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Sarah's Apex > Autonomic nervous system > Flashcards

Autonomic nervous system Flashcards

1
Q

What are the 4 classifications of receptors?

A

A receptor receives the signal and instructs the cell to perform a specific function. Signal transduction is the process by which a cell converts this extracellular signal into an intracellular response.

Receptor classifications:
* Ion channel
* G-protein
* Enzyme-linked receptor
* Intracellular receptor

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2
Q

Describe the general architecture of the G protein second messenger system.

A

This is one area where it’s easy to get lost in the details. Your life will be easier if you understand the general architecture of the G protein system BEFORE trying to memorize the specifics about each receptor.
* 1st messenger (extracellular signal)
* Receptor (responds to the extracellular signal)
* G protein ( turns on or turns off an effector)
* Effector (activates or inhibits the second messenger)
* Enzymatic cascade ( a bunch of steps you don’t have to worry about)
* Cellular response (causes a physiologic change)

Remember that second messengers are tissue specific. For example, cAMP may cause a response in one cell type while causing a different response in a different cell type.

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3
Q

What second messenger system is associated with the alpha-1 receptor? what other receptors share a similar pathway?

A

Other receptors that share a similar 2nd messenger pathway:
* Histamine-1
* Muscarinic-1
* muscarinic-3
* Muscarinic-5
* Vasopressin-1 (vascular)

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4
Q

What second messenger system is associated with the alpha-2 receptor? What other receptors share a similar pathway?

A

Other receptors that share a similar 2nd messenger pathway.
* Muscarinic-2
* Dopamine-2 (presynaptic)

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5
Q

what second messenger system is associated with the beta-1 AND beta -2 receptor? What other receptors share a similar pathway?

A

Other receptors that share a similar 2nd messenger pathway:
* Histamine-2
* Vasopressin-2 (renal)
* Dopamine (postsynaptic)

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6
Q

Describe the autonomic innervation of the heart.

A

Heart:
Myocardium: Beta 1
conduction system: Beta 1
-> increased contractility, heart rate, conduction speed
-> M2-> Decreased contractility, heart rate and Conduction velocity

SNS: The cardiac accelerator fibers arise from T1-T4
PNS: Vagus nerve (CN X)

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7
Q

Describe the autonomic innervation of the vasculature

A

Vasculature
Arteries: a1>a2 : Vasoconstriction
Veins: a2>a1 : Vasoconstriction

Specific vascular beds
Myocardium : B2 : vasodilation
Skeletal muscle B2: Vasodilation
Renal: DA : Vasodilation
Mesenteric: DA: Vasodilation

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8
Q

Describe the autonomic innervation of the bronchial tree.

A

Beta-2 receptors are not innervated. Instead, they respond to catecholamines in the systemic circulation or in the airway (inhaled)

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9
Q

Describe the autonomic innervation of the kidney

A

Renal tubules: a2: diuresis (ADH inhibition)
Renin release: B1 : increased renin release

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10
Q

Describe the autonomic innervation of the eye.

A

Sphincter muscle (iris): -: -: M: Contraction (miosis)
Radial muscle (iris): a1: Contraction (mydriasis): -: -
Ciliary muscle: B2: relaxation (far vision): M: contraction (near vision)

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11
Q

Describe the autonomic innervation of the GI tract

A
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12
Q

Describe the autonomic innervation of the pancreas

A

Islet (beta cells): Alpha 2: Decrease insulin release
Beta 2: Increase insulin release

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13
Q

Describe the autonomic innervation of the bladder

A

Trigone & Sphincter: Alpha 1: contraction: M: Relaxation
Detrusor: Beta 2: Relaxation: M: contraction

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14
Q

List the steps of norepinephrine synthesis. What is the rate limiting step?

A

Norepinephrine is the primary neurotransmitter in the sympathetic nervous system.

Notice how and where EPI is synthesized

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15
Q

what are the 3 ways that NE can be removed from the synaptic cleft? Which is the most important?

A

NE is removed from the synaptic cleft in 1 of 3 way:
* Reuptake into the presynaptic neuron (accounts for 80%)
* Diffusion away from the synaptic cleft
* Reuptake by extraneural tissue

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16
Q

What enzymes metabolize NE and EPI? what is the final metabolic byproduct?

