Preoperative

A MI that occurred within six months of planned noncardiac surgery is considered recent . Data shows that the rates of postoperative MI decreased as the length of time from the cardiac event to surgery increased . Surgery should take place at least 60 days after the last cardiac event . Furthermore, the patient’s age also plays an important role. Patients over 55 years of age have a greater prevalence of cardiac risk factors which increases their overall risk for MACE . Patients over the age of 65 have an increased risk of acute ischemic stroke undergoing noncardiac surgery .

Routine revascularization prior to noncardiac surgery to reduce perioperative cardiac events is not recommended . The Coronary-Artery Revascularization before Elective Major Vascular Surgery trial demonstrated that revascularization before elective major vascular surgery does not improve long-term survival . Furthermore, there was no significant reduction in MACE postoperatively. In this trial, patients with clinically significant, stable coronary disease were randomized to undergo coronary revascularization or medical therapy. Patients were carefully screened and those with coronary artery disease not amenable to revascularization, ≥ 50% stenosis of the left main coronary artery, left ventricular ejection fraction <20%, and severe aortic stenosis (AS) were excluded.

Indications for revascularization prior to surgery include: high risk coronary anatomy such as left main disease, unstable angina, MI, or arrhythmias that are ischemic in origin. Patients who require revascularization prior to surgery should be treated according to the CPG for coronary artery bypass grafting (CABG) or percutaneous intervention (PCI) .

In patients who underwent a drug eluting stent (DES) who now require surgery, the decision to continue aspirin or dual antiplatelet therapy (DAPT) should be individualized. DAPT includes an aspirin and a P2Y ₁₂ platelet receptor-inhibitor, which includes clopidogrel, prasugrel, and ticagrelor. Non-operative risk factors for DES thrombosis include: premature discontinuation of DAPT, diabetes, renal failure, low ejection fraction, advanced age, and procedural characteristics. These include type of DES, bifurcation and ostial lesions, long stent length, multiple stents, overlapping stents, small-diameter vessels and suboptimal results such as coronary dissection or under expansion . In the operative setting, multiple factors such as coronary vasospasm, activation of inflammatory pathways, increase in catecholamine secretion, reduction in tissue plasminogen activator, and increased platelet activation and shear stress may also lead to acute stent thrombosis.

In the nonoperative setting, the rates of stent thrombosis with newer-generation DES is low . Several trials have shown that there was no significant difference in the rates of stent thrombosis in patients treated with 3 to 6 months of DAPT as compared to patients treated with longer durations . In the operative setting, studies showed that the risk of stent thrombosis is greater when the surgery is performed soon after stent implantation. The risk of thrombosis was 3.5% within 6 weeks of stent (BMS and first generation DES stents- sirolimus and paclitaxel) implantation and 1% at 6 and 24 months . In a meta-analysis of 839 patients with DES, 2.3% had stent thrombosis within six months of implantation, 1.7% within 6 to 12 months, and 0.86% >12 months after implantation .

The 2016 ACC/AHA Guideline Focused Update on Duration of Dual Antiplatelet Therapy in Patients with Coronary Artery Disease has updated the recommendations of DAPT perioperatively . The decision on timing of surgery and DAPT therapy involve the type of surgery, risk of delaying the surgery, risk of stent thrombosis and ischemia, and the risk of bleeding. In situations where noncardiac surgery needs to be performed urgently, balloon angioplasty may be required and surgery should be postponed for at least 14 days . Patients who had recent BMS stent implantation, surgery should be delayed for at least 30 days. Patients with DES placed within the first 3 months should have their surgery delayed. Proceeding with surgery within the first 3 to 6 months may be considered if the risk of delaying surgery is greater than the risk of stent thrombosis (Class IIb). Patients with DES implanted ≥ 6 months can proceed with surgery (Class I) ( Table 3.3 ).

In those situations where discontinuation of P2Y ₁₂ platelet receptor-inhibitor therapy is required, aspirin should be continued if surgically feasible. The risk of bleeding with DAPT therapy is most likely to be higher than aspirin alone or no antiplatelet therapy but the degree of increase is currently unclear . Clopidogrel and ticagrelor should be stopped 5 days prior to surgery, and prasugrel should be stopped 7 days prior to surgery . Restarting P2Y ₁₂ platelet receptor-inhibitor therapy should be done as soon as the patient is surgically stable .

