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JUL
10

Bloody Evidence

 

Untitled

The use utilization of packed red blood cell (PRBC) infusions has become a staple in many retrieval services all over the world.

"If a patient is losing blood, we should replace it.”

"I do not want to dilute their clotting factors with isotonic or balance crystalloid's.”

These are the statements that are sung from day one of any trauma-related course. Yet, when one tries to dive into what evidence actually supports the concept of giving pre-hospital blood PRBC transfusions, your eyes open up in the realization of the lack of literature support. 

Let's take a look at what we know for sure.

  1. PRBC's offer zero clotting factors.
  1. PRBC's at the time of use must be kept at a temp from 1-9 degrees Celsius.

Knowing these facts, we can without hesitation draw the conclusion that if we are going to transfuse PRBC's it is with the goal to increase the amount of hemoglobin, and if we initiate this transfusion, the blood must be warmed prior to entering the body. If you are hanging cold blood on trauma patients, you are doing an exponential more amount of harm than good.

Increasing the hemoglobin is our primary reason for administering PRBC's in a trauma patient… right?

The D02(amount of oxygen delivered) equation is D0= Q X [(1.34 X Hgb X SaO2) + PaO2 x 0.003]. When one begins to utilize this equation, you will find that the most efficient way of increasing oxygen delivery is by increasing the hemoglobin concentration. However, the amount of hemoglobin available will not matter if cardiac output is compromised. 

So, does this mean that our exsanguinating patient will benefit from a PRBC infusion?

The initial recommendation of transfusing PRBC's came from a paper by Adam and Lundy in 1941. The paper made the statement "when the concentration of hemoglobin is less than 8-10g/dL of whole blood, it is wise to give a blood transfusion before the operation. This 10/30 trigger was universally accepted without any evidence or clinical trials to support it. To this day there have not been any studies to support a transfusion trigger of 10g/dL. Our threshold more commonly acceptable for transfusion now is 7g/dL. This recommendation comes from the American Blood Bank Association (ABBA) in 2012.

There is very little evidence to support increased oxygen utilization when a transfusion is administered to an individual with a hemoglobin higher than 4 g/dL. The reason is that our oxyhemoglobin disassociation curve shifts to the right during shock. This shift increases oxygen extraction above the normal 25%.  The citrate in PRBC’s actually starts to shift this curve to the left due to the bound 2,3-DPG.  As we all know a left shift means oxygen is bound to hemoglobin very strongly and has a hard time disassociating.  The 2,3 DPG will remain bound until the eight-hour mark after transfusion. At this point, approximately 50% of the 2,3-DPG is now unbound and available for facilitating oxygen offloading from the Hgb molecule.  All the 2,3-DPG will not be available until 24 hours after transfusion. This puts the patient at high-risk for poor tissue oxygen until all bound 2,3-DPG is available and fully unbound from citrate.  Citrate toxicity is usually caused by multiple units of PRBC’s.

How Does Our Body React to Anemia?

A reduction in oxygen carrying capacity of blood is met by two intrinsic compensations.

  1. Increase in cardiac output (Q)
  2. Increase in oxygen extraction from the capillaries. 

Our oxygen consumption is calculated by multiplying the D0by the 0extractions (CvO2). In a normal healthy individual the hemoglobin will leave the left ventricle 100% saturated in oxygen and return to the right atrium 75% saturated with oxygen. This explains the physiological oxygen extraction (O2ER) of 25%. 

As hematocrit drops the blood will become thinner and cardiac output will increase until the hematocrit drops below 10%. This is the point in which the increase in oxygen extraction is no longer able to compensate for a decrease in oxygen delivery. The tissue oxygen consumption will begin to fall, and lactate will begin to rise. This is the point where we reach > 40% O2ER.  It’s important to point out that the increased lactate production is simply a result of the increase in glycolysis seen in the anaerobic state.  Simply put, it is an indication of stress. 

Volume Expansion

One of the benefits I can actually see behind the administration of PRBC’s is the lack of third spacing. When trauma patients are resuscitated with 0.9% saline or balanced crystalloids there is a considerable amount of third spacing that occurs within the first few hours. I believe this to be the only benefit in the trauma patient. Are there better volume expander options with less risk? Stay tuned.

