Perioperative Myocardial Infarction

Updated: Sep 27, 2023
Author: Aneeta Bhatia, MD, FFARCS, FASE; Chief Editor: Perin A Kothari, DO 

Practice Essentials

Key points in the management of myocardial infarction (MI) or injury in the perioperative period include the following:

  • Detailed preoperative risk stratification based on the Revised Cardiac Risk Index (RCRI) and the National Surgical Quality Improvement Program (NSQIP) of the American College of Surgeons [1, 2, 3, 4]  
  • Addition of cardiac biomarkers (eg, fourth-generation troponin T [TnT], fifth-generation high-sensitivity TnT [hs-TnT], and N-terminal prohormone of brain natriuretic peptide [NT-proBNP]) to the RCRI to improve prediction of adverse cardiac events in the immediate postoperative period after major noncardiac surgery [5]
  • Preoperative cardiac evaluation using the American College of Cardiology (ACC)/American Heart Association (AHA) guidelines and algorithm [6, 7]
  • Use of invasive monitoring in patients at high risk for adverse events—specifically, arterial blood pressure (BP) monitoring with or without continuous stroke volume–based cardiac monitors, central venous catheterization with or without a pulmonary artery catheter, and intraoperative transesophageal echocardiography (TEE) carried out according to American Society of Echocardiography (ASE) guidelines [8, 9, 10]
  • Prompt recognition of possible clinical signs or symptoms in the perioperative period via electrocardiography (ECG), altered hemodynamics, changes in biomarkers (eg, TnT or hs-TnT), or new changes in imaging - Persistent hypotension, ST-segment depression or elevation, tachyarrhythmias, bradyarrhythmias, conduction changes, new left bundle-branch block (LBBB), wall-motion abnormalities, or cardiac arrest must be managed; changes in biomarkers must be promptly evaluated [11, 12, 5] ; an elevated plasma cardiac TnT (cTnT) concentration above the 99th percentile of a normal reference population is significant in identification of myocardial injury after noncardiac surgery (MINS)
  • Optimization of myocardial perfusion by maintaining a balance between myocardial oxygen demand and supply
  • Minimization of secondary stressors (eg, emergence, extubation, tachycardia, arrhythmias, anemia, hypothermia, hypoxia, acidosis, and sepsis) that place increased stress or demands on the heart
  • Maintenance of coronary perfusion pressure (CPP) with support of aortic diastolic BP (DBP) by fluid challenge, use of vasopressors to improve CPP, or both; CPP is calculated as DBP minus left ventricular end-diastolic pressure (LVEDP)
  • Correction of metabolic abnormalities and anemia
  • Maintenance of myocardial oxygen delivery as a function of CPP and the oxygen content of the blood; correction of anemia and induction of coronary vasodilation
  • Reduction of oxygen demand by correction of dysrhythmias
  • Use of nitroglycerin for coronary dilation and improvement of myocardial supply
  • Institution of inotropic-vasopressor infusions for further hemodynamic support, with consideration given to the possible need for more invasive support via intra-aortic balloon pump (IABP) or extracorporeal membrane oxygenation (ECMO) for cardiogenic shock
  • Prompt conclusion of the surgical procedure in a safe manner and consultation of cardiology for continued postoperative management 

In view of the prevalence and severity of this complication in the perioperative period, the aim of this article is to provide a sound foundation whereby providers can more readily make a prompt diagnosis of perioperative MI (PMI) and institute an effective treatment plan.



Globally, more than 300 million surgical procedures are performed annually.[13]  As life expectancy increases, the surgical population grows. If perioperative death were to constitute its own category in the annual US mortality tables, it would represent the third leading cause of death.[14]

Cardiac complications constitute a major cause of postoperative morbidity and mortality in surgical patients. Worldwide, more than 10 million patients experience serious cardiac events after noncardiac surgery,[15, 16, 17]  and every year, more than 1 million adults die within 30 days of noncardiac surgery.[16]

Myocardial ischemia, with or without subsequent MI, is a common and feared cardiac complication of noncardiac surgery, with an inpatient mortality in the range of 5-17%.[16, 17, 12]  PMI is the most common of the cardiac complications causing postoperative morbidity and mortality. It has a reported incidence of 1-17% in all types of surgery and is an independent risk factor for cardiovascular death. Patients experiencing an MI after noncardiac surgery have an in-hospital mortality of 15-25%,[15, 16, 17, 18, 19, 20, 21, 22, 23, 11]  with mortality being particularly high in the first 30 days. 

As shown in a 2017 study from the VISION (Vascular Events in Noncardiac Surgery Patients Cohort Evaluation) investigators, as many as 65-93% of patients with PMI have no ischemic symptoms,[17, 12]  and 50% of cases of PMI go unrecognized.[24]  Clearly, this poses a diagnostic dilemma.