Postoperative

Perioperative MI is a common complication of major noncardiac surgery. A perioperative MI increases the risk of cardiac morbidity and mortality . Myocardial infarction can be diagnosed based on clinical symptoms, electrocardiographic (ECG) findings, measurement of biomarkers, and imaging. The Third Universal Definition of an MI is defined as detection of a rise and/or fall of cardiac biomarkers with at least one value above the 99 ^th percentile upper reference limit and with at least one of the following: 1) symptoms of ischemia; 2) new or presumed new significant ST-segment-T-wave changes or new left bundle branch block (LBBB); 3) development of pathological Q waves in the ECG; 4) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality; and, 5) identification of an intra-coronary thrombus by angiography or autopsy .

Patients with a perioperative MI and myocardial injury that do not fulfill the Third Universal Definition of a MI have a worse short and long-term outcome . Myocardial infarction is classified in five categories. A spontaneous MI (Type 1) is due to atherosclerotic plaque rupture resulting in intraluminal thrombus . A Type 2 MI is due to an ischemic imbalance. Myocardial injury with necrosis occurs when the demand for myocardial oxygen is greater than the supply. Cardiac death due to myocardial infarction is classified as Type 3. Type 4 and 5 are related to peri-procedural injury in the setting of PCI or CABG respectively. While most perioperative MIs are usually Type 2, clinicians should be vigilant for Type 1 MIs.

Biomarkers of cardiac necrosis include cardiac troponin (T or I) or the MB fraction of creatinine kinase. It is important to distinguish between a rise and/or fall of biomarkers from a chronic elevation. Blood samples should be drawn on first assessment and then repeated 3-6 hours later. The measurement of troponin levels is recommended in the setting of signs or symptoms suggestive of myocardial ischemia or MI (CIass I) . The routine use of biomarkers in patients without signs or symptoms suggestive of myocardial ischemia or MI is not recommended (Class III).

ECG manifestations of acute MI ( Figs. 3.2 and 3.3 ) are defined as: 1) new ST elevation at the J point in 2 continuous leads with the cut-point ≥1 mm in all leads other than leads V2-V3. These leads require ≥ 2 mm in men ≥40 years, ≥ 2.5 mm in men <40 years, or ≥ 1.5 mm in women . In patients with a concern for left circumflex ischemia, leads can be positioned in the left posterior axillary line (V7), left mid-scapular line (V8), and the left paraspinal border (V9). In patients with a suspected inferior or right ventricular infarction, leads can be placed in the right V3 and V4 positions. In addition, ST depression in ≥2 precordial leads (V1–V4) may indicate transmural posterior injury. Multilead ST depression with coexistent ST elevation in lead aVR has been described in patients with left main or proximal left anterior descending artery occlusion . In addition, patients may also present with a new LBBB. In those patients with an existing LBBB, the Sgarbossa criteria can be used: 1) ST-elevation ≥1 mm and concordant with QRS complex (5 points); 2) ST segment depression ≥ 1 mm in lead V1, V2 or V3 (3 points); and, 3) ST-elevation ≥ 5 mm and discordant with QRS complex (2 points). A score of more than 3 points has a 98% specificity .

Anterior wall myocardial infarction, arrows pointing to ST elevations.

Inferior wall myocardial infarction, arrows pointing to ST elevations.

With the exception of a true posterior myocardial infarction, the absence of persistent ST-elevation is suggestive of non-ST segment acute coronary syndrome (NSTE-ACS). These patients can be categorized on the basis of elevated cardiac biomarkers. Patients with elevated cardiac biomarkers in the appropriate clinical context are considered to have non-ST segment myocardial infarction (NSTEMI). ECG changes such as ST depression, transient ST elevation, and/or prominent T-wave inversions may be present but are not required for a diagnosis of NSTEMI. Patients with clinical symptoms but with no elevations in cardiac biomarkers are considered to have unstable angina (UA) .

