Introduction

Pain after cardiac surgery is common; 75% of patients recall experiencing moderate to severe pain on the cardiac ICU. This has significant physiological and psychological consequences, potentially leading to chronic pain, affecting up to 50% of patients. Adequate treatment is essential to recovery.

Basic Pain Physiology

Pain is ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such’ (Association for the Study of Pain Taxonomy). It is an integrated process of peripheral and central events. Modulation and interpretation produce individual reactions, giving meaning to the stimulus–response relationship.

Nociceptors, peripheral projections of primary sensory neurones, are sensitive to physical and chemical stimuli, including heat and acid. These directly activate neuronal ion channels resulting in an action potential (AP). Additionally, inflammatory mediators produced following surgery indirectly sensitize nociceptors to subsequent stimuli, by reducing the AP generation threshold.

First-order neurones transmit APs to the dorsal horn (DH) of the spinal cord via:

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  Aβ fibres – conducting touch

  
  
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  Aδ fibres – causing sharp localized pain

  
  
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  C fibres – producing dull, poorly localized pain

The majority of second-order neurones, transmitting impulses from the DH to the mid-brain, decussate before ascending spinothalamic pathways. Mid-brain fibres project to the sensory cortex where pain perception occurs. This is modulated by past experience and the balance between noxious and inhibitory impulses within the CNS and spinal cord. Pathological changes here are likely responsible for the development of chronic pain.

Causes of Pain Following Cardiac Surgery

Routine cardiac surgery produces a combination of somatic, visceral and neuropathic pain (Box 39.1):

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  Somatic pain: Superficial or deep, arising from skin, muscle and bone. Stimulating dermal nerve endings causes sharp, well-localized superficial pain. In contrast, deep pain, from muscles, is dull and poorly localized.

  
  
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  Visceral pain: From deep, internal tissues. Typically, diffuse and poorly localized pain, associated with autonomic disturbances (e.g. nausea, sweating). Afferents travel alongside autonomic projections; spinal-level convergence leads to referred pain in dermatomes of shared embryonic origin. Cardiac pathways specifically refer pain to the neck and arm (e.g. vagus nerve, cervical sympathetic and upper five thoracic ganglia).

  
  
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  Neuropathic pain: Consequent upon neuronal tissue lesions (central or peripheral). Often accompanied by positive (e.g. allodynia, hyperalgesia) and/or negative symptoms (including loss of sensation: hypoaesthesia or hypoalgesia).

Common cardiac surgery incisions involve cervical, thoracic and lumbar dermatomes (Figure 39.1). Initially, pain is located within wound and drain sites. Over time it may become more generalized to trunk and limb, particularly following internal mammary artery (IMA) conduits.

Figure 39.1 Cardiac surgical incisions and corresponding dermatomes

The physiological and psychological consequences of pain following cardiac surgery are summarized in Table 39.1.

Acute Pain Management

Virtually all cardiac surgical patients experience pain from surgical incisions, medical devices and invasive procedures. As many have co-morbidities associated with chronic pain (e.g. DM, arthritis, heart failure), these must be considered in analgesic planning before surgery.

Regular pain assessment using validated tools improves patient outcomes, both alerting staff to its presence and allowing evaluation of interventions. Self-assessment tools (including numerical, verbal rating, visual analogue or descriptor scales) represent ‘gold standard’ pain evaluation, and these can be adapted for non-verbal patients. Those unable to self-report should be assessed with measures validated in ICU patients, such as the critical care pain observation tool.

Acute pain management should include:

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  Prevention: Attention to patient positioning, choice of incision(s) and operative technique minimizes the risk of postoperative pain. Placing the arms in internal, rather than external, rotation reduces the incidence of shoulder pain. Similarly, bony fractures and excessive sternal retraction, particularly during IMA harvesting, should be avoided. Endoscopic techniques for conduit harvesting may reduce incisional pain.

  
  
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  Patient and caregiver communication: Preoperative discussion regarding expectations and management plans is paramount. Deciding what is achievable and acceptable is especially important in individuals with pre-existing chronic pain; total absence of postoperative pain may be unrealistic. Agreed plans should be documented and communicated to all caregivers, ensuring consistent delivery.

  
  
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  Pharmacological management: Chronic postoperative pain is an emerging research field. It is thought to relate to neuronal plasticity and long-term neurophysiological change following acute pain. Thus, effective acute pain management enhances early comfort and reduces the risk of chronicity.

Moderate to severe nociceptive pain is best managed with opioids. Activation of central and peripheral opioid receptors inhibits release of, and response to, neurotransmitters. Additional benefits are associated with increased vagal tone. Various administration routes are available; however, patient-controlled administration provides better analgesia than nurse-controlled. When titrated intravenously, common drugs (e.g. remifentanil, fentanyl, morphine, oxycodone) show similar efficacy; therefore, choice is based on patient co-morbidities and side effects. Side effects are often dose-related and can be reduced by titration to effect or choosing a different drug (opioid switching).

A ‘multimodal’ approach should be considered, using drugs synergistically to facilitate opioid sparing. Paracetamol is relatively safe in most patients. There is currently little place for NSAIDs in the early postoperative period. Their side-effect profile is concerning (risk of GI bleeding and renal insufficiency) and they are associated with an increased risk of death, re-infarction and cardiac failure in certain cardiac populations. Adjuncts for consideration where opioids and paracetamol are insufficient include α-agonists (e.g. clonidine), N-methyl-d-aspartate-receptor antagonists and α2δ ligands (e.g. gabapentin or pregabalin, which decrease acute pain scores and opioid consumption, and pain 3 months after surgery).

Central neuraxial blockade has failed to demonstrate any impact on either morbidity or mortality following cardiac surgery. Whilst meta-analysis of thoracic epidural analgesia suggests decreased postoperative complications, concerns about epidural haematoma formation limit its use. There is little convincing evidence to support wound infiltration or catheter-based regional nerve blocks in cardiac surgery; however, peripheral local anaesthesia may provide immediate postoperative analgesia.

Related posts:

Chapter 3 – Diagnostic Techniques Chapter 6 – Weaning from Cardiopulmonary Bypass Chapter 11 – Tricuspid and Pulmonary Valve Surgery Chapter 19 – Procedures for Structural Heart Disease Chapter 24 – Temperature Management and Deep Hypothermic Arrest Chapter 35 – TOE for Miscellaneous Conditions