Sometimes when interpreting spiromtery, a patient may have what appears to be a mixed obstructive/ restrictive picture. (Reduced FEV1/FVC and Reduced FVC).

Patients with an obstructive process (i.e COPD) may have gas trapping, which will reduce their FVC due to increased residual volume (RV). This may falsely lead a clinician to interpret it as a mixed obstructive/ restrictive process, while it is truly just obstructive.

NOTE: The next step to confirm pseudo-restriction, is to get a TLC. If normal (and therefore not restrictive) it highly suggests this pathology. Also look at the RV and RV/TLC ratio.

Img Cred: Cleve Clin J Med


  1. Sorino, C et al. Physician’s mistakes in the interpretation of spirometry. European Respiratory Journal 2012 40: P1131
  2. Ranu H, Wilde M, Madden B. Pulmonary Function Tests. The Ulster Medical Journal. 2011;80(2):84-90.
  3. As-Ashkar, F, Mehra, R, Mazzone, PJ. Interpreting pulmonary function tests: recognize the pattern, and the diagnosis will follow. Cleve Clin J Med. 2003;70:866–881.

Pulse oximetry is almost ubiquitous in the acute medicine setting. It can be very useful but has its limitations. Some factors affecting it include:

  • Carbon Monoxide (binds up oxygen at higher affinity)
  • Cyanide (disrupts electron transport chain)
  • Methemoglobin (form of hemoglobin that does not carry oxygen)
  • Anemia (hemoglobin deficiency)
  • Cold extremities (hypothermia)
  • Fingernail polish/ extensive nail pigmentation
  • Intravenous Dyes (i.e methylene blue)



Asterixis is considered a form of myoclonus.

HOW TO DETECT? Have the patient hold their arms outstretched with fingers and wrists extended. There will be intermittent loss of muscular tone causes sudden flexion at the wrists followed by a return to extension, so that the hands flap in a regular or, more often, an irregular rhythm.

See video here.

Major Causes for Asterixis include:

  • Hepatic Encephalopathy
  • Hypercapnia
  • Uremic Encephalopathy


  1. Young RR, Shahani BT. Asterixis: one type of negative myoclonus. Adv Neurol. 1986;43:137-56.
  2. Chapter 11: Movement Disorders. Clinical Neurology, 9e

Spontaneous Pneumothorax

  • Can be either primary (absence of underlying lung pathology) or secondary (due to presence of underlying lung pathology)
  • Classic spontaneous pneumothorax occurs in a tall, thin, young male patient (Marfan Syndrome!)
  • In primary spontaneous pneumothorax: If the pneumothorax is small and symptomatic it usually resolves on its own, but if it is large and symptomatic, patient should be admitted
  • In secondary spontaneous pneumothorax: Most patients will require admission and chest tube drainage. Since, these patients usually have underlying lung pathology, other treatment will also be included (i.e. antibiotics, additional diagnostic tests, etc.)
  • Spontaneous pneumothorax may evolve into tension pneumothorax


Tension Pneumothorax

  • Forms due to a one-way valve where air can enter the pleural space upon inspiration, but not leave (MEDICAL EMERGENCY!!!)
  • Most commonly due to traumatic pneumothorax (due to blunt or penetrating trauma to the chest or due to iatrogenic causes such as diagnostic/therapeutic procedure)
  • Findings to help differentiate from spontaneous pneumothorax: contralateral tracheal deviation, hypotension, tachycardia, hypoxia, increased jugular venous pressure (JVP)
  • Physical exam findings on ipsilateral lung: hyper-resonance, absent breath sounds, decreased vocal fremitus, and diminished chest wall expansion
    • 14-16 gauge needle inserted in second intercostal space at the mid-clavicular line


Symptoms common to both spontaneous and tension pneumothorax include: chest pain localized to affected side and dyspnea. The chest pain may be pleuritic and is usually acute.

Patients with underlying asthma or COPD should be treated urgently if patient has a tension pneumothorax or a symptomatic spontaneous pneumothorax as this can result in life-threatening cardio-respiratory failures.



  • Kemp, Walter L, Travis G Brown, and Dennis K Burns.The Big Picture: Pathology. 1st ed. The McGraw-Hill Companies-Lange, 2007. Print.
  • Ashby  M  et al. Conservative versus interventional management for primary spontaneous pneumothorax in adults. Cochrane Database Syst Rev. 2014 Dec 18;12:CD010565.
  • Bintcliffe  OJ  et al. Spontaneous pneumothorax: time to rethink management? Lancet Respir Med. 2015 Jul;3(7):578–88.
  • Grundy  S  et al. Primary spontaneous pneumothorax: a diffuse disease of the pleura. Respiration. 2012;83(3):185–9.
  • Stone, Keith c. Current Diagnosis and Treatment: Emergency Medicine. 7th ed. New York: McGraw-Hill education, 2011. Print.

