EMCrit Podcast 50 – Acid Base Part IV – Choose the Solution Based on the Problem

This is Part 4 of the Acid Base saga. In this episode, I discuss the acid base effects of fluids and when and how to use sodium bicarbonate.

If you haven’t checked out the previous episodes, you should definitely do that first:

You may need the EMCrit Acid Base Sheet to follow along

The Acid Base of Fluids

Crystalloids will have acid-base effects by their SID and the dilution of extracellular Atot

“Balanced Fluids” are fluids with a SID just low enough to balance the dilution of the weak acid, albumin (SID of 24-28)

For the effects on a patient with altered pH, any fluid with a SID the same as the pt’s bicarb will keep the patient at the same pH. If the SID is greater than the pt’s bicarb, then the fluid will be alkalotic and if less than the pt’s bicarb–acidotic (Intens Care Med 2011;37:461).

Hypertonic fluids are even more acidifying b/c they draw pure water into the extracellular space

Chart with a bunch more fluids is on crashingpatient.com

Sodium Bicarbonate

If not stored in glass, bicarb containing solutions leech CO2 and become not so much bicarbonate.

If given at all, should be given slowly by push over 5-10 minutes or by drip; never by rapid push

In hyperkalemia, NaBicarb isotonic is essentially a potassium-free, non-acidic fluid that dilutes down the potassium.

NaBicarb can be used as a substitute for hypertonic saline in increased ICP (Neurocrit Care 2010;13:24). They used 85 ml of 8.4% sodium bicarb infused over 30 minutes.

Articles

Best Review of the Stewart/Quant Approach to Fluids

Best Review of Sodium Bicarb Use Ever

Balanced solutions (p-lyte) led to lower Cl and higher bicarb (Am J Emerg Med. 2011 Jul;29(6):670-4)

Another incredible review on fluids including the rec. that we use 3 amps of bicarb (J Intens Care Med 2010;25(5):271)

Also of interest may be the previous episode on intubating the patient with the severe metabolic acidosis

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EMCrit Podcast 49 – The Mind of a Resus Doc: Logistics over Strategy

amateurs discuss strategy; experts discuss logistics
–Napoleon?


This Part I of the Mind of a Resus Doc Series, in which we delve into the philosophies that make a good resuscitationist.

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EMCrit Podcast 48 – PhD in EKGs Part II: Left Bundle Branch Block

Left Bundle Branch Block (LBBB) doesn’t = STEMI!

A few months ago, we had Dr. Stephen Smith on the podcast to discuss a variety of EKG issues. Dr. Smith has an EKG blog that is required reading for every ED and ICU doc. This is Part II and I think it discusses an incredibly important issue: right now major medical societies including the AHA and ACEP are asking us to fibrinolyse or PCI patients with new or presumed new LBBB. However, your interventionalists will tell you that this strategy is a ridiculous waste given how few acute occlusions will actually be found. Why this discrepancy?

 

Dr. Smith actually created a post specifically for this podcast; here is the full text:

A 45 year old male with no history of cardiac disease presented with new onset pulmonary edema.  He was intubated prehospital.  BP before and after intubation was 110 systolic, with HR of 120.

There is sinus tach with LBBB.  There is no concordant ST elevation.  V4 has 2 mm of discordant ST elevation (at the J-point, relative to the PR segment) following a 5 mm S-wave.  The ST/S ratio is 0.40 in this lead. Lead II has proportionally excessively discordant ST depression, with 1.25 mm STD and only 4.0 mm R-wave, for a ratio of 0.31.  This is also a sign if ischemia (reciprocal inferior ST depression).              Also, look at V3: complexes vary slightly: 2nd complex has approx 2.5-3.0 mm STE following a 14 mm S-wave; complex 4 has 2-2.5 mm STE following a 10.5 mm S-wave.   So these approach an ST/S ratio of 0.20, but it is not definite.

In a study of 19 patients with LAD occlusion, vs. 129 controls with ischemic symptoms and LBBB, at least one complex in V1-V4 with at least 2mm of STE and an ST/S ratio > 0.20 was highly specific for LAD occlusion (1).   Here is the reference for the abstract on proportionally excessively discordant ST depression (2).

