Hemorrhagic Shock in Emergency Medicine Medication

Updated: May 06, 2016
  • Author: William P Bozeman, MD; Chief Editor: Trevor John Mills, MD, MPH  more...
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Medication

Medication Summary

Achievement of hemostasis, fluid resuscitation, and use of blood products are the mainstays of treatment. Pressor agents may be useful in some settings (eg, spinal shock), but these agents should not be substitutes for adequate volume resuscitation and blood product replacement.

Tranexamic acid (TXA) is an inexpensive antifibrinolytic drug that promotes blood clotting by preventing blood clots from breaking down. It has been shown to reduce mortality in trauma patients with uncontrolled hemorrhage. [17] Further studies are planned to determine specific recommendations for TXA administration.

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Vasopressors

Class Summary

These agents augment both coronary and cerebral blood flow during the low-flow state associated with shock.

Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that in turn produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and renal vasodilation

Norepinephrine (Levophed)

Used in protracted hypotension following adequate fluid-volume replacement. Stimulates beta1-adrenergic and alpha-adrenergic receptors, which, in turn, increase cardiac muscle contractility and heart rate, as well as vasoconstriction; result is increased systemic BP and coronary blood flow.

Vasopressin (Pitressin)

Has vasopressor and ADH activity. Increases water resorption at distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects); however, vasoconstriction also is increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.

Epinephrine (Adrenalin, Bronitin)

Used for hypotension refractory to dopamine. Alpha-agonist effects include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta2-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.

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