Baby Miller: Acute Postoperative Pain Management

Front 1

acute postoperative apin

Back 1

a complex physiologic reaction to:

-tissue injury
-visceral distention
-disease

Front 2

effects of postoperative pain

Back 2

-patients state it is what gives them the most apprehension prior to surgery
-produces adverse physiologic effects on multiple organ systems

Front 3

organ systems affected by postoperative pain

Back 3

-pulmonary
-cardiovascular
-endocrine
-immune
-coagulation
-GI
-GU

Front 4

physiologic effect of pain on the pulmonary system

Back 4

basically decreased lung volumes:

-atelectasis
-ventilation perfusion mismatch
-arterial hypoxemia
-hypercapnea
-pneumonia

Front 5

physiologic effects of pain on the cardiovascular system

Back 5

basically sympathetic stimulation:

-systemic hypertension
-tachycardia
-myocardial ischemia
-cardiac dysrhythmias

Front 6

phyiologic effects of pain on the endocrine system

Back 6

-hyperglycemia
-sodium and water retention
-protein catabolism

Front 7

phyiologic effects of pain on the immune system

Back 7

decreased immune function

Front 8

phyiologic effects of pain on the coagulation system

Back 8

-increased adhesiveness of platelets
-decreased fibrinolysis
-hypercoagulation
-DVT

Front 9

phyiologic effects of pain on the GI system

Back 9

ileus

Front 10

phyiologic effects of pain on the GU system

Back 10

urinary retention

Front 11

ultimate goals of the acute pain service

Back 11

-evaluation and treatment of post-op pain
-identification and management of undesirable side effects related to postop analgesia

Front 12

nociception

Back 12

-the recognition and transmission of painful stimuli generated from thermal, mechanical, or chemical damage

Front 13

what are nociceptors?

Back 13

-free afferent nerve endings of myelinated A delta and unmyelinated c fibers

Front 14

afferent sensory pathway

Back 14

-peripheral afferent nerve endings (nociceptors) send axons to the dorsal horn of the spinal cord, where they synapse with 2nd order neurons; the axons of the 2nd order neurons cross to the contralateral side of the spinal cord and ascend in the spinothalamic tract, which on their way to the thalamus divide and send axons to the reticular formation and the periaqueductal gray matter, then go to the thalamus, where 2nd order neurons synapse with 3rd order neurons, which send axons to the sensory cortex


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Front 15

modulation of nociception

Back 15

-occurs at several different levels along the afferent sensory pathway prior to pain being percieved by the sensory cortex
-can occur at the origin of stimulus (nociceptor), or any point along the ascending pathway
-in addition, can also occur through descending efferent inhibitory pathways originating in the brainstem

Front 16

peripheral modulation of nociception

Back 16

-occurs by either release or elimination of ndogenous mediators of inflammation near the nociceptor

Front 17

endogenous mediators of inflammation

Back 17

-prostaglandins (PGE1>PGE2)
-histamine
-bradykinin
-serotonin
-acetylcholine
-lactic acid
-hydrogen ions
-potassium ions

Front 18

effect of mediators on nociceptors

Back 18

-sensitize and excite them, causing hyperalgesia, especially in tissues subjected to trauma and inflammation

Front 19

effect of aspirin and other NSAIDs

Back 19

-produce analgesia by inhibiting COX, which converts arachidonic acid to PGs
-by inhibitng the production of prostaglandins, they also block (modulate) nociception at peripheral sites

Front 20

modulation of nociception at the level of the spinal cord

Back 20

-done by excitatory and inhibitory neurotransmitters in the dorsal horn, or by spinal reflexes that transmit efferent impulses back to peripheral nociceptors

Front 21

descending efferent inhibitory pathways that modulate nociception

Back 21

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Front 22

excitatory pain modulating neurotransmitters

Back 22

-glutamate
-aspartate
-vasoactive intestinal peptide
-cholecystokinin
-gastrin-releasing peptide
-angiotensin
-substance P

Front 23

inhibitory pain modulating neurotransmitters

Back 23

-enkephalins
-endorphins
-substance P
-somatostatin

Front 24

supraspinal modulation of nociception

Back 24

-occur through descending pathways originating in the brainstem which synapse in the substantia gelatinosa of the dorsal horn of the spinal cord

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Front 25

what specific receptor type is located in these descending pathways?

Back 25

opioids

Front 26

opioid descending pathways

Back 26

-release endorphins and enkephalins which act presynaptically to hyperpolarize nerve fibers and negate action potential propagation to the next synapse and subsequent neurotransmitter release
-morphine and other opiates are agonists at receptors throughout the CNS

Front 27

in addition to opioids, what other receptor type has descending inhibitory pathways?

Back 27

-alpha adrenergic receptors

Front 28

alpha adrenergic inhibitory pathway

Back 28

-terminates in the substantia gelatinosa of the dorsal horn of the spinal cord, where NE is released to rpoduce hyperpolarization of nerve fibers, which negates the action potential propagation and neurotransmitter release from the next synapse

Front 29

the analgesic effect of which drug is likely explained by this pathway?

Back 29

clonidine (alpha 2 agonist)

Front 30

neural activity-dependent plasticity

Back 30

-the dynamic nature of the response to injury by nociceptors

Front 31

plasticity

Back 31

-as peripheral nociceptors are sensitized by local mediators of injury/inflammation (bradykinin, PGs, K ions), the excitability and frequency of neural discharge from nociceptors increases, and this primary hyperalgesia permits previously subnoxious stimuli to generate action potentials which are transmitted to the spinal cord
-as peripheral nerve firing increases, the excitability of spinal cord neurons increases, altering its response to afferent impulses

Front 32

what does this central sensitization of the spinal cord to afferent impulses result from, and what is this called?

Back 32

-results from functional changes in spinal cord processing, called neuroplasticity

Front 33

what is the clinical consequence of neuroplasticity?

Back 33

-action potentials can persist for 1-3 hours after the stimulus is discontinued, and can occur in tissue even after a minor surgical incision, and can last for days in this area

Front 34

what specific substances does spinal cord neuroplasticity involve?

Back 34

-binding of glutamate to NMDA receptors
-binding of substance P and neurokinins