For clinical purposes, MI is often broadly classified as non-ST-elevation MI (NSTEMI) or ST-elevation MI (STEMI). A more explicit classification is provided by the fourth universal diagnosis of MI published in 2018 by the Fourth Global MI Task Force.[25]  The Task Force defined this condition as myocardial necrosis in the setting of myocardial ischemia, characterized by a rise or fall in cardiac biomarkers (eg, troponin), along with any of the following:

  • Cardiac symptoms of ischemia
  • ST-T segment changes or new bundle-branch block
  • Pathologic Q waves
  • Imaging evidence of loss of viable myocardium with new regional wall-motion abnormality (RWMA)
  • Intracoronary evidence of thrombus on angiography

Five types of MI are defined in the fourth universal diagnosis,[25] as follows:

  • Type 1- Spontaneous MI related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries, leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis
  • Type 2 - Myocardial injury with necrosis, in which a condition other than coronary artery disease (CAD) contributes to an imbalance between myocardial oxygen supply or demand (not a coronary event)
  • Type 3 – Cardiac death with suggestive symptoms of MI and new ECG changes or ventricular fibrillation (VF) before biomarkers are available for diagnosis
  • Type 4a – MI related to percutaneous coronary intervention (PCI) with stent stenosis and elevation of biomarkers and symptoms or signs suggestive of MI
  • Type 4b – MI with resultant biomarker elevation related to stent thrombosis diagnosed with coronary angiography or on autopsy
  • Type 4c - MI associated with in-stent stenosis in the same territory as balloon angioplasty without angiographic evidence of other culprit lesions
  • Type 5 – MI associated with coronary artery bypass grafting (CABG)

Evolving evidence suggests that the current diagnostic criteria for MI may be insufficient. Advances in the sensitivity of biomarker assays have led to more accurate diagnosis of PMI, better prediction of risk, and a fuller understanding of their prognostic value.[19, 11, 12, 5]  

A broader and more useful clinical concept is MINS, which is defined as prognostically relevant myocardial injury due to ischemia that occurs within 30 days after noncardiac surgery.[19]  The definition of MINS was introduced to focus on the prognostic relevance of a peak in the Roche fourth-generation Elecsys TnT assay. A plasma cTnT level higher than 0.03 ng/mL secondary to myocardial ischemia within 30 days of noncardiac surgery is significant.

MINS has been independently associated with 30-day mortality after noncardiac surgery, specifically in vascular surgical patients.[19] For an accurate determination of the prevalence of this perioperative complication, it is important to distinguish between MINS and noncardiac elevations in troponin (eg, from sepsis or pulmonary embolism).

The development by Roche of a fifth-generation high-sensitivity cTnT (hs-cTnT) assay has permitted detection of very low levels of cTnT. Using this assay improves overall diagnostic accuracy in patients with suspected PMI, and a negative result also has a high negative predictive value. This assay has proved to be a more sensitive biomarker for picking up PMI and predicting 30-day mortality.[12, 5]

The hs-cTnT assay has proved to have a higher prognostic value in MINS.[12]  Evidence suggests that prediction of postoperative MI can be improved by using hs-cTnT and NT-proBNP biomarker assays. Kopec et al found that the addition of hs-cTnT (>14 ng/L) and NT-proBNP (>300 ng/L) to the RCRI significantly improved the prediction of postoperative MI (event rate, 5.2% [30/572]).[5]

PMI presents a significant challenge to the anesthesiologist in that surgery is a high-stress, high-oxygen-demand state associated with hypercoagulability. A coronary thrombus can compromise the oxygen supply, resulting in a critical mismatch between myocardial demand and supply. Although substantial advances have been made in anesthesia safety, comparable advances have not been made in prevention of organ injury in the perioperative period.

Anesthesiologists have the potential to make a significant impact on patient outcomes by achieving more accurate risk stratification, developing a better understanding of the pathophysiologic mechanisms of organ injury, preventing organ injury, and promptly recognizing and treating PMI. Improved outcomes can avoid postoperative escalation in care and healthcare costs.


The exact pathophysiology of PMI is not yet fully defined but is distinct from that of nonoperative MI. Nonoperative MI is characterized by coronary artery plaque fissuring, plaque rupture, or acute luminal thrombosis in the coronary arteries. In patients with PMI, two distinct mechanisms have been described.

The first mechanism is thromboembolic dynamic obstruction from atherosclerotic plaque instability and rupture caused by an increase in luminal shear stress, endothelial activation, or an inflammatory process.[14, 26] The following can predispose to embolic obstruction:

  • Catecholamines and cortisol increase associated with pain, anemia, and hypothermia causing coronary vasoconstriction and plaque instability
  • Tachycardia and hypertension causing increased vascular shear stress and rupture of vulnerable plaques.
  • Increase in procoagulant levels (fibrinogen and von Willebrand factor), reduction in anticoagulant factors (protein C, antithrombin III, and alpha2-macroglobulin), and increase in platelet aggregation contributing to thrombus formation; surgery-induced procoagulant and antifibrinolytic activity triggers coronary thrombosis in patients with or without CAD
  • Trauma associated with surgery sets off an inflammatory cascade; increases in tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, and C-reactive protein (CRP) can initiate plaque fissuring and acute coronary thrombosis [14, 26, 27, 28, 29]

The second mechanism is an unbalanced myocardial oxygen demand-to-supply ratio in patients with chronic CAD,[14, 26, 27, 28, 29] which can develop from the following:

  • Surgery- or anesthesia-induced increased sympathetic activity or hypotension from hypovolemia, bleeding, anemia
  • Anesthesia-induced tachycardia and arterial hypertension during intubation, extubation, and hypothermia
  • Perioperative hypoxia or hypercarbia from respiratory depression in the setting of significant coronary artery stenosis [15, 3, 6]

Typically, PMI occurs early in the postoperative period (peak occurrence, 100 min after surgery), a time characterized by a combination of these factors.

