This post is inspired by the confusion of intern year.  Since our responsibility in the hospital has increased, the lens through which we interpret information has changed.  For example, the pharmacology of opiates didn’t matter for Step I, Step II, or Step III.  It used to be triaged to the bottom of the what-I-care-about list.  But, now it matters when the well-educated patient comes in with nephrolithiasis, asking about pain medication options.  How long will it last?  When will she start to feel the effects/when will levels peak?  This post will breakdown clinically relevant information about opiates–yes, pain is subjective so the daily utility of this may be of question.  But, I felt it was my responsibility to at least know a little bit about what I prescribe.  The good thing I’ve  learned is that morphine and pain medication dosing hasn’t changed much in the past 20 years, so it’s knowledge I’m ok with memorizing.

Given that patients ideally don’t spend more than 24 hours in the Emergency Department, the first section of this post focuses on the acute effects of pain medication.  The second portion consists of the Morphine Equivalent Daily Dose (MEDD).  It translates the dose and route of the opiates the patient has received in the last 24 hours to an equivalent parenteral form of morphine.  It’s less useful in the ED, but still valuable to be aware of the basics.

Screen Shot 2014-10-10 at 1.42.44 PM

Morphine IV

     Dose – 0.1 mg/kg

     Onset – 5-10 minutes

     Peak – 30 minutes

     Duration – 3-4 hours

Hydromorphone IV (Dilaudid) – about 5-10 times stronger than morphine IV

     Dose – 0.2-1 mg q 2-3 hours

     Onset – 5 minutes

     Peak – 15-30 minutes

     Duration – 3-4 hours

Fentanyl IV – about 100 times stronger than morphine IV

     Dose – 1-2 mcg/kg.  Note: this is for Fentanyl IV; below there is information on the conversion to Fentanyl patches.

     Onset – immediate

     Peak – 3-5 minutes

     Duration – 0.5-1 hour

Morphine Equivalent Daily Dose

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The Morphine Equivalent Daily Dose is a table to find the dose of morphine equivalent to another opioid over 24 hours.

The following example uses oral dosing:

If a patient is receiving 4 mg of Hydromorphone every 4 hours, what is the equivalent amount of morphine?

Notice on the table, the conversion factor for morphine to hydromorphone is 5.  If a patient is receiving 4 mg of oral Hydromorphone every 4 hours, the patient is getting a total of 24 mg in 24 hours.  Using a factor of 5, the oral morphine equivalent for that same time period is 120 mg.


Stanford Anesthesia


Medscape Emergency Medicine


An intimate moment, a case study

Sometimes we get caught up in the details and forget the basics.  This case is relatively straight forward and it involves abdominal pain.  Since abdominal pain accounts for up to 10% of ED visits, it’s crucial to have a broad differential and not forget the basic approach.  So here we go…


(not my actual patient…)

(All identifying information has been removed and details have been changed)

Triage Note:

  • CC: “Patient with suprapubic pain that started last night after sexual intercourse”
  • Vitals: Temp: 98.7 Pulse: 99 Resp: 19 BP: 165/82 SpO2: 100% RA
  • EMS Treatment prior to arrival: 4mg Zofran, 100mcg Fentanyl

History of Present Illness:

32 year-old female presents to the ED via EMS complaining of abdominal pain.  EMS was called to transport the patient from her PCP’s office.  Paramedics report she was doubled over in pain, nauseous and tearful in the exam room upon their arrival.  She received 100mcg of Fentanyl and 4mg of Zofran en route to the hospital with some relief.  Last night around midnight, immediately following intercourse, she had a sudden onset of lower abdominal pain she described as a “dull aching.”  Over the course of the night the pain began to gradually worsen and become more generalized and kept her awake most of the night.  Now the pain is very severe and feels “sharp” with radiation to the back.  Movement causes severe pain that “takes my breath away.”  Pain is worse when she lies flat on her back, and her abdomen feels “bloated.”

