Norepinephrine Mechanism of Action (MOA) - ANSWER A1, A2, B1 agonist.
Primary agent used in distributive shock because it's ability to recruit venous volume and augment
preload, while increasing arterial tone, and increasing cardiac output.
Alpha one causing peripheral smooth muscle contraction. (low dose venous, high dose venous and
arterial).
Alpha 2 adrenoreceptor agonism actually antagonizes the release of norepinephrine in the CNS, but
these receptors are less present in peripheral vasculature and thus, their anti-hypertensive effects are
overtaken by A1 agonism.
These alpha effects can increase SVR and thereby increase cardiac workload, decrease cardiac output,
and increase coronary perfusion pressure.
The slight B1 agonism increases inotropy and chonotropy sufficiently to overcome these A1 effects and
result in a fairly "pure" vasopressor. Increasing contraction of the heart and increasing AV nodal
conduction.
**First line agent in septic shock
Epinephrine MOA - ANSWER A1
A2
B1 - Stimulate Heart Rate through SA node, increase conduction through AV node. Increase contractility
to ATRIAL and VENTRICULAR cardiac muscle.
,B2 - Smooth muscle relaxation. Resulting in dilation of the bronchial tree, coronary arterial dilation. Also
plays a role in insulin and glucagon secretion in the pancreas. Also increases cardiac
inotropy/chonotropy
B3 - Increase lypolysis and thermogenesis in brown adipose tissue.
**Cardiogenic shock or other shock states with a cardiac component.
Adjunctive therapy in severe septic shock
IVP in cardiac arrest to augment CPP
IVP while introducing PPV/intubation
Precedex MOA - ANSWER Dexmetatomadine is an alpha 2 adrenoreceptor agonist that acts both on the
presynaptic neuron and postsynaptic neuron. Inihibiting norepinephrine release pre-synaptically
reduces/halts the transmission of pain, while postsynaptically acts to reduce sympathetic tone. The
combination of these effects is anesthesia with analgesia and anxiolysis.
loading dose is 1 mg/kg while gtt is .2-1.5 mg/kg/hr
**This agent is often used for patients who would not tolerate a precipitous drop in their sympathetic
tone, for those patients in severe alcohol withdrawal.
propofol MOA - ANSWER Propofol is a lypophylic general anesthetic unlike any drugs of the class
benodiazapen, barbituate, or A2 agonist. Its mechanism is proposed to be a GABA (inhibitory
neurotransmitter) agonist causing global CNS depression
Dosing for procedural sedation of .1-.5 mg/kg as a loading dose with repeat doses. gtt titration ranging
from 10-60 mcg/kg/min
**Anesthetic
Sedation for mechanically ventilated ICU patients
Procedural sedation
, Phenylephrine MOA - ANSWER Pure Alpha adrenergic receptor agonist. Causing increase in SVR through
systemic arterial vasoconstriction. This also causes a dose dependent increase in systolic and diastolic
blood pressure and thereby decreasing cardiac output, especially in patients with heart failure.
40-100 mcg IVP for hypotension during anesthesia
Titrated as a drip from .5-9 mcg/kg/min
**used rarely as adjuncitve therapy for patients in septic shock.
Used more often in vasodilatory shock states such as neurogenic shock/ shock from epidural/spinal
blocks.
vasopressin MOA - ANSWER arganine/vasopressin receptor agonist causing potent increase in SVR
through 2 different MOA.
1) regulate extracellular fluid volume acting on renal collecting ducts and distal convoluted tubule to
increase water permeability via v2 receptors
2)Sodium re-absorption across the ascending loop of HENLe.
3)Binding to V1 receptors on vascular smooth muscle, causing vasoconstriction.
Normal concentrations of the drug are below it's vasoactive range, nevertheless in severe hypovolemic
shock, AVP increases do contribute to increase in SVR.
1.8 u/hr
**used as adjunctive therapy in septic shock. Can be used as a first line agent in a pulmonary
hypertensive patient in shock states.
Ketamine MOA - ANSWER NMDA receptor antagonist blocking glutamate and thus introducing a
cateleptic/dissociative (which is dose dependent) state.
N-Methyl-D-Aspartate is a receptor in the CNS responsible for conduction of action potentials associated
with memory. Antagonizing these receptors does not allow for the transmission of these signals.
