningless. Doing the draw correctly is a patient safety intervention, not clerical work.

Verify the order and the required tubes, and check any fasting or timing requirement. Identify the patient with two identifiers and explain the procedure. Perform hand hygiene and don gloves. Position the arm below heart level and select a vein, preferring the median cubital in the antecubital fossa; avoid an arm with a dialysis fistula or graft, an arm on the side of a mastectomy with lymph node dissection, an arm with an infusing IV, and any site with infection, burn, hematoma, or scarring. Apply the tourniquet 3 to 4 inches above the site for no longer than 1 minute. Cleanse with alcohol in a circular or back-and-forth motion and let it air dry fully, and for blood cultures use chlorhexidine and let it dry, scrubbing the bottle tops as well. Anchor the vein below the site, insert the needle bevel up at about 15 to 30 degrees, and fill the tubes in the correct order of draw: blood cultures first, then the light blue citrate coagulation tube, then serum tubes, then green heparin, then lavender EDTA, then gray. Release the tourniquet once blood flows and before removing the needle. Fill the light blue tube completely to the fill line, since the citrate-to-blood ratio must be exact. Invert tubes gently the recommended number of times rather than shaking. Withdraw the needle, activate the safety device, apply pressure, and dispose of sharps at the point of use. Label every tube at the bedside in front of the patient with name, identifiers, date, time, and your initials, and transport promptly, protecting light-sensitive specimens such as bilirubin.

Leaving the tourniquet on longer than a minute causes hemoconcentration and falsely raises potassium, calcium, protein, and hematocrit. Fist pumping falsely raises potassium. Drawing above or proximal to an infusing IV dilutes the sample and can spike glucose or the infused electrolyte to nonsense levels; draw from the opposite arm. Drawing a coagulation study from the arm with a heparin infusion falsely prolongs the aPTT. Not letting alcohol dry stings and hemolyzes the sample. A needle that is too small, excessive suction from a syringe, vigorous shaking, or a difficult traumatic draw hemolyzes the specimen and falsely elevates potassium, magnesium, phosphorus, and LDH while invalidating the sample. Underfilling a citrate tube falsely prolongs PT and aPTT. Drawing out of order causes additive carryover, for example EDTA carryover falsely raising potassium and falsely lowering calcium. Labeling away from the bedside is how specimens get switched between patients.

If the site develops a hematoma, remove the tourniquet and needle immediately, apply firm pressure, and elevate. If the patient feels faint, stop, lower the head, and stay with them. If you cannot obtain the specimen after two attempts, hand off to another nurse or the phlebotomy team rather than continuing to stick. If a result is wildly inconsistent with the patient's clinical picture, suspect a preanalytic error, notify the laboratory, and redraw, but do not delay treatment of a clinically consistent critical value while waiting for confirmation. Report any labeling error immediately and never relabel a tube drawn by someone else.

Label the tubes at the bedside, in the patient's presence, before you leave the room. And never draw a specimen from the arm with the infusing IV, because the diluted or contaminated result will be acted on as if it were real.

Normal adult oral temperature averages 98.6 degrees Fahrenheit (37 degrees Celsius), with an acceptable range of about 96.8 to 100.4 degrees Fahrenheit (36 to 38 degrees Celsius) depending on route and time of day. Rectal and temporal artery readings run roughly 0.5 to 1 degree Fahrenheit higher than oral, and axillary runs about 1 degree Fahrenheit lower. Fever is generally defined as 100.4 degrees Fahrenheit (38 degrees Celsius) or higher. Hypothermia is a core temperature below 95 degrees Fahrenheit (35 degrees Celsius).

Temperature reflects the balance between heat produced and heat lost, regulated by the hypothalamus. A rise usually signals infection or inflammation, but it also occurs with dehydration, tissue injury, thyroid storm, malignant hyperthermia, neuroleptic malignant syndrome, and environmental heat. A fall signals exposure, sepsis in older adults and infants, hypothyroidism, or intraoperative heat loss. In immunocompromised and older patients, the temperature may be the only sign of serious infection, and in older adults a normal temperature does not rule out sepsis, because their baseline is lower and their febrile response is blunted.

