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BNP: Data, Diagnosis and Applications

BNP: Data, Diagnosis and Applications

M Lamberta PGY-3


What are the Biomarkers?

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ACEP Clinical Policy

Natriuretic Peptide (NP) assays gained approval by the FDA around the year 2000 for the evaluation of undifferentiated dyspnea and suspected ADHF.  The first commercially available test detected the biologically active hormone BNP, but many more recent assays also detect the inert Amino-terminal cleavage product of the BNP prohormone: N-Terminal proBNP (NT-proBNP). (Table 1)  Both biomarkers are comparable in their diagnostic accuracy demonstrated by Receiver Operating Characteristic (ROC) curves. 


From 1999 to 2000, Maisel et al. recruited 1,586 participants in the first large multinational randomized control trial (RCT) to evaluate BNP for the diagnosis of heart failure in ED patients presenting with acute dyspnea.[1].  The Breathing Not Properly (BNP) study analyzed a subgroup from this cohort to conclude that adding BNP to clinical judgment would have enhanced diagnostic accuracy from 74% to 81%.  This trial supported BNP as a good rule-out test for Acute Decompensated Heart Failure (ADHF) with a sensitivity of 90% for BNP < 100 pg/mL when compared to the gold standard: blinded assessment of two independent cardiologists.   The authors also argued that BNP ruled-in 14 of the 19 patients that were erroneously diagnosed by clinicians as “CHF improbable,” thereby reducing false negatives from 2% to 0.6%.  The improved sensitivity, however, inevitably reduced specificity to near 74% for a cut-off of BNP ≥100 pg/mL. [2] Furthermore, a secondary analysis pointed out the limited application of this biomarker as clinical judgment seemed to outperform BNP assay when applied to the dyspneic patient at the extremes of pretest probability ie greater than 95% or less than 5% certainty of ADHF. [3] Therefore, a higher rule-in threshold (BNP > 500 pg/mL improved specificity of this assay but also opened up a “gray-zone” in the interpretation of BNP where the test could neither rule-in nor rule-out with good certainty.  

By the mid-2000s, the rule-out and rule-in cut-offs for CHF began to gain modest support by professional organizations including ACEP. [4]  Wang et al. contributed to JAMA’s Rational Clinical Examination series by conducting a meta-analysis of these preceding data in addition to 20 smaller studies on BNP to determine Likelihood ratios for BNP.  The meta-analysis calculated a negative likelihood ratio (LR-) near 0.9 (cut-off <100 pg/mL) again promoting BNP as a strong test to rule-out ADHF.  Yet, comparing BNP to patient history “significant for heart failure” (LR+ 5.8) or  “interstitial edema” on chest X-Ray (LR+ 12), BNP stood as an equivocal test to rule-in HF with LR+ 2.7 (≥100 pg/mL).[5]



In the later 2000s, large RCTs would similarly establish the accuracy of NT-proBNP in ADHF.  The PRIDE (N-Terminal Pro-BNP Investigation of Dyspnea in the Emergency Department) constructed ROC curves to conclude that adding NT-proBNP to the evaluation of patients with dyspnea was superior to clinician-estimated likelihood of CHF alone with area under the curve (AUC) measuring 0.90 for clinician alone versus 0.94 for clinician+NT-proBNP, (p = 0.006).[6]  The Canadian IMPROVE-CHF study affirmed similarly that adding NT-proBNP to clinical judgment alone increased the AUC from 0.83 to 0.90. [7]

Despite showing statistical differences in diagnostic accuracy through Receiver-Operator Characteristic Curves, the application of natriuretic peptides did not appear to add much to clinical judgement at the extremes of pre-test probability, so many began to apply it to patients who were considered intermediate pretest probability  (21% to 79%) or under circumstances of competing diagnoses ie COPD vs PNA vs CHF.  Steinhart et al. attempted to better stratify these “intermediate probability” patients by deriving an algebraic model that capitalized on increased positive likelihood ratios at higher absolute levels of NT-proBNP.  In a validation study, this model appeared to correctly reclassify 44% of the “intermediate” patients to either low risk or high risk.  The strength of this approach is that it provides for practical application of NT-proBNP as a continuous variable rather than just relying on discrete cut-offs, it accounts for age-adjusted variability, and it prompts the clinician to appropriately consider pre-test probability before interpreting the test result.  The weakness lies in the fact that it requires math (yet, an excel model is available for download here), and it does not appear to approve diagnostic accuracy in a majority of cases.  In this study, the model helped to correctly reclassify 10% of the study participants. [8,9]

When NPs came to the scene 15 years ago the hope was that it would be the “super-hero” for the bewildered clinician in the diagnosis of dyspnea, but subsequent trials and meta-analyses gave BNP the persona of  more of a “yes-man” supporting what the clinician already knew and equivocating just as much for cases of “intermediate probability.”    The literature of the last 15 years has elucidated NP test characteristics, confounding variables (Tables 1 and 2), and interpretation, but application of the test still appears rather heterogeneous by anecdote as either a rule-in, rule-out, adjudicator, or prognosticator.   



  • Ruling-in low-probability:  BNP as a rule-in test to diagnose patients who are being treated erroneously for other conditions ie a 65-year-old patient with a history of COPD but no current diagnosis of HF. Rosen even suggests “we abandon the routine obtaining of a BNP level for patients deemed to be having a CHF flare-up, and instead consider it in all dyspnea patients that we don’t believe are having CHF.” [10] This implies a sentiment of screening.  In an older population, where prevalence is higher, it may be a good consideration.
  • Ruling-out high-probability:  As expenditures for heart failure continue to soar, the use of BNP, in concert with other clinical signs and adjunct studies, may have significant application for ruling-out ADHF in known HF patients. This may lead to scoring protocol or institutional decision rules to help identify ED patients who are safe for outpatient management.
  • Adjudicating intermediate risk:  Likely BNP will continue to find application case-by-case by the ED clinician who is interested in detecting the presence of heart strain whether it will change management or not.  Interpretation of BNP should be considered after establishing pre-test probability for the patient, with the knowledge of confounding variables, and can employ tools to interpret the test like that proposed by Steinhart et al. (available for download here).  That said, the same cases of intermediate probability will more likely represent the complex and sicker patients requiring longer hospital stays and extended work-ups and more than half the time the knowledge of BNP will unlikely help to narrow the diagnosis. [9]
  • Prognosticating: Elevated BNP almost always suggests a poor prognosis whether it is used to stratify ADHF, NSTEMI, or PE, but prognosis is often more accurately reflected—and more easily assessed—by patient hemodynamics and renal perfusion. [11,12,13] There is no strong evidence that BNP will consistently help an admitting team in their management, but there is still ongoing research discerning how BNP may help in response-guided therapy and discharge planning.
  • Outcomes: Only a handful of randomized controlled trials have measured changes in outcomes for clinicians who use natriuretic peptide assays in the ED.  Meta-analyses of these trials have shows trends towards decreased cost and length of stay, but no reproducible significant difference in these outcomes or in regards to therapy or mortality.  [14,15]




