Peripheral Nervous System- SNS Flashcards
What adrenergic receptors are most common on vascular smooth muscle
A1
What adrenergic receptors are most common in the brain and spinal cord
A2
What adrenergic receptors are most common in myocardium
B1
What adrenergic receptors are most common in airway smooth muscle
B2
What receptors are on smooth muscle of blood vessels, direct vasodilation, and kidney?
D1 (dopamine)
What receptors are most common of post-ganglionic sympathetic nerve terminals, glomeruli, renal cortex and renal tubules, adrenal cortex, chemoreceptor trigger zone, and indirect vasodilation?
D2 dopamine
What are the direct acting sympathoMIMETICS
*Catecholamines* Epinephrine Norepinephrine Isoproterenol Dopamine Dobutamine
How should catecholamines be administered?
By injection
Absorbed from respiratory tract
Poorly absorbed after oral administration-> high first pass effect
Do catecholamines cross the BBB?
No
What is the onset and duration of Catecholamines ?
Rapid
Emergency use
What are the adverse effects of catecholamines ?
Narrow safety margin
Short half life
Predispose myocardium to tachycardia and tachyarrhythmias
Anxiety, restlessness, tremors
Altered perfusion-> direct to “flight tissue”
Extravasation of Norepinephrine or Dopamine can cause tissue damage and sloughing
Cerebral hemorrhange
What adrenergic receptor does epinephrine not have affinity for?
Dopamine
What receptor does norepinephrine not have receptor affinity for ?
B2 and Dopamine
What receptors does Isoproterneol have affinity for?
B1 and B2
What receptors does dopamine have affinity for?
Dopamine (low dose)
B1 (med dose)
A1 (high dose)
How is norepinephrine degraded/removed form the nerve endings?
Active uptake (50-80%) Diffusion Destruction -MAO= mono-amine oxidase (nerve endings) -COMT= catecholamine O-methyl transferease (tissue)
How is norepinephrine / epinephrine removed from the circulation
COMT destroy in tissues
Liver
Effects peak 10-30seconds, absent by 1 min
What is the mechanism of action of epinephrine
Direct acting catecholamine sympathomimetic
Competitive agonist at all alpha and beta receptors
Epinephrine will cause _________ at the B1 receptors
Cardiac contraction
Epinephrine will cause _________ at B2 receptors
Bronchodilation and vasodilation
Epinephrine will cause ___________ at a1 receptors
Vasocontriction
Epinephrine can be administered by what routes?
IV, IM, SQ, inhaled, IO
What are the systemic indications for using Epinephrine?
- *Cardiopulmonary arrest (CPA)
- *Anaphylaxis
- *Increase mean arterial pressure by increasing systolic arterial pressure (SAP)
Vasopressor
Positive inotrope
What local effects can epinephrine be used for?
Local anesthetic (i.e. Lidocaine) to produce regional vasoconstriction -> delay systemic absorption
Topically to treat local hemorrhage
What are precautions to using epinephrine?
Causes massive sympathetic output
-increase myocardial workload and oxygen demand
–> increased myocardial oxygen consumption (MvO2)
Can result in myocardial ischemia
Cardiac arrest is possible
What is the MOA of norepinephrine
Direct catecholamine sympathomimetic
Mainly through a1 agonism
What are the indications for using Norepinephrine ?
Vasopressor support of CV is needed
Treat hypotension
Eg. Septic shock = sepsis and hypotension leading to refractory volume expansion
What is the main clinical effect of using Norepinephrine
Vasocontriction (a1 agonist-> MOST important catecholamine vasopressors)
Less of an increase in MvO2 than with epinephrine
What re the precautions and contraindications to using Norepinephrine
Cardiac arrhythmias/ tachyarrhythias -> major adverse effect of concern
-> used cautiously and with ECG
Do not use in hypertensive patients