My list of publications (updated regularly). Click here.

Powered by

Sunday, August 16, 2015

Life Threatening Asthma - Some Pearls and Pitfalls

My talk on Life Threatening Asthma talk in 2nd NECCS Ipoh

Some may not agree with the ventilation strategy I borrowed from Scott Weingart's, i.e., a PEEP of 0 or zEEP.  I guess if you are familiar on how to play around with the PEEP in severe airway obstruction without causing a disaster in barotrauma, then go ahead. But to be on the safe side, I'll stick with the strategy mentioned by Scott Weingatt. Listen to the 2nd podcast listed below on Dominating the Vent: Part II for a clearer picture.

Here are the compilation of podcasts and lectures I referred to prepare the talk on asthma:
1. Scott Weingatt's Dominating the Vent: Part I
Download mp4 lecture:

2. Scott Weingatt's Dominating the Vent: Part II
Download mp4 lecture:

**These 2 lectures are very easy to understand and form the basis of ventilation strategy in ED in general. Some people may not agree with Weingatt's strategy. Different people have different opinion but Weingatt's strategy is very simple - only two strategies that you need to concern in ED: obstructive strategies and lung protective strategies. Even if patient initially does not have lung injuries, ARDS, ALI, the patient may eventually end up with some form of lung injuries if ventilation strategies not appropriate. So, treat the patient as if having a lung injury. Only 4 settings to adjust in ED: TV, IFR, PEEP/FiO2 (use ARDSnet table) and RR.
Notes in pdf is available for download

3. Scott Weingatt - Severe asthmatic podcast

4. Scott Weingatt - Coding Asthmatic

5. Management of the Crashing Asthmatic

6. RAGE session 3 on life threatening asthma
And RAGEBack session 3:

And here are some of the articles referred to:
1 Oddo M, Feihl F, Schaller MD, et al. Management of mechanical ventilation in acute severe asthma: practical aspects. Intensive Care Med 2006;32(4):501-10.  
2. Alvarez GG, Schulzer M, Jung D, et al. A systematic review of risk factors associated with near-fatal and fatal asthma. Can Respir J 2005;12(5):265-70.
3. Restrepo RD, Peters J. Near-fatal asthma: recognition and management. Curr Opin Pulm Med 2008;14(1):13-23
4. The 3Mg-Trial on the use of MgSO4
Goodacre S, Cohen J, Bradburn M, et al. The 3Mg trial: a randomised controlled trial of intravenous or nebulised magnesium sulphate versus placebo in adults with acute severe asthma. Health Technol Assess 2014;18(22):1-168

Saturday, August 08, 2015

Five Compelling Reasons Why New or Presumed New LBBB (without any other qualification such as Sgarbossa’s or Smith’s criteria) Should NOT be treated as STEMI

My presentation (contra-argument) during the "debate" with Prof Dr. Rashidi Ahmad from UMMC during the 2nd National Emergency and Critical Care Symposium 2015 in Ipoh (08 August 2015)


The 6-page companion notes below can also be downloaded at: OR at the following URL in

1. Recent evidences suggest that new or presumed LBBB does not predict STEMI any more than old LBBB or no LBBB

a.  Chang et al (2009): observational, 7937 patients with CP admitted to ED; 55 with new or presumed new LBBB, 136 had old LBBB, and 7746 had no LBBB. The rate of AMI was not significantly different between the 3 groups (7.3% vs 5.2% vs 6.1%; P = 0.75). Authors conclude, “ED patients with a new or presumed new LBBB are not at increased risk of AMI. The presence of LBBB, whether new or old, did not predict AMI.”

b.  Jain et al (2011): Retrospective, n = 892, only 36 (4%) of whom had new LBBB. Out of these 36, only 14 patients (39%) had final diagnoses of acute coronary syndromes (12 – AMI, 2 UA), 13 (36%) had cardiac diagnoses other than acute coronary syndrome (e.g. acute heart failure, complete heart block, AF, aortic stenosis, hypertensive emergency) and 9 (25%) had noncardiac diagnoses. Which means, only approx 1/3 of new or presumed new LBBB ultimately has AMI. Out of these 36 patients, almost all patients - 32 underwent PCI (3 in the non-ACS cardiac diagnoses and 1 non-cardiac group did not). Which means, new or presumed LBBB results in up to 2/3 of unnecessary PCIs.

