Test 4: Multimodal Acute vs Chronic Pain Flashcards
What is Acute Pain (basic definition)?
Pain caused by noxious stimuli due to traumatic injury (chemical, thermal, or mechanical), surgery, or acute illness.
What is Chronic pain (basic definition)?
Pain with no apparent biological value that lasts longer than 3 months or beyond the normal course of healing.
-Associated with insomnia, lost work days, impaired mobility & emotional distress (anxiety, anger, fear, depression)
-Hyperexcitable state. Nerves are constantly activated from damage.
-Two general classifications: Malignant or Non-Malignant
-Challenging to treat (multimodal approach)
What is Malignant pain?
Pain caused by or related to cancer and its treatment.
What is Non-Malignant pain?
Neuropathic
Inflammatory
Musculoskeletal
Idiopathic
Combination of one or all of the above
What triggers responses with acute pain?
SNS triggers neuroendocrine responses in response to surgical stress.
What factors can impact the SNS response with Acute Pain?
SNS response impacted by:
-Size of the surgical field
-Number of nerve/pain receptors in the area
-Bleeding, infection, anxiety
-Coexisting diseases
What are the Cardiovascular Effects associated with acute pain?
-Increases catecholamines from SNS and increases cortisol = inc HR, inc vascular resistance (peripheral, systemic, and coronary), increased myocardial oxygen contractility, and increased arterial BP.
-Leads to increase in Myocardial O2 demand & consumption (!)
-Potential for rupture of artherosclerotic plaque from vascular walls (further decreases O2 supply to tissues)
-Can lead to Dysrhythmias, angina, myocardial ischemia & infarct
-Risk of MI due to increased myocardial O2 demand/consumption (!)
T/F: Aggressive pain management is essential to preventing post-op cardiac complications.
True (Blue Box!)
What are the Respiratory Effects associated with acute pain?
-Most problematic for pts with trauma/surgery in the upper ABD area & thorax
-Pain ⬇TV due to ⬇thoracic and abdominal movement
-⬇Vital capacity, ⬇inspiratory capacity & ⬇FRC
-⬇ability to clear the airway due to pain
-Muscle spasms = ⬇limited respiratory muscle movement (dec ventilation)
-Poor cough, splinting ⇒atelectasis & pneumonia
-Effects are worse in pts with pre-existing pulm dysfunction (Asthma, COPD) or ⬇FRC at baseline (morbidly obese, elderly)
How does acute pain increase the risk for DVT or PE?
Pain decreases/delays mobilization
What physiological changes associated with acute pain do you need to know (basic overview)?
-Inc HR, PVR, and ABP: all things we assess to see if they’re experiencing pain
-Decreased VC, TV, and TLC
-V/Q mismatch, atelectasis, PNA
-Decreased ability to cough leads to hypoxia and hypercarbia
-Decreased gastric emptying, decreased intestinal motility
-Inc plt aggregation (thrombosis). compounded if they aren’t moving
-Decreased immune function (increased risk of infection)
-Inc urinary sphincter tone (urinary retention)
What is Sensitization?
-Non-associative learning. Behavior toward a stimulus changes in the absence of any apparent associated stimulus or event (such as a reward or punishment)
-Repeated administration of a stimulus results in the progressive amplification of a response
-Often characterized by an enhancement of response to a whole class of stimuli in addition to the one that is repeated
-Post-op surgical pain can trigger chronic pain of a different kind
What is Central Sensitization?
-Pain modulation is enhanced due to neuroplastic changes in the CNS
-Repetitive stimuli to injured nerves alters neurotransmitter levels
-Associated with chronic pain states
What is Peripheral Sensitization?
-Environmental chemical changes of peripheral nerves
-Release of algogenic substances and neurotransmitters, such as Bradykinin, serotonin, Substance P, glutamate, etc.
-Enhanced excitability of nerves
-Reduces nociceptive thresholds
-High-threshold nerve endings become responsive to non-noxious stimuli
How does acute pain transition to chronic pain?
Pain goes from Nociceptive to Neuropathic.
