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Has no relationships with any proprietary entity producing health care goods or services consumed by or used
on patients.
Disclosure of Financial Relationships;
Charles Read, M.D.
The American College of Physician 2008 The Core of Internal MedicineA Re-Certification Preparation CoursePulmonary & Critical Care Medicine
Charles A. Read, M.D.
Director of Adult Critical Care
Associate Professor of Pulmonary & CCM
Georgetown University Medical Center
Question #1 Sepsis
• 28 yo man with diffuse petechial rash diagnosed with menigococcemia
• LP are compatible with bacterial meningitis
• Given IV penicillin and his CXR is normal
• T: 39 P: 120 RR: 20 MAP: 68 on NE
• FiO2 50% and Peep 5 SaO2 = 100%
Question #1: Shock
• In past 6 hours he has received 3 L NS• Urine Output has decreased to 0.25 ml/kg• WBC: 22,000 Plat: 40,000Which of the following interventions is the most
appropriate at this time?(A) Transfuse Platelets(B) Increase NE to achieve MAP > 75 mmHG(C) Switch from NE to DA(D) Administer 1000 ml bolus NS(E) Administer furosemide
Question #1
• Correct answer : D
• Give 1000 ml fluid bolus– Despite the 3 l already he is oxygenating
reasonably well and there is still evidence of organ hypoperfusion
– Only need to keep Plat >50 K if active bleeding or procedure planned
– No evidence that DA better than NE
Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock
Critical Care Medicine 2004 :32(3) 858-873
Surviving Sepsis A: Initial Resuscitation
• 1: Should begin as soon as syndrome recognized. An elevated serum lactate helps to identify . – During first 6 hours the goals should include :
• CVP 8-12mm Hg ( 12-15 mmHg on vent)• MAP > 65 mm Hg• Urine output > 0.5ml/kg/hr• Central Venous or mixed venous O2 sat > 70
• Grade B
Surviving Sepsis A: Initial Resuscitation
• Resuscitation directed for the aforementioned goals within the first 6 hours of presentation improved the 28-day mortality
• Panel judged CV and mixed venous saturation to be equivalent
• Target a higher CVP ( 12-15 mm Hg) in mechanically ventilated patients
Rivers E et al.: Early goal-directed therapy in the treatment of severe sepsis and septic shock N Engl J Med 2001;345:1368-77
Oxygen Delivery
CaO2 = (Hgb x SaO2 x 1.36) +(PaO2 x 0.003)
DO2 = CaO2 x CO x 10
DO2 : Oxygen Delivery Hgb : Hemoglobin
CaO2: Oxygen Carry capacity
SaO2 : Oxyhemoglobin Saturation
PaO2 : Arterial Oxygen Tension
CO : Cardiac Output
Physiologic forms of shock
• Hypovolemic: Dehydration/ hemmorhagic
• Distributive: Sepsis, adrenal Insufficiency, neurogenic, anaphylactic, liver failure
• Cardiogenic: Ischemic or non-ischemic cardiomyopathies, negative inotropes
• Obstructive: Pulmonary HTN, PE, Cardiac Tamponade, valvular, pregnancy
Question # 2 : Solitary Pulmonary Nodule
• 65 yo man with severe alzheimer’s dementia and multiple aspiration pneumonias with 2.5 cm RLL nodule. Prior CXR from 9 yrs ago showed it to be 1.5 cm.
• Current CT shows focal areas of both very high and very low attenuation within the mass.
Question # 2 : Solitary Pulmonary Nodule
Which of the following would be the most appropriate management of the pulmonary lesion at this time.A) referral to thoracic surgeryB) No further evaluationC) Positron emission tomographyD) Fiberoptic bronchoscopy with TBBXE) Transthoracic needle biopsy
Question #2:Correct answer: B
• Hamartoma is the commonest benign pulmonary neoplasm.
