Index
Module 15 • Shock & Hemodynamics
Shock Syndromes I
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Data Tables
Shock Syndromes I
Gretchen L. Sacha ~3 min read Module 15 of 20
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Shock Syndromes I

4

Inotropes exert a pharmacodynamic effect that increases CO after adequate fluid administration.

Dobutamine is a β-agonist that improves cardiac function by improving SV and CO. Because of

its β1 activity, dobutamine may induce tachyarrhythmias and, given its β2 activity, hypotension.

Isoproterenol is also a β-agonist, but because it has stronger β2 activity than dobutamine, it causes

more hypotension. For this reason, isoproterenol is not commonly used in the ICU as an inotrope.

Milrinone is a phosphodiesterase type 3 (PDE3) inhibitor. PDE3 inhibition potentiates cyclic

adenosine monophosphate, leading to increased ventricular contractility and vasodilation.

Milrinone may be desirable for patients receiving β-antagonists before critical illness or for

patients having tachyarrhythmias while receiving dobutamine.

ii.

Milrinone may also be favored in patients with pulmonary hypertension (PH) because it

decreases cardiac filling pressures and pulmonary vascular resistance (PVR).

iii.

Milrinone may increase or decrease blood pressure, depending on the individual patient’s

SVR and CO when it is administered. In general, a decrease in blood pressure is more common

with milrinone than with dobutamine.

iv.

The half-life of milrinone is significantly longer (2.3–2.4 hours) than that of dobutamine (2

minutes) and isoproterenol (2.5–5 minutes) and thus limits its utilization in emergent scenarios.

d.Levosimendan is a calcium channel sensitizer that also activates adenosine triphosphate (ATP)-

sensitive potassium channels.

Levosimendan’s pharmacodynamic effects are similar to those of milrinone.

ii.

Like milrinone, levosimendan may be preferred in patients receiving β-antagonists before

critical illness or in those with PH.

iii.

Levosimendan is not available for use in the United States.

D.Administration of Vasoactive Agents
1

Vasopressor agents should be administered through central venous access to minimize the risk of

extravasation and tissue necrosis.

2If central access cannot be obtained, it may be necessary to administer vasopressors peripherally until

central access is established.

3

Clinical trials comparing central and peripheral administration of vasopressors are lacking.

4

The Surviving Sepsis Campaign (SSC) guidelines suggest initiating vasopressors peripherally to restore

MAP rather than delaying initiation until a central venous access is secured.

5

There are no specific guidelines on the characteristics of the peripheral access to use for peripheral

vasopressor administration, but some common best practices are to use a vein proximal to the antecubital

fossa, use ultrasonography to confirm intravenous placement, and administer peripherally for a short

time (48 hours).

6

If vasopressors are administered peripherally, protocolized monitoring should be developed to ensure

frequent monitoring of the infusion site and for signs of extravasation.

E.Outcomes Studies
1

Studies of therapies in patients with sepsis and septic shock will be discussed in section VII, Sepsis.

2Fluid and resuscitation studies in ICU patients

Resuscitation fluids are commonly given for patients in the ICU, with 25%–37% of patients

receiving this therapy in a 24-hour period in cross-sectional studies.

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