the Respiratory II framework, filled in. Tap "Hide answers" to quiz yourself.
Respiratory II picks up where Respiratory I stopped. Respiratory I was the upper airway and the physiology of gas exchange. This one is everything below the vocal cords: alveoli that collapse, alveoli that fill with pus, pleural spaces that fill with air or fluid, and the lungs finally failing. Every highlighted answer was a blank on the paper handout.
This does not replace lecture or ATI. It exists so you can follow along, connect patho to assessment findings, and practice thinking like a nurse instead of memorizing slides.
The whole module splits into two failures: a VENTILATION problem (air will not move → CO₂ rises) or an OXYGENATION problem (air moves fine but O₂ will not cross → PaO₂ falls). Name the failure and the intervention picks itself.
Ask Claire AI: "Explain the pathophysiology simply." · "Why does this symptom happen?" · "Walk me through the nursing priorities." · "Help me recognize early vs late signs." · "Give me NCLEX questions about this topic." Focus her on: gas exchange, hypoxia, respiratory distress, chest tube management, mechanical ventilation, prioritization.
Atelectasis = collapsed alveoli. Extremely common after surgery. An alveolus that is not periodically inflated to its full volume collapses shut, and the surfactant film sticks it closed.
Answer first: it is usually silent. The earliest clues are a low-grade fever in the first 24–48 hours after surgery, diminished or absent breath sounds over one area, fine crackles at the bases, a slightly increased respiratory rate and heart rate, and restlessness with a small drop in SpO₂.
Why the fever? Collapsed lung tissue releases inflammatory mediators — it is inflammation, not infection, which is why the treatment is lung expansion and not antibiotics.
Frank dyspnea, marked tachypnea and tachycardia, hypoxemia that does not fix with a nasal cannula, cyanosis, dullness to percussion over the collapsed lobe, absent breath sounds, anxiety progressing to confusion — and with a large lobar collapse, the trachea deviates TOWARD the affected side because the collapsed lung pulls the mediastinum with it.
Trachea toward the bad side = collapse. Trachea away from the bad side = tension pneumothorax.
Why does pain increase atelectasis risk?
Pain makes the patient splint — shallow, guarded breaths that never fully inflate the alveoli, and a suppressed cough that leaves secretions sitting in the airways. Untreated pain is therefore a respiratory problem, not just a comfort problem.
Why does immobility increase risk?
Lying flat compresses the dependent (posterior/basal) lung, drops functional residual capacity, and lets secretions pool by gravity instead of being mobilized. Immobile patients also stop taking the periodic deep breaths (sighs) that normally re-inflate alveoli.
Ask Claire AI: "Why is pain management considered respiratory care?" ATI: look up Atelectasis, Incentive spirometry, Pulmonary hygiene.
| Intervention | Why? |
|---|---|
| Incentive spirometer | Produces a slow, sustained maximal INSPIRATION that pops collapsed alveoli back open. Sit upright, seal the lips, inhale slowly and hold 3–5 seconds, then cough. 10 breaths every hour while awake. The work is on the way IN — blowing hard into it does nothing. |
| Ambulation | The single best pulmonary hygiene measure. Walking increases tidal volume and depth automatically, mobilizes secretions, and improves V/Q matching. Early ambulation prevents both atelectasis and VTE. |
| Turn / cough / deep breathe | Re-inflates alveoli and moves secretions out of dependent lung fields. Turn every 2 hours; splint the incision with a pillow so the cough is actually effective. |
| Pain management | Medicate BEFORE spirometry, coughing, and ambulation — a patient who cannot take a deep breath because it hurts will not expand a lung. Balance it: enough analgesia to breathe deeply, not so much that the respiratory drive drops. |
Pneumonia is NOT just an infection. Once the alveoli fill, it becomes a GAS EXCHANGE problem — and that is what you assess, treat, and prioritize.
