CRNA Interview Exam Questions and
Answers
Norepinephrine Mechanism of Action (MOA) - Answers -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 - Answers -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 - Answers -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 - Answers -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 - Answers -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 - Answers -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.
Answers
Norepinephrine Mechanism of Action (MOA) - Answers -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 - Answers -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 - Answers -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 - Answers -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 - Answers -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 - Answers -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.