Choose the route based on the patient. Oral requires a cooperative, alert patient who can keep the mouth closed and breathe through the nose; place the probe in the posterior sublingual pocket beside the frenulum and wait 15 to 30 minutes after hot or cold intake, smoking, or chewing gum. Tympanic requires a straight canal, so pull the pinna up and back in an adult and down and back in a child under 3, and it is not reliable with cerumen impaction. Temporal artery scanning requires a dry forehead swept to the hairline, sometimes with a behind-the-ear confirmation per the manufacturer. Axillary is the least accurate but is safe for newborns and for anyone at risk from other routes; place the probe in the center of the axilla with the arm held down against the chest. Rectal is the most accurate noninvasive reflection of core temperature; position the patient in Sims position, lubricate, and insert about 1 to 1.5 inches in an adult, never forcing it, and never leave the patient. Use the same route and the same device each time you trend a patient, and document the route with the value.

An oral reading taken right after hot coffee reads falsely high, and after ice chips or with mouth breathing and oxygen by mask, falsely low. A tympanic probe not aimed toward the tympanic membrane or used with impacted cerumen reads falsely low. A sweaty forehead or a hat or blanket over the temporal area gives a falsely low temporal reading. A loosely held axillary probe or one placed on clothing reads falsely low. A rectal probe embedded in stool reads inaccurately. Comparing a rectal value today to an oral value yesterday manufactures a fever or hides one, which is why route consistency matters.

For fever, verify with an appropriate route, obtain a full set of vital signs, and assess for a source: lungs, urine, wounds, IV sites, and abdomen. Obtain cultures before antibiotics if ordered. Give antipyretics as ordered, increase fluid intake unless contraindicated, remove excess covers, and provide tepid, not cold, sponging, since cold causes shivering and raises temperature. Monitor for dehydration and for febrile seizures in young children. Fever in a neutropenic patient or a fresh postoperative patient with new onset rigid muscles and rapidly rising temperature under anesthesia demands immediate escalation, the latter being malignant hyperthermia treated with dantrolene. For hypothermia, warm gradually with blankets and warmed fluids, and monitor for dysrhythmias, because rapid rewarming causes vasodilation and hypotension.

Route changes the number, so document the route and trend the same route. A temperature of 100.4 degrees Fahrenheit in a neutropenic or postoperative immunosuppressed patient is an emergency even though the same number in a healthy adult is not.

Adult resting heart rate 60 to 100 beats per minute. Below 60 is bradycardia and above 100 is tachycardia. Normal ranges are higher in children, roughly 100 to 160 in a newborn and 70 to 120 in a school-age child.

The pulse is the palpable wave of blood ejected with each ventricular contraction, so it tells you about rate, rhythm, and the strength of the ejection. It is your fastest bedside indicator of hemodynamic change: heart rate rises before blood pressure falls in hypovolemia, pain, fever, hypoxia, and anxiety. Rhythm irregularity may be the first sign of atrial fibrillation, which carries stroke risk, and pulse quality tells you about perfusion to that limb.

Palpate the radial pulse with the pads of the first two or three fingers, never the thumb, which has its own pulse. Count for a full 60 seconds if the rhythm is irregular or the patient is a child, an infant, or on cardiac medication; 30 seconds doubled is acceptable only for a regular adult rhythm. Grade amplitude as 0 absent, 1+ weak and thready, 2+ normal, 3+ full or bounding. For the apical pulse, place the diaphragm of the stethoscope at the fifth intercostal space at the left midclavicular line and count for a full minute; use the apical site for infants and young children, for irregular rhythms, and before digoxin. To assess a pulse deficit, one nurse counts apical while a second simultaneously counts radial for a full minute; a difference means some beats are too weak to perfuse the periphery, which is classic in atrial fibrillation. Assess peripheral pulses bilaterally and compare, and use a Doppler when a pulse cannot be palpated.

Using the thumb makes you count your own pulse. Counting for 15 or 30 seconds on an irregular rhythm produces a wrong rate. Pressing too hard obliterates a weak pulse and makes you report it as absent; pressing too lightly misses a thready one. Counting radially in atrial fibrillation underestimates the true ventricular rate. Taking the pulse right after activity, pain, smoking, or caffeine, or while the patient is anxious, gives a falsely elevated resting rate. Not comparing sides misses a unilaterally diminished pulse from arterial occlusion.

Assess the patient, not just the rate: level of consciousness, blood pressure, skin color and temperature, chest pain, dizziness, and shortness of breath determine whether an abnormal rate is being tolerated. For a new irregular rhythm or a symptomatic rate abnormality, obtain a 12-lead ECG, place the patient on a monitor, check electrolytes and digoxin level if applicable, and notify the provider. Hold digoxin and notify the provider if the apical pulse is below 60 in an adult, below 70 in a child, or below 100 in an infant, and assess for toxicity signs of anorexia, nausea, vomiting, visual halos, and dysrhythmia. Hold beta blockers per parameters for bradycardia or hypotension. A newly absent or diminished peripheral pulse with a cold, pale, painful limb is an arterial emergency; after cast application or arterial catheterization, check pulses distal to the site frequently.

