Pulmonology
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| Indications for Mechanical Ventilation = SaO2 <90%, elevated PCO2 , and PaO2 of: | <60 mmHg
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| Treatment of ARDS induced hypoxemia usually requires | positive pressure ventilation
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| Normal mechanical ventilator tidal volume (___ ml/kg IBW) | 10-15
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| Large tidal volumes cause _____ in stiff lungs | high inflation pressures
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| ARDS has a ___% mortality rate | 30-40 (90% in pts with sepsis)
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| Arterial blood gas values consistent with RF: PaO2 value < 60 mmHg, PaCO2 value > __ mmHg, SaO2 value < 90% | 50
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| Resp failure: ABG = PaO2 <60 mmHg, SaO2 <90%, PaCO2 = | >50 mm Hg
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| The tip of the endotracheal tube should rest at the level of the | aortic arch; 2 cm above the carina
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| respiratory compromise is evident whe the PaO2 is < __mm Hg on room air | 60
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| respiratory compromise is evident when the PaCO2 is > __mm Hg | 45
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| Adequacy of ventilator settings needs to be determined with repeated: | arterial blood gas levels
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| ILD & chest tightness 2/2 cotton dust inhalation | Byssinosis
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| Secondary causes of ARDS | Sepsis, Pancreatitis, Hypotension (shock)
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| ARDS PE/ auscultation | crackles
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| ARDS is characterized by PaO2/FIO2 of: | </= 200
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| Primary causes of ARDS | Aspiration, Lung contusion and trauma, Inhalational injury, Pneumonia, Near -drowning
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| ARDS mechanism of action | Alveolar injury -> inflamm cytokines (TNF, IL6, IL8) -> neutrophil recruitment: release toxic mediators (proteases) -> lung capillary endothelial & alveolar epithelial injury -> edema
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| TRALI mechanism of action (2 hits): | 1) neutrophil sequestration & priming in lung microvessels (due to endothelial injury); 2) neutrophil activation by blood product favctor -> cytokines -> inflamm -> lung capillary edema
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| Pulse oximetry of ___ at rest is required for O2 therapy | <88%
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| Low DLCO with restriction = | interstitial lung disease, pneumonitis
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| Low DLCO with obstruction = | emphysema, cystic fibrosis, bronchiolitis
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| Low DLCO with normal spirometry = | anemia, pulmonary vasculitis, early interstitial lung disease
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| Noncaseating granulomas and inflammation of alveoli, small bronchi and small blood vessels = | Sarcoidosis (tx: long-term steroids)
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| Triad of symptoms for Wegener’s Granulomatosis: | Small vessel vasculitis, Granuloma formation inflammation, Necrosis
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| Idiopathic: alveolar (lung) hemorrhage & rapidly progressive glomerulonephritis = | Goodpasture
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| Goodpasture pathophysiology: | glomerular antibodies
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| Goodpasture treatment = | Immunosuppressive therapy
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| Standard for diagnosing ILD = | surgical lung bx
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| PFT result interpretation: obstruction vs restriction | Obstruction: low FEV1/VC (<50% is severe); restriction: low VC, low FEV1, normal FEV1/VC
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| Sweat chloride test is to dx: | Cystic fibrosis
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| Transudative pleural effusions: usual etiologies | [low protein] CHF; cirrhosis, nephrotic syndrome
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| Exudative pleural effusions: usual etiologies | [high protein] Inflammatory or malignant dz: TB, PNA, Ca, infarction, trauma, chylothorax
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| Pleural fluid: Fluid:serum protein ratio = | >0.5 exudative; <0.5 transudative
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| Pleural fluid analysis: | total protein, LDH, WBC & diff, glucose, pH; Gram stain, cx, cyto. Consider also AFB
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| pHTN is defined as: | mean PA pressure >25mmHg at rest or >30mmHg with exercise
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| Classifications of pHTN | WHO: PAH; pHTN with left heart dz; pHTN assoc w/lung dz +/- hypoxemia; pHTN 2/2 chronic thrombotic / embolic dz; multifactorial / idiopathic. Also I-IV (least -> most severe)
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| 5 categories of pHTN etiology | 1. reduced area of PA bed 2/2 COPD, ILD, SCD; 2. increased PV pressure (pericarditis, LVF, MV stenosis; 3. increased pulmo blood flow (congenital L-R shunt); 4. vixcosity (P vera); 5) Misc (HIV, portal HTN)
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| pHTN sxs | DOE, retrosternal CP, syncope, LE edema, ascites, hoarseness (2/2 recurrent laryngeal nerve impingement)
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| pHTN physical exam: | Narrow & split S2, loud P2, LLSB heave, mid-diastolic gallop (S3), right sided gallop (S4), systolic click, JCD
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| Idiopathic pHTN Tx | 1. prostaglandins (eg, epoprostenol); 2. phosphodiesterase-5 inhibitors (sildenafil); 3. endothelium antagonist (eg, bosentan). ALSO continuous IV prostacyclin
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| Clinically significant OSA = | Apneic episodes last >10 seconds & occur 10-15 times/hour.
