My Foolproof Guide for Treating Hypotension on Rounds
As an anesthesiologist, I treat many patients with hypotension. Sometimes, it’s my fault, but in those cases, it’s expected and correctable with the right medication. Of course, outside of the OR, the workup of hypotension, whether chronic or acute, can present more of a problem. In those cases, the question becomes why is the patient hypotensive, and there are many possible reasons.
To help you treat different types of patients with low blood pressure in an efficient way, I’ll share with you a framework spelled out to me by one of my favorite mentors. This approach focuses on five underlying factors—and is so foolproof that you will not only be able to treat your hypotensive patient, but also do so correctly.
The 5 Components of the Framework
Let’s begin with a review. Remember Physiology 101? It was there, so many years ago, that you learned:
Pressure (P) = Flow (Q) * Resistance (R)
In physiologic terms, that would be:
MAP = CO * SVR
And considering the cardiac output is the product of heart rate and stroke volume, we get:
MAP = (Stroke volume * Heart Rate) * SVR.
In its simplest terms, blood pressure only depends on those three things—stroke volume, heart rate, and systemic vascular resistance (afterload). But stroke volume and heart rate can actually be separated into a couple more determinant factors.
What determines one’s stroke volume? How does the heart know how much blood to eject? Well, of course, it depends on how much blood gets put into the heart—preload.
How much of that blood leaves the heart? As a corollary, what’s the difference between a strong, young, athlete’s heart, and the patient waiting for a VAD? Contractility.
So, stroke volume is determined by the preload, or how much blood gets into the heart, and by contractility, or the ability of the heart muscle to contract.
As for heart rate, let’s say a patient has a rate of 110. Sinus tachycardia is going to get you a much higher blood pressure, all other things being equal, than the wonky, dyssynchronous contractions of atrial fibrillation. So in addition to the heart rate, we care about the rhythm.
To summarize, the five components of our hypotension framework are rate, rhythm, preload, afterload, and contractility.
Treating Each Component of Hypotension
Now let’s talk about how the five components can become perturbed, and what you can do to correct them in each case.
Increasing heart rate will typically increase cardiac output. This is true up until the point that diastolic filling is compromised because the heart is beating too fast and doesn’t have enough time to fill.
A hypotensive patient with a heart rate in the 30s needs their heart rate jacked up. Reach for atropine or epinephrine for the immediate fix. Alternatively, if you have the resources, transcutaneous or intravenous pacing can get the heart moving at a more normal rate.
Hypotensive with an HR of 150? Too fast! Give some esmolol to slow things down and allow time for diastolic filling. Now, this is all assuming a sinus rhythm. But what if it’s not?
Sinus rhythm is the rhythm of life! It’s the way in which our perfect, embryologically designed heart prefers to beat—but not every patient’s heart behaves this way.
Rapid A-fib with hypotension? Sounds like it’s time to try and cardiovert this patient back to a normal rhythm. Pharmacologic cardioversion is another option with tools like amiodarone or lidocaine.
This one can be hard to assess without an echo probe. But you might have the luxury of markers like CVP, or arterial line waveform variations.
Short of that, fall back on the physical exam. Does the patient look dry? Do they have a reason to be dry (e.g., overdiuresis, diarrhea, blood loss)? If so, give them fluid or blood products.
A low SVR state will lead to low blood pressure. The way to fix this one is with medication, not fluid. That septic patient needs some norepinephrine after they have failed their fluid challenge, not another 4 liters of crystalloid.
A bad heart is often the most difficult problem to correct. If you have a sense (based on history or symptomatology) that poor heart function is to blame for hypotension, your typical response is going to be inotropy (epinephrine, dobutamine).
Those medications are not without their risks, but in a hypotensive patient, they are probably risks you are willing to take.
The Patient Will Show You the Way
As usual, you have to let the patient’s story be your guide. If they lost a liter of blood into their belly (and another liter onto the road), you can be pretty sure you’ve got a preload problem.
What if the patient with chest pain and EKG changes is hypotensive? Take a look at their heart, and bolster its ability with an inotrope.
The real magic is in your “sick” patient, who needs ICU-level care. They have low SVR from infection, their heart wasn’t strong to start with, they are overloaded with fluid but intravascularly depleted, and they are having occasional arrhythmias. You might be facing many of these problems at once. Do what you can to support the patient and work through the disease process so that they can return to normal physiology ASAP.
One more tool that has become a boon to answering the question, “Why is this patient hypotensive?,” is point-of-care ultrasound. With a simple peek at the heart through a basic transthoracic echo view, you can get a gross sense of your preload and contractility. You can quickly rule out a heart that’s sick and needs some help pumping, or an empty heart that simply needs some volume added to the tank. Proficiency with this technology will amplify your clinical acumen.
Use it Anytime, Anywhere
The beautiful thing about this framework is that it can be applied to any hypotensive patient. Did someone pass out in the clinic with a blood pressure of 84/40? Did you walk into an ICU patient’s room and see 67/40 on the monitor? Or maybe during a surgical procedure, the A-line unexpectedly reads 77/52. No matter where you are, the framework and physiology are the same. Use it!
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