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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

Table 4. Vasoactive Pharmacology and Pharmacodynamic Effectsa

DA

α1

β1

β2

Other

Mechanism

HR

CVP

CO

SVR

PVR

Vasopressors

Dopamineb

< 5 mcg/kg/min

++++

— or ↑

— or

— or

Dopamineb

5–15 mcg/kg/min

+

++++

+

— or

— or ↑

— or

Dopamineb

> 15 mcg/kg/min

++++

++

++

— or ↑

— or

Epinephrinec

< 5–10 mcg/min

++

++++

+++

— or

Epinephrinec

> 5–10 mcg/min

++++

+++

+

— or

Norepinephrine

++++

+++

+

↓ or —

or ↑

— or

— or

Phenylephrine

+++

— or ↓

— or

— or

Vasopressin

N/A

V1R and V2R

agonism

— or ↓

— or

— or

Angiotensin II

N/A

AT-R1 and

AT-R2 agonism

— or

?

Inotropes

Dobutamine

+

++++

++

— or

— or

— or

Isoproterenol

++++

++++

— or

— or

— or

Levosimendan

N/A

Ca2+

sensitization and

KATP activation

— or

Milrinoned

N/A

PDE3

inhibition

— or ↑

— or

aReceptor activity ranges from no activity (0) to maximal (++++) activity.

bDopamine has dose-dependent effects. At lower doses (< 5 mcg/kg/min), activity at dopamine receptors predominates. At moderate doses (5–15 mcg/kg/min), β1 effects

predominate, and at doses > 15 mcg/kg/min, α1 effects predominate. However, there is overlap in these effects, and these dose ranges are not exact.

cEpinephrine has dose-dependent effects. At lower doses (˂ 5–10 mcg/min), activity at β receptors predominates. At higher doses (typically ˃ 10 mcg/min), α1 receptor

activity becomes more prominent. However, there is overlap in these effects, and these dose ranges are not exact.

dNormal half-life is 2.5 hr, but milrinone is eliminated renally. Loading dose rarely used in routine management.

AT-R1 = angiotensin receptor type 1; AT-R2 = angiotensin receptor type 2; DA = dopaminergic; KATP = adenosine triphosphate-sensitive potassium channels; N/A =

not applicable; PDE3 = phosphodiesterase type 3; V1R = vasopressin receptor type 1; V2R = vasopressin receptor type 2; ? = unclear.

Information from: Bangash MN, Kong ML, Pearse RM. Use of inotropes and vasopressor agents in critically ill patients. Br J Pharmacol 2012;165:2015-33; Hollenberg

SM. Vasoactive drugs in circulatory shock. Am J Respir Crit Care Med 2011;183:847-55; Antonucci E, Gleeson PJ, Annoni F, et al. Angiotensin II in refractory septic

shock. Shock 2017;47:560-6; Chawla LS, Busse L, Brasha-Mitchell E, et al. Intravenous angiotensin II for the treatment of high-output shock (ATHOS trial): a pilot

study. Crit Care 2014;18:534; and Khanna A, English SW, Wang XS, et al. Angiotensin II for the treatment of vasodilatory shock. N Engl J Med 2017;377:419-30; Jentzer
JC, Coons JC, Link CB, et al. Pharmacotherapy update on the use of vasopressors and inotropes in the intensive care unit. J Cardiovasc Pharmacol Ther 2015;20:249-60.
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