Functional capacity is an established predictor of perioperative cardiac events, with poor functional capacity correlating to increased adverse events. Functional capacity is often defined in terms of metabolic equivalents (METS) and ranges from 1, which is defined as a resting state, to >10. Perioperative risk for cardiac events increases if an individual cannot achieve 4 METS which is defined as climbing a flight of stairs, walking up a hill, walking on level ground at >4 mph, or heavy house or yard work [4].

The prognostic significance of a preoperative electrocardiogram is unclear; however, it provides a baseline standard that can be compared to in the postoperative period. Timing should be approximately one to three months prior to the planned procedure. A 12-lead electrocardiogram is reasonable in patients undergoing elevated–risk procedures with history of coronary artery disease, arrhythmias, structural heart disease, or peripheral/neurovascular disease. There is no benefit of routine preoperative electrocardiograms in asymptomatic patients undergoing low–risk procedures .

Reduced left ventricular function with ejection fraction <35 % correlates with a significant increase in perioperative events, particularly with risk for postoperative acute decompensated heart failure [5]. It is reasonable to evaluate left ventricular function preoperatively in patients who report dyspnea of unclear etiology or if there is evidence of clinical heart failure on preoperative examination. For patients with known left ventricular dysfunction and no assessment within the past 1 year, an echocardiogram is also reasonable prior to surgery. There is no evidence that routine echocardiogram is useful prior to surgery in other patient groups and is not recommended .

Pharmacological stress testing may be useful in patients with poor functional capacity (<4 METS) in which clinical history and physical findings are concerning for an active or unstable coronary syndrome prior to surgery. Both dobutamine stress echocardiogram testing and pharmacological stress nuclear perfusion imaging have been studied in numerous studies prior to elevated-risk surgery; however, no randomized controlled trials exist. Regardless of the modality chosen, the presence of a moderate to large area of ischemia is associated with increased risk of perioperative myocardial infarction and/or death [6]. Evidence of prior myocardial infarct on rest imaging, however, is of little predictive value for perioperative cardiac events. A normal pharmacologic stress test has a high negative predictive value for myocardial infarction or cardiac death during the perioperative period.

Routine coronary angiogram is not recommended for patients undergoing elevated-risk noncardiac surgery. The indication for coronary angiogram in the preoperative period is the same as the indication in the nonoperative period, i.e., unstable and active coronary syndromes.

Preoperative risk stratification may lead the identification of obstructive coronary artery disease. Many factors play a role in deciding whether preoperative coronary revascularization should be performed and via which approach, i.e., surgical versus percutaneous coronary intervention (PCI) . PCI should be performed in patients with high-risk coronary artery anatomy (left main disease) and prohibitive risk for surgical revascularization and those patients that have active unstable coronary syndromes and are candidates for revascularization. For patients with planned time-sensitive surgery, bare-metal stents (BMS) or balloon angioplasty is favorable. In these circumstances, preferably 4–6 weeks of aspirin and P2Y-12 platelet receptor blockers are given followed by aspirin perioperatively. If noncardiac surgery can be delayed >12 months, then drug-eluting stents (DESs) are a therapeutic option and allow 1 year of aspirin and P2Y-12 receptor blocker therapy. Some data demonstrate safety in termination of dual antiplatelet therapy with the use of newer-generation DESs at 6 months. Average recovery times for surgical revascularization need to be considered when considering preoperative surgical revascularization strategy. Currently, there are no randomized controlled trials demonstrating that coronary revascularization (either surgical or PCI) reduces hard end points of postoperative mortality or cardiac events. The Coronary Artery Revascularization Prophylaxis (CARP ) trial is the largest available trial of 510 patients that were randomized to either surgical/percutaneous revascularization or medical management with the exclusion of urgent/emergent surgery, unstable angina, left main disease, severe left ventricular function (EF <20 %), or aortic stenosis prior to elevated high-risk vascular surgery [7]. The CARP trial demonstrated no difference in postoperative death or myocardial infarctions at 30 days but did show that coronary revascularization led to longer delays in patients getting their planned surgical procedure.

Patients already receiving long-term beta-blocker treatment should continue in the perioperative period; this is supported by multiple retrospective and observational studies [8–10]. If beta-blockers are to be initiated prior to surgery, it is important to allow sufficient time to assess patient tolerability and safety. It is our practice to start patients on beta blockade 1 week prior to their surgery. For patients with moderate- to high-risk myocardial ischemia on preoperative testing, it is reasonable to start beta-blockers regardless of whether or not a coronary revascularization approach is decided. In addition, for a patient with greater than three cardiac risk factors of either coronary artery disease, heart failure, diabetes, chronic renal disease, or history of cerebrovascular accident, it is reasonable to start a beta-blocker if not previously prescribed.

