The active-learning packet with model answers, so you can test yourself first and then check.
This packet strengthens your understanding of the respiratory content from lecture. It does not replace your notes or the PowerPoint — use it to actively quiz yourself, find your gaps, and practice clinical judgment.
Use these together: Lecture · PowerPoint slides · ATI Engage Med-Surg · MCR topics · Claire (ATI AI).
Do not simply reread your notes. Test yourself first, then use your resources to fill in what you missed.
🔒 Every answer on this page is hidden behind a Model answer button. Say your answer out loud — or write it — before you tap. If you tap first, you have not studied; you have read.
Choose one respiratory condition. Without looking at your notes, answer the five question groups below. Every condition on this page uses the same five groups — that repetition is the point.
Airflow out of the lungs is chronically limited and not fully reversible — a mix of chronic bronchitis (inflamed, mucus-filled airways) and emphysema (destroyed alveoli).
Expected findings: barrel chest, prolonged expiration, pursed-lip breathing, tripod position, accessory muscle use, chronic productive cough, wheezes or diminished breath sounds, hyperresonance to percussion, clubbing, activity intolerance, weight loss
Diagnostics: spirometry is definitive — a post-bronchodilator FEV1/FVC below 0.70; ABG showing chronic respiratory acidosis; chest x-ray with hyperinflation and a flattened diaphragm; CBC that may show polycythemia from chronic hypoxemia
Their usual baseline SpO₂: 88–92% — titrate oxygen to that target, not to 98%
🚨 Deterioration: rising respiratory rate then a falling one as they tire, inability to speak a full sentence, new drowsiness or confusion (CO₂ narcosis), a silent chest, and a PaCO₂ climbing above their baseline with a falling pH
In COPD, a change in mental status outranks the pulse-ox number.
Priority nursing: sit them upright or let them tripod, give the prescribed bronchodilator, titrate O₂ to 88–92%, coach pursed-lip breathing, clear secretions, and reassess — open the airway before you order tests
Medications:
| Class | Example | Job |
|---|---|---|
| Rescue SABA | albuterol | Fast bronchodilation — give first in distress |
| Anticholinergic | ipratropium, tiotropium | Dries secretions and dilates — tiotropium is maintenance only, never rescue |
| LABA | salmeterol | Long-acting control — scheduled, not PRN |
| Inhaled steroid | fluticasone | Reduces inflammation — rinse the mouth after to prevent thrush |
| Systemic steroid | prednisone, methylprednisolone | Short burst during an exacerbation — watch glucose |
| Antibiotic | per culture | Only when sputum turns purulent / infection is suspected |
Anticipated orders: ABG, chest x-ray, sputum culture, nebulized bronchodilators, systemic corticosteroids, controlled oxygen, and BiPAP if the CO₂ keeps climbing
Never crank oxygen up to 10 L/min in a COPD patient without assessing ventilation — because high-flow O₂ worsens V/Q matching and can blunt the drive to breathe, raising CO₂ further.
Respiratory therapist (nebs, ABGs, BiPAP), pulmonologist, dietitian (small frequent high-calorie meals — eating is work), physical/occupational therapy and pulmonary rehab, pharmacist for inhaler technique, smoking-cessation counseling, case management/social work for home O₂ and equipment, and palliative care in advanced disease.
Complications: acute exacerbation, pneumonia, acute respiratory failure, cor pulmonale (right-sided heart failure from pulmonary hypertension), spontaneous pneumothorax from ruptured bullae, polycythemia and clotting risk
Teaching / preventing exacerbations:
Emphysema sits under the COPD umbrella. Map what makes it different.
The alveolar walls are destroyed. Alveoli merge into large floppy sacs (bullae), which destroys surface area for gas exchange and destroys the elastic recoil that normally pushes air out.
