“Humans Are Not Yeast”: (almost) everything we believe about lactate is a myth. 

5 Ott 4e193a6c-13de-44f2-aabe-2b095321f652_1-8a517f942153f96606ebbde8331f1dc8

4e193a6c-13de-44f2-aabe-2b095321f652_1-8a517f942153f96606ebbde8331f1dc8On September issue of Emergency Medicine News, Paul Marik wrote an article entitled “Humans are not yeast”

This is a game changer article about the current concepts on lactic acid and its clinical meaning in emergency medicine.

The author illustrate simple but well established concepts about lactic acid metabolism that revert most of the common conceptions about its significance in clincal medicine.  

I will resume below some of the most relevant concepts expressed in the article. The italic bullet point text is from the original article.

I really encourage all of you to read the full text of original article to completely understand the whole rationale behind those statements and to access the complete list of references.

It is free open access.

Let’s start with some biochemistry.  

Piruvate, the product of glycolysis, can enter in Krebs cicle to produce energy through aerobic (oxygen driven) process or can take a shorter and faster (x100 times) way to produce energy when is transformed to lactate (the basis of lactic acid) using NADH (so reduced to NAD+ and ready to take another H+) and H+.

  • No hydrogen ions are present in glycolysis. In fact, the conversion of pyruvate to lactate consumes hydrogen ions. It is actually a lactic alkalosis. (J Mol Cell Cardiol 1997;9[11]:867.)
  • Increased lactate may simply occur because of increased production of pyruvate due to in- creased glycolysis there is no oxygen debt. We spoke about the muscles exporting lactate; the same thing happens in shock: lactate is used as a fuel for oxidative metabolism. Lactate is transported into the mitochondrion through specific transport proteins, and then is converted to pyruvate in the mitochondrial intermembrane space. Pyruvate then moves into the mitochondrial matrix and undergoes oxidative metabolism.
    Lactate is, therefore, a fuel for oxidative metabolism. It’s consumed by the brain and heart, and that is absolutely vital to survival when someone is in shock
So why is lactate produced and used for?
Lactate is aerobically producted by muscle and is a more efficient source of energy for the brain and the heart.
  • Lactate is a much more efficient bioenergetic fuel than glucose so as someone exercises, the muscles make lactate to fuel the heart. The heart works much more efficiently with lactate. What happens to the brain? The exact same thing. As someone exercises, brain lactate goes up, and the brain starts using lactate preferentially as a source of fuel. This is a brilliant design: Muscles make lactate aerobically as a source of energy for the brain and heart.
Lactic metabolic acidosis is a biochemical myth! It’s more a lactic alkalosis.
  • The lactic acidosis explanation of metabolic acidosis is not supported by fundamental biochemistry, and has no research basis. Acidosis is caused by reactions other than lactate production.  
  • No hydrogen ions are present in glycolysis. In fact, the conversion of pyruvate to lactate consumes hydrogen ions. It is actually a lactic alkalosis. (J Mol Cell Cardiol 1997;9[11]:867.)
Hypoxia does not induce lactate serum level elevation, and in sepsis oxygen cellular level is not decreased. 
  • There is this pervasive idea that people with sepsis have cellular hypoxia and bioenergetic failure, but this concept was debunked in 1992. Compared with limited infection, the muscle O2 goes up in patients with severe sepsis.
  • Increased lactate may simply occur because of increased production of pyruvate due to increased glycolysis there is no oxygen debt. We spoke about the muscles exporting lactate; the same thing happens in shock: lactate is used as a fuel for oxidative metabolism. Lactate is, therefore, a fuel for oxidative metabolism. It’s consumed by the brain and heart, and that is absolutely vital to survival when someone is in shock. The body makes lactate, which is then used as a metabolic fuel.
Iperlactic state is generated, by epinephrine and not by hypoxia, in case of extreme physiological stress as protective mechanism.
  • The clinical plausibility was that lactate increases during adrenergic states and in the absence of an oxygen debt. Lactate increases with epinephrine infusion; lactate increases with hyperdynamic sepsis. All of the states have a high cardiac output, high oxygen delivery, and not a single trace of hypoxia. It’s driven by epinephrine, not by hypoxia.
  • We do know that lactate is associated with increased mortality because the sicker a patient is, the higher his epinephrine levels. It’s a protective mechanism. The association is related to the fact that lactate is a biomarker of physiological stress. And clearly the greater the physiological stress, the greater the risk of death. But lactate itself is a survival advantage, and it’s not an evolutionary accident that we make lactate.