Several specific disease states warrant detailed review in terms of cardiovascular preoperative assessment.

Heart failure is a very common disease which is more prevalent in the elderly. Estimates are that >10 % of patients older than 65 years of age suffer from the condition [11]. Congestive heart failure is a clinical syndrome characterized by the heart’s inability to meet the metabolic demands of the body at normal ventricular filling pressures. Heart failure can be classified according to the predominant ventricle involved: left ventricular (LV), right ventricular (RV), or mixed LV/RV failure. In LV heart failure, patients present with shortness of breath, fatigue, exercise intolerance, and/or signs of RV failure. In RV heart failure, patients present with lower extremity edema, early satiety, abdominal distension, fatigue, and exercise intolerance. Heart failure can also be categorized into systolic, diastolic, or mixed systolic/diastolic. In systolic heart failure, there is evidence of reduced LV function manifest by a reduced EF. In diastolic heart failure, the LV is non-dilated with normal or near-normal systolic function but may shows signs of structural changes (i.e., hypertrophy) and/or diastolic dysfunction.

Heart failure is a well-recognized risk factor for perioperative morbidity and mortality [1, 12]. The single most important piece of information to be obtained from a patient with a history of heart failure is their preoperative symptom complex . Using the standard New York Heart Association scale (Table 6.4) for symptoms, patient’s status and risk can be determined. The higher the NYHA class, the higher the risk for perioperative complications.

Transthoracic echocardiography (TTE ) is the single most important diagnostic tool used preoperatively to assess patients with known or suspected heart failure. Parameters which can be determined on TTE include LV size, wall thickness, LVEF, right and left atrial size, and RV size and function, as well as assessment for any significant valvular lesions. Additional information which can be obtained on a standard 2D TTE include diastolic function, estimated central venous pressure, and estimated pulmonary artery systolic pressures (PASP). It is our practice to obtain a preoperative TTE in all patients with a history of HF undergoing elevated-risk noncardiac surgery.

In addition to TTE , there is significant literature to support the use of perioperative levels of natriuretic peptides (BNP or NTproBNP) in the risk stratification of heart failure patients undergoing noncardiac surgery [13]. Elevated natriuretic peptide levels are strongly correlated to perioperative morbidity and mortality.

All patients with HF who are scheduled to undergo elective noncardiac surgery should be “optimized” from a medical standpoint. This includes diuresis to achieve a euvolemic volume status, stable heart rates, and adequate blood pressures with optimal end-organ perfusion. Patients should be instructed to continue their HF medications (beta-blockers, ACE inhibitors/angiotensin receptor blockers, aldosterone antagonists, diuretics) until the day of surgery. In patients with heart failure, judicious use of fluids in the perioperative period is required to avoid issues of volume overload and pulmonary edema. In patients with advanced heart failure, it is reasonable to have a cardiac anesthesiologist (if available) to perform anesthesia for the case using invasive monitoring with pulmonary artery catheter and/or transesophageal echocardiogram as needed. In all patients, HF medications should be reinstituted postoperatively as soon as clinically indicated.

Patients with significant valvular heart disease (VHD ) are at increased risk of perioperative morbidity and mortality [1, 12]. The risk is dependent upon the type and severity of VHD and the nature of the procedure being performed.

As with HF, a comprehensive history and physical exam (looking for overt signs/symptoms of HF or angina) is the first step in assessing a patient with VHD. The NYHA HF scale is a useful tool to determine a patient’s functional status. TTE should be performed in any patient with known or suspected VHD. A high index of suspicion for VHD should be present in any patient with a history of cardiac murmur.

Aortic stenosis (AS ) is the most common VHD particularly among the elderly [14]. AS causes a fixed obstruction at the aortic valve level resulting in pressure overload of the left ventricle resulting in concentric hypertrophy of the LV. Valvular AS has several causes including congenital, rheumatic, bicuspid, and calcific (senile). In the USA, severe AS in the elderly (>70 years of age) is most commonly related to calcific degeneration, while severe AS in younger patients (50–70) is typically related to the bicuspid aortic valve (1–2 % of the general population). Severe aortic stenosis is defined as an aortic valve area (AVA) <1 cm², Vmax >4 m/s, and/or a mean aortic valve gradient >40 mmHg [15].