• Can be diagnosed by CT
• Presence of focal areas of fat and calcium are characteristic/pathognomonic
Definition of Solitary Pulmonary Nodule
• Solitary Pulmonary Nodule
• Solitary: Single well demarcated lesion No associated adenopathy or effusion
• Pulmonary: Completely surrounded by lung parenchyma
• Nodule: well demarcated lesion less than 3 cm. Lesions greater than 3 cm are masses
Epidemiology: Differential Diagnosis for Benign Nodules (70%)
• Infectious Granuloma (80%)– Coccidiodomycosis, histoplasmosis & mycobacteria
• Hamartomas (10%)• Intrapulmonary lymph nodes• Arteriovenous malformations• Parasitic: Echinococcus or Dirofilaria• Pulmonary Infarcts/ Contusions
Differential Diagnosis of Malignant SPN (30%)
• Primary Lung ( 70-90%)– Usually Non-small cell
– Small Cell accounts for only 4 %
• Metastatic Lesions ( 10-30%)– Head & neck, breast, kidney, sarcomas
– Distinguishing metastatic from primary is not so obvious on presentation clinically in
– 44 pt with breast cancer and SPN 43% were Mets and 52% Primary Lung -Casey, Surgery 1984;96:801-804
Patient Characteristics Which Increase Likelihood of Malignancy
• Age: In patient with age greater than 50, the likelihood of cancer approximates their age. In patients less than 35, the likelihood of cancer is low.
• Exposure History– Smoking– Asbestosis
• Previous History of Cancer
Characteristic of the Nodule That Alter the Odds: Shape
Smooth and round more likely benignalthough 21% of malignancies have
smooth marginsSpiculated or Corona radiata sign are highly
suspicious for cancer, 88-94% are cancerLobulated or scalloped border are
intermediate probability of cancer. 25% of benign nodules are lobulated
Characteristic of the Nodule That Alter the Odds
• Calcifications: – Laminated or Central is typical for granuloma– Pop-corn or areas of fat and calcium are
hamartomas– Eccentric or stippled does not exclude cancer
Characteristic of the Nodule That Alter the Odds
• Size: less than 1cm increases likelihood of benignity whereas greater than 2 cm increases likelihood of malignancy (80% are malignant)
• Stability of more than two years makes it likely benign
• Growth makes cancer more likely. The doubling time for cancer is between 3months to 1 year. Benign lesions have doubling times of less than 30 days or greater than 450 days.
PET Scanning Nodules
• False negatives occur with bronchoalveolar carcinoma, carcinoids and tumors less than 1 cm.
• False Positive occur with active infectious and inflammatory processes
• It is useful once diagnosis is made in staging as well as to stage the mediastinum preoperatively
Question #3: Flow-volume loop
• 67 yo man with COPD with 3 months of progressive dyspnea and wheezing.
• One year ago he had a CABG complicated by prolonged ICU for ARDS
• PE: Persistent wheeze and JVP normal.
• PFTS: as follows
Question #3: Flow-volume loop
FEV1 2.22 L ( 64%)
FVC 4.96 L (107%)
FEV1/FVC 45%
FEF 25-75% 2.13 l/sec (60%)
Question #3: Flow-volume loop
Which of the following is most likely the cause of his dyspnea?
A) Exacerbation of COPD
B) Congestive Heart Failure
C) Late Sequela of ARDS
D) Tracheal Stenosis
E) Constrictive Pericarditis
Question #3: Flow-volume loop
• Correct Answer : D Tracheal Stenosis
Question #4: RA and the Lung
67 yo man with subtle decrease in exercise tolerance and dry cough. 2yr history of seropositive RA. His joint disease is well controlled since the addition 3 months ago of MTX. 12.5mg q week to prednisone 5mg qd. Smokes 2ppd but no exposure history.
Question #4: RA and the Lung
• PE afebrile with joint deformities
• Subcutaneous nodules on extensor surfaces
• No adenopathy. No JVD or edema
• Bibasilar inspiratory crackles
CXR: Subtle bilateral reticular infiltrates
Question #4: RA and the LungPFTs demonstrate :
FEV1 78% predicted
FVC 75% predicted
FEV1/FVC 86%
TLC 70% predicted
RV 72% predicted
DLCO 66% predicted
Which of the following is the most appropriate next step in the management of the patient?
A) Cardiopulmonary exercise testingB) Begin a tumor necrosis factor- antagonistC) Initiate antibiotic therapyD) Stop methotrexate therapyE) Surgical Lung Biopsy
Question 4: RA and Lung disease
Question 4: RA and Lung diseaseCorrect Answer: D
• Associations:– Pleural Effusions: Exudate Low pH low Glucose– Pulmonary Rheumatoid Nodules & Caplan Nodules– Capillaritis– Pulmonary Hypertension– Pulmonary Fibrosis– Bronchiolitis Obliterans– Drug Induced disease– Upper Airway Obstruction
Question 4: RA and Lung disease
• When patient with RA develops ILD, infection (particularly when immunosupressed), Drug-induced lung disease abd complication of RA is in the differential
• No specific test for MTX induced disease but temporal relationship noted.
