Perioperative myocardial ischemia is one of the serious complications of surgical treatment. Myocardial ischemia can cause significant changes in cardiac function and induce a series of serious events, such as myocardial infarction, arrhythmia, pulmonary edema, and even death. The assessment, prevention and effective treatment of perioperative myocardial ischemia are the keys to reduce cardiac accidents and complications, and contribute to the patient’s immediate recovery and long-term prognosis.
I. Metabolic and physiological mechanisms of myocardial ischemia
Myocardial ischemia occurs when the coronary blood supply cannot meet the energy needs of the myocardium. Therefore, myocardial ischemia can occur either when the coronary blood supply is significantly reduced or when the myocardial need for energy is significantly increased. In myocardial ischemia, there is not only a lack of oxygen to the myocardial tissue, but also a failure to remove potentially toxic metabolites, resulting in the accumulation of lactate, carbon dioxide and hydrogen ions. In addition, the restoration of blood flow may further aggravate the extent of the injury (reperfusion).
Under normal conditions, the myocardium is completely dependent on carbon for aerobic metabolism, with very little intracellular oxygen and ATP. Fatty acids are the primary mode of energy supply for myocardial oxidative phosphorylation, and other substrates include glucose, amino acids, pyruvate, and lactate. Once myocardial ischemia occurs, the myocardium rapidly shifts from aerobic to anaerobic metabolism, resulting in the production of large amounts of lactic acid.
After coronary occlusion, there is an outward migration of K+ from the ischemic cells in less than 1 minute, and the extracellular K+ concentration increases. The loss of intracellular K+ in the myocardium leads to alterations in myocardial cell membrane polarization and abnormalities in the ST segment of the electrocardiogram and underlies ventricular arrhythmias in the early stages of myocardial ischemia.
Calcium homeostasis is a key factor in maintaining normal cardiac function, and dysregulation of calcium homeostasis is an important pathogenetic factor in myocardial cell injury. The increase in intracellular calcium ions in ischemic myocardium is responsible for the contracture that occurs in ischemic myocardium.
In myocardial ischemia, the above metabolic changes lead to progressive membrane function changes and ion homeostasis dysregulation, and the early membrane function changes are characterized by ion pumps and ion channels becoming impaired one after another, the earliest being potassium ion efflux from ischemic myocardial cells, which occurs before Na+-K+-ATPase dysfunction, and when ATP is reduced to When ATP is reduced to a certain level, Na+-K+-ATPase becomes significantly impaired, so Cl- and water accumulate in the cell, K+ is further lost, and the cell loses the ability to regulate its own volume, and intracellular edema occurs. As ischemia increases, ion pump transport is dysregulated, and large amounts of calcium ions enter the cell and activate phosphatidic acid and lipase, resulting in irreversible changes due to structural damage to the cell membrane and cell disintegration.
In terms of mechanics, acute myocardial ischemia can affect the systolic and diastolic functions of the heart. Diastolic dysfunction often precedes changes in systolic function. The immediate effects of myocardial ischemia on ventricular compliance are related to the etiology of the ischemia. Decreased oxygen supply begins with increased ventricular compliance, and increased oxygen demand is associated with an immediate and significant decrease in ventricular compliance (i.e., the ventricles become stiff). The ventricle requires a higher filling pressure (LVEDP) to maintain a certain volume per beat. At this point, the patient may exhibit abnormal wall motion, arrhythmias, and conduction block. An 80% decrease in coronary blood flow may cause ventricular systolic weakness; a 95% decrease in coronary blood flow may result in ventricular dyskinesia. In severe myocardial ischemia, elevated LVPEDP can cause pulmonary edema. Ischemic myocardium can be irreversibly damaged (infarction) or immediately recovered, while there are other physiological pathways. After transient severe myocardial ischemia, myocardial systolic function can be gradually recovered, i.e. myocardial depression; while chronic severe ischemia can cause a decrease in cardiac systolic function such as chronic ventricular wall motion abnormalities, i.e. myocardial hibernation.
