Westermark’s Sign


Other Known Aliasesnone


Definitionfocal peripheral hyperlucency resulting from collapsed vessels distal to a pulmonary thromboembolism.



Clinical SignificanceOccurs as a result of oligemia of perfusion to the lung parenchyma and can be seen in up to 10% of patients with acute PTE.  Similar to Hampton’s Hump, it has a low sensitivity, but a high specificity


History – Named after Nils Johan Hugo Westermark (1892-1980), a Swedish radiologist who first described this finding in his 1938 paper entitled ” On the roentgen diagnosis of lung embolism”.  He was also an accomplished sailor and won a silver medal in the 1912 Olympics.




  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Up To Date. www.uptodate.com
  6. Krishnan AS, Barrett T. Images in clinical medicine. Westermark sign in pulmonary embolism. NEJM. 2012; 366(11):e16. [pubmed]
  7. Radiopaedia.  Westermark Sign. https://radiopaedia.org/articles/westermark-sign-1
  8. Westermark N. On the roentgen diagnosis of lung embolism. Acta Radiol 1938;19:357‑72.

PAINE #PANCE Pearl – Pulmonary


57yo man is referred to your practice due to an incidental 1.1cm single pulmonary nodule found on computed tomography.  He is a never smoker and denies any known family history of lung cancer.  He has no pulmonary medical history and reports no pulmonary symptoms.


Image result for single pulmonary nodule ct


What is the next step in the management of this patient?


Hampton’s Hump


Other Known Aliasesnone


Definitionwedge-shaped opacity in the periphery of the lung on chest radiography usually with its base along the pleural margins.


Clinical SignificanceOccurs as a result of infarction and subsequent hemorrhage from the bronchial arteries classically due to a pulmonary embolism, but can also be from anything that causes infarction of lung parenchyma.  The sensitivity and specificity of this finding is not robust and is, by definition, a late finding that is really no longer seen in modern medicine.


History – Named after Aubrey Otis Hampton (1900-1955), an American radiologist who received his medical degree from Baylor University in 1925.  He rose through the ranks quickly in the field of radiology ultimately taking a position as chief of radiology at Massachussetts General in 1941.  He first described his eponymous finding in 1940 in his manuscript entitled “Correlation of postmortem chest teleroentgenograms with autopsy findings”.

Image result for Aubrey Otis Hampton



  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Up To Date. www.uptodate.com
  6. Radiopaedia. Hamptons’ Hump. https://radiopaedia.org/articles/hampton-hump-2
  7. Schatzki R, Lingley JR. Aubrey O. Hampton, 1900-1955. The American journal of roentgenology, radium therapy, and nuclear medicine. 1956; 75(2):396-7. [pubmed]
  8. Ladeiras-Lopes R, Neto A, Costa C, et al. Hampton’s hump and Palla’s sign in pulmonary embolism. Circulation. 2013; 127(18):1914-5. [pubmed]
  9. Hampton AO, Castleman B.  Correlation of postmortem chest teleroentogenograms with autopsy findings.  Am J Roentgenol Radium Ther. 1940;34:305-326.

#36 – Basics of the Ventilator with Wes Johnson, PA-C



Guest Information


Wes Johnson, MSPAS, PA-C, (soon to be), DHSc was a former student of mine at UAB and was a respiratory therapist prior to PA school.  He is the Regional Director of Clinical Education for Island Medical Management Emergency group in North Alabama.  He won the Preceptor of The Year award from UAB in 2016 and currently finishing up his doctorate degree from A.T. Still University.

Twitter – @wesj2288



For the purposes of this podcast and post, we will be using the Puritan Bennett 840 ventilator (pictured below).  All the term we use are synonymous with all vents, but the screens will be different.