Tachycardia is a well-known determinant of myocardial energy demand, as well as supply. It is well recognized that an elevated heart rate (HR) in the presence of stable coronary artery stenosis causes impairment of subendocardial and epicardial blood flow distribution because of the shortened diastolic time interval, resulting in subendocardial ischemia and myocardial dysfunction. The short-term effects of tachycardia-induced ischemia on myocardial perfusion-contraction matching have been demonstrated in patients (as well as animals) with limited coronary blood flow.[28]

The frequent combination of increased HR and ST-segment depression, detected during Holter monitoring before the event, suggests that prolonged ischemia rather than thrombosis can be the cause of PMI and that most PMIs occur in the absence of ST-segment elevation on ECG.[29]  Landesberg et al found that the rise in cardiac troponin I (cTnI; peak, 21.1 ± 26.5 ng/mL; range, 3.3-100.2 ng/mL) occurred during or shortly after prolonged (>100 min), silent, postoperative ischemia. The majority (67%) of ischemic events, including those converting to PMI, started within 2 hours from the end of surgery and emergence from anesthesia.

Anesthesia in and of itself, whether general or regional, is not a risk factor for high-risk cardiac patients undergoing noncardiac surgery if it is administered without complications. Postoperative stress (including emergence) precipitates ischemia, infarction, or both.

Perioperative myocardial ischemia peaks during the early postoperative period and is significantly associated with MI and cardiac complications. Intraoperative ischemia is less common and is infrequently associated with PMI. Most important is an imbalance between oxygen demand and supply, which is responsible for most cases of PMI.[14, 26, 27, 28, 29]  Preexisting CAD is a strong predictor of PMI, with type 2 NSTEMI being more common than type 1 STEMI.[29]


Timely detection of PMI is of paramount importance. Given that most patients are asymptomatic, the anesthesiologist must rely on clinical signs and technology, not symptoms, to make the diagnosis.

In the awake patient, either pre- or postoperatively, the classic symptom of chest pain is unreliable for detecting PMI because of the presence of confounding variables in the perioperative period (eg, use of pain medications). In pooled data from multiple studies, Devereaux et al[15]  found that only 14% of patients experiencing a PMI will have chest pain.

One of the most common initial findings in the perioperative period is the onset of persistent hypotension, with possible nausea and diaphoresis.[30]  Other signs include decreased oxygen saturation and ECG changes.


An analysis from Bijker et al showed that 64% of patients under anesthesia experienced episodes of systolic BP (SBP) lower than 90 mm Hg and that more than 93% patients had at least one episode of mean arterial pressure (MAP) that was 20% below baseline.[31] In elderly patients, this resulted in adverse outcomes.

The clinical relevance and short and long-term implications of intraoperative hypotension remain controversial. However, Monk et al observed that 1-year mortality increased by 3.6% for each minute that SBP was lower than 80 mm Hg.[32]  In a retrospective review of perioperative deaths, Lienhart et al found that intraoperative hypotension and anemia were closely associated with postoperative myocardial ischemic events.[30, 33]  The etiology of hypotension should be sought and treated in accordance with the algorithm developed by Singh et al.[30]

Electrocardiographic changes

A standard 12-lead ECG is valuable and must be obtained. Characteristic ECG changes include new T-wave inversion and ST-segment depression. ST-segment changes can best be seen in leads V3-5, II, and aVF. Changes reflective of subendocardial or transmural ischemia (ST elevation >1 mm) may be seen. The ACC defined the following ECG changes as meeting the diagnostic criteria for PMI[24] :

  • New Q-wave changes (≥30 ms) present in any two contiguous leads fulfill the definition of the development of pathologic Q waves
  • ECG changes indicative of ischemia are ST-segment elevation (≥2 mm in leads V1, V2, or V3 and ≥1 mm in the other leads) or ST-segment depression (≥1 mm) in at least two contiguous leads, or symmetric inversion of T waves (≥1 mm) in at least two contiguous leads

The majority of PMIs are of the non-Q-wave type, preceded by episodes of ST-seg­ment depression and T-wave inversion.[29]

Postoperative ECG changes concomitant with a troponin leak are independent predictors of mortality.[34] In the VISION study,[11] postoperative ECG changes that were independently associated with 30-day mortality in the presence of a troponin elevation included ST-segment changes, LBBB, and anterior-lead ischemic changes.


Troponin biomarkers have near-absolute myocardial tissue specificity. Only 4-6% of troponin leaks are associated with nonspecific cytosolic leaks. Elevated TnT levels should be evaluated by repeat measurements at 3 and 6 hours, including a delta between these time points, to determine whether the elevation is acute or chronic.

The fourth-generation cTnT assay has a limit of detection (LoD) of 0.01 ng/mL (10 ng/L), a 99th percentile cutoff point of 0.01 ng/mL (10 ng/L), and a 10% coefficient of variation (CV) of 0.03 ng/mL (30 ng/L). For the diagnosis of acute MI (AMI), this is considered the standard assay.

The fifth-generation hs-cTnT assay is a modification of the fourth-generation cTnT assay. In all cases of suspected myocardial injury or MI, this assay should also be checked to confirm the diagnosis.[35]  The fifth-generation assay is more sensitive than the previous-generation assay. Specifically, the LoD is 0.003 ng/mL (3 ng/L), the 99th percentile cutoff point is 0.014 ng/mL (14 ng/L), and the CV is 10% at 0.013 ng/mL (13 ng/L). By virtue of its lower LoD and increased precision, the hs-cTnT assay is able to detect more subtle elevations indicative of cardiac injury.[35]

The VISION study showed that peak postoperative hsTnT during the first 3 days postoperatively was significantly associated with 30-day mortality.[12]  In this study, a measurement of at least 20 ng/L (0.02 ng/mL) in men and 14 ng/L (0.014 ng/mL) in women was considered significant.