Infection → inflammation → the alveoli fill with…
This causes impaired oxygenation (blood flows past a fluid-filled alveolus and never picks up oxygen — a shunt), increased work of breathing (stiff, wet lungs are hard to inflate), and hypoxia.
| Symptom | WHY does it happen? |
|---|---|
| Crackles | Fluid and exudate in the small airways and alveoli. The popping is stuck alveoli snapping open on inspiration. Bronchial breath sounds over peripheral lung fields and increased fremitus mean consolidation. |
| Tachypnea | Compensation for hypoxemia. Chemoreceptors sense the low PaO₂ and drive the rate up to recruit more alveoli — the earliest and most reliable vital sign change. |
| Productive cough | The airway clearing exudate. Sputum is purulent, thick, sometimes rust-colored or blood-tinged (classic with S. pneumoniae) because RBCs leak into the alveoli. |
| Confusion | Cerebral hypoxia. The brain has no oxygen reserve, so it shows the deficit before anything else — and in an older adult this may be the ONLY sign. |
| Low oxygen saturation | V/Q mismatch / shunt — the alveoli are perfused but not ventilated, so blood returns to the left heart still desaturated. This is why a shunt responds poorly to low-flow oxygen alone. |
What may be one of the FIRST signs of hypoxia in older adults?
New-onset confusion / an acute change in mental status. Older adults with pneumonia are often afebrile, may have no cough, and may present only as "not acting right," a new fall, incontinence, or sudden functional decline. Treat new confusion in an older adult as hypoxia until proven otherwise — check the SpO₂ first.
WHY? Fever, crackles and a productive cough are expected consequences of the infection. Confusion with an SpO₂ of 84% means oxygen is no longer reaching tissue — that is organ-level hypoxia and it kills first. Act now: sit them upright, apply oxygen, stay with the patient, recheck the saturation and level of consciousness, and notify the provider.
Prevention teaching: pneumococcal and annual influenza vaccination, smoking cessation, oral care, early mobility, and head of bed elevated 30–45° for anyone being tube fed.
| Test | Purpose |
|---|---|
| Chest x-ray | Confirms the diagnosis. Shows infiltrates/consolidation, tells you which lobe and how much lung is involved, and reveals a pleural effusion or empyema. The x-ray may lag behind the symptoms early and stays abnormal for weeks after the patient feels better. |
| ABGs | Tells you how badly gas exchange is failing. Early: low PaO₂ with a low PaCO₂ and high pH (respiratory alkalosis from blowing off CO₂). Late/tiring: rising PaCO₂ with a falling pH = respiratory acidosis = the patient is failing. |
| CBC | Shows the systemic infection response. WBC elevated with a left shift (more bands/immature neutrophils). A normal or LOW WBC in an older or septic patient is more ominous, not reassuring. |
| Sputum culture & sensitivity | Identifies the organism and which antibiotic will kill it. Collect BEFORE the first antibiotic dose. Best specimen: early morning, deep cough from the lungs (not saliva), after rinsing the mouth with water. |
The priority is oxygenation, not the antibiotic. Antibiotics fix the cause over days; hypoxia kills in minutes. Do not send a hypoxic patient off the unit for a test before stabilizing breathing.
| Intervention | Purpose |
|---|---|
| High Fowler's | Maximizes lung expansion and lowers work of breathing. Sitting up lets the diaphragm drop and keeps abdominal contents off the lungs. With unilateral pneumonia, "good lung down" puts gravity-driven blood flow where the alveoli still work. |
| Oxygen | Corrects hypoxemia and reduces the cardiac work of compensating. Titrate to the ordered target — commonly SpO₂ 92–95%, but 88–92% in a known CO₂ retainer with COPD. Use the lowest FiO₂ that achieves it. |
| Fluids | Thins thick secretions so they can actually be coughed up and replaces losses from fever and tachypnea. Aim 2–3 L/day unless heart failure or kidney disease requires a restriction. |
| Cough / deep breathe | Clears exudate and re-opens alveoli so the antibiotic-treated lung can participate in gas exchange again. Add incentive spirometry, repositioning, and ambulation. |
| Antibiotics | Kill the causative bacteria. Empiric broad-spectrum first (after cultures), narrowed once sensitivities return. Teach: finish the entire course even after feeling better, or the survivors become resistant. Antibiotics do nothing for viral pneumonia. |
All of these lose the reflexes that protect the airway — the swallow, the gag, and the cough. Gastric contents or oral secretions enter the trachea instead of the esophagus. The acid causes an immediate chemical burn of the alveoli, and the oral bacteria that ride in on it cause the infection that follows. Because the right mainstem bronchus is wider and more vertical, aspiration lands most often in the right lower lobe.