In patients with severe AS , determination of symptoms directly attributable to the valve is critical. Cardinal symptoms of AS include angina, HF, and syncope. In patients with severe symptomatic AS who are scheduled for elective surgery, serious consideration must be made to intervening upon the AV prior to noncardiac surgery to lower the risk of perioperative complications. There are essentially three different interventions that can be performed in a patient with severe symptomatic AS : balloon valvuloplasty (BAV), percutaneous valve replacement (TAVR), or surgical valve replacement (SAVR). Balloon valvuloplasty is used as a bridging strategy aimed at temporarily improving hemodynamics by reducing the severity of AS. A successful BAV results in a 50 % improvement in AVA and a 50 % reduction in pressure gradients [16]. Risks of BAV include stroke (up to 10 % of patients), acute aortic regurgitation, and vascular access site complications [17]. BAV is not an effective long-term therapy for severe AS, as 50% of patients will have restenosis of the AV within 6 months [18]. TAVR is a newer procedure that has a proven mortality benefit in inoperable patients with severe AS and is an attractive alternative for high-risk patients with severe AS [19]. The recovery from TAVR is significantly shorter than with SAVR, which can require 2–3 months for an elderly patient to return to their baseline. Uncomplicated TAVR patients are typically discharged from the hospital within 2–3 days and are back to their baseline with 2–3 weeks post-procedure.

In patients with severe asymptomatic AS , the decision to intervene upon the AV prior to elective surgery is more difficult and requires a case-by-case analysis. The absence of symptoms should be confirmed with exercise stress testing. In those patients with severe symptomatic AS who must undergo an urgent or emergent noncardiac surgery, if BAV is not available, invasive hemodynamic monitoring, avoidance of rapid volume shifts/loads, careful administration of vasodilators, and maintenance of normal sinus rhythm are all essential.

Mitral stenosis (MS ) secondary to rheumatic heart disease was once the most common form of VHD worldwide and is still the leading cause of VHD in developing nations [20]. With the introduction of rapid screening for strep infections and prompt antibiotic treatment, the incidence of rheumatic fever and its sequelae is now exceedingly rare in the USA except for in patients who have emigrated from endemic areas [21]. MS can also occur secondary to congenital malformation, prior mitral valve surgery (including repaired and replaced valves), and from systemic diseases which can cause valvular fibrosis (e.g., carcinoid, lupus, rheumatoid arthritis). The normal mitral valve has an orifice which is 4–5 cm². As the mitral orifice narrows, a pressure gradient between the left atrium (LA) and LV develops. This pressure gradient is added to the LV diastolic pressure causing an increase in the LA pressure which leads to LA dilatation, elevated pulmonary arterial pressures, and pulmonary congestion. As the severity of MS progresses, LV diastolic filling is impaired, ultimately resulting in reduced cardiac output. Symptoms of severe MS mimic symptoms of combined LV systolic/diastolic HF. Severe MS is defined as an MV area (MVA) <1.5 cm² which corresponds to a transmitral gradient of >5–10 mmHg at a normal heart rate [15]. In general, noncardiac surgery can be performed safely in patients with MS with an MVA >1.5 cm² and in asymptomatic patients with severe MS and estimated PASP <50 mmHg. As with asymptomatic AS, if feasible, the absence of symptoms should be confirmed with exercise stress testing. In asymptomatic patients with severe MS and estimated PASP >50 mmHg and in symptomatic patients with severe MS , the risk of perioperative morbidity and/or mortality is significantly increased, and consideration for mitral valve intervention (either percutaneous BAV or open surgical repair) must be entertained. Medical management of all patients with significant MS includes optimization of volume status, avoidance of volume shifts/loads, and maintenance of normal sinus rhythm with a slow heart rate to allow for diastolic filling.

In general, nonsignificant regurgitant valvular disease (aortic insufficiency or mitral regurgitation) is well tolerated and does not increase the risk of perioperative complications as the LV is conditioned to tolerate typical volume shifts associated with perioperative care. Patients with severe asymptomatic regurgitant valvular disease (aortic insufficiency or mitral regurgitation) and preserved LVEF can safely be sent to the operating room for noncardiac surgery. For patients with severe asymptomatic regurgitant valvular disease and reduced LVEF (<30%) or for those patients with severe symptomatic regurgitant valvular disease, there is an increased risk of cardiac complications, and management must be tailored based upon a risk-benefit analysis for the proposed noncardiac procedure [22]. If a patient requires noncardiac surgery, pharmacologic optimization (with the use of diuretics and afterload-reducing agents) prior to the OR can lower the cardiac risk.