Puritan Bennett 840

Big Concepts of The Ventilator


  1. Mode
    1. Assist Control (AC)
      1. Every breath is either a machine driven (set by rate) or fully assisted (initiated by the patient)
        1. Uses either pressure (ACPC) or volume (ACVC)
    2. Synchronized Intermittent Mechanical Ventilation (SIMV)
      1. Set number of machine driven breaths, and patient intitated breaths are partially assisted
    3. Pressure Support (PS)
      1. No machine driven breaths and all breaths are initiated by the patient and partially assisted
  2. Delivery
    1. Pressure
      1. Static Controls
        1. Pressure
        2. Time (inspiratory)
        3. Peak flow
      2. Variable Factors
        1. Volume
        2. Total flow
    2. Volume
      1. Static Controls
        1. Tidal volume (cc)
        2. Flow (L/min)
      2. Variable Factors
        1. Pressure
  3. Positive End Expiratory Pressure (PEEP)
    1. The pressure left in the circuit at the end of expiration
    2. Prevents alveolar collapse and improves oxygenation
    3. Can cause barotrauma and affect hemodynamics

Static Controls


(For this section, refer back to the vent picture above)

  1. Fraction of Inspired Oxygen (FiO2)
    1. Start at 100% and titrate down to 21%
  2. f (machine breath rate)
  3. Control
    1. Pressure Control (PC)
      1. Inspiratory pressure (Pi)
        1. Peak pressure in circuit
        2. Initial setting = < 20 cm H20
      2. Inspiratory time (I-time)
        1. Initial setting = 1.25 seconds
    2. Volume Control (VC)
      1. Vt (tidal volume of each breath)
        1. Initial setting = 6-8 cc/kg IBW
      2. Vmax (flow rate)
  4. Spontaneous Support
    1. Trigger for spontaneous support
      1. Volume = V-trig
      2. Pressure = P-trig
    2. Pressure Support (PS)
      1. I was always taught at least 5 cm H20 to overcome circuit resistance

Real-Time Controls


  1. Flashing “C” and “S”
    1. Lets you know what breaths are controlled (machine) or spontaneous (patient)
  2. Airway Pressure
    1. Ppeak (max airway pressure)
      1. A marker of resistance
    2. Pmean (average airway pressure)
      1. A measure of alveolar pressure
    3. Pplat (small airway and alveoli pressure)
      1. A measure of compliance
  3. fTotal (machine + spontaneous breaths)
  4. I:E (inspiratory:expiratory ratio)
    1. Normal = 1:2 (at rest)
    2. Inverse ratio (2:1) can improve oxygen due to intention auto-PEEP

Wes Johnson’s Approach to Setting Up a Ventilator (after RSI)


Mode: AC

Vt: 6-8 mL/kg based on pt’s IBW

Rate: 12-16 bpm

FiO2: 100%

PEEP: 5.0

At the 5-minute mark:

  • Check an ABG
    • Titrate FiO2 off of PaO2 and pulse oximeter
    • Adjust minute ventilation off of PaCO2 and/or ETCO2


  1. Respiratory Review YouTube Channel https://www.youtube.com/channel/UCtaRF58UDVthvH36YYCttng
  2. Deranged Physiology.  Mechanical Ventilation. http://www.derangedphysiology.com/main/core-topics-intensive-care/mechanical-ventilation-0
  3. Weingart SD – “Spinning Dials – How to Dominate the Ventilator” – https://emcrit.org/wp-content/uploads/vent-handout.pdf
  4. Weingart SD. Managing Initial Mechanical Ventilation in the Emergency Department. Annals of emergency medicine. 2016; 68(5):614-617. [pubmed]
  5. Air Link Regional West – “Initial Adult Ventilator Settings” – https://www.rwhs.org/sites/default/files/airlink-factsheet-ventsettings.pdf
  6. Open Anesthesia. Modes of Mechanical Ventilation. https://www.openanesthesia.org/modes_of_mechanical_ventilation/
  7. Modern Medicine Network.  A Quick Guide to Vent Essentials. http://www.modernmedicine.com/modern-medicine/content/tags/copd/quick-guide-vent-essentials
  8. Tobin MJ. Extubation and the myth of “minimal ventilator settings”. American journal of respiratory and critical care medicine. 2012; 185(4):349-50. [pubmed]