Thanks to the author and to Aidan Baron who originally shared the article.


  1. The Science of Emergency Medicine: Humans Are Not Yeast. Emergency Medicine News: September 2016 – Volume 38 – Issue 9 – pp 1,29–30 doi:10.1097/01.EEM.0000499522.28133.48



How Ultrasound (really) improved my clinical practice

24 Ago echo for dum like me

Beyond theories and protocols, here we are three (real) clinical prehospital scenarios  in which without ultrasound my own practice would have been different with (probably!!!) some (bad!!) consequence on patients final outcome.

Case #1



pic 2

Apparently 45 yrs old female found unconscious in a secondary street by people accidentally passing by. No witness of the event. No other information on the patient.

When the first medical team arrived, the patient was unconscious with some non coordinated vocal response (if stimulated) and no finalized movements of the extremities; she was spontaneously breathing with an apparent good respiratory drive a RR of 24 and O2 sat of 98% on room air.  Good breath sounds were (apparently) bilaterally transmitted (not easy to appreciate when you perform auscultation of the chest on the roadside).

She had a good palpable radial pulse (bilaterally), the HR was 72 and her BP 110 over 70. To a quick external exam multiple minor signs of trauma where present on her face, forehead and left anterior chest wall. No sign of major external bleeding was present.

When we arrived the above clinical scenario was confirmed. The cops, on the scene, were investigating about what happened, but at the moment no other new information was available.

As first thing I was concerned, cause of the low level of consciousness, about patient’s competence to maintain airway patency , so I decided to protect the airways with tracheal intubation. 

But first to proceed to RSI, during the preox period and despite the apparent hemodynamic stability I decided to perform an extended FAST ultrasound exam; it takes 2 min, is safe and free.  The EFAST revealed a pneumothorax on the left, no abdominal bleeding, no pericardial fluid effusion. At this point we decide to open the chest (finger bougie tecnique, Ketamin pre-medication) before intubating the patient in prevision  of the mechanical positive pressure ventilation, and air transport.

The patient arrived well compensated (from both respiratory and hemodynamic point of view) at the trauma  center where was discharged 3 weeks later without major clinical consequences.

But what without ultrasound???

We don’t have a clinical guidance (and practice) to open the chest simply ‘cause of the presence of external sign of chest trauma when the patient is in a well compensated respiratory status and had a good hemodynamic balance.

In this case the chance to find clear US signs of penumothorax, prevented a possible worsening of respiratory and hemodynamic status  after intubation.  Intubation itself, PPV and high altiutde transport, are all factors that can precipitate a prior stable pneumothorax.

Case #2

pic 1

28 yrs male victim in a car accident extricated after several minutes by the firefighters. At the arrival of the fire crew he was still breathing but when the first medical crew arrived found him in CA. Advanced life support started and was ongoing when we arrived.

The patient was intubated on the field, two thoracic tubes were bilaterally placed (emo-thorax on the right side no pneumo bilaterally)  and a bolus of 2 liters of fluids administered via two large bore venous accesses.

He had an organized cardiac electric activity and an EtCO2 value of 35 mmHg (without chest compressions in place). The US of the heart shown some weak wall motion (coordinated with electric activity), so we decided to rapidly transport the patient to the nearest trauma center where he was reanimated for more than 1 hour and then called  without any evidence of possible cause of death.

