Pulmonary Flashcards
A-a gradient
Description
Shorthand formula
A-a gradient = Measured PaO2 - Calculated PaO2
Quick A-a formula: 150 – (PaCO2 x 1.2 + PaO2)
Elevated A-a gradient ddx
V/Q Mismatch
–(PE, pneumonia, asthma)
Impaired O2 diffusion
–(interstitial pneumonia, PCP)
Right to Left Shunt
–(congenital heart disease)
Normal A-a gradient ddx
Hypoventilation
–(opioid OD)
Decreased FiO2
–(high altitude)
Central cyanosis clinically apparent with hemoglobin greater than
saturated carboxyhemoglobin looks like SaO2
saturated methemoglobin looks like SaO2
5 g/dL
100%
85%
Asthma pathophysiology
Bronchial *** and ***
Mucous ***
Increased *** cells
Bronchial muscle ***
Bronchial constriction and edema
Mucous plugging
Increased goblet cells
Bronchial muscle hypertrophy
Samter’s triad
asthma, recurrent sinus disease with nasal polyps, and a sensitivity to aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs)
Asthma miscellaneous
measurement predicting need for admission
Hemodynamic sequelae
FEV1
hypotension, pulsus paradoxus
Death risk factors (just for review)
- Hx of sudden severe exacerbations
- Prior intubation
- Prior ICU admit
- >1 admission or >2 ED visits in past year
- ED visit in past month
- >2 adrenergic MDIs per month
- Current/recent systemic steroid use
- “Poor perceivers”
- Concomitant disease – cardiopulmonary or psychosocial
- Illicit drug use
Asthma
beta-2 agonists comparison review
–Inhaled superior to oral and parenteral routes, fewer side effects
–Intermittent equal to continuous administration
–MDIs equal to nebulizers
–Racemic equal to “R” enantiomer preparations (levalbuterol)
Asthma, mechanism of action
steroids (3)
inhaled anticholinergic
magnesium
ketamine
steroids: immunomodulatory, up regulates beta receptors, immediately causes vasoconstriction
inhaled anticholinergic: relaxes bronchial smooth muscle
magnesium: relaxes bronchial smooth muscle
ketamine: sedation and bronchodilation
Cardiac arrest, intubated asthma patient steps (4)
1 Disconnect ventilator
2 Compress chest
3 Bilateral chest tubes
4 Fluid bolus
Bronchiolitis medication for congenitally ill child
Ribavirin
COPD
unique pathophysiology from asthma
–Different inflammatory markers from asthma (e.g. neutrophils, not eosinophils)
–Proteases and oxidants result in tissue destruction
- airflow reduction is not fully reversible and generally progressive
COPD
long-term natural history (4)
–Destruction of pulmonary vascular bed and thickened vessel walls
–Pulmonary hypertension
–Polycythemia
–Right sided heart failure (cor pulmonale)
In the setting of COPD exacerbation
Deep sulcus sign on the left suggestive of occult pneumothorax
COPD pneumothorax caveat
Blebs can mimic pneumothorax as shown on the x-ray
In the setting of COPD exacerbation
Lobar atelectasis distinguished from pneumonia by
sudden decompensation
volume loss on the affected side
may be treated by bronchoscopy
COPD therapy
indication for antibiotics
disease altering interventions (3)
abx: increased sputum production and purulent
smoking cessation and home oxygen (for PaO2 < 55 or Cor Pulmonale)- > mortality benefit
pneumococcal vaccination
ARDS
description
diagnostic criteria (3)
Non-cardiogenic pulmonary edema due to leaky alveolar capillary membranes
Diagnosis:
1 HypoxiaPaO2 < 60 mm Hg with FiO2 > 0.5
2 Normal ventricular function: PCWP < 18 mm Hg
3 Diffuse alveolar infiltrates: with normal heart size