Cases with excessive discordance of at least 5mm [Sgarbossa criteria 3] that did not have proportional discordance, did not have LAD occlusion.  The mean highest ST/S ratio for those without occlusion was 0.10 (95% CI: 0.09-0.11); the mean highest ST/S ratio for those with occlusion was 0.44 (95% CI: 0.19-1.05)

Because of this study, I believe the following rule is as good for diagnosis of STEMI in the setting of LBBB as standard interpretation of STEMI in the absence of BBB (and that it is more sensitive and specific than the Sgarbossa rule):

Smith modified Sgarbossa rule:

1) at least one lead with concordant STE (Sgarbossa criterion 1) or
2) at least one lead of V1-V3 with concordant ST depression (Sgarbossa criterion 2) or
3) proportionally excessively discordant ST elevation in V1-V4, as defined by an ST/S ratio of equal to or more than 0.20 and at least 2 mm of STE. (this replaces Sgarbossa criterion 3 which uses an absolute of 5mm)

It is important to remember that this is not sensitive for “MI” which is diagnosed by biomarkers. The lack of sensitivity of the Sgarbossa rule in previous studies is because the ECG is always (even without BBB) insensitive for MI.  It is, however, much more sensitive for occlusion.

Followup:
Because of proportionally excessive discordance in lead V4, (and, of course, clinical instability), the patient was taken for immediate angiography, which confirmed a 100% mid-LAD occlusion.

For a case with more than 5 mm of ST elevation in V1-V4, but without excessive proportional discordance, see this post:
http://hqmeded-ecg.blogspot.com/2011/02/new-lbbb-and-massive-st-elevation-do.html

Tom Bouthillet has done a great job of describing my ratio rule here:
http://ems12lead.com/2010/12/29/excessive-discordance-as-a-marker-of-acute-stemi-in-lbbb/

To learn more about the meaning of New LBBB, look here:
http://hqmeded-ecg.blogspot.com/2010/03/new-left-bundle-branch-block-is-poor.html

Caution: these data have not been published in a peer review journal, and the ACC/AHA still (though I believe wrongly, and this recommendation is rarely followed) recommends reperfusion for patients with ischemic symptoms and new LBBB, even without any specific findings of STEMI.

 

1. Dodd KW. Aramburo L. Broberg E. Smith SW. For Diagnosis of Acute Anterior Myocardial Infarction Due to Left Anterior Descending Artery Occlusion in Left Bundle Branch Block, High ST/S Ratio Is More Accurate than Convex ST Segment Morphology (Abstract 583). Academic Emergency Medicine 17(s1):S196; May 2010.

2. Dodd KW. Aramburo L. Henry TD. Smith SW. Ratio of Discordant ST Segment Elevation or Depression to QRS Complex Amplitude is an Accurate Diagnostic Criterion of Acute Myocardial Infarction in the Presence of Left Bundle Branch Block (Abstract 551). Circulation October 2008;118 (18 Supplement):S578.

Additional References


(1) Jain S, et al. Utility of left bundle branch block as a diagnostic criterion for acute myocardial infarction Am J Cardiol 2011;107(8):1111-6.
(2) Poon K, et al. Abstract 4317: Does a New or Presumed New Left Bundle Branch Block Have Equivalent Mortality to an Acute ST-Elevation Myocardial Infarction? Circulation 120: S935.
(3) Kontos MC, 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.
(4) Chang AM, 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.

If you want a .doc or .pdf of these abstracts, email: dr.smiths.ecg.blog@gmail.com

 

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EMCrit Podcast 47 – Failure to Plan for Failure: A Discussion of Airway Disasters

Cliff Reid of Resus.Me fame put out an incredible post on NAP4, the audit done on all of the airway complications in Great Britain. It was such a phenomenal post that I got in touch with Cliff and asked if he wanted to come on the podcast to speak about it. He did me one better and got an interview with one of the authors of the Emergency and Critical Care Section.

So in this podcast, we interview Dr. Jonathan Benger, professor of Emergency Medicine with a particular interest in the management of the airway.

