Pulmonary

What is Acute Respiratory Distress Syndrome (ARDS)?

ARDS is acute noncardiogenic pulmonary edema caused by diffuse alveolar-capillary membrane injury, producing refractory hypoxemia and bilateral infiltrates within one week of a known insult.

What are the Berlin diagnostic criteria for ARDS?

Onset within 1 week of a known clinical insult, bilateral opacities on chest imaging not fully explained by effusion or collapse, respiratory failure not fully explained by cardiac failure or fluid overload, and impaired oxygenation with PaO2/FiO2 ratio of 300 or less on at least 5 cm H2O PEEP.

How is ARDS severity graded by PaO2/FiO2 ratio?

Mild 201 to 300, moderate 101 to 200, severe 100 or less (all on PEEP of at least 5 cm H2O).

What is the most common cause of ARDS in the ED?

Sepsis (especially pneumonia); other causes include aspiration, trauma, pancreatitis, massive transfusion, and near-drowning.

What ventilator strategy reduces mortality in ARDS?

Low tidal volume lung-protective ventilation at 6 mL/kg predicted body weight with plateau pressure kept under 30 cm H2O, higher PEEP, and permissive hypercapnia.

What rescue therapy improves mortality in severe ARDS?

Prone positioning for 12 to 16 hours per day; neuromuscular blockade and ECMO are additional options in refractory cases.

How is ARDS distinguished from cardiogenic pulmonary edema at the bedside?

ARDS has normal cardiac filling pressures, normal or low BNP, no cardiomegaly or Kerley B lines, and does not improve with diuresis, whereas cardiogenic edema has elevated BNP, cardiomegaly, and responds to preload reduction.

What is Acute Respiratory Failure?

Acute respiratory failure is the inability of the respiratory system to maintain adequate oxygenation or ventilation, defined by PaO2 under 60 mm Hg or PaCO2 over 50 mm Hg with acidemia.

What distinguishes type I from type II respiratory failure?

Type I is hypoxemic failure (PaO2 under 60 mm Hg with normal or low PaCO2) from V/Q mismatch or shunt; type II is hypercapnic failure (PaCO2 over 50 mm Hg with respiratory acidosis) from inadequate alveolar ventilation.

What clinical findings signal impending respiratory arrest?

Altered mental status, inability to speak in full sentences, paradoxical abdominal breathing, silent chest, rising PaCO2 with fatigue, bradypnea, and cyanosis.

Which patients benefit most from noninvasive positive pressure ventilation?

COPD exacerbation with hypercapnic acidosis and cardiogenic pulmonary edema; NIPPV reduces intubation rates and mortality in these groups.

What are contraindications to NIPPV?

Cardiac or respiratory arrest, altered mental status with inability to protect the airway, active vomiting or upper GI bleeding, facial trauma or burns, and hemodynamic instability.

What is the standard rapid sequence intubation drug approach in respiratory failure?

Preoxygenate, then give an induction agent (etomidate or ketamine) immediately followed by a paralytic (succinylcholine or rocuronium), with ketamine preferred in bronchospasm and avoidance of succinylcholine in hyperkalemia, burns over 24 hours old, or crush injury.

What confirms correct endotracheal tube placement?

Sustained waveform capnography is the gold standard, supported by direct visualization of the tube through the cords, bilateral breath sounds, and chest radiograph for depth.

What is Hypoxia?

Hypoxia is inadequate oxygen delivery to the tissues, most often resulting from hypoxemia (low arterial oxygen content) but also from low cardiac output, anemia, or impaired oxygen utilization.

What are the five mechanisms of hypoxemia?

V/Q mismatch (most common), right-to-left shunt, hypoventilation, diffusion impairment, and low inspired oxygen tension such as high altitude.

Which cause of hypoxemia fails to correct with supplemental oxygen?

Right-to-left shunt (pneumonia consolidation, ARDS, pulmonary edema, atelectasis); V/Q mismatch and hypoventilation improve with oxygen.

How does the A-a gradient help localize the cause of hypoxemia?

A normal A-a gradient points to hypoventilation or low inspired oxygen, while a widened gradient indicates V/Q mismatch, shunt, or diffusion impairment; expected normal is roughly age divided by 4 plus 4.

When is pulse oximetry unreliable?

Carbon monoxide poisoning (falsely normal), methemoglobinemia (reads near 85 percent regardless of true saturation), severe anemia, poor perfusion, and certain dyes or nail polish.

