Protocol for Vasopressor Use in the ICU

Vasopressors increase vasoconstriction, which leads to increased systemic vascular resistance (SVR).
Increasing the SVR leads to increased mean arterial pressure (MAP) and increased perfusion to organs.
Inotropes increase cardiac contractility, which improves cardiac output (CO), aiding in maintaining MAP
and perfusion to the body. The equation that connects the 2 is MAP= CO x SVR.

The major vasopressors include phenylephrine, norepinephrine, epinephrine, and vasopressin.

Dopamine is a vasopressor with inotrope properties that is dose-dependent. Dobutamine and milrinone
are inotropes.

Indications for use of Vasopressors:

Vasopressors should be initiated when there is evidence of hypotension, defined as a systolic blood
pressure (SBP) <90 mmHg or mean arterial pressure (MAP) <65 mmHg, despite adequate fluid
resuscitation.

In patients with septic shock, vasopressors should be initiated after adequate fluid resuscitation
(30mL/kg) has been completed and persistent hypotension is present.

Step 1: Assess and optimize fluid status

Determine the cause of hypotension and address any reversible causes such as hypovolemia.

Administer an initial fluid bolus of 500-1000 mL of crystalloid or colloid solution.

Reassess fluid status and hemodynamic response.

Step 2: Choose appropriate vasopressor

First-line vasopressor: norepinephrine (NE)

Second-line vasopressor: vasopressin or epinephrine

Dopamine may be used as an alternative in select patients with low cardiac output and low systemic
vascular resistance (SVR).

Step 3: Initiate vasopressor infusion

Start with norepinephrine infusion at 0.05-0.1 mcg/kg/min and titrate to maintain MAP > 65 mmHg.

If persistent hypotension despite adequate norepinephrine dose, add vasopressin at 0.03 units/min.

If persistent hypotension despite adequate norepinephrine and vasopressin, add epinephrine at 0.03-
0.05 mcg/kg/min.
In patients with low cardiac output and low SVR, dopamine may be used at 5-10 mcg/kg/min.

Step 4: Titrate vasopressors to goal

The goal of vasopressor use is to maintain adequate organ perfusion while avoiding end-organ damage
from excessive vasoconstriction.

Titrate vasopressors to maintain a MAP of 65-90 mmHg and avoid excessive vasoconstriction by
monitoring for signs of tissue hypoperfusion (e.g., lactate level, urine output, mental status, skin
perfusion).

Step 5: Consider other interventions

In patients with refractory shock, consider adjunctive therapies such as corticosteroids or inotropic
agents.

Consult with a critical care specialist for guidance on further management.

Step 6: Wean vasopressors

Once the underlying cause of shock has been addressed and hemodynamic stability has been achieved,
taper vasopressors gradually to avoid rebound hypotension.

Consider switching to a lower-dose vasopressor (e.g., vasopressin) or tapering off the vasopressor
entirely, if possible.

Monitoring:

Continuous monitoring of blood pressure, heart rate, and urine output.

Frequent reassessment of fluid status and response to therapy.

Monitor for signs of tissue hypoperfusion (e.g., lactate level, urine output, mental status, skin perfusion).

Complications:

Vasopressors can cause vasoconstriction, which can lead to tissue hypoperfusion and ischemia.

Excessive vasoconstriction can lead to organ dysfunction, such as acute kidney injury or mesenteric
ischemia.

Monitor for signs of complications and adjust vasopressor therapy as needed.