Pulmonary artery catheter and cardiac output from arterial pressure waveform

Reduced left ventricular compliance from ischemia results in increased pulmonary artery occlusion pressure (PAOP) and LVEDP. The presence of tall atrial V waves is seen in the tracing if papillary muscles are involved and mitral insufficiency ensues. Impairment of systolic function can lead to decreased cardiac output and mixed venous oxygen saturation.

Indirect evidence can be also be obtained from the measurement of stroke-volume variation (SVV). SVV measurement can rule out hypovolemia, leaving myocardial ischemia as a more probable cause of decreased cardiac output in a patient with cardiac risk factors.

Transesophageal echocardiography

A landmark study by Smith et al provided evidence that segmental wall-motion abnormalities detected via TEE are highly sensitive and specific indicators of myocardial ischemia.[9]  In this study, which involved both TEE and ECG monitoring, new segmental wall-motion abnormalities were detected in 24 of 50 high-risk vascular and coronary artery bypass patients (48%). ECG detected ST-segment changes in only six patients (12%), all of whom also had wall-motion abnormalities. Intraoperative MI occurred in three patients; persistent wall-motion abnormalities had been detected in all three, but ST-segment changes were seen in only one.

TEE is now an integral part of monitoring for PMI.[10]


Once PMI is confirmed by biomarker assays or TEE, all patients should undergo coronary angiography as soon as it is feasible. Prompt diagnosis of the cause of ischemia is needed to further guide appropriate management. In particular, in the setting of NSTEMI, angiography is needed to detect whether the ischemia is type 1 (plaque rupture or thrombosis) or type 2 (supply-demand imbalance). For STEMI or type 1 NSTEMI, invasive intervention will be needed, which can be guided only by angiography.



Addressing the problem

Prevention of perioperative myocardial ischemia is always the goal of the anesthesiologist. The fundamental purpose of a thorough history and a meticulous physical examination is to ascertain the presence of CAD, myocardial ischemia, or both preoperatively and to stratify risk so that aggressive preventive measures can be applied. In the patient with prior heart disease, every attempt should be made to contact the primary cardiologist and obtain records of recent visits and testing.

According to the 2014 ACC/AHA guidelines,[6] in a patient without acute coronary syndrome (ACS), the risk of major adverse cardiac events (MACE) should be estimated according to patient- and surgery-specific factors when there is a known or elevated risk of CAD. This can be done by using the online NSQIP risk calculator developed by the American College of Surgeons[3] or by incorporating the RCRI[2] along with an estimation of surgical risk that is based on the type and invasiveness of the procedure.[21]

Patient-specific factors that increase the risk of MACE include prior diagnoses of the following:

  • CAD
  • Heart failure
  • Cerebrovascular disease
  • Diabetes
  • Renal disease

Guidelines on cardiac assessment and care of patients undergoing noncardiac surgery have recommended preoperative cardiac stress testing in patients with limited functional capacity who, on the basis of clinical factors, are considered to have a risk of MACE higher than 1% and in whom the test result would influence treatment.[16]

After quantification of the risk for ischemia, significant CAD or ACS should be treated by a cardiologist with appropriate revascularization and the surgery delayed for the recommended time according to the type of intervention being performed (ie, balloon angioplasty vs bare-metal stent vs drug-eluting stent vs CABG).

For patients without active cardiac conditions or with stable disease, invasive cardiac investigation and treatment are not generally recommended. This approach derives from the landmark CARP (Coronary Artery Revascularization Prophylaxis) trial, which compared preoperative coronary artery revascularization with no revascularization before elective vascular surgery.[22] In this trial, there was no difference in all-cause mortality at 2.7 years between patients who received preoperative revascularization (22%) and those who did not (23%); there also were no differences in secondary outcomes (eg, postoperative MI within 30 days or stroke).

For these patients, therefore, the focus should be on stabilizing their medical condition and minimizing the surgical stress response.[4] Several classes of drugs have been proposed for use in reducing the risk of ischemic complications of anesthesia and surgery.

Pharmacologic treatment and prophylaxis

Aspirin has been an integral part of the acute treatment of spontaneous ACS and also plays a role in preventive strategies. It eliminates the diurnal variation in plaque rupture, reduces platelet aggregation, and has an anti-inflammatory effect that may be additive to its antithrombotic effect in patients with plaque instability.[36]  However, although some PMIs are due to thrombosis, the POISE (Perioperative Ischemic Evaluation)-2 trial showed that aspirin did not reduce the risk of MI but did increase the risk of major bleeding.[16]

If the patient is on dual antiplatelet therapy (DAPT) with an additional agent (eg, clopidogrel) besides aspirin, it is preferable that monotherapy with aspirin only be initiated 5 days preoperatively so as to reduce the risk of bleeding, provided that there are no contraindications for cessation of DAPT.

