Common Lab Values: Practice Questions & Explanations

Normal serum potassium is 3.5-5.0 mEq/L (or 3.5-5.0 mmol/L). Potassium is the major intracellular cation and is critical for normal cardiac, neuromuscular, and cellular function. Hypokalemia (below 3.5) causes muscle weakness, cramping, arrhythmias (U waves on ECG, flattened T waves, ST depression), constipation, polyuria. Common causes: diuretics (loop and thiazide), vomiting, diarrhea, inadequate intake, insulin therapy, alkalosis. Hyperkalemia (above 5.0) causes muscle weakness, paresthesias, life-threatening cardiac arrhythmias (peaked T waves, widened QRS, ventricular fibrillation, asystole). Common causes: renal failure, ACE inhibitors/ARBs, potassium-sparing diuretics, rhabdomyolysis, hemolysis, acidosis. NCLEX frequently tests potassium because of its narrow therapeutic range and severe consequences of imbalance.

Normal fasting blood glucose is 70-100 mg/dL (3.9-5.5 mmol/L). Values 100-125 mg/dL indicate prediabetes (impaired fasting glucose); 126 mg/dL or higher on two separate tests indicates diabetes. Hypoglycemia (below 70) causes shakiness, sweating, anxiety, hunger, confusion, and at severe levels (below 40-50) seizures, loss of consciousness, and death. Treatment of hypoglycemia in a conscious client: 15-20 grams of fast-acting carbohydrate (4 oz juice, 3-4 glucose tablets, 1 tbsp honey), then recheck in 15 minutes; repeat if still low; once normal, provide complex carb and protein snack. For unconscious clients: IV dextrose (D50) or IM/SQ glucagon. Hyperglycemia symptoms: polyuria, polydipsia, polyphagia, fatigue, blurred vision. Diabetic ketoacidosis (DKA) is a serious complication of type 1 diabetes with glucose typically over 300, ketones, acidosis.

Normal serum sodium is 135-145 mEq/L. Sodium is the major extracellular cation, essential for fluid balance and neuromuscular function. Hyponatremia (below 135): symptoms based on rate of change — acute hyponatremia is more dangerous than chronic. Symptoms include nausea, headache, confusion, lethargy, seizures (especially below 120), coma. Causes: SIADH, diuretics, vomiting/diarrhea, heart failure, kidney failure, excessive water intake. Correction must be slow (no more than 8-10 mEq/L in 24 hours) to avoid osmotic demyelination syndrome. Hypernatremia (above 145): symptoms include thirst, dry mucous membranes, restlessness, irritability, weakness, seizures, coma. Causes: dehydration, diabetes insipidus, excessive sodium intake, certain medications. Treatment: gradual rehydration with hypotonic fluids. Both extremes require careful, controlled correction to prevent brain injury from rapid fluid shifts.

Normal hemoglobin (Hgb): 12-16 g/dL for adult females; 14-18 g/dL for adult males. Lower values indicate anemia; higher values indicate polycythemia. Anemia (Hgb below normal): symptoms include fatigue, weakness, pallor, shortness of breath, tachycardia, palpitations, dizziness. Common causes: blood loss (acute or chronic), iron deficiency (most common cause worldwide), B12 deficiency, folate deficiency, chronic disease, kidney disease (decreased erythropoietin), bone marrow disorders, hemolysis. Workup includes hematocrit (Hct, typically 3× the Hgb value, 36-48% females, 42-54% males), MCV (mean corpuscular volume — distinguishes microcytic, normocytic, macrocytic anemias), reticulocyte count, iron studies, B12, folate, kidney function. Polycythemia (Hgb above normal): causes include dehydration, chronic hypoxia (COPD, smoking, sleep apnea, high altitude), polycythemia vera. Transfusion thresholds vary but generally: symptomatic anemia or Hgb below 7-8 g/dL in stable patients; higher threshold for cardiac patients (around 8-10). NCLEX commonly tests hemoglobin ranges and indications for assessment of bleeding.