• CPEX will define impact of the ILD but not help define it
• No other evidence of active RA to begin alternative tx.
Question # 5: Steroids in Sepsis
• 29 yo with active SLE hospitalized with pneumonia. Had been on Prednisone 30 mg/d but weaned off 6 months ago
Febrile WBC 6,000 with left shift Hgb 10 and Plat: 20,000 Mild renal insufficiency
She is hypotensive with BP: 70/40
In addition to fluids and vasopressors which of the following is the most appropriate next step in this patient’s management?
A) Perform an ACTH stim test and initiate steroid therapy if abnormal
B) Initiate therapy with fludroocortisoneC) Administer methylprednisolone, 2g IVD) Administer IV Dexamethasone, and perform and
ACTH stim test
Question #5: steroids in Sepsis
Question #5: Steroids in Sepsis
Correct Answer: D Administer Dexamethasone and do ACTH stim test
Empiric steroids are indicated but hydrocortisone and Methylprednisolone interferes with cortisol measurement
Surviving Sepsis H. Steroids
Rationale: One Multi-centered RCT in patients with severe septic shock showed a significant shock reversal and reduction in mortality in relative adrenal insufficiency (post stim cortisol < 9).
Annane D et al: Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA 2002;288:862-71
Surviving Sepsis H. Steroids
Rational: Two randomized prospective trials and meta-analyses concluded that high-dose steroids for severe sepsis or septic shock are ineffective or harmful.
Bone RC et al: A Controlled clinical trial of high dose methylprednisolone in the treatment of severe sepsis and septic shock. N Engl J Med 1987; 317:653-58
Cronin L et al: Corticosteroid treatment for sepsis: A critical appraisal and meta-analysis of the literature. Crit Care Med 1995;23:1430-39
The VA systemic Sepsis Cooperative Study Group: Effect on high-dose glucocorticoid therapy on mortality in patients with clinical signs of sepsis. N Engl J Med 1987; 317: 659-65
Question # 6: Cough
47 yo man 6 months of cough, episodic, worse at night and when exposed to cold air. Brought on with deep breathing and laughter. No PND or GERD symptoms
PE, CXR and Spirometry normal. No benefit from acid suppression, nasal steroids or anithistamines
He has a family history of allergies
Question # 6: Cough
Which of the following would likely provide the diagnosis of this patient’s chronic cough?a) 24-hour pH-probeb) CT scan of sinusesc) Bronchoscopyd) Trial of inhaled albuterole) CT of the chest
Question # 6: CoughIrwin RS, Madison JM: The Persistent troublesome cough
Am J Resp Crit Care Med 2002; 165:1469-74
• Correct answer is D
• Patient has cough variant asthma or post-infectious reactive airway disease (PIRAD)
Differential Diagnosis Diagnostic study Therapy
Sinusistis/PND
Upper airway cough syndrome (UACS)
CT sinuses Decongestants/anti-inflamatory
Reactive Airways PFT/ methacholine Bronchodilators
GERD 24 Hour Ph PPI
ACE 0 D/c Med
Asthma- Airway hyperresponsiveness
• Histamine, methacholine, exercise
• Positive methacholine challenge- fall in FEV1 of 20% or greater( PC 20 )with 8 mg/ml or less of methacholine
• other causes of nonspecific airway responsiveness: COPD, CHF, bronchiectasis, allergic rhinitis
• Negative methacholine challenge excludes a diagnosis of asthma with 95% certainty
Classification of Severityof Asthma:Clinical Features Before Treatment
Step 4 • Continuous symptoms Frequent • FEV1 or PEFR 60%Severe • Limited physical activity predictedPersistent • Frequent exacerbations • PEFR variability >30%
Step 3 • Daily symptoms >1x/wk • FEV1 or PEFR >60%-Moderate • Daily use of inhaled 80% predictedPersistent short-acting beta2- • PEFR variability >30%
agonist• Exacerbations 2x per
week
Step 2 • Symptoms >2x/wk but >2x/mo • FEV1 or PEFR 80%Mild Persistent <1x/d predicted
• PEFR variability 20%-30%
Step 1 • Symptoms 2x/wk 2x/mo • FEV1 or PEFR 80%Mild • Asymptomatic and predictedIntermittent normal PEFR between • PEFR variability <20%
exacerbations
SymptomsNighttimeSymptoms Lung Function
National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. Bethesda, MD: National Heart, Lung, and Blood Institute. National Institutes of Health (NIH); April 1997. NIH publication No. 97-4051.