What is the treatment of symptomatic methemoglobinemia?

Methylene blue 1 to 2 mg/kg IV; avoid in G6PD deficiency, where exchange transfusion or hyperbaric oxygen is used instead.

What oxygen delivery device provides the highest FiO2 without positive pressure?

Nonrebreather mask at 15 L/min delivers roughly 70 to 90 percent; high-flow nasal cannula delivers up to 100 percent with heated humidified flow and some PEEP effect.

What is Hypercapnia?

Hypercapnia is elevated arterial carbon dioxide (PaCO2 over 45 mm Hg) resulting from inadequate alveolar ventilation relative to CO2 production.

What are the major causes of acute hypercapnia in the ED?

Central respiratory depression (opioids, sedatives, CNS injury), neuromuscular weakness (myasthenic crisis, Guillain-Barré), chest wall restriction, and severe airway obstruction from COPD or asthma.

How do you distinguish acute from chronic hypercapnia on ABG?

In acute hypercapnia pH falls about 0.08 for every 10 mm Hg rise in PaCO2 with minimal bicarbonate change; in chronic hypercapnia the pH is near normal with a markedly elevated bicarbonate from renal compensation.

What are the clinical features of CO2 narcosis?

Headache, flushing, bounding pulses, asterixis, somnolence progressing to coma, and papilledema from cerebral vasodilation.

Why is uncontrolled high-flow oxygen risky in chronic hypercapnic COPD?

Excess oxygen worsens hypercapnia through V/Q mismatch and the Haldane effect (and to a lesser degree loss of hypoxic drive), so target SpO2 is 88 to 92 percent.

What is the first-line therapy for hypercapnic respiratory failure in COPD?

BiPAP, which unloads respiratory muscles and augments alveolar ventilation, reducing intubation rates and mortality.

What is permissive hypercapnia?

Deliberate acceptance of elevated PaCO2 and mild acidemia in obstructive disease or ARDS to avoid barotrauma and breath stacking, tolerating pH down to roughly 7.20.

What is Airway Obstruction?

Airway obstruction is partial or complete blockage of airflow anywhere from the nasopharynx to the bronchi, which may be caused by foreign body, edema, infection, secretions, mass, or loss of muscle tone.

What does the character of stridor localize?

Inspiratory stridor indicates extrathoracic (supraglottic or glottic) obstruction, expiratory stridor indicates intrathoracic obstruction, and biphasic stridor suggests fixed obstruction at the subglottis or trachea.

What are the danger signs of impending complete airway obstruction?

Stridor at rest, drooling, tripod positioning, muffled or hot potato voice, hoarseness, agitation, and accessory muscle use.

What distinguishes histaminergic from bradykinin-mediated angioedema?

Histaminergic angioedema has urticaria and pruritus and responds to epinephrine, antihistamines, and steroids; bradykinin-mediated angioedema (ACE inhibitor or hereditary C1 esterase inhibitor deficiency) has no urticaria and does not respond to those agents.

How is hereditary angioedema with airway involvement treated?

C1 esterase inhibitor concentrate, icatibant, or ecallantide; fresh frozen plasma is a backup when those are unavailable, and airway management takes priority.

What is the surgical airway of choice in a can't-intubate can't-oxygenate adult?

Cricothyrotomy through the cricothyroid membrane; in children under about 10 to 12 years needle cricothyrotomy with jet insufflation is preferred over surgical cricothyrotomy.

What is Foreign Body Aspiration?

Foreign body aspiration is inhalation of an object into the airway, most often food or small toys, producing sudden choking, coughing, and potentially complete obstruction.

Which age group and which bronchus are classically involved?

Children under 3 years are at highest risk, and aspirated objects most often lodge in the right mainstem bronchus because it is wider, shorter, and more vertical in adults and older children.

What radiographic findings suggest a bronchial foreign body?

Most objects are radiolucent, so look for unilateral hyperinflation with air trapping and mediastinal shift away from the affected side on expiratory or lateral decubitus films; a normal film does not exclude the diagnosis.

What is the management of a conscious adult with complete airway obstruction?

Abdominal thrusts (Heimlich maneuver) until the object is expelled or the patient becomes unresponsive, then begin CPR with airway inspection before each ventilation attempt.

How does foreign body relief differ in infants under 1 year?

Alternate 5 back blows with 5 chest thrusts; abdominal thrusts are avoided because of the risk of intra-abdominal organ injury.