c.   Kontos et al (2011): observational, n= 401 LBBB undergoing their institutional MI rule-out protocol, including serial cardiac biomarkers and PCI. LBBB were classified as chronic, new, or if no ECG was available, as presumably new. 37% new LBBB, 27% presumed new LBBB. A total of 116 patients (29%) had MI, with no significant difference in terms of frequency as well as the infarct size of MI was similar among patients with chronic LBBB, new LBBB, or LBBB of unknown duration. Concordant ST changes were the most important predictor of MI (odds ratio 17, 95% CI 3.4-81, P < .001) and an independent predictor of mortality (odds ratio 4.3, 95% CI 1.3-15, P < .001); “new” or “presumably new” (a.k.a. chronicity) was neither predictive.

d.   Wong et al (2005) in the HERO-2 (Hirulog and Early Reperfusion or Occlusion) trial; n= 300 with LBBB (92 with and 208 without ST-segment changes) and 15,340 no LBBB. AMI occurred in 80.7% of LBBB patients and 88.7% of controls (p = 0.006). What’s more interesting is when they analyzed LBBB with or without concordant ST changes: LBBB with ST-segment changes similar risk of 30-day mortality (even slightly higher) compared to STEMI patients without LBBB (odds ratio [OR] 1.37, 95% confidence interval [CI] 0.78 to 2.47). It is those STEMI patients with LBBB that has NO concordant ST-segment changes that has demonstrated lower mortality than STEMI patients without any LBBB (OR 0.52, 95% CI 0.33 to 0.80).  LBBB with concordant ST-segment elevation or lead V1 to V3 ST-segment depression independently predicted higher 30-day mortality but the absence of concordant ST-segment elevation or lead V1 to V3 ST-segment depression during LBBB independently predicted a lower 30-day mortality rate than that of patients with no LBBB.

2. Questionable historical origin - Recognition of LBBB in AMI dates back to 1917 in an account by Oppenheimer and Rothschild. As noted by Bauer (1965) many of the patients with BBB had many other confounding risks: they were significantly older, higher frequency of HPT, CHF, previous MI, and cardiogenic shock. Therefore, it is difficult to discern whether increased mortality risk (approximately 2-fold) in BBB were actually due to the BBB it self or it was confounded by age and comorbid conditions. Furthermore, in her article published in the Journal of Electrocardiology Vol. 33 (2000), Sgarbossa questioned whether many of the ECGs recorded in the pre-thrombolytic era were actually recorded in real time when the patients were having acute myocardial infarction or not. In that article the authors say:

“In the prethrombolytic era, however, the management of patients with myocardial infarction (MI) consisted only of pain relief, observation, and treatment of complications. In patients with ECG confounders, such as LBBB, the diagnosis of MI was confirmed through biochemical determinations over several hours or days after admission. Because there was no incentive to collect information on early ECG signs of MI, most studies on the diagnosis of MI in the presence of LBBB included ECGs with old infarctions as well as recordings obtained at widely scattered time-points after acute infarction”

Furthermore, the recommendation by ACC/AHA to use the criteria of new or presumed new LBBB is based on the findings more than 20 years ago. It was based on the pooled data of 9 trials in the FTT group (FTT = Fibrinolytic Therapy Trialists) back in 1991 (more than 20 years ago) showing that STEMI patients with BBB treated with fibrinolysis had lower mortality rate than placebo (18.7% vs 23.6%) but this is at the expense of increased major bleeding risk (1.3% vs 0.3%) and increase in stroke (2.1% vs 1.1%). Furthermore, there are three important caveats in interpreting the FTT group results:

o   these trials did not specify whether the ECG showed RBBB or LBBB

o   whether the conduction abnormalities were new, or whether there were associated ST-segment changes (a.k.a. the chronicity of the BBB unknown)

o   the cohort of STEMI patients with BBB in FTT group was very small, 3.6% of the total cohort

3.   3. Confounding pathogenetic mechanisms:

