Critical Care Fundamentals: Management of Shock Part 1

Shock is defined as circulatory failure leading to decreased organ perfusion. In a shock state there is an inadequate delivery of oxygenated blood to tissues that results in end-organ dysfunction. Effective resuscitation includes rapid identification and correction of inadequate circulation. the finding of normal hemodynamic parameters (i.e. normal blood pressure) doe not exclude shock itself. In this 11 minute and 40 second video, I will review the management shock – part 1 (The goals of shock management, signs of adequate organ perfusion, the etiology of shock, and some basic terminology).

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The goal of shock is restore and maintain end organ perfusion!!!

Each organ has a critical perfusion pressure Cerebral Perfusion Pressure 50-70 mm Hg Coronary Perfusion Pressure 60-80 mm Hg Renal Perfusion Pressure 65-70 mm Hg

Optimize hemodynamics: CO=SV x HR, SVR

Balance perfusion to vital organs with over vasoconstriction to prevent ischemia (ie gut ischemia)

Literature would support MAP 65 mm Hg (at least to start) then frequently reassess your patients perfusion as some patients may need higher MAP to maintain perfusion however some may need less

Some (not so perfect) signs for adequate organ perfusion include:

Mental Status

Capillary refill

UOP

Mottled extremities

Lactate (See the Basics of Shock)

Etiology of Shock (Based on the SOAP II Trial):

Obstructive Shock (2%)

Hypovolemic Shock (16%)

Cardiogenic Shock (16%)

Distributive Shock (66%) Septic (62%) – most common shock in the ICU Non-septic (4%)



Terminology:

Vasopressor : induce vasoconstriction Phenylephrine, Vasopressin, Angiotensin II, Selepresin

induce vasoconstriction Inotrope : increase cardiac contractility

increase cardiac contractility Inopressor : Induce vasoconstriction & increase cardiac contractility Norepinephrine, Dopamine, Epinephrine

Induce vasoconstriction & increase cardiac contractility Inodilator : increase cardiac contractility & cause vasodilation Dobutamine, Milrinone, Levosimendan, isoproterenol

increase cardiac contractility & cause vasodilation

Important Receptors:

Alpha 1: On the vasculature and cause vasoconstriction

Beta-1: On the heart and cause inotropy and chronotropy

Beta-2: On the vasculature & lungs and cause vasodilation and bronchodilation

V1: On the vasculature and cause vasoconstriction

Angiotensin II: On vasculature and cause vasoconstriction

References:

Walsh M et al. Relationship between intraoperative mean arterial pressure and clinical outcomes after noncardiac surgery: toward an empirical definition of hypotension.Anesthesiology 2013. PMID: 23835589 De Backer D et al. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. NEJM 2010. PMID: 20200382

Critical Care Education Curriculum

Please watch Critical Care Fundamentals – Mgmt of Shock Part 2A & Mgmt of Shock Part 2B as well

Mgmt of Shock – Educational Reinforcement Material

Mgmt of Shock – Supplemental Educational Material

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)