| A | B |
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| Pulse oximetry measures _____; not ___________. | Oxygenation; ventilation |
| How is pulse oximetry affected by the presence of anemia? | With less Hg to oxygenate; you can have a normal Sa02 reading in the presence of decreased oxygenation. |
| An asthmatic presents with wheezing and DIB; but a normal pulse ox. What does it mean? | Not much-just that the patient has good oxygenation. His ventilation; however; probably sucks. |
| How does carbon monoxide effect pulse oximetry? | To a pulse oximeter; carboxyhemoglobin looks like hemoglobin. Therefore; the reported saturation is too high (and tends to be 100%). |
| How does methemoglobin effect pulse oximetry? | To a pulse oximeter; metHb looks like 85% O-Hb and 15% reduced Hb. Therefore; the reported sat is too high (and tends to be 85%). |
| What are the causes of an inaccurately low pulse ox? | Hypothermia nail polish vasospasm ambient light (especially fluorescent) |
| What are the causes of an inaccurately high pulse ox? | Carboxyhemoglobinemia and methemoglobinemia |
| Give a qualitative definition of the A-a gradient. | The A-a gradient is the difference between calculated alveolar p02 and measured arterial p02. |
| What is a normal A-a gradient? | < 10 - 15 mmHg |
| What are the causes of an increased A-a gradient? | Age adjusted gradient: 10 + (age/10) decreased diffusion (interstitial lung disease) V/Q mismatch is most common cause of A-a grad R to L shunt (ASD; VSD) |
| What is the "quick and dirty" formula for A-a gradient? | 140 - (PaC02 + PaO2) |
| What is the role of bedside spirometry in asthma? | Measures degree of large airway obstruction; measures severity and response to therapy; and predicts need for admission. |
| What is the role of ABG in acute asthma. | Indicated only for severe cases. Normal or mildly elevated pCO2 suggests impending respiratory failrue. |
| What are the signs of severe asthma? | Absence of wheezing; inability to speak; pulsus paradoxus > 20 mmHg; hypoxemia; normocarbia or hypercarbia; PEFR < 80 mmHg. |
| All that wheezes is not ashtma. | CHF; FB; obstruction; infection. Also; remember that asthma doesn't always wheeze. |
| List the asthma death risk markers. | Hx of sudden severe attacks prior intubation ICU admit 2 or more hosp in prior 12 mos 3 or more ED visits in 12 mos asthma related ED visit within last mo use of more than two beta-aerosol MDIs per mo current or recent systemic steroid use cardiac dz other resp dz pysch dz psychosocial probs drug use poverty urban |
| First line therapy for asthma? | Aerosolized beta agonists. |
| Discuss beta-1 vs. beta-2. | Beta-1: cardiac. Beta-2: bronchodilation (via increased adenyl cyclase activity). Remember: "1 heart; 2 lungs." |
| What are the side effects of beta-2 agonists? | Tremor (most common); anxiety; palpitations; headache; tachycardia |
| T or F: subcutaneous beta agonists have no proven benefit over nebulized betas. | True! |
| What are the side effects of aerosolized anticholinergics? | Dried secretions; tachycardia; mental status changes; blurry vision. |
| What is the role of corticosteroids in acute asthma? | Corticosteroids reduce inflammation; increase beta agonist effect; and prevent recurrence. |
| When are corticosteroids indicated in acute exacerbation of asthma? | Always. |
| T or F: IV steroids are slighly more effective and rapid in onset than oral steroids. | False. |
| What is the principle effect of adding theophylline to beta-2 agonists? | Increase toxicity; but not efficacy. |
| Theophylline is metabolized by ____ | Cytochrome p450 |
| T or F: intermittent adminsitration of inhaled adrenergics results in similar outcomes when compared to continuous nebs. | True! |
| T or F: early use of steroids may decrease the admission rate in the setting of SEVERE asthma. | True. |