A

There are 2 metabolic pathways for norepinephrine and epinephrine
* Monoamine oxidase (MAO)
* Catechol-O-methyltransferase (COMT)
the final byproduct of NE and EPI metabolism is vanillylmandelic acid (VMA). Another name for this compound is 3-mthoxy-4-hydroxymandelic acid. An elevated level of VMA in the urine aids in the diagnosis of pheochromocytoma

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17
Q

List the 3 types of cholinergic receptors. Where are each of these found inside the body?

A

Nicotinic Type M (muscle):
* Neuromuscular junction

Nicotinic Type N (nerve):
* Preganglionic fibers at autonomic ganglia (SNS & PNS)
* Central nervous system

Muscarinic:
*Postganglionic PNS fibers at effector organs
* Central nervous system

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18
Q

Describe the synthesis, release, and metabolism of acetylcholine.

A
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19
Q

list the 5 components of the autonomic reflex arc

A

sensor -> afferent pathway -> control center-> efferent pathway -> effector

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20
Q

compare and contrast the architecture of the SNS and PNS efferent pathways

A

Both Pathways contain a pre- and postganglionic nerve fiber

PNS:
* Preganglionic: Long, myelinated, B-fiber, releases Ach
* Post-ganglionic: Short, unmyelinated, C-Fiber, release Ach

SNS:
* Preganglionic: Short, myelinated, B-Fiber, releases Ach
* Postganglionic: Long unmyelinated, C-fiber, releases NE (*Ach is released at sweat glands, piloerector muscles, and some vessels)

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21
Q

what is the origin of the efferent SNS pathways?

A

Thoracolumbar:
*T1-L3
* Cell bodies arise from the intermediolateral region of the spinal cord and axons exit via the ventral nerve roots
* Preganglionic fibers usually synapse with postganglionic fibers in the 22 paired sympathetic ganglia (mass effect)

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22
Q

what is the origin of the efferent PNS pathways?

A

Craniosacral:
* CN 3,7,9,10
* S2-S4
* preganglionic fibers synapse with postganglionic fivers near or in each effector organ (precise control of each organ)

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23
Q

Describe the innervation of the adrenal medulla. How is it different then the typical SNS efferent architecture?

A

The innervation of the adrenal medulla is unique; there are no postganglionic fibers.

The preganglionic fibers release Ach onto the chromaffin cells, and the chromaffin cells release EPI and NE into the systemic circulation at a ratio of 80% and 20% respectively

You can think of the adrenal medulla as an autonomic ganglion that is in direct communication with bloodstream

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24
Q

Describe the hemodynamic management of the pt with pheochromocytoma.

A

Understanding the hemodynamic management of this pt is critical to the success of your anesthetic. You must alpha block before you beta block! just remember that A comes before B.

Commonly used alpha antagonists include:
*Non-selective: phenoxybenzamine and phentolamine
* alpha-1 selective: Doxazosin and prazosin

Problems that arise from blocking the beta receptor first:
* Beta-2 blockade inhibits skeletal muscle vasodilation and increases SVR
* Beta-1 blockade reduces inotropy and can precipitate CHF in the setting of increased SVR.