Prevention: HOB 30–45° during and for 30–60 minutes after feeding, swallow screen before the first sip after a stroke, chin-tuck and small bites, thickened liquids if ordered, sit fully upright to eat, aggressive oral care, verify tube placement before use.
Never give oral fluids or meds to a stroke patient who has not passed a swallow screen.
Empyema = a collection of thick, infected PUS inside the PLEURAL SPACE — the potential space between the visceral and parietal pleura. It is usually a complication of pneumonia, a lung abscess, chest trauma, or thoracic surgery: an infected effusion that was not drained.
Pneumonia affects:
Empyema affects:
Pneumonia is fluid INSIDE the lung. Empyema is pus AROUND the lung. That difference is exactly why one is treated with antibiotics and pulmonary hygiene and the other needs drainage — thoracentesis or a chest tube — plus antibiotics.
Why does empyema cause hypoxia?
The pus takes up space in a closed chest. It compresses the lung from the outside so that region cannot inflate, and it stiffens/thickens the pleura so the chest wall cannot expand. Less ventilation to still-perfused lung = V/Q mismatch = hypoxemia. Pleuritic pain makes it worse because the patient splints and breathes shallowly on that side.
Nursing care after drainage: chest tube care, deep breathing and incentive spirometry to re-expand the lung, full antibiotic course, and monitor drainage amount and character.
To remove fluid (or air) from the pleural space through a needle/catheter inserted between the ribs. Two reasons: diagnostic — sample the fluid for culture, cell count, protein, LDH, glucose, cytology; and therapeutic — relieve the compression so the lung can re-expand and the patient can breathe.
What complication are we watching for MOST closely?
PNEUMOTHORAX — the needle passes right next to the lung, so a puncture lets air into the pleural space. Also watch for re-expansion pulmonary edema if more than about 1,000–1,500 mL is removed at once, plus bleeding/hemothorax and infection. A post-procedure chest x-ray is standard.
What assessment matters MOST?
Respiratory status — specifically breath sounds on the procedure side, plus RR, work of breathing, and SpO₂. Sudden sharp chest pain, new dyspnea, diminished or absent breath sounds on that side, and a falling SpO₂ = pneumothorax until proven otherwise. Report immediately.
Also: apply a dressing and position the patient on the unaffected side for about an hour so the puncture site can seal, monitor VS frequently, and document the amount, color, and consistency of the fluid removed.
TB is BOTH a respiratory disorder and a public health / infection-control issue. Caused by Mycobacterium tuberculosis, an acid-fast bacillus spread by tiny droplet nuclei that stay suspended in the air for hours. That is why the isolation answer is what it is.
TB requires:
Room type: a private, NEGATIVE-pressure room (airborne infection isolation room / AIIR) with 6–12 air exchanges per hour, air exhausted outside or through a HEPA filter, and the door kept closed at all times.
Mask: The nurse wears a fit-tested N95 respirator (or a PAPR) every time she enters. The patient wears a surgical mask — not an N95 — whenever they must leave the room, and transport is limited to essential trips only. Also teach the patient to cover coughs with tissues and dispose of them in a lined bag.
Never leave the door of a negative-pressure room open, and never rely on a surgical mask to protect yourself from TB.
Cough > 3 weeks + night sweats + weight loss = screen for TB and mask the patient now.
| Latent TB | Active TB | |
|---|---|---|
| Symptoms? | None. The person feels completely well — the organism is walled off inside granulomas and dormant. | Yes — cough > 3 weeks, night sweats, fever, weight loss, fatigue, hemoptysis. |
| Contagious? | NO — cannot transmit TB to anyone. No isolation is needed; the person can work and go to school. | YES — highly contagious by the airborne route. Airborne precautions until treated and non-infectious. |
| Skin test / IGRA | Positive | Positive |
| Chest x-ray | Normal (or old calcified scar) | Abnormal — infiltrates/cavitation, classically the upper lobes |
| Sputum AFB | Negative | Positive |
| Treatment | Treat anyway to prevent progression — usually INH for 6–9 months, or rifampin for 4 months | Multi-drug therapy (RIPE) for 6–9+ months, often with directly observed therapy |
Roughly 5–10% of latent infections progress to active disease; the risk jumps with HIV, immunosuppressants, diabetes, and malnutrition — which is why we treat people who feel fine.