| What are the early effects of steroids in acute asthma? | Vasoconstriction; decreased capillary permeability; decreased mucus production |
| What are the delayed effects of steroids in acute asthma? | Decreased inflammation; mediator production; cell migration and activation; stabilization of mast cell membranes; and upregulation of beta receptors to increase responsiveness to adrenergics. |
| What is the role of arachidonate in acute asthma? | Arachidonate is released on exposure to allergens. Breakdown of arachidonate produces three cysteinal leukotrienes; which cause bronchoconstriction; vascular permeabilty; and proinflammatory cellular migration. |
| T or F: one of the effects of steroids is to prevent/suppress leukotriene production. | False. |
| T or F: leukotriene-modifying agents have been shown to prevent hospitalizations and relapses in acute asthma. | False. No consistent data exists. |
| T or F: Leukotriene-modifying agents may decrease the need for steroids or allow lower steroid doses in acute asthma. | True. The effect of LMAs and steroids may be complimentary. |
| Discuss the Churg-Strauss syndrome. | Described as an allergic angiitis and granulomatosis; similar to polyarteritis nodosa. Patients have marked eosinophilia and multiorgan vasculits. Pulmonary symptoms predominate; and may present as refractory asthma. Steroids are the treatment-but has been associated with chronic high-dose steroid use and subsequent withdrawl. |
| Although mechanical ventilation in the setting of asthma decreases the work of breathing; protects the airway; and may improve oxygenation; it is important to remember that it does NOT treat _______. | Obstruction. |
| What are the fundamental prinicples to keep in mind when treating asthma with mechanical ventilation. | Strongly consider RSI Keep patient paralyzed Minimize risk of barotrauma Allow pCO2 to rise (permissive hypercapnia) Ketamine for sedation and bronchodilation (smooth muscle relaxant) |
| What are the goals of permissive hypercapnia in ventilation of acute asthma? | Keep airway pressures down Prevent barotrauma and hemodynamic side effects Keep SaO2 > 90% Normalization of pCO2 is NOT a goal |
| The key to permissive hypercapnia is a _____ inspiratory flow rate and a ______respiratory rate. | Rapid; reduced |
| The most common etiology of pediatric bronchiolitis is _____ | Respiraotry syncytial virus (RSV) |
| A 6 mo old infant presents with a hx of URI sxs last week; now with rapid breathing; decreased feeding; retractions; and wheezing. CXR shows air trapping; peribronchial cuffing and atelectasis. What's your diagnosis? | Bronchiolitis; probably RSV. |
| What are the high risk factors in pediatric bronchiolitis? | Preemies; congenital heart disease; lung disease |
| What is the treatment for pediatric bronchiolitis? | Supportive care fluids humidified O2 bronchodilators if responsive steroids do not alter course rarely need intubation ribavirin reserved for intubated pts or those with underlying heart or lung disease |
| What are admission criteria in patients with pediatric bronchiolitis? | Respiratory distress hypoxia hypercarbia PO fluid intolerance apneic spells underlying cardiac or pulmonary disease |
| What are the two pathologic components of COPD? | Emphysema-dilation and destruction of airspaces Chronic bronchitis-excessive mucus secretion. Most patients have components of both. |
| What are the mainstays of treatment of acute COPD exacerbation? | 02 to keep SaO2>90% Beta-2 agonists aerosolized anticholinergics steroids (for severe cases) antibiotics? Mechanical ventilation |
| What are the criteria for long-term O2 therapy in COPD? | Room air PaO2 <55. PaO2 56-59 plus cor pulmonale |
| ARDS is most succinctly described as a _____________ | Noncardiogenic pulmonary edema |