Why dyspnea is the main complaint: because without elastic recoil the patient must actively force air out, and with less alveolar surface, less oxygen crosses into the blood — so they work harder for a worse result
Common cause: smoking; in a young patient with no smoking history think alpha-1 antitrypsin deficiency
Findings: thin, underweight, barrel chest with increased AP diameter, pursed-lip breathing, tripod position, minimal cough or sputum, hyperresonance on percussion, markedly diminished breath sounds, prolonged expiration
Diagnostics: spirometry with a low FEV1/FVC and a raised residual volume, a reduced diffusing capacity (DLCO), CT/chest x-ray showing hyperinflation and bullae
🚨 Deterioration: increasing drowsiness — that is hypercarbia, and it is more worrying than the SpO₂. Also sudden sharp chest pain with unilateral absent breath sounds, which is a ruptured bulla causing pneumothorax.
Priority: support ventilation, not just oxygenation — upright position, bronchodilator, controlled low-flow O₂ to a SpO₂ of 88–92%, and escalate to BiPAP if CO₂ rises and they are getting sleepy
Meds and orders: bronchodilators, inhaled and sometimes systemic corticosteroids, antibiotics for infection, oxygen, ABG monitoring, and pulmonary rehabilitation. Lung volume reduction surgery or transplant in selected advanced cases.
Respiratory therapy, pulmonology, dietitian (these patients burn calories breathing and are often underweight), pulmonary rehab/PT, thoracic surgery if a bulla ruptures or for lung volume reduction, and home O₂ and equipment through case management.
Complications: hypercarbic respiratory failure, spontaneous pneumothorax, cor pulmonale, recurrent pneumonia, severe weight loss and muscle wasting
Teaching: smoking cessation, vaccines, pursed-lip breathing, energy conservation, high-calorie/high-protein small frequent meals, avoid crowds during flu season, and never turn the home oxygen up on their own
Three things at once, and all of them are reversible: bronchoconstriction (smooth muscle spasm), airway inflammation and edema, and thick mucus plugging
Why the wheeze is on expiration: because airways narrow further as the chest deflates, so air is squeezed through narrowed tubes on the way out — and air is trapped behind the narrowing
The key difference from COPD: asthma is episodic and reversible with a bronchodilator; COPD is chronic and only partly reversible
Findings: expiratory wheezing, cough (often at night), chest tightness, dyspnea, prolonged expiratory phase, tachypnea, accessory muscle use, anxiety, and an inability to speak in full sentences when it is severe
Diagnostics: spirometry showing obstruction that improves after a bronchodilator, peak expiratory flow rate compared with the patient's personal best, and ABGs in an acute attack
Peak flow zones: Green 80–100% of personal best = good control. Yellow 50–79% = caution, use the rescue inhaler and follow the action plan. Red under 50% = emergency, rescue inhaler and get help.
🚨 The two findings that mean it is getting worse, not better:
Priority in an acute attack: sit upright, give the short-acting beta-agonist (albuterol) immediately, apply oxygen, stay with the patient and coach slow breathing, then reassess — the drug that opens the airway comes before any test
| Rescue (quick relief) | Control (daily, prevents) |
|---|---|
| Albuterol (SABA), ipratropium, systemic corticosteroids in an exacerbation, IV magnesium sulfate in severe attacks | Inhaled corticosteroids (first-line), LABAs — only combined with an ICS, never alone — montelukast, cromolyn, and biologics such as omalizumab for severe allergic asthma |
Anticipated orders: continuous or back-to-back nebulized albuterol, IV or oral corticosteroids, oxygen, peak flow measurement, ABG, chest x-ray to rule out pneumonia or pneumothorax
A LABA alone, without an inhaled steroid, is never appropriate in asthma.
Respiratory therapist, pulmonologist or allergist/immunologist, pharmacist for inhaler and spacer technique, school nurse or occupational health, and case management for medication access.
Complications: status asthmaticus (an attack that does not respond to treatment), respiratory failure requiring intubation, pneumothorax, and airway remodeling from years of poor control
Teaching: identify and avoid personal triggers (allergens, smoke, cold air, exercise, aspirin/NSAIDs, stress, respiratory infections), use a written asthma action plan with peak flow zones, correct inhaler technique with a spacer, rinse after steroid inhalers, premedicate before exercise if prescribed, take the controller every day even when well, and get the annual flu vaccine
Needing the rescue inhaler more than twice a week means the asthma is not controlled — that is a call to the provider, not a refill.
