Intraoperative myocardial ischemia can occur when there is an oxygen supply and demand imbalance. This can lead to such perioperative events as:
Congestive heart failure (CHF)
Arrhythmias
Myocardial infarction (MI)
Cardiogenic shock and end-organ damage
Death
A thorough preoperative cardiac evaluation can identify the severity (and presence) of disease in patients with diagnosed or suspected coronary artery disease (CAD). History and physical exam, combined with laboratory, EKG, and stress testing (stress EKG, echocardiography, nuclear scans), can confirm or refute myocardium at risk for ischemia.
Epidemiology
Incidence
CAD, the primary contributing factor to myocardial ischemia, affects over 11 million Americans.
The incidence of perioperative myocardial ischemia is unknown as its detection is largely a function of monitoring technique (simple or multilead EKGs with or without computer ST segment analytic enhancement, pulmonary artery catheter, TEE, etc.) and the skill of the monitoring personnel.
Prevalence
CAD in the general population increases with age.
Age 15–44 years: 4 per 1,000
Age >65 years: 80 per 1,000
Morbidity
Myocardial ischemia can lead to infarction, arrhythmias, heart failure.
Mortality
Perioperative MI remains the leading cause of postoperative death in the elderly (1) [C].
Etiology/Risk Factors
Preoperative risk factors:
Increasing age
Previous MI
Angina
Arrhythmias
Hypertension
Diabetes mellitus
Peripheral vascular disease
Hypercholesterolemia
Cigarette smoking
Perioperative risk factors:
Hypertension
Hypotension
Hypoxia
Hemodilution
Tachycardia
Increased cardiac work/tension
Physiology/Pathophysiology
Ischemia can result from a decrease in oxygen supply or an increase in oxygen demand.
Decreased myocardial oxygen supply is the result of a decrease in coronary blood flow or blood oxygen content:
Decreased coronary artery perfusion pressure can result from decreased diastolic blood pressure or increased left ventricular end-diastolic pressure. CPP = DBP - LVEDP, where CPP is coronary perfusion pressure, DBP is diastolic blood pressure, and LVEDP is left ventricular end-diastolic pressure.
Coronary artery stenosis (fixed) or vasospasm (variable) obstructs coronary blood flow. Distal to the stenosis, the vessel becomes maximally dilated over time to maintain blood flow. However, it lacks the ability to further compensate for decreases in blood flow.
Thromboembolic phenomenon. Stasis, inflammation, and tachycardia can dislodge clots and block coronary arteries, decreasing coronary blood flow.
Tachycardia decreases diastolic time, and, thus, the duration that the LV is perfused. During systole, LV intracardiac pressures exceed CPP; thus, blood flow only occurs during diastole.
Decreased blood oxygen-carrying capacity can result from red blood cell loss/anemia, decreased oxygen saturation, or hypoxemia.
Increased myocardial oxygen demand occurs when there is an increase in cardiac work:
Tachycardia increases the number of times that the myocardium depolarizes and repolarizes as well as mechanically contracts and relaxes.
Increased contractility. Mechanical contraction follows myocyte depolarization and involves the energy consuming process of sarcomere shortening.
Increased ventricular wall tension can occur with
Increased afterload (pressure work): Increased systemic (or pulmonary) vascular resistance, intraventricular pressures and radius, as well as hyperviscosity, and decreased aortic compliance
Increased preload (volume work)
Ventricular hypertrophy. The increased muscle mass requires a greater amount of energy for each contraction. Additionally, the "watershed" subendocardium is more likely to become ischemic during times of decreased supply or increased demand.
Prevantative Measures
Optimize myocardial oxygen supply
Maintain mean arterial pressures. General anesthesia with volatile or IV medications as well as neuraxial blocks can decrease BP. Consider the use of nitrous oxide to allow decreased doses, low-dose vasopressor infusions, and fluid and/or blood administration, as appropriate.
Decrease LVEDP. Consider enhancing inotropy to improve emptying as well as decreasing preload
Decrease the risk for thromboembolic phenomenon.
Discuss with the surgeon and primary care doctor/cardiologist the perioperative management of platelet inhibitors or other anticoagulants in patients currently on medications or at high-risk for cardiac events.
The pleiotropic effects of statins have been shown to improve endothelial function, enhance the stability of atherosclerotic plaques, decrease oxidative stress and inflammation, and inhibit the thrombogenic response. Certain patient populations may benefit from de novo preoperative administration; additionally, abrupt withdrawal in patients taking statins has been associated with an increase in myocardial events.
Decrease the heart rate with beta-blockers, calcium channel blockers, and opioids. Additionally, avoid increases in heart rate from drugs with sympathetic or vagolytic properties as well as hypotension (reflex). Anticipate increases during laryngoscopy, incision, surgical stimulation, and extubation.
Optimize blood oxygen content with adequate hemoglobin levels and oxygen partial pressure. Consider transfusing blood, increasing the FIO2, adjusting ventilator settings (respiratory rate, tidal volumes), and administering positive end-expiratory pressure (PEEP).
Decrease myocardial oxygen demand
As above, decrease the heart rate and anticipate inciting medications or events that can cause tachycardia.
Decrease inotropy, if appropriate, by removing sympathetic stimulation, administering beta-blockers, and avoiding drugs with positive inotropy. However, decreases in ejection fraction/stroke volume can increase the LVEDP (thus decreasing the CPP) as well as forward flow.
Decrease preload. Consider diuretics, venodilators, fluid restriction, and enhancing forward flow with inotropy, as appropriate.
Decrease afterload. Maneuvers to decrease systemic vascular resistance may jeopardize the mean arterial pressure and should be done cautiously.