| What is the pathophysiology of ARDS? | Primary insult is disruption of alveolar capillary membranes; resulting in leaky capillaries; interstitial and alveolar edema; reduced compliance; and pulmonary shunting. |
| What are the diagnostic criteria of ARDS? | PCWP < 18 mmHg. PaO2 < 60 mmHg with FiO2 > 50%. Diffuse alveolar infiltrates with normal heart size. |
| What are the causes of ARDS? | Sepsis (most common) trauma drowning/aspiration toxic gases/smoke drugs pneumonia pancreatitis lung embolism CNS injury high altitude |
| What is the most common cause of ARDS? | Sepsis |
| Name three drugs that can cause ARDS | ASA; opiates; paraquat |
| What is the treatmen of ARDS? | Supportive care. Correct underlying disorder. Mechanical ventilation. Consider CPAP; BiPAP; PEE |
| pThe most common cause of bacterial pneumonia is ______ | The aptly named pneumococcus. |
| What are the common organisms in bacterial pneumonia and their associated "demographics?" | Pneumococcus (most common) Hflu (COPD; elderly; smokers) S. Aureus (post-viral; IVDA; hematogenous; NH; immunosuppressed) Klebsiella (alcoholics; chronic lung dz; aspiration) Pseudomonas; enterobacter (nosocomial) Moraxella (winter; COPD) Anaerobes (aspiration) |
| What are the host risk factors for pneumonia? | Decreased cough/gag Impaired immunity Impaired mucociliary transport Chronic disease Increasted secretions |
| What are the histologic criteria for an adequate sputum sample? | < 10 epis; > 25 WBCs /HPF |
| What are the three most important causes of atypical pneumonia? | Mycoplasma; Chlamydia; Legionella. |
| A patient with pneumonia has a sputum gram stain demonstrating gram positive diplococci. What is the most likely organism? | Pneumococcus. |
| A patient with pneumonia has a sputum gram stain demonstrating small gram-negative bacilli. What is the most likely organism? | H. Flu |
| A patient with pneumonia has a sputum gram stain demonstrating short gram negative paired bacilli. What is the most likely organism? | Klebsiella pneumoniae. |
| An ill patient with pneumonia has a sputum gram stain demonstrating few PMNs and no dominant bacterial species. What is the most likely organism? | Legionella |
| A patient with pneumonia has a sputum gram stain demonstrating gram negative bacilli. What is the most likely organism? | E. Coli; Pseudomonas |
| A patient with pneumonia has a sputum gram stain demonstrating mononuclear cells and no dominant organism. What is the most likely organism? | Mycoplasma. |
| A patient with pneumonia has a CXR demonstrating lobar infiltrate. What is the most likely organism? | Pneumococcus |
| A patient with pneumonia has a CXR demonstrating patchy; mulitlobar basilar infiltrates. What are the most likely organisms? | H. Flu; Pseudomonas; E. Coli; anaerobes |
| An alcoholic; homeless patient with pneumonia has a CXR demonstrating patchy; multilobar infiltrates in the upper lobes and a bulging fissure. What is the most likely organism? | Klebsiella |
| What organisms are most associated with pleural effusion in the setting of pneumonia? | Pneumococcus; staph (empyema; pneumothorax); Group A Strep. |
| What organims are most commonly associated with lung abscess? | Klebsiella (bulging fissure); Staph; Psuedomonas. |
| What is the differential for nosocomial (hosp > 5 days) pneumonia? | Enterobacter; Pseudomona; Acinetobacter; Staph; H. Flu |
| What is the differential for pneumonia in patients with COPD; smokers; and the elderly? | Pneumococcus; H. Flu; M. Catarrhalis. |
| What is the differential for pneumonia in ICU patients; patients on broad-spectrum abx; and patients on the vent? | Pseudomonas; Pseudomonas; Pseudomonas |
| What si the differential for pneumonia in nursing home patients? | Pneumococcus; gram negatives (E Coli; Pseudomonas); Staph. |
| ACEP PNEUMONIA POLICY: What are the determinants of the Pneumonia Severity Index? | Age and sex ; Coexisting Illness; Physicial Findings; Labs; and CXR. (Mnemonic: ACP Loves CXRs.) |
