Top Ten Tips to Optimize Vasopressor Use

Written by Eriny Hanna

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Here are the top 10 points for optimizing vasopressor use in critically ill patients.

Why does this matter?
Hypotension is associated with increased morbidity and mortality, so it’s important to use vasopressors correctly.

MAPing it out

Set goals of mean or diastolic pressures. Organ perfusion pressure is determined by mean arterial pressure (MAP). In patients with coronary artery disease or pulmonary hypertension, setting a diastolic pressure goal helps with coronary perfusion. Consider an arterial line if using high doses of vasopressors for a prolonged time.

Individualize target pressures. Studies suggest that 65 is a good MAP goal, even in patients with a history of hypertension.^1,2 If markers of perfusion (urine output, cap refill, mental status) suggest hypoperfusion, trialing a higher MAP is reasonable.³ If so, reassess every few hours and adjust vasopressor dose to avoid adverse events.

Vasopressors recruit endogenous fluid. Vasopressors increase systemic vascular resistance which helps recruit endogenous fluid into circulation leading to increased venous return and cardiac output.⁴ Norepinephrine also reduces capillary leakage. The authors recommend starting vasopressor early in patients with a MAP <50-55 mmHg in addition to a fluid bolus.

Reassess fluid status and cardiac output after starting vasopressors. Higher doses of vasopressors can lead to ischemia due to excessive vasoconstriction, which can alter cardiac output.

Consider a different mechanism of action when needing a second agent. Norepinephrine is the first line for distributive shock.⁵ Adding a second vasopressor with a differing mechanism of action, most commonly vasopressin, can limit side effects. Angiotensin II is a newer agent that can help mitigate septic acute kidney injury.⁶

Consider adding hydrocortisone when requiring high doses of vasopressors. Hydrocortisone decreases the amount of required vasopressors, especially in those with multiorgan failure.⁵

Consider using vasopressin plus an inotrope in right ventricular failure. Pulmonary arteries do not have V1-receptors, therefore vasopressin does not increase pulmonary vascular resistance. Norepinephrine should still be first line because it has inotropic effects that improves right ventricle function.

There is no maximum dose of vasopressors. The authors argue that limiting the maximum dose of vasopressors may limit the likelihood of recovery or lead to tolerating hypotension.

Enteral feeding can be started with low-dose vasopressor use. The authors suggest enteral nutrition is safe in doses of norepinephrine that are less than 0.3 micrograms/kg/min. They note to avoid enteral feeling with higher norepinephrine doses, epinephrine, and/or dobutamine to avoid mesenteric ischemia.⁷

Vasopressors can be safely administered through a peripheral line. Do not delay initiation of vasopressors if there is no central access.

Editor’s note: Sorry, this is only obliquely related to IV fluid week, but hey…still relevant! ~Clay Smith

Source
Ten tips to optimize vasopressors use in the critically ill patient with hypotension. Intensive Care Med. 2022 Jun;48(6):736-739. doi: 10.1007/s00134-022-06708-y. Epub 2022 May 3.

Works Cited

1. Lamontagne F, Richards-Belle A, Thomas K et al (2020) Effect of reduced exposure to vasopressors on 90-day mortality in older critically ill patients with vasodilatory hypotension: a randomized clinical trial. JAMA 323:938–949. https://doi.org/10.1001/jama.2020.0930
2. Asfar P, Meziani F, Hamel J-F et al (2014) High versus low blood-pressure
   target in patients with septic shock. N Engl J Med 370:1583–1593. https:// doi.org/10.1056/NEJMoa1312173 4528
3. Redfors B, Bragadottir G, Sellgren J et al (2011) Effects of norepinephrine on renal perfusion, filtration and oxygenation in vasodilatory shock and acute kidney injury. Intensive Care Med 37:60–67. https://doi.org/10. 1007/s00134-010-2057-4
4. Monnet X, Jabot J, Maizel J et al (2011) Norepinephrine increases cardiac preload and reduces preload dependency assessed by passive leg raising in septic shock patients. Crit Care Med 39:689–694. https://doi.org/10. 1097/CCM.0b013e318206d2a3
5. Evans L, Rhodes A, Alhazzani W et al (2021) Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021. Intensive Care Med 47:1181–1247. https://doi.org/10.1007/ s00134-021-06506-y
6. Leisman DE, Fernandes TD, Bijol V et al (2021) Impaired angiotensin II type 1 receptor signaling contributes to sepsis-induced acute kidney injury. Kidney Int 99:148–160. https://doi.org/10.1016/j.kint.2020.07.047
7. Piton G, Le Gouge A, Boisramé-Helms J et al (2022) Factors associated with acute mesenteric ischemia among critically ill ventilated patients with shock: a post hoc analysis of the NUTRIREA2 trial. Intensive Care Med. https://doi.org/10.1007/s00134-022-06637-w