Count apically for a full 60 seconds whenever the rhythm is irregular or the patient is receiving digoxin, and hold digoxin for an adult apical rate below 60 beats per minute.

Adult 12 to 20 breaths per minute, quiet, regular, and unlabored. Below 12 is bradypnea and above 20 is tachypnea. Newborns run about 30 to 60 and toddlers about 20 to 30 breaths per minute.

Respiratory rate is the most sensitive and most frequently missed early warning sign of deterioration. It rises before blood pressure falls in sepsis, before oxygen saturation drops in early pneumonia and pulmonary embolism, and it is part of every clinical deterioration score for that reason. It also reflects acid-base status, since the lungs compensate for metabolic acidosis by increasing minute ventilation.

Count respirations without telling the patient, immediately after taking the pulse while your fingers are still on the wrist, because awareness changes the pattern. Observe or feel the rise and fall of the chest for a full 60 seconds if the pattern is irregular or the patient is an infant, otherwise 30 seconds doubled is acceptable. Assess more than rate: depth (shallow, normal, deep), rhythm (regular or irregular), effort (use of accessory muscles, nasal flaring, retractions, tripod positioning, pursed-lip breathing), symmetry of chest expansion, and audible sounds such as stridor, wheezing, or grunting. Note the patient's position and oxygen delivery device and flow rate along with the value. Learn the abnormal patterns: Kussmaul breathing is deep and rapid in diabetic ketoacidosis, Cheyne-Stokes alternates crescendo and decrescendo with apnea and is seen in heart failure and near end of life, and apnea is the absence of breathing.

Telling the patient you are counting their breathing changes the rate in either direction and is the most common error. Counting for 15 seconds and multiplying magnifies any miscount by four and misses irregular patterns entirely. Recording an assumed number of 18 or 20 without actually counting is both falsification and a missed early warning. Counting immediately after exertion, suctioning, or a painful procedure gives a falsely high rate. Documenting rate alone while ignoring effort misses the patient who is maintaining 18 breaths per minute with visible accessory muscle use and is about to tire out.

Correlate rate with oxygen saturation, breath sounds, mental status, and skin color. Restlessness, anxiety, and confusion are early hypoxia; cyanosis is late. Position the patient upright in high Fowler position, encourage deep breathing and coughing or incentive spirometry, apply oxygen as ordered, and suction if secretions are the problem. A respiratory rate under 12 with a sedated patient on opioids means holding the drug, stimulating the patient, supporting ventilation, and having naloxone available. A sustained rate over 20 to 24 with increased work of breathing warrants provider notification and consideration of arterial blood gases even if the pulse oximetry still looks acceptable. Silence in a previously wheezing asthmatic is an ominous sign of no air movement, not improvement.

Count respirations without the patient knowing, for a full minute when anything is irregular, and treat a rising respiratory rate as the earliest sign of deterioration even when every other vital sign is still normal.

Normal is less than 120/80 mm Hg. Elevated is systolic 120 to 129 with diastolic less than 80. Stage 1 hypertension is systolic 130 to 139 or diastolic 80 to 89. Stage 2 hypertension is systolic 140 or higher or diastolic 90 or higher. A hypertensive crisis is above 180 systolic or above 120 diastolic. Hypotension is generally systolic below 90 mm Hg or a drop of more than 40 mm Hg from the patient's baseline. Normal pulse pressure, the difference between systolic and diastolic, is about 30 to 40 mm Hg.

Blood pressure is the force of blood against the arterial wall and is the product of cardiac output and systemic vascular resistance, so it tells you whether the patient is perfusing organs. Sustained elevation silently damages the brain, heart, kidneys, and retina and is the leading modifiable risk factor for stroke. Low pressure means inadequate perfusion, and a mean arterial pressure below about 60 to 65 mm Hg does not perfuse the kidneys and brain.

