This is the first in a series of pieces that are designed to give a new flight clinician a frame of reference for some types of flights they will be on, and some of the problems they may see.
The story goes…
Walking in through the double doors to this ED was in stark contrast to the last time we were there. It was a brand new stand alone facility that seemed like it picked up and move 5 miles away over night. The way the new construction smelled, the mixture of fresh paint and dry wall gave the impression of a new state of the art facility delivering world class care.
Little did we know that this would not be the case…
The staff escorted us to a room where we saw her. She did not look as old as her 69 years, and she was not resting peacefully. She was intubated. Her hands were restrained with soft restraints as were her feet, her legs writhing at the bottom of the bed and her fists clenched tight. A vent cooed an alarm for high pressure, which the RT deftly cleared with the push of a button.
This did not look incredibly complicated… but then it got really complicated really fast. We seemed to have arrived and interrupted an attempt to stop the patient’s writhing with prolonged paralysis. A nurse walked in as we finished getting the monitor transferred to ours.
At first glance, this might be what you would expect to see with a head bleed. Hypertension, after all, is not unheard of with intracranial hemorrhages. But this is not exactly a textbook portrayal of a Cushing’s Response. I would expect to see bradycardia and some bizarre respiratory patterns as well, which are not present here. Instead we see hypertension, tachycardia, and a regular respiratory pattern.
What else is the problem? What are we not seeing?
“What is she on for pain control?” My partner chimes in.
“Fifteen of propofol…” was the reply. I chuckle to myself. Definitely not enough…
“How long has she been at fifteen of Cardene?” I asked
“We just went up to fifteen about five minutes before you got here. She also got twenty of labetalol.”
Hubris
Hubris – noun – excessive pride or self-confidence.
My partner and I share the same knowing look as she pops the security tag on the narcotics box. She holds up a vial of fentanyl and tilts it back and forth at me, to which I gave a nod of agreement. Quickly she gets 100mcg of fentanyl drawn up and connected to the patient’s IV. We both knew that the patient’s paralytics had worn off a long time ago and the propofol was all that was left leaving the patient with nothing for pain control. While propofol does provide sedation, it does nothing for pain, and an ET tube in the throat is quite painful. Now the restraints made sense to me. We had seen this before and we knew that the fentanyl was the answer here.
“Hold on to that next dose of paralytics, we are going to push some fentanyl and see how that treats her.” Our request was followed by an inevitable exasperated sigh.
The changeover of the equipment from the ED’s to ours was relatively uncomplicated. Drips were changed over to our pumps and the ventilator was all set up and ready to go. The patient was notably less tachycardic and we paused to let the blood pressure cycle before we slid her over to our cot.
I thought to myself, “that seemed like a big drop.” In reference to the blood pressure. With our BP now within our target parameter, we started to back off on the Cardene, which had been at max dosing for twenty or thirty minutes now.
Ten more minutes have passed and we have finished loading her into the aircraft. Thinking that all of the jostling from getting her loaded would stimulate her, another 50mcg of fentanyl was given and we let that work while we settled in for the flight.
The engine spools as the BP cycles:
Now we are in trouble. Hypotension and intracranial hemorrhage are not a great combination. The Cardene is backed off again (10mg/min).
“Dude, turn it off.” My partner suggested. I paused for a moment, because if we just shut it off we can have a rebound of the hypertension… and then it hit me. Pain. Pain was the source of the hypertension. It was not the result of the body trying to regulate CBF… and now we had a real problem on our hands.
“Cardene is off.” She said.
“I’m mixing up the Levo.” I said as I reached into the bag for a vial of the drug.
We certainly had our hands full for the rest of the flight…
Neuro emergencies are a common reason CCT is requested. In fact, it was the number one reason my base was requested to move a patient at that time. The management of these patients is not always as straight forward as controlling the BP with vasoactive agents, making sure they have some seizure prophylaxis, and then ensuring they behave with the ventilator… and you are not always set-up for success. As was the case with this particular episode.