What is the definitive management of a retained airway foreign body?

Rigid bronchoscopy for removal; flexible bronchoscopy may be used diagnostically in stable cooperative adults.

What is café coronary?

Sudden collapse during eating from complete upper airway obstruction by a food bolus, often mistaken for myocardial infarction because the patient cannot speak or cough.

What is Anaphylaxis?

Anaphylaxis is a rapid-onset, IgE-mediated systemic hypersensitivity reaction involving two or more organ systems or hypotension after allergen exposure, and it is potentially fatal.

What are the clinical diagnostic criteria for anaphylaxis?

Acute onset with skin or mucosal involvement plus either respiratory compromise or hypotension; or two or more organ systems involved after likely allergen exposure; or hypotension alone after exposure to a known allergen.

What is the first-line treatment and dose of epinephrine in anaphylaxis?

Epinephrine 0.3 to 0.5 mg of the 1 mg/mL (1:1000) concentration IM into the anterolateral thigh, repeated every 5 to 15 minutes as needed; pediatric dose is 0.01 mg/kg up to 0.3 mg.

What is the role of antihistamines and corticosteroids in anaphylaxis?

They are adjuncts only, treating cutaneous symptoms and possibly reducing prolonged symptoms; they never replace or delay epinephrine and do not prevent airway or cardiovascular collapse.

How is anaphylaxis refractory to IM epinephrine managed?

Start an IV epinephrine infusion, give aggressive IV crystalloid, and add glucagon 1 to 5 mg IV for patients on beta-blockers who fail to respond to epinephrine.

What is a biphasic reaction and how does it affect disposition?

Recurrence of symptoms typically 4 to 12 hours after resolution without re-exposure; patients are observed 4 to 6 hours or longer if severe presentation, and all are discharged with epinephrine autoinjectors and allergy follow-up.

What is Asthma Exacerbation?

An asthma exacerbation is an acute episode of reversible bronchospasm, airway edema, and mucus plugging producing wheezing, dyspnea, cough, and expiratory airflow obstruction.

What findings indicate a severe or life-threatening asthma exacerbation?

Inability to speak in full sentences, accessory muscle use, peak flow under 40 percent predicted, SpO2 under 90 percent, altered mental status, and a silent chest from minimal air movement.

Why is a normal or rising PaCO2 ominous in acute asthma?

Tachypneic asthmatics should be hypocapnic; a normalizing or rising PaCO2 signals respiratory muscle fatigue and impending respiratory failure.

What is the initial ED treatment of an asthma exacerbation?

Continuous or repeated inhaled short-acting beta-agonist, inhaled ipratropium for moderate to severe attacks, and early systemic corticosteroids (prednisone 40 to 60 mg PO or methylprednisolone IV) within the first hour.

What adjuncts are used in severe refractory asthma?

IV magnesium sulfate 2 g over 20 minutes, heliox, ketamine as the induction agent for its bronchodilating effect, and epinephrine IM in near-arrest presentations.

What ventilator strategy is used in intubated asthmatics?

Low respiratory rate, low tidal volume, high inspiratory flow with prolonged expiratory time, and permissive hypercapnia to prevent breath stacking and auto-PEEP.

What should you do if an intubated asthmatic suddenly becomes hypotensive?

Disconnect the ventilator to allow full exhalation of stacked breaths (auto-PEEP), push on the chest to assist exhalation, and evaluate for tension pneumothorax.

What is COPD Exacerbation?

A COPD exacerbation is an acute worsening of dyspnea, cough, or sputum production beyond baseline in a patient with chronic airflow limitation, most often triggered by infection.

What are the Anthonisen criteria for antibiotic use in COPD exacerbation?

Increased dyspnea, increased sputum volume, and increased sputum purulence; antibiotics are indicated with two or three cardinal symptoms (purulence must be one) or if mechanical ventilation is required.

What is the target oxygen saturation in COPD exacerbation?

88 to 92 percent, using controlled oxygen to avoid worsening hypercapnia and acidosis.

What intervention reduces mortality and intubation in COPD exacerbation with hypercapnic acidosis?

Noninvasive positive pressure ventilation (BiPAP).

What is the standard corticosteroid regimen for COPD exacerbation?

Prednisone 40 mg orally daily for 5 days; oral is as effective as IV in patients able to take PO.

What bronchodilators are used in COPD exacerbation?