If the patient is already receiving a beta blocker, statin, or angiotensin-converting enzyme (ACE) inhibitor, these medications should be continued during the perioperative period. The POISE trial showed that the use of statin and aspirin therapy was associated with cardiovascular protection in patients who had a perioperative cardiovascular event.[34, 37]

If ACE inhibitors are withheld, they should be restarted as soon as possible postoperatively.[21]  If patients are not already on beta blockers, therapy can be initiated in the perioperative period, even on the day of surgery if indicated for acute tachycardia. However, it is not recommended to begin on the day of surgery for the sole purpose of risk reduction. It is preferable to initiate therapy 2-7 days before surgery to allow assessment of the effectiveness and tolerability of the dose.[21]

Alpha2-adrenergic receptor agonists have been advocated as alternatives to perioperative beta blockers for attenuating the stress response, on the grounds that they presumably could reduce cardiovascular morbidity and mortality after cardiac and noncardiac surgery by decreasing perioperative hemodynamic instability, inhibiting central sympathetic discharge, reducing peripheral norepinephrine release, and dilating poststenotic coronary vessels.[38]  Again, however, the POISE-2 trial showed that whereas alpha2 agonists might have these proposed benefits, they had no effect on overall rates of MI, stroke, or death.[16]


Regardless of risk stratification and reduction strategies, the anesthesiologist must be prepared to manage perioperative myocardial ischemia acutely in all patients. The postoperative and intraoperative periods are extremely critical. It is crucial that myocardial injury be promptly identified, carefully evaluated, and aggressively managed. Secondary stresses  that increase the stress or demand on the heart (eg, anemia, sepsis, and extubation) must be minimized.

To ensure prompt recognition, vigilance should be maintained, and all obligatory American Society of Anesthesiologists (ASA) monitoring should be carried out with the recommended alarms audible. In addition, high-risk patients should be considered for more invasive monitoring, including arterial line placement with continuous hemodynamic and cardiac output (CO) or cardiac index (CI) monitoring (via a Flotrac- or Vigileo-style monitoring device), central line placement with a pulmonary artery catheter, and perhaps TEE.  

Goals and critical actions

The most important goals in the management of PMI are as follows:

  • Confirmation of the diagnosis by means of ECG and biomarker assays, with or without imaging
  • Relief of ischemia
  • Assessment of hemodynamic status and correction of any abnormalities present
  • Initiation of reperfusion

Critical actions in the intraoperative period include the following:

  • Immediately communicate to the surgery team and the operating room (OR) staff that the patient’s status may be compromised.
  • Ensure adequate oxygenation; increase the fraction of inspired oxygen (FiO 2) to 100% to improve oxygen saturation as measured by pulse oximetry (SpO 2)
  • Decrease anesthetic depth
  • Expand monitoring to include 12-lead ECG, or order it immediately if in the pre- or postoperative area
  • Initiate fluid challenge, and give a routine dose of phenylephrine for temporizing management of hypotension
  • Assess hemodynamic stability, and rule out other major acute causes of cardiovascular compromise (eg, hypovolemia, concealed hemorrhage, anaphylaxis, septic or neurogenic shock, anesthetic overdose, local anesthetic toxicity, and tension pneumothorax)
  • Initiate supportive measures to maintain BP - Give  vasopressin or epinephrine to maintain coronary perfusion pressure (CPP) and cerebral perfusion pressure
  • If necessary, correct arrhythmias pharmacologically, electrically, or both -  Amiodarone 150-300 mg bolus for ventricular or atrial arrhythmias, followed by subsequent infusion as needed; synchronized cardioversion or defibrillation as indicated; epinephrine 1 mg q3-5min for asystole per advanced cardiac life support (ACLS) guidelines
  • Carry out standard cardiopulmonary resuscitation (CPR) per ACLS guidelines for cardiac arrest if needed
  • Minimize myocardial work and oxygen demand while optimizing supply - Ensure adequate oxygenation and ventilation; lower HR with beta blockers; transfuse blood products to replace hemoglobin for improved oxygen delivery; avoid hypothermia; and correct acidosis or other metabolic derangements
  • Administer nitroglycerin to decrease preload while also dilating coronary arteries
  • If possible, administer aspirin or another antiplatelet agent
  • Immediately order laboratory tests, including arterial blood gases, electrolytes, basic metabolic panel (BMP), and complete blood count (CBC)
  • Immediately order a cardiac biomarker assay (cTnT or, if available, fifth-generation hs-TnT)
  • Consider the ACC/AHA guideline for surveillance for troponin
  • Establish central access (or, if it is already present, confirm it) to permit large-volume supportive resuscitation with fluids or blood products and inotropic infusions with vasopressors, if indicated
  • Use other invasive monitoring, if it is not already established - Initiate arterial line–based, real-time, continuous CO and SVV cardiac monitoring (eg, with Flotrac or Vigileo); if a pulmonary artery catheter is already in place, assess CI and systemic vascular resistance (SVR); look for pulmonary diastolic pressures and prominent a and v waves suggestive of papillary muscle dysfunction and acute mitral regurgitation (MR); use TEE to evaluate systolic and diastolic function, preload and afterload, and valvular function (specifically looking for evidence of new MR)
  • Consider an IABP for hemodynamic stability if the patient has a large anterior-wall MI
  • Consider ECMO
  • Notify cardiology for further treatment, and communicate the possibility of an emergency need for coronary reperfusion therapy - Few randomized studies have been specifically directed at PMI and the outcomes of treatment initiated postoperatively, and in most cases, guidelines for  treatment of spontaneous ACS are used, with obvious specific considerations in the perioperative setting; in the case of ST-segment elevation, thrombolytic therapy is contraindicated because of the risk of bleeding, and consequently, prompt primary angioplasty in a cardiac catheterization laboratory is indicated [39]
  • In patients who have asymptomatic NSTEMI, those in whom invasive reperfusion therapy is not indicated on the basis of angiography, and those with an isolated elevation in cardiac biomarkers (ie, MINS), guideline-directed medical management should be initiated in collaboration with the surgery team and cardiology; as is the case during intraoperative management, postoperative medical management of BP, HR, and pain should be aggressive to minimize stress and correct supply-demand imbalance.