| ACEP PNEUMONIA POLICY: What are the classes of severity? | Class I: <51 pts. Class II: 51-70 pts; mort 0.6%. Oral abx or brief admit. Class III: 71-90 pts; mort 0.9%. Same tx as Class II. Class IV: 91-130 pts; mort 9.5%. Admit for IV abx. Class V: >130 pts. 26.7% mort; ?ICU/IV Abx. |
| ACEP PNEUMONIA POLICY: True of false: The ACEP Pneumonia Severity Index is not so much a clinical decision instrument as a predictor of mortality. | Abso-fucking-lutely |
| T or F: Blood cultures; sputum cultures; grams stain; and empiric abx therapy are all considered level C (based on preliminary; inconclusive or conflicting results). | True. |
| What are the historical risk factors for increased morbid/mort in pneumonia? | Extremes of age Mech vent Hosp within last year for pneumonia Malnutrition COPD Diabetes CHF Chronic renal failure Liver dz Aspiration Splenectomy Alcoholism Immunosuppression |
| What are the exam findings that place a pneumonia patient at increased risk for morbid/mort? | Altered mental status Heart rate > 140 RR>30 Diastoli BP<60 Systolic <90 Temo >38 Suspected concomittant extrapulmonary sites of infection |
| What are the ancillary (lab) findings that place a pneumonia patient at increased risk for morbi/mort? | WBC < 4000 or > 30;000 Absolute PMN < 1000 PaO2 < 60 PCO2 > 50 Cr >1.2 or BUN > 20 Multilobar involvement Cavitary lesion Effusion Rapidly progressive metabolic acidosis DIC Hg < 9 or Hct < 30% |
| A patietn with pneumonia is less than 60 yo. What are the options for empiric outpatient therapy? | Doxycycline; macrolide; quinolone |
| A patient with pneumonia is > 60 yo. What are the options for empiric outpatient therapy? | Quinolones; macrolide + cephalosporin |
| What are the common clinical features and treatment of streptococcal pneumonia? | Often post viral Abrupt onset Fevers; chills; rigors Chest pain Cough may be absent in early disease Rusty; heme + sputum Inc WBC Lobar consolidation Pleural effusion Tx = pcn (hi incidence of resist); macrolid; quinolone |
| What are the common clinical features and tx of H Flu pneumonia? | Common in debilitated; COPD and peds Winter to early spring Clinically similar to pneumococcal pneumonia. Tx = augmentin; macrolide; 3d Cephalosprorin; quinolone |
| What are the common clinical features and tx of Mycoplasma pneumonia? | Most common atypical pneumonia. Insidious onset 14-day incubation Young adults Meningitis Bullous myringitis Encephalitis hemolysis Erythemia multiforme Guillan-Barre patchy interstitial infiltrates complement fixation titers elevated Tx = macrolides |
| What are the typical clinical features and tx of Chlamydia pneumonia? | Caused by obligate intracellular parasite Preceding URI; stacatto cough Dx by serology and PCR Seen in young adults (outbreaks) Tx = macrolides |
| What are the clinical features of chlamydia pneumonia in children? | Acquired at birth; seen at 13-19 wks. Conjunctivitis Retractins; rales Afebrile; alert; tachypneic CXR - hyperinflation; bil diffuse infiltrates Differs from RSV (no wheezes; conjunctivitis) |
| What are the two forms of Legionella? | Pontiac fever |
| What is the clinical presentation of Legionella pneumonia? | Elderly male; chronic underlying disease; with pleuritic chest pain; GI sxs (N/V/D); toxic appearance; relative bradycardia; and mental status changes. |
| What are the lab and radiographic findings in Legionella pneumonia? | Increased WBC count Sputum with few PMNs; no orgs Hyponatremia Hypophosphatemia Microscopic hematuria Elevated LFTs Positive serology (hi spec; low sens) CXR shows unilateral patchy alveolar inf progressing to consolidation and pleural effusion with hilar adenopathy. |
| What is the treatment for Legionella pneumonia? | Erythromycin for 3 weeks |