  1. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347:161-167.
  2. McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation 2002;106:416–22
  3. Schwam E. B-type natriuretic peptide for diagnosis of heart failure in emergency department patients: a critical appraisal. Acad Emerg Med. 2004;11:(6)686-91.
  4. Silvers SM, Howell JM, Kosowsky JM, Rokos IC, Jagoda AS. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute heart failure syndromes. Ann Emerg Med 2007;49:627–69. (BNP Clinical Policy)
  5. Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT. Does this dyspneic patient in the emergency department have congestive heart failure? JAMA 2005;294:1944–56
  6. Januzzi JL Jr, Camargo CA, Anwaruddin S, et al. The N-terminal Pro-BNP Investigation of Dyspnea in the Emergency Department (PRIDE) study. Am J Cardiol. 2005;95:948-954.
  7. Moe GW, Howlett J, Januzzi JL, Zowall H, for the Canadian Multicenter Improved Management of Patients With Congestive Heart Failure (IMPROVE-CHF) Study Investigators. N-terminal pro-B-type natriuretic peptide testing improves the management of patients with suspected acute heart failure: primary results of the Canadian prospective randomized multicenter IMPROVE-CHF study. Circulation 2007;115:3103–10
  8. Emergency Medicine Journal Club. Does BNP Augment Acue Decompensated CHF ED Management. WUSM-St. Louis. Journal Club November, 2009.
  9. Steinhart B, Thorpe KE, Bayoumi AM, Moe G, Januzzi JL, Mazer CD. Improving the diagnosis of acute heart failure using a validated prediction model. J Am Coll Cardiol 2009;54:1515–21.
  10. Carpenter CR, Keim SM, Worster A, Rosen P, BEEM (Best Evidence in Emergency Medicine). BRAIN NATRIURETIC PEPTIDE IN THE EVALUATION OF EMERGENCY DEPARTMENT DYSPNEA: IS THERE A ROLE? The Journal of Emergency Medicine. 2012;42(2):197-205.
  11. Heeschen C, Hamm CW, Mitrovic V, et al. N-terminal pro-B-type natriuretic peptide levels for dynamic risk stratification of patients with acute coronary syndromes. Circulation. 2004 Nov 16. 110(20):3206-12.
  12. Binder L, Pieske B, Olschewski M, et al. N-terminal pro-brain natriuretic peptide or troponin testing followed by echocardiography for risk stratification of acute pulmonary embolism. Circulation. 2005 Sep 13.
  13. Singer AJ, Birkhahn RH, Guss D, et al. Rapid Emergency Department Heart Failure Outpatients Trial (REDHOT II): a randomized controlled trial of the effect of serial B-type natriuretic peptide testing on patient management. Circ Heart Fail 2009;2:287–93.
  14. Trinquart L, Ray P, Riou B, Teixeira A. Natriuretic peptide testing in EDs for managing acute dyspnea: a meta-analysis. Am J Emerg Med. 2011;29:(7)757-67
  15. Lam LL, Cameron PA, Schneider HG, et al. Meta-analysis: effect of B-type natriuretic peptide testing on clinical outcomes in patients with acute dyspnea in the emergency setting. Ann Intern Med 2010; 153: 728−735.



LB Daniels, AS Maisel. Natriuretic Peptides. J Am Coll Cardiol. 2007 Dec 18. 50(25): 2357-68. (Tables 1-2)


Continued Reading

JM Kosowsky, JL Chan. Acutely Decompensated Heart Failure: Diagnostic and Therapeutic Strategies. EB Medicine Review (2006).

Mueller TT. Head-to-head comparison of the diagnostic utility of BNP and NT-proBNP in symptomatic and asymptomatic structural heart disease.. Clinica chimica acta. 2004-03;341:41-48.


Why Not Dobutamine?

Why Not Dobutamine?

PGY3 Neil McCormack


A patient rolls into the emergency room. You don’t need this. You’ve got a lot of other patients. This patient however is in shock. They are hypotensive and with a decreased mental status. You need to give them something and the attending asks what vasopressors you would like. “Why not dobutamine” the intern asks. With a sigh and a heavy eye roll you turn away. But… Why not dobutamine?



Dobutamine            Dobutamine is a synthetic catecholamine used primarily for cardiac stress testing outside of the hypotensive patient (8). This is due to the positive inotropic effects it plays on the heart. Dobutamine acts via a 3:1 selective agonist effect on β1 and β2 receptors respectively. This causes increased contractility of the heart (9). There is, however, a side effect of reflexive decrease in systemic vascular resistance (SVR) causing potential for worsening of hypotension. This is not seen in higher doses of dobutamine and the reason for this is because of dobutamine’s partial α1 agonist effect (9). Given this information, we can intuitively think that giving dobutamine would be a good option for use in a hypotensive patient. But what does the literature say?

There have been a few studies that look at the use and effectiveness of dobutamine in the setting of hypotension (1, 2, 9, 10, 12, 13). Partially due to the α1 partial agonist effect, dobutamine is not a first line recommended treatment option alone in patients with septic or hypovolemic shock (3, 4, 9). It has been proposed as a first line treatment for sepsis patients if used in conjunction with another vasopressor (example: norepinephrine) to prevent the reflexive SVR decrease and hypotension. In the absence of using multiple vasopressors, dopamine and norepinephrine have been listed as the first line drugs of choice for septic shock patients. According to the “Surviving Sepsis” guidelines (3, 4), norepinephrine is the first line vasopressor of choice for sepsis patients. However, dobutamine is the recommended inotropic agent to be used in combination to improve cardiac output (without going to supranormal levels of cardiac output) (3).



But what if this patient has a bad heart? The evidence for use of dobutamine in patients with cardiogenic shock is more favorable (7, 12, 14). Patients who need inotropic support primarily are recommended to undergo dobutamine therapy as their vasopressor of choice in the beginning. This is due to the positive effect that dobutamine has on the contractility of the heart muscle itself. It has been shown as well that dobutamine appears to have a more favorable effect on right ventricular (RV) contractility than on left ventricular (LV) though it is effective in both settings (14). The downside of dobutamine alone is, as mentioned, it is only a partial α1 agonist and thus, if the blood pressure does not respond to the increased inotropic effects, a second line agent will need to be added. In a trial looking at epinephrine vs dobutamine/norepinephrine, there was no difference in the overall outcomes of patients but the epinephrine patients had more side effects (including arrhythmias).

What does all this mean? Well what this means is that the intern may have, in fact, been correct to suggest that we use dobutamine for our now hypotensive patient. It all depends on the suspected cause (IE: cardiogenic vs septic vs other causes of hypotension). It is important to keep in mind, though, that unless this patient has a purely cardiogenic cause (such as severe heart failure), they may also require a second pressure support in order to maintain a healthy blood pressure.



1) Bangash, Mansoor N, Ming-Li Kong, and Rupert M Pearse. “Use of Inotropes and Vasopressor Agents in Critically Ill Patients.” British Journal of Pharmacology 165, no. 7 (April 2012): 2015–33. doi:10.1111/j.1476-5381.2011.01588.x.

2) Beale, Richard J., Steven M. Hollenberg, Jean-Louis Vincent, and Joseph E. Parrillo. “Vasopressor and Inotropic Support in Septic Shock: An Evidence-Based Review.” Critical Care Medicine 32, no. 11 Suppl (November 2004): S455–65.

3) Campaign, Surviving Sepsis. “Leitlinienempfehlungen Zur Sepsistherapie.” Sepsis Und MODS, 2015, 377.

4) Dellinger, R. Phillip, Mitchell M. Levy, Jean M. Carlet, Julian Bion, Margaret M. Parker, Roman Jaeschke, Konrad Reinhart, et al. “Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008.” Critical Care Medicine 36, no. 1 (January 2008): 296–327. doi:10.1097/01.CCM.0000298158.12101.41.