A clot — usually a DVT that broke off from a leg vein — lodges in the pulmonary circulation and blocks blood flow to part of the lung.
Why the pain is sharp and worse on inspiration: infarcted lung tissue irritates the pleura — pleuritic pain
Virchow's triad (why clots form): venous stasis, endothelial injury, and hypercoagulability — immobility, surgery, and cancer or estrogen therapy are the classic examples
Findings: SUDDEN dyspnea, pleuritic chest pain, tachypnea, tachycardia, hypoxemia, anxiety or a sense of impending doom, cough, hemoptysis, low-grade fever, and hypotension if the embolus is large
Diagnostics: CT pulmonary angiography is the gold standard; D-dimer is useful mainly to rule PE out; V/Q scan when contrast is contraindicated (renal impairment, allergy); lower-extremity duplex ultrasound to find the source DVT; ABG usually shows respiratory alkalosis with hypoxemia; ECG most often shows sinus tachycardia
🚨 Deterioration: a rising respiratory rate, falling SpO₂ despite oxygen, falling blood pressure, JVD, and a change in level of consciousness — that is right heart failure and obstructive shock
Sudden onset is the tell. "Suddenly short of breath" after surgery or immobility means PE until proven otherwise.
Priority order:
Medications: IV heparin infusion or low-molecular-weight heparin (enoxaparin) first, transitioning to warfarin or a DOAC such as apixaban or rivaroxaban; thrombolytics (alteplase) for a massive PE with hemodynamic instability
Lab monitoring: aPTT for IV heparin, INR for warfarin (therapeutic 2–3 for VTE), platelets for heparin-induced thrombocytopenia; antidote for heparin is protamine sulfate, for warfarin it is vitamin K
Anticipated orders: CT pulmonary angiogram, D-dimer, ABG, ECG, troponin and BNP for right-heart strain, oxygen, heparin protocol, and possibly an IVC filter if anticoagulation is contraindicated
Rapid response team, hospitalist or pulmonologist, radiology, pharmacy for the heparin protocol and dosing, anticoagulation clinic for follow-up, physical therapy for safe mobilization, and interventional radiology or vascular surgery for thrombectomy or an IVC filter.
Complications: obstructive shock and cardiac arrest, pulmonary infarction, right ventricular failure, chronic pulmonary hypertension, recurrent PE, and bleeding from the treatment itself
Prevention — this is the high-yield part: early and frequent ambulation, sequential compression devices, prophylactic subcutaneous heparin or enoxaparin, leg and ankle exercises, adequate hydration, and no pillows under the knees or crossing of legs
Discharge teaching on anticoagulants: use a soft toothbrush and an electric razor, report black stools, bleeding gums, unusual bruising, or a bad headache, keep vitamin K intake (green leafy vegetables) consistent rather than eliminated if on warfarin, keep lab appointments, and carry medical identification
Malignant cells grow in lung tissue, obstruct airways, invade nearby structures, and spread.