| What are the clinical features of Klebsiella pneumonia? | Gram neg CAP Alcoholics; diabetics; COPD Sudden onset cough and chest pain "Currant jelly" sputum CXR: RUL predominance with "bulging fissure" often complicated by empyema and abscess |
| What is the tx of Klebsiella pneumonia? | Hospitalize; 3d gen cephalosporin plus aminoglycoside |
| Briefly discuss Psittacosis | Chlamydia Psittaci Bird handlers Renal failure; endocarditis; encephalitic; DIC Tx = doxycycline; erythromycin |
| Briefly discuss Q fever. | Coxiella burnetii Sheep; goats; cattle seen in vets and farmers pneumonia; endocarditis; hepatitis Tx = doxycycline |
| What are the risk factors for hospital-acquired pneumonia? | Mechanical ventilation; ICU; previous Abx; elderly; debilitated; immunocompromised; risk fxs for aspiration. |
| What are the most typical aspirated FBs in children? | Coins (upper airway) and food (peanuts; popcorn) |
| What the common aspirated FBs in adults? | Bones and dentures |
| What are the clinical features of FB aspiration? | Primarily children Often R mainstem Recent episode choking or wheezing Chronic cough Wheezing unresponsive to tx Life-threat if not detected early In the diff dx for new-onset wheezing Ball-valve effect causes hyperinflation on side of aspiration |
| What are the typical CXR finding with FB aspiration? | Hyperinflation on side of FB Shift of mediastinum away from object Shit; you may even see a FB |
| When is bronchosopy indicated in the setting of suspected FB aspiration? | Always. Come on; it's not going to pass. |
| What are the risk factors for aspiration pneumonia? | Seizure; alcoholic; obtunded; depressed gag |
| What are the features of aspirate that have an impact on the severity of aspiration pneumonia? | pH (lower is worse) volue (>25 ml) Presence of particles (food; etc) Bacterial contamination (usually anaerobes) |
| What is the clinical presentation of aspiration pneumonia? | Immediate resp distress due to chemical burn. Hypoxemia. Respiratory alkalosis. Wheezes; rales. Hypotension. CXR often negative initially. Localization related to dependent lung. |
| What is the treatment of aspiration pneumonia? | Supportive. Anaerobes often a factor-metronidazole; clindamycin. |
| Primary infection in tuberculosis is usually in the _______ lobes. | Lower! |
| What is the treatment for suspected new pulmonary TB? | Quadruple therapy at least until culture back (approx 8 weeks) to avoid missing MDR TB: INH; rifampin; pyrazinamide; ethambutol or streptomycin |
| Discuss the typical course of primary TB infection. | A self-limited; mild pneumonic process; typically undiagnosed; usuallyin the middle and lower lobes. Hematogenous spread leads to upper lobe reactivation (80-85%) or activation in other sites (15%). 5% of cases will reactivate (most within two years). Immunocompent patients usually heal-fibrose-calcify. |
| Discuss the classic active TB. | Fever; wt loss; hemoptysis; night sweats; coff; pleuritic pain; hemoptysis; middle and lower lob infiltrates with hilar nodes. |
| What are the side effects of the first line drugs for TB? | INH - liver; neuropathy. RIFAMPIN - flu sx; orange discoloration of secretions and urine; drug interactions PYRAZINAMIDE - hyperuricemia; decreased glucose control STREPTOMYCIN - nephro/ ototoxi. ETHAMBUTOL - vision and red-green discrimination problems |
| T or F: Extrapulmonary TB is generally no more difficult to treat than pulmonary TB. | True. |
| T or F: Even if they are compliant with multi-drug regimens; HIV patients have an increased risk of treatment failure in tuberculosis. | False. |
| Multidrug resistant TB is; by definition; resistant to at least ____ and ____. | INH; Rifampin |
| For average-risk individuals; a PPD is considered postive at ____ mm. | 10 mm. |
| When is a 5mm PPD considered positive? | Depressed immunity (steroids; HIV) Recent exposure High likelihood for TB (pos CXR) |
