Acute respiratory disease Notes

NOTES NOTES ACUTE RESPIRATORY DISEASE GENERALLY, WHAT IS IT? DIAGNOSIS PATHOLOGY & CAUSES ▪ Acute respiratory disorders induced by changes in atmospheric pressure/direct communication between atmosphere, vasculature/pulmonary conditions, diseases (e.g. pulmonary trauma, pneumonia, sepsis, severe burns) ▪ Impaired alveolar gas exchange → hypoxemia ▪ Can lead to potentially fatal conditions SIGNS & SYMPTOMS ▪ Hypoxemia: dyspnea, tachypnea, chest pain DIAGNOSTIC IMAGING ▪ Medical imaging OTHER DIAGNOSTICS ▪ Clinical presentation, history ▪ Arterial blood gases TREATMENT OTHER INTERVENTIONS ▪ Oxygen therapy ▪ Mechanical ventilation ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) osms.it/ards PATHOLOGY & CAUSES ▪ Acute lung condition ▪ Widespread diffuse inflammation → increased vascular permeability, loss of pulmonary tissue ▪ Triggered by pulmonary conditions, diseases (e.g. pulmonary trauma, pneumonia, sepsis) PATHOLOGY ▪ Refractory hypoxemia, reduced pulmonary compliance, pulmonary edema without cardiovascular cause (noncardiogenic pulmonary edema) ▪ Alveolar barrier cells damaged → alveolar sacs flooded → impairs air exchange ▫ Pro-inflammatory cytokines released: tumor necrosis factor (TNF), interleukins ▫ Interleukins (IL-1, IL-6, IL-8) → neutrophil activation → toxic substances (reactive oxygen species) released → alveolar and capillary damage → oncotic gradient lost → no fluid resorption → fluid in interstitium ▪ Damaged Type II pneumocytes → surfactant layer malfunction OSMOSIS.ORG 867

▪ Acute inflammatory response → abnormal extravascular fibrin deposition ▫ Increased activity of extrinsic coagulation pathway ▫ Impaired fibrinolysis CAUSES ▪ Systemic infections/septic shock ▪ Acute lung injury ▫ Compromises ability to regulate gas exchange → lungs fill up with fluid in interstitium, alveoli ▪ Gastric contents aspiration ▪ Severe pneumonia ▪ Serious burns ▪ Mechanical (e.g. near drowning) ▪ Inflammatory (e.g. pancreatitis) SIGNS & SYMPTOMS ▪ Usually begin within first few hours, 1–2 days ▪ Dyspnea, tachypnea, tachycardia, diaphoresis, low blood oxygenation → cyanosis, diffuse crackles on lung auscultation DIAGNOSIS DIAGNOSTIC IMAGING Chest X-rays ▪ Bilateral alveolar infiltrate, pulmonary edema with no cardiovascular cause CT scan ▪ Bilateral airspace opacities Ultrasound ▪ Subpleural consolidations, pleural line irregularities, no lung gliding LAB RESULTS ▪ Respiratory alkalosis → respiratory acidosis 868 OSMOSIS.ORG Figure 123.1 A chest radiograph demonstrating diffuse, bilateral, coalescent opacities resembling ground glass. OTHER DIAGNOSTICS 2012 Berlin definition ▪ Acute pulmonary injury within week of clinical consultation ▪ Bilateral opacities on chest X-ray/CT scan unexplained by other pulmonary pathologies (e.g. pleural effusion, lung collapse) ▪ Respiratory failure without heart failure (noncardiogenic) ▪ Minimum positive end expiratory pressure (PEEP) of 5cmH20 ▪ Reduced oxygen in arteries, reduced partial pressure arterial oxygen/fraction of intake of oxygen (PaO2/FiO2) ratio ▫ Mild: 201–300mmHg ▫ Moderate: 101–200mmHg ▫ Serious: < 100mmHg TREATMENT MEDICATIONS ▪ Antibiotic therapy ▫ After microbiological culture, determines appropriate course of antibiotics ▪ Diuretics ▫ Manage fluid output

Chapter 123 Acute Respiratory Disease OTHER INTERVENTIONS Figure 123.2 The histological appearance of diffuse alveolar damage, the pathological correlate of ARDS. There is a diffuse inflammatory cell infiltrate and pink, hyaline membranes in the alveolar spaces. Mechanical ventilation ▪ Maintain gas exchange to meet metabolic demands ▪ Endotracheal intubation/tracheostomy (prolonged intubations) ▪ Monitor parameters ▫ PEEP: keep alveoli from collapsing, improve oxygenation ▫ Mean airway pressure: recruit alveoli to open ▫ Plateau pressure: monitor alveoli for overdistension ▪ Extracorporeal membrane oxygenation (ECMO) ▫ Removes blood from body, artificially removes CO2, oxygenates red blood cells Figure 123.3 The gross pathological appearance of ARDS. There is a diffuse, vaguely nodular infiltrate, most easily visible at the apices. OSMOSIS.ORG 869

