Introduction
Myocardial ischemia, whether in the anesthesia, prebypass, immediate post–cardiopulmonary bypass (CPB) settings, or early postoperative period in the intensive care unit (ICU), is stressful for the surgeon, medical and nursing staff, and the patient. It occurs in coronary artery bypass graft surgery (CABG) with an incidence of 2%–10% .
There can be numerous causes, many specifically related to the surgery, or patient journey. There can be challenges in recognition of the ischemia, and establishing its causes, which need to be corrected immediately. Uncorrected severe myocardial ischemia or established perioperative myocardial infarction will result in a significantly higher perioperative mortality, a reduced ejection fraction long-term, and a poorer prognosis and survival .
This chapter will outline a practical approach and consider perioperative myocardial ischemia in the following conditions:
- 1.
The anesthetic and prebypass setting.
- 2.
While handling of the heart during surgery—especially in off-pump CABG (OPCAB).
- 3.
Surgery related/iatrogenic technical problems leading to immediate postbypass or early postsurgery ischemia.
- 4.
Recognition and management in the ICU setting (first 24 hours).
- 5.
Myocardial ischemia occurring in other (non-CABG) cardiac surgery.
Diagnosis of myocardial ischemia/myocardial infarction
EKG diagnosis of perioperative myocardial ischemia is challenging, particularly in the intraoperative setting, as the number of monitoring leads is limited—often only leads II and V. A number of abnormal parameters occurring concurrently will help reinforce the suspicion or diagnosis.
These include:
- 1.
Significant ST-segment depression or elevation.
- 2.
Associated hypotension.
- 3.
Concurrent elevation of the pulmonary artery pressures.
- 4.
New, regional wall motion abnormalities (NWMA) on intraoperative transesophageal echocardiography (TEE). These NWMAs can be the most sensitive and earliest of the ischemia related changes and makes an important case for routine TEE in all cardiac surgery procedures, including CABG . New or worsening mitral regurgitation is also suggestive of myocardial ischemia.
In the immediate postoperative setting, these parameters can be reinforced by:
- 1.
A rise in troponin levels. A rise of three to five times baseline is suggestive and a rise of more than 10-fold is diagnostic of significant ischemic event or perioperative myocardial infarction . The appropriate threshold of high sensitivity troponin for myocardial injury/infarction following on-pump CABG is at present unclear.
- 2.
New Q waves.
- 3.
A reduced and progressively declining cardiac output/index and rising lactate .
Myocardial ischemia in the anesthetic and pre–cardio pulmonary bypass phase
Predisposing factors include severe hypertension, which increases afterload, and cardiac work, and tachycardia that increases myocardial oxygen demand.
Hypotension is, however, much more important with a more profound effect in causing ischemia.
Patients with severe/critical left main coronary stenosis, severe critical triple vessel disease, acute coronary syndromes/unstable angina, severe left ventricular (LV) dysfunction, minimal functional reserve, and critical aortic stenosis are the most vulnerable.
Difficult intubation or prolonged episodes of hypoxia can be predisposing factors.
Severe hypertension is managed with intravenous nitroglycerin, ensuring adequate analgesia—morphine or fentanyl, and judicious anesthesia—propofol, sevoflurane, or other inhalation of agents.
Tachycardia is treated by intravenous short-acting beta-blockers such as esmolol or metoprolol .
Nitroglycerin reduces preload (venous vasodilator), retains aortic diastolic pressure and coronary perfusion pressure, reduces LV end-diastolic pressure and enhances the subendocardial perfusion gradient, reduces afterload (although a relatively weak effect), maximizes coronary vasodilatation, especially in the smaller unobstructed vessels and collateral channels, and helps reverse any coronary spasm .
Hypotension that triggers myocardial ischemia is corrected by placing the patient in the Trendelenburg position, rapid administration of intravenous fluids, and alpha agonist such as metaraminol or norepinephrine.
If the patient is or known to be potentially unstable (e.g., critical left main coronary stenosis with ongoing chest pain, episodes of LV dysfunction, and intermittent ST-segment changes) before coming to the operating room, elective placement of an intraaortic balloon pump (IABP) to reduce afterload, enhance diastolic pressure and coronary perfusion, and maintain cardiac output would allow a safer anesthetic induction and pre-CB period while grafts are being harvested, etc. .
Occasionally, despite having the abovementioned maneuvers, the patient can be so unstable that it is best to rapidly establish CPB, and to then harvest the conduits (even though this may be more awkward and associated with more bleeding), and then proceed with the predetermined grafting strategy/cardiac surgery, in the predetermined manner.
Strategies to prevent or limit perioperative ischemia, especially in the pre-CPB or pregrafting period, include beta-blockers, calcium antagonists , direct coronary and remote ischemic preconditioning, cyclosporine, steroids, and glucose/insulin/potassium infusions. The results have been mixed at best and no strong recommendations exist .
Severe aortic stenosis can be problematic. Hypotension, especially in the setting of concomitant coronary artery disease, may provoke severe ischemia. This is best managed with volume and an alpha agonist such as metaraminol.
Rapid atrial fibrillation that causes hypotension should be immediately electrically reverted.
Ischemia while handling the heart (pre–cardiopulmonary bypass)
Occasionally, myocardial ischemia may manifest while preparing the heart for CPB—when opening the pericardium, placing the purse-string sutures, or inspecting areas of the heart/coronary arteries to plan for grafting—the possible lengths of grafts required, etc.