In this case the presence of wall motion at the US exam (well supported from EtCO2 values and and by an organized cardiac electric activity) strongly influenced the decision to transport the patient in TCA to the hospital for definitive care.

Ultrasound can be a further hint in the decision to carry on the resuscitative efforts in patients in CA with PEA and no evidence of reversible causes on the field. It can be also the decisive tool in deciding  to transport those patients to the hospital for second level diagnostic assessment and advanced care.

Case #3

pic 3

24 yrs old pedestrian male hit by a motorbike while crossing the road. He was found unconscious by first responders. When we arrived the patient was lying down on the spinal board wearing a cervical collar with eyes closed but responsive when called and able to execute simple commands with no apparent deficit of the limbs. He suffered a severe facial trauma  with  avulsion of several frontal teeth and a profound total tickness wound to the superior lip with presence of a lot of blood in the mouth and  the first part of the airways; his breathing was laborious and noisy. Anyway  the patient was able to maintain an ox sat of 93% on room air (that easily improved to 98% with 2 liters of oxygen administered via simple O2 mask). 

The radial pulse was present at a rate of 90/min and the BP was 100 over 70. The rest of external exam highlighted a profound wound at the internal part of the calf with exposition of muscular plan and some hemorrhage well controlled with external manual compression.

We provided (with not much success due to the unstoppable bleeding) to clear the airways from blood and secretions, but still the respiration was difficult and noisy even if the ox sat was on a satisfying 98% on O2 non rebreather mask . In the meanwhile two large bore venous accesses were placed and some fluids keep going.

The EFAST exam revealed no signs of pneumo but presence of blood in the right and left upper quadrant of the abdomen.

We decided to do not insist further on airways control because at this point the control of abdominal bleeding became the first priority. After a rapid transport in ED the total body CT (he was still hemodynamically compensated)  confirmed the presence of internal bleeding and the patient proceeded straight to OR.

Often the suspect of internal bleeding is not clear just by considering clinical signs, especially when we have to deal with young patients who have a large compensation range. POCUS can give us the chance to see the presence of blood in the abdomen and to prioritize our clinical pathway pondering these findings.

Take home points


Performing a chest US before intubating a even stable chest trauma patient, prevents possible  (pre, intra and post) intubation hemodynamic disasters.


Prehospital arrested trauma patients with an organized electric activity and good EtCO2  might have some cardiac activity even in absence of palpable carotid or femoral pulse. They deserve a strong effort on addressing reversible causes and a rapid transport to a  trauma center for advanced in hospital care.


The presence of internal bleeding (revealed by US) can revolve clinical priorities enabling a fast track toward the OR. This virtuous path can start from the prehospital environment.

Getting to the Start Line

18 Ago

The Collective

We can debate the value of this advanced team model vs that advanced team model. We can debate videolaryngoscopy vs direct laryngoscopy for days. People do. Its all chump change compared to the real challenge. Getting that team where they need to be. Dr Alan Garner and Dr Andrew Weatherall have a bit reviewing a paper they’ve just had published trying to add to this discussion. 

You may just have noticed that there are things happening in Brazil. They are called Olympics and they are a curious mix of inspiring feats of athleticism and cynical marketing exercise inflicted upon cities that can probably barely afford them and which will be scarred for a generation afterwards. I’d hashtag that but it turns out the IOC will take you on if you mess with their precious sponsor money.

Now, you might think the obvious segue from a mention of the Olympics at the…

View original post 3.112 altre parole

“Best Practice” preospedaliera: Arresto cardiaco da trauma

4 Ago img_2166

Tra tutte le “Best Practices”, quella che rappresenta più di tutte un cambio radicale di mentalità nell’approccio clinico e terapeutico, è la gestione dell’arresto cardiaco da causa traumatica. Vi prego quindi di leggere attentamente le raccomandzioni raccolte nel documento sottostante e di non esitare a esprimere le vostre riflessioni nei commenti.