Currently, there is little data on the management of myocardial infarction and injury in the post-operative setting. In patients who fulfill the diagnostic criteria for an acute MI, immediate consultation with a cardiologist, cardiac catheterization laboratory, and surgical team should be done in order to facilitate immediate revascularization when possible. These patients should receive guideline-directed medical therapy (GDMT) according to the AHA Guideline for the Management of ST-Elevation Myocardial Infarction . Patients who develop NSTE-ACS following noncardiac surgery should receive GDMT with limitations imposed by the specific surgical procedure and the severity of the NSTE-ACS .

Preoperative

Heart failure is a diverse clinical syndrome due to any structural or functional impairment of left ventricular filling or ejection of blood . Patients with heart failure can have a reduced left ventricular ejection fraction, <40%, (HFrEF), or a heart failure with preserved left ventricular ejection fraction, >50%, (HFpEF) . Common symptoms include fatigue, orthopnea, shortness of breath either at rest or exertion, dyspnea, tachypnea, cough, lower extremity edema, increasing abdominal girth or discomfort, and loss of appetite. Prior to surgery, the presence of pulmonary or systemic congestion should be determined. Patients with pulmonary congestion may have rales, dullness to percussion, or diminished breath sounds. However typical lung exam findings may be absent in patients with elevated left ventricular filling pressures due to compensatory changes in lymphatic and perivascular tissue. The presence of increased jugular venous pressure (JVP) has a good sensitivity (70%) and specificity (79%) for estimating an increased left ventricular filling pressure . Patients with decompensated CHF should be treated according to GDMT for heart failure . A two-dimensional echocardiogram should be performed in patients who have newly diagnosed heart failure, develop a significant clinical change, or receive treatment that affects cardiac function.

Postoperative

Patients with active or stable heart failure have an increased risk for perioperative morbidity and mortality . The presence of a severely decreased, <30%, left ventricular ejection fraction, is an independent risk factor in perioperative outcome and increased long-term mortality in patients undergoing elevated-risk noncardiac surgery .

There is limited data on the use of pulmonary artery catheters perioperatively. The routine use of pulmonary artery catheters perioperatively is not recommended . They may be considered in patients who are unable to have medical conditions that may affect hemodynamics corrected prior to surgery . According to the 2013 ACCF/AHA Guideline for the Management of Heart Failure, pulmonary artery catheters should be used in those patients who have respiratory compromise or impaired perfusion that cannot be adequately assessed clinically (Class I) .

Preoperative

Since the progression of VHD may be slow, patients may not exhibit symptoms due to a gradual decrease in their daily activities. A detailed examination may reveal signs of severe VHD. Echocardiography is recommended in patients with suspected moderate or greater degree of stenosis or regurgitation who have not had an echocardiogram within one year or who exhibit a change in their clinical status on examination . In patients who meet the criteria for treatment of the valvular disease, intervention prior to elective surgery is indicated .

Patients who have severe AS should be evaluated for a change in their clinical symptoms. The Class I recommendations for aortic valve intervention include: 1) symptomatic patients; 2) asymptomatic patients with severe AS with a LVEF <50%; and, 3) patients with severe AS who are undergoing other cardiac surgery . Options for treatment include surgical aortic valve replacement (SAVR), transcatheter aortic valve replacement (TAVR), and balloon valvuloplasty. Current indications for TAVR include patients who have a prohibitive surgical risk and a predicted post-TAVR survival of >12 months. Balloon aortic valvuloplasty may be considered as a bridge to SVAR or TAVR in those patients who require emergent or urgent surgery (Class IIb) .

Patients with severe mitral stenosis (MS) should also be evaluated prior to surgery. Class I indications for intervention include patients who are symptomatic. Patients with suitable anatomy can undergo a percutaneous mitral balloon commissurotomy.

Patients with chronic aortic insufficiency and chronic mitral insufficiency should be managed according to the Guidelines for Management of Patients with Valvular Heart Disease .