ABG INTERPRETATION uses a systematic four-step approach: STEP 1 — pH: 7.28 is BELOW 7.35 → ACIDOSIS; STEP 2 — Identify the cause: PaCO₂ 58 mmHg is ABOVE 45 mmHg → RESPIRATORY cause (CO₂ is an acid; elevated CO₂ causes acidosis); STEP 3 — Check compensation: HCO₃ 26 mEq/L is within normal range (22-26) → NOT COMPENSATED (kidneys haven't retained bicarb yet); STEP 4 — Oxygenation: PaO₂ 68 mmHg is BELOW 80 mmHg → MILD HYPOXAEMIA.

Interpretation: Uncompensated Respiratory Acidosis with mild hypoxaemia. COMMON CAUSES of respiratory acidosis: COPD exacerbation; opioid-induced respiratory depression; neuromuscular disease (Guillain-Barré, myasthenia gravis); severe pneumonia; atelectasis.

Nursing priorities: Assess airway and breathing immediately; prepare for possible intubation and mechanical ventilation if severe; administer supplemental oxygen; for COPD patients, target SpO₂ 88-92% (avoid hypoxic drive suppression); if opioid-induced: naloxone; stimulate patient to breathe, reposition; treat underlying cause.

The rome mnemonic: Respiratory Opposite (pH and CO₂ move in opposite directions); Metabolic Equal (pH and HCO₃ move in the same direction).

HYPERKALEMIA (K+ above 5.0 mEq/L) produces a predictable progression of ECG changes that correlates with potassium level and toxicity: K+ 5.5-6.5 mEq/L: PEAKED T WAVES — tall, narrow, symmetrical T waves; this is the first ECG sign; K+ 6.5-7.5 mEq/L: prolonged PR interval, widened QRS, loss of P waves; K+ above 7.5 mEq/L: sinusoidal wave pattern → VENTRICULAR FIBRILLATION → asystole.

The urgency: Peaked T waves indicate the cardiac conduction system is being affected and the patient is at immediate risk of fatal dysrhythmia; this takes priority over subjective symptoms like weakness.

Nursing priorities with peaked t waves: (1) CONTINUOUS CARDIAC MONITORING — apply immediately if not already in place; (2) NOTIFY PROVIDER IMMEDIATELY; (3) PREPARE FOR EMERGENCY TREATMENT: Calcium gluconate IV — cardiac membrane stabiliser; does not lower K+ but protects the heart; fastest-acting intervention; Sodium bicarbonate IV — drives K+ into cells (alkalosis shifts K+ intracellularly); Dextrose 50% + Regular insulin — drives K+ into cells (faster-acting); Kayexalate (sodium polystyrene) — GI potassium binder; removes K+ from body; slower (hours); Dialysis for severe refractory hyperkalemia.

Causes of hyperkalemia: Renal failure (most common); ACE inhibitors; potassium-sparing diuretics; excessive supplementation; acidosis; tissue destruction (rhabdomyolysis, haemolysis).

SEVERE HYPONATRAEMIA (sodium below 120-125 mEq/L with symptoms) is a neurological emergency.

Pathophysiology: When serum sodium falls rapidly, the extracellular fluid becomes hypotonic; water moves by osmosis into brain cells; brain cells swell (cerebral oedema); the skull cannot accommodate the swelling; this causes increased intracranial pressure.

Signs by severity: Mild (130-135): nausea, headache, fatigue; Moderate (125-130): confusion, disorientation; Severe (below 120-125): stupor, seizures, coma, herniation, respiratory arrest.

Nursing priorities: NEUROLOGICAL ASSESSMENT — level of consciousness, orientation, seizure precautions (padded side rails, suction at bedside); NOTIFY PROVIDER IMMEDIATELY; STRICT I&O — fluid restriction (often the first treatment for dilutional hyponatraemia); SEIZURE PRECAUTIONS.