Review of Systems:

  • Constitutional: No fevers, chills
  • CV: No Chest Pain
  • Resp: Reports that waves of pain “take her breath away,” no shortness of breath, no cough
  • GI: Nausea, improved with Zofran. No vomiting, diarrhea, constipation or melena
  • GU: No vaginal pain or discharge, no abnormal vaginal bleeding, no urinary symptoms

Medical History:

  • Medical History: G2 P2
  • Surgical History: c-section x2 (low transverse)
  • Medications: IUD
  • Allergies: None

Physical Exam:

  • Vitals: T: 97.8  P:96  BP:103/64  RR: 18
  • Gen: A+Ox3, sitting upright in bed holding abdomen, in obvious pain
  • CV: RRR, no MRG, symmetric pulses in all extremities
  • Resp: Lungs CTAB, no respiratory distress
  • Abd: Protuberent abdomen, soft, not tympanic. Moderate diffuse TTP, no rebound or guarding, no palpable organomegaly or masses.
  • GU/GI: Unable to perform speculum exam as patient could not tolerate positioning due to pain. Bimanual exam with mild uterine tenderness and mild left adenexal tenderness. No blood or discharge noted. Rectal exam normal, heme negative.
  • Back: Normal appearance, no CVA tenderness
  • Ext: Atraumatic, no cyanosis or edema
  • Otherwise unremarkable exam

Lab Data:

  • Urine Preg: Negative
  • UA: Normal
  • CBC: WBC: 13.0  Hb: 11.5  PLT: 304
  • CMP: Normal
  • Lipase: Normal

Moving forward…

We were unable to perform a bedside trans-vaginal ultrasound due to her discomfort (she was unable to lie flat).  Trans-abdominal ultrasound was unremarkable.  We decided to move forward with a CT of the abdomen and pelvis…

Before I give away the diagnosis, let’s take a step back and summarize:

  • 32 y/o female, negative pregnancy test, suprapubic pain immediately following intercourse, now has peritoneal signs, hemodynamically stable

This helpful image from Rosen’s is good for localizing abdominal pain.  Our patient had diffuse pain but could also localize it to the lower quadrants.  Obviously female-specific pathology is important here, but don’t forget about gender-neutral pathology such as appendicitis, diverticulitis, ureteral calculi, pancreatitis, biliary disease, etc.

abd pain

Back to our patient…

History is very important!  This lady initially had suprapubic pain, immediately after intercourse, that became diffuse over a short period of time.  It was worse with movement, and took her breath away.

Exam is very important!  She was doubled over in pain, had a protuberant abdomen, and couldn’t lie flat on the bed.

So we finally got the CT.  You might expect to see something causing peritoneal signs.  And the diagnosis was…

Large, ruptured, functional left ovarian cyst with hemorrhagic ascites.

Ruptured Ovarian Cyst

Ruptured ovarian cysts are very common and symptoms may vary widely.  Rarely, intraperitoneal hemorrhage results.  They usually occur following strenuous activity, and the most common time is mid-cycle.  They can be associated with nausea/vomiting, vaginal bleeding, weakness, shoulder tenderness (due to diaphragmatic tickling), and ultimately (and rarely) circulatory collapse.

The most important thing in the workup is to rule out ectopic pregnancy.  The presentation can be a close mimic to ectopic, so get that UPT cooking as soon as you can.  And get the ultrasound in there!  Unfortunately we couldn’t with our patient, but it may have spared her the radiation of a CT.

One of the main points I took away from this case was conservative management.  The management for ruptured ovarian cysts really involves three components:

  1. rule out ectopic
  2. hemodynamic stability
  3. pain control

If there is no ectopic, they are stable, and their pain is controlled, they can go home.

So in summary, this is a pretty basic case and a common presentation.  As I move forward in my education, it’s tempting to focus on the new, sexy details of EM and skip over the basics.  Hopefully this will help.  Please let us know if you have any other pearls for dealing with ruptured ovarian cysts or female abdominal pain in general.  Thanks.


Rosen’s Emergency Medicine – Concepts and Clinical Practice, 8th edition

Tintinalli’s Emergency Medicine Manual, 7th edition

Emedicine.Medscape.com, Ovarian Cyst Rupture

Intraosseous (IO) infusion

Just a quick rundown on the intraosseous (IO) lines that we’d better get more familiar with as we enter residency.  Especially during traumas or codes, the intraosseous line is invaluable in securing access in a volume depleted pt or small child.  IO lines infiltrate the spongy, cancellous bone that’s inside of the hard, outer compact bone.  Ideal locations are those with large networks of vascular, trabecular meshwork of red bone marrow.  These sites are at the end of long bones (femur, humerus, tibia, and sternum) where the intraosseous vasculature drains quickly into the central venous canal and central circulation.