Mild IntermittentAsthma Classification: Step 1
• No daily medicationneeded
• Short-actingbronchodilator: inhaledbeta2-agonists asneeded for symptoms
•Use of short-actinginhaled beta2-agonistsmore than two times aweek may indicate the need to initiate long-term control therapy
•Teach basic facts aboutasthma
•Teach inhaler/spacertechnique
•Discuss roles ofmedications
•Develop self-management plan
•Discuss appropriateenvironmental controlmeasures to avoidexposure to knownallergens and irritants
Long-Term Control Quick Relief Education
National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. Bethesda, MD: National Heart, Lung, and Blood Institute. National Institutes of Health (NIH); April 1997. NIH publication No. 97-4051.
Mild PersistentAsthma Classification: Step 2
Daily medication:
• Anti-inflammatory:either inhaledcorticosteroid (lowdose) or cromolyn ornedocromil.
• Sustained-releasetheophylline.Zafirlukast or zileutonmay be considered forpatients 12 yrs of age,although their positionin therapy is not fullyestablished.
• Short-actingbronchodilator: inhaledbeta2-agonists asneeded for symptoms.
• Use of short-acting inhaled beta2-agonists on a daily basis, or increasing use, indicates the need for additional long-term-control therapy.
Step 1 actions plus:
• Teach self monitoring.
• Refer to groupeducation if available.
• Review and updateself-management plan.
Long-Term Control Quick Relief Education
National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. Bethesda, MD: National Heart, Lung, and Blood Institute. National Institutes of Health (NIH); April 1997. NIH publication No. 97-4051.
Moderate PersistentAsthma Classification: Step 3
Daily medication:
• Either
• Anti-inflammatory:inhaledcorticosteroid(medium dose)OR
• Inhaled corticosteroid(low-medium dose)and add a long-actingbronchodilator: eitherlong-acting inhaledbeta2-agonist, SRtheophylline, or long-acting beta2-agonisttablets.
• Short-actingbronchodilator: inhaledbeta2-agonists asneeded for symptoms.
• Use of short-acting inhaled beta2-agonists on a daily basis, or increasing use, indicates the need for additional long-term-control therapy.
Step 1 actions plus:
• Teach self monitoring.
Refer to groupeducation if available.
• Review and updateself-management plan.
Long-Term Control Quick Relief Education
National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. Bethesda, MD: National Heart, Lung, and Blood Institute. National Institutes of Health (NIH); April 1997. NIH publication No. 97-4051.
Severe PersistentAsthma Classification: Step 4
Daily medication:
• Anti-inflammatory:inhaled
corticosteroid(high dose) AND
• Long-actingbronchodilator:
eitherlong-acting inhaledbeta2-agonist, SRtheophylline, or long-acting beta2-agonisttablets AND
• Oral corticosteroid
• Short-actingbronchodilator: inhaledbeta2-agonists asneeded for symptoms.
• Use of short-acting inhaled beta2-agonists on a daily basis, or increasing use, indicates the need for additional long-term-
control therapy.
Steps 2 and 3 actions,plus:
• Refer to individualeducation/counseling
Long-Term Control Quick Relief Education
National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. Bethesda, MD: National Heart, Lung, and Blood Institute. National Institutes of Health (NIH); April 1997. NIH publication No. 97-4051.
Question # 7: Pulmonary Hypertension
52 yo women with 1 yr history of progressive dyspnea. She is short of breath climbing one flight. Former heavy smoker and has hypertension.
PE: elevated JVP, Increased P2, pitting edema
CBC, Chem 20, HIV, RF, ANA, and anti-Scl-70 are negative
CXR: Prominent central arteries and clear lung fields
Question # 7: Pulmonary Hypertension
Echo: concentric LVH, EF=55%, dilated RV, normal valves and PA systolic of 59.
PFT normal except DLCO of 40%
V/Q scan: normal ventilation, heterogeneity of perfusion
RHC: RAP= 10, RVP = 50/10, PAP = 50/20, PCWP (PAOP)= 26 CO: 3.1 CI: 2.0
Question # 7: Pulmonary Hypertension
Which of the following is the most likely cause of the patient’s pulmonary hypertension ?