| Test | What does it tell us? |
|---|---|
| PPD (Mantoux skin test) | Screening only — it says the person has been INFECTED/exposed, not that they have active disease. Inject 0.1 mL intradermally to raise a wheal; read at 48–72 hours; measure the INDURATION (the firm raised area) in mm, not the redness. Positive at ≥5 mm for HIV/immunosuppressed/recent close contacts/abnormal CXR, ≥10 mm for higher-risk groups such as healthcare workers, recent immigrants and IV drug users, and ≥15 mm for people with no risk factors. A positive PPD always requires a chest x-ray to rule out active disease. |
| QuantiFERON (IGRA blood test) | Blood test that measures the immune (interferon-gamma) response to TB antigens — same information as a PPD, but one visit with no return trip to read it, and it is not falsely positive from prior BCG vaccination. Still cannot distinguish latent from active. |
| NAAT (nucleic acid amplification) | Detects TB genetic material directly in sputum — results in hours instead of weeks. Used for rapid confirmation of active pulmonary TB and can flag rifampin resistance, so treatment and isolation decisions do not have to wait on culture. |
| Acid-fast sputum culture | The GOLD STANDARD — it confirms ACTIVE disease and gives drug sensitivities, but takes 1–6 weeks to grow. Collect early-morning sputum on 3 consecutive days. Three consecutive negative AFB smears on therapy = the patient is no longer considered infectious and can come off airborne precautions. |
Four drugs together for the first 2 months (intensive phase), then usually INH + rifampin for 4–7 more months. Multiple drugs are used because TB mutates to resistance fast against any single agent.
| Medication | Major side effect & nursing teaching |
|---|---|
| Rifampin | Harmless ORANGE-RED discoloration of urine, sweat, saliva and tears — teach it up front so the patient does not stop the drug, and warn that it permanently stains soft contact lenses and clothing. Also hepatotoxic, and it is a strong liver enzyme inducer that makes oral contraceptives fail — teach a backup barrier method. Watch for drug interactions with warfarin, protease inhibitors, and many others. |
| INH (isoniazid) | HEPATOTOXICITY and PERIPHERAL NEUROPATHY. Give pyridoxine (vitamin B₆) with it to prevent the numbness and tingling of the hands and feet. Monitor LFTs; teach the patient to report jaundice, dark urine, RUQ pain, nausea, and unusual fatigue, and to avoid alcohol completely. Take on an empty stomach, 1 hour before or 2 hours after meals; avoid tyramine-rich foods (aged cheese, cured meats) and histamine-rich fish. |
| Ethambutol | OPTIC NEURITIS — the EYE drug. Causes decreased visual acuity and loss of red-green color discrimination. Get a baseline eye exam and teach the patient to report ANY vision change immediately — it is reversible if the drug is stopped early. Generally avoided in young children who cannot report vision changes. |
| Pyrazinamide | HEPATOTOXICITY plus HYPERURICEMIA — it raises uric acid and can trigger gout: joint pain, especially a hot swollen great toe. Teach increased fluid intake, monitor uric acid and LFTs, and report joint pain or jaundice. Also causes photosensitivity — use sunscreen. |
The lungs are failing at oxygenation and/or ventilation.
| Early Signs (compensating) | Late Signs (crashing) |
|---|---|
| Restlessness, anxiety, agitation, "impending doom" — the very first sign of hypoxia is a change in behavior, because the brain notices first | Confusion → lethargy → somnolence → coma — the same brain, now beyond compensating |
| Tachypnea and tachycardia, often with a mildly elevated blood pressure — the body recruiting rate and cardiac output to deliver oxygen | BRADYCARDIA, hypotension, dysrhythmias, and a falling respiratory rate — the myocardium is now hypoxic itself; this precedes arrest |
| Dyspnea, accessory muscle use, nasal flaring, and an inability to speak in full sentences; pale skin, headache from rising CO₂ | Cyanosis, diaphoresis, paradoxical (see-saw) abdominal breathing, and a QUIET chest with poor air movement |
A suddenly QUIET respiratory patient may actually be:
TIRING OUT — respiratory muscle fatigue and impending respiratory arrest. When a struggling patient suddenly settles down, stops fighting, gets sleepy, and the chest goes silent, that is not improvement — it means so little air is moving that there is nothing left to make sound with. A silent chest in a wheezing asthmatic and a "finally calm" patient in distress are both emergencies. Get help and prepare for intubation.