PAINE #PANCE Pearl – Pulmonology


When following low-risk, small single pulmonary nodules,

  1. What is the time sequence for the follow-up CT scans?
  2. How long do you re-image them for?


  1. It depends on the size of the nodule and consistency after the initial CT scan.  The current guidelines state:
    1. For solid nodules:
      1. < 6mm recommend no further imaging
      2. > 6mm but < 8mm recommend CT scan at 6-12 months
      3. > 8mm recommend CT scan at 3-6 months, 9-12 months, and 18-24 months
    2. For non-solid (ground glass) nodules:
      1. < 5mm recommend no further imaging
      2. > 5mm recommend annual CT for 3 years
    3. For part-solid (>50% ground glass) nodules:
      1. < 8mm recommend CT scan at 3 months, 12 months, 24 months, and annual for 1-3 years
      2. > 8mm recommend CT scan at 3 months and PET or biopsy
  2. Low-risk nodules can be serially scanned for 2 years and if no change, can stop repeat imaging as malignant nodules will show some form of change in 2 years.


  1. Gould MK, Donington J, Lynch WR. Evaluation of individuals with pulmonary nodules: when is it lung cancer? Diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2013; 143(5 Suppl):e93S-e120S. [pubmed]

#32 – Pulmonary Thromboembolism




  • 300,000-600,000 cases per year in the United States
  • It is estimated that up to 50% will have post-thrombotic syndrome

Why Are We So Scared?

  • As many as 20% of patients with 1st onset PTE have no identifiable risk factors
  • 10-30% 1-month mortality with up to 25% presenting as sudden death
  • Fear of litigation is #1 reason clinicians work-up low risk PTE

Why Can’t We Test Everyone?

  • Up to $16,000 per patient in total health care costs
  • 6 times more deaths with testing and treatment

Signs and Symptoms

The majority of the classic signs and symptoms come from PIOPED II study and EMPEROR registry.  These include:

  • Dyspnea (73%)
  • Chest Pain (64%)
  • Tachypnea (57%)
  • DVT findings or leg pain/swelling (47%)
  • Tachycardia (26%)
  • Dizziness (12%)
  • Hemoptysis (10%)

The EMPEROR registry took it a step further and determined mean vital sign measurements of:

  • Heart rate – 95 bpm
  • Respiratory rate – 20 bpm
  • Oxygen saturation – 95%

A recent trail in the NEJM called PESIT concluded as many as 1 in 6 patients with first time syncope has a PTE on inpatient work-up.  This study has been largely panned by the EM community and you can read their take from the links below:

Pre-Test Probability Scores

The most well know score is the Wells Criteria first published in 1998 and then revised and simplified in 2000 and 2001.


A second calculation is the Geneva Score first published in 2001 and revised and simplified in 2006 and 2008.


The Pulmonary Embolism Rule-Out Criteria was published in 2008 by Jeff Kline and is a second set of criteria to definitively rule-out PTE in patients ALREADY SCORE AS LOW RISK by Wells or Geneva.


What about just good ol’ clinical gestalt?  An interesting study was performed in 2013 looking at the accuracy of Wells vs Geneva vs Gestalt and found:

  • Clinical gestalt had a lower missed rate of PTE in low-risk patients
  • Clinical gestalt had a high accuracy of diagnosing PTE in high-risk patients

The Work-Up of Suspected PTE

  1. Electrocardiogram is not senstitive nor specific for PTE but should be ordered on every patient with chest pain and/or shortness of breath to rule-out ACS
    1. The EMCMD talks about the 10 ECG findings of PTE in the best video I have every scene
  2. D-Dimer
    1. High senstivity = good for rule-out
    2. Should only be used after pre-test probability due to the false positives and unnecessary work-ups
    3. ADJUST-PE Study
      1. Found D-Dimer go up with age and created an age adjusted D-Dimer cutoff of:
        1. Age (yr) x 10 as diagnostic threshold
  3. Radiographic Imaging
    1. Computed tomography is gold standard but has higher radiation exposure and contrast loads
    2. Image result for CT PTE
    3. Ventilation/Perfusion scan is safer in renal patients but up to 2/3rd are non-diagnostic
    4. Image result for V/Q PTE

Risk Assessment

Once you diagnose a patient with a PTE, you have determine the patient’s risk and severity of disease.

