3.2 Core Workflows and Decision Points
Key Takeaways
- First-line status asthmaticus care: continuous nebulized albuterol (5-20 mg/hr), ipratropium, and systemic corticosteroids, with IV magnesium sulfate 2 g over 20 min for refractory cases.
- Target SpO2 88-92% in COPD; uncontrolled high-flow oxygen can suppress the hypoxic drive and worsen hypercapnia.
- Start BiPAP for COPD exacerbation when ABG shows pH <= 7.35 with PaCO2 > 45 mmHg; it cuts intubation rates by ~60%.
- Massive PE (SBP < 90 mmHg) with no major contraindication warrants systemic thrombolysis; anticoagulation alone is given for hemodynamically stable PE.
- Tension pneumothorax is a clinical diagnosis treated immediately by needle decompression, then a chest tube - do not wait for a chest x-ray.
Asthma and Status Asthmaticus
Status asthmaticus is severe bronchospasm that does not respond to initial bronchodilators and threatens respiratory arrest. The escalation ladder is heavily tested:
- Continuous nebulized albuterol (short-acting beta-2 agonist), commonly 5-20 mg/hour, plus ipratropium (anticholinergic) for additive bronchodilation.
- Systemic corticosteroids early (e.g., methylprednisolone or oral prednisone) - they do not work for 4-6 hours, so give them up front.
- IV magnesium sulfate 2 g over 20 minutes for refractory severe asthma - it relaxes bronchial smooth muscle.
- IM epinephrine for impending arrest or anaphylactic component.
- BiPAP as a bridge; intubation only when the patient is failing despite maximal therapy.
Danger Signs
- Silent chest (no wheezing because almost no air moves)
- Inability to speak in full sentences
- Rising PaCO2 (fatigue)
- Altered mental status, bradycardia, cyanosis
Intubating an asthmatic is high-risk: use the largest tube, expect high airway pressures, allow a long expiratory time (low rate, permissive hypercapnia) to avoid breath-stacking and auto-PEEP.
COPD Exacerbation
In chronic obstructive pulmonary disease (COPD), the workflow centers on controlled oxygen and noninvasive ventilation.
- Oxygen target: SpO2 88-92%. Driving SpO2 to 100% with uncontrolled high-flow oxygen can blunt the patient's drive and worsen CO2 retention (and via the Haldane/V-Q effects, raise PaCO2). Titrate to the 88-92% window using a Venturi mask or nasal cannula.
- Bronchodilators + steroids + antibiotics when infection is suspected.
- BiPAP is first-line for acute hypercapnic respiratory failure: start it when ABG pH <= 7.35 with PaCO2 > 45 mmHg. A Cochrane review shows NIV reduces mortality ~50% and intubation ~60%.
| Modality | When to use |
|---|---|
| Controlled O2 (88-92%) | Every COPD exacerbation |
| BiPAP | pH <= 7.35, PaCO2 elevated, alert and cooperative |
| Intubation | NIV failure, apnea, unable to protect airway, hemodynamic instability |
A COPD patient who becomes drowsy and flushed on oxygen may be developing CO2 narcosis - recheck the ABG and consider BiPAP.
Pulmonary Embolism and Tension Pneumothorax
Pulmonary Embolism (PE)
Risk-stratify, then treat by hemodynamics:
- Stable PE -> therapeutic anticoagulation (heparin/LMWH or a DOAC).
- Massive PE = SBP < 90 mmHg for > 15 minutes, a >= 40 mmHg drop, or needing pressors -> systemic thrombolysis (e.g., alteplase) if no major bleeding contraindication; catheter-directed therapy or embolectomy if thrombolysis is contraindicated.
- Submassive PE = normotensive with right-ventricular strain (elevated troponin/BNP, RV dilation) -> anticoagulation, monitor closely; thrombolysis is individualized.
Classic clue: sudden dyspnea, pleuritic chest pain, tachycardia, hypoxia with a clear chest x-ray. CT pulmonary angiography (CTPA) is the confirmatory test.
Tension Pneumothorax
This is a clinical diagnosis - treat before imaging. Findings: severe dyspnea, absent breath sounds and hyperresonance on the affected side, tracheal deviation away from the side, distended neck veins, hypotension. Immediate treatment: needle decompression (large-bore catheter, traditionally 2nd intercostal space midclavicular line, increasingly 4th/5th intercostal space mid-axillary line), followed by a chest tube.
Putting the Workflows Together
The value of organizing respiratory care into workflows is that each one begins with a recognition cue and ends with a specific next action, which is exactly how CEN questions are constructed. For the asthmatic, the cue is wheezing or a silent chest with a prolonged expiratory phase, and the action ladder starts with continuous beta-agonists. For the COPD patient, the cue is a known history with a rising carbon dioxide and respiratory acidosis, and the pivotal action is controlled oxygen followed by noninvasive ventilation.
For pulmonary embolism, the cue is sudden pleuritic dyspnea with hypoxia and a clear chest film, and the branch point is whether the patient is hypotensive. For tension pneumothorax, the cue is unilateral absent breath sounds with hemodynamic collapse, and the action is immediate decompression.
A frequent test trap is to offer an action that is correct for a different pathway. Giving a bronchodilator to a patient with a tension pneumothorax, or ordering a chest x-ray before decompressing one, or pushing oxygen to 100 percent in a carbon-dioxide retainer, are all plausible-sounding distractors that solve the wrong problem.
Decision Anchors by Condition
| Condition | Recognition cue | Pivotal action |
|---|---|---|
| Status asthmaticus | Silent chest, rising CO2 | Continuous albuterol, then escalate |
| COPD exacerbation | History + pH <= 7.35, high CO2 | Controlled O2, then BiPAP |
| Massive PE | Sudden dyspnea + SBP < 90 | Systemic thrombolysis |
| Submassive PE | Normotensive + RV strain | Anticoagulate, monitor closely |
| Tension pneumothorax | Absent sounds + shock | Needle decompression, then tube |
Memorizing this cue-to-action map, rather than free-floating facts, is what lets you answer quickly when the stem buries the diagnosis inside a paragraph of vital signs. Notice that several of these conditions share overlapping presentations — dyspnea, tachycardia, and hypoxia appear in nearly all of them — so the differentiating cue is rarely the chief complaint and almost always a specific physical finding or value. Unilateral absent breath sounds point to a mechanical problem, a clear chest film with sudden hypoxia points to embolism, audible wheezing points to obstruction, and a known retainer with acidosis points to hypercapnic failure.
Training yourself to scan for the one finding that separates the look-alikes is the difference between a confident answer and a guess on test day.
A COPD patient arrives with SpO2 84%. The nurse applies a non-rebreather at 15 L/min and the SpO2 rises to 100%, but the patient becomes increasingly drowsy. What is the priority action?
A trauma patient has sudden severe dyspnea, absent breath sounds on the right, tracheal deviation to the left, hypotension, and distended neck veins. What is the most appropriate immediate intervention?