Evidence-based recommendations

Debate continues regarding the use of routine surveillance of cardiac biomarkers postoperatively to detect asymptomatic myocardial injury. Given that PMI is mostly silent and that the ECG is often difficult to interpret and frequently does not exhibit characteristic ST-segment elevation or Q-waves, it is to be expected that the true incidence of PMI is considerably underreported, a situation that possibly obscures its etiology.[26]

As noted earlier (see Problem), the diagnosis of MINS was introduced to focus attention on the prognostic relevance of ischemic troponin elevations after noncardiac surgery.[19]

In a prospective observational study by Biccard et al, the incidence of MINS in vascular surgery patients was 19.1%, and 30-day all-cause mortality in the vascular cohort was 12.5% in patients with MINS, compared with 1.5% in those without MINS.[40] MINS was independently associated with 30-day mortality in vascular patients. The 30-day mortality was similar in MINS patients with (15.0%) and without (12.2%) an ischemic feature. The percentage of vascular surgery patients who sustained MINS without overt evidence of myocardial ischemia was 74.1%. Most patients with MINS were asymptomatic and would have gone undetected without routine postoperative troponin measurement.

In a study that used the more sensitive biomarker, hs-TnT, an absolute hs-TnT change of 5 ng/L or more was associated with an increased risk of 30-day mortality.[12] An elevated postoperative hs-TnT (ie, hs-TnT 20 to < 65 ng/L with an absolute change ≥5 ng/L or hs-TnT ≥65 ng/L) without an ischemic feature was associated with 30-day mortality. Of the 3904 patients with MINS (17.9% of the total population), 3633 (93.1%) did not experience an ischemic symptom.

Evidence suggests that prediction of postoperative MI can be improved by evaluating the cardiac biomarkers hs-TnT and NT-proBNP.[37, 36] Kopec et al found that the addition of hs-cTnT (>14 ng/L)  and NT-proBNP (>300 ng/L) to the RCRI significantly improved the prediction of postoperative MI.[5]

Among patients with CAD who undergo vascular surgery, a perioperative elevation in cardiac troponin levels is common and, in combination with diabetes, is a strong predictor of long-term mortality. These data support the utility of cardiac troponin assays as a means of stratifying high-risk patients after vascular operations, as per the CARP trial.[22]

These findings are not going unnoticed. For example, Canadian Cardiovascular Society guidelines on perioperative cardiac risk assessment for patients undergoing noncardiac surgery strongly recommended (on the basis of moderate-quality evidence) obtaining daily TnT measurements for 48-72 hours postoperatively in patients whose baseline risk for cardiovascular death or nonfatal MI at 30 days after surgery is higher than 5%. This applies to patients older than 65 years, those aged 45-65 years with significant cardiovascular disease, those with an RCRI score of 1 or higher, and those with elevated preoperative plasma BNP concentrations.[5, 36]


Case Example 1

Clinical scenario

A 60-year-old man presents with a history of recurrent ventricular tachycardia (VT). He has a history of ischemic cardiomyopathy and has an automated implantable cardioverter-defibrillator (AICD) that provides him with shock intermittently and a bioprosthetic aortic valve. He has chronic kidney disease (CKD), hypertension, and diffuse CAD. His home medications include amiodarone, aspirin, carvedilol, prasugrel, furosemide, lisinopril, and zolpidem. 

Six years previously, the patient underwent stenting of the left anterior descending artery (LAD) and the circumflex branch of the left coronary artery (LCX); 3 years previously, he underwent CABG (left internal mammary artery [LIMA] to the LAD and saphenous vein grafts [SVGs] to the diagonal, ramus, and second marginal branch). He has undergone multiple percutaneous transluminal coronary angioplasties (PTCAs) for occluded SVGs, the most recent procedure being stenting for 100% occlusion of the drug-eluting stent previously placed in the LCX.

ECG shows normal sinus rhythm, left atrial enlargement, abnormal QRST angle, prolonged QT interval, and septal infarct. Echocardiography is technically difficult, but the ejection fraction (EF) is estimated to be 40%, and moderate anterior-wall hypokinesis is noted. The left ventricle (LV) and right ventricle (RV) are normal in size, and RV function is normal.

The patient is scheduled to undergo VT ablation; he is no longer a candidate for reperfusion intervention. His 5-hour-long intraoperative course is complicated by hypotension that necessitates epinephrine and norepinephrine infusions. After an extended period of intubation in the postanesthesia care unit (PACU), he is extubated when he meets all the relevant criteria. He is not receiving any vasopressors.

