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Vasopressors
Dr. Ahmad Nabries
Introduction
Inotropes :
Primarily increases myocardial contractility, by
increasing the velocity and the force of
myocardial fibre shortening; also have effect on
peripheral vasculature dan HR
Vasopressors : increases SVR
BP = CO X SVR
CO = SV X HR
SV
Preload
Afterload
Contractility
Introduction
Sympatomimetics
Mimic the effects of neurotransmitter
substances of the sympathetic nervous
system
Receptors
1. Alpha : 1 & 2
2. Beta : 1, 2 & 3
3. Dopamine
Figure 2. Schematic representation of postulated mechanisms of intracellular action of 1adrenergic agonists. 1-Receptor stimulation activates a different regulatory G protein (Gq),
which acts through the phospholipase C system and the production of 1,2-diacylglycerol
(DAG) and, via phosphatidyl-inositol-4,5-biphosphate (PiP2), of inositol 1,4,5-triphosphate
(IP3).
Figure 1. Simplified schematic of postulated intracellular actions of -adrenergic agonists. Receptor stimulation, through a stimulatory Gs-GTP unit, activates the adenyl cyclase
system, which results in increased concentrations of cAMP.
Overgaard C B , and Davk V Circulation. 2008;118:10471056 Copyright American Heart Association, Inc. All rights reserved.
Sympatomimetics
Catecholamine
Non-catecholamine
Catecholamine
Is a monoamine, an organic compound that
has acatechol (benzene with
two hydroxylside groups) and a sidechain amine
Catecholamine
Epinephrine (adrenaline),
Norepinephrine (noradrenaline) and
Dopamine
All of which are produced from phenylalanine
and tyrosine
Dobutamine (synthetic)
Isoproterenol (synthetic)
Non-catecholamine
Ephedrine
Pseudoephedrine
Amphetamine,
Cocaine,
Phenylephrine,
Tetrahydrozoline,
Naphazoline,
Oxymetazoline,
Ritodrine,
Metaproterenol,
Albuterol,
Terbutaline,
Salbutamol
Inotropic Agents
Phosphodiesterase
Inhibitors
Phosphodiesterase 3 is an intracellular
enzyme that breaks down cAMP into AMP.
(PDIs) increase the level of cAMP by
inhibiting its breakdown within the cell, which
leads to increased myocardial contractility
These agents are potent inotropes and
vasodilators and also improve diastolic
relaxation (lusitropy), thus reducing preload,
afterload, and SVR
Vasopressors
Isoproterenol
Norepinephrine
Epinephrine
Ephedrine
Phenylephrine
Vasopressin
Dobutamine
Dopamine
Pharmacology
Drug
Clinical Indication
Dose Range
Receptors
-1
-2
-1
-2
+++
++++
++
+++++
Severe hypertension
(especially in
patients taking nonselective
-blockers)
Ventricular arrhythmias
Cardiac ischemia
Tissue ischemia/gangrene
(high doses
or due to tissue
extravasation)
Catecholamine
Dopamine
Shock (cardiogenic,
vasodilatory)
HF
Symptomatic
bradycardia
unresponsive to atropine
or pacing
2.0 to 20 mcg
/kg/min
max 50 mcg
/kg/min
Dobutamine
Low CO
(decompensated HF,
cardiogenic shock,
sepsis-induced
myocardial
dysfunction)
Symptomatic
bradycardia
unresponsive to atropine
or pacing
2.0 to 20 mcg
/kg/min
max 40 mcg
/kg/min
+++++
+++
N/A
Tachycardia
Increased ventricular
response rate in
patients with atrial fibrillation
Ventricular arrhythmias
Cardiac ischemia
Hypertension (especially
nonselective
beta-blocker patients)
Hypotension
Norepinephrine
Shock (vasodilatory,
cardiogenic)
0.01 to 3
mcg/kg min
+++++
+++
++
N/A
Arrhythmias
Bradycardia
Peripheral (digital) ischemia
Hypertension (especially
nonselective
beta-blocker patients)
Drug
Clinical Indication
Dose Range
Receptors
-1
-2
-1
-2
+++++
++++
+++
N/A
Ventricular arrhythmias
Severe hypertension
resulting in
cerebrovascular hemorrhage
Cardiac ischemia
Sudden cardiac death
+++++
++++
+
N/A
Ventricular arrhythmias
Cardiac ischemia
Hypertension
Hypotension
Catecholamine
Epinephrine
Shock (cardiogenic,
vasodilatory)
Cardiac arrest
Bronchospasm/anaphyl
axis
Symptomatic
bradycardia or
heart block
unresponsive to
atropine or pacing
Isoproterenol
Bradyarrhythmias
(especially
torsade des pointes)
Brugada syndrome
Infusion: 0.01 to
0.10
mcg /kg/min
Bolus: 1 mg IV
every 3 to 5
min (max 0.2
mg/kg)
IM: (1:1000):
0.1 to 0.5 mg
(max 1 mg)
2 to 10 mcg/min
Drug
Clinical Indication
Dose Range
Receptors
-1
-2
-2
PDI
Milrinone
Low CO
(decompensated HF,
after cardiotomy)
N/A
N/A
Amrinone
Vasopressin
Shock (vasodilatory,
cardiogenic)
Cardiac arrest
Ventricular arrhythmias
Hypotension
Cardiac ischemia
Torsade des pointes
V1 receptors (vascular
smooth muscle)
V2 receptors (renal
collecting duct system)
Arrhythmias, enhanced AV
conduction
(increased ventricular response
rate in
atrial fibrillation)
Hypotension
Thrombocytopenia
Hepatotoxicity
Arrhythmias
Hypertension
Decreased CO (at doses 0.4
U/min)
Cardiac ischemia
Severe peripheral
vasoconstriction
causing ischemia (especially
skin)
Splanchnic vasoconstriction
Inotropes
Dopamine
Dobutamine
Dose
Mechanis
m of
Action
1-5
mcg/kg/
min
Dopamine
rgic
agonist
6-10
mcg/kg/
min
HR
Systolic
Diastolic
Myocard
demand O2
SVR
PVR
Increase
Minimal
No effect
Minimal
increase
Minimal
increase
No effect
Beta 1
agonist
Increase
Increase
No effect
Increase
Increase
Minimal
increase
11-20
Alpha
agonist
Increase
Increase
No effect
increase
Significan
t increase
Minimal
increase
1-10
mcg/kg/
min
Beta 1
agonist,
alpha anti
agonist
increase
increase
No effect
increase
Minimal
effect
/decrease
Minimal
decrease
Inotropes
Dose
Mechanis
m of
Action
HR
Systolic
Diastolic
Myocard
demand
O2
SVR
PVR
Epinephrine
0.01-1
mcg/kg/
min
Beta 1
agonist>A
lpha
agonist
Increase
Significant
increase
No effect
Significant
increase
Increase
Minimal
increase
Norepineph
rine
0.01-1
mcg/kg/
min
Beta 1
agonist<A
lpha
agonist
Increase
Some
Increase
No effect
Increase
Significant
increase
Minimal
increase
Milrinone
0.1-1
mcg/kg/
min
PDI
No
Change
Increase
Improves
Minimal
increase
Decrease
Decrease
Therapeutic
Use
Grazie
Muchas gracias
Thank you
Tarimo kasiah
Arigato Gozaimasu
Danke schon
Matursuwun
Merci