CRNA Reviewed Questions
And Correct Answers
GRADED A+
Norepinephrine Mechanism of Action (MOA) - ANS-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 - ANS-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 - ANS-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 - ANS-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 - ANS-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 - ANS-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 - ANS-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.
And Correct Answers
GRADED A+
Norepinephrine Mechanism of Action (MOA) - ANS-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 - ANS-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 - ANS-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 - ANS-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 - ANS-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 - ANS-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 - ANS-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.
