Giving our patients the best chance to survive shock

Erik Diringer, DOIntensivist – Kenmore Mercy Hospital

Disclosures

None

Vasopressors

Powerful class of IV medications that induce vasoconstriction

Not to be confused with inotropes

Surprisingly a dearth of studies exist comparing their use in different shock states2

Shock States (Adult)

“The rude unhinging of the machinery of life” 2

Significant reduction of systemic tissue perfusion

Oxygen consumption > Oxygen delivery (VO2 > DO2)

Cellular effect

Systemic effects

Cell death, end-organ damage, MSOF, death

Often happens prior to hypotension

Shock States

MAP = (CO x SVR) + CVP

CO = HR x SVSV influenced by preload, afterload, contractility

Shock States

Types:Distributive: dec. SVR

Eg) septic shock, SIRS, anaphylaxis, neurogenic, toxins

Cardiogenic: dec. contractility (inc. SVR, HR)Eg) CMP, arrhythmia, mechanical, obstructive

Hypovolemic: dec. preload (inc. SVR, HR)Eg) fluid loss, hemorrhage

Vasopressor/Inotrope Receptors

Alpha adrenergicα-1 in vessels, induces vasoconstriction

Beta adrenergicβ-1 in heart, increases inotropy and chronotropy, mild vasoconstrictionβ-2 in vessels induces vasodilation

Dopamine: renal, splanchnic, coronary, cerebral vascular beds

Generally induce vasodilationSubtype induces vasoconstriction by inducing NE release

Vasopressor ChoicesNorepinephreine (Levophed) – 0.02-1 mcg/kg/min IV

α-1 and β-1 activityPotent vasoconstriction, modest inc. CO

Phenylephrine (Neo-Synephrine) – 40-60 mcg/min IVα-1 activityPotent vasoconstriction, dec. SV

Epinephrine – 2-10 mcg/min IVPotent β-1 activity, modest α-1, β-2inc. CO, dec. SVRα-1 predominates at higher dosesBeware of arrhythmias, splanchnic vasoconstriction

Vasopressor Choices

Dopamine1-2 mcg/kg/min: selective renal, splanchnic, cerebral, coronary vasodilation

5-10 mcg/kg/min: β-1 activity

>10 mcg/kg/min: α-1 activityBeware of arrhythmias

Vasopressor Choices

Vasopressin (ADH)Second-line agent in distributive shock

Doses >0.03 U/min associated with coronary and mesenteric ischemia

Inotrope Choices

Dobutamine (Dobutrex)β-1 activity: inc. contractility, dec. SVR

Isoproterenol (Isuprel)β-1, β-2 activity: inc. HR, dec. SVR

MilrinonePDE inhibitor

Non-adrenergic, but similar physiological effect to dobutamine

Pre-Pressor Problems

ABCs

Volume resuscitation

Central access, monitoring

Why is my patient in shock? What determinant of tissue perfusion is being adversely affected?

HR, preload, afterload, contractility, SVR

Distributive Shock

Distributive Shockdec. SVR

Compensatory inc. HROften dec. contractility in septic shockGoal is to maintain adequate SVR without adversely affecting CO

Septic shock most common causeEGDT, volume resuscitationNorepinephrine is first-line vasopressor therapy in septic shock despite adequate fluid resuscitation3 (Grade 1B)Epinephrine second-line (Grade 2B)Vasopressin (0.03 U/min) to achieve MAP goal, decrease NE (UG)Dopamine only in low-risk for arrhythmia, absolute/relative bradycardia (grade 2C)

Septic Shock

Phenylephrine is not recommended, except (grade 1C):

When norepinephrine is associated with serious arrhythmias

When CO is high and BP persistently low

As salvage therapy when combined inotrope/vasopressor drugs and low-dose vasopressin have failed to achieve the MAP target

Phenylephrine is an appropriate pressor in neurogenic shock

Cardiogenic Shock

Cardiogenic Shock

dec. contractility

Compensatory inc. SVR and HR

Only vasopressors with β activity are indicated!

Avoid α-1 agents that only increase SVR

Inotropes preferred when BP adequate

Sometime secondary to dec. HR

Provide optimal supportive care (pH, temp, O2)

May require device (VA-ECMO, IABP, VAD, TVP)

Cardiogenic Shock – Obstructive

Generally no role for vasopressors

Treatment aimed specifically at underlying causeCardiac tamponade, tension pneumothorax, massive PE

Hypovolemic Shock

Hypovolemic Shockdec. preload

Compensatory inc. SVR and HR

Why is my patient hypovolemic?Fluid loss, hemorrhage

Treat the underlying cause

Generally vasopressors indicated as temporizing supportie) BP support during intubation, procedures

Specific casesEsophageal varices: Vasopressin decreases portal blood flow and improves hemostasis

Take Home Messages

Shock often occurs before hypotensionOxygen consumption > Oxygen delivery (VO2 > DO2)

Tissue perfusion influence by CO and SVRCO influenced by HR, preload, afterload and contractility

Shock can be distributive, cardiogenic, hypovolemic or a combination

Vasopressor choice directed at mechanism of shock

Take Home Messages

Always ask “Why?”Direct your therapy based upon the answer

References1. Müllner M, Urbanek B, Havel C, et al. Vasopressors for shock. Cochrane

Database Syst Rev 2004; :CD003709.

2. Simeone FA: Shock, trauma and the surgeon. Ann Surg 1963; 158: 759–774.

3. Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012 (http://www.survivingsepsis.org/Guidelines).