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25
what is the transcellular potassium shift, and what causes it to occur?
The transcellular K+ shift describes a number of processes that alter serum K+ by shifting K+ into or out of the cells * Things that shift K+ into cells (ICF) leads to hypokalemia * Things that shift K+ into the ECF lead to hyperkalemia K shift in: Alkalosis, beta-2 agonists, theophylline, insulin K shift out of cell: acidosis, cell lysis, hyperosmolarity, succinylcholine
26
Describe the anatomy and physiology of the baroreceptor reflex.
the baroreceptor reflex regulates short term blood pressure control. * When the blood pressure rises, the baroreceptor reflex decreases heart rate, contractility, and systemic vascular resistance * When blood pressure falls, the baroreceptor reflex increases heart rate, contractility, and systemic vascular resistance longer term pressure control is mediated by the RAAS and ADH.
27
describe the anatomy and physiology of the Bainbridge reflex.
The bainbridge reflex increases heart rate when venous return is too high. This is beneficial, because it minimizes venous congestion and promotes forward flow. * Sensor: SA node, RV, pulmonary veins * Afferent: Vagus * Control: Vasomotor center in the medulla * Efferent: vagus (inhibition) * Effector: SA node increases HR Treatment: None required Example: Autotransfusion during childbirth
28
describe the anatomy and physiology of the Bezold-Jarisch reflex.
The Bezold-Jarisch reflex decreases the heart rate when venous return is too low. This gives an empty heart adequate time to fill. * Sensor: Cardiac mechanoreceptors (venous return) & cardiac chemoreceptors (ischemia) * Afferent: Vagus * Control: Vasomotor center in the medulla * Efferent: Vagus * Effector: SA node decreases heart rate & AV node decreases conduction velocity Treatment: Restore preload (IVF and leg elevation) and increase heart rate (EPI is best) Examples: * Cardiac arrest during spinal anesthesia * Massive hemorrhage * Myocardial ischemia *shoulder arthroscopy + interscalene block w/EPI + sitting position
29
describe the anatomy and physiology of the oculocardiac reflex
the oculocardiac reflex as the five (V) and dime (X) reflex * Sensor: pressure on the eye or globe * Afferent: Long and short ciliary n. -> ciliary ganglion -> opthalamic V1 of trigeminal n (CN V)-> gasserian ganglion * Control: Vasomotor center in the medulla * Efferent: Vagus * Effectors: SA node decreases heart rate & AV node decreases conduction velocity treatment: * Ask the surgeon to remove the stimulus. This is usually enough to terminate the reflex * Administer 100% oxygen, ensure proper ventilation, and deepen anesthetic * Administer an anticholinergic (atropine or glyco) Examples: * Strabismus surgery * Ocular trauma * Retrobulbar block (Can cause or prevent the OCR)
30
what is the primary determinant of cardia output in the pt with a heart transplant? What is the consequence of this?
The transplanted heart is severed from autonomic influence, so the heart rate is determined by the intrinsic rate of the SA node. This explains why these pts often have a resting tachycardia (HR: 100-120 bpm) If CO is the product of HR and SV ( and the heart rate is fixed), then CO becomes dependent on preload. Indeed, CO is highly dependent on cardiac filling. This feature makes these pts very sensitive to hypovolemia.
31
What drugs can be used to augment heart rate in the pt with a heart transplant?
Central to understanding this is knowing that there is no autonomic input from the cardiac accelerator (T1-4) or the vagus nerve. * Drugs that directly stimulate the SA node can be used to increase HR (epi, isoproterenol, glucagon) * Drugs that indirectly stimulate the SA node can NOT be used (atropine, glyco, and ephedrine)
32
A pt presents for removal of a glomus tumor. What are you primary concerns when planning your anesthetic?
Glomus tumors (glomangiomas) originate from neural crest cells. They tend to grow in the neuroendocrine tissues that lay in close proximity to the carotid artery, aorta, glossopharyngeal nerve, and the middle ear. These tumors usually aren't malignant. * They can release several vasoactive substances that can lead to exaggerated hyper- or hypotension (NE, 5-HT, histamine, bradykinin). * Octreotide can be used to treat carcinoid-like s/sx. * Cranial nerve dysfunction (glossopharyngeal, vagus, and hypoglossal) can cause swallowing impairment, aspiration of gastric contents, and airway obstruction. * Surgical dissection of a glomus tumor that has invaded the internal jugular vein increases the risk of air embolism.