  1. Echocardiogram
    1. Looking for RV strain
      1. RV:LV ≥ 1
      2. RV hypokinesis
      3. Paradoxical septal movement
      4. Tricuspid regurgitation
  2. Biomarkers
    1. Brain Natriuretic Peptide (BNP)
      1. > 90 pg/mL has been associated with increased mortality
    2. Troponin
      1. > 0.01 ng/mL suggests evidence of RV dysfunction
  3. Pulmonary Embolism Severity Index (PESI)
    1. Published in 2005 and simplified 2010
    2. Developed to help prognosticate 30d mortality and found low-risk patients (PESI – 0) can be safely treated as outpatient

Definitions/Grades of PTE

Treatment Strategies for PTE

  1. Anticoagulation
    1. Started with confirmation of PTE or with high pre-test probability during workup
    2. Lots of options (heparin, LMWH, direct thrombin inhibitors, Factor Xa inhibitors)
  2. Fibrinolytics
    1. Lots of recent research on who to lyse and who not to
    2. Original research showed benefit if full dose lytics were given to massive PTE, but harm in submassive patients
    3. This led to MOPPET in 2013 evaluating 1/2 dose lytics in submassive patients and found:
      1. Reduction in overall mortality
      2. No difference in bleeding complications
      3. Reduction in hospital stay
    4. PEITHO came next in 2014 and looked at full dose lytics vs anticoagulation only for submassive PTE and found:
      1. No mortality benefit
      2. Reduction in hemodynamic compromise
      3. Increase in major bleeding and intracranial hemorrhage
  3. Catheter Directed Therapy
    1. Good options in patients with a high risk of bleeding with systemic fibrinolytic therapy
    2. This can include:
      1. Focal fibrinolytic therapy at the clot
      2. Mechanical thombectomy
        1. AngioJet system
        2. AngioVac system
      3. Ultrasound Assisted Local Fibrinolytic Therapy
        1. ULTIMA and SEATTLE-II studies found reduction in RV:LV ratio and decreased bleeding complications
  4. Surgical Thrombectomy
    1. Can be used as a last resort option and mortality from these procedures has dramatically improved from 57% in the 1960s to < 6% in 2005

Putting It All Together

This is a graphic I modified from Jeff Kline and EmCrit that encompasses everything into a nice, neat package and as I have said before “algorithms will set you free”