5) Huang, Xuan, Shu Lei, Mei-fei Zhu, Rong-lin Jiang, Li-quan Huang, Guo-lian Xia, and Yi-hui Zhi. “Levosimendan versus Dobutamine in Critically Ill Patients: A Meta-Analysis of Randomized Controlled Trials.” Journal of Zhejiang University. Science. B 14, no. 5 (May 2013): 400–415. doi:10.1631/jzus.B1200290.

6) Levy, Bruno, Pierre Perez, Jessica Perny, Carine Thivilier, and Alain Gerard. “Comparison of Norepinephrine-Dobutamine to Epinephrine for Hemodynamics, Lactate Metabolism, and Organ Function Variables in Cardiogenic Shock. A Prospective, Randomized Pilot Study.” Critical Care Medicine 39, no. 3 (March 2011): 450–55. doi:10.1097/CCM.0b013e3181ffe0eb.

7) Lewis, Tyler, Caitlin Aberle, Diana Esaian, and John Papadopoulos. “EFFICACY AND SAFETY OF MILRINONE VERSUS DOBUTAMINE IN CARDIOGENIC SHOCK.” Critical Care Medicine 43, no. 12 Suppl 1 (December 2015): 34. doi:10.1097/01.ccm.0000473960.43621.41.

8) Miller, Todd D., J. Wells Askew, and Nandan S. Anavekar. “Noninvasive Stress Testing for Coronary Artery Disease.” Heart Failure Clinics 12, no. 1 (January 2016): 65–82. doi:10.1016/j.hfc.2015.08.006.

9) Müllner, M., B. Urbanek, C. Havel, H. Losert, F. Waechter, and G. Gamper. “Vasopressors for Shock.” The Cochrane Database of Systematic Reviews, no. 3 (2004): CD003709. doi:10.1002/14651858.CD003709.pub2.

10) Rudis, M. I., M. A. Basha, and B. J. Zarowitz. “Is It Time to Reposition Vasopressors and Inotropes in Sepsis?” Critical Care Medicine 24, no. 3 (March 1996): 525–37.

11) Smith, Maria A. “Use of Vasopressors in the Treatment of Cardiac Arrest.” Critical Care Nursing Clinics of North America 17, no. 1 (March 2005): 71–75, xi. doi:10.1016/j.ccell.2004.09.010.

12) Steltzer, H., P. Simon, A. N. Owen, M. Thalmann, and A. F. Hammerle. “The Effects of Dobutamine Therapy in Critically Ill Patients Measured by Transoesophageal Echocardiography and Intracardiac Monitoring.” Anaesthesia 49, no. 5 (May 1994): 432–37.

13) “Vasopressors and Inotropes in Shock.pdf,” n.d.

14) Vincent, J. L., C. Reuse, and R. J. Kahn. “Effects on Right Ventricular Function of a Change from Dopamine to Dobutamine in Critically Ill Patients.” Critical Care Medicine 16, no. 7 (July 1988): 659–62.


Dilt v. Metoprolol in Afib/RVR

by Najm Haque, PGY2


Atrial fibrillation with rapid ventricular response is a common emergency room problem. Patient with stable blood pressure who present in Afib with RVR need medications to control their heart rate (unstable patients require more cardioversion). Traditionally, these patients receive beta blockers or calcium channel blockers in IV form for rate control. The most common medications used in the US are metoprolol and diltiazem, but it is unclear which is superior.


Fromm et al Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department

This study was published in the Journal of Emergency Medicine in April 2015 and compared how fast rate control was achieved in diltiazem vs metoprolol. This was a prospective, double-blind study which compared the effects of both medications at 30 minutes, as well as looking at mean decrease in heart rate, and adverse effects. Patients were randomized and either received Diltiazem 0.25 mg/kg IVP (maximum dose of 30mg) or Metoprolol 0.15mg/kg IVP (maximum dose of 10mg). A second escalation dose of 0.35mg/kg of diltiazem (max of 30mg) or 0.15mg/kg of metoprolol (max of 10mg) was given at 15 minutes if target HR was not achieved. The results of the study showed that diltiazem reached the target HR of <100 much more frequently at 5 minutes (50% vs 10.7%) and at 30 minutes (95.8% vs 46.4%) when compared to metoprolol. There was no difference in adverse effects.



Demircan C, Cikriklar HI, Engindeniz Z, et al. Comparison of the effectiveness of intravenous diltiazem and metoprolol in the management of rapid ventricular rate in atrial fibrillation.

This study was published in the Journal of Emergency Medicine in 2005. Similar to the study by Fromm et al, this study compared diltiazem (0.25mg/kg, max of 25mg) and metoprolol (0.15mg/kg, max of 10mg), was prospective and randomized, and used a target heart rate < 100. They compared the two medications at intervals of 2, 5, 10, 15, and 20 minutes. In each interval, the success rate of diltiazem was higher than metoprolol, and at 30 minutes 90% of patients receiving diltiazem reached the target heart rate while 80% of patients receiving metoprolol reached the target heart rate. In addition, the decrease in heart rate was higher in the group receiving diltiazem than the group receiving metoprolol.


Scheuermyer FX, Grafstein E, Stenstrom R, et al. Safety and efficiency of calcium channel blockers versus beta-blockers for rate control in patients with atrial fibrillation and no acute underlying medical illness.

This study was published in 2013 and compared the effect of calcium channel blockers and beta blockers in ER patients with known Afib who present with Afib with RVR. The primary outcome of this retrospective cohort study was hospital admissions and patients with underlying medical conditions requiring hospitalization were excluded (which means this study looked for patients who were admitted to the hospital for Afib with RVR and no other medical problem). The study enrolled 259 patients over a 4 year period and noted patients receiving CCBs were more likely to be admitted (31% vs 27%) although this was statistically insignificant. Secondary outcomes were ED length of stay, adverse effects, return visits in 7 or 30 days, and the incidence of stroke or death in 30 days. In all categories, both CCBs and beta blockers were essentially equal.


What do these studies tell us?

The studies by Fromm et al and by Demircan et all are essentially the only two studies published which compare diltiazem and metoprolol directly in an emergency room population. The first of these studies (Demircan) noted that diltiazem was slightly better than metoprolol in achieving a target heart rate while the most recent study by Fromm noted that diltiazem was significantly better than metoprolol. Of note, Fromm did use a higher maximum dose of diltiazem (30mg vs 25mg). Both studies did an adequate job of excluding patients with other conditions which caused the afib with RVR. The third study compared the broad group of CCBs vs beta blockers and concluded there was no difference, but it does not specify which medications were used and it’s primary end point was not heart rate but whether or not a patient was admitted to the hospital. So what should you do in the emergency room? In patients who present with Afib with RVR with no other underlying condition like infection, ingestion, STEMI, it appears diltiazem is more effective than metoprolol in achieving rate control. However, if there is an underlying condition like sepsis, there is currently no published data about what agent should be given.



What about using both?

If a patient is given 2 doses of metoprolol without resolution of rapid ventricular response, the instinct is to give diltiazem to try and achieve better rate control. However, there is a theoretical risk of causing the patient to go into complete heart block if this is done. There are no published case reports of this happening, so the risk is purely theoretical, but the administration of both medications should be avoided.

Demircan C, Cikriklar HI, Engindeniz Z, et al. Comparison of the effectiveness of intravenous diltiazem and metoprolol in the management of rapid ventricular rate in atrial fibrillation. Emerg Med J 2005;22(6):411-4. Erratum in: Emerg Med J 2005;22(10):758.  PubMed PMID: 15911947.