Arresto cardiaco adulto traumatico

Chi è interessato ad approfondire il razionale che sta alla base  delle raccomandazioni può scaricare e leggere il documento completo: Arresto cardiaco nell’adulto da causa traumatica full













“Best Practice” preospedaliera: Arresto cardiaco nel neonato

29 Lug IMG_1655

Continua la pubblicazione di una serie di monografie dedicate alle Best Practices per l’emergenza preospedaliera.

La quarta della serie riguarda l’arresto cardiaco nel neonato.

Potete scaricare il documento cliccando sull’icona sottostante.

Arresto cardiaco neonato






“Best Practice” preospedaliera: Arresto cardiaco in età pediatrica

16 Lug Arresto cardiaco pediatrico

Continua la pubblicazione di una serie di monografie dedicate alle Best Practices per l’emergenza preospedaliera.

La terza della serie riguarda l’arresto cardiaco in età pediatrica.

Potete scaricare il documento cliccando sull’icona sottostante.Arresto cardiaco pediatrico







“Best Practice” preospedaliera: Arresto cardiaco in gravidanza

1 Lug Arresto cardiaco gravidanza_Page_1

Continua la pubblicazione di una serie di monografie dedicate alle Best Practices per l’emergenza preospedaliera.

La seconda della serie riguarda l’arresto cardiaco in gravidanza.

Potete scaricare il documento cliccando sull’icona sottostante.

Arresto cardiaco gravidanza_Page_1






“Best Practice” preospedaliera

25 Giu Arresto cardiaco adulto non traumatico_Page_1

Da oggi inizia la pubblicazione di una serie di monografie dedicate alle Best Practices per l’emergenza preospedaliera.

La prima riguarda l’arresto cardiaco nel paziente adulto da causa non traumatica.

Potete scaricare il documento cliccando sull’icona sottostante.

Arresto cardiaco adulto non traumatico_Page_1





Emorragia post-traumatica

2 Giu DCR copy

References link:


Drug-to-drug interaction. New evidences on Morphine and delayed onset of action of antiplatelet agents.

8 Mag Logo MEDEST2

A recently published article entitled  “Chest pain relief in patients with acute myocardial infarction” (European Heart Journal: Acute Cardiovascular Care April 22, 2015) address in a very well documentrd way the topic about drug-to-drug interactiono between morfine and antiplatelets agents in STEMI patients.

Guido Parodi, a lead interventional cardiologist in Cardiovascular and Thoracic Department of Careggi Hospital in Florence, (Italy) author of the article, highlights the fact that “despite the complete absence of rigorous studies designed to assess the impact of morphine administration in patients with AMI, clinical practice guidelines for the management of patients with STEMI strongly recommend the use of morphine for analgesia.”

As indicated in the article recent literature indicates an increased risk of mortality in STEMI patients treated with Morphine.

The analysis of CRUSADE registry in 2005 has shown how patients treated with morphine had a higher adjusted risk of death than patients not treated with morphine even after using a propensity score matching method. This is a non randomized trial and so influenced from potential bias, and the hypothesis that morphine was administered to higher-risk patients is also to be considered. But an additional potential explanation of morphine’s negative impact on AMI outcome may be related to drug-to-drug interactions.

Biologically a cause effect relation can be explained, because morphine inhibits gastric emptying, delaying absorption and so decreasing peak plasma levels of orally administered drugs in general and antiplatelet agents in this particular case.
This was very well demonstrated in a 2015 study from the same author “Morphine is associated with a delayed activity of oral antiplatelet agents in patients with ST elevation acute myocardial infarction undergoing primary PCI” (Parodi G, Bellandi B, Xanthopoulou I, et al. Circ Cardiovasc Interv Epub ahead of print January 2015) in whom the negative impact of morphine on platelet inhibition was not only limited to patients who vomited (patients with vomiting were excluded), but morphine-treated patients clearly showed higher residual platelet reactivity compared with patients who did not receive morphine.