  1. Beckman MG. Venous Thromboembolism: A Public Health Concern. Am J Prev Med. 2010;38(4S):S495-S501
  2. Spyropoulous AC. Direct medical costs of venous thromboembolism and subsequent hospital readmission rates: an administrative claims analysis from 30 managed care organizations. J Manag Care Pharm. 2007;13(6):475-486
  3. Calder KK. The mortality of untreated pulmonary embolism in emergency department patients. Ann Emerg Med. 2005;45(3):302-310
  4. Stein PD. Silent pulmonary embolism in patients with deep venous thrombosis: A systematic review. Am J Med. 2010;123:426-431
  5. Stein PD. Clinical Characteristics of patients with acute pulmonary embolism. Am J Med. 2007;120:871-879
  6. Pollack CV. Clinical characteristics, management, and outcoms of patients diagnosed with acute pulmonary embolism in the emergency department. JACC. 2011;57(6):700-706
  7. Wells PS. Use of a clinical model for safe management of patients with suspected pulmonary embolism. Ann Intern Med. 1998;129:997-1005
  8. Wells PS. Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer. Thromb Haemost. 2000;83:416-420
  9. Wells PS. Excluding pulmonary embolism at the bedside without diagbnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and D-dimer.  Ann Intern Med. 2001;135:98-107
  10. van Belle A. Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography. JAMA. 2006;295(2):172-179
  11. Wicki J. Assessing clinical probability of pulmonary embolism in the emergency ward: a simple score. Arch Intern Med. 2001;161:997-92-97
  12. Le Gal G. Prediction of pulmonary embolism in the emergency department: the revised Geneve score. Ann Intern Med. 2006;144:165-171
  13. Klok FA. Simplication fo the revised Geneva score for assessing clinical probability of pulmonary embolism. Ann Intern Med. 2008;168(19):2131-2136
  14. Kline JA. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria. J Thromb Haemost. 2008;6:772-780
  15. Penaloza A. Comparison of the unstructured clinical gestalt, the wells score, and the revised Geneva score to estimate pretest probability for suspected pulmonary embolism. Ann Emerg Med. 2013;62(2):117-124
  16. Righini M. Age-adjusted D-dimer cutoff levels to rule-out pulmonary embolism: the ADJUST-PE study. 2014;311(11):1117-1124
  17. Stein PD. Clinical characteristics of patients with acute pulmonary embolism: data from IOPED II. Am J Med. 2007;120:871-879
  18. Anderson DR. Computerized tomographic pulmonary angiography versus ventilation perfusion lung scanning for the diagnosis of pulmonary embolism. Curr Opin Pulm Med. 2009;15:425–429
  19. Rudoni RR. Use of two-dimensional echocardiography for the diagnosi of pulmonary embolus. J Emerg Med. 1998;16(1):5-8
  20. Taylor RA. Point-of-care focused cardiac ultrasound for prediction of pulmonary embolism adverse outcomes. J Emerg Med. 2013;45(3):392-399
  21. Kiely DG. Elevated levels of natriuretic peptides in patients with pulmonary thromboembolism. Resp Med. 2005;99:1286-1291
  22. Jaff MR. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, chronic thromboembolic pulmonary hypertension: a scientific statement form the American Heart Association. Circulation. 2011;123:1788-1830
  23. Keller K. Cardiac troponin I for predicting right ventricular dysfunction and intermediate risk in patients with normotensive pulmonary embolism. Neth Heart J. 2015;23:55-61
  24. Aujesky D. Derivation and validation of a prognostic model for pulmonary embolism. Am J Respir Crit Care Med. 2005;172:1041-1046
  25. Jimenez D. Simplification of the pulmonary embolism severity index for prognostication in patients with acute symptomatic pulmonary embolism. Arch Intern Med. 2010;170(15):1383-1389
  26. Tapson VF. Treatment of pulmonary embolism: anticoagnulation, thrmbolytic therapy, and complications of therapy. Crit Care Clin. 2011;27:825-839
  27. Sharifi M. Moderate pulmonary embolism treated with thrombolysis. Am J Cardiol. 2013;111:273-277
  28. Zhang Z. Lower dosage of recombinant tissue-type plasminogen activator (rt-PA) in the treatment of acute pulmonary embolism: a systematic review and meta-analysis. Thrombosis Research. 2014;133:357-363
  29. Meyer GM. Fibrinolysis for patients with intermediate-risk pulmonary embolism. NEJM. 2014;370(15):1402-1411
  30. Chatterjee S. Thrombolysis for pulmonary embolism and risk of all-cause mortality, major bleeding, and intracranial hemorrhage: a meta-analysis. JAMA. 2014;311(23):2414-2421
  31. Curtis GM. Risk factors associated with bleeding after alteplase administration for pulmonary embolism: a case control study. 2014;34(8):818–825
  32. Kennedy RJ. Thrombus resolution and hemodynamic recovery using ultrasound-accelerated thrombolysis in acute pulmonary embolism. J  Vasc Interv  Radiol. 2013;24:841-848
  33. Kucher N. Randomized, controlled trial of ultrasound-assisted catheter-directed thrombolysis for acute intermediate-risk pulmonary pulmonary embolism. Circulation. 2014;129:479-486
  34. Cross FS. A survey of the current status of pulmonary embolectomy for massive pulmonary embolism. Circulation. 1967;35:186-191
  35. Stulz P. Decision making in the surgical treatment of massive pulmonary embolism. Eur J Cardio-thorac Surg. 1994;8:188-193
  36. Leacche M. Modern surgical treatment of massive pulmonary embolism: result in 47 sonsecutive patients after rapid diagnosis and aggressive surgical approach. J Thorac Cardiovasc Surg. 2005;129:1018-1023
  37. Prandoni P, et al (PESIT Investigators). Prevalance of Pulmonary Embolism amount Patients Hospitalized for Syncope.  NEJM.  2016;375:1524-1531
  38. John MA, Klok FA, van Es N. D-dimer Interval Likelihood Ratios for Pulmonary Embolism.  Acad Emerg Med.  2017;4;1-5.
  39. Konstantinides SV, et al. Impact of Thrombolytic Therapy on the Long-Term Outcome of Intermediate-Risk Pulmonary Embolism.  JACC.  2017;69(12):1536-1544
  40. Sharifi M, et al (PEAPETT Investigators). Pulseless electrical activity in pulmonary embolism treated with thrombolysis.  Am J Emerg Med.  2016;34(10):1963-1967
  41. Piazza G, et al. (SEATTLE-II Investigators). A prospective, single arm, multicenter trial of ultrasound-facilitated , catheter-directed, low-dose fibrinolysis for acute massive and submassive pulmonary embolism.  JACC. 2015;8(1):1382-1392


