hemoptysis, vague symptoms Partial or complete occlusion of blood flow in pulm artery from DVT lower extremities; tissue frag, foreign body, air, fat embolus from fx, amniotic fluid; triggers released of serotonin, histamine, catecholamines, ang II inflam mediators, toxic oxygen free radicals— vasoconstriction, impedes blood flow, increase in pulm art pressure— RV dilation, increased afterload, V/Q mismatch, decrease in surfactant, atelectasis, hypoxemia, lung infarction,
decreased CO, shock, death Pulmonary Edema Left sided HF, ARDS, inhalation of toxic gases causing cap injury-fluid to alveolar space Dyspnea, CP, hypoxia, orthopnea, paroxysmal nocturnal dyspnea, rales, dullness to percussion, S3 heart sound, frothy sputum Accumulation of water in alveolar sacs; prevents exchange of gases HF- back up of blood into lungs, increase cap hydrostatic pressure, pushes fluid out of alveolar sacs Post-obs pulm edema- relieving airway obs, inspiration against occluded airway- excessive intrathoracic neg pressure- increase venous return to R side heart-increase pulm blood volume/pressure= edema Differentiate between the etiology, clinical manifestations, and pathophysiology of pneumothorax and pleural effusion: Disease Etiology Clinical Manifestations Pathophysiology Pneumothorax Primary Secondary Iatrogenic Tension Spontaneous-occur in young 20-40, tall thin males, result of bleb rupture in person with emphysema, smoking; bleb rupture usually at apexes-during exercise, rest or while asleep- rupture allows air in, family hx/genetic Sudden pleural pain, tachypnea, dyspnea, decreased breath sounds, hyperresonance to percussion Complete lung collapse- deviated trachea, SOB, low BP Presence of air/gas in pleural space, air may cause lung to collapse completely 2ndary- trauma; tension pneumo-air becomes trapped in thoracic cavity and cant escape; site of injury on pleural injury acts as one way valve(air in); complete lung collapse may occur Pleural Effusion Respiratory Failure
2. Evaluate the difference between the etiology, clinical manifestations, and pathophysiology of hypoxic and hypercapnic respiratory failure, ARDS and acute lung injury. Acute resp failure-direct injury, triggered by injury or dsyfxn of one or more body system/organ, post op 2ndary to anesthesia/narcotics; main dysfxn is impairment in diffusion resulting in low o2 or high CO2; most pulm dx can cause resp failure as well as brain/spinal cord injuries Disease Etiology Clinical Manifestations Pathophysiology Hypoxic Respiratory Failure PaO2<50mmHg, caused by pulmonary edema, embolus, PNE Inadequate diffusion of oxygen from alveoli to capillary Hypercapnic Respiratory Failure PaCO2>50mmHg , resp dep by meds (opiods/benzos), abn of spinal cord conducting system, medulla, dx of neuromuscular junction, chest wall abn, obs of lg airways or COPD Inadequate alveolar ventilation Acute Lung Injury / Acute Respiratory Distress Syndrome (ARDS) (elderly & immunocompromised have high mortality) PNE, burns, aspirations, DIC, pancreatitis, inhaled toxic gases Indirect from circulating inflammatory
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