Inhaled short-acting beta-agonist combined with a short-acting anticholinergic such as ipratropium.

What complications must be excluded in a COPD patient who deteriorates abruptly?

Pneumothorax (from bleb rupture), pulmonary embolism, pneumonia, and acute decompensated heart failure.

What is Bronchiectasis?

Bronchiectasis is permanent, irreversible dilation and destruction of bronchial walls from chronic infection and inflammation, resulting in impaired secretion clearance and recurrent infection.

What is the classic clinical presentation of bronchiectasis?

Chronic cough with copious foul-smelling purulent sputum, recurrent pneumonias, hemoptysis, and crackles with or without wheezing; digital clubbing may be present.

What are the major causes of bronchiectasis?

Cystic fibrosis (most common in the United States), prior severe or recurrent infection including tuberculosis, allergic bronchopulmonary aspergillosis, immunodeficiency, and ciliary dyskinesia.

What imaging finding confirms bronchiectasis?

High-resolution CT showing dilated thick-walled airways with the signet ring sign and tram-track opacities; chest radiograph may be normal or show nonspecific crowded markings.

Which organisms commonly colonize and infect bronchiectatic airways?

Haemophilus influenzae, Pseudomonas aeruginosa, Staphylococcus aureus, and nontuberculous mycobacteria.

How is an acute exacerbation of bronchiectasis managed in the ED?

Airway clearance and chest physiotherapy, bronchodilators, and antibiotics targeting prior sputum cultures with Pseudomonas coverage such as a fluoroquinolone when indicated.

How is massive hemoptysis from bronchiectasis managed?

Protect the airway, position the patient with the bleeding lung down to protect the healthy lung, correct coagulopathy, and arrange urgent bronchoscopy or bronchial artery embolization.

What is Carbon Monoxide Poisoning?

Carbon monoxide poisoning is tissue hypoxia caused by inhaled CO binding hemoglobin with roughly 240 times the affinity of oxygen, shifting the oxyhemoglobin curve left and impairing cellular respiration.

What is the classic presentation of CO poisoning?

Headache, nausea, dizziness, and flu-like symptoms without fever, often affecting multiple household members or pets simultaneously, especially in winter with faulty heaters or generator use.

Why can pulse oximetry and PaO2 be misleading in CO poisoning?

Standard pulse oximetry cannot distinguish carboxyhemoglobin from oxyhemoglobin and reads falsely normal, and PaO2 measures dissolved oxygen which is unaffected, so diagnosis requires co-oximetry carboxyhemoglobin level.

What is the initial treatment of CO poisoning?

High-flow 100 percent oxygen by nonrebreather or endotracheal tube, which reduces the CO half-life from about 4 to 5 hours on room air to roughly 60 to 90 minutes.

What are indications for hyperbaric oxygen therapy in CO poisoning?

Loss of consciousness, neurologic deficits, cardiac ischemia, severe metabolic acidosis, carboxyhemoglobin over 25 percent (or over 15 to 20 percent in pregnancy), and pregnancy with fetal distress.

What co-exposure must be considered in an enclosed-space fire victim with CO poisoning?

Cyanide toxicity, suggested by profound lactic acidosis and hemodynamic collapse; treat empirically with hydroxocobalamin, avoiding nitrites in patients with concurrent CO poisoning.

What is Inhalation Injury?

Inhalation injury is damage to the airway and lung parenchyma from heat, smoke particulates, and toxic gases, and it is the leading cause of early mortality in burn patients.

What findings predict airway compromise from inhalation injury?

Facial burns, singed nasal or facial hair, carbonaceous sputum, soot in the oropharynx, hoarseness, stridor, and closed-space exposure with loss of consciousness.

Why is early intubation emphasized in suspected inhalation injury?

Progressive airway edema over hours makes later intubation technically difficult or impossible, so intubate early when airway compromise is anticipated rather than waiting for failure.

What is the diagnostic gold standard for inhalation injury?

Fiberoptic bronchoscopy showing airway edema, erythema, soot, ulceration, or mucosal sloughing.

What are the three components of inhalation injury?

Upper airway thermal injury, lower airway and parenchymal chemical injury from smoke particulates, and systemic toxicity from carbon monoxide and cyanide.

Which fire-related toxin causes profound lactic acidosis with normal or high mixed venous oxygen saturation?

Cyanide, which inhibits cytochrome oxidase and blocks cellular oxygen utilization; treat with hydroxocobalamin.

