Acute Pain Management Flashcards
- Common sources and key features of acute pain?
sources: surgery, trauma, childbirth, acute disease states, medical procedures.
features: proportional to damage, reflects activation of nociceptors or sensitized central neurons; often associated with autonomic hyperactivity and protective reflexes (splinting, muscle spasm)
- Methods of assessment of acute pain?
- subjective scales both at rest & w/ activity
- ask about intensity, , onset, duration and location
- reassessment after analgesic, interventions and timed intervals
- not reasonable to completely resolve pain, goals to comfort at rest, ambulating and with cough, ideal no interference with mood or sleeping
- Hormonal response to acute pain.
increased ACTH–> protein catabolism
increased cortisol –> lipolysis
increased glucagon/epi, decreased insulin–> decreased protein anabolism
decreased testosterone and insulin–> decreased protein anabolism
increased cortisol, catecholamines and angiotensin II–> CHF, vasoconstriction, increased contractility and HR
increased aldosterone and ADH–> salt and water retension
- Physiologic stress response to acute pain.
CV- Tachy, HTN, increased SVR, increased myocardial O2 consuption, arrhythmogenic, altered regional blood flow
Pulm- surgery reduces VC, TV, RV< FRC and FEV1, causes V/Q mismatch; increased abd down
GI/GU- ileus, N, V, hypomobility or urethra and bladder
Immune: lymphopenia, depression of reticuloendothelial system, leukocytosis, reduced killer T cell
Coagulation: increased platelet adhesion, increased fibrinogen, diminished fibrinolysis,, activation of coag
general: immobility, insomnia, anxiety, fatigue, weakness, feeling helpless
- Role of opioids in acute pain management.
used for moderate to severe pain, ***more effective in nociceptive pain (over neuropathic)
effects: analgesia, sedation, resp depression, euphoria/dysphoria/hallucinations, vasodilation, bradycardia, myocardial depression, miosis, NV, delayed gastric emptying, smooth muscle spasm (constipation, urinary retention, biliary spasm, sk muscle rigiditiy and pruritis
- Chronic physiologic effects opioids.
tolerance- PCA with basal therapy may be necessary; SE faster NV, impairment, sedation and resp depr v slower constipation and miosis
withdrawal- physiologic dependence
addiction- pattern of behaviors
- Commonly used narcotics: morphine
slow onset, metabolized by liver
avoid in renal failure, metabolite3-glucoronide
causes histamine release
slow release prep unsuitable for acute pain
- Commonly used narcotics: hydromorphone
fewer adverse SE than morphine
5-7x more potent than morphine
metabolite 3-glucorinde (no analgesic, neurosecitatory properties
- Commonly used narcotics: Meperidine
more lipid soluble than morphine, 1/10 as potent
fast analgesic effect, short duration, +/- endorphin effect
atropine like side effects
large doses can cause myocardial depression and orthostatic hypotension
AVOID with MAO-Is
generally only given for shivering post procedure metabolite normeperidene (CNS excitation, less potent analgesia, long half life (15-20hr)
avoid background infusion rate
- Common narcotics: fentanyl
highly lipid soluble, rapid onset, short duration
NO histamine release
inactive metabolites
transdermal contraindicated in acute pain
- Common narcotics: mixed opioid agonists/antagonists (nubain)
kappa opioid receptors, limited resp depression
may precipitate withdrawal, lower abuse potential
attenuates opioid induced side effects w/o reversing analgesia
- Common narcotics: tramadol
Avoid concurrent MAOIs and SSRIs no histamine release less resp depression no adverse effects on HR, LVF, CI increase seizure risk may precipitate withdrawal in dependent patients
- Benefits/ contraindications of PCA
benefits: peaks and valleys avoided, better satisfaction
***contra: untrained providers, patient rejection, inability to comprehend technique (age or cognitive impairment)
role in acute pain is to “titrate” opioid plasma concentration near to the “min effect, analgesic concentration” (MEAC)
- Features of adjuncts: NSAIDS
stops PGE2 injur/ inflammation
no reduction in gastric motility
***SE: gastropathy, inhibition of platelet function, renal effects, inhibits bone osteogenesis
(ketorolac is the only parenteral NSAID, no preoperative use, 5 d max)
COX-2 inhibitors can be used preoperatively (does not impair homeostasis)
- Features of adjuncts: ketamine
NMDA receptor antagonist
may reduce pre-operative nausea vomiting
may have preemptive analgesia effect
