Sympathetic Nervous System Flashcards
Peripheral collection of nerve cell bodies
Ganglion
Number of paired sympathetic ganglia
22
SNS preganglionic pathway to sympathetic chain
Myelinated B fibers exit spinal cord via ventral nerve roots > white communicating rami > sympathetic chain
Preganglionic sympathetic axons (C fibers) that traverse uninterrupted through the sympathetic trunk form____
Splanchnic nerves
Collection of plexuses that surrounds the abdominal aorta
Abdominal prevertebral plexus
Abdominal prevertebral plexuses
Celiac plexus
Aortic plexus
Superior hypogastric plexus
Inferior hypogastric plexus (pelvic)
Location of cell bodies of preganglionic sympathetic fibers
Interomediolateral horn of the spinal cord (Rexed’s lamina 7)
Inferior cervical ganglion + T1 ganglion
Stellate (cervicothoracic) ganglion
SNS innervation of the stellate ganglion
Ipsilateral head, neck, and upper extremity
Indications for blocking stellate ganglion
Treatment of:
Upper extremity sympathetic dystrophy
Complex regional pain syndrome
Increase blood flow to the upper extremity
Provide relief from intractable post-MI pain
Horner’s syndrome symptoms
Ipsilateral ptosis, miosis, anhidrosis, flushed skin, nasal congestion, and enopthalmos
Alternate name for adrenal glands
Surarenal glands
Two divisions of adrenal glands
Medulla
Cortex
Adrenal medulla function
Secretes catecholamines
Adrenal cortex function
Secretes glucocorticoids, mineralcorticoids, and androgens
Autonomic innervation of adrenal glands
Preganglionic sympathetic nerves T5-T9
No postganglionic nerves
Mechanism of adrenal stimulation
Preganglionic fibers release ACh onto chromaffin cells > NnACh receptor stimulaiton > chromaffin cells release epinephrine and norepinephrine directly into circulation
Rate/ ratio of catecholamine release from adrenal medulla at rest
Epi: 0.2mcg/ kg/ min (80%)
NE: 0.05mcg/ kg/ min (20%)
Catecholamine- secreting tumor usually arising from the adrenal gland or extra chromaffin tissue
Pheochromocytoma
Pheochromocytoma triad of symptoms
Headache
Diaphoresis
Tachycardia
Pheochromocytoma diagnostic
Elevated level of VMA
Pheochromocytoma preoperative treatment
Alpha blockade THEN beta blockade
Non-selective alpha blockers
Phenoxybenzamine
Phentolamine
Alpha-1 selective blockers
Doxazosin
Prazosin
What happens if beta is blocked before alpha in the presence of pheochromocytoma?
Heart failure
Anesthetic considerations for pheochromocytoma removal surgery prior to tumor ligation
Treat hypertension
Treat tachycardia
Monitor serum glucose throughout (anticipate hyperglycemia)
Intraoperative/ preoperative treatments for htn in patients undergoing pheochromocytoma removal surgery
Sodium nitroprusside
nitroglycerine
Clevidipine
Nicardipine
Deepening anesthetic
Intraoperative/ preoperative treatments for tachycardia in patients undergoing pheochromocytoma removal surgery
Short-acting beta blockers like esmolol (caution with cardiomyopathy)
Intraoperative/ preoperative considerations following removal of a pheochromocytoma
Hypotension = tx with phenylephrine, NE, vasopressin, or IVF
Consider steroid supplementation if both adrenal glands were removed or manipulated during surgery
Drugs to avoid in pheochromocytoma removal surgery
Histamine- releasing drugs (succinylcholine, atracurium, mivacurium, morphine)
Indirect-acting sympathomimetic agents
SNS activators: desflurane, ketamine, pancuronium, naloxone
SNS activation effects on serum glucose and potassium
Stimulates hepatocytes to release more glucose and potassium
SNS activation effects on insulin
Stimulates pancreatic beta cells to increase insulin output
Two phases to K+ response to SNS stimulation
Initial rise (short-lived)
Longer term effect is decreased K+
Why does K+ decrease with SNS stimulation
Adrenal medulla secretes catecholamines > epi binds to beta-2 receptors on skeletal muscle and erythrocytes = Na+/K+ pump activation = decrease in K+ concentration
Factors that impact serum K+ concentration
Beta-2 agonism (Epi, albuterol)
Methylxanthines (Theophylline)
Nicotinic type-M agonism (succinylcholine)
Destruction of cell membranes (rhabdomyolysis)
Activating H+/K+ exchanger (acidosis)
Hyperventilation (alkalosis)
Activating the Na+/ K+ exchanger (Epi, insulin)