Pain activates a general hormonal and inflammatory reaction is a main determinant in postsurgical patient’s recovery that may negatively affect the CV system, especially in high-risk patients. Pain can also become chronic, increasing the risk for CV dysfunctions. Epidural analgesia has various beneficial effects on patient’s outcome, including the reduction of stress response and sympathetic activation after surgery. Some data suggest a protective role of EA on CV morbidity, especially on ischemia and dysrhythmias. However, serious CV complications may be expected with neuraxial anesthesia. Traditional CV drugs such as alpha-2 agonists and beta-blockers display important role in pain treatment. Clonidine may also protect from CV morbidity perioperatively, by improving hemodynamic and sympathetic stabilities and reducing stress response, while beta-blockers display beneficial effects in cardiac surgery but may be deleterious in noncardiac surgery. On the other hand, common drugs that are effective for analgesia may also improve the risk for CV morbidity. COX-2 inhibitors are contraindicated for chronic use in pain patients; however, they may not be unsafe in the perioperative setting. Available data are sparse to conclude that short-time administration of COX-2 inhibitors in the perioperative setting is associated to higher risk of CV morbidity, except for patients at higher risk for cardiac events. As well, new data suggest that acetaminophen, which is traditionally considered safe in terms of CV risk, may not be as safe as believed. Opioids are safe, but can harm CV homeostasis in specific cases or when associated with other drugs; neuraxial opioids may protect from hemodynamic impairment and positively affect analgesia. Protecting heart function during pain flares means acting on nociceptive stimulus and on the organic response to pain; the concept should be to stabilize and bring homeostasis to a pain patient’s CV system, always balancing beneficial and detrimental effects of any treatment.
Bugada, D., Bellini, V., Bignami, E., Lorini, F. (2020). Analgesic Control During Acute Pain to Protect Heart Function. In S. Govoni, P. Politi, E. Vanoli (a cura di), Brain and Heart Dynamics (pp. 633-647). Springer Nature [10.1007/978-3-030-28008-6_42].
Analgesic Control During Acute Pain to Protect Heart Function
Lorini F
2020
Abstract
Pain activates a general hormonal and inflammatory reaction is a main determinant in postsurgical patient’s recovery that may negatively affect the CV system, especially in high-risk patients. Pain can also become chronic, increasing the risk for CV dysfunctions. Epidural analgesia has various beneficial effects on patient’s outcome, including the reduction of stress response and sympathetic activation after surgery. Some data suggest a protective role of EA on CV morbidity, especially on ischemia and dysrhythmias. However, serious CV complications may be expected with neuraxial anesthesia. Traditional CV drugs such as alpha-2 agonists and beta-blockers display important role in pain treatment. Clonidine may also protect from CV morbidity perioperatively, by improving hemodynamic and sympathetic stabilities and reducing stress response, while beta-blockers display beneficial effects in cardiac surgery but may be deleterious in noncardiac surgery. On the other hand, common drugs that are effective for analgesia may also improve the risk for CV morbidity. COX-2 inhibitors are contraindicated for chronic use in pain patients; however, they may not be unsafe in the perioperative setting. Available data are sparse to conclude that short-time administration of COX-2 inhibitors in the perioperative setting is associated to higher risk of CV morbidity, except for patients at higher risk for cardiac events. As well, new data suggest that acetaminophen, which is traditionally considered safe in terms of CV risk, may not be as safe as believed. Opioids are safe, but can harm CV homeostasis in specific cases or when associated with other drugs; neuraxial opioids may protect from hemodynamic impairment and positively affect analgesia. Protecting heart function during pain flares means acting on nociceptive stimulus and on the organic response to pain; the concept should be to stabilize and bring homeostasis to a pain patient’s CV system, always balancing beneficial and detrimental effects of any treatment.
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