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acure respiratory distress syndrome non-cardiogenic pulmonary edema
Cor pulmonale R heart failure
hemoptysis coughing up blood
orthopnea difficulty breathing when lying down
paroxysmal nocturnal dyspnea difficulty breathing at night
positive end-expiratory pressure (PEEP) extrinsic PEEP uses an impedance valve to increase volume of air remaining in lungs at end of expiration to improve gas exchange
subcutaneous emphysema crackling under the skin upon palpation due to trapped air. typically found in chest, neck or face
tidal volume volume of air inhaled or exhaled w/each breath
Upper airway structures nasopharynx, oropharynx, larynx
lower airway structures larynx, trachea, bronchi, alveoli
inspiration active process of ventilation
exhalation passive process of ventilation
external respiration movement of o2 from the alveoli into the bloodstream and movement of CO2 from the blood stream to the alveoli
internal respiration exchange of gases between the bloodstream and the tissues in the body
normal adult tidal volume 500 mL
minute volume RR x TV
s/s of respiratory compromise tripod breathing cyanosis ALOC difficulty speaking full sentences difficulty breathing accessory muscle use(nasal flaring, intercostal retractions) abnormal resp. rate or TV SpO2 below 95% abnormal lungs sounds
management of respiratory compromise ABCs monitor SpO2 monitor ETCO2 monitor ECG O2 if hypoxia suspected IV access support ventilations consider Hs & Ts consider CPAP consider pharmacologic interventions as indicated transport
acute respiratory distress syndrome (ARDS) Pulmonary edema that can lead rapidly to fatal respiratory failure; causes include trauma, sepsis, OD, drowning, and toxic inhalation
s/s of ARDS progressive decline in respiratory status dyspnea ALOC, agitation, confusion fatigue pulmonary edema tachypnea tachycardia possible cyanosis low SpO2
management of ARDS monitor SpO2 position pt upright, legs dangling descending rapidly to lower altitude if HAPE suspected considering CPAP w/PEEP
pathophysiology of COPD slowly progressive respiratory disease w/high mortality rates includes emphysema and chronic bronchitis typically caused by smoking and environmental toxins
s/s of COPD possible hx of smoking or exposure to cigarette smoke cough w/increased mucus production air trapping w/prolonged expiratory phase signs of R heart failure, including JVD and pedal edema chronic dyspnea, worsening on exertion tachypnea accessory muscle use possible flushed or cyanotic skin pursed lip breathing low SpO2 abnormal lung sounds, such as diminished rhonchi clubbing of the fingers
management of COPD pts may have chronically low SpO2; target o2 admin to an SpO2 of about 95% only a small percent of COPD pts are on a hypoxic drive. bronchodilators such as albuterol or ipratropium are likely indicated CPAP may help avoid progression to respiratory failure and need for intubation or BVM ventilation
pathophysiology of asthma chronic inflammatory airway disease death rates rising not falling about half of all asthma deaths occur before reching the hospital triggers include allergens, exercise, foods, stress, and meds
s/s of asthma dyspnea wheezing cough pulsus paradoxus tachypnea tachycardia low SpO2
management of asthma monitor peak expiratory flow rates(PEFR) if possible aggressive use of bronchodilator meds are indicated to reverse bronchospasm
status asthmaticus severe, prolonger asthma attack not reversible w/bronchodilator meds
pneumonia lung infection often leading to death in elderly and immunosuppressed pts
s/s of pneumonia suspect pneumonia in any pt w/hx of chest pain w/associated fever, chills, or cough weakness cough pleuritic chest pain dyspnea tachypnea abnormal lung sounds
Management of Pneumonia dehydration is common, consider IV fluids
pathophysiology of PE blockage in a pulmonary artery that decreases blood flow, leading to potentially fatal hypoxemia
risk factors of PE prolonged immobility of the extremities recent surgery long bone fx smoking use of birth control meds
s/s of PE acute, unexplained dyspnea pleuritic chest pain cough presence of risk factors listed above tachypnea, often w/normal lung sounds tachycardia possible indications of deep veins thrombosis
management of PE aggressive o2 therapy prepare for possible sudden cardiac arrest rapid transport
pathophysiology of pneumothorax not related to blunt or penetrating trauma recurrence rate is high (50%) much more common in males and smokers
s/s of pneumothorax acute onset of sharp pleuritic chest pain or shoulder pain possible localized diminished lung sounds coughing fit or heavy lifting may precipitate symptoms tachypnea possible subcutaneous emphysema
management of pneumothorax closely monitor SpO2 o2 transport in position of comfort
Hyperventilation syndrome significant until confirmed otherwise; anxiety is most common cause, may other dangerous possibilities
s/s of hyperventilation syndrome tachypnea possible chest pain possible anxiety possible numbness possible carpopedal spasm due to alkalosis and hypocalcemia
causes of hyperventilation syndrome anxiety metabolic disorders respiratory disorders pulmonary emolism cardiac disorders CNS disorders various meds
management of hyperventilation syndrome supportive care monitor SpO2 and administer o2 as indicated transport breathing into a paper bag, breath holding or other attempts to raise the pts CO2 levels are NOT recommended
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