ALTITUDE SICKNESS osms.it/altitude-sickness PATHOLOGY & CAUSES ▪ Reaction to exposure to low oxygen concentrations when traveling to high altitude ▫ AKA high altitude illness (HAI), acute mountain sickness (AMS) ▪ Partial pressure of oxygen of inspired air calculated by PiO2 (mmHg) = FiO2 (%) x [Pb (mmHg) - 47mmHg] ▫ FiO2: fraction of inspired oxygen, not affected by altitude, remains unchanged in 21% ▫ Pb: barometric pressure ▫ 47mmHg: vapor pressure of water at 37°C/98.6°F ▪ In high altitudes, ↓ Pb → ↓ PiO2 ▪ Partial pressure of alveolar oxygen (PAO2) ▫ Pressure in alveolar space after equilibration with blood ▪ PAO2 lower than PiO2 ▫ Air enters lungs, humidified by upper airway, partial pressure of water vapor reduces partial pressure of oxygen ▫ Continual uptake of oxygen from alveoli by pulmonary capillaries ▫ Continual diffusion of CO2 from capillaries into alveoli ▪ ↓ PiO2 → ↓ PAO2, ↓ PaO2 → hypoxemia ▪ HAI starts at 1.5km/5,000ft, symptoms noticeable above 2.4km/8,000ft Adaptive mechanisms ▪ Hypoxemia → hyperventilation → ↑ expiration of CO2 by lungs → ↓ PCO2 → ↑ pH (respiratory alkalosis) ▪ ↓ PCO2 , ↑ pH inhibit central, peripheral chemoreceptors, decrease ventilation rate ▪ Within several days ↑ HCO3-, ↓ H+ kidney excretion → ↓ pH → stimulation of respiratory center to further increase ventilation ▪ ↑ erythropoietin production → ↑ red blood 870 OSMOSIS.ORG cell production ▪ ↑ 2,3 BPG synthesis → ↓ hemoglobin affinity for O2 → ↑ release of oxygen to tissues Measures to avoid HAI ▪ Acclimatization: ascending slowly to high altitudes, to adjust to decreasing oxygen levels ▪ Preventative medications: acetazolamide (diuretic); increases bicarbonate kidney excretion RISK FACTORS ▪ ▪ ▪ ▪ History of HAI episodes Prior exercise/alcohol consumption Rapid ascent to high altitude Comorbidities that affect breathing (e.g. asthma) COMPLICATIONS ▪ Can lead to potentially fatal conditions ▫ High altitude cerebral edema (HACE), high altitude pulmonary edema (HAPE) SIGNS & SYMPTOMS ▪ Usually appear within 6–12 hours of ascent ▪ Headache, dizziness, fatigue, nausea, vomiting, loss of appetite, sleep disturbance ▪ Often improves with time if person does not ascend to higher altitude ▪ HACE ▫ Excessive fatigue, confusion, neurologic deficits (e.g. ataxia, altered mental state) ▪ HAPE ▫ Dry cough, dyspnea

Chapter 123 Acute Respiratory Disease DIAGNOSIS LAB RESULTS ▪ Arterial blood gases ▫ ↓ PaO2, ↑ PaCO2, respiratory alkalosis OTHER DIAGNOSTICS ▪ Clinical presentation, history of living at low altitude, recent ascent at high altitude TREATMENT MEDICATIONS ▪ Symptom relief ▫ E.g. analgesics for headache, antiemetics for nausea ▪ Carbonic anhydrase inhibitors (e.g. acetazolamide) ▫ Increase HCO3- excretion; treat respiratory alkalosis Figure 123.4 A chest radiograph demonstrating acute pulmonary edema in an individual who ascended to 2700m. OTHER INTERVENIONS ▪ Rest ▪ Descent ▪ Symptom relief ▫ E.g. oxygen to improve breathing ▪ HACE, HAPE ▫ Medical emergencies; require immediate descent/oxygen administration DECOMPRESSION SICKNESS (DCS) osms.it/decompression_sickness PATHOLOGY & CAUSES ▪ Gas embolism, occurs when individuals experience sudden decreases in atmospheric pressure ▫ AKA diver’s disease ▪ Air breathed at relatively high pressure (e.g. diver descends from water surface) → inspired gases compressed to higher pressure of surrounding water → ↑ partial pressure of oxygen, nitrogen → ↑ oxygen, nitrogen dissolved in blood, loaded in body tissues ▫ Henry’s law: at constant temperature, amount of gas dissolved in liquid directly proportional to partial pressure ▪ If oxygen, nitrogen quantities high enough → oxygen toxicity/nitrogen narcosis, respectively OSMOSIS.ORG 871

▪ Pressure drops too rapidly (e.g. ascent to water surface) → sum of gas tensions in tissue exceeds ambient pressure → liberation of free gas from tissues due to excess dissolved gases → gas bubbles → vessels blocked, tissues compressed, clotting cascade, inflammation ▪ Occurs in scuba, deep sea divers, underwater construction workers; during rapid ascent of an unpressurized aircraft ▪ Caisson disease (chronic decompression sickness) ▫ Tunnel workers, moving from caisson to atmospheric pressure RISK FACTORS ▪ Right-to-left shunt (e.g. patent foramen ovale/atrial/ventricular septal defect) ▪ Air travel after diving ▪ More common in individuals who are biologically male SIGNS & SYMPTOMS ▪ Usually develop within one hour of surfacing ▪ Excessive fatigue, headache ▪ Depend upon size, location of gas bubbles Type I DCS ▪ Skeletal muscles, joints ▫ Painful condition, AKA “the bends”; arching of back, posture reminiscent of Grecian bend ▪ Skin ▫ Itching, rash Type II DCS (more severe) ▪ Nervous system ▫ Paresthesia, amnesia, weakness, paralysis ▪ Lungs ▫ Edema, hemorrhage, atelectasis, emphysema → respiratory distress, AKA “the chokes”; cough, chest pain, dyspnea ▪ Can progress to permanent injuries/fatal damage 872 OSMOSIS.ORG DIAGNOSIS OTHER DIAGNOSTICS ▪ Clinical presentation, history of exposure to sudden decreases in atmospheric pressure ▪ Confirmed if symptoms relieved after recompression TREATMENT OTHER INTERVENTIONS ▪ Hyperbaric oxygen therapy in recompression chamber ▫ Under high pressure gas bubbles forced back into solution; slow decompression permits gradual gas elimination via lungs, prevents obstructive bubbles reforming

Chapter 123 Acute Respiratory Disease OSMOSIS.ORG 873