In ATLANTIC Trial (Montalescot G, van ‘t Hof AW, Lapostolle F, et al.; ATLANTIC Investigators. Prehospital ticagrelor in ST-elevation myocardial infarction. New Engl J Med 2014; 371: 1016–1027), STEMI patients who did not receive morphine had a significant improvement in the ECG-based primary end point (ST-segment resolution), reflecting better myocardial reperfusion,with a significant “p” value for interaction between morphine use and time of ticagrelor administration. Professor Montalescot one of the lead authors of this Trial noted:“Co-administration of morphine in the ambulance may have delayed ticagrelor’s onset of action. To what extent this interaction may have affected our results remains unknown at this stage.”

So what to do with analgesia strategy in STEMI patients?

Given the key importance of platelet inhibition in patients treated by PPCI for STEMI and the absence of data that may support a potential clinical benefit of morphine in patients with acute myocardial infarction, more caution should be used regarding morphine administration in STEMI patients, and a restricted morphine use seems to be reasonably recommended.

Morphine administration has to be reserved, as suggested in the article, just for level of pain ≥ 7 on the base of a numerical rating scale (NRS) related value.

Courtesely from Dott. Guido Parodi

Courtesely from Dott. Guido Parodi

For lower chest pain intensity (NRS ≤ 7) alternative strategies has to be persecuted.
The author indicates paracetamol (1 g) or aspirin (≥300 mg) as alternative of choice to reduce chest pain as well demonstrated in letterature.
It has also to be considered how first line agents, currently indicated from STEMI guidelines, as Beta- blocker and Nitrates are able to reduce AMI-related chest pain until the definitive pain relief effect obtained with myocardial mechanical reperfusion.

Bottom Line

The first impact to reduce chest pain has to be reserved to Nitrates or B-blockers (where all contraindications are excluded).

After this NRS has to be evaluated and the use of Morphine is indicated only for values above 7. For lower values Paracetamol or Aspirin are the agents of choice.



  • Parodi G. Chest pain relief in patients with acute myocardial infarction. Eur Heart J Acute Cardiovasc Care. 2015 Apr 22. pii: 2048872615584078. [Epub ahead of print] Review.PMID:25904757

  • Meine TJ, Roe MT, Chen AY, et al. Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the CRUSADE Quality Improvement Initiative. Am Heart J 2005; 149: 1043–1049.

  • Parodi G,Valenti R, Bellandi B, et al. Comparison of prasugrel and ticagrelor loading doses in ST-segment elevation
    myocardial infarction patients: RAPID (Rapid Activity of Platelet Inhibitor Drugs) primary PCI study. J Am Coll Cardiol 2013; 61: 1601–1606
  • Parodi G, Bellandi B, Valenti R, et al. Comparison of double (360 mg) ticagrelor loading dose with standard (60 mg) prasugrel loading dose in STEMI patients: The Rapid Activity of Platelet Inhibitor Drugs (RAPID) primary PCI 2 study.
    Am Heart J 2014; 167: 909–914.
  • Nimmo WS, Heading RC, Wilson J, et al. Inhibition of gastric emptying and drug absorption by narcotic analgesics. Br J Clin Pharmacol 1975; 2: 509–513.
  • Parodi G, Xanthopoulou I, Bellandi B, et al. Ticagrelor crushed tablets administration in STEMI patients: The MOJITO study. J Am Coll Cardiol 2015; 65: 511–512.
  • Montalescot G, van ‘t Hof AW, Lapostolle F, et al.; ATLANTIC Investigators. Prehospital ticagrelor in ST-elevation myocardial infarction. New Engl J Med 2014; 371: 1016–1027
  • Duggan ST and Scott LJ. Intravenous paracetamol (acetaminophen). Drugs 2009; 69: 101–113.
  • Zijlstra F, Ernst N, de Boer MJ, et al. Influence of prehospital administration of aspirin and heparin on initial patency of
    the infarct-related artery in patients with acute ST elevation myocardial infarction. J Am Coll Cardiol 2002; 39: 1733–1737
  • Yusuf S, Sleigh P, Rossi P, et al. Reduction in infarct size and chest pain by early intravenous beta blockade in suspected
    acute myocardial infarction. Circulation 1983; 67: 132–141.
  • Kim YI and Williams JF Jr. Large dose sublingual nitroglycerin in acute myocardial infarction: Relief of chest pain and reduction of Q wave evolution. Am J Cardiol 1982; 49: 842–848.