Kussmaul Breathing


Other Known AliasesNone

DefinitionForm of hyperpnea (hyperventilation) characterized by a rhythmic, labored, and deep respiration pattern


Clinical Significance Compensatory mechanism of profound metabolic acidosis, classically associated with diabetic ketoacidosis

History – Named after Adolph Kussmaul (1822-1902), a German physician, who noticed it in patients with severe diabetes mellitus and first published the finding in 1874.  Dr. Kussmaul was a prolific physician in the late 1880’s and this is just one of many eponymous distinctions that bears his name.  I am sure his name will come again in this series.


  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com/
  5. A. Kussmaul: Zur Lehre vom Diabetes mellitus. Über eine eigenthümliche Todesart bei Diabetischen, über Acetonämie, Glycerin-Behandlung des Diabetes und Einspritzungen von Diastase in’s Blut bei dieser Krankheit., Deutsches Archiv für klinische Medicin, Leipzig, 1874, 14: 1-46.
  6. Young P, Finn BC, Bruetman JE, Buzzi A, Zylberman M. [The outstanding achievements of Adolf Kussmaul]. Revista medica de Chile. 2012; 140(4):538-44. [pubmed]

PAINE #PANCE Pearl – Emergency Medicine


What are 3 pretest probability scoring systems used to evaluate patients with a suspected pulmonary thromboembolism?


There are 3 validated pretest probability scoring systems that can be used to help clinicians decide who can be sent home, who needs a D-dimer, and who goes straight to CT for suspected PTE.


Wells Criteria


Developed – 1998

Revised – 2000

Simplified – 2001



Geneva Score


Developed – 2001

Revised – 2006

Simplified – 2008



Pulmonary Embolism Rule-Out Criteria (PERC) Score


Developed – 2008

This score is used AFTER the patient is determined to be low-risk using the Well’s or Geneva score.  In patients who are low-risk and PERC negative, there is only a 1.6% false-negative rate for missed PTE.  Any one of these would deem the patient PERC positive.



Why is this so important?

Although it does help us in deciding who maybe at higher risk of PTE, I personally feel these scoring systems help us document who DOES NOT need work-up.  There are quite a few patients who come in with non-specific chest pain or shortness of breath, and you should ALWAYS entertain the idea of PTE in these patients.  But, not every single one of these patients need a d-dimer or CTA.  Better yet, some of these patients can be discharged home without any investigation if they are low-risk and PERC negative.


Below is an algorithm I modified from Jeff Kline using these clinical decision instruments.


All these images are slides from my talk at the 2015 AAPA Conference


  1. Wells PS, Ginsberg JS, Anderson DR. Use of a clinical model for safe management of patients with suspected pulmonary embolism. Annals of Internal Medicine. 1998;129(12):997-1005. [pubmed]
  2. Wells PS, Anderson DR, Rodger M. Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer. Thrombosis and Haemostasis. 2000;83(3):416-20. [pubmed]
  3. Wells PS, Anderson DR, Rodger M. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer. Annals of Internal Medicine. 2001;135(2):98-107. [pubmed]
  4. Wicki J, Perneger TV, Junod AF, Bounameaux H, Perrier A. Assessing clinical probability of pulmonary embolism in the emergency ward: a simple score. Archives of Internal Medicine. 2001;161(1):92-7. [pubmed]
  5. Le Gal G, Righini M, Roy PM. Prediction of pulmonary embolism in the emergency department: the revised Geneva score. Annals of Internal Medicine. 2006;144(3):165-71. [pubmed]
  6. Klok FA, Mos IC, Nijkeuter M. Simplification of the revised Geneva score for assessing clinical probability of pulmonary embolism. Archives of Internal Medicine. 2008;168(19):2131-6. [pubmed]
  7. Kline JA, Courtney DM, Kabrhel C. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria. Journal of Thrombosis and Haemostasis. 2008; 6(5):772-80.  [pubmed]

#23 – Essentials of Intubation


This is actually a special episode for the PAINE Podcast as I have the opportunity to do a joint-interview podcast with Chip Lange from TOTAL EM.  This was the first time I got to dabble with a conversational-style podcast and I think it went pretty good.  Chip and I had a great time doing it and will most definitely be doing more of these in the future.

One of the many saying my Army Airborne Ranger dad has instilled in me growing (and one that I still use today) is the seven “P” approach to accomplishing tasks:










What is nice about this saying is that it applies very nicely to the steps of intubation as well.


You need to to have everything at the bedside you MIGHT need prior to any intubation attempt.  This includes equipment, medications, and any personnel or team members who will assist.  If you even suspect this could be a difficult airway, you should have your plan B and plan C options in the room to ward off the evil spirits.

  • Endotracheal tubes (3 sizes), stylets, bougies, syringes
    • Test the balloons on all the tubes
  • Laryngoscope
    • Multiple blades and handles
    • Check the lights
    • If using video, plug it in and make sure it turns on
  • Patent IV lines x 2
  • Suction
  • Cardiac and pulse oximetry monitor
  • Bag-valve mask
  • End-tidal CO2 monitor
  • Medications
    • Drawn up and labeled
    • Concentration read aloud

This also gives you the opportunity to talk with you team about the plan for intubation (how many attempts, progression should plan A, steps of what will happen during the intubation and everyone’s roles during the procedure, etc..), as well as reviewing assisting maneuvers (external laryngeal manipulation, etc.).



In order to decrease any deoxygenation-related issues during the intubation attempt, your patient should recieve 100% oxygen at 15 liters per minute through a non-rebreather mask for 3-5 minutes.  This will properly de-nitrogenate and super-saturate all the hemoglobin and give you the time you need to visualize and intubate.