Two families: non–small cell lung cancer (about 85%, includes adenocarcinoma and squamous cell — often treated surgically if caught early) and small cell lung cancer (aggressive, spreads early, treated with chemotherapy and radiation rather than surgery)
Why the symptoms: a tumor obstructing an airway causes cough, wheeze, and post-obstructive pneumonia; invasion of vessels causes hemoptysis; pleural involvement causes pain and effusion; pressure on the laryngeal nerve causes hoarseness
Biggest risk factor: tobacco smoke; then radon, asbestos and other occupational exposures, air pollution, and family history
Findings: a persistent cough or a change in a chronic cough, hemoptysis, dyspnea, chest or shoulder pain, hoarseness, recurrent pneumonia or bronchitis, unexplained weight loss and fatigue, and clubbing
Diagnostics: chest x-ray and CT to find it, PET to stage it, and bronchoscopy or needle biopsy for the definitive tissue diagnosis; sputum cytology and mediastinoscopy for lymph node involvement
Screening: annual low-dose CT for adults roughly 50–80 years old with a 20 pack-year history who currently smoke or quit within the past 15 years
🚨 Deterioration: facial and neck swelling with distended neck veins (superior vena cava syndrome — an oncologic emergency), sudden severe dyspnea with absent breath sounds on one side (effusion or pneumothorax), massive hemoptysis, or new neurologic changes suggesting brain metastases
Treatment: surgical resection (wedge, lobectomy, or pneumonectomy) for early non–small cell disease, chemotherapy, radiation, immunotherapy, and targeted therapy based on tumor markers
Priority nursing: maintain a patent airway and oxygenation first, manage pain so they can breathe deeply and cough, promote nutrition, monitor for infection during myelosuppression, and address the psychosocial and end-of-life needs directly rather than around them
Postoperative thoracotomy care: chest tube management, splinted coughing and deep breathing, incentive spirometry, early mobility, and pain control before pulmonary hygiene — not after
After a pneumonectomy: position on the back or the operative side as prescribed so the remaining lung can expand; that side has no lung to re-expand and usually no chest tube to suction
Oncologist, thoracic surgeon, radiation oncologist, pulmonologist, respiratory therapy, pain management and palliative care, dietitian, social work and case management, chaplain, and home health or hospice.
Complications: superior vena cava syndrome, malignant pleural effusion, pneumothorax, airway obstruction, hemorrhage, metastasis to brain, bone, liver, and adrenals, and paraneoplastic syndromes such as SIADH with small cell disease or hypercalcemia with squamous cell
Prevention and teaching: smoking cessation at any stage still helps, avoid secondhand smoke, test the home for radon, use occupational protection from asbestos and other carcinogens, keep screening appointments, report new hoarseness/hemoptysis/weight loss, and infection precautions during chemotherapy
Something has entered the pleural space that does not belong there — air (pneumothorax), blood (hemothorax), or fluid (effusion) — and it has destroyed the negative pressure that holds the lung open, so the lung collapses.
The chest tube's job: remove the air or fluid and restore negative intrapleural pressure so the lung can re-expand
Placement tells you what they are draining: a high/apical tube (about the 2nd–3rd intercostal space) removes air, because air rises; a low/basal tube (about the 5th–6th intercostal space, midaxillary) removes fluid or blood, because fluid settles
| What you see | Expected ✅ | Report / act ❌ |
|---|---|---|
| Water-seal chamber | Tidaling — the fluid level rises and falls with breathing. Intermittent bubbling is expected with a pneumothorax as trapped air escapes. | CONTINUOUS bubbling = an air leak in the system. Check all connections first, then work toward the patient. |
| Tidaling stops | If the patient is comfortable and breath sounds are back — the lung has re-expanded. | If the patient is dyspneic — the tubing is kinked, clamped, obstructed, or dependent-looped. Assess the patient, not just the box. |
| Suction chamber (wet) | Gentle continuous bubbling — that is the suction working, not an air leak. | No bubbling = suction is not connected or is turned too low. |
| Drainage | Gradually decreasing, changing from bloody to serosanguineous to serous. | More than 100 mL/hr of fresh bright red blood, or a sudden stop with distress — notify the provider. |
| Insertion site | Occlusive dressing intact, site clean and dry. | Crepitus (subcutaneous emphysema — crackling under the skin), redness, drainage, or fever. |
🚨 Signs of tension pneumothorax: severe dyspnea, absent breath sounds on one side, tracheal deviation AWAY from the affected side, distended neck veins, hypotension — this is an emergency
Routine care: keep the drainage system upright and BELOW the level of the chest, keep tubing free of kinks and dependent loops, assess breath sounds and respiratory status every shift and with any change, encourage deep breathing, coughing, and incentive spirometry to help the lung re-expand, mark and record drainage on the outside of the chamber, and keep sterile water and an occlusive dressing at the bedside
Never clamp a chest tube routinely — because trapped air has nowhere to go and can build into a tension pneumothorax. Brief clamping is only for changing the system or checking a leak, on an order. Never strip or milk the tubing routinely and never empty the drainage chamber.