Stable ischemia syndrome may occur as a result of increased oxygen demand based on fixed plaques in the coronary arteries. In contrast, the unstable ischemic syndrome is generally considered to be a plaque rupture with local embolization and local vascular response, resulting in an intermittent decrease in oxygen supply to the critical coronary vessels. endothelial cell function is impaired in patients with CAD or hypertension, resulting in increased vasoconstriction. Patients with left ventricular hypertrophy in this state will have even worse subendocardial perfusion due to minimal coronary vasodilation and a rapid decrease in myocardial reserve capacity in the event of myocardial ischemia. The early manifestation of myocardial ischemia after noncardiac surgery is almost always ST-segment depression rather than ST-segment elevation. ST-segment depression usually precedes postoperative cardiac complications. Most perioperative myocardial infarctions present with a non-Q-wave pattern.
Patients during the postoperative period are often characterized by adrenergic stress, which can induce myocardial ischemia in patients with CAD, causing coronary vasoconstriction and promoting platelet aggregation. Tachycardia shortens cardiac diastolic and coronary perfusion times and can also reduce coronary artery diameter.
The surgery itself can induce hypercoagulability due to increased platelet count and function, decreased fibrinolysis, decreased levels of natural anticoagulants (including protein C and from antithrombin III), and increased procoagulants (fibrinogen, coagulation factor VIII, and vW factor). These postoperative changes may increase the likelihood of postoperative coronary thrombosis, but their significance remains to be clarified.
II. Risk factors
Lee et al. recently identified preoperative risk factors associated with adverse outcomes as.
1, pre-existing CAD.
2, high-risk surgery.
3, history of ischemic heart disease.
4, history of congestive heart disease.
5, history of cerebrovascular disease.
6, preoperative treatment with insulin.
7, preoperative serum creatinine greater than 110 μmol/L.
Other possible risk factors include peripheral vascular disease, advanced age, severe physical limitation, uncontrolled hypertension with left ventricular hypertrophy, and those on digitalis. Decompensated cardiac disease such as arrhythmias or chronic congestive heart failure is particularly associated with poor outcomes.
Clinically controllable factors that increase postoperative myocardial ischemia include: tachycardia, anemia, hypothermia, shivering, hypoxemia, endotracheal suction, and inadequate analgesia. Perioperative myocardial infarction in patients undergoing noncardiac surgery may be associated with a faster postoperative heart rate and a higher pain threshold, but may not be associated with angina pectoris (mostly resting).
Postoperative myocardial ischemia does increase the risk for surgical patients. The Perioperative Myocardial Ischemia Study (SPI) group showed that 20% of preoperative patients and 41% of intraoperative and postoperative patients had ischemic ST-segment changes; inpatients with postoperative myocardial ischemia had a 9-fold increased risk of cardiac events, and Landesberg et al. showed a 32-fold increased risk of cardiac events in patients with acute myocardial ischemia for more than 2 h. Both studies concluded that postoperative myocardial infarction is usually preceded (>24h) by prolonged and severe ST-segment depression. Perioperative myocardial infarction is associated with 15-30% in-hospital death and is an indicator of poor patient prognosis after hospital discharge.
III. Monitoring and diagnosis of myocardial ischemia
1.Electrocardiogram
Standard 12-lead ECG is the most commonly used method to monitor perioperative myocardial ischemia, and the diagnosis is mainly based on ST-segment and T-wave changes. Confirmation criteria.
a, ST-segment elevation or decrease greater than 0.1mv.
b, ST-segment elevation greater than 0.15mv in leads without Q waves.
c, T-wave hypoplasia or inversion.
The number and location of ECG leads can affect the detection of myocardial ischemia. Most scholars recommend the use of II/V5 leads, and London et al. showed that the detection rate of myocardial ischemia was only 80% in II/V5 leads and 96% in II/V5/V4 leads; Landesberg et al. suggested that the highest detection rate was achieved in V3, 4 and 5 leads.
2.Exercise ECG
The more ST-segment decrease, the longer the duration, and the more the number of leads with ST-segment decrease, the more severe or extensive ischemia is indicated. Exercise ECG can detect occult myocardial ischemia, but its results are affected by many factors, such as the location and severity of the coronary lesion, the number of branches of the lesion, the presence of collateral circulation, the patient’s age, gender and the presence of symptoms.
