Pain in the Cardiac Surgical ICU Patient

1. Shana Winchel, BSN, RN-BC MSN Student MSN 621-Alverno College Shana.Winchel@gmail.com Pain in the Cardiac Surgical ICU Patient

2. Objectives Upon completion of this tutorial the learner will: Know the definition of pain Have an increased understanding of the pathophsyiology of pain Have a better understanding of why pain is masked due to hemodynamics Understand the implications of undertreated pain and utilize appropriate interventions to improve patient outcomes

3. Tutorial Guide Return to the main menu at any time by using button Easy navigation forward or backward by using or To return to last slide viewed use the button

4. Main Menu Definitions Pain Myths Pathophysiology Pharmacology Genetics Fifth Vital Sign Nursing Considerations References

5. What is pain? Pain means that there is an increase in vital signs. True False

6. Pain Defined Margo McCaffery is a registered nurse and pioneer of the field of pain management nursing. She defines pain as “whatever the experiencing person says it is, existing whenever and wherever the person say it does” (McCaffery, 1968, p. 95). This has become the prevailing conceptualization of pain for clinicians over the past few decades.

7. What are some pain myths? 1. Addiction is common in patients taking pain medication 2. All people in pain look uncomfortable or sick 3. If a person can sleep, they are not in pain 4. It is just anxiety, their pain is not that bad 5. People who take narcotics will become so sedated that they cannot function.

8. Myths Debunked 1. Addiction to narcotics is rare and usually occurs in patients who have a prior history of drug abuse. When narcotics are properly prescribed and monitored for pain relief, there should be little concern about addiction. Weiner, Peterson, and Keefe (1999)

9. Myths Debunked 2. Pain is invisible. You will come across many, many people in your life who are in pain and look fine. Each person is different in the way he or she feels and exhibits pain. A person’s pain is what they perceive it to be and cannot be judged by anyone else. McCaffery and Pasero (1999)

10. Myths Debunked 3. Prolonged pain can exhaust the body to the point where sleep occurs, even though the pain continues. McCaffery and Pasero (1999)

11. Myths Debunked 4. Excess anxiety and tension can cause the experience of heightened anxiety, increased pain and slower healing times. Anxiety, which is a stress response can cause numerous negative problems. McCaffery and Pasero (1999)

12. Myths Debunked 5. When patients start to take a narcotic, they often feel drowsy. But their bodies usually will very quickly build up a resistance to the sedating effects. Some people, however, become more alert as they finally achieve pain relief. McCaffery and Pasero (1999)

13. What is not a pain myth? • All people in pain look uncomfortable or sick • If a person can sleep, they are not in pain • Pain is whatever the patient says it is • It is just anxiety, their pain is not that bad

14. Pathophsyiology of Pain Complex process that is mediated by multiple pathways in the spine and brain It is a sensory experience

15. Forms of Pain 1. Nociceptive/Inflammatory -Normal processing of stimuli that damages normal tissue or has the potential to damage tissue if prolonged. 2. Neuropathic -Stimuli “abnormally” processed by the central nervous system McCaffery and Pasero (1999)

16. Pain Mechanism 1. Transduction: Noxious stimuli causes tissue damage and initiates the pain mechanism 2. Transmission: Action potential continues from site of damage and ascends to brain 3. Perception of pain: Conscious experience 4. Modulation: Attempt to inhibit pain experience

17. Transduction Cell damage releases sensitizing substances -prostaglandin -bradykinin -serotinin -histamine McCaffery and Pasero (1999)

18. Transmission This phase of transmission occurs in the dorsal horn of the spinal cord -The signal moves up from the site of injury or damage to the brain McCaffery and Pasero (1999)

19. Perception of pain The pain experience happens in this phase -An individual will be aware of pain at this point McCaffery and Pasero (1999)

20. Modulation Neurons from the brain stem release serotinin, norepiphrine and endogenous opioids -These are substances our body releases to fight pain -An example might be if you burn your hand, your brain will tell you move it away from the heat McCaffery and Pasero (1999)

21. Used with permission from McCaffery and Pasero (1999)

22. Pain sensation Mediators, as previously listed, heighten nociception and facilitate the communication of painful sensations to the spinal cord and the brain. Porth and Matfin (2009)

23. What is nociceptive pain? • Stimuli abnormally processed by the central nervous system • Normal processing of stimuli that damages normal tissue or has the potential if prolonged • Processing of pain through the liver

24. Pain Mediators Some of the pain mediators: adrenocorticotropic hormone (ACTH), glucocorticoids, catecholamines, substance P, prostaglandins, leukotrienes, bradykinin, histamine, and serotonin