A) Left ventricular diastolic dysfunction
B) Chronic Pulmonary Embolism
C) Primary Pulmonary Hypertension
D) Pulmonary Veno-Occlusive disease
E) Constrictive Pericarditis
Question # 7: Pulmonary Hypertension
• Correct answer : A
Left ventricular dysfunction
5 10
25 125
Normal Hemodynamic Pressure: “nickel, dime, quarter and a buck twenty five for inflation”
RAP/CVP=5
RV/PAP= 25
PAOP/LA=10
LVSBP= 125
Hemodynamic Profiles
Disease CVP PAP PAOP CO SVR
Normal 5 25/15 10 5 1000
Distributive
Sepsis/AI3 12/6 4 8 600
Hypovolemic 3 12/6 4 3 1200
Obstructive (PE/PHTN)
18 40/20 6 2 1600
Cardiogenic 15 30/20 18 2 1600
Hemodynamic Profiles
Disease
Normal
CVP
5
PAP
25/15
PAOP
10
CO
5
SVR
1000
RV Infarct 20 15/10 6 3 1200
Tamponade 15 30/15 15 3 1200
Question # 7: Pulmonary HypertensionCorrect Answer: A
Disease CVP/RAP
5
RVP
25/5
PAP
25/12
PAOP/PCWP
10
CO
5
A: LV failure
10 50/10 50/20 26 3.1
PPH, VOD
PEConstrictive Pericarditis 10 30/10 30/12 12 3
Question # 8: Pleural Effusion
75 yo man with 80-pack yr & 3 months fever, night sweats weight loss, and dyspnea. Dull left chest pain.
T: 36.8 P:112 RR: 26 Trachea shifted to right, dullness and decreased
breath sounds on leftLabs; WBC: 6.8 Liver and renal normal, Protein
5.0g/dl, LDH 188 U/L.CXR complete opacification on left hemithorax with
shift of mediastinum to right.
Question # 8: Pleural Effusion
Pleural Fluid analysis:
Cell Count: 980 20% Neutro 55% Lymph
10% mesothelial15% eos
Total Protein: 4.5 mg/dl LDH: 1200 U/L Glucose 45 mg/dl
pH: 7.2
Gram stain negative; cytology pending
Question # 8: Pleural Effusion
What is the most likely diagnosis?
A) Transudative pleural effusion
B) Malignant pleural effusion
C) Parapneumonic effusion
D) Rheumatoid pleural effusion
E) Pleural Effusion associated with esophageal rupture
Question #8:Pleural EffusionsCorrect Answer: B
Light’s criteria:Exudates
1) Pleural Fluid protein/Serum protein >0.52) Pleural Fluid LDH/Serum LDH >0.63) Absolute pleural fluid LDH > 2/3 upper limit of normal (> 200)
Only need one to make an exudate This effusion is a exudative with lymphocytic
predominance
Question # 8: Pleural Effusion
• Most common cause of transudates in decreasing order are CHF, hepatohydrothorax, nephrotic syndrome, other low albumin states, atelectasis
• CHF usually bilateral (R>L) orthopnea, S3 and evidence of pulmonary edema on CXR
• Nephrotic syndrome has small bilateral effusions and abnormal UA
• Low albumin states have bilateral effusions albumin less than 1.8
Pleural effusions: Results of tests
• Low pH and Low Glucose– Most common : malignancy & infections– Also seen in rheumatoid arthritis– Are prognostic factors for malignancy– Can be used to decide on need to drain a parapneumonic
effusion
• Lymphocytic Predominant Exudates: Malignancy and Tb.– Malignancy: cytology only positive around 40%– Tb: The presence of greater than 5% mesothelial cells
rules this diagnosis out.
Question # 8: Pleural Effusion
• Effusion is a lymphocytic exudative effusion• If it were a massive parapneumonic it would be
neutrophilic and patient would be more toxic.• Rheumatoid effusions usually seen in setting of
other manifestations of RA• Rupture esophagous would expect low pH 4.0
history of wretching vomitting and are usually not massive
Question # 9: Sleep
45 yo man alternates day, evening and night shifts at work. Drink 6-8 cups of coffee a day to stay awake. His wife reports that he snores and moves his legs when he sleeps.
The accompany image represents one segment of his overnight polysomnogram:
A Pause in ventilation accompanied by desaturation and persistent thoracic cage movement ending with a burst on the EEG.
Question # 9: Sleep
Which of the following disorders does this polysomnogram show ?