3.Other methods
Such as echocardiography, radionuclide, coronary angiography. It has also been proposed that elevated PCWP and its characteristic wave pattern are indicators of ischemia. However, most studies have concluded that PAC is not a sensitive indicator and should not be used as a primary monitoring method.
TEE is a highly sensitive indicator for monitoring myocardial ischemia. myocardial ischemia on TEE is manifested by new segmental ventricular wall motion abnormalities (RWMAs), reduced systolic wall thickening, and ventricular dilatation. the presence of RWMAs after extracorporeal shutdown during CABG surgery is associated with poor clinical outcome. In contrast, ECG-detected ischemia or RWMAs prior to extracorporeal circulation are not associated with perioperative cardiac event rates. disadvantages or problems of TEE include: high cost; inability to obtain changes prior to TEE insertion; and intraoperative real-time analysis of TEE images can reduce the accuracy of the analysis. It is generally accepted that there is little value in combining ECG and TEE monitoring in non-cardiac surgery patients. However, TEE is twice as valuable as ECG in predicting the occurrence of myocardial infarction in patients with CABG. Moreover, patients with both ECG and TEE showing myocardial ischemia have the highest relative risk (RR) of myocardial infarction.
4.Laboratory tests
Serum glutamic oxalacetic transaminase is increased within 1 hour of myocardial ischemic damage, lactate dehydrogenase is decreased within 2 hours, myocyte creatine phosphatase is imbalanced and serum CPK is increased, which has a sensitivity and specificity of 95% for the diagnosis of acute myocardial infarction.
Prevention of myocardial ischemia
1. Make adequate preoperative preparation, correct anemia and electrolyte imbalance, control blood pressure and heart rate at appropriate levels, and stop the medication for those treated with β-blocker before surgery.
2. Select appropriate anesthesia, use reasonable drugs, maintain stable, prevent too shallow or too deep anesthesia, prevent too wide plane of intravertebral anesthesia, and avoid drastic changes in blood pressure and heart rate.
3. Strengthen anesthesia management and monitoring, timely detection and early treatment.
V. Treatment of myocardial ischemia
1, the rational use of anesthetic sedative and analgesic drugs, for suspected cases of coronary artery disease or previous myocardial ischemia, preoperative morphine and valium are used to eliminate fear and tension and cardiovascular reactions. High-dose sufentanil can reduce the stress response to improve recovery after abdominal aortic aneurysm surgery. A study showed that the application of 1 μg?Kg-1?h-1 sufentanil after CABG reduced the incidence of myocardial ischemia.
2. β-blockers: β-blockers can inhibit perioperative tachycardia and reduce myocardial oxygen consumption, and are considered to be the most effective drugs for the prevention and treatment of perioperative myocardial ischemia, and can reduce distant cardiac events. Beta blockers have been shown to be used in the treatment of hypertension, supraventricular tachycardia, ventricular arrhythmias, angina pectoris and myocardial infarction. This class of drugs reduces the incidence of reinfarction after myocardial infarction and is therefore the basis for long-term therapeutic use after myocardial infarction. During adrenergic excitation such as tracheal intubation, tracheal extubation and chest opening, β-blockers can exert their anti-hypertensive effects and also reduce tachycardia. This is the main mechanism of its anti-myocardial ischemia. Most recent studies have concluded that beta blockers are the most effective agents in patients with many clinical high-risk factors or stress states.
The ACC/AHA 2002 guidelines for perioperative cardiovascular evaluation of patients undergoing non-cardiac surgery recommend perioperative ① control of recent episodes of angina symptoms or symptomatic arrhythmias or hypertension requiring beta blockers (long-term beta blockers should not be withdrawn); ② preoperative myocardial ischemia found in patients proposed for vascular surgery who are at high cardiac risk, beta blockers are appropriate.