25. Bradykinin Bradykinin is a molecule produced by enzymes at the site of an injury and then binds to receptors to cause pain. McCaffery and Pasero (1999)

26. Serotinin Serotonin also is an important regulator for pain sensation, and abnormal levels of serotonin can contribute to painful events such as migraine headaches. McCaffery and Pasero (1999)

27. Substance P Substance P is a protein found in the brain and spinal cord, and is associated with some inflammatory processes. Its function is to cause pain. McCaffery and Pasero (1999)

28. Prostaglandins Prostaglandin is produced during inflammatory responses, and it helps to mediate some of the cardinal features of inflammation, including pain, edema, and fever Stock, Shinjo, Burkhardt, Roach, Taniguchi, Ishikawa, Kim, Flannery, Coffman, McNeish, and Audoly, (2001).

29. Histamine Histamine is released by mast cells. Substance P is released which causes mast cells to release histamine, which in turn stimulates the nociceptors Overproduction of histamine promotes inflammation by causing vasodilatation and increased capillary permeability.

30. Effects of Mediators Each of these has one or more effects on the body. And many of these bio-chemicals are inflammatory -- that is, they cause the injury site to swell up.

31. Inflammation and Pain Nociceptive stimulation perpetuates the inflammatory response. Inflammation of peripheral tissues can cause the vicious cycle of pain Porth and Matfin (2009)

32. Inflammation Some of the chemical mediators that are released during injury and inflammation: -Prostaglandins -Leukotrienes -Histamine

33. Inflammation Inflammation can cause pain with pressure and tissue damage.

34. Inflammation causes pain However, if the inflammation is prolonged or out of control, it can cause destruction. This is what occurs in arthritis, where the inflammation actually destroys the joints. Destruction causes pain

35. Inflammation and Pain Inflammation can serve to compound problems by actually causing pain itself.

36. Stress Response to Pain Stress causes the Endocrine System to release excessive amounts of: -Adrenocorticotrophic Hormone (ACTH) -Cortisol -Growth Hormone -Catecholamines -Glucagon Porth and Matfin (2009)

37. Function of Catecholamines Click to learn more Decrease in insulin-which allow more serum glucose in the blood stream Increase in glucagon-which increases serum glucose Increase in heart rate Increase in cardiac contractility Catecholamines

38. Function of ACTH Click to learn more Stimulates release of cortisol Adds to the effect of catecholamines Adds to the effect of glucagon-increase in blood sugar ACTH Cortisol

39. Stress Catecholamines and cortisol are released during the stress response to alert the individual to a threat or challenge.

40. What are Catecholamines NOT responsible for: a. Decrease in insulin b. Increase in glucagon c. Increase in heart rate d. Increase in cardiac contractility e. Decrease in heart rate

41. Pattern developing? Stress and pain mediators overlap Inflammation and pain mediators overlap Inflammation and Stress can increase pain

42. Pain as the fifth vital The importance of the adequate assessment and optimal management of pain has received a great deal of attention Green, Wheeler, and LaPorte (2003) Pain, “the fifth vital sign” as defined by Ruth Massaro, an executive vice president of the Joint Commission on Accreditation of Healthcare Organizations (JCAHO)

43. Hemodynamics and Pain As nurses we have been educated to look for hypertension and tachycardia as a symptom of pain but we now know that this is not an accurate to way evaluate pain. Why…….

44. Rationale for vitals Healthy individuals will seek an equilibrium to return to the stable vital signs despite severe pain Some individuals will have medical conditions that cause bradycardia and hypotension and severe pain will not change the vital signs McCaffery and Pasero (1999)

45. The Fifth Vital Using the pain rating as the fifth vital sign will remind all staff to assess pain regularly. This makes pain visible and raises awareness of the importance of pain management. McCaffery and Pasero (1999)

46. How can I tell if my patient has pain? • Ask them • Check their vitals • Look for grimacing or other outward signs

47. Genetics and pain Genetics can influence effective pain management We all have polymorphisms that can affect the effectiveness of pain medication

48. CYP2D6 Polymorphism The CYP2D6 enzyme is involved in metabolism of up to 25% of drugs. About 10% of Caucasians and 3% of Asian people have this genetic polymorphism. Used with permission from P. Jannetto

49. What does CYP2D6 polymorphism really mean Polymorphism is a genetic mutation that changes the rate of the conversion codeine to morphine. Of note, Morphine is a metabolite of codeine that relieves pain Consequently, some individuals do not achieve analgesia from codeine

50. Categories of CYP2D6 Polymorphisms Super Metabolizers: Clear the drug rapidly and need higher dose Intermediate Metabolizers: Slow to obtain relief and build up effect Poor Metabolizers: Have no ability to clear the drug and become toxic easier Used with permission from P. Jannetto