Scheuermeyer FX, Grafstein E, Stenstrom R, et al. Safety and efficiency of calcium channel blockers versus beta-blockers for rate control in patients with atrial fibrillation and no acute  underlying medical illness. Acad Emerg Med 2013;20(3):222-30. PubMed PMID: 23517253.


Fromm C, et al. Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department. J Emerg Med. 2015 Apr 22. [Epub ahead of print]


Stephanie Haimowitz, PGY3


AS is a 43 yo F, on OCPs for menorrhagia, h/o recent left ACL tear and as a result decreased ambulation x3 weeks, p/w SOB, worse on exertion x2 weeks but acutely worsening on the day of presentation. On the day of presentation, the patient complained of an episode of acutely worsening dyspnea, now occurring at rest and associated with lightheadedness, chest pressure, and diaphoresis.

On Exam, the patient was mildly tachycardic with an O2 sat of 98% on RA at rest. She appeared to be breathing comfortably, although at times noted to take shallow breaths, and the remainder of her exam was unremarkable.

Labs were notable for an elevated troponin of 0.302. EKG showed sinus tach with a ventricular rate of 106 and an incomplete RBBB. CT w/PE protocol showed large bilateral pulmonary emboli in both the right and left main pulmonary arteries with extension into segmental and subsegmental branches, as well as flattening of the interventricular septum with dilatation of the right ventricle.


The patient was started on a heparin drip and admitted to the CCU for hemodynamic monitoring and catheter directed thrombolysis via EKOS, which uses ultrasound to enhance the effects of catheter directed thrombolysis. The patient underwent the endovascular intervention with improvement in her symptoms and repeat echo showed improved RV function. She was switched to Lovenox and discharged home on xarelto.

There are many factors to consider when choosing the appropriate treatment modality for a patient with a PE. In a well-appearing hemodynamically stable patient with evidence of a peripheral or subsegmental PE, anticoagulation with either heparin, a low molecular weight heparin such as lovenox, or one of the newer factor Xa inhibitor oral agents is the most common treatment modality. Factors to consider when deciding whether to escalate treatment include hemodynamic instability, evidence of right heart strain, a large central thrombus on CT, and overall clinical appearance.

While this patient was hemodynamically stable, she had clear evidence of right heart strain (e.g. troponemia, dilated right ventricle, flattening of interventricular septum, and McConnell’s sign- diminished RV systolic function with sparing of the apical wall seen here), and large bilateral pulmonary emboli on CT scan. The RV dysfunction seen on echo is often considered to be predictive of a poor short-term prognosis, thus warranting more aggressive therapeutic measures.[1]

The decision was made to use ultrasound enhanced catheter directed fibrinolysis.

The SEATTLE II Study, published in August of this year, investigated the efficacy of this technique. The use of full dose systemic thrombolysis has fallen out of favor over the past few years due to the risks of severe bleeding and intracranial hemorrhage. By using the ultrasound guided catheter directed approach, a lower dose of thrombolytic can be used because it is injected adjacent to the PE. The study was a single-arm, multicenter design with the inclusion criteria of a proximal PE, age >18, PE symptom duration <14 days, and RV/LV diameter ratio >0.9 on CT. A total of 150 patients were enrolled at 22 sites across the US, at urban, non-urban, teaching, and non-teaching hospitals. The primary outcome was a change in RV/LV diameter ratio pre and post procedure. The primary safety outcome was major bleeding within 72 hours of initiation of therapy. Major bleeding was defined as either intracranial hemorrhage or bleeding causing hemodynamic compromise and requiring intervention such as blood transfusion. Patients enrolled in the study had a mean difference RV/LV diameter of 0.42. There were 16 major bleeding events, however none of these were intracranial hemorrhage.[2]

The most glaring limitation of the study was the lack of a comparator group, such as full dose systemic fibrinolysis, half dose systemic fibrinolysis, or a/c alone. Thus, while the results of the study appear promising, additional comparative clinical studies are necessary to help define the role of ultrasound facilitated catheter directed fibrinolysis in the treatment of acute PE.




[1] 14.Grifoni S, Olivotto I, Cecchini P, et al. Short-term clinical outcome of patients with acute pulmonary embolism, normal blood pressure, and echocardiographic right ventricular dysfunction. Circulation 2000; 101:2817.

[2] Piazza, Gregory, Benjamin Hohlfelder, Michael R. Jaff, Kenneth Ouriel, Tod C. Engelhardt, Keith M. Sterling, Noah J. Jones, John C. Gurley, Rohit Bhatheja, Robert J. Kennedy, Nilesh Goswami, Kannan Natarajan, John Rundback, Immad R. Sadiq, Stephen K. Liu, Narinder Bhalla, M. Laiq Raja, Barry S. Weinstock, Jacob Cynamon, Fakhir F. Elmasri, Mark J. Garcia, Mark Kumar, Juan Ayerdi, Peter Soukas, William Kuo, Ping-Yu Liu, and Samuel Z. Goldhaber. “A Prospective, Single-Arm, Multicenter Trial of Ultrasound-Facilitated, Catheter-Directed, Low-Dose Fibrinolysis for Acute Massive and Submassive Pulmonary Embolism.”JACC: Cardiovascular Interventions 8.10 (2015): 1382-392. Web.

Goodbye MONA? Oxygen in AMI

Goodbye MONA?

From: Best Mona Lisa Parodies @

Dr. Mayuri Patel PGY3

CC: Chest pain and Shortness of breath

HPI: 72F w/ PMHx of Rheumatic fever (s/p AVR repair 9 years prior), pHTN, hFrEF (EF 30%), HLD, DVT (on coumadin) s/p IVC filter BIBEMS for progressive DOE over 1 month. Prior to arrival to ED, pt developed substernal chest pain radiating to jaw associated with diaphoresis and nausea. EMS placed patient on NRB.

Triage VS afebrile BP 129/85 HR 74 RR 24 02 96%RA

General: awake, mild distress, oriented to person, place and time


Pulm: CTA – b/l

Abd: +bs, soft, nt/nd

Ext: 2+ pulses, no cyanosis or edema

EKG – Sinus rhythm, HR 74, STE II, III, aVF with reciprocal changes

Troponin – 12; CPK – 377


MEHEART was activated, patient transferred to Weiler for cardiac catheterization.

Patient given Heparin 5000 Units, NTG Sl, Plavix 600mg, ASA 162mg. En route to Weiler hospital, pt placed on 2L NC.

Hospital course:

Cardiac cath showed mild coronary artery disease for the left ventricle. The 1st acute marginal artery to the right ventricle occluded (possibly culprit). Intervention – medical management.

Patient was admitted to telemetry s/p cardiac cath. ECHO showed dilated left ventricle, EF 20-25%. Patient was elevated by heart failure team for ICD placement, because patient met NYS Class IIa criteria. Patient opted for medical management instead of ICD placement. Patient was evaluated for LifeVest and discharged after medical management.


Traditionally, we are taught that administration of high flow oxygen is the standard of care for patients presenting with cardiac emergencies. However, where does this dogma come from? The earliest evidence comes from 1900, when Steele observed that oxygen relieved pain during episodes of angina pectoris(1). The evidence for this observation came in 1928, when the cause of angina was attributed to hypoxia of the myocardium (2).