In addition to the conventional uses of IO lines, I thought it’d be interesting to wrap up this post with a couple articles/case reports that further showcase the utility of IO infusion.  It has potential as a means for invasive systemic blood pressure monitoring and for hastening the delivery of vasoactive drugs especially in the setting of out of hospital cardiac arrest.  These articles will be at the end.

What is it?  When is it indicated?

Per Wikipedia, the IO infusion is the process of injecting directly into the bone marrow to provide a non-collapsible (2/2 the hard cortex keeping things patent) entry point into the systemic vasculature.  What this means for us: IV blown or can’t be attained?  US currently being used for FAST?  Grab the IO kit.  In short, American Heart Association guidelines recommend IO infusion if IV cannot readily be obtained.  Don’t perform IO infusion when there’s overlying infection, high risk of fracture or IVC injury (drugs/fluids will extravasate).

For historical perspective, the IO route was first mentioned in the 1920’s literature when the sternum was suggested as a site for potential blood transfusion.  During WWII, IO infusion was used; however, subsequent popularity of the plastic catheter overshadowed the adoption of IO until the 1970’s.

In general, the IO kit contains a driver and needle tips.  The FDA has approved three devices for adult trauma pts in whom IV access cannot be obtained.  The pictures (largely from the Critical Care Nurse article) are below, but the one I’ve seen most in the hospital are the EZ-IO (for proximal and distal tibia as well as proximal humerus).  The two others are FAST 1 (for sternum) and Bone Injection Gun (proximal tibia and proximal humerus).  There’s a couple pics of the FAST 1 and Bone Injection Gun, but we’ll focus on the EZ-IO.

Finally, in terms of pain, the IO method doesn’t seem to be as horrible as it may first look.  On a scale of 1-10, an observational study found an average of  a 3.9 rating for insertion with a removal score of 2.2.  Doesn’t seem to be too bad, but I don’t think I’ll try it on myself yet…




What are the risks?  

As the benefits are fairly obvious when thinking intuitively about the whole thing, the risks of IO infusion should not be overlooked.

Compartment syndrome – Can occur when IO improperly placed and there’s extravasation of fluid into surrounding tissue space.  Specifically, there is risk of IO needle passing through both sides of bone cortex and infiltrating soft tissue space.  Prevent this by removing improperly placed IO needle when does not flush cleanly.  Can also confirm proper placement by aspirating bone marrow.

Infection/osteomyelitis – An intuitive risk of IO infusion since we’re creating a pathway from outside to inside.  More often due to poor aseptic technique or leaving the IO in for longer than 24 hrs.  The goal is generally to leave the IO in for no longer than 3-4 hrs.

Extravasation – Specific to more dangerous fluids, the extravasation of caustics/hypertonics like sodium bicarb, dopamine or calcium chloride can cause muscle necrosis.

How do you do it?

The proximal tibia is the site I’ve seen most commonly in my few years in the hospital.  Its flat surface, easily identifiable landmarks and distance from the thorax (where resus attempts are happening) make it ideal.  Grab driver; put on needle tip; aim slightly medial and 2 cm distal to tibial tuberosity; push hard (lidocaine prior to this if pt awake).  Passage through cortex and infiltration of the marrow space  will be identified by sudden drop in resistance or pop feeling.

For distal tibia, aim slightly proximal to the medial malleolus.  Drill into flat portion of tibia here.  Make sure to angle 15 degrees cephalad to avoid growth plate.

For proximal humerus, drill 90 degrees directly into the greater tuberosity.

Confirm proper placement via infusion of fluid without extravasation to surrounding area.  Make sure to flush line adequately upon insertion; a decently forceful infusion helps push away the bone spicules in the bony medulla.  If there’s a need for fast fluid administration, pressure bags, 60 cc boluses and IV pumps can be used.



IO as invasive blood pressure monitors

Now, for the recent developments on IO infusion…

A recent article in the American Journal of Emergency Medicine published a case report that supports the ability of intraosseous pressure (IOP) to consistently reflect systemic blood pressure.  Prior to this, animal studies had shown the parallel relationship between intraosseous and intravenous environments.  The correlation between IO and IV readings for blood pressure and arterial waveform (yes, even despite the IO reading being venous and the IV being arterial) have sparked some thoughts on the structural relationship and the future potential for monitoring that IO may possess.  The thought is that since there’s similarities between the structure of intraosseous vasculature and the overlying venous vasculature there may be some therapeutic potential by studying the two.