33
What are the anesthetic considerations for multiple system atrophy?
Multiple system atrophy (previously known as Shy-Drager syndrome) causes degeneration of the locus coeruleus, intermediolateral column of the spinal cord (where the cell bodies for the SNS efferent nerves live), and the peripheral autonomic nerves. * Autonomic dysfunction (orthostatic hypotension) * Treat HoTN with volume and direct acting sympathomimetics * Exaggerated HTN response to ephedrine and possibly ketamine
34
Compare and contrast low, intermediate, and high dose epinephrine.
Low dose Epi (0.01-0.03 mcg/kg/min) * at low doses, non-selective beta effects predominate. Beta-1 stimulation increases heart rate and contractility, while beta-2 stimulation mediates vasodilation in the skeletal muscle. The net effect is typically an increased CO with a reduction in blood pressure. Pulse pressure is increased (wider). Intermediate dose epi (0.03-0.15 mcg/kg/min) * This dose range is characterized by mixed beta and alpha effects High dose epi (>0.15 mcg/kg/min): * in this dose range, the alpha effects prevail and blood pressure rises. Supraventricular tachyarrhythmias are common, and these limit the usefulness of high dose EPI.
35
Describe the cardiovascular effects of isoproterenol
Isoproterenol is a synthetic catecholamine that stimulates beta 1 and beta 2 receptors * it increases heart rate, contractility, and myocardial oxygen consumption * It decreases SVR, which reduces diastolic BP. This may reduce coronary perfusion pressure (CP= AoDB-LVEDP) * It causes severe dysrhythmias and tachycardia * IT vasodilates nonessential vascular beds, such as those in the muscle and skin. This characteristic precludes its use in septic shock.
36
list 4 clinical indications for isoproterenol.
1. Chemical pacemaker for bradycardia unresponsive to atropine. 2. Heart transplant 3. Bronchoconstriction 4. Cor pulmonale
37
in what situations should ephedrine NOT be use to treat hypotension?
Uses endogenous catecholamine stores from the presynaptic sympathetic nerve. Multiple doses can cause tachyphylaxis (Progressively smaller response to a given dose after multiple administrations) * Ephedrine doesn't work well when neuronal catecholamine stores are depleted (sepsis) or absent (heart transplant) * Risk of hypertensive crisis in pts on MAO inhibitors * Conditions where increased HR or contractility is detrimental to hemodynamics
38
How does vasopressin increase blood pressure?
Vasopressin restores blood pressure in two ways: * V1 receptor stimulation causes intense vasoconstriction * V2 receptor stimulation increases intravascular volume by stimulating the synthesis and insertion of aquaporins into the walls of the collecting ducts. This increases water (but not solute) reabsorption and lowers serum osmolarity Aldosterone increases water and sodium reabsorption (serum osmolarity is unchanged). This is an important difference between vasopressin and aldosterone
39
what is the best treatment for vasoplegic syndrome?
Refractory HoTN is also called vasoplegic syndrome. The key here is that hypotension does not respond to conventional therapies such as adrenergic agonists, hydration, and reducing depth of anesthesia. * Vasopressin is the best treatment (0.5-1 unit IV bolus followed by an infusion of 0.03 units/min) * the incidence of vasoplegic syndrome is increased by ACE inhibitors or angiotensin receptor antagonists * Methylene blue is the next best choice
40
the 6 drugs that are selective for the beta 1 receptor
these drugs are beta-1 selective * Atenolol * Acebutolol * Betaxolol * Bisoprolol * Esmolol * Metoprolol Knowing what you know about the beta-1 and beta-2 receptor, you should be able to predict their side effects A's B's E, beginning of alphabet plus M
41
list 6 non-selective beta antagonists
they antagonize beta 1 and beta 2 receptors * Carvedilol * Labetolol * Nadolol *Pindolol * Propranolol * Timolol Knowing which receptors they target you can predict their side effects Lower alphabet plus C
42
what is the primary site of metabolism of the commonly used beta blockers? What are 2 exceptions?