There are just too many confounders to the pathogenetic mechanism of LBBB in AMI. In a commentary article for example, Neeland et al (2012) say that for an AMI to result in LBBB, it would have required a rather large infarct. This is because, unlike the RBB, which is a discrete bundle that can be injured by a small focal insult, the LBB is a large bundle that is further branched into the anterior superior and posterior inferior fascicles, and therefore, the infarct would have either affected the LBB just distal to the bundle of His or an infarct that affect both anterior and posterior fascicles. As such, although LBBB can occur de novo in AMI, LBBB is more likely a pre-existing marker of underlying structural heart disease such as a fibrotic conduction system – thus, a reflection of the patient’s baseline CVS risks such as long standing HPT causing LVH or left ventricular remodeling resulting from CHF. This is consistent with the observations by Bauer (1964) that show that LBBB in AMI, although can be transient or permanent but most permanent LBBB in AMI are not due to true AMI-related LBBB because these true-AMI related LBBB has very high mortality.

4.   4. Ethical issue of giving fibrinolytics when it is not needed

The bleeding risk: E.g., FTT group data: bleeding risk of fibrinolysis 1.1 – 1.3%. NNT for streptokinase is 25; based on the studies like Chang et al (2009) where the incident of STEMI is the same in the new LBBB vs old LBBB vs no LBBB, and the incident of STEMI is only 1/3rd of the total cases of new or presumed LBBB, is it ethical to subject the patient to fibrinolytic merely because of new or presumed new LBBB per se? To quote Neeland et al (2012):

“In centers where primary PCI is not readily available, these issues obviously are more concerning given the risks of bleeding, particularly intracranial bleeding, with fibrinolytic therapy; the risks of fibrinolytic therapy may be magnified in patients with LBBB who generally are older and have higher rates of hypertension.”

5.   5. Unnecessary PCIs. As commented in Neeland et al (2012), presumed LBBB has emerged as a frequent reason for false activation cath lab. In a single study of 1335 patients, Larson et al (2007) – overall false +ve cath lab activation was 14%, but in the LBBB cohort, the rate was 44%! Lopes et al (2011) – 39% out of 98 patients with new LBBB, even including those with concordant ST-changes on ECG did not have positive angio finding. Even worse is in centers that do not have 24/7 PCI service.

ADDITIONAL NOTES: What’s the alternative?

If new or presumed new LBBB per se should not be treated as STEMI equivalents, what are the alternatives?

1. Add on the Sgarbossa’s 3 criteria

Concordant ST elevation >/= 1 mm, weighted score 5;

Concordant ST depression >/= 1 mm in V1-V3, weighted score 3;

Discordant ST elevation >/= 5 mm, weighted score 2

Tabas et al (2008) in a meta-analysis on the Sgarbossa’s criteria,

N = 2100

11 trials

For a total score of >/= 3 points,

sensitivity is 20% (95% CI 18 – 23%); specificity of 98% (95% CI 97 – 99%)

For a total score of >/= 2 points,

sensitivities ranged from 20% to 79%; specificities ranged from 61% to 100%

Sokolove et al (2000)

Sgarbossa’s criteria has an excellent inter-observer agreement (kappa=0.81, 95% CI  0.80 to 0.83) between cardiologists and emergency physicians for diagnosing AMI.

Concordant STE is the single most specific criteria (Lopes et al, 2011; Jain et al, 2011)

Although Sgarbossa’s criteria is specific, it is not sensitive. But we should remember Sgarbossa’s for LBBB is an add-on criteria for STEMI. Without Sgarbossa’s, the usual definition of STEMI should be applied.

2. Smith’s et al (2011)

Address the weak criteria of discordant ST elevation

Absolute 5 mm was used by Sgarbossa et al

Changed it to ST/S </= -0.25 (meaning magnitude of at least 25% of the R or S whichever greater) increases sensitivity from 52% to 91% at the expense of reducing specificity from 98% to 90%.