At removal: medicate for pain first, then have the patient take a deep breath and bear down (Valsalva) or hold the breath as the tube is pulled, and apply an airtight petroleum-gauze occlusive dressing. A chest x-ray follows to confirm the lung stayed up.
The provider or thoracic surgeon who inserts and removes the tube, respiratory therapy, radiology for the confirming chest x-ray, and physical therapy for safe mobility with the drainage system.
Complications: tension pneumothorax, infection at the site or empyema, subcutaneous emphysema, bleeding, re-expansion pulmonary edema if a large effusion is drained too fast, and re-collapse after removal
Prevention and teaching: keep the system below the chest and upright, do not lie on the tubing, sit up and use incentive spirometry regularly, report new shortness of breath or chest pain immediately, and ambulate with the drainage unit carried below chest level
The patient cannot maintain adequate oxygenation, ventilation, or a patent airway on their own.
Indications: hypoxemic respiratory failure, hypercarbic respiratory failure (a rising PaCO₂ with a falling pH), inability to protect the airway, apnea, and severe work of breathing that is exhausting them
The key physiologic change: normal breathing pulls air in with NEGATIVE pressure; a ventilator pushes air in with POSITIVE pressure. Positive pressure in the chest reduces venous return, so it can lower cardiac output and blood pressure — especially with high PEEP.
Common settings: FiO₂ (percent oxygen), tidal volume (roughly 6–8 mL/kg of ideal body weight, and 6 mL/kg in ARDS to prevent volutrauma), respiratory rate, and PEEP (usually starting around 5 cm H₂O) which holds alveoli open at the end of exhalation
Confirming ET tube placement: continuous waveform capnography (ETCO₂) plus equal bilateral breath sounds and symmetric chest rise; a chest x-ray is the definitive confirmation. Note and document the centimeter marking at the lips every shift so you know if it migrates.
If breath sounds are heard only on the right: the tube has slipped into the right mainstem bronchus — notify the provider so it can be repositioned
| HIGH pressure alarm | LOW pressure alarm | |
|---|---|---|
| Means | Something is RESISTING the breath | Air is ESCAPING — a leak or disconnect |
| Causes | Secretions, biting the tube, kinked tubing, coughing, bronchospasm, water in the circuit, pneumothorax, decreasing lung compliance | Circuit disconnection, a cuff leak, or the tube coming out |
| You do | Assess the patient, suction if secretions, unkink tubing, drain condensation, use a bite block if needed — and if breath sounds are absent on one side, suspect pneumothorax and escalate | Trace the circuit from patient to machine, reconnect, check the cuff, and confirm the tube is still at the correct depth |
🚨 If the patient is in distress and you cannot fix it fast: disconnect from the ventilator and manually ventilate with a bag-valve device on 100% oxygen while someone gets help. Think DOPE — Displacement, Obstruction, Pneumothorax, Equipment failure.
Never silence a ventilator alarm without assessing the patient first.
The VAP prevention bundle: head of bed elevated 30–45 degrees, oral care with chlorhexidine per protocol, subglottic suctioning, daily sedation interruption with a spontaneous breathing trial, DVT prophylaxis, and stress ulcer prophylaxis
Suctioning: suction when indicated (secretions audible or visible, high pressure alarm, desaturation, restlessness) rather than on a schedule; hyperoxygenate first, limit each pass to about 10–15 seconds, and apply suction only while withdrawing
Comfort and safety: establish a communication method (board, writing, eye blinks) before sedating, reorient frequently, assess pain and sedation with a scale, and prevent unplanned extubation by securing the tube and using restraints only per policy and order
Anticipated orders: ABGs after every settings change, daily chest x-ray, continuous pulse oximetry and capnography, sedation and analgesia protocols, enteral nutrition, and a weaning/spontaneous breathing trial protocol
Readiness to wean: the underlying cause is improving, they are hemodynamically stable, they can initiate their own breaths, oxygenation is adequate on low FiO₂ and PEEP, and they are awake enough to protect the airway
Respiratory therapist (settings, weaning trials, ABGs), intensivist or pulmonologist, pharmacist for sedation and analgesia, dietitian for enteral feeding, speech-language pathologist after extubation or with a tracheostomy for swallow evaluation, PT/OT for early mobility, and palliative care and social work for goals-of-care conversations with the family.