Most beta blockers depend on the liver as their primary site of metabolism. Examples include: propranolol, metoprolol, labetalol, and carvedilol. There are 2 exceptions: * Esmolol is metabolized by RBC esterases (not pseudocholinesterase) * Atenolol is eliminated by the kidneys (caution in renal failure)
43
which beta blockers have local anesthetic properties? what is another name for this?
Membrane stabilizing properties is another way of saying that a drug has local anesthetic-like effects. This effect reduces the rate of rise of the cardiac action potential, however it probably only occurs when these drugs reach toxic levels. Examples include: * propranolol * acebutolol
44
what is intrinsic sympathomimetic activity? which drugs exert this effect?
Beta blockers that exert a partial agonist effect, while simultaneously blocking other agonists that have a higher affinity for the beta receptor are said to have intrinsic sympathomimetic activity. * Examples: labetalol and pindolol
45
What bronchodilator is the prototype nonselective PDE inhibitor?
Theophylline
46
In vascular smooth muscle, cAMP inhibits what enzyme?
Myosin light chain kinase
47
List 2 ways cAMP augments myocardial performance.
1. Increasing intracellular calcium and the force of contraction 2. Increasing the rate of relaxation by accelerating the return of calcium to sarcoplasmic reticulum- this is called lusitropy
48
What enzymes metabolize cAMP to 5'-AMP?
PDE 3 and PDE 4
49
The major neurotransmitter released from postganglionic sympathetic neurons is:
norepinephrine
50
What is the rate-limiting step in catecholamine synthesis?
Tyrosine hydroxylase
51
Neurotransmitter release from presynaptic terminals is triggered by influx of:
Ca^+2
52
Stimulation of which presynaptic adrenergic receptor augments NE release?
Beta-2
53
Catecholamines are removed from the synaptic cleft by what 3 mechanisms?
1. Reuptake into the presynaptic nerve 2. Reuptake by extraneural tissue 3. Diffusion away from the synaptic cleft
54
Which NE termination of action mechanism consumes ATP?
Reuptake
55
Which local anesthetic blocks reuptake of NE at the synapse?
Cocaine
56
What 2 enzymes metabolize NE in the liver and kidney?
1. MAO (monamine oxidase) 2. COMT (catechol-O- methyltransferase)
57
What percentage of NE undergoes reuptake?
80%
58
What is the end-product of NE and Epi metabolism?
VMA (vanillymandelic acid)
59
What is the major metabolite of dopamine metabolism?
Homovanillic acid
60
What 2 enzymes metabolize catecholamines?
MOA (monamine oxidase) COMT (catechol-O- methyltransferase)
61
How specific is VMA excretion in the urine for diagnosis of pheochromocytoma?
97% specific
62
What is the rate-limiting factor for ACh synthesis?
the availability of the substrates, choline and acetyl-CoA
63
Name the 2 types of messages in the efferent ANS
Electrical (action potentials Chemical (neurotransmitters)
64
List the 2 locations of neurotransmitter release in the efferent ANS
1. Ganglia 2. Effectors (targets)
65
Where do cell bodies of preganglionic sympathetic fibers lie?
The interomediolateral (IML) horn of the spinal cord, also known as the lateral horn and Rexed's lamina 7
66
List the 4 abdominal prevertebral (peripheral) plexuses.
1. Celiac 2. Aortic 3. Superior hypogastric 4. Inferior hypogastric (pelvic)
67
Stellate ganglion block causes what syndrome?
Horner's syndrome Mnemonic: Very Homely PAM Vasodilation, Horner, Ptosis, Anhidrosis, Miosis
68
What is another name for the stellate ganglion?
Cervicothoracic ganglion
69
Which peripheral nerve block can result in Horner syndrome?
Brachial plexus block
70
Describe the sympathetic innervation to the adrenal medulla.
Preganglionic sympathetic B fibers arise from the thoracic region of the spinal cord (T5-T9) and travel uninterrupted to the adrenal medulla
71
What neurotransmitter is released at the adrenal medulla by the SNS?
ACh
72
What receptor on the Chromaffin cells binds ACh?
Type- N nicotinic ACh (NN)
73
What is the classic presentation of pheochromocytoma?
Headache, diaphoresis, tachycardia
74
What consequences follow removal of a pheochromocytoma?
HoTN and hypoglycemia
75
What 2 molecules are released by SNS stimulation of hepatocytes?
Glucose and potassium
76
what 4 factors shift potassium into the cell?
1. Alkalosis 2. Beta- 2 agonist 3. theophylline 4. Insulin
