Intubating the Hypotensive Patient

Intubating the Patient with Hypotension

Before you intubate your next hypotensive patient, think twice and read below.

Positive pressure ventilation has multiple hemodynamic affects on your patient, mostly reduced venous return resulting in reduced preload, and increased right ventricular afterload. The combination of these two along with the systemic affects of your sedation for induction can result in rapid hemodynamic compromise in the already unstable patient.


58 y/o M with cough fevers and chills with body aches presents to the ED.

VS: 40.1, 135 (ST), sat 90% on NRB and he is breathing a real 30x’s/min, BP 85/55.

You determine the patient would benefit from endotracheal intubation, how do you proceed?

Step 1: Emergent or not?

The first question you always have to ask yourself is this going to be emergent, and do I have time. As ED doctors we are quick to jump to intubation when we know someone needs it, but the reality is most patients can be intubated urgently rather than emergently, while getting everything you need prior to induction. If they are agonal, severely hypoxic and cannot be BVM ventilated then godspeed.

But if you decide this is an urgent intubation, and have 5 minutes proceed

Step 2: What is my access?

The nurses should have 3 minutes to get you two working IV’s before you go to a humerus I/O. If you use the tibia be sure you use a pressure bag to augment the infusion rates, which usually are 65 ml/min vs. 165 ml/min with a pressure bag. In the Obese, sickle cell patient, or patient on hemodialysis this is the rapid IV of choice and results in fewer errors than placing a sterile semi-emergent CVC.

Why 3 minutes?

-Because while that is happening another nurse should be grabbing you two bags of crystalloid and a pressure bag ready to give to this patient.

-If you have a pharmD ask for a vasopressor drip on the pump ready to go, if they can make phenylephrine fastest or epinephrine take what you can get. Otherwise someone should be getting central pharmacy to make you drip, this is preferable to you making the drip yourself.

By now you should have two IV’s and one of the IV’s should be designated for induction medications. Have one bag of crystalloid running wide open on the IV that has been established as the line that will have the meds pushed through. This way we know if the IV is infiltrated (the bag isn’t running, or the skin around the IV has blown up) or if it just so happens that the BP cuff is on the same arm as the designated IV you realize before pushing the meds  (cause’ its just embarrassing trying to figure out why your patient isn’t paralyzed).

Now this is where I don’t expect most ED doctors to follow, but I would recommend this. Place an arterial line. You can argue there have been no studies that show that A-lines save lives and that it is a waste of time and not an ED skill, and you may be right. What I will argue is that’s true of chest x-ray’s, MRI’s and most innovative technologies and it is all about what you do with the information that makes the difference.

 The A-line gives you beat-to-beat information. There is no recycling of the blood pressure because the cuff couldn’t read and people start feeling for a pulse. CPR? Hit restart, that can’t be right! I know this has happened to all of us.

An US guided A-line doesn’t take much time to put in, once you are familiar with the technique. I believe it allows for a smoother more hemodynamically stable intubation. Are they hypertensive during laryngoscopy, (your unsecured aneurysms that have leaked but not ruptured!?) give him more propofol and take the blade out. Has my patient’s pressure just dropped? bolus him phenylephrine or epinephrine.

This also makes getting an ABG after intubation much easier than asking RT to do radial A-line sticks in hypotensive patients and prevents the dreaded; oh we couldn’t get an ABG so we didn’t do one.

Step 3: Induction Medications:

You can use whatever you want, just know they all cause hypotension. Ketamine seems to be en vogue, and is a good choice, but since we don’t have it in our omnicell in the ICU most of the ICU anesthesiologists here use an opiate like fentanyl first followed by a low dose of propofol; as in 10mg boluses up to 30mg until they are unresponsive to jaw thrust. I personally don’t think 20mg of etomidate is the best answer, but don’t have any science to back this up.  Use whatever you like and markedly reduce the dose of the sedative.

Step 4: You were ready for hypotension

It was going to happen, but now atleast you are ready for it. First continue your fluid bolus, which should now be on a pressure bag if the MAP starts to get a little soft.

Then if it is apparent that there is a loss of vasomotor tone, you should replace the lost endogenous catecholamines with temporary vasopressors. I suggest blousing aliquots of phenylephrine 100 mcg Q 1 minute unless the MAP has precipitously dropped, then start with 300mcg. Once you have stabilized their MAP see if you have to keep pushing phenylephrine, if you do they need a drip, if you don’t congratulations you have successfully intubated a sick hypotensive patient without killing them.

If you are slick with the echo probe and see the LV or RV is down consider epinephrine 10mcg boluses instead and an epi infusion if needed.

Step 5: How do I sedate my hypotensive patient?

Let me start off by saying I think there is enough good evidence to recommend avoidance of benzodiazepines completely in most ICU patients not seizing. BZDs result in increased delirium, prolonged ventilator days, and worse patient outcomes compared with alternatives. This is never truer than in the elderly.

With that said the first thing to address is pain. It’s uncomfortable to sit in a firm bed without moving for hours, while having a toothbrush shoved in the back of your throat and the IV monitor beeping over and over again. If you treat pain first you will have a marked reduction in the requirement for “sedation/amnesia”. I like a dilaudid push of 1mg after hemodynamics have settled out followed by a drip 0.5-2mg/hr.

The sedation choice for me is between low dose propofol (10-30 mcg/kg/min) and dexmedetomidine. I prefer dex, 0.1-0.7mcg/kg/hr and it is going generic this year. If people give you a hard time about choosing this “expensive medication” show them the data on benzodiazepines and hospital LOS, and ventilator days. If you use ketamine, as I know ACMC has, you are ahead of the curve.

When giving these meds you don’t need to SNOW the patient, just make them calm enough that they can be awoken with loud verbal stimuli (we use the RAAS scale, target -1 to -2).  Having them be comatose makes repeat exams with fluctuating mental status difficult to monitor.

This isn’t the sexy part of medicine but if you are in the business of saving lives and making your patients comfortable the nuances listed above is worth the extra effort.

The most important part of intubating the hypotensive patient is to be prepared for the rapid hemodynamic consequences that will follow. You shouldn’t sit after an intubation followed by PEA arrest wondering why that happened, it’s usually right in front of your face.

SIDE PEARL HYPOTENSION from obstructive shock:

If by chance you know the patient has a large pulmonary embolism as the cause of their distress you should be aware that intubation is likely to result in rapid hemodynamic deterioration. WHY? The RV is a low-pressure, high compliance chamber and rapid increases in afterload (PE) result in RV dilation. The RV dilation results in bowing of the interventricular septum to the left and causes reduced compliance of the LV, and the LV becomes more underfilled.  Since the RV is perfused during diastole and systole, any reduction in MAP (caused by LV dysfunction) will cause a stiffening of the RV again impeding forward flow. The now more dilated RV causes tricuspid annulus dilation and significant tricuspid regurgitation and again impedes forward flow. Intubation will exacerbate the RV failure by decreasing MAP, and increasing RV afterload especially if they become hypoxemic or hypercarbic as both increase pulmonary vascular resistance.

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