Points that came out of the show

  • Mortality is higher in the ED and ICU compared to the operating room. Our patients are sicker, so we must be more diligent in planning
  • Quantitative wave-form ETCO2 should be the standard of care for EVERY ED and ICU intubation
  • Needle cricothyrotomy seems to fail more often than surgical cricothyrotomy
  • Awake intubation was not used when it was indicated
  • Junior resident anesthesiologists were often responding to the ED and ICU
  • There was a failure to plan for failure
  • Obesity figured into a large percentage of the airway disasters

For more from the NAP4

Executive Summary

Full Report (Skip to the EM/ICU Chapter)

How to subscribe to Cliff Reid’s Brand New Podcast

Great Conferences Coming Up


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EMCrit Podcast 46 – Acid Base: Part III

This is the 3rd part of a 4 part series on acid base.

You should listen to Acid-Base Part I first where you will learn about the underlying chemisty of acid base. Part II then delves into the underpinnings of the mathematics of acid base. In part III, we will go through two actual problems and show how the EMCrit method plays out. Part IV delves into the acid-base of solutions.
Before we get to the clinical stuff, I am giving three lectures at the 8th annual NY Symposium on Neurological Emergencies and Neurocritical Care. Should be a great conference. If you are free for some of the days between June 14-17, 2011; consider coming.

Ok back to acid base stuff.

For this podcast to be optimally effective, you need to print out my acid base sheet:

EMCrit Acid Base Method

Here is the 1st problem from last podcast:

 

Here is the same patient after we treated his DKA:

Mike asked if there was any literature to support the simplification I am using to make the incredible complex quantitative formula more approachable. The answer is yes and here is the pdf you want to read:

Story DA, Morimatsu H, Bellomo R. Strong ions, weak acids and base excess: a simplified Fencl-Stewart approach to clinical acid-base disorders. Br J Anaesth. 2004 Jan;92(1):54-60.

 

Want an incredible program that will do all of the work for you and teach you about the quantitative method at the same time? Look no further than this incredible site:

AcidBase.org’s analysis model

 

Need an Audio Only Version?
Acid Base Part III MP3 [Play] [Play](Right Click and Choose Save as)

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EMCrit Podcast 45 – Acid Base: Part II

This is the second part of a 4 part series on acid base.

You should listen to Acid-Base Part I first. In Part III, we solve the problem below and reunify everything. Part IV discusses the acid-base of administered solutions.
For this podcast to be optimally effective, you need to print out my acid base sheet:

EMCrit Acid Base Sheet

Here is the problem to work on for the next podcast:

 

I gave some shout-outs during the talk, here are the links:

  • The Air Medical Memorial honors those flight medics, docs, pilots, and nurses who have fallen in the line of duty.
  • Josh Mularella developed the free app call ERRES, search for it on itunes.
  • Casey Parker created a site for outback EM and Crit Care called Broome Docs.
  • Ivor Kovic donated three free codes to his cpr app, CPRPRO. Sign up for the mailing list if you want to enter to win one.

 

 

Need an Audio Only Version?
Acid Base Part II MP3 [Play] (Right Click and Choose Save as)

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EMCrit Podcast 44 – Acid Base: Part I

I have spoken about it for a while, but I’ve finally gotten it done: the acid-base podcast. The podcast is going to be in 3 or 4 parts. They are segmented from a lecture I gave to my residents recently. Part II discusses the mathematics of acid base and Part III goes through actual problems. Part IV then discusses the acid-base of administered solution.

This lecture discusses a quantitative approach to acid base management. This is also known  as the Fencl-Stewart approach, the strong-ion approach or the physicochemical approach. It provides explanations for why acid base disorders occur in human pathophysiology. The classic method used in the USA is the Henderson-Hasselbalch (misspelled on my slides) approach. I find this method to provide no comprehensive explanation for why things are as they are. Through the quantitative approach, you can also understand the H&H approach and continue to use it with new insight.

This first part deals with the preliminaries. Part II will go into clinical applications.

After listening to the podcast, I recommend reading this article:

Kaplan LJ,Frangos S. Clinical review: Acid–base abnormalities in the intensive care
unit. Critical Care 2005;9(2):198
For the next part of the series, you will need a print out of this sheet:
EMCrit Acid-Base Sheet

Want to read more?