This situation is readily resolved by rapid institution of CPB, and if necessary cross-clamping, and initiating myocardial protection of the heart. In our practice, this would be with a combination of antegrade (700 mL) and retrograde (300 mL) of blood cardioplegia at 20°C to maintain myocardial temperature of approximately 25°C.
In reoperative cardiac surgery, particularly in redo CABG, prebypass ischemia can be highly problematic, and potentially fatal.
Myocardial ischemia can occur while displacing the heart and dividing adhesions to expose and mobilize the ascending thoracic aorta and the right atrium for cannulation. This may be due to excessive retraction, compression, or inadvertent bleeding and hypotension. Right atrial bleeding can be immediately rectified with 5/0 polypropylene sutures or local compression with a gauze square. A minimal amount of dissection may suffice to expose enough right atrium and ascending thoracic aorta for cannulation and CPB.
Alternatively after local control of any bleeding, peripheral CPB can be instituted, and then further cardiac, pericardial, and retrosternal dissection can occur safely.
A most serious, hazardous, and potentially fatal cause of ischemia in redo CABG is the inadvertent handling, and distal embolization (trashing) in diseased but patent saphenous vein grafts (SVGs), particularly those on the right side. Consequences can be ischemia manifested by dramatic ST-segment changes in the inferior leads, hypotension, and complete heart block. Hence diseased but patent SVGs should be avoided if possible, or if mobilization of the heart behind or distal to these grafts is required, it should be performed after CPB is instituted.
Off-pump coronary bypass surgery is almost always associated with some degree of myocardial ischemia.
Retraction of the heart, especially to expose the circumflex, compresses the right ventricle and to some degree the right atrium and impedes venous return to the heart and subsequent cardiac output. This is managed by placing the patient in Trendelenburg position, rotated to the right, opening the right pleura, displacing the heart very slowly, administration of appropriate fluids, close communication with the anesthetist, and the transient use of vasopressors to ensure adequate systemic pressure. An IABP may also be required .
Essential additional monitoring during such cardiac manipulations includes continuous central right atrial (RA) or pulmonary artery (mixed) venous oxygen saturation and continuous TEE .
If it is predicted that access to the lateral wall will be difficult (large heart) or that myocardial ischemia persists despite taking great care, then the normal cardiac position should be restored and an elective “conversion” to CPB would be appropriate. Patients can be converted to a beating heart approach if there are contraindications to aortic cross-clamping.
Myocardial ischemia while grafting/performing the distal anastomosis is avoided by routinely using intracoronary shunts to maintain distal myocardial perfusion and by grafting the most ischemic territory first, and allowing 5–10 minutes of unencumbered graft and native coronary perfusion, before embarking on the next distal coronary anastomosis.
Elective conversion to on-pump CABG is associated with a standard perioperative mortality (1%–2%), whereas those cases converted as an emergency have a perioperative mortality of 10%–15% .
Technical reasons for myocardial ischemia, detection, prevention, correction
Myocardial ischemia is seen occasionally, after grafting, and after weaning from CPB, and sometimes earlier, in the interval between releasing the cross-clamp and weaning from CPB. This is usually associated with severe and persistent ST-segment changes and regional wall motion abnormalities on TEE. Occasionally, these changes may be transient and physiologic. For example, a period of time is taken for myocyte recovery after reperfusion, especially if the aortic clamp times have been relatively short (1 or 2 bypass grafts) or following an air embolus (when the left-sided cavities have been opened), especially to the right coronary artery (RCA) distribution. Air bubbles can be seen in the acute marginal branches on the anterior aspect of the right ventricle. Both of these situations are transient and will resolve over 5–20 minutes with appropriate cardiac support and high perfusion pressures on CPB.
However, a number of technical problems may be the culprits, and each will be addressed in turn.
Aortic valve regurgitation (AR) which is not severe enough to warrant aortic valve surgery but may be problematic. Even mild degrees of AR should be seriously planned for as:
- 1.
It may lead to inadvertent and unrecognized LV distention while antegrade cardioplegia is being administered, which in turn may lead to severe, and even irrevocable myocardial damage. Awareness of this and placement of an LV vent both to cover the time of administration of cardioplegia and also to help wean the patient off CPB once the cross-clamp is released.
- 2.
The AR may mitigate against adequate myocardial protection, especially by antegrade cardioplegia. This should be preempted by retrograde cardioplegic induction and performing a small transverse aortotomy just above the sinotubular junction to administer additional direct ostial cardioplegia, especially to the RCA.
Coronary spasm is a real entity, difficult to recognize intraoperatively, and is sometimes a diagnosis of exclusion. Correction is by intravenous nitroglycerin (10–50 µg/min) being the usual dose ( Figs. 23.1A–23.3B ). Nitroglycerin can be administered directly into the coronary arteries via the aortic cardioplegic tack when the aortic clamp is in place or through a free graft prior to completion of the proximal anastomosis or with a fine needle into a completed vein graft.
Coronary graft spasm may occur especially in arterial grafts and should be prevented by topical or intraluminal vasodilators (nitroglycerin, papaverine, milrinone, diltiazem, phenoxybenzamine). Spasm may also occur in SVGs ( Fig. 23.4A–C ).