What is Drowning?

Drowning is the process of respiratory impairment from submersion or immersion in liquid, with outcomes classified as fatal or nonfatal; terms such as near-drowning, wet, dry, and secondary drowning are obsolete.

What is the primary pathophysiologic insult in drowning?

Hypoxemia from laryngospasm, aspiration, and surfactant washout leading to pulmonary edema, atelectasis, and shunt physiology; the resulting hypoxia drives cardiac arrest and neurologic injury.

Does salt water versus fresh water drowning change ED management?

No; despite theoretical osmotic differences, clinically significant electrolyte and volume shifts are rare and management is identical, focused on oxygenation and ventilation.

How does drowning resuscitation differ from standard cardiac arrest care?

Because the arrest is hypoxic, begin with rescue breaths and prioritize airway and ventilation rather than compression-only CPR.

When is cervical spine immobilization indicated in drowning?

Only when there is a mechanism suggesting trauma such as diving, surfing, high-impact fall, or signs of injury or intoxication with unclear history; routine immobilization is not recommended.

What is the appropriate ED disposition of an asymptomatic drowning patient?

Observe for 4 to 6 hours with pulse oximetry; patients who remain asymptomatic with normal oxygen saturation and lung exam may be discharged.

What therapies are NOT recommended after drowning?

Prophylactic antibiotics and corticosteroids; antibiotics are given only for grossly contaminated water exposure or documented infection.

What is Blunt and Penetrating Chest Trauma?

Chest trauma is blunt or penetrating injury to the thoracic cage, lungs, heart, and great vessels, accounting for a large share of trauma mortality and often manageable with a chest tube rather than thoracotomy.

What are the immediately life-threatening chest injuries identified in the primary survey?

Airway obstruction, tension pneumothorax, open pneumothorax, massive hemothorax, flail chest with pulmonary contusion, and cardiac tamponade.

What is flail chest and what causes the associated hypoxia?

Three or more contiguous ribs fractured in two or more places producing paradoxical chest wall motion; hypoxia is driven mainly by the underlying pulmonary contusion, and treatment centers on analgesia, pulmonary toilet, and oxygenation.

How does pulmonary contusion present and evolve?

Hypoxia with patchy nonanatomic infiltrates that often lag 6 to 24 hours behind injury and peak at 24 to 72 hours; management is supportive with judicious fluids and oxygenation support.

What findings suggest traumatic aortic injury and what is the diagnostic test?

Widened mediastinum, loss of the aortic knob, left apical cap, deviation of the trachea or nasogastric tube to the right, and first or second rib fracture; CT angiography of the chest is the test of choice.

What are the indications for ED resuscitative thoracotomy?

Penetrating thoracic trauma with witnessed arrest or signs of life within roughly 15 minutes, or blunt trauma arrest with signs of life within about 10 minutes; outcomes are best with penetrating cardiac wounds.

How is an open pneumothorax (sucking chest wound) initially managed?

Apply an occlusive dressing taped on three sides to create a flutter valve, then place a chest tube at a separate site; a fully sealed dressing risks converting it to a tension pneumothorax.

What is Pneumothorax?

Pneumothorax is air in the pleural space causing partial or complete lung collapse, classified as spontaneous (primary or secondary), traumatic, or iatrogenic.

Who is at highest risk for primary spontaneous pneumothorax?

Tall thin young men who smoke, from rupture of apical subpleural blebs; secondary spontaneous pneumothorax occurs in COPD, cystic fibrosis, and Pneumocystis pneumonia.

What are the clinical findings of tension pneumothorax?

Severe respiratory distress, hypotension, distended neck veins, absent breath sounds and hyperresonance on the affected side, and late tracheal deviation away from the side of injury; it is a clinical diagnosis requiring immediate decompression before imaging.

Where is needle decompression performed?

Fifth intercostal space at the anterior axillary line is now preferred in adults, with the second intercostal space at the midclavicular line as an alternative, followed immediately by tube thoracostomy.

What is the deep sulcus sign?

An abnormally deep and lucent lateral costophrenic angle on a supine chest radiograph indicating an anterior pneumothorax in a patient who cannot sit upright.

Which imaging modality is most sensitive for pneumothorax in trauma?

Bedside ultrasound, showing absent lung sliding, absent comet-tail artifacts, and the lung point sign; it outperforms supine chest radiography.