N4S1 Critical Care: ARDS, Pulmo Embolism, Respi Failure

ARDS

Severe inflammatory process causing diffuse alveolar damage with sudden progressive pulmonary edema, refractory hypoxemia, and reduced lung compliance.

Acute lung injury

Term commonly used to describe mild ARDS.

Exudative phase

First 24–48 hours after injury: alveolar-capillary membrane damage, protein-rich fluid leakage into alveoli, loss of surfactant, atelectasis, refractory hypoxemia.

Proliferative phase

Occurs ~2–7 days after injury: Type II alveolar cell proliferation, granulation tissue, thickened alveolar walls, ↓ lung compliance, possible pulmonary hypertension.

Fibrotic phase

End-stage with extensive fibrosis/scarring, alveoli replaced by collagen → very stiff noncompliant lungs and long-term respiratory insufficiency.

ARDS pathophysiology

Inflammatory mediators injure alveolar-capillary membrane → fluid/protein/inflammatory cells flood alveoli, surfactant dysfunction, V/Q mismatch, intrapulmonary shunting → refractory hypoxemia.

Phase 1 (ARDS)

Injury reduces normal lung blood flow; platelets aggregate and release histamine, serotonin, bradykinin.

Phase 2 (ARDS)

Released substances inflame and damage alveolar-capillary membrane, increasing capillary permeability and shifting fluid to interstitium.

Phase 3 (ARDS)

Capillary permeability increases further; proteins and fluids leak into alveoli, raising interstitial osmotic pressure and causing pulmonary edema.

Phase 4 (ARDS)

Decreased blood flow and alveolar fluid damage surfactant production → alveolar collapse (atelectasis) and impaired gas exchange.

Phase 5 (ARDS)

Oxygenation is severely impaired while CO₂ can still cross membranes; blood O₂ and CO₂ levels become low.

Phase 6 (ARDS)

Pulmonary edema worsens and inflammation causes fibrosis → gas exchange is further impeded.

ARDS hallmark

Hypoxemia that does not improve with supplemental oxygen and occurs without elevated left atrial pressure.

PaO2/FiO2 >200 but ≤300 mmHg

ARDS is classified as ___ (mild ARDS).

PaO2/FiO2 >100 but ≤200 mmHg

ARDS is classified as ___ (moderate ARDS).

PaO2/FiO2 ≤100 mmHg

ARDS is classified as ___ (severe ARDS).

Chest X-ray (ARDS)

Bilateral infiltrates that can progress to a ground-glass appearance and eventual “white-out” of both lung fields.

Alveolar dead space (ARDS)

Increased dead space → ventilation without perfusion, worsening gas exchange.

Lung compliance (ARDS)

Decreased (“stiff lungs”), making ventilation more difficult.

ABG initial (ARDS)

PaO₂ < 60 mmHg and PaCO₂ < 35 mmHg (as initial pattern noted in the file).

ABG later (per file)

Later findings include changes noted in ABG such as PaO₂ values and ↓ HCO₃⁻ (<22 mEq/L) with persistent hypoxemia despite therapy.

BNP test (ARDS)

Plasma BNP can help distinguish ARDS from cardiogenic pulmonary edema.

Echocardiography (ARDS)

Transthoracic echo used when BNP is inconclusive to evaluate cardiac contribution to pulmonary edema.

Oxygen therapy (ARDS)

Start supplemental O₂ and escalate as hypoxemia worsens; mainstay supportive therapy.

Endotracheal intubation & mechanical ventilation

Primary life-saving therapy in severe ARDS to maintain oxygenation and ventilation.

PEEP purposes

Keeps alveoli open, increases functional residual capacity, improves oxygenation, reduces V/Q mismatch, and allows lower FiO₂ to avoid oxygen toxicity.

Ventilation goal (ARDS)

Target PaO₂ > 60 mmHg or SpO₂ > 90% using the lowest FiO₂ possible.

Circulatory support (ARDS)

Treat hypotension from hypovolemia or high PEEP; give fluids cautiously; use inotropes/vasopressors if needed.

Monitoring (ARDS)

Serial ABGs, pulse oximetry, ventilator settings, hemodynamics, intake/output, sputum, labs, and chest imaging.

Neuromuscular blocking agents

Used to improve patient-ventilator synchrony, reduce oxygen consumption, and help manage severe hypoxemia.

Inhaled nitric oxide

Inhaled pulmonary vasodilator that can transiently improve oxygenation and reduce V/Q mismatch.

35–45 kcal/kg/day

Caloric requirement for patients with ARDS is ___ per day (enteral feeding preferred).