| When is a 15mm cutoff used for the PPD? | For those with a very low risk of infection. |
| An immigrant with a history of BCG vaccination presents with a positive PPD. What is the CDC guideline for such an eventuality? | Ingore the BCG history and proceed as if not vaccinated. |
| What is the treatment of a positive PPD? | 9-10 most of INH. |
| What is sarcoidosis? | A multi-system; non-infectious; non-caseating granulomatous disease of unknown cause; usually benign. Usually in young to middle-age adults. |
| What is the presentation of sarcoidosis? | Young to middle-aged adults; presenting with bilateral hilar adenopathy; pulmonary infiltrates; ocular and skin lesions; cough; SOB; eye pain; fever; night sweats. |
| What is the laboratory profile in sarcoid? | Increased calcium and alkaline phosphatase; anemia; increased serum ACE. |
| What is the specific treatment of sarcoidosis? | None. Treat the complications: cardiac; CNS; ocular; hypercalcemia. |
| What are the pulmonary manifestations of AIDS? | INFECTIOUS: bacterial; mycobacterial (TB; MAI); parasitic (toxo); viral (herpes; CMV); fungal (histo; crypto). MALIGNANT: Kaposi's; Non-Hodgkin's |
| What's the most important thing to remember about fungal pneumonia in AIDS patietns? | Often associated with concomitant meningitis; disseminated disease; candidiasis and aspergillosis. |
| What is the most common pulmonary infection in HIV+ patients? | Bacterial pneumonia - same organisms as in non-HIV pts. |
| How do CD4 counts correlate with pulmonary manifestations of AIDS? | CD4 200-500: TB CD4 < 200: PCP CDR < 50: CMV; MAI |
| A patient with AIDS presents with pulmonary sxs and diffuse interstitial infiltrates on CXR. What are the most likely causes? | PCP; CMV; TB; MAI; histoplasmosis; coccidiomycosis. |
| A patient with AIDS presents with pulmonary symptoms and a focal consolidation on CXR. What are the most likely causes? | Bacterial pneumonia; TB; PCP; MAI |
| A patient with AIDS presents with pulmonary symptoms and a cavitary lesion. What are the most likely causes? | PCP; TB; bacterial; fungal |
| What is the most common presnting illness in AIDS? | PC |
| pWhat is the clinical triad in PCP? | Fever; exertional dyspnea; cough |
| Usually the CD4 count has to drop below _____ for PCP to develop. | 200 |
| What serum lab test is classically associated with PCP? | LDH increased (>450) |
| What imaging study is most sensitive for PCP | Gallium scan |
| What is the radiographic appearance of PCP? | Classic "bat-wing" bilateral interstitial infiltrates. Effusions are rare. Can present with spontaneous pneumothorax. |
| What is the most sensitive diagnostic approach to PCP? | BAL with brushings and transbronchial biopsy. |
| What is the treatment of PCP? | TMP/SMX (high incidence of allergy in HIV) Pentamidine (watch for hypotension and hypoglycemia) Steroids if pO2<70 or Aa gradient >35 |
| What is the differential diagnosis for an anterior mediastinal mass? | Remember the five Ts: Thymoma (think myasthenia gravis); Thyroid (retrosternal); Teratoma (teeth and hair) T cell lymphoma Terrible (carcinoma) |
| What is the most common mediastinal mass? | Bronchogenic carcinoma |
| What is the most common cause of superior vena cava syndrome? | Bronchogenic carcinoma |
| What is the presentation of SVC syndrome? | Facial edema; upper extremity edema; headache; plethoric facies; visual changes; syncope; dyspnea |
| What is the treatment of SVC syndrome? | Treat underlying cause if known Diuretics and steroids for increased ICP Radiation therapy for malignant causes |
| What are the two types of spontaneous pneumothorax? | Primary (no lung disese) and Secondary (due to underlying lung disease) |
| What are the characteristics of primary spontaneous pneumothorax? | Often seen in tall; thin young men; smokers; those who have performed Valsalva; etc. Often present as a ruptured bleb at the apex. Tend to recur. |
