©SIRJOEL EXAM SOLUTIONS
10/14/2024 11:14 PM
Comprehensive CRNA Interview Review
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
, ©SIRJOEL EXAM SOLUTIONS
10/14/2024 11:14 PM
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
, ©SIRJOEL EXAM SOLUTIONS
10/14/2024 11:14 PM
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.
, ©SIRJOEL EXAM SOLUTIONS
10/14/2024 11:14 PM
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.
.1-.5 mg/kg IVP analgesia
1-5 mg/kg IVP dissociation (procedural)
15-90 mcg/kg/min or 1-6 mg/min for maintenence of anesthesia.
Care is to be taken as to not induce a subdissociative like state.
DSI/RSI/RSA
adjunct analgesic in opiate dependent patients.
Nicardapine MOA - answer✔Voltage sensitive calcium channels regulate the influx and release
of calcium in response to action potential and depolarizing signals. Nicardapine inhibits the
influx of calcium through these channels thus affecting calcium concentrations. This inhibition
results in vasodilation more specific to coronary and cerebral vessels. This vasodilation
decreases SVR and opens up the afterload of the heart, increases oxygen delivery and blood flow
during vasospastic states, regulates blood pressure during hypertensive emergencies and post
transplantation where goal blood pressures need to be tightly met.
Has little affect on SA/AV nodal conduction velocity.
Begin infusion at 5 mg/hr and titrate by 2.5 every 5-15 minutes for goal blood pressure.
Clavidipine MOA - answer✔Inhibiting influx of Calcium in L-type calcium channels in arterial
smooth muscle to decrease SVR.
10/14/2024 11:14 PM
Comprehensive CRNA Interview Review
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
, ©SIRJOEL EXAM SOLUTIONS
10/14/2024 11:14 PM
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
, ©SIRJOEL EXAM SOLUTIONS
10/14/2024 11:14 PM
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.
, ©SIRJOEL EXAM SOLUTIONS
10/14/2024 11:14 PM
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.
.1-.5 mg/kg IVP analgesia
1-5 mg/kg IVP dissociation (procedural)
15-90 mcg/kg/min or 1-6 mg/min for maintenence of anesthesia.
Care is to be taken as to not induce a subdissociative like state.
DSI/RSI/RSA
adjunct analgesic in opiate dependent patients.
Nicardapine MOA - answer✔Voltage sensitive calcium channels regulate the influx and release
of calcium in response to action potential and depolarizing signals. Nicardapine inhibits the
influx of calcium through these channels thus affecting calcium concentrations. This inhibition
results in vasodilation more specific to coronary and cerebral vessels. This vasodilation
decreases SVR and opens up the afterload of the heart, increases oxygen delivery and blood flow
during vasospastic states, regulates blood pressure during hypertensive emergencies and post
transplantation where goal blood pressures need to be tightly met.
Has little affect on SA/AV nodal conduction velocity.
Begin infusion at 5 mg/hr and titrate by 2.5 every 5-15 minutes for goal blood pressure.
Clavidipine MOA - answer✔Inhibiting influx of Calcium in L-type calcium channels in arterial
smooth muscle to decrease SVR.