Treatment depends on cause and acuity: SIADH (most common cause): fluid restriction; slow correction with 0.9% NS or 3% hypertonic saline if severe/symptomatic; CRITICAL SAFETY POINT — CORRECTION RATE: Sodium must be corrected slowly — no faster than 8-12 mEq/L per 24 hours; rapid correction can cause OSMOTIC DEMYELINATION SYNDROME (formerly central pontine myelinolysis) — permanent, devastating neurological damage from myelin destruction.

Causes of hyponatraemia: SIADH (most common inpatient cause); excessive hypotonic fluid administration; heart failure; cirrhosis; hypothyroidism; psychogenic polydipsia.

ELEVATED WBC (LEUKOCYTOSIS) in a post-operative patient should trigger assessment for infection.

Normal post-surgical wbc: A mild leukocytosis (WBC up to 12,000-15,000) is expected immediately after major surgery as part of the normal inflammatory response — this typically resolves within 24-48 hours.

Abnormal post-op wbc: A WBC of 16,800 on post-op day 2 (when the initial surgical inflammation should be subsiding) is suspicious for an INFECTIOUS process.

Assessment priorities: (1) WOUND — inspect the incision: erythema, warmth, swelling, purulent drainage, dehiscence; (2) VITAL SIGNS — fever (temperature above 38°C/100.4°F) confirms infection; tachycardia (>90 bpm); (3) LOCALISING SYMPTOMS — pain level and location; urinary symptoms (CAUTI risk); respiratory symptoms (pneumonia, especially common after abdominal surgery — atelectasis leading to pneumonia); (4) DRAINS/TUBES — assess drainage character; (5) IV SITES — inspect for phlebitis or CLABSI signs.

Common post-op infectious complications: Surgical site infection (SSI) — most common post-op day 3-5; Urinary tract infection (CAUTI) — foley catheter risk; Pneumonia — especially in abdominal/thoracic patients, immobile patients; C. difficile colitis — antibiotic-associated; CLABSI.

Report to provider: WBC trend; temperature; wound assessment findings; any localising signs.

Severe HYPERKALEMIA (normal potassium 3.5-5.0 mEq/L) is a medical emergency because of its effect on the HEART — it causes CARDIAC DYSRHYTHMIAS. ECG changes progress: PEAKED T waves → widened QRS → and potentially fatal arrhythmias (ventricular fibrillation, cardiac arrest/asystole). NCLEX physiological/electrolytes. The cardiac effects make hyperkalemia life-threatening — this is the priority concern. TREATMENT (severe): calcium gluconate (protects the heart), insulin with glucose and/or sodium bicarbonate (shift K+ into cells), and measures to remove potassium (diuretics, dialysis, potassium-binding agents). Causes: renal failure, potassium-sparing diuretics, tissue damage. Recognizing the cardiac danger of hyperkalemia (and its ECG changes) is a heavily tested NCLEX concept.

A client with prolonged NASOGASTRIC (NG) SUCTION or excessive VOMITING is at risk for METABOLIC ALKALOSIS — because they lose HYDROCHLORIC ACID (stomach acid, which contains H+ and chloride) from the stomach, raising blood pH (less acid = more alkaline). NCLEX physiological/acid-base. Also lost: potassium and chloride (risk of hypokalemia, hypochloremia).

Monitor: electrolytes, acid-base status, replace fluids/electrolytes as ordered.

Acid-base quick reference: vomiting/NG suction → metabolic alkalosis; diarrhea → metabolic acidosis (loss of bicarbonate); hypoventilation → respiratory acidosis (CO2 retention); hyperventilation → respiratory alkalosis (CO2 blown off). Knowing that loss of stomach acid (vomiting/NG suction) causes metabolic alkalosis is a commonly tested NCLEX acid-base concept.