Within 30 minutes, the patient becomes diaphoretic, pale, and nauseated. He becomes hypotensive, requiring reinstitution of support. ECG shows nonspecific ST-T changes in inferior leads and multiple premature ventricular contractions (PVCs). As the patient's sensorium continues to worsen, he is reintubated and mechanically ventilated. He goes into cardiogenic shock and pulmonary edema, requiring milrinone, epinephrine, and vasopressin infusions.

A holosystolic murmur is heard radiating to the axilla. Bilateral basal rales can be auscultated. The PA tracing develops new v waves. Transthoracic echocardiography (TTE) shows acute severe MR with a new inferior-wall abnormality. Chest x-ray reveals mild congestion of the lungs. Over the following 2 days, biomarkers rise from 2.9 ng/L to 74 ng/L. NSTEMI is diagnosed. The patient's subsequent course in the cardiac critical care unit (CCU) is complicated by cardiogenic shock and multiple episodes of nonsustained VT.


The patient was taken to the catheterization laboratory and was found to have 80% ostial stenosis in the right coronary artery (RCA). PCI to the RCA was carried out. Subsequently, the patient developed acute kidney injury (AKI) with severe acidosis, which necessitated continuous renal replacement therapy (CRRT). He experienced cardiac arrest and was found to be in pulseless electrical activity (PEA), probably secondary to acidosis and hypoxia. Hypoxia was secondary to pneumonia and bilateral pleural effusions.

The patient was resuscitated. Thereafter, he developed worsening pneumonia, heparin-induced thrombocytopenia (HIT), and sepsis. ECG documented a change from PVCs to atrial fibrillation (AF) and then to wide QRS tachycardia. Six days after the procedure, he succumbed to multiorgan failure. 


Case Example 2

Clinical scenario

A 53-year-old woman with aortoiliac disease presents for revision of the right iliac limb of an aortobifemoral bypass graft placed 6 months previously under general anesthesia. She has a history of smoking, anxiety, familial hyperlipidemia, hypertension, sleep apnea, and CAD with 50% RCA stenosis and an EF of 55%. Her ECG shows normal sinus rhythm. Her medication list includes atorvastatin, carvedilol, hydrocodone-acetaminophen, and potassium chloride.

The patient's intraoperative course is remarkable for episodes of hypotension 2 hours into the procedure. These episodes respond to routine boluses of phenylephrine. After the procedure is completed and the patient extubated, the dorsalis pedis pulse is not palpable, and reexploration and thrombectomy are therefore indicated.

During the second surgical procedure, periods of hypotension necessitate an infusion of phenylephrine and transfusion of a unit of blood for anemia due to blood loss. The phenylephrine infusion is turned off at extubation as BP normalizes. The patient is normotensive for 30 minutes but soon develops persistent hypotension in the PACU and becomes progressively clammy. Vasopressor administration is restarted, and another unit of blood is given. Aspirin and a beta blocker are administered as well.

Subsequently, the patient's ECG shows ST elevation in the inferior leads. Troponin increases from 0.1 ng/L to 57 ng/L over the following 24 hours. Echocardiography reveals mild-to-moderate RV dysfunction with preserved left ventricular ejection fraction (LVEF) and no valvular heart disease.


The patient was diagnosed with inferior-wall STEMI and underwent coronary angiography through the ulnar artery (because the femoral and radial arteries had severe disease). She underwent angioplasty and stenting of her completely occluded RCA with a Promus drug-eluting 3.0 × 32 stent (Boston Scientific, Marlborough, MA). After stent placement, a TIMI (Thrombolysis in Myocardial Infarction) 3 flow was established. LVEDP was 8 mm Hg. The patient was placed on aspirin, beta blockers, and ticagrelor and was discharged on postoperative day 7.

On postoperative day 9, the patient returned with symptoms of chest pain. Her NT-proBNP was 3889 pg/mL, and her troponin was 0.2 ng/mL. Because she had advanced vascular disease that made a second cardiac catheterization difficult, she was managed medically. No new RWMA was seen on TTE. In a follow-up phone conversation, the patient reported that she was stable and that her wound was healing well.


Case Example 3

Clinical scenario

A 65-year-old Caucasian man presents with worsening shortness of breath due to worsening congestive heart failure (CHF) symptoms from his aortic valve (New York Heart Association [NYHA] class III). His history includes known CAD (for which he has undergone CABG), a failed bioprosthetic aortic (21 mm) valve with moderate calcific aortic stenosis, severe paravalvular aortic valve insufficiency, acute-on-chronic diastolic heart failure, hypertension, peripheral vascular disease (PVD; treated with patch repair of the femoral artery), peripheral neuropathy, osteoarthritis, and obesity (body mass index [BMI], 33.2).

In view of his accompanying comorbidities and age, the patient is deemed to be a high-risk candidate for an open aortic valve replacement. He is determined to be a better candidate for a valve-in-valve transfemoral transcatheter aortic valve replacement under monitored anesthesia care. His intraoperative course is stable, and a 23-mm Evolut Pro Valve in Valve (Medtronic, Minneapolis, MN) is placed.

Upon successful positioning of the device, deployment results in sudden asystole. Acute total occlusion of the left main coronary artery (LMCA) is seen on fluoroscopy, accompanied by complete aortoventricular uncoupling. Continuous CPR is performed, and the patient is intubated and mechanically ventilated on an emergency basis. As surgeons prepare to go on peripheral cardiopulmonary bypass (CPB), with CPR continuing, TEE reveals severe myocardial stunning. On bypass, a mean systemic pressure of 65 mm Hg is maintained. 