“Intraosseous arterioles are similar histologically to arterioles located throughout the body, and include an intima, media and an adventitia. This suggests intraosseous arterioles regulate blood flow in a similar manner to arterioles located in other anatomic locations.”

IO infusion vs. IV infusion for vasoactive drugs

Relevant considerations when comparing IO vs. IV access are the different pharmacodynamics of the two methods.  Specific to pressors in cardiac arrest, studies have looked at the differences between IO and IV.  At the heart of the discussion is the unquestionable speed with which IO can be placed.  On the other hand, the utility of expeditious placement is offset by the delay that IO infusion has in achieving peak drug levels along with generally diminished absorption (which also varies amongst IO sites like tibia vs. sternum).  A recent article in Resuscitation brought up additional interesting discussion points specific to IO access in out of hospital cardiac arrests.  “Lastly, it is worth noting that the optimal pharmacodynamic approach to intra-arrest medication administration remains unclear, both experimentally and clinically. Whether achieving high peak levels is preferable over strategies in which a lower drug concentration is sustained over a longer period of time is not known. It is also possible that the delay to peak concentration and lower absorption associated with tibial IO administration of medications can be overcome by higher doses.”  If IO is going to become more readily utilized, there are many more discussions to be had on resuscitation protocol.


Day MW. Intraosseous devices for intravascular access in adult trauma patients. Critical Care Nurse. 2011;31:76-90.

Gluckman W, Forti R, Lamba S. (2012, Jun 13). Intraosseous cannulation. Emedicine. Retrieved 03/07/14 from http://emedicine.medscape.com/article/908610-overview#aw2aab6b6.

Frascone RJ, et al. Use of an intraosseous device for invasive pressure monitoring in the ED. Am J Emerg Med. 2014. http://dx.doi.org/10.1016/j.ajem.2013.12.029.

Davis DP. The use of intraosseous devices in cardiopulmonary resuscitation: is this the answer for which we have been searching? Resuscitation. 2012;83(1):7-8.

Normal saline solution is THE RESUSCITATION FLUID?!

My resident told me that resuscitation fluid is normal saline.  I was told to go write the order for normal saline at 100 cc/hr for my middle-aged severe sepsis pt with acute on chronic renal failure.  We were stopping it only if signs of difficulty breathing or shortness of breath developed.  I couldn’t remember why normal saline might not be the definitive answer for resuscitation, but when I asked about using lactated Ringer’s, I was told that normal saline is the resuscitation fluid of choice.  Dilutional hyperchloremic acidosis didn’t spring to mind; but, something didn’t sit right with me.

So, being the diligent 4th year medical student, I decided to educate myself by breaking down major papers on resuscitation fluid choices.  Much of my reading eventually honed in on the difference between normal saline and  “balanced” crystalloid solutions (e.g. Ringer’s lactate or Plasma-Lyte).  The science behind strong ion differences and the chemistry of fluids are complex and beyond the scope of this post.  But, my hope is to distill major studies on crystalloids–specifically, normal saline (“unbalanced” solutions) vs. “balanced” solutions.  This simplified approach detailed below should give us an idea of the themes that influence our fluid choices.  Furthermore, I have a feeling much of this relates to the glycocalyx and microenvironment/context/whatever you want to call it in which we administer resus fluids.  The study populations below are heterogeneous (i.e. some are healthy pts, some are septic pts), so no frank conclusions can be drawn.  I just thought it interesting that there’s so much normal saline-bashing happening recently.

A theme that seemed to be pervasive in my literature search: isotonic saline is nonphysiologic with a higher [Cl-] load compared to plasma; this may contribute to hyperchloremic metabolic acidosis, renal vasoconstriction, and a decrease in GFR.

(Full citations are at bottom of post)

Yunos et al. JAMA. 2012

Showed that period of higher Cl- use (i.e. like normal saline) was associated with greater adverse renal outcomes

–> Prospective, open-label study of 1533 pts admitted to the ICU

–> Compared control period (6 months of using chloride-rich fluids) vs. intervention period (6 months of using “balanced/physiologic” low chloride fluids)

* Keep in mind, normal saline has 154 mmol/L [Cl-] while lactated Ringer’s has 109 mmol/L [Cl-]

–> Primary outcomes of increased creatinine, increased incidence of AKI

–> Chloride restrictive strategy (the intervention period) was associated with lower creatinine, decreased incidence of AKI when compared to chloride-rich strategy, and a significant decrease in dialysis

Chowdhury et al. Ann Surg. 2012

Found greater adverse renal effects in healthy pts given normal saline rather than balanced solutions

