Pulmonary Flashcards
Alveolar O2 formula?
Normal A-a gradient?
PAO2 = 713*FiO2 - PaCO2/0.8
On room air (21% O2), this is:
PAO2 = 150 - PaCO2/0.8
Normal A-a gradient is <15 mm Hg.
Increases with aging but should always be <30 mm Hg
Cause(s) of hypoxemia with a normal A-a gradient
Hypoventilation, low inspired oxygen
(Everything else that causes hypoxemia - V/Q mismatch, shunts, barriers to diffusion - causes an elevated A-a gradient).
Light criteria for an exudative effusion
At least one of:
- Pleural fluid protein / serum protein ratio > 0.5
- Pleural fluid LDH / serum LDH ratio > 0.6
- Pleural fluid LDH > 2/3 the upper limit of normal for serum LDH
Diagnostic workup of new pleural effusion
Thoracocentesis, unless clearly due to CHF
Berlin Criteria (2012) for diagnosis of ARDS
- Acute onset within 1 week of insult
- Bilateral CXR opacities not explained by other lung pathology
- Respiratory failure not explained by heart failure or volume overload
- Decreased PaO2 / FiO2 ratio, <300, on at least 5 cm H2O of pEEP
How can the severity of ARDS be graded?
PaO2 / FiO2 (P/F) ratio:
<100: Severe
<101-200: Moderate
<201-300: Mild
CXR finding in ARDS?
What else can cause a similar image?
Bilateral lung opacities (pulmonary edema)
Can also be seen in CHF and volume overload
What is a key intervention in ARDS?
PEEP, up to 15-20 cm H2O
O2 saturation goal in ARDS
88-95% saturation (PaO2 55-80)
In a ventilated patient with volume control, what can cause an elevated peak inspiratory pressure (PIP)?
How can you tell the difference?
Increased airway resistance or decreased pulmonary compliance
Check with inspiratory hold:
- The “Plateau Pressure” here reflects only pulmonary compliance.
- The difference between this and PIP (the “Delta Pressure” reflects airway resistance.
Extrapulmonary involvement of sarcoidosis (5)
- Skin lesions (e.g. erythema nodosum)
- Uveitis
- Arthralgias
- Hypercalcemia
- Heart disease
Sarcoidosis on CXR
Bilateral hilar lymphadenopathy, reticular infiltrates, +/- scattered opacities
What is Lofgren syndrome?
Acute sarcoidosis with erythema nodosum and arthralgias
Manifestations of sarcoidosis heart disease
- Restrictive cardiomyopathy early, dilated cardiomyopathy late
- AV block and other conduction defects
- Arrhythmias and sudden cardiac death
(Seen in 5% of sarcoidosis patients, due to noncaseating granuloma in the heart)
Mechanism of hypercalcemia in sarcoidosis?
Treatment?
Mechanism: 1-alpha hydroxylse in the granuloma activates viatmin D (converts 25-vitamin D to 1,25-vitamin D)
Treatment: Glucocorticoids (reduce activation by the granuloma)
Treatment for sarcoidosis
Monitor if asymptomatic.
Glucocorticoids if symptomatic
Hypoxia with a petechial rash and neurological signs after trauma
Fat embolism from long-bone fracture to lungs
Mechanism of secondary spontaneous pneumothorax
Rupture of alveolar blebs due to chronic destruction of alveolar sacks
(seen in chronic lung disease like COPD and CF)
Diagnostic test for aspiration pneumonitis?
Treatment?
Diagnosis: upright CXR
Treatment: supportive care only
Pattern of PFTs and DLCO in interstitial lung disease
Restrictive pattern and decreased DLCO (restrictive pattern with normal DLCO seen with chest wall deformities)
Time course of aspiration pneumonitis and pneumonia
Pneumonitis: cough +/- hypoxemia within hours of aspiration of gastric contents
Pneumonia: symptoms several days after aspiration of oropharyngeal secretions
Hypersensitivity pneumonitis:
Presentation?
CXR findings?
Presentation: cough, dyspnea, fever, malaise (so it is pneumonia-like) in association with trigger (bird droppings, molds in farming)
CXR: Ground glass / hazy opacities
Secondary polycythemia in an obese man - likely diagnosis?
Obstructive sleep apnea
Three most common causes of chronic cough?
An initial test/trial in each?
- Postnasal drip (upper-airway cough syndrome) (try empiric antihistamine)
- Asthma (PFTs)
- GERD (try empiric PPI)
Mechanism of chronic nonproductive cough in ACEIs
Decreased metabolism of kinins and substance P
Most effective treatment for allergic rhinitis
Glucocorticoid nasal sprays (fluticasone, mometasone)
Oropharyngeal physical exam finding that may be seen in allergic rhinitis?
Pharyngeal cobblestoning (streaks of lymphoid tissue)
Appearance of flow-volume loop in obstructive lung disease
Scooped-out pattern during exhalation (low flow in later, effort-independent phase)
Pattern of PFTs and DLCO in asthma
PFTs: Obstruction (FEV1/FVC < 0.7) that is reversible, >12% increase in FEV1 w/ bronchodilator
DLCO: normal
Pattern of PFTs and DLCO in COPD
PFTs: Obstruction (FEV1/FVC < 0.7) that is irreversible or only partially reversible
DLCO: often reduced but may be normal in early disease
Patient with severe asthma attack has normal PaCO2. Next step?
Intubation (impending respiratory failure)
Pulsus paradoxus with a normal heart, pericardial space, and pericardium
Severe asthma and COPD (when generating highly negative (up to 40 mm Hg) intrathoracic pressures during inspiration, so blood pools in lungs)