Always Alpha block then Beta block 

Surgeon should tell you when lifting the tumor to ligate b/c pt willhave massive vasodilation 

Catecholamine depletion

Down regulation of beta receptors 

Site of involuntary control

Principle site of ANS organization 

Highest level of ANS integration

Controls the ANS during periods of extreme stress 

Thirst Center- fluid balance 

Uterine contractions and milk production

Satiety 

Temperature

Endocrine hormone secretion

Medulla and Pons Controls

(Brainstem)

Momentary Hemodynamics

Tonic quality of vessels- partial vasoconstriction

Ventilation- respiratory center 

T1-T12

L1-L3 

(Thoracolumbar) 

Crianal nerves 3,7,9,10

Sacral 2-4 

(Craniosacral)

Directly innervated by preganglionic sympathetic fibers

Causes chroffain cells to release Epi (80%) and NORE (20%) 

Short Preganglionic Fibers that release ACTH to Nicotinic receptors on Long postganglionic fibers.

Long Postganglionic fibers release catecholamines (Epi, NORE, Dopa) to effector organs which have adrenergic receptors (alpha, beta, dopa) 

Long preganglionic fibers that release ACTH to nicotinic receptors on short postganglionic fibers.

Short postganglionic fibers release ACTH to muscarinic receptors on effector organs 

Unipolar

Myleinated

Sensory Neurons 

(Somatic or Autonomic) 

Afferent Fibers

Enter through the dorsal root ganglia 

Bipolar 

Preganglionic myleinated

Postganglionic unmylinated 

Bradycardia

Decreased Inotropism

Miosis (pin-point)

Salivation

GI Motility

Increased Gastric acid secretion 

Increased BP

Increased Left ventricular contractility 

(Minimal Effect on HR) 

Decreased Systolic duration

Increased HR 

Left Stellate Ganglia Controls 

(Area of the Heart)

Right Stellate Ganglia Controls

(Area of the Heart)

Phrenic Blockade- dyspnea

Recurrent Laryngeal Nerve Blockade- Horseness

Accidential Injection

Pneumothorax

Hematoma

Direct nerve injury 

Horner's Syndrome (myosis, ptosis, anhidrosis, vasodilation) 

Strong effect on ventricular contractility

Less effect on HR

SA node, AV node, and Atria

Strong vagal discharge- effects HR

Minimal effect on contracility 

alpha produces vasoconstriction

beta produces vasodilation 

Vasodilation only in the genitals 

Bronchodilation (B2)

Pulmonary vasoconstriction 

Bronchoconstriction 

No pulmonary vasodilation (cannot override hypoxic pulmonary vasoconstriction) 

Survery Resistance and Afterload

Carotid sinus --> Glossopharyngeal-->Hering's Nerve--> Medulla 

Located in the large system arteries (Carotids)

Increase in afterload tell CNS to tell ANS to reduce normal artieral pressure and vice versa 

Venous Baroreceptor Reflex

(Bainbridge Relfex)

Most important for moment to moment control

Detects the degree of stretch in the atria- Increased stretch causes increased HR, decreased stretch causes decreased HR

Prevents blood from backing up into lungs 

Atria-->Vagal Stimulation-->Medulla 

Buffer for blood pressure from extreme highs and lows

Decreases daily variation to 1/2 or 1/3

Down regulation of receptors makes system less responsive (CHF, sleep deprived) 

Occurs within 1-2 days 

Onset of acute HTN, barorecptors will reset to new high 

Low O2

High CO2

Low pH 

Follow the same path as barorecptors

Carotids: Hering's-->medulla

Aortic: Vagus-->medulla 

Most powerful of all the SNS vasoconstriction system

When the brain realizes it isnt getting enough O2 it will have massive arterial vasoconstriction as a last ditch effort to get O2 to the brain 

(Decreased blood flow to medullary center)

ICP level are increased to Aterial Pressure

Cerebral arteries compress to low or no blood flow

Causes arterial BP to rise (vasoconstriction) above CSF 

This leads to reflex bradycardia 

Prolonged ischemia leads to cell death and loss of autoregulation which cause arterial BP to fall and death 

Nerve innervation is lost

Atropine will NOT work

Need direct beta agonist (isopril and maybe Epi)

Barorecptor reflexs do not work 

Flaccid paralysis, loss of sensation, loss of spinal reflexes, bradycardia, hypotension, loss of temp regulation

Shock usually resolves in 1-3 weeks

Incidence in 85% quadraplegics and high paraplegics (T6 or higher)

Stimulation below transection causes sympathetic reponse with no high brain function modulation 

Stimulation caused by full bladders, pain, debridments, catherization, pelvics

Tyrosine Hydroxalase 

It converts Tyrosine-->Dopa-->Dopamine-->NE

NE prevents Tyrosine Hydroxalase therefore creating feedback inhibition

Causes increased intracellular calcium

Can cause constriction or relaxation

cAMP is deactivated by phosphodiesterase 

Alpha 2: Inhibits further NE release

Beta 2: Accelerates NE release in synaptic cleft

DA 2: Inhibits NE release

NE itself inhibits conversion of tyrosine to dopa 

Inhibit reuptake of NE, serotonin, and dopamine

Can have exaggerted response to catecholamines

Inhibit the metabolism of NE and Epi by blocker MOA

Can have exaggereated response to catecholamines 

5 mg in adult 

Dose: 0.04-0.08 mg/kg 

Onset: 5 min

Peak: 10 min

Duration 60 min

Adm with 0.2 mg/kg Glycoparrulate 

Irreversible cholinesterase inhibitor

Used to treat glaucoma 

May cause a prolonged effect of Succinylcholine in pts

SLUDGEM

Treat with atropine

Can be caused by too much anticholinesterases (neostigmine) or sarin nerve gas

35-70 mcg/kg every 3-10 mins 

From antimuscarinic overdose (atropine, scopalamine, glycopyrrulate)

Stupor, coma, delirum, hallucinations, dry mouth, blurred vision, hot, dry, flush

Give Physostigmine -1 mg