VASOPRESSORS &

INOTROPES
Critical Care Internship
Program
Dr. T. Madayag

Sympathomimetics & Catecholamines

Dopamine, epinephrine &

norepinephrine
Produced naturally in the body to
activate the sympathetic nervous
system by
Initiating the fight or flight
Stimulating the alpha and beta receptors
thus
Increased cardiac output
vasoconstriction

 Cholinergic transmission is
mediated by Ach
Adrenergic transmission is
mediated by
epinephrine (adrenal medulla)
norepinephrine (post ganglionic
neurons)

Ach Effects

HEART
Decreased heart rate by reduction in
SA firing
Increased conduction through the AV
node

VESSELS
Vasodilation

Receptor Physiology

Alpha 1
Alpha 2
Beta 1
Beta 2
Dopaminergic
Vasopressin (V1)

Alpha 1

Located in the arteriolar walls

inducing vasoconstriction
Present in the heart
Stimulation leads to constriction of
the vascular smooth muscle,
splanchic vessels
Increases SVR

Alpha 2

When blocked causes vasodilation by

inhibiting the release of
norepinephrine

Beta Receptors

Beta 1
Most common in the heart
Stimulation causes
Increased rate (Chronotropic effect)
Contractility (Inotropic effect)
Increased CO & performance

Relaxation of smooth muscles

Vasodilation

Dopamine Receptors

7 sub-types
Present in renal, splanchnic, coronary
& cerebral vascular beds
D4 receptors identified in the heart

Increases CO by
Improving contractility
Heart rate

D1, D2 receptors stimulate

diuresis & naturesis in the kidneys

Vasopressin (V1) Receptors

Present in smooth muscles of

peripheral arterioles
Stimulation causes
Increased vascular resistance
**Main compensatory mechanism in
hypovolemic shock

Increased BP due to baroreflex

Rationale for Vasopressor &

Inotrope Use
Shock
A final common pathway in

MI
Sepsis
Pulmonary embolism
Trauma
Anaphylaxis

 Types of shock
Hypovolemic
Cardiogenic
Neurogenic
Obstructive
Distributive
Septic

 Pathologic processes in septic

shock
Vasodilation (vasoplegia)
Maldistribution of blood flow
Myocardial depression

Management of Shock

Management of adequate
systemic pressure for optimal
tissue perfusion
Maintain MAP of 60 mm Hg

Fluid resuscitation
Optimize LV function via
inotropes and vasopressors

Vasopressors & Inotropes

Vasopressors
Increase SVR increase BP

Inotropes
Increases CO by contractility

 Note
Drugs may influence several
receptor sites
May be dose dependent
BP may increase via direct &
indirect responses

Phenylephrine (neosynephrine)
Vasopressin
Norepinephrine (Levophed)
Epinephrine
Dopamine
Dobutamine

Increased SVR

Decreased CO

Phenylephrine (neosynephrine)
Vasopressin
Norepinephrine (Levophed)
Epinephrine
Dopamine
Dobutamine

Decreased SVR

Increased CO

 Treatment of shock

Characterized by inadequate tissue perfusion

Results in impairment of oxygen & nutrient delivery
Causes hypotension
Progresses to multi organ system dysfunction

Reversal of the problem & correcting

hemodynamics
Fluid and/or blood resuscitation-initial
management of hypotension
Vasopressors -refractory hypotension despite
adequate resuscitation
Inotropes in low cardiac output states

Drug Overview

Phenylephrine (Neosynephrine)
Useful in neurogenic shock
Also when the SVR700 & CO not impaired
Hyperdynamic sepsis

Pure alpha activity veno & arteriororal

constriction
Minimal direct effects on inotropy or chronotropy
s/dBP, MAP
Reflex bradycardia
Minimal effects on heart rate or contractility
(arrhythmia potential minimal)
Decreased renal & splanchnic perfusion

Epinephrine

Potent beta-1 receptor activity

Beta-2 and alpha-1 receptor effects
CO, SVR, variable effects on MAP
Beta-1 effects may provoke arrhythmias
Greater degree of splanchnic
vasoconstriction
ACLS, anaphylaxis, second line agent in
shock, hypotension post CABG/open
heart

Vasopressin (ADH)

Regulates retention of water (not

salt)
Stimulates smooth muscle V-1
receptors
Vasoconstriction

Used in
DI
Esophageal variceal bleeding

Norepinephrine (Levophed)

Acts on Alpha-1 and Beta-1

receptors
Potent vasoconstriction venous
return increases
Less increase in CO
Reflex bradycardia
Low doses (2 mcg/min)- beta
adrenergic receptors
3 mcg/min- alpha receptors
vasoconstriction

Dopamine (Intropin)

Precursor of epinephrine
&norepinephrine
Mediated by dopaminergic
receptors
Dose dependent
Low doses (2-5 mcg/kg/min)
D-1 receptors in renal, mesenteric,
coronary, & cerebral beds leads to
vasodilation
Use of dopamine for acute renal failure not
supported and should be eliminated

Dopamine (Intropin)

Moderate doses (5-10 mcg)

Stimulates B-1 receptors
Increases CO by increasing SV
Variable effects on HR

Higher Doses
Pure alpha
Vasoconstriction
Increases SVR

Dopamine (Intropin)

Adverse Effects
Tachycardia,
Tachyarrhythmia
Excessive vasoconstriction (dose
dependent)
Increased myocardial O2 demand

Dobutamine (Dobutrex)

Not a vasopressor
Inotrope that causes vasodilation
Predominant beta-1 receptor activity
inotropy & chronotropy
LV filling pressures

Net effect:
CO
Decreased SVR (with or without a small
reduction in BP)
*CO may be decreased as a result of marked
decrease in SVR (afterload)

Deciding on the right vasopressor

In all shock states

Vasopressors should only be initiated with/after
adequate resuscitation is provided with
crystalloids, colloids, and/or blood products

Septic shock
Maintain MAP 65 mm Hg
Norepinephrine (Levophed) is the first line
agent when vasopressors indicated

Refractory septic shock

Add vasopressin, dopamine or epinephrine

 Cardiogenic shock
In low output cardiogenic shock,
Norepinephrine (Levophed), Dopamine +/Dobutamine

Hypovolemic shock
FLUIDS

Shock of unknown etiology

Dopamine

Neurogenic shock
Dopamine