A) Obstructive Sleep Apnea
B) Restless leg syndrome
C) Narcolepsy
D) Central Sleep Apnea
E) Cheyne-Stokes breathing
Question # 9: SleepCorrect Answer: A
Obstructive Sleep Apnea:Diagnosis: Cessation of flow but persistent effort accompanying with desaturation. At least 15 apnea/hypopnea /HR
Central Apnea:Diagnosis: Cessation of flow and effort
Narcolepsy: document sleep latency less than 5 min on multiple sleep latency test and early onset of REM.
Question # 9: Sleep
• CPAP is considered the most consistently effective intervention.
• Some find CPAP cumbersome BiPAP may be better
• Uvuloplasty: 40% effective. Reserve for those not tolerating CPAP. Same applies for oral appliances
• Weight loss is difficult to achieve
Question # 10:
55 yo male with severe dyspnea and right sided pleuritic chest pain.
PMH: anaphylaxis after normal coronary angiogram
PE: T:38.1 P:115 R: 24 BP: 110/70
Portable CXR: normal
ABG: (RA) pH: 7.44 PaCO2: 35 PaO2: 60
100% NRB 7.44 PaCO2: 35 PaO2: 150
Question # 10:
Which of the following is the most appropriate next step in the evaluation of the patient?
A) Ultrasound Left Pleural Space
B) Ventilation/perfusion lung scanning
C) Echo with air contrast injection
D) Azithromycin therapy
E) Non-contrast helical (spiral) CT scanning
Question 10: Correct answer BPulmonary Embolism
• Helical Ct without contrast won’t detect PE• Contrast echo is good for shunt however patient
hypoxemia corrects with supplemental O2 and shunt would not cause chest pain
• Ultrasound good for small effusions but these would not have such a profound effect
• Clear CXR does not support diagnosis of pneumonia
Question 10: Pulmonary embolismcorrect answer: E
• Suspicion is that of Pulmonary Embolism– Modified Wells Criteria
• Clinical Signs of DVT 3.0 points• HR > 100 1.5 points• Immobilization 1.5 points• Previous DVT/PE 1.5 points• Hemoptysis 1.0 points• Cancer 1.0 points• PE more likely than any
other diagnosis 3.0 points
< 2.0 = low 2-6 = moderate >6 is high suspicion
Pulmonary Embolism
• Work up: If suspicion is low to moderate a negative d-Dimer helps rule out DX. Positive d-Dimer not helpful
• If suspicion if moderate to high and sign of DVT then Venous Dopplers
• If Suspicion is High: CT scan with PE protocol• If Dye Allergy: Dopplers and V/Q scan• Unstable patient: Dopplers and ECHO to look for
RV strain
Question # 10: Pulmonary embolism : Correct answer: B
• High Probability VQ: 85% will have PE– High Prob & High clinical suspicion: 95% will
have PE
• Low probability VQ: 13 % will have PE– Low probability with high clinical suspicion:
43% have PE
• Normal V/Q: only 5% have PE and these have no clinical sequela left untreated
Question # 11: Abnormal CXR
28 yo woman with a persistent cough. Never smoked and travels to Mexico to vacation yearly. CXR shows mild interstitial abnormalities with hilar and mediastinal fullness. PFT’s are normal. A PPD is negative
Question # 11: Abnormal CXR
Which of the following findings would warrant a trial of oral corticosteroid therapy?A) Bilateral Anterior uveitisB) HypercalcemiaC) Fever and tender red nodules over the anterior shinsD) Abnormal LFTs
Question # 11: Sarcoid• Absolute indication for steroids
– Neurologic Sarcoid– Cardiac Sarcoid– Hypercalcemia + renal failure– Occular (treated with topical steroids)
• Relative:– Disabling lung disease– Disfiguring cutaneous
• Patients with adenopathy and no symptoms have 50-90% spontaneous resolution.
• Lofgren’s syndrome: fever, E. Nordosum and adenopathy do well with just NSAIDS.
Question 11: Sarcoid
STAGE CXR Response to systemic steroids
0 Normal N/A
I Adenopathy & Normal Parenchyma
60-80%
II Adenopathy & Infiltrates 50-60%
III Parenchyma & no adenopathy
< 30%
IV Fibrosis & Honey combing < 10%
Question 12: Resp Failure on Vent
37 yo admitted to ICU with severe CAP and ARDS. HIV positive not on HAART,. Intubated, BAL performed and begun on Trimethoprim/Sulfa and steroids.
Originally doing well on lung protective vent strategy but over 20 minutes SaO2 drops to 87% despite FiO2 100% PEEP 12. Pulse 132 RR 22 Lung sounds diminished on right
Peak insp Pressure gone from 28 to 38 and SBP down to 80 mmHg
Question 12:
Which of the following is the most appropriate next step in the management of the patient?