–> Randomized, double-blind, cross-over study of 12 healthy adult males

–> Compared effects of normal saline infusion with effects of Plasma-Lyte (a “balanced solution”) infusion

–> Found the following adverse effects after normal saline: greater expansion of extracellular fluid volume, greater reduction in mean renal artery flow velocity, and greater reduction in renal cortical tissue perfusion

Shaw et al. Ann Surg 2012

Observed greater morbidity associated with normal saline in a population of abdominal surgery pts

–> Retrospective analysis of adult pts undergoing major abdominal surgery

–> 30,994 pts received only normal saline while 926 pt received only balanced fluid

–> Used a bunch of fancy models to find associations between fluid type given and endpoint of major morbidity defined as composite of one or more major complications

–> No significant difference between the two groups with rates of acute kidney injury (AKI), but normal saline group had increased dialysis (4.8% vs. 1%)

–> Mortality higher in the normal saline group (5.6% vs. 2.9%)

–> The authors conclude that the association between normal saline use and major morbidity appears to be stronger than chance; however, no explanation is clearly found

Karakala et al. Curr Opin Crit Care 2013

Briefly summarizes the aforementioned studies and points out many more interesting assocations with normal saline

–> An interesting, current review of different IV fluids in sepsis

–> Points out that normal saline/”physiological” fluid actually has 1.5x the [Cl-] as the human body

–> Cites Wilcox et al. experiment in dogs where rise in plasma [Cl-] demonstrated renal afferent vasoconstriction; infusion of chloride-containing solutions were associated with reduced renal blood flow

So, there you have it.  There’s no paucity of studies willing to look at the danger of normal saline.  Of particular interest to me was in the Karakala review.  They cited the difficulty in differentiating lactic acidosis (often in sepsis) from hyperchloremic metabolic acidosis (often 2/2 iatrogenic fluid loading).  It mentions that with the challenging  differentiation of the two pathphysiologies, we often volume load without knowing the etiology.  My question from looking at these studies has to do with the dogma of normal saline.  Its ubiquitous presence in the hospital makes it difficult to tease out the influences or systematic error in studies.  From a cursory glance, it seems that without a large RCT, the many studies may be hindered by our gut reaction to administer normal saline quickly and without pause.  As such, we don’t know if the RRT requirements are 2/2 the saline itself or preexisting tissue hypoperfusion states.

Chowdhury AH et al. A randomized, controlled, double-blind crossover study on the effects of 2-L infusions of 0.9% saline and Plasma-Lyte 148 on renal blood flow velocity and renal cortical tissue perfusion in healthy volunteers. Ann Surg. 2012;256(1):18-24.

Yunos et al. Association between a chloride-liberal vs chloride-restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. JAMA. 2012;308(15):1566-1572

Shaw et al. Major complications, mortality, and resource utilization after open abdominal surgery. Ann Surg 2012;255(5):821-829.

Karakala et al. Intravenous fluids in sepsis: what to use and what to avoid. Curr Opin Crit Care 2013;19(6):537-543.


This is a brief synopsis of the literature surrounding the glycocalyx and its role in resuscitation.  After some recent coverage of Marik’s opposition to the tenets of Early Goal Directed Therapy, I thought it would be useful to delve into some work covering the glycocalyx.  It is an interesting thing to think about in terms of the Starling principle which was engrained into us during our undergraduate and medical school careers.  The Starling model described transvascular exchange in terms of hydrostatic and oncotic pressure gradients.  At the arteriolar end of a capillary, the dominant hydrostatic pressure caused net fluid movement to filter into the interstitium.  Conversely, the venular end experienced a dominant colloid osmotic pressure causing net fluid movement back into the capillary.  (Note: colloid osmotic pressure is the same thing as oncotic pressure)

What is the endothelial glycocalyx layer (EGL)?

The endothelial glycocalyx layer (EGL) lines the lumen of vessels and consists of glycosaminoglycans and proteoglycans.  It interacts with the lumen contents and plays a role in the physiology of volume status regulation.  It can be thought of as a layer lining the lumen of the vessel, contributing to oncotic pressure and reacting to the environment around it.  The presence of specific glycoasminoglycans (heparan sulphate, chondroitin sulphate, and hyaluronic acid) and proteoglycans in the plasma can be taken as signs of damage to the EGL.  For example, rapid crystalloid infusion in volunteers resulted in elevated plasma levels of hyaluronic acid and may be indications of injury to the patient.

