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Flashcards in Pulmonary Deck (23)
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-Lower resp track infection, viral, usually rsv or influenza, Starts as URI -> progresses
-CXR: peribronchial thickening, bronchial wall thickening, hyperexpansion, patchy atelectasis
-Supportive care - not recommending using bronchodilators, rac epi or corticosteroids



-Infection of subglottic airway, larynx, trachea, bronchi
-Common causes - para flu t1 and t2
-Mucosal airway edema ->epithelial necrosis -> decreased airway diameter and increased air resistance
-Barky cough, worse at night
-XR: lateral neck film with "steeple sign"***
-Humidified or cool mist, rac epi, heliox
****dexamethasone 0.6mg/kg IV/IM x1****



-Chronic reversible disorder resulting in inflammation, bronchoconstriction, airway hype-responsiveness
-Triggers: extrinsic (allergic), intrinsic (infection, viral more likely), exercise induced


Status asthmaticus

-Progressively worsening bronchospasm/ airway flow obstruction unresponsive to standard therapy
-Cough, esp at night that wakes child up, Pulsus paradoxus (mod/severe) r/t lower airway obstruction, Fever if associated with infectious trigger
-CXR: hyperinflation, flattened diaphragms, peribronchial thickening, narrowed cardiac silhouette -> air-trapping
-**anticipate hypocarbia/ respiratory alkalosis when compensating -> normal or rising CO2 measurement shows unable to compensate
-Mgmnt: supplemental O2, inhaled beta agonists (albuterol, levalbuterol - bronchial smooth muscle relaxation, reduce histamine release), corticosteroids (decrease inflammation), anticholinergic (atrovent - bronchodilation), magnesium sulfate (smooth muscle relaxation ... hypotension), heliox (low density gas, facilitates oxygen delivery), invasive ventilation (allow permissive hypercapnia)
**ketamine for induction --> bronchodilator effects**



-Bordatella pertussis - grm neg coccobacillus, toxin mediated disease (paralyzed cilia, causes inflammation), aerosolized droplets, v contagious, high risk when starting vaccinations
-3 stages: catarrhal, paroxysmal (cough at night, paroxysmal coughing spams, young infants present with apnea**), convalescence
-Diagnosis: DFA, PCR, CBC (leukocytosis, lymphocyte predominance)
-ABX: erythromycin (avoid in infants <1mo r/t hypertrophic, pyloric stenosis), clarithromycin, azithromycin ***
Post exposure antimicrobial prophylaxis for all persons within 21d of exposure



-H. Influenzae, staph aureus, strep pneumo
-severe inflammation of epiglottis, may obstruct breathing - sudden onset of symptoms, difficulty swallowing, drooling, dysphasia, tripod position
-XR: enlarged epiglottis and distended hypopharynx "thumbprint sign"**
-Avoid noxious stimuli, humidified O2, IVF, systemic steroids, abx (3rd gen cephalosporin plus vancomycin)


Retropharyngeal abscess

-Strep pyogenes, staph aureus, h flu
-follows trauma or infection, ages 1-5yr
-sore throat, fever, dysphagia, trismus, leukocytosis
-CT scan with IV contrast
-surgical drainage, broad spectrum ABX


Peritonsillar abscess

-local cellulitis progresses to abscess, older children/adolescents
-strep pyogenes, staph aureus, h flu
-swollen tonsils with uvula deviation (may obstruct airway), leukocytosis, threat culture for group a strep
-CT scan with IV contrast
-surgical drainage, ABX (ampicillin-sulbactam, clindamycin, vancomycin)**


Obstructive sleep apnea

-cessation of airflow
-d/t hypertrophy of tonsils +\- adenoids, craniofacial abnormalities, neurological abnormalities, decreased muscle tone, genetic disorders
-snoring, restless sleep, morning headaches (from chronic CO2 retention), pulmonary hypertension, cor pulmonale / right sided heart failure
-tx: tonsillectomy, adenoidectomy, cpap, bipap