It is indeed a strange phenomena that our current day practices are based on studies in early 1900s. There have been multiple subsequent studies showing the harmful effects of oxygen. In 1950, Russek et al. showed that administration of 100% oxygen prolonged EKG changes during exercise tolerance testing and had no effect on anginal pain (3). A 1964 study reported that breathing high concentrations of oxygen (85% to 90%) for at least 30 minutes in the first 24 hours after MI resulted in decreased heart rate, reduced cardiac output, and increased systemic vascular resistance (4). In the following year, a study by Thomas et al. showed that giving 40% oxygen for 20 minutes to patients following MI resulted in a 17% decrease in cardiac output and a 5% rise in arterial blood pressure (5). Certainly not an ideal situation after an AMI. In 1969, a study by Neill showed that in “normal subjects” the availability of oxygen for myocardial metabolism was not affected until arterial oxygen saturation falls as low as 50% (6). However, in patients with CAD, myocardial ischemia was observed in some patients when oxygen saturation fell below 85%. In a subset of patients with triple-vessel disease, 6 minutes of high-flow oxygen reduced coronary blood flow sufficiently to induce myocardial ischemia (7).


The first randomized, double blinded controlled trial of oxygen therapy was conducted in 1976. The study randomized 200 consecutive patients thought to have MI to treatment with oxygen (given via medium concentration mask at 6L/min) or air for the first 24 hours. Patients with CHF, chronic pulmonary disease, or breathlessness from any cause other than AMI were excluded. The group receiving oxygen therapy had a higher level of serum aspartate aminotransferase level than the group receiving room air, indicating greater myocardial damage. Forty-three patients were excluded post-hoc when the diagnosis of MI was revoked. There was a mortality rate of 11% (9/80) in the oxygen group vs. 4% (3/77) in the air group, but this did not achieve statistical significance. The relative risk of mortality in oxygen group 2.9 (95% CI 0.81-10.3; P=0.08). The authors concluded that the results are suggestive of “deleterious effect” of oxygen and that administration of it in patients with uncomplicated MI is not beneficial (8).


What causes the deleterious effects of oxygen therapy? It is theorized that reactive oxygen species are responsible for vasoconstriction. This was shown by McNulty et al. in 2007 in patients with AMI. The study showed that breathing 100% oxygen for 10 minutes increased vascular resistance in the LAD by 23% (9). Interestingly, this increase could be prevented by co-administration of the antioxidant ascorbic acid. The diameter of the large conduit coronary arteries was not appreciably affected, suggesting that vasoconstriction occurs at the level of the myocardial microcirculation.

A Cochrane review in 2013 meta-analyzed available studies on oxygen therapy in patients with AMI. Combing the 4 randomized controlled trials (430 patients with 17 deaths) generated a relative risk of mortality of 2.11 (95% CI 0.78 to 5.68) in participants with confirmed AMI. The authors concluded that due to the small number of deaths, it could be a chance occurrence (10).

The AVOID trial from Australia might be the last straw in the age-old dogma of oxygen for AMI. It is a prospective, multicenter trial with both pre-hospital and in-hospital treatment comparing oxygen (8L/min) with air. It included patients that met STEMI criteria, had symptoms for less than 12 hours and initial 02 saturation >94%. Exclusion criteria included 02 saturations <94%, AMS, and oxygen administration prior to randomization. Primary end points for the study were infarct size measured by Troponin T (TnT) and CK-MB. Secondary endpoints were recurrent myocardial infarction, cardiac arrhythmia and myocardial infarct size assessed by cardiac magnetic resonance (CMR) imaging at 6 months. There were 638 patients randomized, of which 441 were confirmed STEMI who underwent primary endpoint analysis (218 in oxygen group vs. 223 in no oxygen group). The baseline characteristics were similar except for 38% in the oxygen group had anterior infract vs. 33 % in no oxygen group. There was a statistically significant increase in mean CK-MB, however mean TnT was similar. There was an increase in the rate of recurrent myocardial infarction in the oxygen group compared to the no oxygen group (5.5% vs. 0.9%, P=0.006) along with increase in frequency of cardiac arrhythmia (40.4% vs. 31.4%; P=0.05). At 6 months, the oxygen group (139 patients) had an increase in myocardial infarct size on CMR (20.3grams vs. 13.1grams; P=0.04) (11).

The AVOID trail concludes that supplemental oxygen in normoxic STEMI patients increased myocardial injury along with cardiac arrhythmia, and recurrent MI. It was also associated with larger myocardial infarct size. However, the study is not without its flaws. The use of 02 at 8L/min seems excessive and could account for the differences. Also, patients in no oxygen group were given oxygen either during catheterization or in the hospital stay (if 02 saturation dropped below 94%).

Where do we go from here? It seems that every patient who arrives via EMS with complaint of chest pain is placed on a NRB. The literature does not support this notion, and we may in fact be doing disservice to our patients. If there is to be a change in practice, it has to come from both pre-hospital setting as well as ED. There is no denying the importance of oxygen in patients who are hypoxic and having AMI. However, for normoxic patients it might be prudent to stay away from oxygen.


  1. Steele C. Severe angina pectoris relieved by oxygen inhalations. BMJ1900, 2:1568.
  2. Keefer CS, Resnik WH. Angina pectoris: a syndrome caused by anoxemia of the myocardium. Arch Intern Med 1928, 41:769-807.
  3. Russek HI, Regan FD, Naegele CF. One hundred percent oxygen in the treatment of acute myocardial infarction and severe angina pectoris. JAMA 1950, 144:373-375.
  4. MacKenzie GJ, Flenley DC, Taylor SH, McDonald AH, Stanton HP, Donald KW. Circulatory and respiratory studies in myocardial infarction and cardiogenic shock. Lancet 1964, 2:825-832.
  5. Thomas M, Malmcroma R, Shillingford J. Haemodynamic effects of oxygen in myocardial infarction. Brit Heart J 1965,27:401-407.
  6. Neill WA. Effects of arterial hypoxemia and hyperoxia on oxygen availability for myocardial metabolism: patients with and without coronary artery disease. Am J Cardiol 1969, 24:166-171.
  7. Bourassa MG, Campeau L, Bois MA, Rico O. The effects of inhalation of 100 percent oxygen on myocardial lactate metabolism in coronary heart disease. Am J Cardiol 1969, 24:172-177.
  8. Rawles JM, Kenmure AC:Controlled trial of oxygen in uncomplicated myocardial infarction. Br Med J 1976, 1:1121-1123.
  9. McNulty PH, Robertson BJ, Tulli MA, Hess J, Harach LA, Scott S, Sinoway LI. Effect of hyperoxemia and vitamin C on coronary blood flow in patients with ischemic heart disease. J Appl Physiol 2007, 102:2040-2045.
  10. Cabello JB, Burls A, Emparanza JI, Bayliss S, Quinn T:Oxygen therapy for acute myocardial infarction. Cochrane Database Syst Rev2013, 8:
  11. Stub D, Smith K, Bernard S, Bray JE, Stephenson M, Cameron P, Meredith I, Kaye DM: A randomized controlled trial of oxygen therapy in acute myocardial infarction Air Verses Oxygen In myocarDial infarction study (AVOID Study). American Heart Journal 2012, Volume 163, Issue 3, 339 – 345.e1.





Why We Do What We Do Critical Care Edition: Is there an Echo? What is all This I Keep Hearing About ECMO?