In this case, the patient was somewhat mismanaged prior to our arrival. One number became the focus for the team that was treating her and they lost visibility on the big picture. I wrote about a similar case last year when I talked about the phrase “we are getting ready to re-paralyze them” always makes me stop and look at everything else that is going on. While we did see the problem, once we started treating it, we soon found ourselves chasing the blood pressure back the other direction.
Take Home Points and Items of Interest
The MKD
The Monroe-Kellie Doctrine traces its origins back close to 200 years ago. It remained largely unchallenged and the explanation was “perfected” in the 1920s. The MKD is how the body regulates cerebral blood flow in order to maintain CPP (Cerebral Perfusion Pressure).
There is a balance of tissue, CSF, and blood in the skull. These things fluctuate in response to the other taking up more or less room in the cranial vault. It is about 80% brain, 10% blood (150mL), and 10% CSF (150mL). The basic premise of the Monroe Kelly hypothesis is that if there is an increase in one of the intracranial components then the other two have to decrease. We influence two of these elements either brain tissue or blood.
Another compensatory mechanism is movement of CSF. Cerebrospinal fluid gets drained down the spinal column but this compensation takes hours today’s to accomplish it’s effect of reducing ICP.
In the uninjured brain, this is exactly how things work and the changes are minimal with MAPs of 50-150. The normal brain autoregulates blood flow to provide a constant flow regardless of the BP by vasoconstriction or vasodilation of cerebral blood vessels. But in the injured brain this natural compensatory mechanism is dysregulated, and we have to do it for the patient.
Numbers and Targets
Maintaining cerebral blood flow is necessary to prevent secondary injury, and the only ways that we can ensure that the brain remains perfused in the presence of increased intracranial pressure is to either increase the MAP or decrease the ICP. Remember: CPP = MAP – ICP
There’s a few different ways that we can do that. First, we can change the cerebral vascular resistance by influencing the level of carbon dioxide in the brain. For those who are conscious and defending their own ETCo2, airway management may not be necessary, but any alteration of mentation in the presence of suspected head injury necessitates airway management so we can control the PaCO2. In the brain, PaCO2 is how we regulate cerebral vascular resistance. Hypercapnia results in vasodilation while hypocapnia results in vasoconstriction. The goal is to maintain ETCO2 between 30-35.
In general, our first move is to increase the MAP, our second move is to decrease the ICP.
Chasing the Blood Pressure (The easiest way to look like a dummy).
There are some blood pressure parameters for different types of ICH and different teams have different parameters. Here is the important thing to remember. If you are having to rely on on the blood pressure to make titrations of medications, you have to ensure that there is nothing influencing that number. In this case, a pain response from the ET tube was creating a sky-high blood pressure. Once that stimulation was removed, the Cardene was working as it should. Control pain and get sedation on board with these patients before aggressively titrating vasoactive agents. That is not to say you should delay getting something like cardene started, but take it easy until you know the patient’s pain is controlled and they are not fighting the tube.
The problem was that the patient likely never needed the one-two punch of labetalol and Cardene for the blood pressure. Relying on propofol for adequate sedation may not be a bad idea, but you must absolutely provide pain control as well. Especially in the transport setting.
The thing about numbers and targets is that we sometimes get caught up in the pursuit of forcing the patient into a situation to make the numbers look right, without making things right. As was the case with this particular patient.
What Do You Need To Do?
Remember that there are problems, targets, and strategies (channeling some Sarah Crager). Hypertension and hypotension are problems for patients experiencing neurological emergencies. The targets, dictated by evidence and protocol, exists so that we know how much of the problem to fix and how fast. The strategies are how we get to the target and solve the problem. There is an old adage of “there’s more than one way to skin a cat,” and while this is true, there is still a most right answer. In this case, the mistake was made in thinking that the numbers were the problem to fix, and the initial strategy to fix them was failing to achieve the targets they sought.
Key and essential in what we do in the CCT and prehospital environment is to ensure you completely understand the problem that you are trying to fix, and completely understand the secondary and tertiary effects of the strategies you select.