1) Initiated by either peripheral or central mechanisms:
-Peripheral Sensitization
-Central Sensitization
2) Hyperexcitable nerve endings:
-Changes resulting from direct nerve injury
-Sprouting of new nerve endings. Fire ectopically
3) Neuroma formation:
-Abnormal growth or tumor of the nerve
-Abnormal mechanosensitivity
4) Damaged nerves have reduced pain thresholds:
-Respond to non-noxious stimuli
What is Neuropathic pain?
-Initiated or caused by changes in the PNS or CNS
-“shooting” “burning” “stinging”
-Accompanied by hyperalgesia and allodynia.
What is Mechanosensitivity?
Physiological foundation for the senses of touch, hearing and balance, and pain is the conversion of mechanical stimuli into neuronal signals.
What is “Wind Up”?
Sensitization of the Wide Dynamic Range (WDR) neurons in the posterior column of the spinal cord.
-With chronic stimulation, these increase cellular calcium, increase release of inflammatory substances (ex: Substance P, Bradykinins, and Glutamate), and produce cyclooxygenase.
-Prostaglandins are also synthesized, which are responsible for the reduction of our neuropathway inhibition (reduction of inhibition = excitability)
-Sustained stimulation of afferent C Fibers leads to a longer sustained depolarization. Afferent input sensitizes low threshold afferents, increasing the neuronal field.
-Increased neurologic pathway excitation and formation of hyperalgesia = “Wind Up”.
-Very hard to treat this. Complex.
What is Glutamate?
Theorized to play a key role in the development of “Wind Up”.
-The primary excitatory neurotransmitter
-Released by Primary afferents in the dorsal horn (A Delta & C fibers)
Acts on receptors within the Dorsal Horn:
-Metabotropic
-Kainite
-AMPA
-NMDA
What occurs when Glutamate stimulates the NMDA Receptor?
-Activation of the receptor
-Released of 2nd messengers: Kinases and Lipases
What causes upregulation of 2nd Messengers?
Substance P and Calcitonin Gene Related Peptide.
-Produces hyperexcitability of the NMDA Receptors.
-Leads to long term neuronal plasticity, excitability, and eventually produces gene transcription changes.
-Contributes to central sensitization and chronic pain states.
What are the different techniques used in treating acute pain?
-Preemptive analgesia
-NSAIDS (Ketorolac, Acetaminophen (not rly a NSAID), and Celecoxib)
-Opioids
-NMDA Antagonists
-Alpha2 Adrenergic Agonists
-Local Anesthetics
-PCA
What are different techniques to treat Chronic pain?
-Anticonvulsants
-Antidepressants
-Corticosteroids
-Methadone
Why are Anticonvulsants used to treat Chronic pain?
2nd gen Anticonvulsants: Gabapentin and Pregabalin
-Inhibit neuronal excitation and stabilize nerve membranes
-Decrease repetitive neural ectopic firing (neuropathic pain). Used in the tx of postherpetic neuralgia, diabetic neuropathy, and trigeminal neuralgia.
Why are Antidepressants used to treat Chronic pain?
-Ex: TCAs, SSRIs, SNRIs
-Descending inhibitory pathway is altered in central sensitization.
-Antidepressants increase the availability of inhibitory neurotransmitters
-Can also act on other sites.
-Dose is lower than normal recommended antidepressant doses (effects may not occur until 4-10 days)
What other sites do Antidepressants work on?
-Blocking of sodium and calcium channels
-Decreasing PGE2 and TNF-α
-Blocking NMDA receptors
-Enhancing opioid receptors
What Tricyclics (TCAs) are used in chronic pain treatment?
-Ex: amitriptyline (Elavil), nortriptyline
-C/I in recent MI, prolonged QT, dysrhythmias, unstable CHF
-Used to treat postherpetic neuralgia, headaches, fibromyalgia
What SNRIs are used in chronic pain treatment?
-Ex: duloxetine (Cymbalta), venlafaxine (Effexor)
-Preferred for pts with cardiac disease
What SSRIs are used in chronic pain treatment?
-Ex: Prozac, Paxil, Celexa, Zoloft, Lexapro
-weak data
