cells dt trauma sepsis blood transfusions ARDS most severe form ARDS bil lung

Cells dt trauma sepsis blood transfusions ards most

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cells d/t trauma, sepsis blood transfusions ARDS most severe form ARDS- bil lung infiltrates on CXR, low ratio PaO2 to fraction of inhaled o2, dypnea, hypoxemia, hyperventilation, resp alkalosis, organ dysfxn, metabolic acidosis, decreased tidal vol, hypercapnia, decreased CO, low BP Massive lung inflammation, disseminated alveolar capillary damage, impairs gas exchange, o2 problems, pulm edema, hypoxemia ARDS-3 phases
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1. Inflammatory- w/in 72hr, inflam cascade triggered by insult/injury to cap membranes- increase permeability—fluid, blood cells, proteins leak into interstitium/alveoli—impair gas exchange, surfactant inactivated/production impaired; lungs lose compliance, work of breathing increases, alveolar ventilation decreases, hypercapnia develops 2. Proliferative- 1-3 wks; pulm edema resolves, surfactant produced again; intra-alveolar exudate turns into cellular granulation tissue and worsens hypoxemia 3. Fibrotic-14-21 days; alveoli undergo fibrosis, causes decrease in pul fxn which may be permanent; leads to decrease in residual capacity and continuing V/Q mismatch with right to left shunting; causes pul HTN PF ratio classify dx PF 201-300= mild dx PF 101-200= moderate dx PF <100= severe dx Obstructive Respiratory Disorders 3. Explain the differences between the etiology, clinical manifestations and pathophysiology of asthma, chronic bronchitis, and emphysema. Disease Etiology Clinical Manifestations Pathophysiology Asthma Triggered by allergy, high among adult females, African Americans, people older than 65, familial, exposure to allergen during childhood Dyspnea, expiratory wheezing, asymptomatic b/w attacks-PFTs normal During- chest constriction, expiratory wheezing, prolonged expiration, tachy, tachypnea Severe attacks-accessory muscle use, inspiratory/expiratory wheezing Silent chest and PaO2<70mmHg= impending death IgE mediated rxn, airway narrows, cellular changes include bronchial smooth muscle hypertrophy, goblet cell hyperplasia, thickening/hyalinization of basement membranes, proliferation of eosinophils, bronchial mucous plugs, cause air trapping—decreased alveolar perfusion, increased alveolar gas pressure, decreased vent, decreased V/Q ratio, increased lung volumes- hyperventilation, lungs hyperexpanded-cause CO2 retention/resp acidosis----RESP FAILURE Chronic Bronchitis- blue Smoking-chronic irritant, Productive cough 3 consecutive mos Mucus secreting cells hyperplasia, secrete
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bloater COPD-obs of airflow; preventable/ tx occupational dusts, chemicals, indoor air pollutants; Hypoxemia, low tidal volumes, hypercapnia, hypoventilate, poor exercise tolerance, wheezing, dyspnea, decreased FEV1, polycythemia, cyanosis, pul HTN and cor pulmonale excessive amt of mucus, impaired ciliary fxn & viscosity makes it hard to clear, plug airway/impair o2; starts in lg airway to sm airway, airways narrow- obs and air retention, thorax expands, Emphysema-pink puffer inherited mutation in alpha 1 antitrypsin (look if nonsmoker and <40 y/o) Hypoxemia, hypercapnia, hypoventilation, pursed lipped breathing, tripod pos., high metabolic rate, shallow rapid resp, thin,
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