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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).