Enteral feeding

Preferred route for nutrition in ARDS; parenteral used if enteral not possible or insufficient.

Nursing — airway care (ARDS)

Maintain patent airway, perform tracheal suctioning and ET tube care per facility policy.

Nursing — PEEP caution

PEEP may lower cardiac output — monitor for hypotension, tachycardia, and ↓ urine output; suction only as needed to maintain PEEP.

Prone positioning (ARDS)

Repositioning (including prone) to improve alveolar recruitment and oxygenation in selected patients.

Pulmonary embolism (PE)

Obstruction of the pulmonary artery or its branches by a thrombus (or other embolus) that reduces blood flow, causes V/Q mismatch, and leads to hypoxemia.

Embolus origin (PE)

Most commonly a dislodged deep vein thrombosis (DVT) from the venous system.

Other emboli types

Air, fat, amniotic fluid, and septic emboli are possible non-thrombotic causes.

Gas exchange disruption (PE)

Obstruction increases alveolar dead space: ventilation continues but perfusion decreases or is absent.

Hemodynamic consequences (PE)

↑ Pulmonary vascular resistance → pulmonary hypertension → right ventricular strain/failure → ↓ cardiac output → systemic hypotension/shock.

Pulmonary infarction (PE)

Multiple small emboli may cause pulmonary infarctions with ischemic necrosis of lung tissue.

Dyspnea (PE)

Most frequent symptom; often sudden in onset.

Tachypnea (PE)

Most common sign on exam.

Chest pain (PE)

Often sudden and pleuritic; can be substernal and mimic angina.

Cough / hemoptysis (PE)

Cough may occur and sputum can be blood-tinged.

Cardiac signs (PE)

Tachycardia, weak/rapid pulse, hypotension, palpitations, syncope; with large embolus — JVD and RV strain signs.

Systemic symptoms (PE)

Fever (low-grade), diaphoresis, anxiety, restlessness, lightheadedness, pallor, cyanosis.

Peripheral DVT signs

Warmth, tenderness, redness, and edema of the affected lower leg.

33%

About ___ of people with a pulmonary embolism die before the condition is diagnosed and treated.

D-dimer (PE)

Blood test often elevated in PE but nonspecific — useful to rule out PE in low-risk patients.

ABG (PE)

May show hypoxemia and hypocapnia (from tachypnea) but can also be normal.

CT Pulmonary Angiography (MDCTA)

Gold standard imaging for rapid, high-quality visualization of pulmonary arteries and parenchyma.

V/Q scan

Ventilation-perfusion scan used when contrast is contraindicated (e.g., renal failure or allergy); sensitive but less specific than MDCTA.

Pulmonary angiography

Invasive definitive test showing filling defects or abrupt cutoffs; requires specialized team.

Doppler ultrasound (legs)

Identifies DVT as a source of PE.

Echocardiogram (PE)

Detects right ventricular strain or dysfunction secondary to PE.

Chest X-ray (PE)

Often normal; may show infiltrates, atelectasis, pleural effusion or elevated hemidiaphragm — mainly used to rule out other causes.

ECG (PE)

May show sinus tachycardia, nonspecific ST-T changes, right axis deviation, RBBB, or atrial fibrillation.

Anticoagulant therapy (PE)

Mainstay treatment to prevent new clots and extension of existing thrombus (LMWH, UFH, DOACs).

Initial anticoagulants (PE)

LMWH (e.g., enoxaparin), unfractionated heparin (UFH), or DOACs (dabigatran, rivaroxaban, apixaban, edoxaban).

Long-term therapy (PE)

Warfarin (INR monitoring) or DOACs; duration typically 3–6 months, longer if high risk.

Monitoring (PE therapy)

Monitor PT/INR, aPTT, and platelet counts as appropriate for the chosen anticoagulant.

Thrombolytic therapy (PE)

tPA and similar agents used in hemodynamically unstable or massive PE to rapidly lyse clot; carries major bleeding risk.

Thrombolytic contraindications (PE)

Recent stroke, intracranial disease, active bleeding, recent surgery/trauma, labor, severe uncontrolled HTN.

Embolectomy (PE)

Catheter-based or surgical removal of clot for patients with contraindications to thrombolysis or persistent instability.

IVC filter (PE)

Consider for recurrent PE despite anticoagulation or contraindication to anticoagulants; not recommended as initial therapy.

Supportive care (PE)

Oxygen for hypoxemia, hemodynamic support (fluids/vasopressors), and prevention of DVT (compression stockings, early ambulation).

Stable PE management

Hemodynamically stable → immediate anticoagulation; some low-risk patients may be outpatient-managed with follow-up.

