4.3 Pulmonary Embolism, Pneumothorax, COPD & Asthma

Pulmonary Embolism, Pneumothorax, COPD & Asthma

This section covers four acute conditions that recur on the CCRN: pulmonary embolism, pneumothorax (especially tension), COPD exacerbation, and status asthmaticus.

Pulmonary Embolism (PE)

A pulmonary embolism is obstruction of a pulmonary artery, usually by a thrombus from a lower-extremity deep vein thrombosis (DVT). It increases dead space (ventilated but not perfused lung), causes acute right-ventricular (RV) strain, and produces hypoxemia with a widened A-a gradient. Classic presentation: sudden dyspnea, pleuritic chest pain, tachycardia, tachypnea, and hypoxemia; the ECG may show sinus tachycardia or the S1Q3T3 pattern.

Wells criteria stratify pretest probability:

In the two-tier model, a score <= 4 = PE unlikely and > 4 = PE likely. For low/moderate probability, a normal high-sensitivity D-dimer safely rules out PE without imaging; an elevated D-dimer or a high-probability score prompts CT pulmonary angiography (CTPA), the gold standard.

Management follows the hemodynamics:

• Stable PE -- anticoagulation with low-molecular-weight heparin, unfractionated heparin, or a direct oral anticoagulant (DOAC). Start empirically when suspicion is high and there is no contraindication.
• Massive PE (sustained hypotension, SBP < 90 mmHg, or shock with RV failure) -- systemic thrombolysis (alteplase/tPA) if no contraindication, or catheter-directed thrombolysis or surgical embolectomy. Avoid aggressive diuresis and fluid restriction, which drop RV preload and worsen output.
• Submassive PE (RV strain but normotensive) -- anticoagulate and consider thrombolysis case-by-case.

An IVC filter is reserved for patients with an absolute contraindication to anticoagulation.

Pneumothorax and Tension Pneumothorax

A pneumothorax is air in the pleural space causing lung collapse. A tension pneumothorax is the life-threatening variant: a one-way valve lets air accumulate under pressure, collapsing the lung, shifting the mediastinum, and compressing the great veins so venous return and cardiac output fall.

Recognize tension pneumothorax clinically -- do not wait for a chest x-ray:

• Absent breath sounds and hyperresonance on the affected side
• Tracheal deviation away from the affected side
• Hypotension, distended neck veins, severe respiratory distress
• In a ventilated patient, sudden high peak airway pressures with desaturation

Immediate treatment is needle decompression -- a large-bore needle into the 2nd intercostal space, midclavicular line (or the 4th/5th intercostal space, anterior axillary line per updated trauma guidance) -- followed by chest-tube (tube thoracostomy) placement. A small simple (non-tension) pneumothorax may be observed; a larger or symptomatic one gets a chest tube. Contrast this with cardiac tamponade (Beck's triad: hypotension, elevated CVP/JVD, muffled heart tones) where breath sounds are equal and clear.

COPD Exacerbation

Patients with chronic obstructive pulmonary disease (COPD) present with worsening dyspnea, increased sputum, and hypercapnic (Type II) failure. Management bundle:

• Controlled oxygen to SpO2 88-92% -- over-oxygenation worsens V/Q matching and can raise CO2; do not aim for 100%.
• Short-acting bronchodilators -- albuterol (SABA) plus ipratropium (SAMA) by nebulizer.
• Systemic corticosteroids to reduce airway inflammation.
• Antibiotics when sputum is purulent/increased or the patient is ventilated.
• Noninvasive positive-pressure ventilation (BiPAP) -- first-line for hypercapnic respiratory acidosis in an alert, cooperative patient who protects the airway; it reduces intubation and mortality.

A chronically compensated ABG (high PaCO2, high HCO3, near-normal pH) is the patient's baseline -- treat the patient, not the gas.

Status Asthmaticus

Status asthmaticus is severe asthma unresponsive to initial bronchodilators, with intense bronchospasm and air trapping. Management: continuous or repeated nebulized SABA (albuterol) with ipratropium, early systemic corticosteroids, IV magnesium sulfate for severe cases, and oxygen to correct hypoxemia. Ominous signs of impending arrest include a "silent chest" (no air movement), fatigue, altered mental status, and a rising or normalizing PaCO2 -- in a tachypneic asthmatic, a normal CO2 means the patient is tiring, not improving. If intubated, beware auto-PEEP (dynamic hyperinflation) from air trapping: use a low respiratory rate, prolonged expiratory time, and permissive hypercapnia. Rising plateau pressures with hypotension suggest breath-stacking -- briefly disconnect the circuit to allow full exhalation.

VTE Prophylaxis and Prevention

Because most pulmonary emboli originate from a DVT, prevention is a core ICU responsibility. Mechanical prophylaxis (sequential compression devices) and pharmacologic prophylaxis (low-dose heparin or LMWH) are standard unless contraindicated by active bleeding. Early mobility, adequate hydration, and removing unnecessary central lines lower risk further. Recognize DVT signs -- unilateral calf swelling, warmth, and tenderness -- and never massage a suspected clot.

Spontaneous Pneumothorax and Auto-PEEP Recap

A primary spontaneous pneumothorax classically strikes tall, thin young smokers from a ruptured bleb; a secondary one complicates COPD or other lung disease and is more dangerous because pulmonary reserve is already low. On the ventilator, the shared danger across asthma, COPD, and any obstructive process is auto-PEEP: incomplete exhalation stacks breaths, raises intrathoracic pressure, and drops cardiac output. The fix is always to lengthen expiratory time -- lower the rate, shorten inspiratory time, and treat the bronchospasm -- rather than adding tidal volume. Apply the right escalation order in obstructive crises: optimize inhaled bronchodilators and corticosteroids first, add IV magnesium for severe asthma, and reserve intubation for exhaustion, a silent chest, or a climbing PaCO2. Once intubated, a low rate with permissive hypercapnia guards against the hemodynamic collapse that auto-PEEP can trigger.