A) Inhaled Nitric OxideB) Start inverse ratio ventilationC) Insert a needle in the right hemithorax,
2nd anterior spaceD) Use prone positioning
Question 12: Correct answer C
• Acute tension pneumothorax, a known complication in patients with Pneumocystis Jiroveci pneumonia.
Peak pressure is the pressure to push the breath in and thus overcome lung/chest wall compliance and air way resistance
Plateau pressure only to hold breath in. Only overrcomes lung/chest wall compliance
Question #13: ARDS/Vent
72yo women is evaluated in the ER for fever & flank pain. Obese BW: 90kg ( IDBW: 60kg)
Febrile: BP: 85/50 P: 132 RR: 28Lungs clear R CVA tendernessGiven fluids and AntibioticsShe goes into progressive respiratory failure
and decision to intubate her.
In addition to 100% FiO2, PEEP of 5 and rate of 24, which would be the most appropriate vent setting?
A) PCV PIP 30, Peep 10 I:E 2:1
B) AC tidal Volume 360
C) AC tidal volume 540
D)PS of 10 cm
Question #13: Pneumonia/Vent
• ARDS-net clinical trial 6ml/kg IBW was superior to 12 ml/kg IBW in terms of survival and development of MODS.
• IBW is based on sex and height
Question # 13Correct Answer : B
ARDS Mechanical VentilationARDS-Net
ARDS-Net
• Multi-centered• Randomized prospective trial• Hypothesis: In patients with ALI and ARDS
would lower tidal volume improve outcome• Randomized to : 6 ml/kg ( Plat 30-25) vs. 12 ml/kg ( plat <50) predicted BW Stopped after 4th interim analysis ( n=861)
ARDS-Net
ARDS-Net
Ventilator modes
• Full support: Patient in arrest, shock– i.e: AC, CMV
• Partial support: Weaning of patients– i.e: PS, SIMV
• Super-duper: Sick lungs where full support does not work– i.e PCV, APRV
Basic Modes: Assist/Control (CMV)
Set: Fio2 Peep Rate TV
Represents two separate modes:
Control mode:
Cycle on: Time Target: Volume Cycle off: Volume
Assist mode:
Cycle on: pressure/flow Target: Volume Cycle off Volume
The rate set is the rate it changes from on to the other.
FULL SUPPORT: UNWEANABLE
Basic Modes: (S)IMV
• Set TV, Peep, FiO2 and Rate
• Cycle on: either Time (control) or Pressure/flow (assist or Synch)
• Target: Volume
• Cycle Off: Volume
• Similar Characteristic to AC
• Full or Partial Support depending on Rate
Basic Modes: Pressure Support(Power Steering)
• Set FiO2 Peep(Cpap) and Pressure• Cycle on: Pressure/Flow (Pure Assist)• Target: Pressure• Cycle Off: Flow
• Pure assist mode. Volume delivered changes based on Compliance
• Can be Full Support ( Psmax) or Partial support depending on level of pressure
Basic Modes: Pressure Control
• Cycle on: Pressure Flow (assist) or Time (control)• Target: Pressure• Cycle off: Time
– Can maintain inspiratory effort and dwell time beyond patient’s effort.
– Recruit alveola with longer time constants– As flow reaches Zero yet the pressure is maintained,
the Pressure set is the Plateau pressure
• Can prolong inspiratory phase to the point of reversing I:E ratio (Needs sedation)
Question #14: Interstitial lung disease
60 yo man with 1 yr progressive severe DOE and 3 month non-productive cough
Smoked 2ppd x 30 yrs quit 3 yrs ago
PE: pain both knees without swelling, bibasilar crackles No edema
SaO2 on RA at rest 94% with exertion 84%
CXR: Lower lobe interstitial linear markings
Question #14: Interstitial lung disease
HRCT: reticular infiltrates in periphery lower lobes, sub-pleural cysts patchy ground glass opacities, centrilobular emphysema in the apices
PFTs: FEV1 =84% FVC = 82%
DlCO = 39%
ANA = 1:160 ( one dilution above normal)
Question #14: Interstitial lung disease
Which of the following is the most likely diagnosis?
A) Emphysema with “smoker’s lung”
B) Systemic lupus erythmatosus with pulmonary involvement
C) Idiopathic pulmonary fibrosis
D) Idiopathic pulmonary fibrosis with emphysema
E) Systemic sclerosis ( scleroderma) with lung involvement
Question #14: Interstitial lung diseaseCorrect Answer: C
• Counterbalance restrictive effect of fibrosis and obstructive effect of emphysema account for normalization of lung volume.