-upper airway lacking cartilaginous rigidity (floppy), associated with feeding problems, expiratory stridor and cough, worse with agitation, harsh and barky cough, decreased symptoms when prone
- direct visualization when awake with flexible bronchoscope for airway collapse
-observation in most cases, resolution before 18months in most cases


Acutely respiratory distress syndrome (ARDS)

-injury to alveolar capillary membrane
-stages: exudative (injury to alveolar capillary barrier, increased pulmonary congestion, pulmonary edema, depletion of surfactant), proliferative (healing begins), fibrotic (remodeling, fibrotic scarring) --> leads to pulmonary hypertension, bronchoconstriction, hypovolemia, increased pulmonary vascular resistance
-ABG with PaO2/FiO2 ration <200 (predicts shunt), CXR with bilateral infiltrates
-Mgmnt: supportive care, ventilation (permissive hypercapnia, low tidal volumes, avoid PIP >30)


Cystic fibrosis

-autosomal recessive multi system disorder
-abnormal protein impairs movement of salt and water across epithelial walls in exocrine glands--> sticky secretions
-meconium ileus, cholestatic jaundice, nasal polyps, pancreatic insufficiency, chronic metabolic alkalosis
-Mgmnt: airway clearance techniques, high calorie unrestricted fat diet, pancreatic enzymes


Pulmonary embolism

-materials traveling in blood stream become lodged in pulmonary artery bed, thromboembolism most common
-decreased perfusion to affected alveolar units distal to emboli -> increased alveolar dead space -> impaired ability to eliminate CO2 -> ventilation/perfusion mismatch
-pleuritic chest pain, sense of doom, elevated d dimers**
-VQ scan, helical CT scan (useful if other lung disease present), evaluate for DVT
-Mgmnt: anticoagulation, thrombolysis, thrombectomy


Tracheoesophageal fistula

-congenital or acquired communication between trachea and esophagus
-associated GU defects (horseshoe kidney, polycystic kidney), GI defects (imperforated anus, duodenal atresia, malrotation), MSK defects, VATER syndrome (vertebral/vascular, anal atresia, tracheoesophageal fistula, esophageal atresia, renal or radial anomalies)
-symptoms worse with feeding
-pre-op: reduce risk of aspiration (continuous auctioning and gastric decompression) --> operative repair


ABG interpretation

Normal Values
-pH: 7.35-7.45
-CO2: 35-45
-HCO3: 22-26
-PaO2: 80-100

-measurement of oxygenation, ventilation, acid/base status


Respiratory acidosis

-CO2 retention: hypoventilation, CNS depression, trauma, COPD


Respiratory alkalosis

-excess CO2 loss: hyperventilation, anxiety, pain, fever, excessive ventilatory support


Metabolic acidosis

-increased acids: diabetic ketoacidosis, renal failure, lactic acidosis
-loss of base: diarrhea***


Metabolic alkalosis

-excess base: excess antacids, citrate in blood transfusions, sodium bicarbonate administration
-loss of acids: vomiting***, NG suctioning


Non-invasive ventilation

-positive pressure ventilation increases surface area available to participate in gas exchange, can stent open upper airways
-continuous positive airway pressure (CPAP): one set pressure throughout respiratory cycle
-bilevel positive airway pressure (BiPAP): higher pressure during inspiration, lower pressure in between respirations, keeps lungs open for entire respiratory cycle, can be timed or spontaneous


Invasive ventilation

-provide positive pressure and oxygenation, override work of breathing, monitor with capnography

-pressure support only: no rate, two leaves of pressure (one for inspiration and one for end of expiration and in between breaths)

-pressure control pressure support: set pressure with each breath, volume of breath depends of lung compliance

-volume control pressure support: set volume with each breath --> high pressure to achieve set volume indicate poor lung compliance


Invasive ventilator adjustments to eliminate more CO2

-increase rate (blow off more CO2)
-increase pressure control (increase size of breath delivered)
-increase tidal volume (increase size of breath delivered)
-decrease inspiratory time (shorter time for inspiration allows more time for expiration)


Invasive ventilator adjustments to increase oxygenation

-increase FiO2
-increase positive end expiratory pressure (PEEP)
-increase inspiratory time (increases mean airway pressure)