Have the patient rest quietly for 5 minutes with no caffeine, smoking, or exercise for the prior 30 minutes, and an empty bladder. Position with back supported, both feet flat on the floor, legs uncrossed, and the arm bared and supported at heart level. Select a cuff whose bladder width is about 40 percent of arm circumference and whose bladder length encircles about 80 percent of the arm. Center the bladder over the brachial artery with the lower edge about 1 inch above the antecubital fossa. Palpate the radial pulse while inflating to estimate systolic, then deflate fully and wait 30 seconds. Place the stethoscope diaphragm or bell lightly over the brachial artery, inflate 20 to 30 mm Hg above the estimated systolic, and deflate at 2 to 3 mm Hg per second. The first Korotkoff sound is systolic and the disappearance of sound is diastolic. Do not reinflate mid-reading; deflate completely and wait 1 to 2 minutes before repeating. Take it in both arms at the first visit and use the higher arm thereafter. For orthostatic vital signs, measure blood pressure and pulse supine, then again 1 and 3 minutes after sitting and standing; a drop of 20 mm Hg systolic or 10 mm Hg diastolic, or a rise in heart rate of 20 beats per minute, with symptoms is a positive finding. Avoid the arm with a dialysis access, a mastectomy with node dissection, a PICC or infusing IV, an injury, or a cast.

A cuff too narrow or too short falsely raises the reading, and a cuff too wide falsely lowers it, which is why a regular cuff on an obese arm produces a false diagnosis of hypertension. The arm held below heart level falsely raises the reading and above heart level falsely lowers it. An unsupported arm or the patient holding the arm up isometrically raises the reading. Legs crossed at the knee, an unsupported back, a full bladder, talking, or the cuff over clothing all falsely raise it. Deflating too fast underestimates systolic and overestimates diastolic; deflating too slowly causes venous congestion and a falsely high diastolic. Reinflating without a full pause gives a falsely high diastolic. Pressing the stethoscope too hard falsely lowers the diastolic. Failing to first palpate the systolic can cause you to miss an auscultatory gap and record a falsely low systolic or falsely high diastolic.

Verify an abnormal reading manually in the other arm before acting, especially if the value came from an automatic cuff, and compare it to the patient's own baseline. For hypotension, assess perfusion: mental status, urine output, skin temperature and color, and capillary refill; lower the head of the bed and raise the legs unless contraindicated, hold antihypertensives per parameters, ensure IV access, and notify the provider. For a hypertensive crisis, assess for target organ damage with headache, blurred vision, chest pain, dyspnea, epistaxis, and neurologic change, place the patient in a quiet environment with the head of the bed elevated, and notify the provider immediately. Teach hypertensive patients daily home monitoring with technique instruction, sodium restriction, the DASH eating pattern, weight loss, alcohol moderation, regular activity, and that they must not stop antihypertensives abruptly because of rebound hypertension. Teach rising slowly to prevent orthostatic falls.

Cuff size and arm position determine the number. A cuff that is too small or an arm below heart level falsely elevates the pressure, and a patient should never be diagnosed or medicated off a single reading taken with poor technique.

Normal SpO2 is 95 to 100 percent on room air. Below 95 percent warrants assessment and below 90 percent is generally considered hypoxemia requiring intervention, corresponding to a PaO2 of roughly 60 mm Hg. For patients with chronic carbon dioxide retention such as advanced COPD, a target of 88 to 92 percent is often acceptable and intentional.

Pulse oximetry noninvasively estimates the percentage of hemoglobin saturated with oxygen, giving continuous or spot feedback on oxygenation without an arterial stick. It is the standard monitor during procedural sedation, opioid administration, weaning, and any respiratory illness. Understand its key limitation from the oxyhemoglobin dissociation curve: saturation stays near normal over a wide range of PaO2 and then falls off a cliff, so once the SpO2 starts dropping below 90 percent, the PaO2 is falling fast.

Select a well-perfused site, usually a finger, and remove nail polish or artificial nails, or use an alternate site such as the earlobe, forehead, or toe. Warm a cold extremity. Position the sensor so the light source and detector are directly opposite each other, and place it on the side opposite an automatic blood pressure cuff, since cuff inflation interrupts the signal. Confirm that the displayed pulse rate on the oximeter matches the patient's palpated or monitored heart rate; if they do not match, the saturation reading is not trustworthy. Document the value along with the oxygen delivery device and flow rate and the patient's activity level, since a resting saturation of 94 percent means something different from a saturation of 94 percent while ambulating. Rotate a continuous probe site and inspect the skin at least every 4 hours or per policy to prevent pressure injury.

Nail polish, especially dark shades, artificial nails, and dried blood or dirt block light transmission and falsely lower the reading. Poor perfusion from hypothermia, vasoconstriction, hypotension, or vasopressors gives a low or absent reading. Motion and shivering produce artifact. Bright ambient or procedural light interferes; cover the probe. Severe anemia gives a falsely reassuring saturation, because the small amount of hemoglobin present is fully saturated while total oxygen content is low. Carbon monoxide poisoning gives a falsely high, often normal, reading, because standard oximeters cannot distinguish carboxyhemoglobin from oxyhemoglobin, so a smoke inhalation patient needs co-oximetry or arterial blood gases. Methemoglobinemia drives the reading toward the mid 80s regardless of true saturation. Deeply pigmented skin is associated with occult hypoxemia, meaning the device can overestimate true arterial saturation, so weight the clinical assessment accordingly.