Education and entertainment for the ultrasound enthusiast




Emergency medicine resuscitation - When minutes matter...

Songs or Stories

Sharing the Science and Art of Paediatric Anaesthesia


"Live as if you will die tomorrow; Learn as if you will live forever"


Navigating resuscitation


Taking the hocus out of pocus and bringing hospital care to the streets.

LITFL: Life in the Fast Lane Medical Blog

Emergency medicine and critical care medical education blog


Emergency Medicine Education

The Collective

A Hive Mind for Prehospital and Retrieval Med

Dave on Airways

Thoughts and opinions on airways and resuscitation science


A Free Open Access Medical Education Emergency Medicine Core Content Mash Up

Broome Docs

Rural Generalist Doctors Education


Emergency Medicine #FOAMed


Bringing the Boring to EM

"CardioOnline"Basic and Advanced Cardiovascular medicine" Cariology" concepts and Review -Dr.Nabil Paktin,MD.FACC.دکتـور نبــــیل "پاکطــــین

این سایت را به آن دکتوران و محصلین طب که شب و روز برای رفاه نوع انسان فداکاری می کنند ، جوانی و لذایذ زندگی را بدون چشمداشت به امتیاز و نفرین و آفرین قربان خدمت به بشر می کنند و بار سنگین خدمت و اصلاح را بدوش می کشند ، اهداء می کنم This site is dedicated to all Doctors and students that aver the great responsibility of People’s well-being upon their shoulders and carry on their onerous task with utmost dedication and Devotionاولین سایت و ژورنال انتــرنتی علـــمی ،تخـصصی ، پــژوهشــی و آمــوزشــی طبـــی در افغــانســـتان


Free Open Access Medical Education

Little Medic

Learning everything I can from everywhere I can. This is my little blog to keep track of new things medical, paramedical and pre-hospital from a student's perspective.

Prehospital Emergency Medicine Blog

All you want to know about prehospital emergency medicine

Italy Customized Travel Blog

Local Travel Agent, sommelier, food & wine expert in Florence, Italy


The FOAM Search Engine

EM Lyceum

where everything is up for debate . . .

Pediatric EM Morsels

Pediatric Emergency Medicine Education

EM Pills

curiosità-novità-aggiornamenti in medicina d'urgenza


Free Open Access Medical Education for Paramedics


Free Open Access Meducation 4 General Practice

Rural Doctors Net

useful resources for rural clinicians

Auckland HEMS

Unofficial site for prehospital care providers of the Auckland HEMS service




Prehospital Emergency Medicine


Just another WordPress.com site

EM Basic

Your Boot Camp Guide to Emergency Medicine

KI Doc


Emergency Live

Prehospital Emergency Medicine


Academic Medicine Pearls in Emergency Medicine from THE Ohio State University Residency Program

ERCAST Emergency Medicine Podcasts

Emergency medicine, podcasts, reviews, opinion and curbside consults

Prehospital Emergency Medicine

 Academic Life in Emergency Medicine

Prehospital Emergency Medicine

Prehospital Emergency Medicine

Greater Sydney Area HEMS

The Pre-hospital & Retrieval Medicine Team of NSW Ambulance

%d blogger cliccano Mi Piace per questo: