Recently I was asked to come in and speak to a critical care paramedic class on the topic of hemodynamics - not monitoring them, just the dynamics. I have often imagined the ideal way to teach a class on hemodynamics would be to build a simplified plumbing system of the body. This would consist of:
1. Hand Pump
2. Large flexible/compliant tubing for the venous side
3. Stiff tubing for the arterial side
4. Resistance Appliance
The pump would shuttle blood from the venous tube into the arterial tube. Once the fluid entered the arterial side, rather than just circulating without resistance, it would meet a narrowing of circumference and begin to build a pressure head (AKA: capillaries). If this pressure head eventually overpowered the pump, we would then have flash pulmonary edema ;).
If I wanted to represent a patient in hypovolemic shock, I would have an extension set connected inline with the circulation and attached to a three-way-stopcock. Imagine I open up the stopcock and allow fluid to leak into a bucket beside the table. As the volume diminishes the pump will be primed with less and less fluid. With the consistent draining of blood from the arteries through the capillaries and into the venous system- I will quickly lose my pressure head. What would the body naturally do in this situation?
Baroreceptors would quickly tell my brain that I need to shut off urine output by releasing vasopressin. Circulating catecholamines would run through my vessels shunting blood away from my extremities and into my central circulation. My body would try to form a clot over the source of bleeding.
The students (cataecholamines) would grab the pressure bag that is encompassing the "venous" flexible tubing (latex free), and try to reduce the size of the large venous pool of fluid that is available, but not under stress. Now that it is stressed, we are using fluid that was just taking up space - now to increase pre-load.
I would pretend to be a surgeon, plug the hole, and everyone would high-five and leave me tremendous reviews at the technical college.
Now imagine I am an old man, 70 years old and currently on more medications than I care to admit. My strength is not what it use to be, and I INSIST on cleaning my own gutters. One fall day while cleaning my gutters and listening to Taylor Swift, I slip back and fall 7 feet onto the drive way. A few right ribs are fractured, lung sounds are clear bilateral, I am unresponsive, and have a blood pressure of 78/60.
You jump in the back of the ambulance to intercept with the local paramedics who report some seizure activity and bleeding from the ears. They decided it was a good idea to intubate me for airway protection. 1 liter of 0.9% saline is in and my current blood pressure is 70/42.
The RUQ scan is positive for free fluid. In fact, you can barely see the liver from all the blood.. ahem.. I mean free fluid.
Blood transfusion begins and the pressure is still dropping. Your partner asks if you should elevate my feet - you look at him like he's an idiot and carry on gaining additional access (Psh). 30 minutes out from the hospital, blood is giving you temporary increases in MAP that fade by the next cycle. You grab the blood and squeeze it with your hands to expedite the transfusion. The warmer seems to be diminishing your flow and you even consider taking it off. You wonder:
Is the 5 degree Celsius blood that you railroaded through the buddy-lite actually helping ?
Sure it is! It's a colloid that will not third-space. Now whether or not it helps with clotting is up to the product you are using and whether or not you are infusing cold blood that works in opposition of clot formation. Ask yourself the following questions given the scenario above.
How much of my circulating catecholamines are bleeding out?
How diluted are my endogenous stress response hormones?
How much cerebral perfusion is actually taking place at a MAP of 51?
Do Pressors Have Any Role In Trauma?
Funny you ask.. Recently I did a blog called "The Levophed Assisted Transfusion." I paint a picture of a very specific type of patient that may benefit from a TRANSIENT levophed infusion. However to understand why this makes sense, you have to understand something called the mean systemic filling pressure (MSFP).
A gnarly dude by the name Arthur Guyton did some interesting experiments between 1950 and 1960. Arthur was an American physiologist with a particular passion on understanding venous return. In 1955 he developed the idea of MSFP. This was the static pressure within the venous system in the absence of flow. The number would be generated by dividing stressed volume over compliance.
What Is Stressed Volume?
If you were to drain all the blood from your veins, you would die. However, if you did it on someone else and only refilled the vessel until it is full- but not exerting any stress against vessel walls, you would have what is defined as unstressed volume. As you pump more and more fluid back into the vessel, the walls of the vessel will begin to stretch. The amount of volume you add that increases that stretch is know as stressed volume.
As that vessel expands it will begin to generate a hydrostatic pressure within the vessel. This pressure as mentioned above, is a product of vessel compliance & stressed volume. This pressure is also the root of venous return. If we plot venous return against right atrial pressure, we can begin to see how flow is influenced.
As right atrial pressure increases, flow decreases. This because right atrial pressure is the downstream pressure for venous return. As you move RAP to the right while maintaining the same MSFP, preload will drop.
The reason this concept is important to fully comprehend is because we can heavily influence the MSFP by interventions and/or medications. For example, sedating and paralyzing a patient will increase venous compliance and drop MSFP. As you can imagine dropping MSFP and increasing intrathoracic pressure within a few minutes is not ideal- and explains the majority of post-intubation hypotensive events.
As illustrated above, we manipulate several physiological mechanisms in the process of necessary airway protection. In order for flow to occur- there needs to be a pressure gradient. The delta pressure(gradient) between RAP and MSFP narrows during PPV. This happens regardless of a medical or trauma patient.
The bodies natural compensatory mechanism when diastolic pressures are inadequate, is to decrease venous compliance. This action will tap into the venous capacitance system and increase MSFP (once again the root or venous return). This is the evolutionary response to hypovolemia.
Knowing the extreme compliance of the venous system, we can imagine that adding large amounts of fluid will result in very minimal increases in pressure. The normal physiological compensation would be to manipulate vascular compliance with endogenous catecholamines. However, as seen above - this mechanism is compromised in the sedated and intubated patient.
This is where I feel filling the tank with blood could be augmented with a levophed assisted manipulation in venous compliance. As the stressed volume is repleted, the MSFP will increase above physiological norms, this is when the levophed could be titrated down or off.
"But the literature shows that pressors are associated with an increase in mortality"
It is very important when we evaluate evidence we understand its limitations. Papers evaluating pressors in trauma are not high quality evidence and have questionable methodology that is not routinely used to guide practice. Here are a few reasons why I do not buy into a strong positive linear correlation between pressors and mortality.
As I have mentioned before, the patients who end up getting pressors in observational studies are those who are peri-arrest. These are without-a-doubt sicker patients. More cases of open thoracotomies, higher volumes of transfusion, higher injury severity scores (ISS), and the list goes on. Compare the two arms of any of these observational secondary analysis blah blah blah studies, and you will see that when left to individuals- the sickest of the trauma patients are the ones in whom are receiving pressors.
I think we can all agree that a study showing fentanyl was associated with higher mortality would be useless if we couldn't see the dosing regimen used. A a very smart physician once said " the difference between a medication and a poison is the dose." These prospective observational secondary analysis studies report administration of a variety of pressors with no insight on the dosing that was used. If experience is of any relevance, physicians routinely give 500mcg of epi to maintain a pulse in a crashing patient. This is very different from a levophed infusion at 10 mcg/min.
1.The 1st line agent for an exsanguinating patient is and always will be blood.
2.There may be circumstances in which MSFP needs to be adjusted in order to compensate for changes we cause through the process of intubation and PPV.
3. The only reason we have literature showing pressors associated with an increase in mortality in trauma is because this intervention is performed on a daily basis in emergency departments and operating rooms. We need a well designed study that reports dosing regimens, a control arm, and patients randomly allocated.
Plurad, D. S., Talving, P., Lam, L., Inaba, K., Green, D., & Demetriades, D. (2011). Early Vasopressor Use in Critical Injury Is Associated With Mortality Independent From Volume Status. The Journal of Trauma: Injury, Infection, and Critical Care, 71(3), 565–572.doi:10.1097/ta.0b013e3182213d52
Gupta, B., Garg, N., & Ramachandran, R. (2017). Vasopressors: Do they have any role in hemorrhagic shock?. Journal of anaesthesiology, clinical pharmacology, 33(1), 3–8. doi:10.4103/0970-9185.202185
Henderson, W. R., Griesdale, D. E., Walley, K. R., & Sheel, A. W. (2010). Clinical review: Guyton--the role of mean circulatory filling pressure and right atrial pressure in controlling cardiac output. Critical care (London, England), 14(6), 243. doi:10.1186/cc9247