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Levophed Assisted Transfusion

There is an internal clock that begins ticking when I see a patient with a MAP below 65. That ticking gets even louder when the patient has a known head bleed. As clinicians we have several ways to raise someones mean arterial pressure:

 

Fill The Tank: Fluids and blood products.

 

Manipulate The Pump Dynamics: Inotropes and chronotropes .

 

Change The Size or Compliance of The Container: Vasopressors and regional occlusion (REBOA). 

 

The most common reflex when a clinician is attempting to increase MAP - is to open up the roller clamp on fluids. Our hope is that by increasing venous return we will increase cardiac output.

 

When our MAP is low because of bleeding, the reasonable intervention would be to stop the source of bleeding - and then if needed replace that volume (with blood). What if that source of bleeding is non-compressible? There is evidence to support permissive low MAP's until surgery can correct the bleed. However, this permissive hypotension takes on a new face when increased intracranial pressure is suspected. 

 

We all remember the formula to calculate cerebral perfusion pressure (CPP). CPP is the pressure you have remaining when you subtract the intracranial pressure from your MAP. It would only make sense that it becomes harder to put your hands in your pockets when our legs take up more space in our jeans (even white pants at FAST19 :). Soooo if our blood pressure is low, but our ICP is consistent - we run into an issue of getting perfusion to the brain. 

 

Let's imagine a scenario where you have a trauma patient with a positive RUQ FAST Exam. You see the liver swimming in a pool of "free fluid" in which you suspect to be blood knowing the mechanism of injury. You are picking this patient up from a smaller referring facility who confirms this patient has a subarachnoid bleed. As you walk into the room you note the current MAP is 55, the patient is intubated and poorly sedated. No blood has been administered and the patient has received 2 liters of 0.9% saline. The physician states " I was afraid to give this guy any more sedation because of the blood pressure."

 

What's your next move?

While the strategies for sedation in the presence of hypotension will be covered in a future blog, we can deduce that a patient fighting the ventilator and agitated is not helping their ICP. I believe the majority of my colleagues are going to an analgesic first (A1) approach, and utilizing hemodynamic dose reduction in this scenario. For example, if this guy is 100 kg, I most likely will be giving 50 mg bumps of ketamine until the patient looks comfortable. I also am completely cool with fentanyl.  I believe we are finding that it's the dose and not the drug that matters, but anyways..

 

The main topic I want to discuss it what we should do with the blood pressure. If we evaluate the methods discussed in the beginning of this blog to elevate MAP, my mind processes them like this.

 

Manipulate The Pump Dynamics: Heart rate is typically already elevated and contraction is hyper-dynamic. It is very rare for a hypotensive trauma patient to be bradycardic with a hypo-dynamic heart. 

 

Fill The Tank: Yes, start a blood transfusion. It may take a few minutes to get blood in the room. Replenishing volume with balanced crystalloids can be used with the known end-goal of blood product. 

 

What about starting a pressor? 

Change The Size or Compliance of The Container:

No, but seriously! This is the area that is of interest to me as of lately. It takes sometime for the volume to increase preload enough to increase stroke volume. As that ticking begins to get louder, many will result to shit-loads of saline or push dose pressors to elevate the blood pressure while waiting for blood products to increase hydrostatic pressure enough to elevate MAP. I think push dose epi is the wrong move because of the reasons mentioned in why "manipulating the pump dynamics" is rarely the right move. So what do I do?

 

I believe a temporary levophed assisted transfusion is entirely reasonable in this situation while waiting for blood product to catch-up with preload requirements. Levophed begins its actions by increasing unstressed volume to stressed volume. This is like giving a fluid bolus, but without the negative sequela of crystalloids. Squeezing the venous capacitance system will directly increase pre-load and expedite ascension of cerebral perfusion.

I have found that this usually is only needed for the first 15 minutes of a transfusion. Parenthetically this levophed can eventually be "weened off." The logistics of getting a blood transfusion initiated can vary depending on whether you routinely bring your blood cooler into the hospital with you, and how quickly the hospital can get you blood. Sometimes it's easier to just have the pilot make a run to the aircraft for the cooler (kidding.. not kidding). The levophed Bump & Drip can occur anywhere in this period.

Sometimes we don't have time to wait for the bathtub to fill up, and we need to change the compliance of the container by jumping in. I believe that levophed has utility to be the fat kid in the swimming pool when seconds are critical to brain perfusion.

 

Hypotension, Hypoxia, & Hyperventilation

In May of 2019 JAMA published the Excellence in Prehospital Injury Care (EPIC) study that looked at preventing the three H's that are known to be deleterious to positive outcomes in patients with a TBI.

The study included more than 130 EMS services and implemented special training that stressed the importance of avoiding the three H's. This study probably included too broad of spectrum of patients to accurately detect a difference between the moderate, severe, and critical subgroups. There is obviously not much that will change the outcome of a critical traumatic head bleed in way of intervention. 

 

When the outcome was adjusted to evaluate the effect of this bundle on just the moderate to severe group- the moderate group doubled in survival, and the severe group tripled. This study does not tell us anything that we did not already know, but it should increase the volume of the ticking you hear when your TBI patient has a plummeting MAP. 

 

How will you respond?

 

References are hyperlinked throughout blog.

 

Original author: Tyler Christifulli
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