In this episode I’ll review the vasopressors norepinephrine, vasopressin, epinephrine, dopamine, and phenylephrine. Fluids, vasopressors, and inotropes are the essential parts of the treatment of shock.
Shock is the syndrome that results when the cardiovascular system fails to maintain adequate tissue perfusion.
The immediate treatment goal for shock is to maintain hemodynamics while the cause can be addressed.
For more details, find my favorite review of vasoactive drugs in shock here. Before I dive into discussing each vasopressor, I’ll talk dosing and administration.
My starting rate always depends on how close the patient is to death. If they are in extremis I will start at the maximum rate and titrate down. If they are stable then I will start at the bottom and work up.
Maximum doses vary greatly between institutions. It is likely that your hospital has arbitrarily set a maximum dose for each vasopressor. I wouldn’t get too hung up on it as long as there is agreement across disciplines on your institutional max. Maximum doses were invented to be exceeded, so don’t be shocked when your doc squeezes the IV bag in while trying to stabilize that young OD patient long enough for ECMO to be started.
Peripheral vs. central line
Any port in a storm.
Let’s be realistic. Many patients would suffer organ damage from profound hypotension if you waited for a central line to be placed to give them vasopressors. If you are using vasopressors in a peripheral line, you should choose a small bore in the largest vein possible. If the need for vasopressors persists, a central line should be placed ASAP. In a Cochrane review the average infusion duration that resulted in complications was 55 hours. This is especially important given the phentolamine shortage. I wouldn’t count on phentolamine alternatives (terbutaline and topical nitro paste) if I were you.
If you were going to choose one vasopressor to start first in shock of essentially any etiology, norepinephrine would be the one to choose. Sepsis guidelines say to use this first, and there is data suggesting lower mortality with norepinephrine vs dopamine in cardiogenic shock. Norepinephrine is a potent α-adrenergic agonist with less pronounced β-adrenergic agonist effects. It causes vasoconstriction and to a lesser extent increases cardiac output and stroke volume. Reported dose ranges for norepinephrine are 0.01 to 3.3 mcg/kg/min. My institutional maximum is 0.6 mcg/kg/min and starting concentration is 8 mg in 250 mL normal saline.
Vasopressin is an endogenously secreted hormone. It constricts vascular smooth muscle directly via V1 receptors and also increases responsiveness of the vasculature to catecholamines. In septic shock, endogenous supplies are quickly depleted, and patients are often exquisitely sensitive to “vasopressin replacement therapy” at a dose of 0.03 or 0.04 units/min. Sepsis guidelines recommend adding vasopressin to norepinephrine. This combination usually allows for a lower dose of norepinephrine to be used. Don’t be surprised to see your cardiac surgeons using vasopressin at higher doses for low cardiac output postoperatively. At my institution we use up to 0.1 units/min for this indication, and vasopressin is titrated to effect in this setting (as opposed to fixed dosing in sepsis).
Epinephrine is a more even mix of α and β agonist activity compared to norepinephrine. It is reasonable to use 2nd line when other therapies are not enough. Epinephrine causes more tachycardia and lactic acidosis than 1st line agents, and it should be weaned off first due to the risk of gut ischemia. My institution’s starting concentration is 8 mg in 250 mL normal saline and maximum dose is 1 mcg/kg/min.
The lazy clinician’s vasopressor. Phenylephrine is absolute garbage in septic shock. You don’t want to use this vasopressor if you don’t have to, unless there is something benign going on like systemic vasodilation from drug effect (propofol) or epidural anesthesia. The problem with phenylephrine is that it reduces cardiac output and decreases venous return. It is a pure α agonist. My institutions starting concentration is 50 mg in 250 mL normal saline and maximum dose is 5 mcg/kg/min.
DO NOT BE FOOLED into thinking that phenylephrine is first-line in tachycardic patients because it has no β activity!
Your shocked patient’s tachycardia is probably a compensatory mechanism (see episode 3) and will resolve after the shock is appropriately addressed.
Dopamine Dopamine is like having 3 pressors in 1. Depending on the dose you can get dopamine to do a whole host of things. Dopamine’s activity is traditionally split into 3 categories with specific dose ranges, but in the critically ill patient there is often overlap between these categories:
- < 5mcg/kg/min – vasodilation in renal and mesenteric bed via dopaminergic receptors
- 5-10 mcg/kg/min – increased heart rate and contractility via β1 receptors
- >10 mcg/kg/min – arterial vasoconstriction via α1 receptors
That is wonderful information to have, but it is more important to know that dopamine has essentially no benefit over other vasopressors and comes with a higher risk of ventricular arrhythmia. Don’t expect to use it much. Starting concentration is 400 mg in 250 mL normal saline and institutional max is 20 mcg/kg/min. The one advantage dopamine does have is that it comes premixed with extended stability. This means you will more likely find it in a code cart. Like the saying goes, you go to the code with the vasopressors you have, not the vasopressors you want to have.
If you like this post, check out my book – A Pharmacist’s Guide to Inpatient Medical Emergencies: How to respond to code blue, rapid response calls, and other medical emergencies.