Under fluoroscopic guidance, with the use of a 7-French EBU 3.5 guide catheter (Medtronic, Minneapolis, MN), the LMCA was accessed and wired with a Whisper extra support wire (Abbott, Santa Clara, CA) from the LMCA into the LAD. The totally occluded left main ostium was stented with a 4.0 × 12 mm Vision bare-metal stent (Abbott, Santa Clara, CA), with immediate restoration of flow to the left coronary artery (LCA) system. The RCA could not be cannulated.

By this time, the patient had entered into polymorphic VT necessitating defibrillation. Defibrillation restored normal sinus rhythm and electrical mechanical coupling, with return of systolic and diastolic arterial waveforms. Interrogation with aortography and TEE revealed trace to no paravalvular leak. Final interrogation of the valve revealed trace to no perivalvular leak and a hemodynamically inconsequential gradient across the aortic valve. EF was 25% with severe global LV stunning and severe global LV hypokinesis (LVHK). The patient was placed on ECMO and transferred to the intensive care unit (ICU).

This was a case of intraoperative MI secondary to occlusion of the LMCA by prosthetic valve leaflet shift and ostial left main dissection of unknown etiology. Complete cardiac asystole with myocardial standstill was followed by myocardial stunning after resuscitation.


Case Example 4

Clinical scenario

A 48-year-old woman with a preoperative history pertinent for a 25-pack-year smoking history, gastroesophageal reflux disease (GERD), and hypothyroidism presents with complaints of worsening dyspnea, fatigue, and intermittent chest tightness for the past 6 months.

A recent chest x-ray has identified a right lung mass. Follow-up computed tomography (CT)/positron emission tomography (PET) has confirmed the presence of a 4 × 6 cm right-lower-lobe mass, and needle biopsy has identified it as primary lung adenocarcinoma. The patient is scheduled for a right lower lobectomy. Pertinent negatives include the absence of a prior cardiac history and a negative result on Cardiolite stress testing.

After uneventful induction of general anesthesia and placement of a double-lumen endotracheal tube, the procedure is started, but the planned right lower lobectomy is converted to a complete right-side pneumonectomy because of positive margins. The procedure is completed without apparent complications, with an estimated blood loss of 500 mL. Adequate fluid replacement is followed by good urine output.

During wound closure, the patient becomes hypotensive, with MAP in the 40s. Oxygen saturation and HR remain normal, and no ECG changes are noted. The hypotension is treated with intermittent bolus doses of vasopressors and responds within 1-2 minutes. During emergence from general anesthesia, arterial BPs swing to opposite extremes, with highs in the 200s/100s, and the patient becomes tachycardic, with HR in the 120s. Again, oxygenation and ventilation remain adequate, and the patient is extubated.

In the PACU, the patient’s hemodynamics stabilize, and she is able to follow commands appropriately. She is discharged from the PACU to the floor, and she is comfortable with epidural infusion. The following morning (postoperative day 1), she goes into PEA arrest in the ICU.


Reintubation was successfully accomplished, and CPR led to return of spontaneous circulation (ROSC), but the patient remained hemodynamically unstable, with SBP in the 60s and HR in the 40s. Chest radiography was negative for tension pneumothorax. A 12-lead ECG showed nonspecific ST-T wave changes in leads V2 and V3.

Central access was achieved and inotropic-vasopressor support initiated. Assays for cTnT yielded a value of 2.92. TTE was significant for severe hypokinesis of the apex of the heart, dyskinesia of the interventricular septum, and a reduced EF of 35-40%. Right-heart pressures, structure, and function were normal. Infarction of LAD territory was suspected, and the patient underwent an urgent cardiac catheterization, which revealed no significant CAD.

In view of the characteristic apical hypokinesis and ballooning in the absence of ischemic disease, the patient was diagnosed with Takotsubo stress-induced cardiomyopathy. This condition is thought to result in myocardial stunning as a consequence of overwhelming catecholamine release during stress with a large density of receptors found in the apex of the heart.

Approximately 10% of patients with stress cardiomyopathy develop cardiogenic shock. However, the development of shock may not correlate with the extent of LV systolic dysfunction. One explanation for this discordance between ventricular dysfunction and risk of shock is that some shock is caused by LV outflow tract (LVOT) obstruction, which has been described in 10-25% of patients with stress cardiomyopathy.

Further workup revealed deep vein thrombosis (DVT) without evidence of pulmonary embolism (PE), and appropriate anticoagulation therapy was started. Inotropic and vasopressor support with dobutamine and norepinephrine was continued, and the patient was stabilized. Her postoperative course was then complicated by paroxysmal atrial fibrillation (PAF) with rapid ventricular response (RVR), and the development of a dynamic LVOT obstruction from reduced stroke volume and tachycardia raised concerns about stress-induced cardiomyopathy.

PAF with RVR was treated with sotalol, and long-term beta-blocker therapy with carvedilol was initiated. The patient's condition began to improve, and she was weaned from inotropic-vasopressor support. Mechanical circulatory support (eg, IABP) can be the preferred therapy when there is marked LV dysfunction associated with severe hypotension or shock that does not respond to pharmacologic therapy.[41]

After continued improvement and extubation, the patient was eventually transferred out of the ICU and discharged home to be followed by cardiology on an outpatient basis. Stress-induced cardiomyopathy is typically a transient disorder that generally resolves after removal of the stress-inducing event or environment and provision of supportive care.