Issues pertinent to the cardiac procedure and the physiologic impact of CPB and circulatory arrest include the following:

1. Prior surgery in the chest, which technically complicates surgery.

2. Evidence of aortic and cerebrovascular disease—symptomatic or documented carotid arterial disease may warrant endarterectomy. Aortic disease can affect cannulation strategies for bypass and may sometimes require concomitant repair with the cardiac operation.

3. History of bleeding, anticoagulation regimens, and prothrombotic tendencies may reveal a condition responsive to perioperative therapy.

4. A history of heparin-induced thrombocytopenia (HIT) alerts the potential for the development of life-threatening thrombotic complications when exposed to heparin. HIT is discussed later in the chapter.

5. Renal insufficiency may indicate the need for intraoperative renal protective measures.

6. Patients with pulmonary disease can develop severe post-CPB pulmonary dysfunction and may benefit from preoperative antibiotics, bronchodilators, steroids, or chest physical therapy.

7. Liver dysfunction (eg, cardiac cirrhosis) may indicate derangements in coagulation and platelet function and the need for transfusion of coagulation factors, platelets, and fibrinogen.

Cardiac evaluation determines the major anatomic and physiologic characteristics of the cardiovascular system, to predict intraoperative ischemia and functional reserve of the heart.

1. Radionuclide imaging may demonstrate the regions and extent of myocardium at risk for ischemia. Radionuclide ventriculography characterizes cardiac chamber volume, ejection fraction, and right-to-left stroke volume ratios.

2. Viability studies in patients with severe LV dysfunction can help distinguish areas of myocardial necrosis from hibernation; the latter may recover after revascularization. Current modalities include nuclear imaging (SPECT or PET), dobutamine stress echocardiography, and magnetic resonance imaging (MRI).

3. Echocardiography provides an assessment of ventricular function and valve function. Regional wall motion abnormalities (WMAs) may reflect ischemia or prior myocardial infarction.

4. CT scan and f-MRI are noninvasive modalities to assess for coronary vascular disease. They can be useful in patients who are not candidates for cardiac catheterization.

5. Cardiac catheterization remains the gold standard diagnostic test for most forms of cardiac disease.

   1. Anatomic data. Coronary angiography reveals the location and extent of coronary stenoses, distal runoff, collateral flow, and coronary dominance. Significant stenosis implies a greater than 70% reduction in luminal diameter. The dominant coronary artery supplies the atrioventricular node and the posterior descending coronary artery.

   2. Functional data. Ventriculography may demonstrate WMA, mitral regurgitation (MR), and intracardiac shunts. LV ejection fraction is normally greater than 0.6. Impaired ventricular performance is a useful predictor of increased surgical risk.

   3. Hemodynamic data are compiled from both right and left heart catheterization. Intracardiac and pulmonary vascular pressures reflect volume status, valvular function, and the presence of pulmonary vascular disease (normal values are presented in Table 29.1). An

      elevated LV end-diastolic pressure (LVEDP) may be due to ventricular failure and dilation, volume overload (mitral or aortic insufficiency [AI]), poor compliance from ischemia or hypertrophy, or a constrictive process. The LVEDP may rise substantially in patients with coronary artery disease (CAD) after dye injection for ventriculography or coronary angiography, despite otherwise normal hemodynamic values.

      
      TABLE 29.1 Normal Intracardiac Pressure and Oxygen Saturation

      	Pressure (mm Hg)	O2 Saturation (%)
      Superior vena cava	—	71
      Inferior vena cava	—	77
      Right atrium (mean)	1–8	75
      RV (systolic/diastolic)	15–30/0–8	75
      PA (systolic/diastolic)	15–30/4–12	75
      PA occlusion pressure (mean)	2–12	—
      Left atrium (mean)	2–12	98
      LV (systolic/diastolic/end diastolic)	100–140/0–8/2–12	98
      Aorta (systolic/diastolic)	100–140/60–90	98

      LV, left ventricle; PA, pulmonary artery; RV, right ventricle.

   4. Left-to-right intracardiac shunts are demonstrated by an arterial oxygen saturation (SaO₂) “step up” in the right heart.

