Physiological Adaptation and Medical Emergencies: Practice Questions & Explanations

Post-operative fever has a timing-based differential using the '5 W's' mnemonic: WIND (POD 1-2): ATELECTASIS — partial alveolar collapse from splinting (guarding breathing to avoid pain), anesthesia effects, and secretion retention; causes fever due to inflammatory response; TREATED with: ambulation, deep breathing exercises, incentive spirometry (IS), coughing, adequate pain control so client CAN breathe deeply; WATER (POD 3-5): URINARY TRACT INFECTION — from Foley catheter; increased urinary frequency, urgency, dysuria, cloudy urine; prevent with early Foley removal; WOUND (POD 5-7): WOUND INFECTION — surgical site infection; redness, warmth, swelling, purulent drainage; WALKING (POD 5+): DEEP VEIN THROMBOSIS (DVT)/PULMONARY EMBOLISM — calf pain, swelling, tachycardia, dyspnea; prevent with early ambulation, SCDs, anticoagulants; WONDER DRUGS (any time): DRUG FEVER — particularly from medications like antibiotics, phenytoin, allopurinol; diagnosis of exclusion. INCENTIVE SPIROMETRY (IS): device that provides visual feedback on inspiratory effort; goal is maximum sustained inspiration; hold breath at peak for 2-3 seconds; typical post-op goal: 10-15 breaths per hour while awake; must be used CORRECTLY — slow, deep breath; many clients use it incorrectly as a blowing (expiratory) device when it requires INHALATION.

Pn role: teach and reinforce IS use pre-operatively (before surgery — better compliance than teaching when in pain); encourage early ambulation (most powerful preventive measure for multiple complications); assess lung sounds for crackles; administer antipyretics and analgesics as ordered; document and report persistent or high fever.

OXYGEN THERAPY IN COPD requires special consideration.

Normal physiology: the primary drive to breathe is a RISE IN CO2 (CO2 chemoreceptors are the dominant stimulus).

Copd hypoxic drive: some patients with SEVERE CHRONIC COPD retain CO2 chronically (hypercapnia); their CO2 receptors have adapted ('reset') to high CO2; in these patients, the HYPOXIC DRIVE (low O2 stimulating breathing) becomes relatively more important.

Risk of high o2: in HYPERCAPNIC COPD patients, giving HIGH-FLOW OXYGEN can: suppress the hypoxic drive → decreased respiratory rate → CO2 retention worsens → possible CO2 narcosis (confusion, somnolence) → respiratory failure.

Current evidence: the 'hypoxic drive' theory is somewhat simplified; contemporary evidence emphasizes that excessive O2 in COPD also causes: HALDANE EFFECT (oxyhemoglobin shifts, releasing CO2); V/Q mismatch changes.

Clinical practice: target SpO2 of 88-92% for known or suspected hypercapnic COPD patients receiving supplemental oxygen; use lowest flow that achieves this target; adjust based on clinical response and ABG results; MONITOR for DROWSINESS, CONFUSION, DECREASED RESPIRATORY RATE — may indicate CO2 buildup; titrate down if this occurs; do NOT withhold O2 from a hypoxic client — hypoxia is still dangerous; balance is key.

Contraindication is false: O2 is NOT contraindicated in COPD; it is simply managed carefully.

Pn role: administer oxygen as ordered; apply and use SpO2 monitoring; document O2 flow rate and SpO2; report drowsiness, decreased respiratory rate, SpO2 outside target range to RN; titrate within ordered parameters.

HYPONATREMIA is defined as serum sodium below 135 mEq/L. Normal: 135-145 mEq/L. A value of 125 mEq/L is SIGNIFICANTLY LOW.

Pathophysiology: sodium is the primary extracellular osmole; when sodium drops, serum osmolality drops; water moves by osmosis from the low-sodium ECF INTO cells (following osmotic gradient); BRAIN CELLS SWELL → neurological symptoms are the hallmark. CLINICAL MANIFESTATIONS based on severity and rate of onset: MILD (130-135 mEq/L): may be asymptomatic or have nausea, headache, malaise; MODERATE (125-130 mEq/L): headache, nausea, vomiting, lethargy, confusion, muscle cramps; SEVERE (<125 mEq/L): seizures, coma, respiratory arrest, death.

Rate matters: ACUTE hyponatremia (rapid drop) is more dangerous than chronic hyponatremia (brain has had time to adapt).

Causes: HYPERVOLEMIC (too much water, normal sodium): heart failure, cirrhosis, nephrotic syndrome, SIADH; HYPOVOLEMIC (lost sodium and water, but more sodium than water): GI losses, diuretics, adrenal insufficiency.

Euvolemic: SIADH (syndrome of inappropriate antidiuretic hormone secretion — common cause; ADH causes water retention without sodium retention; causes: malignancy, CNS disorders, medications); water intoxication (rare). CONTRAST WITH HYPERNATREMIA (high sodium, >145 mEq/L): extreme thirst, dry mucous membranes, fever, decreased urine output, concentrated urine, confusion, seizures (cells shrink); treated with free water replacement.

Treatment of hyponatremia: depends on cause and severity; mild-moderate: fluid restriction (for SIADH); replace sodium if depleted.

Caution: correct SLOWLY (no more than 8-12 mEq/L per 24 hours) — rapid correction causes OSMOTIC DEMYELINATION SYNDROME (ODS, formerly central pontine myelinolysis) — irreversible brain damage.