77
What 4 factors shift potassium out of the cell?
1. Acidosis 2. Cell lysis 3. Hyperosmolarity 4. Succinylcholine
78
Identify 4 key point of integration between the ANS and endocrine system.
1. Renin-Angiotensin-Aldosterone System (RAAS) 2. Vasopressin (ADH) 3. Glucocorticoids 4. Insulin
79
The ANS influences all tissues except:
Skeletal muscle
80
Which component of a feedback control arc compares and multiplies signals?
Control center (feedback controller)
81
Mnemonic for cardiac reflexes:
Three Bees in the CV....Ouch Baroreceptor Bainbridge Bezold-Jarisch Chemoreceptor Vasovagal Oculocardiac
82
Baroreceptor Reflex is a:
High-pressure arterial baroreceptor reflex increased BP -> Decreased HR, contractility, and SVR decreased BP-> increased HR, contractility and SVR Attempts to preserve cardiac output during acute blood loss and shock Crucial for going from sitting to standing
83
What two procedures can activate the baroreceptor reflex?
Carotid endarterectomy due to manipulation of the carotid bifurcation Mediastinoscopy due to pressure from the scope on the transverse aortic arch both cause bradycardia
84
What 2 vascular locations contain high-pressure barorecepotrs?
1. Aortic arch 2. Carotid sinus
85
What is the spinal cord origin of cardioaccelerator fibers?
T1-T4
86
Bainbridge reflex is a...
Low-pressure cardiopulmonary baroreceptor reflex Afferent pathway is the vagus to the nucleus tractus solitarius (control center) efferent: both parasympathetic and sympathetic pathways to the SA node Effector: SA node-> increased HR Goal is forward flow for high volume, prevents sludging general rule, during volume loading, the bainbridge reflex prevails, whereas during volume depletion, the high-pressure baroreceptor reflex dominates Cardiac congestion also leads to decreased ADH and increased atrial natriuretic peptide release-> diuresis and decreased intravascular volume
87
Bezold-Jarisch reflex triad and function
Triad: Bradycardia, HoTN, and coronary artery dilation * Cardio-inhibitory reflex that may play a prominent role in cardioprotective reflexes in response to noxious stimuli (MI, Low venous pressure, thrombolysis) sensor: chemo- and mechanoreceptors in the LV wall control center: NTS efferent: vagus nerve Effector and response: SA node-> decreased HR, AV node-> decreased dromotopy
88
Clinical relevance, when may you not see BJR What can augment the BJR
* Less pronounced in a pt with cardiac hypertrophy or atrial fibrillation * The bradycardia and HoTN during a spinal or epidural block have attributed to the BJR * Also seen in shoulder surgery with regional anesthesia in the sitting pt
89
comparing the three
* The bainbridge reflex increases the HR in the setting of venous congestion (preload is too high) * the BJR slows the heart rate in the setting of profound hypovolemia (preload is too low) * these reflexes tend to override the baroreceptor reflex
90
What is the strongest stimulus at the peripheral chemoreceptors?
Hypoxia
91
What affects are caused by hypoxemia
signals are sent via the carotid and aortic bodies through the nerve of Hering (CN 9: glossopharyngeal) and the vagus. Sent to the NTS The effector responses to hypoxia are increased RR and tidal volume -> increase MV Cardiovascular: acute- activation of the PNS -> decreased HR and decreased inotropy (contractility) Persistent hypoxemia leads to SNS activation, causing increased HR and increased inotropy -> increased CO subanesthetic concentration of most volatile inhaled agents (<0.1 MAC) blunt the chemoreceptor reflex Opioids and nitrous oxide also attenuate the chemoreceptor reflex in a dose-dependent manner
92
Vasovagal reflex is AKA: and what are the triggers?
Vasovagal syncope or neurocardiogenic syncope Triggers: Psychological stress (phlebotomy, blood, acute pain) Peritoneal stretching or distension
93
Physiologic changes from Vasovagal reflex:
* Massive vasodilation with a fall in BP that fails to activate the baroreceptor reflex * bradycardia + decreased SV = decreased CO * A sudden decrease in both SVR and CO-> profound decrease in MAP * Decreased MAP causes global cerebral ischemia. If decreased CBF persists-> dizziness or faintness. > 10 seconds = loss of consciousness after regaining consciousness increased vasopressin causes oliguria Profound vasovagal reaction to rapid peritoneal distension during insufflation has been implicated in acute CV collapse and cardiac arrest