Need an Audio Only Version?
Acid Base Part I MP3 [Play] (Right Click and Choose Save as)

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EMCrit Podcast 42: A phD in EKG with Steve Smith

Today, I got to interview Dr. Stephen Smith. Dr. Smith is faculty at the Hennepin Program and author of one of the best books on EKGs in the ED, The ECG in Acute MI.

Dr. Smith’s EKG Blog is probably the best free EKG site out there for Emergency Physicians and Intensivists.

Here are the points we covered:

1. Ischemia Doesn’t Localize

If you see depressions in just one anatomic area, think reciprocal changes to subtle ST-elevations elsewhere

2. If you see Inferior Depressions, think High Lateral Wall STEMI

here are two good cases from Dr. Smith’s Blog:

  • Case: This is a 35 yo woman who had LAD occlusion that was very subtle on ECG, but easily seen with inferior ST depression
  • Case: This is one of a high lateral MI due to OM-2 occlusion that shows up mostly with inferior ST depression.

3. Lateral Wall STEMIs are often Subtle

4. Absolute millimeter criteria for STEMI will often fail you, it is the Pattern that Matters.

5. Benign Early Repolarization and LAD Occlusion can look very similar–You may need to do the math.

Dr. Smith derived this formula:

(1.196 x STE60 in V3 in mm) + (0.059 x computerized QTc in milliseconds) – (0.326 x RA in V4 in mm),

where RA is R-wave amplitude and STE60 is ST elevation at 60ms after the J-point relative to the PR interval.

If the value of the formula is greater than or equal to 23.4, it is MI (Sens, spec, accuracy all around 90%); if less, then it’s early repolarization.

  • Case: Here is a case that illustrates this, it shows a very subtle anterior STEMI, and how use of the complicated new rule that he developed. One need not use the complicated rule; among other  features, it was the long QTc of 455ms that made it unlikely to be normal.   The followup ECG is also very instructive.

You can also see a video of the concept

6. If you are calling it BER, there need to be R waves in the Precordial Leads

7. Q-waves can develop instantly after a STEMI

qR waves can develop instantly and are not indicative of poor response to lytics or PCI (J Am Coll Cardiol 1995;25:1084); this concept is not  applicable to a QS pattern.

8. If you see a wide (>190 ms) QRS, think Hyperkalemia

9. The treatment for VT with hyper-K is Calcium, Calcium, Calcium

10. Check Out these Two Other Great Sites

HQMEDED: High Quality Medical Education and Ultrasound

The Prehospital 12-lead ECG Blog which despite the name, is great for all levels

 

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EMCrit Podcast 41 – Interview with Cliff Reid of RESUS.me

I was able to cajole Cliff Reid of the amazing blog, resus.me on to the EMCrit program. Cliff is truly a doc after my own heart as you will hear from the cast.

He is currently an EMS physician and Director of Training at the New South Wales Ambulance Service.

Cliff’s blog, resus.me is an incredible collection of timely articles on emergency medicine, ems, critical care and resuscitation.

Cliff mentions the HEMS service in London. This amazing service sends a physician/paramedic team to the scenes of bad traumas by helicopter and response cars. A well done video is available on youtube:

The winner of the Toxicology Handbook is Jenny Mendelson. Yeah!!!

photo by Mad Scientist

Click Here to Play the Podcast

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EMCrit Podcast 40 – Delayed Sequence Intubation (DSI)

Update: Want more on DSI after you listen to the podcast below. My friend Minh Le Cong interviewed me on DSI on his amazing PHARM Podcast. It is an additional 45 minutes on newest thoughts on DSI.

Here is the reference for the incredible guidelines on ketamine in the ED.

On to Delayed Sequence Intubation (DSI)

The Case

You have a 50 y/o male with bad bilateral pneumonia. BP 108/70, HR 96, RR 28. He is delirious, agitated, and looks sick, sick, sick! Saturation is 70% on a nasal cannula; when you try to place the patient on a non-rebreather (NRB) he just swats your hand away and rips off the mask. It is obvious to everyone in the room that this patient needs intubation, but the question is how are you going to do it?