3. Neeland et al’s algorithm (2013)

If hemodynamically unstable, e.g. cardiogenic shock, refer for PCI/thrombolytics

If stable, use a more specific criteria (Sgarbossa’s)

If Sgarbossa’s criteria suggestive STEMI – PCI/thrombolytics

If Sgarbossa’s criteria not suggestive – depends on other clinical parameters including echo/serial biomarker

Suggested free web resources:

1.  A MUST READ - Neeland IJ, Kontos MC, de Lemos JA. Evolving considerations in the management of patients with left bundle branch block and suspected myocardial infarction. J Am Coll Cardiol 2012;60(2):96-105. Available at:

2.  Amal Mattu's ECG Case of the Week: Nov 4, 2013. Available at URL:

3.  Modified Sgarbossa Criteria: Ready for Primetime? In: Academic Life in Emergency Medicine (ALiEM) website Available at URL: 


  • Chang AM, Shofer FS, Tabas JA, et al. Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients. Am J Emerg Med 2009;27(8):916-21. 
  • Jain S, Ting HT, Bell M, et al. Utility of left bundle branch block as a diagnostic criterion for acute myocardial infarction. Am J Cardiol 2011;107(8):1111-6.
  • Kontos MC, Aziz HA, Chau VQ, et al. Outcomes in patients with chronicity of left bundle-branch block with possible acute myocardial infarction. Am Heart J 2011;161(4):698-704.
  • Wong CK, French JK, Aylward PE, et al. Patients with prolonged ischemic chest pain and presumed-new left bundle branch block have heterogeneous outcomes depending on the presence of ST-segment changes. J Am Coll Cardiol 2005;46(1):29-38.
  • Sgarbossa EB. Value of the ECG in suspected acute myocardial infarction with left bundle branch block. J Electrocardiol 2000;33 Suppl:87-92.
  • Neeland IJ, Kontos MC, de Lemos JA. Evolving considerations in the management of patients with left bundle branch block and suspected myocardial infarction. J Am Coll Cardiol 2012;60(2):96-105.
  • Fibrinolytic Therapy Trialists' (FTT) Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients.  Lancet 1994;343(8893):311-22.
  • Larson DM, Menssen KM, Sharkey SW, et al. "False-positive" cardiac catheterization laboratory activation among patients with suspected ST-segment elevation myocardial infarction. JAMA 2007;298(23):2754-60.
  • Lopes RD, Siha H, Fu Y, et al. Diagnosing acute myocardial infarction in patients with left bundle branch block. Am J Cardiol 2011;108(6):782-8.
  • Tabas JA, Rodriguez RM, Seligman HK, et al. Electrocardiographic criteria for detecting acute myocardial infarction in patients with left bundle branch block: a meta-analysis. Ann Emerg Med 2008;52(4):329-36
  • Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med 2012;60(6):766-76.
  • Sokolove PE, Sgarbossa EB, Amsterdam EA, et al. Interobserver agreement in the electrocardiographic diagnosis of acute myocardial infarction in patients with left bundle branch block. Ann Emerg Med 2000;36(6):566-71.

Tuesday, June 16, 2015

Giving Oxygen in COPD - A Goldilocks Principle Is Required

Effects of hypoxia in COPD

The most dangerous effects of hypoxia in COPD are sudden cardiac arrest and irreversible damage to the vital organs. Significant hypoxia for more than 4 - 6 minutes is already enough to cause sudden cardiac arrest. (Murphy et al, 2001)

A number of studies recommend keeping a PaO2 of 50 mmHg in COPD to prevent sudden death of hypoxia (Hutchison et al, 1964; Smith et al, 1968; Jeffrey et al 1992).

Effects of hypercapnia in COPD

The most dangerous effects of hypercapnia in COPD (especially during acute exacerbations) are depression of neurological and cardiopulmonary function

Although these effects do not occur as quickly as in hypoxia, yet these effects can last from hours to days. Progressive respiratory failure secondary to hypercapnia in COPD can be fatal (Murphy et al, 2001).

A pH of less than 7.3 is associated with increased risk of ICU admission (Plant et al 2000). Not surprisingly, in COPD, pH has been shown to be a much more important indicator of severity and prognosis than PaCO2 (Murphy et al, 2001).

Reduction in pH also results in a rightward shift in the oxyhaemoglobin dissociation curve.
The paradox is the highest PaCO2 levels have been noted AFTER oxygen therapy has been given. This was found by McNichol and Campbell back in 1965. They found that patients with acute exacerbations of COPD rarely have a PaCO2 of more than 80 mm Hg and almost impossible for the PaCO2 to be above 100 mm Hg or the pH to be below 7.16 unless they have been given oxygen.