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| Apnea-hypopnea Index classifications | AHI (A & H episodes / total sleep time): mild (5-15), moderate (15-30), severe >30
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| OSA workup | PSG, MSLT, ABG, CXR, ECG, CBC (high RBC is common), TSH
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| Diffuse Parenchymal Lung Disease, AKA = | interstitial lung disease (ILD)
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| Incidence of ILD | 81 per 100K men & 67 per 100K women
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| ILD pathophysiology | >150 dz etiologies. Extensive disruption of alveolar tissue, loss of fuctional alveoli, & replacement of functional tissue by scar tissue
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| BOOP pathophysiology | If larger airways (eg, bronchioles) are involved in the inflammatory process -> bronchiolitis obliterans with organizing PNA
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| In ILD from a rheumatic source (RA, SLE, PM/DM, Sjogren), common sx is: | pleuritic pain
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| If pleuritic pain & suddenly worse SOB in ILD, suspect: | PTX (assoc with lymphangioleiomyomatosis, NF1/NF2, tuberous sclerosis, or Langerhans cell histiocytosis)
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| Hemoptysis may be sx of: | malignancy, diffuse alveolar hemorrhage syndromes, PE, or superimposed infxn
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| ILD lab workup | ESR (usually high); cryo-Ig; serolgic tests for collagen vascular dz, RF, ANA, complement
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| ECG in ILD may show: | RV and atrial strain
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| Mainstay of ILD tx is: | corticosteroids (if not tolerated or recalcitrant sxs: cyclophosphamide or azathioprine)
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| Type I respiratory failure = | hypoxemic resp failure (failure of gas exchange)
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| Type II respiratory failure = | hypercapnic RF with or without hypoxemic RF (failure of ventilation)
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| Increased dead space = | areas of lung are ventilated but not perfused (or when decrease in perfusion exceeds decrease in ventilation; eg, COPD, asthma, CF, fibrosis)
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| Most common cause of death in pts with resp failure = | multi system organ failure
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| Hypoxic resp failure definition/criteria: | PaO2 <60 mmHg, or SaO2 <90%
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| Most common risk factor for ARDS = | sepsis
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| Risk factor for ARDS include: | sepsis, SIRS, shock, trauma, aspiration, near-drowning, pancreatitis, DIC, burns
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| Hypoxic resp failure can occur as result of: | Shunting, V/Q mismatch, low inspired O2 tension (eg high altitude, toxic gases), hypoventilation (retained CO2), diffusion impairment (ILD), low mixed venous oxygenation
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| Hypercapnic resp failure definition/criteria: | condition causing acute CO2 retention -> PaCO2 = 45-50 mmHg and resp acidosis (pH <7.35)
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| increased PaCO2 (as in hypercapnic RF) is result of (3): | increased CO2 production (fever, sepsis, trauma, burns, CHO intake, hyperthyroid), decreased tidal ventilation, or increased dead space ventilation
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| Primary goal of therapy in respiratory failure = | maintaining adequate PaO2 levels
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