By: Moses Washington, MD
central  ecmo cannula pic

Figure 1: Central ECMO cannulation, image courtesy of google images, N Engl J Med 2011; 365:1905-1914

Extracorporeal Membrane Oxygenation (ECMO) is a procedure that over the past several years has seen a tremendous resurgence in its use in adults. ECMO is effectively a type of mechanical cardiopulmonary bypass that temporarily (days to weeks) supports the cardiovascular and/or respiratory system in severe illnesses. It has often been used as a last ditch effort in treating refractory illnesses such as ARDS (most commonly), peri-transplant, cardiogenic shock, and post-cardiac arrest. The original technology has been in existence since early 1970s, but very small trials showed its poor outcome resulted in its abandonment in adult population. ECMO only recently saw a resurgence beyond the cardio-thoracic operating rooms in adults during and since the 2009 H1N1 influenza pandemic. This review will cover how it works, indications, contraindications, trials showing outcomes, common complications, and its relevance to Emergency Medicine Critical Care.

The two main methods to implement ECMO are veno-venous (VV) and veno-arterial (VA). The goals of ECMO are to either improve oxygenation, CO2 removal, or allow cardiac unloading or resting the lung.The ECMO circuit consists of cannulas, a pump (which coordinates flow), heat exchanger, and an oxygenator. ECMO cannulas can be inserted centrally (via great vessels) or peripherally (femoral vessels). In VV ECMO blood is drained from the venous system goes to the membrane oxygenator and pumped back to the venous system in series via a circulatory pump and heat exchanger (1). This is typically achieved by cannulating both femoral veins. VV ECMO is reserved for only respiratory disease. VA ECMO in contrary supports failing cardiac and respiratory function or just cardiac failure. In VA ECMO blood is drained from the venous system and pumped into the arterial system. It effectively improves tissue oxygenation, circulatory flow (most importantly cerebral perfusion) and coronary artery perfusion by allowing the heart to rest and unloading the RV (1). This can be performed centrally or peripherally. Central access requires thoracotomy and is only performed by cardio-thoracic surgeons since one cannula is inserted to the right atrium and another into the arch of the aorta. Peripheral VA ECMO requires one to cannulate the femoral vein and artery. The second approach is very much akin to inserting central lines but just requiring larger dilators and cannulas (3). A very simplistic way of understanding how to improve oxygenation and C02 removal in ECMO is mainly all about the blood flow. Essentially, the longer the blood is contact with the membrane oxygenator the better the oxygenation. Since C02 is more rapidly diffuse just increasing the blood flow can improve C02 removal. Since using the circulatory pump can cause clotting consequences low dose heparin and heparin coated cannulas are used (3).

peripheral ECMO pic


Figure 2: Peripheral VA ECMO cannulation, image courtesy of google images,

The most common indications for ECMO in the acute setting are for refractory respiratory failure secondary to ARDS, cardiogenic shock and in peri-arrest. By far the most data showing benefit of ECMO is in ARDS. The idea behind ECMO improving mortality in ARDS effectively is allowing the lungs to rest. This typically has been considered after maximizing low tidal ventilation via ARDSnet protocol, proning, attempting high flow oscillatory ventilation and inhaled nitrous oxide. For VA ECMO indications are refractory cardiogenic shock heart failure, or cardiac arrest. In order to be considered for this costly and labor intensive procedure the disease must have a presumed reversible cause like cardiac ischemia, cardiotoxicity, or viral myocarditis. Contraindications typically include age greater than 65 or 75, metastatic cancer, multi-organ failure, severe irreversible brain damage, and contraindications to anticoagulation (3).

Following the 2009 H1N1 pandemic there was an increase use of ECMO. One study most often quoted was a retrospective case series which documented their experience with ECMO. The study was conducted across 15 ICU’s and ECMO centers in New Zealand and Australia. Out of the 252 patients referred to ICU’s for the influenza pandemic 68 received ECMO.  At the time the data was reported there were a few still remaining in the ICU, those treated with ECMO only had 21% mortality compared to typically 30% which has been seen in the literature (4). This led to the authors saying that the results of their study should help clinicians in healthcare planning during the pandemic. Another study and the largest study was the Efficacy And Economic Assessment of Conventional Ventilatory Support versus Extracorporeal Membrane Oxygenation for Severe Adult Respiratory Failure (CESAR) trial. The CESAR trial was a multi center study conducted in the UK of 180 patients randomized in a 1:1 ratio comparing patients who received conventional mechanical ventilation to those who would be considered to receive ECMO for respiratory failure. Interestingly not only did this study assess for survivability to discharge but also assessed neurologic disability after 6 months of discharge.  At first glance the results seemed very astounding in which 63% (ECMO group) compared to 47% of conventional management group did not  die or have severe disability after 6 months. The study comes under a lot of scrutiny since 68/90 patients randomized to receive ECMO and of those sixty-eight, forty-one survived without severe disability. The remainder were sent to a ECMO center but received conventional management. The study did not achieve its primary objective in effectively comparing ECMO vs conventional management in a 1:1 ratio. This has led to many criticizing that just being referred to an ECMO center in which the staff is better equipped to taking care of the sickest patients may be a confounder in this study. Nevertheless when analyzing the data for face value it can’t be ignored that those who received VV ECMO did have a better outcome (5). Overall, many experts feel that VV ECMO has promise with anecdotal evidence in treating respiratory failure but to date there are not concrete studies that has shown it should be the mainstay treatment in refractory severe ARDS.

VA ECMO and its implication in being a salvation mechanism in refractory cardiogenic failure and specifically cardiac arrest is where most ED physicians are intrigued in its utility. To date only early CPR and defibrillation has been shown to be beneficial in cardiac arrest. The use of VA ECMO in post-cardiac arrest has been referred to as extended cardiac life support (ECLS) or ECPR. Even the AHA is recommending considering ECLS in patients who are presumed to have a reversible cause of cardiac arrest. This is based on some key studies, one study in Taiwan by Chen et al, which looked back at 172 patients over a 3 year period who underwent witnessed in-hospital cardiac arrest secondary to a reversible cause. Out of the studied patients, 113 fit the conventional CPR group to 59 who received VA ECMO after receiving standard ACLS for 10 minutes. They did an intention to treat analysis in which the primary endpoint was survival to hospital discharge. Their results showed that 20% patients showed neurologically intact survival to hospital discharge in the ECMO group. The ECMO group also saw an earlier first rhythm of Ventricular tachycardia or fibrillation although not statistically significant (6). Those in the ECMO group also had ROSC faster than the conventional CPR group. Guen et al, evaluated 51 patients over 32 months, who received ECMO by a cardio-thoracic team who suffered cardiac arrest. All initial rhythms were included for analysis. This study only saw two survivors at 28 days, which reflects the known poor results from most out of hospital cardiac arrest studies. In contrast to the last study median time of onset to ECLS was 75 minutes. This led the authors to conclude using ECMO in the patient population suffering from OHCA should be restricted to selective patients (7). The experience of Dr. Shinar and Dr. Bellezzo, ED doctors, has shown that not only can VA ECMO be life saving but can also be done by trained ED doctors. They documented their experience over a 1 year period. They described a 3 stage approach to initiating VA ECMO in the ED. Stage 1 consists activating the ECLS nurse and ECLS circuit, then cannulating the femoral vessels while CPR is ongoing with angioplasty catheters. Stage 2 proceeds with replacing those catheters with larger cannulas with progressive dilators up to 23 French for the ECMO cannulas and priming and preparing the ECLS circuit. Finally stage 3 is hooking up the ECLS circuit to the cannulas and establishing flow. If ROSC was obtained before completion of stage 3 the protocol stops and standard ACLS care resumes. Eight of twelve patients completed all stages and five out of those eight survived with good neurological outcome to hospital discharge. Interestingly one of those survivors was a patient whose cause of cardiac arrest was an aortic dissection, which typically is a contraindication to initiating ECMO (8).  Another small study (26 patients) was a retrospective observational study at University of Pennsylvania by Johnson also analyzed ECLS for OHCA between July 2007-April 2014. The primary outcome was survival to discharge. This study was interesting in that Emergency medicine team (with senior resident initiating venous access) in concert with CT surgeons following a preset protocol initiated ecmo in post-cardiac arrest patients. The included patients were standard in comparison to other studies and resulted in 4/26 patients surviving to hospital discharge with 75% of those patients being neurologically intact. There was also a significant amount of complications (69%) bleeding and ischemic events (9). These studies show that there is promise that ECMO may be implemented more and taught in the future as truly advanced cardiac life support.