Unstable PE management

Hemodynamically unstable (massive PE) → emergent stabilization, thrombolytics or embolectomy.

PE complications

Pulmonary infarction, pulmonary hypertension, embolic extension, hepatic congestion/necrosis, abscess, ARDS, right-sided heart failure, death.

Nursing (thrombolytic monitoring)

Monitor VS frequently during infusion, maintain bed rest, observe for bleeding, and perform coagulation tests (INR/aPTT) after infusion start.

Nursing (oxygen & respiratory support in PE)

Provide continuous oxygen, monitor SpO₂, encourage deep breathing and incentive spirometry, and mobilize secretions as indicated.

Respiratory failure

Sudden, life-threatening deterioration of gas exchange in the lungs resulting in inadequate oxygenation or ventilation for the blood.

50% ≈ ___ mortality rate for patients with respiratory failure admitted to the intensive care unit.

Chronic respiratory failure

Develops over days or longer allowing renal compensation with ↑ bicarbonate; pH only slightly decreased; common causes include COPD and neuromuscular disease.

Acute hypercapnic respiratory failure

Develops minutes to hours and requires immediate attention; often severe with pH <7.3.

Type I respiratory failure (hypoxemic)

PaO₂ < 60 mmHg with normal or low PaCO₂; primarily oxygenation failure.

Type II respiratory failure (hypercapnic)

PaCO₂ > 50 mmHg with associated hypoxia; ventilation failure leading to CO₂ retention.

Type III respiratory failure (perioperative)

Perioperative resp. failure due mainly to atelectasis after anesthesia, pain, sedatives, or immobility.

Type IV respiratory failure (due to shock)

Inability to oxygenate tissues because of shock (e.g., sepsis, severe blood loss, cardiac events) leading to pulmonary edema and organ hypoperfusion.

Respiratory failure pathophysiology cascade

Impaired ventilation/perfusion → PaO₂

RF risk factors

Accumulated secretions, airway irritants, bronchospasm, CNS depression, COPD, endocrine disorders, heart failure, pulmonary emboli, respiratory infections, thoracic abnormalities, sedative/anesthesia effects.

Early signs of RF

Falling SpO₂ below baseline, dyspnea at rest, air hunger, tachypnea, tachycardia, hypertension, restlessness, anxiety, headache, accessory muscle use.

Late signs of RF

Neurologic depression (lethargy, somnolence, coma), bradypnea, bradycardia, hypotension, cyanosis/mottling, poor respiratory effort, cardiac arrest.

ABG in RF (assessment per file)

pO₂ < 60 mmHg and pCO₂ > 45 mmHg; indicates hypoxemia and hypercapnia in many patients with respiratory failure.

Lab & imaging in RF

Check hemoglobin/hematocrit, blood/sputum cultures, chest X-ray for underlying causes (emphysema, atelectasis, pneumothorax, infiltrates, effusion).

ECG in RF

May show arrhythmias, cor pulmonale, or myocardial ischemia which contribute to respiratory compromise.

Mechanical ventilation (RF)

Endotracheal intubation or tracheostomy with ventilator support to maintain adequate oxygenation/ventilation while treating the underlying cause.

Antacids / H2 blockers (RF)

Given to prevent/treat stress ulcers in critically ill patients.

Antibiotics (RF)

Used to treat or prevent bacterial lung infections that can cause or worsen respiratory failure.

Bronchodilators (RF)

Relax airway smooth muscle to improve airflow in bronchospasm-related respiratory compromise.

Corticosteroids (RF)

Decrease airway inflammation in acute COPD/exacerbations contributing to respiratory failure.

Diuretics (RF)

e.g., furosemide — remove excess fluid, especially when heart failure contributes to pulmonary edema.

Positive inotropes & vasopressors (RF)

Support heart function and blood pressure in hypotension/shock causing respiratory compromise.

Nursing — continuous assessment (RF)

Continuous VS and full-body system assessments since hypoxemia affects all organs.

Nursing — weights & edema (RF)

Daily weight and peripheral edema assessment are key indicators of fluid status and overload.

Nursing — airway & suctioning (RF)

Administer ordered O₂ and humidification, maintain airway, and suction ET/trach after hyperoxygenation as needed.

Nursing — rehabilitation & secretion clearance (RF)

Encourage pursed-lip breathing, incentive spirometry, reposition q1–2h, postural drainage, and chest physiotherapy to mobilize secretions.

Nursing — prevention measures (RF)

Strict intake/output, oral care at least once per shift to prevent ventilator-associated pneumonia, IV fluids and urinary catheter for close monitoring when indicated.