Pain Management



Pain Management





Acute Pain Management

Barash, Chapter 55; Cousins, Chapter 26; Miller, Chapter 72


ACUTE PAIN MANAGEMENT



1. Which nerve fibers mediate pain sensation?

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1. Pain is mediated by the following:



  • Class A delta nerve fibers,


  • Class C (unmyelinated) nerve fibers,


  • Free nerve endings (nociceptor).



2. Which substances act as mediators of pain?

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2. Substances that mediate pain include allogenic mediators such as the following:



  • Potassium and hydrogen ions,


  • Lactic acid,


  • Serotonin,


  • Bradykinin,


  • Histamine,


  • Prostaglandins.



3. What common mechanism of action is shared by opioid and alpha-2 receptors?

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3. The common mechanism of action shared by opioid and alpha-2 receptors is that the receptors are coupled with a G protein, which exerts its membrane function through a secondary messenger protein capable of converting guanosine triphosphate to guanosine diphosphate. This modulates cellular functions such as ion exchange and adenyl cyclase and phospholipase C activity. Hyperpolarization of the nerve probably occurs because of the opening of potassium ion channels and the inhibition of calcium ion channels.



4. What are the endocrine/hormone responses to stress?

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4. Stress causes the following:



  • Release of hormones such as catecholamines, cortisol, angiotensin II, antidiuretic hormone (ADH), adrenocorticotropic hormone, growth hormone, and glucagon (which causes hyperglycemia, catabolism, lipolysis, and a negative nitrogen balance);


  • Less release of insulin and testosterone (anabolic hormones);


  • Sodium and water retention with potassium expenditure → increased extracellular volume.

Catecholamines sensitize peripheral nociceptive endings → propagation of more intense pain.



5. How are the cardiovascular effects of pain mediated?

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5. The cardiovascular effects of pain are mediated by the following:



  • Catecholamines from sympathetic nerve endings and the adrenal medulla,


  • Aldosterone and cortisol from the adrenal cortex,


  • ADH from the hypothalamus,


  • Activation of the renin-angiotensin system.



6. What are the effects of pain on respiration?

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6. The effects of pain on respiration include reflex increases in skeletal muscle tension → decreased total lung compliance, splinting, and hypoventilation. This promotes atelectasis and ventilation-perfusion abnormalities that result in hypoxemia. Functional residual capacity (FRC) may decrease by 25% to 50%. Prolonged increases in the work of breathing may result in hypercapnic respiratory failure.



7. What are the effects of pain on the gastrointestinal system?

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7. Pain affects the gastrointestinal (GI) system by causing a sympathetic hyperactivity → reflex inhibition of GI function → postoperative ileus (nausea/vomiting and discomfort).



8. What are the benefits of epidural anesthesia in reducing postoperative complications?

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8. Benefits of epidural anesthesia include the following:



  • Maintaining or improving left ventricular (LV) ejection fraction and LV wall motion (as long as volume loading is limited);


  • Restoring vital capacity and FRC to near preoperative levels, which is associated with a reduced work of breathing, reduced requirement for postoperative mechanical ventilation, and facilitation of chest physiotherapy;


  • Reduced incidence of deep vein thrombosis, pulmonary embolism, and hypercoagulability in vascular surgery patients;


  • Improved fibrinolytic function.


PHARMACOLOGY OF ACUTE PAIN MANAGEMENT



1. How do nonsteroidal anti-inflammatory drugs (NSAIDs) prevent or reduce pain?

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1. Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce prostaglandin synthesis, blocking the nociceptive response to endogenous mediators of inflammation such as bradykinin, acetylcholine, and serotonin. Acetaminophen and ketorolac tromethamine (Toradol) inhibit cyclooxygenase; they have potent antipyretic and analgesic properties.



2. What are the adverse effects of NSAIDs?

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2. Adverse effects of NSAIDs include the following:



  • GI discomfort: Heartburn, nausea/vomiting, dyspepsia, and epigastric discomfort in 5% to 25% of those taking aspirin and 3% to 9% of those taking NSAIDs;


  • Central nervous system (CNS) disturbance: Headache, dizziness, and drowsiness;


  • Prolonged bleeding (this effect on platelet prostaglandin synthesis is reversed 24 to 48 hours after discontinuing NSAID therapy or 1 week after discontinuing aspirin);


  • Bronchospasm and rhinitis;


  • Direct irritation of the gastric mucosa: Ulceration and bleeding;


  • Acute renal insufficiency with hyperkalemia, peripheral edema (due to prostaglandinmediated effects on renal blood flow), proteinuria, interstitial nephritis, and papillary necrosis.



3. What is the site of action of morphine and its derivatives?

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3. Morphine sulfate and its derivatives act as agonists by interacting with stereoselective and saturable membrane-bound receptors. These are found primarily in the periaqueductal and periventricular gray matter, nucleus reticularis gigantocellularis, medial thalamus, mesencephalic reticular formation, lateral hypothalamus, raphe nuclei, and spinal cord.



4. What are the types of opioid receptors and what are their actions?

View Answer

4. Five types of opioid receptors have been identified:



  • Mu1 Supraspinal analgesia, prolactin release, and euphoria;


  • Mu2: Respiratory depression and physical dependence;


  • Kappa Spinal analgesia, miosis, and sedation;


  • Delta Spinal analgesia;


  • Sigma Dysphoria and hallucinations.



5. What is the difference between the two groups of agonist-antagonist analgesics?

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5. Two types of agonist-antagonist analgesics are as follows:



  • High mu-receptor affinity (activity less than or similar to morphine): buprenorphine (Buprenex) and dezocine (Dalgan);


  • Moderate affinity without activity at the mu-receptor, high affinity with at least moderate activity at the kappa receptor, and at least moderate affinity and some activity at the sigma receptor: pentazocine (Talwin), butorphanol tartrate (Stadol), and nalbuphine.



6. Which analgesics have active metabolites?

View Answer

6. Opioids with active metabolites include the following:



  • Morphine: morphine-6-glucuronide;


  • Codeine: morphine;


  • Meperidine (Demerol): normeperidine;


  • Propoxyphene (Darvon): norpropoxyphene.



7. What is the duration of action of epidural morphine?

View Answer

7. Epidural morphine may last ≥12 hours. Approximately 2% to 10% of the drug diffuses across the dura and binds to spinal opiate receptors → pain relief.



8. What is the benefit of using epidural morphine versus fentanyl in lumbar epidurals?

View Answer

8. Compared to epidural fentanyl, epidural morphine follows the rostral spread of the cerebrospinal fluid and saturates the entire length of the spinal cord. So it may be injected at a lumbar level and still provide analgesia for surgery performed on the upper abdomen and thorax. Lipophilic opiates (fentanyl) provide more of a segmental analgesia. Pain relief also lasts longer with morphine.



9. How do alpha agonists provide analgesia?

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May 28, 2016 | Posted by in ANESTHESIA | Comments Off on Pain Management

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