Those taking beta blockers are less likely to develop supraventricular tachycardia after cardiac surgery and thoracic surgery. The peak incidence of postoperative supraventricular tachycardia and atrial fibrillation is 2 to 3 days after surgery. Selective beta blockers are less likely to induce bronchospasm, even in patients with airway hyperresponsiveness. Of course, beta blockers are relatively contraindicated in patients with asthma and COPD, but selective short-acting beta blockers can usually be applied without increasing airway resistance.
3, calcium channel blockers: slow down the heart rate, dilate the coronary arteries and peripheral vessels, the dilating effect on the coronary arteries and peripheral arteries is 7 to 10 times stronger than the inhibitory effect on the myocardium. Such as nifedipine, verapamil, nicardipine. The short-acting calcium antagonist nifedipine can increase mortality after acute myocardial infarction and should not be used as a first-line drug to control acute hypertension.
4. Nitroglycerin, which has a dilating effect on systemic size A and V, can reduce left ventricular end-diastolic pressure and ventricular wall tension, which facilitates coronary blood flow from epicardium to endocardium, thus improving myocardial ischemia. A study showed that prophylactic application of nitroglycerin did not reduce the incidence of perioperative myocardial ischemia in patients with pre-existing or suspected CAD who underwent noncardiac surgery. This may be related to compensatory tachycardia.
5, epidural analgesia: epidural analgesia can reduce cardiac preload and afterload, reduce adrenergic response and coagulation response, and thoracic epidural analgesia can also dilate coronary vessels. This suggests that epidural analgesia may reduce perioperative myocardial ischemia. However, the basis for improved recovery of cardiac function after epidural analgesia is not well established; and there are concerns about respiratory depression and epidural hematoma. Two recent studies suggest that regional anesthesia does reduce the incidence of myocardial infarction by 1/3, especially with the application of thoracic epidural anesthesia.
6. NSAIDS/modulation of blood homeostasis: NSAIDS are used in many CAD patients for pain relief and antiplatelet effects, but the exact effect is still unknown. Ketorolac can reduce surgical stress without prolonging bleeding time or causing renal insufficiency. A study showed that the addition of ketorolac to morphine PCA reduced the incidence of myocardial ischemia after total arthroplasty. Whether the effect is due to analgesia or antiplatelet is unknown. The main problem is increased bleeding after surgery. COX2 (cyclooxygenase) inhibitors have analgesic but less cardioprotective effects than aspirin and other platelet inhibitors.
7. α2 agonists. α2 adrenergic receptors are located in the presynaptic membrane and mediate a decrease in norepinephrine release at presynaptic terminals, thereby reducing norepinephrine transmission in the central nervous system and producing sedative, anxiolytic and analgesic effects. Preoperative application of colistin reduces hypertension, tachycardia, and norepinephrine levels in patients undergoing aortic reconstruction surgery. Colistin also inhibits the postoperative increase in fibrinogen levels and antagonizes epinephrine-induced platelet aggregation. One study showed that oral administration of colistin 3 mg¤Kg 90 min before admission to the operating room significantly reduced the incidence of perioperative myocardial ischemia in CAD patients undergoing non-cardiac surgery. The more specific α2 agonists dexmedetomidine and mivazerol may also reduce postoperative myocardial ischemia.
8. Management of acute myocardial infarction. Cardiologists should consult patients with suspected myocardial infarction as early as possible. Treatment principles include adequate perfusion (angioplasty or CABG, while thrombolysis is generally contraindicated after surgery), application of aspirin and beta blockers, avoidance of calcium blockers, and selection of ACEI for poor left ventricular function. iABP can improve coronary blood flow and reduce cardiac work in patients with progressive myocardial infarction.
9. Anemia/hypothermia. Anemia is associated with an increased incidence of postoperative myocardial ischemia. In high-risk patients and patients with myocardial ischemia, hematocrit should be adjusted to 30% so that the oxygen-carrying capacity of blood reaches a safer level. Hypothermia is also associated with postoperative myocardial ischemia, and therefore intraoperative and postoperative warming and insulation devices are needed for high-risk patients. Recent studies have shown that the use of hot air warming devices in elderly patients can reduce the incidence of cardiac events.