94
Stimuli of oculocardiac reflex
* Traction on the extraocular muscles, especially the medial rectus * Strabismus surgery, particularly in children * Pressure on the globe * Ocular trauma * Pressure on the conjunctiva * Pressure on the orbital tissue follow enucleation * Retrobulbar block can cause or prevent the oculocardiac reflex
95
Afferent pathway of Oculocardiac reflex
Long and short ciliary nerves -> ciliary ganglion -> ophthalmic division (V1) of CN5 -> trigeminal (gasserian or semilunar) ganglion
96
Control center of OCR
NTS and medullary cardiovascular nuclei and centers efferent: CN10 effector: Decreased activity of the SA and AV nodes
97
Clinical presentation of OCR
* Bradycardia *** * HoTN *** * Junctional rhythm *** * AV block * Asystole
98
Factors that worsen the severity of the OCR
Hypoxemia Hypercarbia Light anesthesia
99
Tx options of OCR
* Ask surgeon to stop stimuli * Administer 100% O2, ensure adequate ventilation, and deepen the anesthetic * administer an anticholinergic such as atropine or glyco * the OCR will fatigue with subsequent occurrences
100
What CV reflex can occlude the peripheral vasculature and increase risk of anuria to increase BP?
CNS ischemic reflex
101
When does the CNS ischemic reflex activate and when is it at peak?
When MAP< 50 Peak MAP of 15-20mmHg
102
What causes Cushing's triad/reflex?
Increased ICP that causes reduced CBF, used to augment cerebral perfusion
103
What 3 things make up cushings triad?
Bradycardia, HTN, and irregular respirations
104
What causes the HTN in Cushings triad?
Increased ICP leads to a sympathetically-mediated increase in BP in an attempt to restore cerebral perfusion pressure (CPP)
105
What causes the bradycardia in Cushings triad?
Intense vasoconstriction activates the baroreceptor reflex * Activation of the parasympathetic medullary centers via the barorecepotor reflex slows the heart but does not overcome sympathetically-mediated HTN
106
Cause of irregular respiration in cushings triad?
Brainstem compression
107
Where is the control center for thermoregulation?
The preoptic area (hypothalamus) serves as the control center in a negative feedback loop. The preoptic area compares the input signal with the setpoint then evokes responses that restore body temperature toward the set point * Cutaneous blood vessels- constriction (retain heat) or dilation (cool) * Brown fat and skeletal muscle for thermogenesis and shivering * Sweat glands for evaporative heat loss * Piloerection for animals with fur Anesthesia sweating threshold is slightly increased, and vasoconstriction and shivering thresholds are decreased markedly
108
What reflex is activated with the valsalva reflex?
The baroreceptor reflex * Increased intrathoracic pressure reduces venous return which decreased cardiac filling and BP which causes the baroreceptors reflex to increase HR * once the glottis opens venous return leads to increase in blood pressure (contractility is still increased). This is then detected by the baroreceptors causing a parasympathetically mediated decrease in HR. No reflex associated with Muller maneuver
109
What are the other names for Mass Reflex?
Autonomic hyperreflexia and autonomic dysreflexia
110
What is the mass reflex?
In response to fear, exercise, and other types of stress, the SNS produces a massive and coordinated output to all end organs simultaneously, and parasympathetic output ceases. Activation of the SNS produces a diffuse physiologic response (mass reflex) rather than discrete effects.
111
Loss of sympathetic drive to which structures is responsible for Horner syndrome?
* Levator palpebrae superior muscle - drooping of the eyelid (ptosis) * Dilator pupillae (radial) muscle- miosis- loss of dilator muscle, allowing unopposed parasympathetic stimulation of the sphincter pupillae (circular) muscle to constrict the pupil * Smooth muscle of cutaneous vessels- Loss of normal sympathetic tone to subcutaneous blood vessels leading to flushing of the skin
112
Which acetylcholine precursor is produced in mitochondria?
Answer: Acetyl- CoA- Kreps cycle glucose and pyruvic acid are components of glycolysis in the cytoplasm Choline is transported into the cell

Sarah's Apex (14 decks)

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