Upper Lobe: SET CAP or FASTEN

S: Silicosis/sarcoidosis
E: Extrinsic allergic alveolitis (hypersensitivity pneumonitis)
T: Tuberculosis
C: Cystic Fibrosis
A: Ankylosing spondylitis
P: Pneumocystis Pneumonitis


F: Farmer’s lung (hypersensitivity pneumonitis)

A: Ankylosing spondylitis

S: Silicosis/sarcoidosis

T: Tuberculosis

E: Eosinophilic granuloma

N: Neurofibromatosis

Lower Lobe: BAD RASH

B: Bronchiectasis
A: Aspiration
D: Desquamative interstitial pneumonia
R: Rheumatoid Arthritis
A: Asbestosis
S: Scleroderma
H: Hamman-Reich Syndrome (Acute interstitial pneumonitis)


  1. Nemec, S. F., Bankier, A. A., & Eisenberg, R. L. (2013). Upper Lobe–Predominant Diseases of the Lung. American Journal of Roentgenology, 200(3). doi:10.2214/ajr.12.8961
  2. Felson B. A new look at pattern recognition of diffuse pulmonary disease. AJR Am J Roentgenol 1979; 133:183.
  3. Genereux GP. Radiologic assessment of diffuse lung disease. In: Radiology, Diagnosis, Imaging, Intervention, Taveras, Ferrucci (Eds), JP Lippincott, Philadelphia 1992. Vol 1, p.1-18.


pH 6.6

130 mEq Sodium

4 mEq Potassium

3 mEq Calcium

109 mEq Chloride

28 mEq Sodium Lactate (provides 9 calories/liter)


Isotonic hydration; replaces (negligible) electrolytes and extra-cellular fluid losses; can buffer mild to moderate acidosis (the lactate is metabolized into bicarbonate which counteracts the acidosis)


  1. Chapter 9. Regulation of Acid-Base Balance. Vander’s Renal Physiology, 8e

Obstructive shock occurs due to obstruction of the cardiovascular system. Commonly due to PE, Tension pneumothorax and Tamponade.

HOW? PE results in elevated RV preload and strain (high CVP and RV dilation).

Typical clinical presentation is hypotension, skin vasoconstriction and distended JVP. A pulsus paradoxus can often be found.


  1. Oxford Desk Reference: Critical Care. Carl Waldmann, Neil Soni, Andrew Rhodes. 2008. Oxford Press.
  2. Emergency Medicine: The Principles of Practice. Gordian W. O. Fulde. 2009. Elsevier Australia.

The JAMA Rational Clinical Examination recommends two clinical signs:

  1. The Lovibond angle (angle between proximal nail bed and nail plate) CLUBBING: >180° (normal is 160° or less)
  2. Distal phalangeal finger depth (DPD) to Interphalangeal finger depth (IPD) ratio. CLUBBING: DPD > IPD (normal is IPD > DPD)
Img Cred: The JAMA Rational Clinical Examination
Img Cred: The JAMA Rational Clinical Examination

NOTE: The Schamroth’s sign (Obliteration of diamond-shaped window between the dorsum of terminal schamroth-testphalanges) is typically taught during bedside rounds but the precision and accuracy of this sign have not been formally tested.


  1. Lampe RM, Kagan A. Detection of clubbing—Schamroth’s sign. Clin Pediatr (Phila). 1983;22(2):125.
  2. Myers KA, Farquhar DRE. Does This Patient Have Clubbing?. JAMA. 2001;286(3):341-347. doi:10.1001/jama.286.3.341
  3. Validity and Reliability of the Schamroth Sign for the Diagnosis of Clubbing.  JAMA. 2010;304(2):159-161. doi:10.1001/jama.2010.935
  1. Smoking Cessation
  2. Long-term Oxygen therapy (>15 hours per day)
  3. Lung volume reduction surgery in certain subsets of COPD patients (Emphysema)
  4. Pulmonary Rehabilitation AFTER a COPD exacerbation


  1. Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease: a clinical trial. Nocturnal Oxygen Therapy Trial Group. Ann Intern Med 1980;93:391-8.
  2. Mannino DM, Kiri VA. Changing the burden of COPD mortality. International Journal of Chronic Obstructive Pulmonary Disease. 2006;1(3):219-233.
  3. Puhan MA, Scharplatz M, Troosters T, Steurer J. Respiratory rehabilitation after acute exacerbation of COPD may reduce risk for readmission and mortality — a systematic review. Respir Res. 2005;6:54.
  4. Young J, Fry-Smith A, Hyde C. Lung volume reduction surgery (LVRS) for chronic obstructive pulmonary disease (COPD) with underlying severe emphysema. Thorax. 1999;54(9):779-789.

A granuloma is a focal, compact collection of inflammatory cells (i.e histocytes).

Caseation” (translation “turning to cheese”). Non caseating aka Non-necrotizing granulomas do not have characteristic necrotic appearance on gross visual examination and generally are of non-infectious etiology. More info here.

  • Seen in conditions such as: ***Sarcoidosis***, hypersensitivity pneumonitis, IBD and chronic Beryllium disease


  1. James DG (1991). What makes granulomas tick? Thorax 46: 734736.
  2. Iannuzzi M, Rybicki BA, Teirstein AS (2007). “Sarcoidosis”. New England Journal of Medicine 357 (21): 2153–2165.
  3. Zumla A, James DG (1996). Granulomatous infections: etiology and classification. Clin Infect Dis 23:146–158
  4. Chapter 390: Sarcoidosis. Harrison’s Principles of Internal Medicine, 19e. Robert P. Baughman; Elyse E. Lower