Primary agent used in distributive shock because it's ability to recruit venous volume and augment
preload, while increasing arterial tone, and increasing cardiac output.
Alpha one causing peripheral smooth muscle contraction. (low dose venous, high dose venous and
arterial).
Alpha 2 adrenoreceptor agonism actually antagonizes the release of norepinephrine in the CNS, but
these receptors are less present in peripheral vasculature and thus, their anti-hypertensive effects are
overtaken by A1 agonism.
These alpha effects can increase SVR and thereby increase cardiac workload, decrease cardiac output,
and increase coronary perfusion pressure.
The slight B1 agonism increases inotropy and chonotropy sufficiently to overcome these A1 effects and
result in a fairly "pure" vasopressor. Increasing contraction of the heart and increasing AV nodal
conduction.
**First line agent in septic shock
Epinephrine MOA - ANSWER A1
A2
B1 - Stimulate Heart Rate through SA node, increase conduction through AV node. Increase contractility
to ATRIAL and VENTRICULAR cardiac muscle.
,B2 - Smooth muscle relaxation. Resulting in dilation of the bronchial tree, coronary arterial dilation. Also
plays a role in insulin and glucagon secretion in the pancreas. Also increases cardiac
inotropy/chonotropy
B3 - Increase lypolysis and thermogenesis in brown adipose tissue.
**Cardiogenic shock or other shock states with a cardiac component.
Adjunctive therapy in severe septic shock
IVP in cardiac arrest to augment CPP
IVP while introducing PPV/intubation
Precedex MOA - ANSWER Dexmetatomadine is an alpha 2 adrenoreceptor agonist that acts both on the
presynaptic neuron and postsynaptic neuron. Inihibiting norepinephrine release pre-synaptically
reduces/halts the transmission of pain, while postsynaptically acts to reduce sympathetic tone. The
combination of these effects is anesthesia with analgesia and anxiolysis.
loading dose is 1 mg/kg while gtt is .2-1.5 mg/kg/hr
**This agent is often used for patients who would not tolerate a precipitous drop in their sympathetic
tone, for those patients in severe alcohol withdrawal.
propofol MOA - ANSWER Propofol is a lypophylic general anesthetic unlike any drugs of the class
benodiazapen, barbituate, or A2 agonist. Its mechanism is proposed to be a GABA (inhibitory
neurotransmitter) agonist causing global CNS depression
Dosing for procedural sedation of .1-.5 mg/kg as a loading dose with repeat doses. gtt titration ranging
from 10-60 mcg/kg/min
**Anesthetic
Sedation for mechanically ventilated ICU patients
Procedural sedation
, Phenylephrine MOA - ANSWER Pure Alpha adrenergic receptor agonist. Causing increase in SVR through
systemic arterial vasoconstriction. This also causes a dose dependent increase in systolic and diastolic
blood pressure and thereby decreasing cardiac output, especially in patients with heart failure.
40-100 mcg IVP for hypotension during anesthesia
Titrated as a drip from .5-9 mcg/kg/min
**used rarely as adjuncitve therapy for patients in septic shock.
Used more often in vasodilatory shock states such as neurogenic shock/ shock from epidural/spinal
blocks.
vasopressin MOA - ANSWER arganine/vasopressin receptor agonist causing potent increase in SVR
through 2 different MOA.
1) regulate extracellular fluid volume acting on renal collecting ducts and distal convoluted tubule to
increase water permeability via v2 receptors
2)Sodium re-absorption across the ascending loop of HENLe.
3)Binding to V1 receptors on vascular smooth muscle, causing vasoconstriction.
Normal concentrations of the drug are below it's vasoactive range, nevertheless in severe hypovolemic
shock, AVP increases do contribute to increase in SVR.
1.8 u/hr
**used as adjunctive therapy in septic shock. Can be used as a first line agent in a pulmonary
hypertensive patient in shock states.
Ketamine MOA - ANSWER NMDA receptor antagonist blocking glutamate and thus introducing a
cateleptic/dissociative (which is dose dependent) state.
N-Methyl-D-Aspartate is a receptor in the CNS responsible for conduction of action potentials associated
with memory. Antagonizing these receptors does not allow for the transmission of these signals.