During the 1950s and 60s, the reason postulated particularly by Campbell was that administration of high concentration oxygen to patients dependent on hypoxia to stimulate their breathing might lead to a progressive decline in this hypoxic respiratory drive (or commonly known as hypoxic drive). Subsequent studies do indeed find that COPD patients with high O2 indeed have slight reduction of minute ventilation.

A one year prevalence study by Plant et al 2000 showed that the injudicious use of oxygen treatment caused acidosis in patients with acute exacerbations of COPD; however, a proportion of these patients were rapidly able to correct their pH once the fraction of inspired oxygen was reduced.

Today, the pathophysiological mechanisms behind hyperoxia-indyeced hypercapnia is thought to be mediated by more complicated set of mechanisms than previously understood including the contributions of hypoxic pulmonary vasoconstriction, absorption atelectasis, respiratory depression, and the Haldane effect; and some even consider some genetic susceptibility to carbon dioxide retention in some individuals.

Hypoxic pulmonary vasoconstriction occurs in COPD patients with poorly ventilated pulmonary regions where hypoxia causes localised vasoconstriction to occur in the pulmonary capillaries, balancing ventilation, and perfusion. Reoxygenation of these pulmonary capillaries causes vasodilatation and creates a significant ventilation‐perfusion (V/Q) mismatch and an increase in physiological dead space in some COPD patients. This mechanism has gained in acceptance over recent years.

Furthermore, higher concentrations of oxygen may also result in absorption atelectasis due to alveolar denitrogenation, further reducing lung function, whilst it is postulated that the Haldane effect (the binding of oxygen and haemoglobin resulting in an increase in unbound CO2 and a reduction in pH) may also result in slight increases in systemic acidity.

Even in prehospital setting, Austin et al (2010) found that titrated oxygen treatment significantly reduced mortality, hypercapnia, and respiratory acidosis compared with high flow oxygen in acute exacerbations of chronic obstructive pulmonary disease (number needed to harm in patients with high flow oxygen is 14 compared to titrated oxygen (i.e., for every 14 patients who are given high flow oxygen, one will die.)

Bottom line:

Too little oxygen is bad
Too much oxygen is bad.
Too much carbon dioxide is bad.
In COPD, if given too much oxygen, it is easy to have too much carbon dioxide.
"Just right" amount of oxygen is optimal.

In other words, maintaining an optimal SaO2 in COPD requires a “just-right” strategy a.k.a The Goldilocks principle (not too much, not too little).

A saturation above 85% avoids the problems of hypoxaemia in the chronically hypoxic patient, whilst minimising the risk of carbon dioxide retention.
Most authors advocate keeping a range of PaO2 of around 50 mmHg with SaO2 of 85%, although some recommends a range of SaO2 between 85 and 92%.

Click here to download a podcast from EM Basic on oxygen therapy in COPD

Why is this called a Goldilocks principle?
It is because in the story of the Goldilocks and The Three Bears, when Goldilocks enters the house owned by three bears, she always find that one set of them is always too much in one extreme compared to the other, and one is “just right” for her (e.g. one porridge is too hot, the other is too cold; one chair is too large, the other is too small; one bed is too hard, the other is too soft, etc).

Recommended readings:

1. New, A.  Oxygen: kill or cure? Prehospital hyperoxia in the COPD patient.  Emerg Med J. 2006 February; 23(2): 144–146. Click here to download this article in pdf.

2. Austin, MA et al. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: Randomised controlled trial. BMJ 2010 Oct 18; 341:c5462. Click here to access this article in full text.

3. Murphy, R, Driscoll, P & O’Driscoll, R. (2001). Emergency oxygen therapy for the COPD patient. Emergency Medicine Journal : EMJ, 18(5), 333–339. doi:10.1136/emj.18.5.333. Click here to access this article in pdf.
There was an error in this gadget


PLEASE NOTE: All contents in this blog are copyrighted materials, unless otherwise stated. Even if you encounter materials in this page without a copyright notice, it does not mean that it is not copyrighted (Click here to read TEN BIG myths on copyright explained). This is especially so as most nations are signatories of the Berne Convention on international copyright law (World Intellectual Property Organization). Nevertheless, I have licensed almost all the materials contained here under Creative Commons licenses strictly for educational, non-commercial purposes only. Kindly email me at should you want to use any of the materials for commercial purposes. Thank you.