CRNA Interview With Complete Solution 2024-2025
Norepinephrine 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).
However, alpha 2 adrenoreceptor agonism paradoxically antagonizes the release of
norepinephrine in the CNS. 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 is sufficient to overcome these A1 effects via increased inotropy
and chonotropy 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 sum 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) regulation of the volume of extracellular fluid through its effects 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, producing vasoconstriction.
Normal concentrations of the drug are below it's vasoactive range, however in profound
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
Norepinephrine 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).
However, alpha 2 adrenoreceptor agonism paradoxically antagonizes the release of
norepinephrine in the CNS. 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 is sufficient to overcome these A1 effects via increased inotropy
and chonotropy 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 sum 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) regulation of the volume of extracellular fluid through its effects 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, producing vasoconstriction.
Normal concentrations of the drug are below it's vasoactive range, however in profound
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