Patients with hypertrophic cardiomyopathy (HCM) have unexplained asymmetric pattern of hypertrophy associated with non-dilated ventricular chambers in the absence of a cardiac or systemic disorder that could explain the hypertrophy . Based on echocardiography, HCM is defined by an end-diastolic wall thickness ≥ 1.5 cm in any myocardial segment accompanied by a normal wall thickness in the other segments. The complex pathophysiology of HCM includes: left-ventricular outflow tract (LVOT) obstruction, diastolic dysfunction, myocardial ischemia, autonomic dysfunction, mitral regurgitation, and atrial and ventricular arrhythmias. Patients may have an implantable cardiac defibrillator (ICD) if there is a history of cardiac arrest, ventricular fibrillation, or hemodynamically significant ventricular tachycardia . There are no large trials examining perioperative risk. However, retrospective data suggests that patients with HCM have an increased operative risk. In one study with 227 patients with HCM, the presence of HCM tripled the risk of perioperative MI and death .

Except in highest risk patients, prophylactic antibiotics are not recommended for patients with VHD undergoing genitourinary (GU) procedures (Class III) . Antibiotic therapy may be reasonable prior to elective cys­toscopy or other urinary tract procedures in patients who are at highest risk for endocarditis with an enterococci urinary tract infection or colonization (Class IIb) . Highest risk patients include: 1) prosthetic cardiac valve; 2) previous infective endocarditis; 3) congenital heart disease (CHD)- unrepaired cyanotic disease, completely repaired CHD with prosthetic material or device during the first six months, repaired CHD with residual defects; and, 4) cardiac transplantation recipients who develop cardiac valvulopathy. If they require urgent procedures, treatment with an antimicrobial effective against enterococci may also be reasonable (Class IIb) .

Postoperative

Patients with AS have a fixed obstruction to forward blood flow. During anesthesia, a decrease in vascular resistance results in hypotension due to an inability to increase cardiac output. This results in an ischemic cascade due to a decrease in coronary perfusion resulting in a further decline in cardiac output. Atrial arrhythmias in the setting of severe AS also lead to hypotension due to the loss of atrial contractility. Patients with severe symptomatic AS undergoing nonemergent procedures had a 2.1% 30-day mortality compared to 1% in patients without severe AS . In addition, there is an increased frequency of postoperative MI. In emergent and urgent noncardiac surgery, patients with severe AS had a 5.9% mortality .

In patients with MS, tachycardia, either sinus tachycardia or atrial arrhythmias, should be avoided. A rapid ventricular rate will lead to a decrease in diastolic filling time leading to an increase in left atrial pressure, resulting in pulmonary edema. In addition, judicious use of intravenous fluids should be used perioperatively to avoid pulmonary edema.

Perioperatively, in patients with aortic or mitral insufficiency, adequate preload should be maintained and significantly elevated blood pressures should be avoided.

In patients with HCM, the effects of anesthesia, perioperative volume loss, arterial vasodilatation, and tachycardia may increase the degree of LVOT obstruction resulting in decreased cardiac output. In addition, increased contractility, such as the use of inotropic agents, will also increase the degree of LVOT obstruction. Maneuvers to improve hypotension include intravenous fluids and beta-blockers. Drugs that increase systemic vascular resistance without increasing heart rate or contractility, such as phenylephrine and vasopressin, can also be used . Perioperative atrial fibrillation may also lead to hemodynamic compromise due to the loss of atrial kick. Pharmacologic or direct current cardioversion may be required.

Preoperative

Patients may have supraventricular or ventricular arrhythmias. Patients with unstable atrial or ventricular arrhythmias should be referred to a cardiologist prior to surgery.

Supraventricular tachycardias (SVT) are a group of arrhythmias with atrial and/or ventricular rates above 100 beats per minute (bpm) with a mechanism that occurs at or above the bundle of His . This definition excludes atrial fibrillation. Patients with SVT may present with palpitations, panic or anxiety, neck pulsations, lightheadedness, or syncope. Patients may have hemodynamic instability due to the presence of a SVT regardless of the ventricular rate . Patients may be managed medically or undergo catheter-based ablation.