Pn role: monitor serum electrolytes; observe for neurological changes; report confusion or seizures immediately; measure I&O; implement fluid restriction if ordered.

SEVERE HYPOGLYCEMIA (blood glucose <54 mg/dL with impaired consciousness) is a MEDICAL EMERGENCY. An unconscious client with a blood glucose of 38 mg/dL requires immediate treatment.

Priority treatment:

IV access available: 50% DEXTROSE (D50W) — 25 grams (50 mL) IV push is standard treatment for severe hypoglycemia with IV access; glucose is administered directly into the bloodstream for rapid correction; blood glucose typically rises within 5-10 minutes; NO IV ACCESS (or if IV is delayed): GLUCAGON — 1 mg IM or SubQ (kit given to family for home use); mechanism: stimulates liver to release stored glucose (glycogenolysis and gluconeogenesis); takes 15-20 minutes to work; less effective with alcohol intoxication or prolonged fasting (depleted glycogen stores); INTRANASAL GLUCAGON (Baqsimi): 3 mg — newer delivery method; easier to administer. DO NOT give oral glucose (juice, glucose tablets) to an UNCONSCIOUS client — aspiration risk.

After regaining consciousness: give a complex carbohydrate snack; monitor blood glucose frequently; assess for the CAUSE of hypoglycemia (missed meal, too much insulin, increased exercise, vomiting). INSULIN SHOULD NEVER BE GIVEN — insulin lowers glucose further; would be fatal. HYPOGLYCEMIA CAUSES in diabetes: too much insulin or oral antidiabetic medication; missed or delayed meals; increased physical activity without adjusting medication or intake; alcohol consumption; liver or kidney disease affecting drug clearance.

Clinical manifestations: MILD (BS 54-69): adrenergic — diaphoresis, shakiness, palpitations, hunger, pallor, anxiety.

Moderate: neuroglycopenic — confusion, difficulty concentrating, headache, visual changes.

Severe: seizures, loss of consciousness, coma. RULE OF 15 for conscious clients with mild hypoglycemia: 15g fast carbs, wait 15 min, recheck.

A CLIENT WITH TRACHEOSTOMY reporting inability to breathe is a RESPIRATORY EMERGENCY. Never leave the client alone during a tracheostomy emergency.

Immediate assessment and actions: STAY WITH CLIENT and CALL FOR HELP (call code/emergency team, call RN and provider).

Assess airway: look-listen-feel at the tracheostomy opening.

Assess tube position: is the tube in the correct position or has it been displaced (dislodged, obstruction)? OBSTRUCTION WITH MUCUS PLUG (most common cause): suction the tracheostomy immediately using sterile technique (inner cannula, suction through tube); can also attempt to IRRIGATE with 1-2 mL normal saline (now less recommended but still used acutely).

Inner cannula: remove and clean or replace disposable inner cannula — this can rapidly relieve blockage.

Tube dislodgement: if tube has come out or is clearly out of the trachea: keep stoma open; position: hyperextend the neck to open the stoma; use an obturator to re-insert same tube if available; OR use 10% smaller tube if same size won't go in easily; EMERGENCY SUPPLIES that must be AT BEDSIDE for every tracheostomy patient: tracheostomy tube of SAME SIZE AND ONE SIZE SMALLER, obturator (used for reinsertion), bag-valve mask (Ambu bag) that fits tracheostomy, suction supplies, extra inner cannula, emergency tracheostomy tray; BAG-VALVE MASK VENTILATION through tracheostomy if client is not breathing.

Oxygen: ensure 100% O2 during emergency.

Pn role: recognize the emergency; call for help; initiate airway management within scope; have emergency supplies organized at bedside; document.

Ongoing care: tracheostomy care every 8 hours or per protocol (clean stoma, change inner cannula, change ties when loose/soiled, assess for complications).

HEMOGLOBIN A1c (HbA1c or glycated hemoglobin) reflects average blood glucose over the PRECEDING 2-3 MONTHS because: glucose binds irreversibly to hemoglobin in red blood cells (RBCs); RBCs have a lifespan of approximately 90-120 days; the percentage of HbA1c reflects average glucose exposure during that period.

Normal values: Normal (non-diabetic): below 5.7%; Prediabetes: 5.7-6.4%; Diabetes diagnosis: 6.5% or above on two separate tests; ADA TREATMENT TARGET for most non-pregnant adults with diabetes: below 7.0%; Individualized targets: less stringent (7.0-8.0%) for elderly, extensive comorbidities, hypoglycemia unawareness; more stringent (<6.5%) for young, newly diagnosed, no significant CVD. CONVERTING A1c TO AVERAGE GLUCOSE: formula: eAG (mg/dL) = 28.7 × A1c - 46.7; A1c 9.8% = approximately 235 mg/dL average.

Clinical implications: A1c 9.8% indicates poor glycemic control over the past 3 months — associated with increased risk of: diabetic retinopathy, nephropathy, neuropathy, and cardiovascular disease; this client needs medication review, diabetes education reinforcement, and lifestyle coaching.

Pn teaching: Explain that A1c reflects their average glucose (not just one moment), so short-term improvements in behavior WILL improve the next A1c; reinforce that even partial improvements reduce complication risk; the value does not define the person — it is a target to work toward.