Complications: ventilator-associated pneumonia, barotrauma and pneumothorax, volutrauma from large tidal volumes, decreased cardiac output and hypotension from positive pressure and PEEP, oxygen toxicity from prolonged high FiO₂, unplanned extubation, tracheal injury from cuff overinflation, ICU delirium, muscle deconditioning, and ventilator dependence
Prevention: the VAP bundle, lung-protective low tidal volumes, the lowest effective FiO₂ and PEEP, cuff pressure monitoring, daily sedation interruption and spontaneous breathing trials to shorten ventilator days, early mobility, and family involvement and reorientation to reduce delirium
Now go back to your lecture notes, the PowerPoint, ATI Engage, and Claire AI. Fill in what you missed and mark the areas that need another pass.
Anything you could not say out loud before tapping the reveal goes on your review list. That list — not the whole packet — is what you restudy tomorrow.
Instead of broad questions, try prompts such as: "Teach me COPD as if I am preparing for NCLEX." · "Compare asthma, COPD, and emphysema in a table." · "Create five ATI-style questions about pulmonary embolism with rationales." · "Walk me through a mechanical ventilation case study." · "Explain hypercarbia using patient examples." · "Help me distinguish assessment findings that require intervention versus continued assessment."
Before selecting an answer, run these in order. Same order, every question.
| Assess further when… | Intervene NOW when… |
|---|---|
| The cue is vague or you cannot name the problem yet — "reports feeling tired," "states the pain is different," a single borderline value in a stable patient. | The cue names a threat to airway, breathing, or circulation — a silent chest, SpO₂ 86%, new confusion, a respiratory rate climbing 20 → 32, absent breath sounds on one side. |
| Nothing will get worse in the next few minutes if you gather more data. | Waiting costs oxygen or perfusion. Then the answer is the action that opens the airway or improves ventilation — not a test, not documentation. |
Diagnostics never beat interventions when the patient is decompensating. ABGs, x-rays, and charting all delay treatment.
Answer all four before you open any reveal. The Answer Key and Rationales is attached to each question — correct answer plus why every distractor is wrong.
Correct: C. The respiratory rate jumped 12 breaths in an hour in a client who already has a clot obstructing pulmonary blood flow. That is a trend, not a number, and it says the client is deteriorating toward respiratory failure or right heart strain.
A — Fatigue with exertion is expected in COPD; it is the disease behaving normally.
B — A routine scheduled medication request. Important, but nobody is unstable.
D — A 0.4°C rise is mild and expected with pneumonia; there is no sign of acute instability.
When a question gives you two numbers, it is asking about the trend.
Correct: B. Increasing drowsiness in emphysema is the classic sign of rising CO₂ and impending respiratory failure. The mental status change matters more than the SpO₂ of 91%, which is acceptable for this client — oxygenation looks fine while ventilation is failing.
A — Pursed-lip breathing helps, but it requires a cooperative, alert client and it is not enough for someone you cannot rouse.
C — Raising the oxygen without assessing treats a number, not the problem. The problem is CO₂ that is not being exhaled, and more oxygen can make the retention worse.
D — Documentation never substitutes for action when a client is deteriorating.
Correct: A. Shallow breathing after chest surgery collapses alveoli. Incentive spirometry expands the lungs, reverses hypoventilation and atelectasis, and improves oxygenation right now — it directly treats the cause.
B — A chest x-ray gives information but moves no air. It delays treatment.
C — Fluids do nothing for impaired lung expansion and could worsen it.
D — Splinting supports the incision and makes deep breathing tolerable, but it is a support for the intervention, not the intervention.
