hemoptysis vague symptoms Partial or complete occlusion of blood flow in pulm

Hemoptysis vague symptoms partial or complete

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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,
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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
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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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