Atrial fibrillation involves uncoordinated atrial activation resulting in an ineffective atrial contraction. ECG manifestations include: 1) irregular atrial activity, 2) absence of distinct P waves; and, 3) irregular R-R intervals . Atrial fibrillation can be paroxysmal, persistent, or permanent. Paroxysmal atrial fibrillation terminates spontaneously or with intervention within seven days of onset. Episodes may occur with variable frequency. Persistent atrial fibrillation is continuous atrial fibrillation that is longer than seven days but less than 12 months. Permanent atrial fibrillation is characterized when the patient or physician has decided to defer further attempts to maintain sinus rhythm . Patients may be treated with beta-blockers, non-dihydropyridine calcium channel blockers, or antiarrhythmic medications. In addition, patients should be treated with anti-thrombotic therapy in order to prevent thromboembolism. For patients with a CHA ₂ DS ₂ -Vasc score (congestive heart failure, hypertension, age ≥ 75 years [2 points], diabetes mellitus, prior stroke or TIA or thromboembolism [2 points], vascular disease, age 65 to 74 years, female sex), ≥1 oral anticoagulation is recommended . Options for anticoagulation include aspirin, warfarin, and target-specific oral anticoagulants. These include a direct thrombin inhibitor, dabigatran, and direct factor Xa inhibitors, rivaroxaban, apixaban, and edoxaban. There is limited data on bridging with low molecular weight heparin (LMWH) or unfractionated heparin . There is also limited data on the management of direct thrombin and factor Xa inhibitors perioperatively. The timing of cessation of and resumption of therapeutic coagulation should be guided by the individual risks and benefits.

Patients may have an SVT due to an accessory pathway. Wolff-Parkinson-White (WPW) syndrome is characterized by patients who have SVT and ventricular pre-excitation on ECG, short PR and delta wave ( Fig. 3.4 ). Patients may also have an accessory pathway that is not evident on the 12-lead ECG (concealed accessory pathway) .

Pre-excitation in patient with WPW Syndrome, closed arrows=delta waves, Open arrows=short PR interval.

Patients with ventricular tachycardia (VT) should be evaluated by a cardiologist in order to determine whether the patient is stable and an appropriate surgical candidate.

Postoperative

Patients who develop tachycardia postoperatively should have a 12-lead ECG. An ECG that reveals a wide complex tachycardia may either have VT or SVT with abnormal conduction. SVT with abnormal conduction may occur in the setting of existing bundle branch block or intraventricular conduction defect, aberrant conduction due to tachycardia, electrolyte and metabolic disorders, conduction over an accessory pathway, paced rhythm, or artifact . It is important to differentiate SVT from VT since the administration of diltiazem or verapamil may result in hemodynamic instability in the setting of VT or atrial fibrillation with pre-excitation. Patients with pre-excitation who develop arrhythmias postoperatively should be managed in consultation with a cardiologist.

Class I recommendations for acute treatment of patients with SVT include vagal maneuvers, adenosine ( Fig. 3.5 ), and synchronized cardioversion for hemodynamically unstable SVT or when pharmacologic therapy is contraindicated .

Narrow complex PSVT, arrow points to P wave and conversion to normal sinus rhythm after administration of adenosine.

Patients who develop complex ventricular ectopy such as ventricular tachycardia should be evaluated for myocardial ischemia, electrolyte abnormalities, or adverse effects from medications.

Bradyarrhythmias postoperatively may be due to sleep apnea, electrolyte abnormalities, myocardial ischemia, medications, or due to increased vagal tone factors such as pain .

Preoperative

There are a wide variety of CIEDs available. Communication between the CIED and surgical teams is required to develop an individualized treatment plan.

Device interaction is generally electrical interference from nonphysiologic electrical sources, such as electrocautery, or rarely direct damage to the generator or leads . In patients undergoing monopolar surgery, inhibition of pacing and inappropriate activation of anti-tachycardia therapies may occur. Patients who have an inhibition of pacing may experience hemodynamic instability. In patients with ICDs, over-sensing results in inhibition of pacing and inappropriate ICD therapy. This includes both anti-tachycardic pacing therapy and ICD shocks. Uncommonly, electrical reset of the pulse generator, permanent damage or failure of the pulse generator, and damage to the lead-myocardial interface may occur .