For ideal visualization, you want to position your patient so that their external auditory meatus lined up to the sternal notch




There are several different medications you can give for premedication purposes to modify the physiologic response during intubation (lidocaine, opiates, atropine, defasculating agents, etc..), but the main one is the sedative.  It is generally poor form to paralyze someone before you sedate them.  There are several medications you can choose from for sedation in intubation:

  • Ketamine – 1-2mg/kg IV
    • My ideal sedative
  • Etomidate 0.3mg/kg IV
    • Less hemodynamic compromise
    • Can cause adrenal suppression
  • Propofol – 1.5-3mg/kg IV
    • Can cause hemodynamic instability



There are 2 choices for classes of paralytics:

  • Depolarizing
    • Succinylcholine – 1.5-2mg/kg IV
    • Rapid onset, shortest duration of action
    • Caution in burn/crush injuries, hyperkalemic patients
  • Non-Depolarizing
    • Rocuronium – 1.2mg/kg IV
    • Vecuronium – 0.3mg/kg IV


Pass The Tube

Once you patient is properly sedative and paralyze, you can proceed to laryngoscopy.


Post-intubation Assessment


This is used for confirmation of correct placement of the endotracheal in the trachea and tests for end-tidal CO2.  There are 2 main types:

  • Qualitative
    • Color change calorimeter
    • Attaches to end of endotracheal tube and detects CO2 by changes in exhaled pH




  • Quantitative
    • Continuous Waveform Capnography
      • Gold standard
      • Gives you a visual waveform to see if the ventilations are adequate


Securing the Tube

Once you know you are in the right spot and have been confirmed by capnography, you need to secure the tube.  There are different ways to achieve and I often defer to the respiratory therapist or nurse on how they want it secured.  There are commercial devices that lock the tube in place and secure using velcro straps, all the way to the old standby of adhesive tape.  This is a great site that shows several different ways you can secure the endotracheal tube (http://aam.ucsf.edu/article/securing-endotracheal-tube).



Chest xray is the gold standard for the radiographical confirmation of endotracheal placement, as well as ensuring the proper depth.  The ideal position for the tube depth should be 3-5cm from the carina or at T3-4 position.


Josh Farkas (PulmCrit) did a great review on endotracheal tube positioning and depth just last week.


Ultrasound is being used more frequently as a confirmatory tool for endotracheal tube placement.


Great review by EmDocs on ultrasound for endotracheal tube confirmation.



Now that the tube is in place, secured, and confirmed, you are done right?  WRONG!!!  Your patient now has a tube shoved into the tracheal and it is a tad uncomfortable.  Postintubation sedation/analgesia is PARAMOUNT for good patient care.

  • Sedation
    • Ketamine – 0.1-0.5mg/kg bolus and 0.1-0.5mg/kg/hr infusion
    • Propofol – 5mcg/kg bolus and 5-50mcg/kg/hr infusion
    • Midazolam – 0.05mg/kg bolus and 0.025mg/kg/hr infusion
  • Analgesia
    • Fentanyl – 2mcg/kg bolus and 1mcg/kg/hr infusion
    • Hydromorphone – 0.5-1mg/kg bolus and 0.5-3mg/kg/hr infusion
    • Morphine – 5-10mg/kg bolus and 2-30mg/hr infusion


You should be shooting for a Richmond Agitation Sedation Scale (RASS) of -1 to -3 for adequate sedation following intubation.



Really good intubation checklist from Scott Weingart of EmCrit


  1. http://lifeinthefastlane.com/ccc/rapid-sequence-intubation/
  2. http://emcrit.org/podcasts/emcrit-intubation-checklist/
  3.  Weingart SD, Levitan RM.  Preoxygenation and Prevention of Desaturation During Emergency Airway Management.  Annals of Emergency Medicine.  2012;59(3):165-175.
  4. http://www.capnography.com/Emergencydevice/emergencyintubtion.htm
  5. http://www.capnography.com/new/emergency-intubations
  6. http://www.capnography.com/new/emergency-intubations?id=216
  7. http://lifeinthefastlane.com/ccc/capnography-waveform-interpretation/
  8. http://www.derangedphysiology.com/main/core-topics-intensive-care/mechanical-ventilation-0/Chapter%201.2.3/endotracheal-tube-detail
  9. http://emcrit.org/podcasts/post-intubation-sedation/
  10. https://coreem.net/core/post-intubation/