| What are the diseases associated with secondary spontaneous pneumothorax? | Asthma COPD Neoplasm Marfan's Ehlers-Danlos CF Pneumonia (esp with abscess or cavitation) HIV Catamenial (endometriosis-related) |
| T or F: spontaneous pneumothorax can often cause peaked T-waves. | False-it may cause INVERTED T-waves. |
| Treatment for spontaneous or iatrogenic ptx. | Observation; high-flow O2; mini-catheter aspiration or formal chest tube. All require re-check for resolution. Patients on ventilators require large-bore chest tubes. |
| What is the diagnostic triad for tension ptx? | JVD; decreased breath sounds; hypotension |
| Aside form the diagnostic triad of JVD; decreased breath sounds and hypotension; what are other signs of tension pneumo? | Unilateral chest expansion; cyanosis; tracheal deviation (late sign). |
| What are the causes of hemoptysis? | 1/4 infectious (non TB); 1/4 neoplastic; 1/4 other (TB; cardiovascular; vasculitis; etc); 1/4 undetermined |
| What is the definition of massive hemoptysis? | >600 ml in 24 hours or 50ml in a single cough. |
| T or F: massive hemoptysis usually causes death by exsanguination | False. The cause of death in massive hemoptysis is asphyxiation. |
| What are the admission criteria for hemoptysis? | Massive TB Hypoxemia requiring O2 Hypercapnia Diffuse alveolar hemorrhage Mycetomas (fungus balls in pulmonary cavities) |
| What is the emergency treatment of massive hemoptysis? | POSITION: place bleeding side down CONSIDER SELECTIVE MAINSTEM INTUBATION of nonbleeding lung ANGIOGRAPHY; bronchoscopy or surgery |
| What are the causes of pneumomediastinum? | PRIMARY: Valsalva; inhalation drug use; vomiting; asthma SECONDARY: Barotrauma (scuba diving); PPB; esophageal rupture; infection; thoracic trauma |
| What is Hamman's crunch? | Sound heard synchronous with heart beat. Indicative of pneumomediastinum. |
| Is pneumomediastinum dangerous in and of itself? | No; unless it progresses to tension pneumomediastinum. Underlying tracheobronchial injury; ptx; and ruptured esophagus are of course dangerous. |
| What are the causes of pleural effusion? | TRANSUDATES are due to incrased hydrostatic or decreased oncotic pressure: CHF; cirrhosis; nephrotic syndrome. EXUDATES: neoplastic (usually lung); inflammatory (SLE; RA; panc); infectious (pneumonia; empyema; TB; abscess) |
| Findings in transudative vs. exudative effusion. | PROTEIN: low in transudate; high in exudate. LDH: low in transudate; high in exudate. |
| What is Virchow's triad? | Risk for VTE: STASIS (immob; obesity; venous insuff; chf) ENDOTHELIAL DAMAGE (trauma; post-op) HYPERCOAGULABLE STATE (ca; preg; OCs; RA; Lupus) |
| What are the EKG findings associated with PE? | Sinus tach and NSST-T changes RBBB Right strain pattern RAD S1Q3T3 pattern in large PE (uncommon) |
| T or F: Few patients with PE have a normal A-a gradient. | True |
| What is the most common xray abnormality in PE? | Elevagted hemidiaphragm. |
| What is Hampton's hump? | A pleural-based density with a rounded border facing the hilum. |
| What is Westermark's sign? | Dilated pulmonary vasculature promixal to embolus with distal oligemia. |
| T or F: a normal V/Q scan virtually rules out PE. | True. |
| A patient with low clinical suspicion for PE has a negative VQ scan. What should you do? | Consider other diagnoses; PE is virtually ruled out in this patient. |
| A patient with a high clinical prob for PE has a high-probability VQ scan. What should y ou do? | Treat for PE. |
| T or F: d-dimer ELISA has a low sensitivity but a high specificity. | False-just the opposite. |
| d-dimer ELISA has a ____ negative predictive value. | HIGH |
| Discuss CT for PE | Accurate for proximal PE May miss small distal PE May identify alternative diagnoses |
| What is the major limitation of echo for PE? | Its low sensitivity. |
