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Resp Failure
Pulmonology
| Question | Answer |
|---|---|
| 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:
Abarnard
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