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Cardiac surgery is associated with significant postoperative pain. Common sources include surgical incision pain, pain associated with rib retraction, and pain from chest tubes and other perioperative appliances. Other potential causes include incomplete revascularization of the myocardium, sternal wires, epicardial pacing leads, and sternocostal and costovertebral pain from retraction.1

The surgical approach has an obvious impact on the severity of postoperative pain. For example, minimally invasive cardiac procedures may produce less overall tissue injury and result in less postoperative pain. Postoperative pain for midline sternotomy has often been described to be moderate, and patients’ anticipated pain level tends to be much greater than the actual pain they experience postoperatively.2 On the other hand, thoracotomy has been associated with a greater degree of both pain and functional limitation, due to the pain associated with breathing and coughing.3 Endoscopic vein graft harvesting has decreased the severity of postoperative leg pain, as well as the infection and wound dehiscence rate.4

Patient risk factors also play a role in the incidence and severity of postcardiac surgical pain, with younger patients (< 60 years old) and those with a higher New York Heart Association (NYHA) class incurring higher pain scores.5,6


The Stress Response

In addition to the discomfort and suffering that postoperative pain accords, the central nervous system responds to the barrage of noxious afferent impulses with a cascade of neurohumoral responses that impair healing and recovery and promote poor clinical outcomes. This so-called stress response is an adaptive mechanism that serves to liberate fuel through catabolism for energy-dependent fight-or-flight activities, increase blood pressure and heart rate, and promote coagulopathy, inflammation, and immune suppression. This is initiated both through the trauma of the surgical procedure and, uniquely in the case of cardiac surgery, through the use of cardiopulmonary bypass.

Pathophysiologic changes include increased oxygen consumption and energy expenditure, increased secretion of adrenocorticotrophic hormone, cortisol, epinephrine, norepinephrine, insulin, and growth hormone, and decreased total tri-iodothyronine levels. Quantifiable metabolic consequences of these changes include hyperglycemia, hyperlactatemia, increased free fatty acid concentrations, hypokalemia, increased production of inflammatory cytokines, and increased consumption of complement and adhesion molecules. Cortisol levels can increase to more than 500% of baseline levels and remain elevated for several days.7 Particularly concerning is the rise in catecholamine levels, as these contribute to postoperative arrythmias.8

Effective attenuation of the entire stress response is not practically achievable, as the effect contributed by cardiopulmonary bypass is difficult to mitigate (see Chapter 17). However, management of postoperative pain is a factor within the anesthesiologist’s control. Control of pain by any means will aid in reducing the stress response, but because of the robust nature of the afferent impulses and the duration over which they are delivered to the central nervous ...

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