EKG. The standard lead monitoring (3 lead: I, II, III) is relatively insensitive, but can be altered by placing the left shoulder lead at the cardiac apex yielding a 3 lead: I, II, modified V5 that allows for ischemic monitoring of the inferior (II) and lateral (V5) LV walls (the areas most vulnerable to ischemia). Diagnostic mode with computer ST segment analytic enhancement is more robust when used with a 5 lead system. Intraoperative 12-lead EKG is generally cumbersome and impractical. However, it may be considered when ischemia is suspected.
ST segment depression or elevation
T wave changes
Arrhythmias
Conduction changes
Pulmonary artery catheters may demonstrate increases in LVEDP or PCWP, reflecting a change in ventricular compliance during ischemic states, or acute mitral insufficiency from papillary muscle ischemia. The etiology of these changes should be determined to distinguish them from false positives. Additionally, decreases in cardiac output and mixed venous oxygen saturation can also suggest ischemia.
Transesophageal echocardiogram (TEE). New regional wall-motion hypokinesis, dyskinesis; systolic thinning/thickening abnormalities; new papillary muscle dysfunction/mitral insufficiency.
Differential Diagnosis
False positive ST-segment changes may result from
Mitral valve prolapse
Pressure overload of the LV in young hypertensive patients can lead to false positive ST-segment changes (2) [B].
Left bundle branch block
Wolff–Parkinson–White syndrome
Right bundle branch block
Digitalis, tricyclic antidepressants, diuretics
Artificial pacemakers
Arrhythmias may be seen with sympathetic agents, metabolic abnormalities, drug toxicities
Treatment⬆⬇
Many of the treatment maneuvers are similar to preventative actions, but can differ in the degree of aggressiveness, level of invasive monitoring, as well as the possible need for discontinuing the surgery and intraoperative or postoperative cardiology evaluation. Additionally, because the heart is the pump for its own blood supply, decreasing oxygen consumption may come at the cost of decreasing the oxygen supply; this requires careful titration and optimization.
Decrease the heart rate with beta-blockers and remove inciting stimuli in order to increase oxygen supply and decrease demand. Beta-blockers need to be titrated appropriately to avoid undesired decreases in inotropy.
Decrease inotropy with myocardial depressants (beta-blockers, volatile anesthetics) in order to decrease myocardial work (3) [B] while maintaining an appropriate forward flow/stroke volume.
Optimize the BP to balance coronary perfusion with myocardial tension (afterload).
Mean arterial pressures can be increased with vasopressors (alpha-agonists such as phenylephrine, norepinephrine, or vasopressin). High-dose dopamine and epinephrine have predominantly alpha-effects, but may be accompanied by tachycardia. Consider removing medications that decrease the systemic vascular resistance (e.g., volatiles, IV medications, and epidural infusions).
Decrease afterload with nitrovasodilators, volatile agents, calcium channel blockers.
Decrease preload with venodilators such as nitroglycerin (immediate) or diuretics such as furosemide (onset 20–30 minutes). Additionally, decreasing the LVEDV/LVEDP can optimize the CPP.
Increase blood oxygen content
Blood transfusion can increase the hemoglobin level, but is associated with metabolic abnormalities, immune reactions, increased viscosity, and worsened outcomes in critically ill patients.
Discontinue or abbreviate the surgical procedure, if appropriate.
Cardiology evaluation may be performed intraoperatively or in the recovery room.
Follow-Up⬆⬇
EKG. Attain a 12-lead EKG and place the patient on continuous monitoring.
Cardiac enzymes should be drawn to evaluate for myocardial damage. Troponin (most cardiac-specific peaks at 12 hours), CK-MB (relatively cardiac-specific peaks at 10–24 hours), LDH (least cardiac-specific peaks at 72 hours).
Cardiology consultation to oversee dynamic cardiac stress or angiographic evaluation, acute interventional management (4) [A] (5) [B], and ongoing risk factors (6) [A].
References⬆⬇
DjokovicJL, Hendley-WhyteJ.Prediction of outcome of surgery and anesthesia in patients over 80. JAMA. 1979;242:2301.
FroelicherVF, YanowitzFG, ThompsonAJ, et al.The correlation of coronary angiography and the electrocardiographic response to maximal treadmill testing in 76 asymptomatic men. Circulation. 1973;48:597.
KemmotsuS, HashimotoY, ShimosatoS.Inotropic effects of isoflurane on mechanics of contraction in isolated cat papillary muscles from normal and failing hearts. Anesthesiology. 1973;39:470.
SinghS, BahekarA, MolnarJ, et al.Adjunctive low molecular weight heparin during fibrinolytic therapy in acute ST-segment elevation myocardial infarction: A meta-analysis of randomized control trials. Clin Cardiol. 2009;32:358–364.
ChenZM, PanHC, ChenYP, et al.Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: Randomized placebo-controlled trial. Lancet. 2005;366:1622–1632.
RussellCL, ConnVS, JantarakuptP.Older adult medication compliance: Integrated review of randomized controlled trials. Am J Health Behav. 2006;30:636–650.
Additional Reading⬆⬇
See Also (Topic, Algorithm, Electronic Media Element)
414.8 Other specified forms of chronic ischemic heart disease
ICD10
I25.89 Other forms of chronic ischemic heart disease
Clinical Pearls⬆⬇
Largely preventable with diligent hemodynamic monitoring and close attention to maintaining baseline hemodynamics and physiologic conditions in the face of surgical interventions.
Accurate EKG lead placement – especially leads II, V5 – is a cornerstone of myocardial ischemia detection.
Treatment should consist largely of restoration of baseline hemodynamic and physiologic conditions.