| What are echocardiographic findings of PE? | RV dilatation; pulmonary artery dilation; dec ejection fraction. |
| Discuss d-dimer for PE. | High sens/low spec test. High neg pred value. Useful for excluding low-prob and possibly interm-prob patients. Stays positive for about a week. Latex not as reliable as ELISA. |
| Spiral contrast CT visualises to at least the ______ arteries. | Segmental |
| What are the contrast requirements of CT and pulmonary angiography for PE? | CT: 120 ml. PA: 300 ml. |
| Discuss the alveolar dead space measurement for PE. | Represents air in alveoli not equilibrated with pulmonary capillary blood due to a regional perfusion defect (occurs with a PE). This test requires use of volumetric capnography; and compares favorably with VQ scanning. Not ready for prime time. |
| What is the problem with A-a gradients in diagnosing PE? | Niether sensitive nor specific. |
| What is the primary rationale behind echocardiography in the diagnosis of pulmonary embolism? | Echo can detect right heart strain and pulmonary hypertension from a major obstruction of the pulmonary arteries. |
| Echo for PE is limited because it requires _____ of the pulmonary vasular bed to be occluded. | 30-40% |
| In echo for PE; which approach is superior; TE or TT? | TE |
| What is BURP in intubation? | Backward; Upward; Rightward Pressure on the the larynx to optimize visualization. |
| What are the three clinical classification systems for identifying a difficult airway? | CORMACK AND LEHANE: std in anesthesiology. Four grades based on ability to see glottis with larngoscope. PERCENTAGE OF GLOTTIC OPENING (POGO) Similar to Cormack and Lehane. MALLAMPATI CLASSIFICATION: Based on the structures that can be visualized with the patient's mouth open. In particualr; how much; if any; of the posterior pharyngeal wall can be visualized. |
| What is the "Rule of Threes" in intubation? | If a patient passes the Rule of 3s; intubation is likely to be successful: 1. Three finger widths can fit between the teeth. 2. Three finger widths between the mandibular genu and the hyoid bone. 3. Three finger widths between the cricoid and the sternal notch. |
| What are the factors affecting speed of desaturation during intubation? | Degree of preoxygenation Patient's body mass Current oxygen utilization associated cardiopulmonary pathology |
| How is the Eschmann bum elastic bougie used? | Placed under laryngoscopy or manually directed to trachea. Serves as a guide over which to slide the tube. Said to cause a palpable "rattle" when it bumps agaisnt tracheal rings. The lighted stylet operates along a similar principle; transiluminating the neck when in the trachea (but not in the esoph). |
| What are the relative contraindications to retrograde intubation? | Bleeding disorder; distorted neck anatomy; laryngeal injury |
| T or F: Fiberoptic bronchoscopic intubation is contraindicated in awake patients. | False: can be done in awake patients after appropriate pretreatment. |
| T or F: The LMA does not entirely protect against aspiration. | True. |
| What are the advantages of the LMA? | Can be inserted without msucle relaxants. Doesn't require direct visualization. Easily taught. May facilitate subsequent fiberoptic intubation |
| What is the difference between the LMA and the ILMA? | The ILMA is an LMA with a large diameter; metallic airway tube and handle; permitting blind passage of an ET tube. |
| What is the combitube? | A dual lumen tube; blindly inserted into the pharynx. It enters the esophagus 90-95% of the time. Ventilation is performed through one of the tubes after tests of location are performed. |
| T or F: In cases of complete airway obstruction and inability to intubate; transtracheal jet ventilation may be a useful adjunct. | False! TTJV cannot be used in complete airway obstruction; since gas cannot passively exit. |