Correct: B. Diminished breath sounds with increased dyspnea means air is not moving — bronchospasm and airway narrowing. The bronchodilator opens the airway and fixes the actual problem within minutes.
A — ABGs tell you how bad it is but delay treatment. Draw them after you have treated.
C — Hydration thins secretions over hours, not in an acute episode — and pushing fluids on a dyspneic client risks aspiration.
D — Old imaging describes the past. It does not treat the present.
Airway before assessment data. Every time.
A 67-year-old client presents with:
Sudden dyspnea, pleuritic chest pain, tachycardia at 124, tachypnea at 34, hypoxemia at 86% on room air, hemoptysis, and recent orthopedic surgery with the immobility that follows it.
The two that carry the most weight: SpO₂ 86% on room air (a direct oxygenation failure) and the word "sudden" combined with hip surgery 10 days ago (the risk factor that names the diagnosis).
Pulmonary embolism, most likely from a DVT that formed in the operative leg during postoperative immobility. Sudden onset, pleuritic pain, tachycardia, hypoxemia, and hemoptysis together are the textbook picture, and orthopedic surgery is a top-tier risk factor.
Why not pneumonia? Pneumonia builds over days with fever, productive purulent sputum, and crackles — it is not sudden. Why not MI? MI pain is usually pressure that does not change with breathing, and it does not produce blood-streaked sputum.
Impaired oxygenation from obstruction of pulmonary blood flow — blood cannot reach ventilated alveoli, so oxygen cannot get into the blood no matter how fast the client breathes. If the clot is large enough, the right ventricle fails against the pressure and the client goes into obstructive shock and arrest.
Support oxygenation, complete a focused respiratory and cardiovascular assessment, notify the provider promptly, establish IV access, and anticipate diagnostic evaluation and anticoagulation.
Prioritize breathing and circulation while escalating care.
Do not ambulate this client and do not leave the room to chart.
SpO₂ rises toward 92% or better, respiratory rate falls back toward normal, heart rate slows, chest pain decreases, the client is calm and oriented, blood pressure stays stable, and anticoagulation labs (aPTT or anti-Xa) reach the therapeutic range without bleeding.
A 72-year-old client with severe emphysema presents with:
Barrel chest, diminished breath sounds, accessory muscle use, respiratory rate 30, and — the one that changed — increasing drowsiness.
Which are chronic and which are new? Barrel chest is chronic and expected. Diminished breath sounds and accessory muscle use are baseline-plus. The increasing drowsiness is NEW, and new is what you act on.
The new drowsiness means worsening carbon dioxide retention (hypercarbia) — the client is breathing fast but shallowly and moving very little air, so CO₂ builds up. High CO₂ is a sedative to the brain, which is why they get sleepy. The SpO₂ of 90% is normal for this client and is falsely reassuring: oxygenation is adequate while ventilation is failing.
SpO₂ measures oxygenation. It tells you nothing about CO₂. Only an ABG and the client's mental status do.
Impending respiratory failure from hypercarbia — respiratory acidosis with a falling pH, progressing to obtundation, apnea, and the need for intubation if nothing changes.
Support ventilation as well as oxygenation, reassess frequently, and notify the provider of the change in condition.
Stay with the client, sit them fully upright, stimulate and reorient them, keep the oxygen at the prescribed rate rather than turning it up, give the prescribed respiratory medications, obtain the ABG, notify the provider immediately, and continue close monitoring with the equipment for BiPAP or intubation ready.
Do not increase the oxygen flow to fix drowsiness — because the problem is CO₂ that is not being exhaled, and extra oxygen does not remove CO₂.
The client becomes more alert and oriented, work of breathing decreases with less accessory muscle use, respiratory rate falls toward baseline, breath sounds improve as air moves, and a repeat ABG shows a falling PaCO₂ with a pH returning toward normal.
The single best indicator here: improved level of consciousness — because that is the sign that went wrong first.
Before the exam, ask yourself — and answer out loud, not in your head:
🤖 After this packet, use ATI Engage Dynamic Quizzing and Claire to generate more questions on anything you had to peek at.