Your first impulse may be to perform RSI, maybe with some bagging during the paralysis period. This is essentially a gamble. If you have first pass success, you (and your patient) may just luck out, allowing you to get the tube in and start ventilation before critical desaturation and the resultant hemodynamic instability. However, the odds are against you: bagging during RSI predisposes to aspiration, conventional BVM without a PEEP valve is unlikely to raise the saturation in this shunted patient, and if there is any difficulty in first-pass tube placement your patient will be in a very bad place.

A Better Way

Sometimes patients like this one, who desperately require preoxygenation will impede its provision. Hypoxia and hypercapnia can lead to delirium, causing these patients to rip off their NRB or non-invasive ventilation (NIV) masks. This delirium, combined with the low oxygen desaturation on the monitor, often leads to precipitous attempts at intubation without adequate preoxygenation.

Standard RSI consists of the simultaneous administration of a sedative and a paralytic agent and the provision of no ventilations until after endotracheal intubation (1). This sequence can be broken to allow for adequate preoxygenation without risking gastric insufflation or aspiration; we call this method “delayed sequence intubation” (DSI). DSI consists of the administration of specific sedative agents, which do not blunt spontaneous ventilations or airway reflexes; followed by a period of preoxygenation before the administration of a paralytic agent.(2)

Another way to think about DSI is as a procedural sedation, the procedure in this case being effective preoxygenation. After the completion of this procedure, the patient can be paralyzed and intubated. Just like in a procedural sedation, we want our patients to be calm, but still spontaneously breathing and protecting their airway.

The ideal agent for this use is ketamine. This medication will not blunt patient respirations or airway reflexes and provides a dissociative state, allowing the application of preoxygenation. A dose of 1–2 mg/kg by slow intravenous push will produce a calmed patient within ~ 30 seconds. Preoxygenation can then proceed in a safe controlled fashion. This can be accomplished with a NRB, or preferably in a patient exhibiting shunt, by use of a non-invasive mask hooked up to ventilator with a CPAP setting of 5-15 cm H20 (or some of the new masks that don’t require a machine, but more on that soon). After a saturation of > 95% is achieved, the patient is allowed to breathe the high fiO2 oxygen for an additional 2–3 min to achieve adequate denitrogenation. A paralytic is then administered and after the 45–60 second apneic period, the patient can be intubated.

In patients with high blood pressure or tachycardia, the sympathomimetic effects of ketamine may be undesirable. While, these effects can be blunted with small doses of benzodiazepine and perhaps, labetalol (3), a preferable sedation agent is available for these hypertensive or tachycardic patients. Dexmedetomidine is an alpha-2 agonist, which provides sedation with no blunting of respiratory drive or airway reflexes (4-5). A dose of 1 mcg/kg administered over 10 minutes will lead to a sedated patient who will accept preoxygenation after 3-5 minutes in most cases.

Another advantage of DSI is that frequently, after the sedative agent is administered and the patient is placed on non-invasive ventilation, the respiratory parameters improve so dramatically that intubation can be avoided. In these cases, we then allow the sedative to wear off and reassess the patient’s mental status and work of breathing. If we deem that intubation is still necessary at this point, we can proceed with standard RSI by administering a conventional sedation agent (e.g. etomidate or additional ketamine) in combination with a paralytic, as the patient has already been appropriately preoxygenated.

A video demonstrating the above concepts is at: http://emcrit.org/misc/preox/

A version of this article originally appeared in ACEP News.
1. Walls RM, Murphy MF. Manual of emergency airway management, 3rd edn. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.
2. Weingart SD. Preoxygenation, reoxygenation, and delayed sequence intubation in the emergency department. J Emerg Med2010 Apr 7. [Epub ahead of print]
3. Aroni F, Iacovidou N, Dontas I, Pourzitaki C, Xanthos T. Pharmacological aspects and potential new clinical applications of ketamine: reevaluation of an old drug. J Clin Pharmacol 2009;49:957–64.
4. Carollo DS, Nossaman BD, Ramadhyani U. Dexmedetomidine: a review of clinical applications. Curr Opin Anaesthesiol 2008;21:457–61.
5. Abdelmalak B, Makary L, Hoban J, Doyle DJ. Dexmedetomidine as sole sedative for awake intubation in management of the critical airway. J Clin Anesth 2007;19:370–3.
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