In 2014 there has been very intriguing studies that have developed that has shown good results involving ECMO for post-cardiac arrest. Like most disease entities often one therapy is not a cure all and post-cardiac arrest specifically likely needs a multi-procedural approach in order to achieve better mortality and neurological outcomes. The first study was by the SAVE-J group out of Japan and led by Dr. Sakamoto. His group in a prospective observational trial compared ECPR vs. conventional ACLS for OHCA over 4 years with the initial rhythm having to be VF/VT. Not only did they use ECPR but also therapeutic hypothermia, and intra-aortic ballon pump. The primary outcome was good neurological outcome at 1 month and 6 months following discharge.  Out of 454 patients, 159 (20 hospitals) patients in the non-ECPR group and 234 (26 hospitals in ECPR group) were analyzed in an intention to treat and protocol to treat fashion.  The ECPR  group had a favorable neurological outcome (CPC 1 or 2) in 12.3% (32/260) at 1 month and 11.2% at 6 months, while the non-ECPR group had 1.5% at 1 month and 2.6% at 6 months (10). Overall the results may look poor but one must take into account that in Japan the EMS paramedics and EMTs are not allowed to pronounce death in the field and are required to bring all cardiac arrests to the hospital in comparison to here in the states. The CHEER trial led by Stub in a pilot study analyzed 26 patients with all rhythms included who received mechanical CPR, pre-hospital initiated therapeutic hypothermia, ECPR and PCI in Melbourne Australia. This trial had a median rapid time (56 minutes) to initiate ECMO and had astounding results with 14/26 or 54% having a CPC score of 1 following hospital discharge.  Although small, this study has shown the most promising data including ECPR as treatment modality with favorable neurological outcomes in post-cardiac arrest care (11).

A procedure this invasive obviously has complications. The most common complication encountered is bleeding which includes not only bleeding due to the cannulation process but also intracranial and GI bleeding. Other common complications are mechanical failure of ECMO circuit and limb ischemia. Limb ischemia is often combated by inserting another cannula to facilitate arterial flow to the lower limbs.


Figure 3: Acute Limb Ischemia, courtesy of google images, 

This technique may become a standard procedure which begins in the Emergency department and taught as advanced cardiac life support. It is feasible to initiate an ECMO protocol in a center which has coordinated effort between the members of the Emergency Department, Vascular or Cardio-thoracic surgeons, and Critical Care Units. With a select patient population with severe respiratory failure and refractory cardiac arrest more lives may be saved with ECMO with excellent neurological outcomes. It is of this author’s opinion like with many other interventions earlier implementation of ECMO in the peri-arrest period or respiratory failure may yield better outcomes on a larger scale.


Gattoni L, et al. Clinical Review: Extracorporeal membrane oxygenation. Critical Care 2011, 15: 243.

Chauhan S and Subin S. Extracorporeal membrane oxygenation, an anesthesiologist’s perspective: Physiology and principles Part 1. Annals of Cardiac Anesthesia 2011. Vol 14, No.3. pp 218-229

Marasco S, et al. Review of ECMO (Extra Corporeal Membrane Oxygenation) Support in Critically Ill Adult Patients. Heart, Lung and Circulation 2008.17S: S41-S47.

The Australia and New Zealand Extracorporeal Membrane Oxygenation (ANZ ECMO) Influenza Investigators. Extracorporeal Membrane Oxygenation for 2009 Influenza A (H1N1) Acute Respiratory Distress Syndrome. JAMA 2009, Vol 302, No 17. pp.1888-1895

Peek G, et al. Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multi-centre randomized controlled trial. Lancet 2009, vol 374. pp.1351-1363

Chen YS, et al. Cardiopulmonary resuscitation with assisted extracorporeal life-support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and propensity analysis. Lancet 2008, Vol 372. pp 554-561

Guen M, et al. Extracorporeal life support following out-of-hospital refractory cardiac arrest. Critical Care 2011, 15:R 29.

Bellezzo J, et al. Emergency physician-initiated extracorporeal cardiopulmonary resuscitation. Resuscitation 2012, 83. pp 966-970.

Johnson NJ, et al. Extracorporeal life support as rescue strategy for out-of-hospital and emergency department cardiac arrest. Resuscitation 2014, 85. pp 1527-1532.

10. Sakamoto T, et al. Extracorporeal cardiopulmonary resuscitation versus conventional cardiopulmonary resuscitation in adults with out-of-hospital cardiac arrest: A prospective observational study. Resuscitation 2014, 85. pp 762-768.

11. Stub D, et al. Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial). Resuscitation 2015, 86. pp 88-94.

Why We Do What We Do: Do We Really Need Contrast CT Scan for Acute Appendicitis?

Surgical Validation of Unenhanced Helical Computed Tomography In Acute Appendicitis.



My_name_is_APPENDIX_20140223_MynameisAPPENDIXImage courtesy of google images: 


by: Sarah Goldman, MD, PGY-2

Bottom Line:


Plain helical CT (without PO or IV contrast) has a sensitivity of 95.4% and specificity of 100% in diagnosis of acute appendicitis.


Major points:

Appendicitis carries a lifetime risk of 8.6% for males and 6.7 for females. Currently the diagnosis of appendicitis is aided by the use of helical CT; however, necessity of oral and/or IV contrast is controversial.  In this study, “Surgical validation of unenhanced helical computed tomography in acute appendicitis” 103 patients diagnosed clinically with appendicitis underwent an unenhanced CT scan of the abdomen and pelvis followed by emergency laparoscopy.  CT scan diagnosed appendicitis in 83 patients (80·6 per cent); laparoscopy identified 87 patients with appendicitis (84·5 per cent). Prospective interpretation of CT images yielded a sensitivity of 95·4 per cent and a specificity of 100 per cent for the diagnosis of acute appendicitis. There were four false-negative scans, including a missed perforated appendicitis.



  • Multicenter, prospective study
  • N=103 patients; all underwent CT and laparoscopy
  • Setting: University Hospital Rotterdam and Medical Centre Rijnmond-Zuid
  • Enrollment: December 1999 and November 2001
  • Primary outcome: diagnosis of appendicitis


Inclusion Criteria:

  • Age 16 or older
  • Clinical diagnosis of acute appendicitis by senior surgeon


Exclusion criteria:

  • signs of acute bowel obstruction
  • contraindication to laparoscopy
  • contraindication to general anesthesia
  • pneumoperitoneum
  • age under 16 years
  • pregnancy
  • sepsis (body temperature of 39°C or above or 35·5°C or less and dependence on catecholamines to maintain normal blood pressure, or positive blood cultures).



