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Resp Failure


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