Never chart "patient resting comfortably" on a patient who was in distress ten minutes ago without laying hands on them and listening to the chest.
| ABG finding | Meaning |
|---|---|
| Low PaO₂ (< 60 mmHg) | HYPOXEMIA — an OXYGENATION failure. Oxygen is not crossing the alveolar-capillary membrane. Normal PaO₂ is 80–100 mmHg. If it stays low even on high FiO₂, that is a shunt (fluid or collapse), and the fix is recruitment — PEEP, positioning, drainage — not just more oxygen. |
| High PaCO₂ (> 45 mmHg) | HYPOVENTILATION — a VENTILATION failure. The patient is not moving enough air to blow off CO₂. Normal is 35–45 mmHg. Causes: fatigue, sedation/opioids, COPD air trapping, neuromuscular weakness. The fix is ventilatory support (BiPAP or intubation), because oxygen alone does not remove CO₂. |
| Low pH (< 7.35) | ACIDOSIS — and with a high PaCO₂, this is ACUTE RESPIRATORY ACIDOSIS. A low pH means the body has NOT compensated — this is happening right now. A patient with a high CO₂ but a normal pH is chronically compensated (a stable COPD baseline); a patient with a high CO₂ AND a low pH is decompensating and needs support now. |
Two rules: oxygenate before you investigate, and if the patient cannot protect the airway or is tiring out, the answer is ventilatory support — not another liter of oxygen.
Not in the handout's blanks, but it is on every respiratory exam and it is the intervention behind half the answers above. Learn the flow rate, the FiO₂, and the one thing that makes each device wrong.
| Device | Flow rate | FiO₂ | Key nursing point |
|---|---|---|---|
| Nasal cannula | 1–6 L/min | 24–44% | Low-flow and variable — the actual FiO₂ depends on how the patient breathes. Roughly +4% per liter. Humidify above 4 L/min; check the nares and behind the ears for breakdown. Patient can eat and talk. |
| Simple face mask | 5–8 L/min | 40–60% | Never run below 5 L/min — lower flow lets exhaled CO₂ accumulate in the mask and be rebreathed. Must be removed to eat. |
| Partial rebreather | 6–11 L/min | 60–75% | Has a reservoir bag and no valve between bag and mask. Keep the bag inflated — it must not deflate more than about a third on inspiration. |
| Non-rebreather | 10–15 L/min | 60–100% | The highest FiO₂ for a spontaneously breathing patient — this is the emergency mask. One-way valves prevent rebreathing. Never let the reservoir bag collapse — turn the flow up until it stays inflated. |
| Venturi mask | 4–12 L/min (per the color-coded adapter) | 24–50%, PRECISE | The most accurate FiO₂ — the device of choice for COPD/CO₂ retainers where an exact, low, titrated oxygen concentration matters. Keep the entrainment ports uncovered. |
| High-flow nasal cannula | up to 60 L/min | 21–100% | Heated and humidified; delivers a small amount of PEEP and washes CO₂ out of the upper airway. Comfortable, and the patient can still talk and eat. |
| Face tent / aerosol mask / trach collar | 8–15 L/min | 24–100%, variable | High humidity. Used for facial trauma, post-extubation, or a tracheostomy. Empty condensation from the tubing away from the patient. |
| CPAP / BiPAP (noninvasive) | Set pressures, not L/min | Titrated | CPAP holds one continuous pressure (OSA, pulmonary edema). BiPAP gives a higher pressure on inspiration and a lower one on expiration, so it actually helps VENTILATION — used for COPD with hypercapnia. Requires an alert patient who can protect the airway. |
The ET tube: creates and protects a patent airway. It is a sealed conduit from the mouth to the trachea — the inflated cuff keeps gastric contents out of the lungs and lets positive pressure be delivered without leaking, and it gives a route for deep suctioning. The tube by itself does not breathe for anyone. Confirm placement with continuous waveform capnography (end-tidal CO₂) plus a chest x-ray; mark and document the cm mark at the teeth/lips (typically 21–23 cm) and check it every shift.