  • Clinical diagnosis of appendicitis established by senior surgeons
  • All patients subsequently underwent both unenhanced abdominal CT* and standardized diagnostic laparoscopy
  • laparoscopy divided into two phases: exploratory and diagnostic. During exploratory phase surgeon was blinded to CT findings. Results were used to interpret value of preoperative CT.  The surgical findings elucidated during exploratory phase of laparoscopy were considered the gold standard
  • All scans were reviewed by radiologists blinded to the clinical history and surgical findings



  • Diagnosis of appendicitis on CT:  appendix greater than

–         appendix >6 mm in transverse diameter.

–         Secondary signs were:

periappendiceal infiltration, thickening of the caecal wall,

presence of an appendicolith, periappendiceal phlegmon or abscess, and adenopathy

– Scans were considered positive if only secondary signs were noted

  • Acute appendicitis was diagnosed by laparoscopy 87 of 103 pts (84.5%)
  • Acute appendicitis was diagnosed by unenhanced CT in 83 of 103 pts (80.6)
  • Sensitivity of unenhanced CT was 95.4; specificity 100%.
  • There were four false negative scans; three cases involved only the tip of appendix and one perforated appendicitis with microabscess



  • Despite that the CTs were reviewed by both residents and expert radiologists, only the scores by expert radiologists were used to evaluated performance of preoperative CT. The correlation between final results of radiology residents vs. experts is unknown
  • Number of patients studied is relatively small
  • False negative did include a case of perforated appendicitis with microabscess
  • Small study and further research is needed before this can become a routine part of the diagnostic work-up.



Van Lankeren, W., et al. “Surgical validation of unenhanced helical computed tomography in acute appendicitis.” British journal of surgery 91.12 (2004): 1641-1645.


How We Do What We Do: Regular Delivery



Below are the steps that you need to know in order to facilitate getting baby out safely as well as protecting mom’s perineum from lacerations (namely 3rd and 4th degree tears).  This will be particularly helpful when you are working at a facility that doesn’t provide OB service.  Print out this post and have it next to you during the delivery.  Enjoy!

2nd stage of Delivery

  • Establish IV access and start IV fluids – increased fluids decreases the length of time for labor.
  • Place mom on Nasal Cannula as it is associated with a decreased incidence of low cord pH (350% actually)


  • Perform your focused H&P: which includes Gestational age, timing and regularity of contractions, rupture of membranes. Cervical exam should be done to ascertain the stage of labor as imminent . Patients who are fully dilated (10 cm) and 100% effaced should be performed in the Emergency Department by the Emergency Physician. 
    • Only one cervical exam should be performed every 2 hours to reduce the incidence of intra-uterine infections. 
    • If patient is not full dilated and effaced, try to help mom avoid pushing
  • Call your back up. This includes OB, Peds ED/NICU depending on the clinical conditions, as well as availability.
  • Know the location of your equipment. Get familiar with the location of the OB pack, as well as neonatal resuscitation equipment in your ED.
  • Identify a supporting person to the head (doula) of the bed. This person acts as a support for the mother, as well as been shown to improve outcomes.
  • Place Mom in the Dorsal Lithotomy Position (semi recumbent at 30 deg to vertical) to avoid aortovagal compression, improved fetal alignment and larger AP and transverse pelvic outlet. 
    • This will also achieve less pain, incidence of operative delivery and decrease incidence of blood loss >500cc.  
    • Make sure she is comfortable – use pillows and have people help hold her legs as needed.
    • The patient should be instructed to postpone pushing (delayed pushing) unless the urge to push is there as it will improve the efficiency of maternal pushing as well as decrease fatigue.
  • As the fetal head is presenting, place one hand on the head while crowning and the other hand on the perineum so as to protect it from severe tears.  Encourage the mother NOT to push while the head delivers to slow down the process. 
    • This has been shown in an educational intervention study decrease the incidence of 4th degree lacerations.
  • As the head delivers, feel for nuchal cord (25-35% of deliveries). 
    • If loose, it should be reduced over the infant’s head. 
    • If tightly wrapped, clamp the cord in two places. Then cut the cord to allow the baby deliver. Once the cord has been cut you have to expedite deliver as the baby’s oxygen supply has been cut off.
  • As the head rotates, the physician’s hands guide the head and provide gentle traction downward to deliver the anterior shoulder.
  • Once delivered, guide the fetus upward to deliver the posterior shoulder.
  • Place hand around one of the legs of the infant to avoid dropping the infant.
  • There is no evidence that suctioning the neonate at this time improves outcomes or stimulates respiration
  • After 1 minute if possible clamp the umbilicus 3 cm distal to insertion at the umbilicus, milk the cord then place another clamp 2-3 cm distally.  Prior to clamping begin the administration of Oxytocin (10 U IM + 20U in a bag of LR) prior to clamping. 
    • This promotes an auto-transfusion of blood to the neonate and helps decrease maternal bleeding (post-partum hemorrhage).
    • Clamping longer than 2 minutes shows only minimal neonatal benefit and promotes potential for PPH.  Transect the umbilicus with sterile scissors.  
  • Baby should be placed on the maternal belly.
  • Dry baby and wrap him trying to note APGAR score at 1 and 5 minutes. 
    • If baby is not breathing spontaneously make the prompt decision to immediately intubate.
    • If no response, begin neonatal resuscitation (1 breath: 3 compressions).

3rd Stage of Labor: Placental Delivery

  • Keep very gentle traction on the clamped umbilical cord.  AVOID EXCESSIVE TRACTION!!!

Too much may cause uterine inversion, tearing the cord or disruption of the placenta causing for severe vaginal bleeding).

  • After delivery, gently massage at the fundus to promote uterine tone.
  • Allow for 10-30 minutes for delivery of the placenta. Signs of placental separation include cord lengthening, a gush of blood, and upward displacement of the uterus.
    • If placenta has not been delivered in 30 min, gentle traction should be placed on the cord to aid in the detachment of the placenta from the uterine wall.
    • If mother is hemorrhaging, the physician should insert hand into the uterus and by using a raking motion remove the placenta from the wall.



 Berghell, V, Baxter,JK, Chauhan, SP, Evidence-based labor and delivery Management, American Jounral of Obstetrics and Gynecolgy, 2008.

 VanRooyen, M & Scott JA, “Emergency Deliver”: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, Seventh Edition, 2011.

 Tuuli, MG et al., Immediate compared with delayed pushing in the Second Stage of labor – A systemic review and Meta-analysis, Obstet Gynecol 2012; 120:660-8.

 Laine, K et al., Decreasing the Incidence of Anal Sphincter Tears During Delivery, Obstet Gynecol 2008;111:1053-7.

 Albers, LL et al., Midwifery Care Measures in the Second Stage of Labor and Reduction of Genital Tract Trauma at Birth: A Randomized Trial, J midwifery Womens Health. 2005; 50(5):365-372.

 Gungor et al. Oronasalpharyngeal suction versus no suction in normal, term and vaginally born infants: A prospective randomized controlled trial., Australian and New Zealand Journal of OB and Gyn 2005; 45:45-6.

Author: Michael Meguerdichian, MD

Editors: Komal Bajaj MD, Cara Taubman MD