Screen Shot 2013-12-10 at 11.23.54 AM

Why is it relevant to resuscitation in the ED and ICU?

– Human studies have shown that the EGL is compromised in systemic inflammatory states like diabetes, trauma and sepsis.

– The EGL makes up a large volume of the intravascular space, excluding large molecules and affecting dilution studies of blood volume.  Therefore, protection of the EGL is an important therapeutic goal.  Patients in septic shock, for example, have been found to have increased plasma concentrations of GAGs, indicating damage to the EGL.

– Using traditional Starling principles, the filtration rate across the capillary is a product of opposing hydrostatic and opposing oncotic pressures.  However, the traditional Starling forces (hydrostatic pressure and colloid osmotic pressure of both capillary and interstitium) have recently been reevaluated and include the colloid osmotic pressure from the subglycocalyx layer.

– Taking into account the subglycocalyx colloid osmotic pressure, the physiology of fluid movement between intravascular and extravascular spaces isn’t as straightforward as an evaluation of the hydrostatic pressures (capillary and interstitial) and the colloid osmotic pressures (again, capillary and interstitial).

– The glycocalyx responds to shear stress, evidenced by its thicker presence in shear stress areas.

How will it affect our practice?

Recent debate amongst ED intensivists has focused on the role of the glycocalyx in our choice for resuscitation fluids.  While large trials such as SAFE have attempted to elucidate the ideal resuscitation fluid, there has been no definitive outcome.  The purpose of this short entry is to give us a chance to think about the complexities of the fluid movement in the setting of the glycocalyx.

In the recent past, crystalloids have been the fluid of choice for expanding intravascular volume in septic patients.  However, given the Starling forces at play in volume-depleted, hypoalbuminemic patients, the intuitive assumption is that colloids would be more useful.  You would think more protein in the blood increases the colloid osmotic pressure pulling fluid in from the interstitium.  The reality is unfortunately not so straightforward.  The glycocalyx is another variable added to the equation of fluid physiology.  It has a protein concentration gradient between that seen in the free-flowing plasma and the endothelial intercellular clefts.

The bottom line is that the investigation of the glycocalyx has been performed in hopes of uncovering the physiologic reasoning behind fluid movement between the vascular and interstitial systems.  The SAFE trial of 2004 looked at the difference of colloids and crystalloids but found no significant hemodynamic resuscitation differences between albumin and saline groups.  There’s been a surge of recent comments in the #FOAMed world regarding fluids and the glycocalyx, so keep a look out for other more detailed analyses and how it pertains to the ideal resuscitation fluid.

Here’s another great #FOAMed resource on the topic: http://thinkingcriticalcare.com/2013/12/10/the-glycocalyx-an-overview-for-the-clinician-foamed-foamcc/


Woodcock TE, Woodcock TM. Revised Starling equation and the glycocalyx model of transvascular fluid exchange: an improved paradigm for prescribing intravenous fluid therapy. Br J Anaesth 2012;108:384-94.

Myburgh JA, Mythen MG. Resuscitation fluids. N Engl J Med 2013;26;369(13):1243-51.

Bicarbonate for lactic acidosis?

After reading some recent posts on emcrit.org and doing some research on quantitative acid-base analysis, I decided to write a simple post on a related subject: the controversy of administering sodium bicarbonate (or simply, “bicarb”) in the setting of lactic acidosis.  With severe sepsis commonly causing lactic acidosis, it’s worth exploring.  At first cursory glance, how could this not work?  Bicarb is a base and the problem with lactic acidosis is acid.  So, one would assume adding a base to an acid would neutralize things.  However, adding NaHCO3 to a patient with lactic acidosis is not a good idea.

We are going to distill some review articles on the subject so us juniors can remember the basics and maybe learn a thing or two about current truth.

To simplify this presentation of complex ideas, I’ve organized this into two parts: the good and the bad.  The good part will detail the intuitive and “advantageous” aspects of using NaHCO3 in lactic acidosis.  The bad part will go into why it’s not so great or intuitive.


I.  NaHCO3 will make solution more basic/raise the pH.


II.  Despite raising arterial pH, NaHCO3 does not raise the intracellular pH nor the CSF pH.

III.  NaHCO3 did not improve hemodynamics or catecholamine responsiveness.

IV.  NaHCO3 may increase lactate.

Continue on for the more detailed explanations.

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