• ANA and RF are often abnormal with IPF
• The patient’s age, sex and paucity of extrapulmonary signs or symptoms 1 year out point to IPF over SLE or scleroderma
Interstitial Fibrosis
• Upper Lobe– Ankylosis Spondylsis
– Sarcoid
– Tb/ Histo
– E. Granuloma (histiocytosis X)
– Cystic Fibrosis
– PCP
• Lower Lobe – Asbestosis
– Rheumatologic (RA/Scleroderma)
– Aspiration
– IPF
Question #15:Lung Cancer
75yo man with cough and weight loss.
Exam: cachectic, right supraclavicular node
CXR 7 cm mass in right lower lobe
CT: Lung mass several enlarged mediastinal lymph nodes, 3 contralateral nodules and an adrenal mass
MRI: Single posterior fossa lesion
Question #15:Lung Cancer
Which is the best next step in management of the patient?
A) Percutaneous biopsy of right adrenal gland
B) Steriotactic biopsy of brain lesion
C) Aspiration biopsy of supraclavicular node
D) Mediastinoscopy
E) Positron emission tomography
Question #15: Lung CancerCorrect Answer: C
Has advanced metastatic disease
Therefore one should biopsy the most accessible site that will diagnose metastatic disease with the least discomfort or risk to the patient.
STAGING:
Small Cell is : Limited ( within a radiation port) or extensive.
Non-small cell staging is TNM
Lung Cancer
• Most common cause of cancer death in US
• Overall 5 year survival of 15%
• More deaths by lung cancer than the next four most common cancers combined (Colorectal, Breast, Prostate, & Pancreas)
NonSmall Cell CancerT Stage
• T1: < 3cm in diameter, contained within visceral pleura.
• T2: > 3cm in diameter, >= 2cm away from carina, invading into visceral pleura, or lobar atelectasis
• T3: any size, extension into chest wall, diaphragm, mediastinum, (but not great vessels) or <2cm from carina or atelectasis of entire lung
• T4: any size invading into great vessels, heart, trachea, esophagus, vertebrae, main carina or malignant pleural effusion.
NonSmall Cell CancerN Stage
• N0: No nodes.
• N1: Ipsilateral hilar or peribronchial.
• N2: Ipsilateral mediastinal, subcarinal.
• N3: Contralateral hilar, contralateral mediastinal or supraclavicular/scalene.
Non Small Cell Carcinoma Staging N0 N1 N2 N3
T1 IA IIA IIIA IIIB T2 IB IIB IIIA IIIB T3 IIB IIIA IIIA IIIB T4 IIIB IIIB IIIB IIIB M1 IV
TREATMENT Surgery
Neoadjuvant/surgery
Non-Surgical
Small Cell Lung Cancer:Staging
• Limited:– 30-40% of small cell lung cancers.– Confined to the hemithorax, mediastinum, and
ipsilateral supraclavicular lymph node.– Within the confines of radiation port.
• Extensive:– 60-70% of small cell lung cancers.– Any distant spread.
Question # 16: Positive PPD
45 yo man with a pre-employment PPD positive at 22 mm. He is asymptomatic
Emigrated from Sri Lanka 15 years ago. No exposure to Tb but did get the “tuberculosis vaccine” as a child .
CXR is normal.
Question # 16: Positive PPD
Which of the following is the most appropriate next step?A) Treatment for active tuberculosis should be initiatedB) Treatment for latent tuberculosis should be initiatedC) Further testing is warranted to look for active
tuberculosis, and sputum induction or bronchoscopy should be performed
D) Skin testing should not have been performed; his reaction is false positive secondary to his earlier vaccination.
Question # 16: Positive PPD
• Correct Answer: B treatment for latent infection
• Positive skin test and negative chest x-ray• BCG: 60-80% reduction in incidence of Tb.
False positive reaction occurs in less than 10% of those vaccinated before 1 yr and 25% in those vaccinated after age 5. It would not cause a 22mm reaction
• 5mm positivity: – HIV
– Intimate exposure,
– CXR compatible with fibrotic changes
– Organ transplant or Immunosuppression with steroid of 15 mg/d of prednisone for > 1 month or the equivalent
• 15mm: No risk factors• 10mm everyone else
Question # 16: Positive PPD