The ventilator: does the work of breathing by pushing air in under POSITIVE pressure — the nurse and provider set the rate, tidal volume, FiO₂, and PEEP, and choose how much the patient triggers versus the machine. It buys time; it does not cure anything. Note that positive pressure is the opposite of normal breathing, which is why it drops venous return and blood pressure.
PEEP helps: keep the alveoli from collapsing at the end of exhalation. Holding a small positive pressure in the chest (usually starting at 5 cm H₂O) increases functional residual capacity and the surface area available for gas exchange, improves oxygenation, and lets you use a LOWER FiO₂ — which protects against oxygen toxicity. It is the main tool for the shunt physiology in ARDS and pulmonary edema.
Why is too much PEEP dangerous?
Because the extra pressure is inside a closed chest. High PEEP raises intrathoracic pressure → compresses the vena cava → less venous return → less preload → falling cardiac output and HYPOTENSION. It also over-distends alveoli and causes barotrauma — a pneumothorax, which can become a tension pneumothorax under positive pressure. Sudden hypotension + falling SpO₂ + absent breath sounds on one side + a high-pressure alarm on a ventilated patient = tension pneumothorax until proven otherwise. High PEEP can also raise ICP and reduce renal perfusion.
| Alarm type | Possible causes |
|---|---|
| HIGH pressure alarm | Something is OBSTRUCTING or resisting the breath. Think: secretions needing suction (most common), the patient biting the tube, kinked tubing, water condensation in the circuit, coughing or fighting the vent, bronchospasm, or decreased lung compliance — pulmonary edema, ARDS, or a pneumothorax. Fix in that order: look, listen, suction, unkink, reposition. |
| LOW pressure alarm | There is a LEAK or a DISCONNECTION. Think: the circuit came apart at a connection, the ET tube cuff is leaking or under-inflated (a gurgling sound or the patient suddenly vocalizing is the tip-off), the tube has become dislodged/extubated, or there is a leak through a chest tube. Trace the circuit from the patient to the machine. |
| APNEA alarm | The patient is not initiating breaths. Think: oversedation or opioids, a neurologic change, respiratory muscle fatigue or arrest, or a disconnection. The vent should deliver backup breaths — but assess the patient first: are they breathing, what is the SpO₂, what is the LOC? |
The universal rule: assess the PATIENT before the machine, and never silence an alarm you have not resolved. If you cannot immediately fix the problem or the patient is deteriorating, disconnect from the ventilator and manually ventilate with a bag-valve device on 100% oxygen while you call respiratory therapy.
Routine care to prevent VAP: HOB 30–45°, oral care with chlorhexidine per protocol, daily sedation interruption and readiness-to-wean assessment, suction only when indicated, hand hygiene, VTE and stress-ulcer prophylaxis.
A chest tube drains air, fluid, blood, or pus out of the pleural space so the lung can re-expand and negative intrapleural pressure is restored.
The water seal is a one-way valve made of about 2 cm of water: air and fluid can leave the chest, but nothing can be sucked back in.
Tidaling means:
The fluid level in the water-seal column RISES with inspiration and FALLS with exhalation. This is EXPECTED and NORMAL. It tells you two things: the system is patent (nothing kinked or clotted), and the lung has not fully re-expanded yet. In a patient on positive-pressure mechanical ventilation the swing is reversed — it falls with inspiration — but the meaning is the same. If tidaling STOPS, it is either good news (the lung has re-expanded) or bad news (the tubing is kinked, clamped, dependent-looped or obstructed) — so assess the patient AND trace the tubing before you decide which.
Continuous bubbling means:
An AIR LEAK. Continuous bubbling in the WATER-SEAL chamber is abnormal and must be tracked down — either a leak in the system (a loose connection, a crack in the tubing, a dislodged dressing exposing the insertion site) or a leak from the patient (a persistent bronchopleural leak). Intermittent bubbling in the water seal that happens only with coughing or exhalation is EXPECTED in a pneumothorax — that is the trapped air leaving, and it should decrease as the lung re-expands. Continuous gentle bubbling in the SUCTION-CONTROL chamber of a wet-suction system is normal and expected — that is just how the suction level is regulated. Vigorous bubbling there only evaporates the water; turn it down.
