What is the CNS nucleus or region of the Sympathetic and Parasympathetic systems?
Sympathetic => Rostral ventrolateral medulla (RVLM) Parasympathetic => Nucleus Ambiguus
What is the exit spinal cord for the Sympathetic and Parasympathetic systems?
Sympathetic => T1-L5 Parasympathetic => CN III, VII, IX, X and S2-4
Describe the pre/post-ganglionic fibers of the Sympathetic and Parasympathetic systems.
Sympathetic => short pre-ganglionic fibers; long post-ganglionic fibers Parasympathetic => long pre-ganglionic fibers; short post-ganglionic fibers
What is the ganglionic transmitter for the Sympathetic and Parasympathetic systems?
The sympathetic and parasympathetic BOTH use ACETYLCHOLINE as their ganglionic transmitter
What do Sympathetic and Parasympathetic post-ganglionic fibers release?
Sympathetic post-ganglionic fibers: - Norepinephrine --> cardiac muscle, smooth muscle, gland cells - Acetylcholine --> sweat glands - Dopamine --> renal vascular smooth muscle - Epinephrine + Norepinephrine --> adrenal medulla Parasympathetic post-ganglionic fibers: - Acetylcholine --> cardiac muscle, smooth muscle, gland cells
Which nerves make and package Ach and NE?
CHOLINERGIC nerves make and package--> Ach NORADRENERGIC nerves make and package --> NE
Name important cholinoceptors in the PNS.
Name important adrenoceptors in the sympathetic nervous system.
Describe what happens when your BP drops
1) Drop in BP is detected by vasomotor centers => activates the sympathetic autonomic nervous system (SANS)
2) SANS => constrict arterioles => increase in SVR/TPR => Increase in BP (MAP)
3) SANS => SA node => Increase in HR => Increase in CO => Increase in BP
4) SANS => LV => Increase contractility => Increases SV => Increase CO => Increase BP
5) SANS => Veins => Increase venomotor tone => Increase venous return => Increase SV
6) SANS => kidneys => Increase NaCl retention => Increase venous treurn => Increase SV
9) SANS => adrenals => Increase NE + Epi
7) Drop in BP is detected by vasomotor centers => depress parasympathetic autonomic nervous system => depression of SA node => Increase HR
8) Drop in BP is detected by baro-receptors => pituitary => Increase ADH => increase water retention => increase SV
Norepinephrine Pharm Card
Also known as: Noradrenaline, Levophed™
Epinephrine Pharm Card
Also known as: adrenaline,EpiPen™
What is the drug class for NE?
NE pharmacologic class: direct acting adrenergic agonist
NE therapeutic class: vasopressor, vasoconstrictor
Describe NE pharmacodynamics.
NE Pharmaco dynamics:
Major action => Vasoconstriction and cardiac stimulation
1) Stimulates peripheral alpha-1 adrenoceptors
- Leads to vasoconstriction (resistance arterioles, increase SVR) and venoconstriction (in capacitance vessels, increase prelaod)
- Increases CO, SVR, and MAP
- Decreases blood flow to skin, muscle, and kidney
2) Stimulates beta-1 receptors in the heart
- Increases HR and contractility
Describe NE pharmacokinetics.
- F ~ 100%
- Given IV ONLY
- Metabolized by COMT and MAO (liver)
- Metabolites are excreted in urine
- T1/2 = 1-2 minutes (can be titrated quickly IV)
- Can cross the placenta, but NOT blood/brain barrier
Describe NE toxicity.
1) Excessive vasoconstriction in mesenteric vessels, peripheral arterioles
- Leads to ischemia, infarction, and gangrene
* Reflex => bradycardia
Describe NE interactions.
1) Use cautiously in patients taking an MAO inhibitor (ie Phenelzine-use lower doses)
2) Risk of excessive hypertension in patints taking propranolol
What are special considerations for NE?
1) Correct volume depletion with IV fluids BEFORE giving NE infusion
2) Select infusion site carefully => extravasation is a major problem
3) Monitor patient and BP continuously in an ICU setting
4) Use catiously in pediatric and geriatric patients
What are the indications for NE use/dose/route?
- Used in adults with acute HYPOTENSION and SHOCK (related to low SVR)
- Infuse 2-12 mcg/min
What should be monitored in patients taking NE?
- Infusion site
- Evidence of extravasation
What is the drug class for Epi?
Epi pharmacologic class => direct acting adrenergic agonist
Epi therapeutic class => vasopressor, cardiac stimulatnt, bronchodilator, adjunct to local anesthetics, treatmetn ofr anaphylaxis
Describe Epi pharmacodynamics.
1) Stimulate peripheral alpha-1 adrenoceptors
- Vasoconstriction => resistance arteriles, increase SVR
- Venoconstriction => capacitance vessels, increase preload
2) Beta-1 receptors
- Tachycardia => increased contractility
3) Beta-2 receptors
- Bronchodilation => helpful in severe allergic reactions by stabilizing mast cells (anaphylaxis)
Describe Epi pharmacokinetics.
1) Can be given by:
- IV => immediate
- Intramuscular => variable
- Subcutaneously => 5-15 minutes
- Inhalation => 1-5 minutes onset
- Opthalmic => topical
2) Metabolized by COMT
3) Renally excreted
Describe Epi toxicity.
1) Excessive vasoconstriction
- Hemorrhagic stroke
Describe Epi interactions.
- Risk of excessive HTN in patients taking propranolol
What are special considerations for Epi?
1) Utility with local anesthetics
2) Drug of choice in severe anaphylactic reactions
What are the indications for Epi use/dose/route?
1) For anaphylaxis:
- 0.1-0.5 mg => Subcutaneously (SC) or Intramuscularly
2) For cardiac arrest:
- 1-5 mg IV push
- 1-4 mcg/min for infusion
What should be monitored in patients on Epi?
-Evidence of extravasation