In patients with a history of prosthetic valve replacement or repair, there is no additional risk for noncardiac surgery provided there is no evidence of valvular and/or ventricular dysfunction. The major risk associated with a history of valve replacement comes from the perioperative management of anticoagulation (discussed separately below) in patients who are chronically anticoagulated .

Management of antithrombotic (antiplatelet ± anticoagulation) therapy in patients undergoing noncardiac surgery is a common situation facing clinicians. Physicians must decide upon the safety of interruption of antithrombotic therapy, optimal timing of preoperative cessation and postoperative resumption of these medications, as well as bridging strategy (if any). Safety of interruption of antiplatelet therapy hinges upon the indication for antiplatelet therapy (recent coronary stenting vs. primary risk reduction in an asymptomatic patient with coronary artery disease) and the type of procedure being planned. Procedural risk is determined by the anatomic site and propensity for bleeding (Table 6.5). Similarly, the approach to anticoagulation is determined by both the indication for anticoagulation (low-risk atrial fibrillation vs. mechanical heart valves/rheumatic heart disease/recent venous thromboembolism) and type of procedure being planned.

Antiplatelet agents include aspirin, nonsteroidal anti-inflammatory drugs, platelet P2Y12 receptor inhibitors including thienopyridines (clopidogrel, prasugrel) and the cyclopentyltriazolopyrimidine (ticagrelor), phosphodiesterase inhibitors (dipyridamole, cilostazol), and glycoprotein IIb/IIIa receptor inhibitors (abciximab, eptifibatide, tirofiban). Platelets have a 10-day life span in the blood. As such the entire platelet pool can be regenerated after 10 days. Aspirin, prasugrel, and ticagrelor are all inhibitors of platelets. Aspirin and prasugrel are both irreversible inhibitors of platelet function, while ticagrelor is a potent reversible inhibitor of platelet function.

In patients (excluding those with a history of coronary stents or recent acute coronary syndrome) who are taking aspirin monotherapy for cardiovascular risk reduction, we recommend that aspirin be held for 5–7 days prior to noncardiac/vascular surgery. Aspirin should be resumed postoperatively once the patient is tolerating oral intake and the risk of major surgical bleeding has passed. This recommendation is based largely upon the results of the POISE 2 trial [23]. Briefly, in POISE 2, investigators used a 2 × 2 factorial design that compared clonidine to placebo and aspirin to placebo in 10,010 patients who were undergoing noncardiac surgery (excluding carotid endarterectomy, retinal surgery, or intracranial surgery) and were at risk for vascular complications. Patients were stratified according to whether they had been taking aspirin (continuation stratum; n = 4382) or not (starting stratum; n = 5628) prior to the study. Patients in the initiation stratum started taking aspirin (at a dose of 200 mg) or placebo just before surgery and continued it daily (at a dose of 100 mg) for 30 days in the initiation stratum and for 7 days in the continuation stratum; after which, patients resumed their regular aspirin dosing. The primary outcome of death or nonfatal myocardial infarction (MI) at 30 days was similar in both the aspirin and placebo group (7.0 vs. 7.1%, respectively; hazard ratio [HR] 0.99, 95% CI, 0.86–1.15). As expected, major bleeding was more common in the aspirin group (4.6 vs. 3.8%; HR 1.23, 95% CI, 1.01–1.49).