Never leave a chest tube clamped while you go look for help. Pinching to locate a leak is momentary — seconds, with your eyes on the patient.
| Nursing action | WHY? |
|---|---|
| Keep the drainage system BELOW chest level | Drainage is by GRAVITY, and the water seal only works upright. If the unit is raised above the insertion site, drainage can siphon back into the pleural space, re-collapsing the lung and reintroducing infection. Keep it upright on the floor or hung on the bed frame — never in the bed and never on its side. |
| Monitor for kinks (and dependent loops) | An obstructed tube is a tube that is not draining — air and fluid re-accumulate in the chest and pressure builds toward a tension pneumothorax. Keep the tubing coiled flat on the bed with a straight drop to the unit, keep it off the floor and out from under the patient or the side rails, and clear dependent fluid-filled loops. |
| Do NOT clamp routinely | Clamping traps air in the pleural space with no way out — pressure rises and a simple pneumothorax becomes a TENSION pneumothorax. The only acceptable reasons to clamp are momentarily: to locate an air leak, to change the drainage unit, or per provider order for a brief trial before removal. Never clamp a chest tube because the patient is being transported or ambulating. Keep it connected and keep it below the chest. |
| Assess breath sounds | They tell you whether the lung is actually re-expanding. Compare both sides every shift and any time something changes: improving breath sounds on the affected side means the tube is working; newly diminished or absent sounds mean the lung is re-collapsing, the tube is blocked, or it has migrated. Also assess RR, SpO₂, pain, the insertion site, subcutaneous emphysema (crepitus), and the amount/color of drainage. |
These two look alike and the answers are opposite. The question to ask is: which end came apart?
Out of the CHEST → occlusive dressing taped on three sides. Out of the SYSTEM → the tube end goes into sterile water.
Air enters: the PLEURAL SPACE — the space between the visceral pleura on the lung and the parietal pleura on the chest wall. It gets there three ways: from outside through a penetrating chest wound (open/"sucking" chest wound), from inside when a bleb or alveolus ruptures (spontaneous, classically a tall thin young man; or secondary to COPD, or barotrauma from a ventilator), or iatrogenically from a central line insertion, thoracentesis, or lung biopsy.
This causes: Loss of the negative intrapleural pressure that normally holds the lung against the chest wall → the lung on that side collapses. Collapsed lung is still perfused but no longer ventilated → shunt → V/Q mismatch → hypoxemia, plus a sudden increase in work of breathing.
Treatment: oxygen, upright position, and a chest tube to evacuate the air (a small stable one may just be observed).
Because the air can get IN but cannot get OUT. The tear acts as a one-way valve, so every breath adds more air and the pressure in that hemithorax keeps climbing. Three things happen fast: (1) the lung on that side collapses completely; (2) the pressure pushes the mediastinum, heart and trachea toward the UNAFFECTED side, compressing the other lung too; and (3) — the part that actually kills — the shifted mediastinum kinks and compresses the vena cava, so venous return collapses, cardiac output falls, and the patient goes into obstructive shock and cardiac arrest within minutes. It is a mechanical problem, so oxygen alone will not fix it: the air must come out NOW.
Needle decompression classically goes in the 2nd intercostal space at the midclavicular line on the affected side (some protocols use the 4th–5th ICS at the anterior axillary line). It is a temporizing measure — a chest tube always follows.
Open ("sucking") chest wound: cover with a sterile occlusive dressing taped on three sides — same flutter-valve logic as the dislodged chest tube. Never tape all four sides — a fully sealed dressing turns an open pneumothorax into a tension pneumothorax.
| Atelectasis / large collapse | Simple pneumothorax | Tension pneumothorax | |
|---|---|---|---|
| Trachea | Pulled TOWARD the affected side | Midline | Pushed AWAY from the affected side |
| Percussion | Dull | Hyperresonant | Hyperresonant |
| Blood pressure | Normal | Usually normal | Severe hypotension + JVD |
| Urgency | Lung expansion measures | Chest tube | Immediate needle decompression |
STOP memorizing isolated diseases. Instead, ask the same six questions on every patient:
| Concept | What you should be thinking |
|---|---|
| Oxygenation | "Are tissues getting oxygen?" — SpO₂, PaO₂, LOC, skin color |
| Ventilation | "Is CO₂ being removed?" — rate, depth, PaCO₂, air movement |
| Compensation | "Is the body trying to keep up?" — tachypnea and tachycardia are the body working, not the body failing |
| Respiratory fatigue | "Is the patient tiring out?" — a rising CO₂, a falling rate, and a quiet chest |
| Prioritization | "What kills first?" — airway, then breathing, then circulation |
| Gas exchange | "Can oxygen cross the alveoli?" — anything filling or collapsing an alveolus says no |
That is how you begin thinking like a nurse instead of memorizing slides.