    

References:

      1.  https://www.medscape.com/viewarticle/760919

  1. National Blood Data Resource Center. Comprehensive report on blood collection and transfusion in the United States. http://www.aabb.org/content/program_and_services/data_center/NBCUS/.2001.Acessed15 May 2007
  2. Wells AW, mounter PJ, Chapman CE, et al. Where does the blood go? Prospective observational study of red cell transfusion in north England. Br Med J. 2002; 325:803-6
  3. 4.Creteur J, Neves AP, Vincent JL. Near-infrared spectroscopy technique to evaluate the effects of red blood cell transfusion on tissue oxygenation. Crit Care. 2009; 13 Suppl 5: S11
  1. Marik PE, Corwin HL. Efficacy of RBC transfusion in the critically ill: a systematic review of the literature. Crit Care Med 2008; 36:2667-74
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APR
04

Challenge Accepted: Tyler's follow up on "What is a normal CVP?"

the strategy win champion the championship

Dr. Dan Davis posed some great questions in response to my last blog/podcast on CVP. Here is my feeble attempt at answering them. 

Question #1: First, can you fill in the missing puzzle piece: the heart?  How do atrial and right ventricular pressures affect the equation?  

 In my first post on this topic we stated that a plethoric IVC and elevated CVP is a pathological condition. A increase in right ventricular pressure will therefore increase right atrial pressure. This congestion can not only cause decreased coronary perfusion of the right ventricle, but also stretch the RV and RA releasing BNP & ANP.  This cascade will cause a break down of endothelial glycocalyx.

Question #2: Could we even have a negative CVP and still observe adequate cardiac output?  And how does the Frank-Starling curve fit into this discussion?

During normal physiological respiratory swings you will and should see a negative value for your CVP during inspiration. A negative value at the end of exhalation may be seen with a right ventricular assist device. Otherwise, your CVP at the end of exhalation should be equal to relative atmospheric pressure (0).

Frank-Starling curve shows the relationship between preload and cardiac output. The healthy heart curve shows early escalations in cardiac output with increased preload. However the relationship is not linear and does meet a point of diminishing returns. The curve plateaus even earlier in patients with heart failure. This is because increased preload and stretching of the ventricle does not equate to increase in contractility due to diseased myocardium.

Question #3: Do different monitors calculate the displayed CVP value differently?  Are there certain clinical scenarios where the displayed CVP value is misleading?

  1. The CVP should be marched out against a capnography waveform tracing. This will give the best location of measuring end of exhalation. This should be done regardless of the device.
  2. There are several situations that can provide false high CVP’s. The most common is positive pressure ventilation. Instead of looking for collapsibility, we look for expansion with respiration variability.

Question #4: Finally, can you give us some general rules to help us negotiate these stormy waters as clinicians?  

Rule #1 - Do not use CVP to guide fluid therapy.

Rule #2 - CVP can be used as a surrogate of RV performance.

Rule #3 - Many things can increase the CVP regardless of volume status.

Rule #4 - Never let Mike Verkest control the audio for your portion of a debate. 😉

Question #5: I've never measured systemic capillary pressure or even peripheral vascular venous pressures, but maybe I should start connecting my antecubital I.V. to the CVP transducer to see what I get?!?

We will do this live at FAST19 and see the effects escalating PEEP has on PVVP. 🤙

Question #6: Should we try a small fluid bolus, look at the CVP reaction, and then reassessing the clinical status of our patients to find the "optimal" CVP?

See Rule #1 - Do not use CVP to guide fluid therapy.

Question #7: What devices look promising to help us identify the optimal CVP for our patients?  Tissue oximetry?  Ultrasonographic stroke volume measurement?  Non-invasive cardiac output measurement using capnometry?

The question really isn’t how to find optimal CVP, but how to assess whether or not a fluid bolus will increase cardiac output. The passive leg raise with pulse pressure variation at this time is the most reliable test.

Reference: 

1. Monnet, X., Marik, P. & Teboul, JL. Intensive Care Med (2016) 42: 1935. https://doi.org/10.1007/s00134-015-4134-1

Dr. Davis challenged Tyler by stating - "If you can answer these questions, you will upend the critical care apple cart..." - Dr. Dan Davis, MD

Tyler's Response - ...
Image 4 4 18 at 1.22 PM

Tyler Christifulli

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