Before you chase a low number, assess the patient. If the patient is comfortable, pink, and alert with a good waveform mismatch, troubleshoot the probe first. If the patient is genuinely hypoxemic, reposition to high Fowler, encourage deep breathing and coughing, suction if indicated, apply or increase oxygen within ordered parameters, and notify the provider. In a COPD patient with chronic retention, do not reflexively crank the oxygen up; titrate to the ordered target and monitor level of consciousness and respiratory rate for carbon dioxide narcosis. Remember that oximetry measures oxygenation only and says nothing about ventilation, so a patient on supplemental oxygen who is retaining carbon dioxide from opioid oversedation can show a saturation of 98 percent while their respiratory rate is 6 and they are in trouble.

Pulse oximetry tells you about oxygenation, not ventilation, and a normal SpO2 never rules out respiratory failure. Verify that the oximeter's pulse rate matches the patient's actual pulse before you trust the saturation.

There is no normal value, because pain is subjective. The standard is the patient's self-report on a validated scale: the 0 to 10 numeric rating scale for adults who can use it, the Wong-Baker FACES or FACES Pain Rating Scale for children roughly 3 years and older and for adults with communication barriers, the FLACC behavioral scale for infants and nonverbal children, and the PAINAD or CPOT for patients with advanced dementia or who are critically ill and nonverbal. Generally 1 to 3 is mild, 4 to 6 moderate, and 7 to 10 severe.

Pain is often called the fifth vital sign because unrelieved pain has physiologic consequences, not just emotional ones: tachycardia, hypertension, increased oxygen demand, splinting with atelectasis and pneumonia, delayed ambulation with thromboembolism, impaired wound healing, delirium, and progression to chronic pain. It is also the assessment most vulnerable to nurse bias, and undertreatment is well documented in older adults, children, and patients of color.

Accept the patient's self-report as the most reliable indicator. Assess systematically: onset and duration, location and radiation, character in the patient's own words such as burning, stabbing, aching, or cramping, intensity now, at worst, and at best, aggravating and relieving factors, associated symptoms, and the effect on sleep, appetite, mood, and function. Establish an acceptable comfort-function goal with the patient rather than a target of zero. Distinguish nociceptive pain, which is somatic and well localized or visceral and diffuse and cramping, from neuropathic pain, which is burning, shooting, and electric and responds to adjuvants such as gabapentin or duloxetine rather than to opioids alone. Use the same scale each time for a given patient. Reassess after every intervention within the drug's expected time to peak effect: roughly 15 to 30 minutes after intravenous administration and 60 minutes after oral administration. Combine pharmacologic and nonpharmacologic measures such as repositioning, ice or heat, splinting an incision when coughing, distraction, music, relaxation, and massage.

Substituting your judgment or the patient's appearance for their self-report is the central error; a patient who is laughing, sleeping, or watching television can still be in severe pain, because sleep and distraction are coping mechanisms, and chronic pain patients often lack the autonomic signs of acute pain. Relying on vital signs to validate pain is wrong, since heart rate and blood pressure normalize with time even while pain persists. Using a different scale on each shift makes the trend meaningless. Using a numeric scale with a young child or a patient with dementia produces unusable data. Asking only about intensity and skipping location and quality misses a new complication, such as calf pain signaling deep vein thrombosis or new chest pain signaling infarction. Waiting for pain to become severe before medicating requires more drug for less relief than dosing around the clock or preemptively.

Medicate within ordered parameters and reassess, documenting the score before and after. For opioids, monitor sedation level and respiratory rate, since sedation precedes respiratory depression, and keep naloxone available; teach bowel regimen because opioid constipation does not resolve with tolerance. With patient-controlled analgesia, teach that only the patient presses the button and instruct family never to press it for them. Investigate new, sudden, or changed pain as a new problem rather than simply increasing the dose, and be alert for pain out of proportion to findings, which suggests compartment syndrome or ischemia. Advocate for adequate analgesia and document the patient's response and any provider notification when relief is inadequate.

Pain is whatever the patient says it is, occurring whenever they say it does. Believe the self-report over the vital signs and over the patient's appearance, and reassess after every intervention.