The approach to perioperative management of antiplatelet therapy in patients with prior percutaneous coronary intervention (PCI ) with stenting warrants specific discussion (Table 6.6). Each year, approximately 500,000 patients in the USA undergo cardiac stent implantation [24]. It has been estimated that up to 10% of patients with coronary stents undergo noncardiac surgery within a year of stent implantation [25]. Following coronary stent implantation, patients are given aspirin and a second antiplatelet agent (clopidogrel, prasugrel, or ticagrelor). This is termed dual antiplatelet therapy (DAPT) . The concern over premature cessation of DAPT following coronary stenting is in-stent thrombosis (acute occlusion of the stent). In-stent thrombosis is a condition that carries a high degree of morbidity and mortality. The highest risk for stent thrombosis following either bare-metal stent (BMS) or drug-eluting stent (DES) is in the first 4–6 weeks after stent implantation [26]. Discontinuation of DAPT during this high-risk period is a strong risk factor for in-stent thrombosis. The “recommended” waiting time prior to proceeding with noncardiac surgery is typically 2–4 weeks following balloon angioplasty (PCI without stent implantation), 4–6 weeks following BMS, and 12 months following DES. In those patients who require noncardiac surgery within the recommended waiting time, strong consideration should be given for continuation of DAPT whenever feasible. If the risk of bleeding with DAPT is considered prohibitive, every attempt possible should be made to continue aspirin throughout the operative period. Once the surgical risk of bleeding has stabilized, the second antiplatelet agent should be resumed. It is critical to note that the recommended time frames for DAPT following coronary stenting are somewhat arbitrary (e.g., in Europe, there are certain DESs which have a recommended DAPT time frame of only 3 months compared to 12 months recommended by the FDA for the same stent) and are based on expert opinions, and thus decisions regarding perioperative management of DAPT must be individualized on a case-by-case basis. With current third-generation DES, our practice is to avoid discontinuing DAPT prior to 6 months post-implantation whenever feasible. To date, there is a lack of evidence to support “bridging” a patient with anticoagulation or IV glycoprotein IIb/IIIa inhibitor following discontinuation of DAPT prior to surgery. The specific antiplatelet management strategy should be communicated and discussed among the cardiologist, surgeon, anesthesiologist, and patient.

Anticoagulants include warfarin, heparin (unfractionated or low-molecular-weight), fondaparinux, direct thrombin inhibitors (recombinant hirudins, bivalirudin, argatroban, dabigatran), and direct Xa inhibitors (rivaroxaban, apixaban, edoxaban). It has been estimated that over 6 million Americans are on chronic anticoagulation for prevention of thromboembolism for atrial fibrillation (AF), mechanical heart valve, or treatment of a thromboembolic disorder. The risks of bleeding for any procedure must be weighed against the benefit of remaining on anticoagulation on a case-by-case basis.

The first step is to determine the risk of thromboembolic event during the period when anticoagulation is to be held. For patients with atrial fibrillation , the daily risk associated with cessation of anticoagulation is extrapolated from yearly risks outside of the surgical period. Two commonly used risk prediction calculators are the CHADS2 and CHA2DS2-VASc score, which can be used to estimate the yearly risk of stroke in patients with non-valvular AF (AF in the absence of rheumatic mitral stenosis , a mechanical or bioprosthetic heart valve, or mitral valve repair) [27, 28] (Table 6.7). In both of these scoring systems, the higher the total score, the greater the yearly risk of stroke (Table 6.8).

In patients with mechanical heart valves, the risk of thromboembolism is determined by the type, number, and location of mechanical valves as well as the presence or absence of any additional risk factors (i.e., heart failure, prior stroke, AF) [29] (Table 6.9). In general, mechanical valves in the mitral position portend a higher risk of embolism compared to the aortic position.

In patients with a history of thromboembolic disease, the risk of recurrent thromboembolism is determined by how recently a clinical event occurred and whether or not the thromboembolism was “provoked” [30] (Table 6.10). The risk of recurrent thromboembolism is greatest within 3 months of a blood clot, and the risk rises in cases of idiopathic thromboembolism. In patients with a history of provoked thromboembolism, risk of recurrence diminishes greatly once the underlying risk factor is corrected.

Cancer patients represent a group with elevated risk for thromboembolism during the perioperative period. Several factors are thought to elevate the risk of clot including prothrombotic activity, cancer therapies (hormonal, radiation, angiogenesis inhibitors), and decreased mobility, as well as the presence of an indwelling central venous catheter (i.e., Mediport) which is common in cancer patients. Many cancer patients are also at increased risk of bleeding due to cancer or treatment-related thrombocytopenia, chemo-related hepatic and renal dysfunction, and tumor friability.

After the risk of thromboembolic event during the period when anticoagulation is to be held is determined, the second step for peri-procedural management of anticoagulation is to determine the risk of bleeding due to the planned procedure. As stated previously, procedural risk is determined by the anatomic site and propensity for bleeding (Table 6.5).

In patients at low risk for thromboembolism undergoing high-risk surgery or patients at high risk for thromboembolism undergoing low-risk procedures, the management is relatively straightforward. The number of days prior to surgery that anticoagulation must be held is determined principally by two factors: the pharmacokinetics of the specific anticoagulant and the patient’s renal function (Table 6.11).