Acute respiratory disease Notes


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Acute respiratory distress syndrome

Decompression sickness

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) 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 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) 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

Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Acute respiratory disease essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Acute respiratory disease by visiting the associated Learn Page.