Prior to surgery, the CIED team should be notified of the type of procedure, anatomic location, use of monopolar electrosurgery, other sources of electromagnetic interference (EMI), surgical venue, post-procedural recovery, and any unusual surgical circumstances. The CIED team will communicate the history of the device, pacemaker (PPM) dependency, and the appropriate perioperative CIED recommendations. Patients with pacemakers are recommended to have the device evaluated every 3 to 12 months, and patients with ICD and cardiac resynchronization therapy defibrillators (CRT-D) every 3 to 6 months either in person or by remote interrogation . Patients who have had a change in their clinical condition should have their devices reevaluated prior to surgery. Devices near Elective Replacement Time may be unreliable and the generator should be changed prior to surgery.

In general, electrosurgery applied below the umbilicus is unlikely to cause pacemaker or ICD/CRT-D interference as compared to above the umbilicus. The greatest risk of over-sensing occurs when the anatomical surgical site and placement of the return electrode occurs across the CIED and/or leads . In order to minimize the effects on the CIED, patients undergoing TURP should have placement of the return pads on the buttock or thigh. Patients who are pacemaker dependent, asynchronous pacing by programming or placement of a magnet over the pulse generator may be required for most procedures above the umbilicus. Inactivation of ICD detection is recommended for all procedures using monopolar electrosurgery above the umbilicus. Intraoperatively external defibrillation equipment should be available. It is important to note that application of a magnet over an ICD will not protect the patient from EMI inhibition of pacing. Changing the pacing mode will require reprogramming of the ICD. All patients should have plethysmographic or arterial pressure monitoring during the procedure since electrocautery may interfere with electrocardiographic monitoring and interpretation of the patient’s underlying rhythm .

Postoperative

Postoperatively, patients with an ICD should have continuous cardiac monitoring until a member of the CIED team reevaluates the ICD and confirms that the appropriate preoperative settings are restored. This is essential since patients with ICDs are considered to be at risk for ventricular arrhythmias perioperatively . Postoperative assessment of the PPM will depend on the operative environment. Patients who have intraoperative reprogramming, unexpected hemodynamic change, emergent surgery above the umbilicus, procedures that have a possibility of affecting device function, or who are unable to logistically have the device evaluated within one month should have the device evaluated prior to transfer from a cardiac telemetry environment . Unless there was a change in the patient’s clinical status perioperatively, patients undergoing transurethral resection of the prostate do not need additional CIED evaluation. Patients who require lithotripsy should have their device evaluated within 1 month unless there was a clinical change during the procedure . Patients undergoing monopolar electrosurgery with no unexpected perioperative complications should have their device evaluated within the month either in person or by remote telemetry .

Preoperative

Pulmonary hypertension is defined by the presence of mean pulmonary artery pressure (mPAP) ≥25 mmHg assessed by right heart catheterization . The classification of pulmonary hypertension is based on groups of patients with similar pathological findings, hemodynamic profiles, and management strategies. Patients can be classified as: group 1, pulmonary arterial hypertension (PAH), mPAP≥25 mm Hg with normal pulmonary artery occlusion pressure ≤15 mm Hg and pulmonary vascular resistance above 3 wood units in the absence of pulmonary parenchymal or thromboembolic disease; group 2, pulmonary hypertension due to left heart disease; group 3, pulmonary hypertension due to lung diseases and/or hypoxia; group 4, chronic thromboembolic pulmonary hypertension; and group 5, pulmonary hypertension with unclear or multifactorial mechanisms ( Box 3.1 ) .

In observational studies, patients with PAH have an increased morbidity and mortality . Risk factors include urgency of surgery, severity of pulmonary hypertension, degree of RV dysfunction, and surgery in a center without expertise in pulmonary hypertension . Given the complex nature of PAH, patients should be managed at a PAH center of excellence . Preoperatively, patients should have a thorough cardiac evaluation and optimization prior to surgery. Signs and symptoms of deterioration may include changes in functional status, presence of elevated jugular venous pressure, congestive heart failure, hypoxia, or syncope. In addition, the patient’s pulmonary hypertension medications and the possibility of additional pulmonary hypertension specific medications should be made available prior to surgery .

Postoperative

Postoperative management requires close coordination between the surgeon and PAH team. Postoperative complications may include respiratory failure, cardiac arrhythmias, congestive heart failure, renal insufficiency, sepsis, hepatic dysfunction, hypertension, cardiac ischemia and stroke .