Answer: 2. Continuous bubbling in the water-seal chamber means an air leak. The first nursing action is the least invasive assessment — check the occlusive dressing at the insertion site and tighten every connection along the tubing, moving from the patient toward the drainage unit.
1 is wrong — and dangerous. Clamping a chest tube in a patient with a pneumothorax traps air in the pleural space and can cause a tension pneumothorax. Clamping is only ever momentary, to localize a leak or change the unit.
3 is wrong. Stripping or milking the tubing is not done routinely; it generates extreme negative intrapleural pressure and damages tissue. It also does not address an air leak.
4 is wrong. Increasing suction does not seal a leak; it just pulls more air through it and evaporates the water in the suction chamber.
Answer: 3 — this requires intervention. The door of a negative-pressure (airborne infection isolation) room must stay closed. Propping it open destroys the negative pressure gradient and lets droplet nuclei escape into the hallway.
1 is correct practice. A fit-tested N95 (or PAPR) is the required respiratory protection for staff entering a TB room; a surgical mask is not adequate.
2 is correct practice. The client wears a surgical mask during unavoidable transport to contain their own droplets. Clients do not wear N95s.
4 is correct practice. Early-morning sputum on three consecutive days is the standard collection for AFB smear and culture.
Answer: 2. This is classic early atelectasis: low-grade fever in the first 48 hours after surgery with diminished bibasilar breath sounds. The treatment is lung expansion, and the patient will not take a deep enough breath while her incision hurts — so medicate first, then spirometry, splinted coughing, and ambulation.
1 is wrong. Post-op atelectasis fever is inflammatory, not infectious. Antibiotics do not re-inflate an alveolus, and cultures are not the priority intervention here.
3 is wrong. An SpO₂ of 93% does not call for the highest-FiO₂ emergency device. Escalating oxygen also does not fix collapsed alveoli — recruitment does.
4 is wrong — it is backwards. Adequate hydration thins secretions so they can be cleared. Restricting fluids makes mucus plugging worse.
Answer: 3. Positive pressure plus PEEP is a set-up for barotrauma. Absent unilateral breath sounds + tracheal deviation away from that side + sudden hypotension + a high-pressure alarm is a tension pneumothorax. It is diagnosed clinically and decompressed immediately — you do not wait for the x-ray.
1 is wrong. A right mainstem intubation causes absent breath sounds on the LEFT (the tube is past the left bronchus), and it does not cause tracheal deviation or shock.
2 is wrong. A mucus plug can absolutely cause a high-pressure alarm and diminished sounds, but it does not cause tracheal deviation or profound hypotension. Suctioning here would delay life-saving decompression.
4 is wrong. A PE causes hypoxemia and hypotension but breath sounds stay present and roughly equal, and there is no tracheal deviation or hyperresonance.
Answer: 2. A patient in distress who suddenly gets quiet is not better — they are exhausted. A falling respiratory rate with a silent chest after an hour of hard work means respiratory muscle fatigue with rising CO₂ and impending arrest. Call for help, stay with the client, be ready to bag-mask and support with BiPAP or intubation.
1 and 3 are wrong — and they are the trap. They interpret decreased effort as improvement. Improvement would show a rate coming down toward normal with improved air movement, better breath sounds, and an alert, comfortable client.
4 is wrong. The problem is now ventilation, not just oxygenation. More oxygen through a cannula does not remove CO₂ and will not reverse fatigue — and in a CO₂ retainer it can further blunt the drive to breathe.
If you remember one sentence: find out whether the problem is air getting IN or oxygen getting ACROSS, then ask whether the patient is compensating or tiring out. Those two answers give you the priority every time.