   5. Cardiac output is determined by thermodilution and can be used to derive the hemodynamic indices (Table 29.2).

      
      TABLE 29.2 Ventricular Function Indices

      Formula	Units	Normal Value
      SV=COHR×1000	mL/beat	60–90
      SI=SVBSA	mL/beat/m2	40–60
      LVSWI=1.36(MAP−PCWP)100×SI	g-m/m2/beat	45–60
      RVSWI=1.36(PAP−CVP)100×SI	g-m/m2/beat	5–10
      SVR=(MAP−CVP)CO×80	dyne-s/cm5	900–1500
      PVR=(PAP−PCWP)CO×80	dyne-s/cm5	50–150

      BSA, body surface area; CO, cardiac output; CVP, mean central venous pressure; HR, heart rate; LVSWI, left ventricular stroke work index; MAP, mean arterial pressure; PAP, mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; RVSWI, right ventricular stroke work index; SI, stroke index; SV, stroke volume; SVR, systemic vascular resistance.

Other studies

1. Routine labs for patients undergoing a cardiac operation usually include a CBC, prothrombin time, activated partial thromboplastin time (aPTT), platelet count, electrolytes, blood urea nitrogen, creatinine, glucose, liver function tests, and thyroid-stimulating hormone level. A heparin-platelet factor 4 antibody detection assay should be considered for patients with a low or rapidly falling platelet count associated with heparin, as these patients are at risk for developing HIT.

2. Chest radiograph and a 12-lead ECG with a rhythm strip.

3. Pulmonary function tests may be appropriate in patients with underlying lung disease.

4. Vascular studies such as carotid duplex and vein mapping.

5. Frailty assessments may aid preoperative evaluation and risk stratification of geriatric patients to identify surgical candidates with adequate physical and cognitive reserve who are likely to benefit and recover from proposed interventions.

Cardiac Medications

1. β-Adrenergic antagonists, calcium channel blockers, antiarrhythmics, and nitrates, including intravenous (IV) nitroglycerin, are routinely continued on schedule until the patient’s arrival in the operating room (OR).

2. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers, and diuretics are usually held before surgery. Patients with

   significant LV dysfunction are prone to vasodilatory shock when they receive an ACE inhibitor preoperatively.

3. Aspirin has a positive effect on graft patency and should be continued in most patients who have significant CAD. Bleeding related solely to aspirin therapy can be overcome with platelet transfusion provided the drug has been cleared from the circulation. Patients receiving multiple antiplatelet agents may or may not be rapidly reversible (Table 29.3).

   
   TABLE 29.3 Antiplatelet Agents

   Drug	Inhibits	Half-Life	Duration	Reversible	Methods to Restore Function
   Aspirin	Cyclooxygenase	15–20 min	7 d	No	Platelet transfusion
   Abciximab (Reopro)	Glycoprotein IIb/IIIa receptor	30 min	48 h	Partially	Platelet transfusion
   Eptifibatide (Integrilin)	Glycoprotein IIb/IIIa receptor	2.5 h	4–8 h	Yes	Delay surgery 8 h after stopping drug
   Tirofiban (Aggrastat)	Glycoprotein IIb/IIIa receptor	1.5–3 h	4–8 h	Yes	Discontinue drug 8 h before surgery
   Clopidogrel (Plavix)	Adenosine diphosphate receptor	8 h	7 d	No	Platelet transfusion
   Prasugrel (Effient)	Adenosine diphosphate receptor	2–15 h	7 d	No	Platelet transfusion
   Cangrelor	Adenosine diphosphate receptor	2–5 min	1 h	Yes	Platelet transfusion or wait 6 h before surgery
   Ticagrelor (Brilinta)	Adenosine diphosphate receptor	6–9 h	5 d	No	Platelet transfusion
   Ticlopidine (Ticlid)	Adenosine diphosphate receptor	12 h–5 d with repeated dosing	7 d	No	Platelet transfusion
   Dipyridamolea (Persantine)	Adenosine uptake; phosphodiesterase	9–13 h	4–10 h	Yes	Platelet transfusion
   Cilostazol (Pletal)	Phosphodiesterase III	11–13 h	48 h	Yes	Platelet transfusion
   Herbal therapiesb	Platelet aggregation	Variable	Variable	Variable	Limited data available

   ^aDipyridamole is available in a formulation with aspirin (Aggrenox).^bIncludes garlic, ginkgo, ginseng, ginger, feverfew, fish oil, and dong quai.

4. P2Y₁₂ inhibitors such as oral clopidogrel and prasugrel are stopped 5 to 7 days prior to surgery. If a bare-metal stent was placed within the past month or a drug-eluting stent within the last year, clopidogrel is often continued up until the time of surgery. Conversely, cangrelor, a reversible P2Y₁₂ inhibitor, may be used for bridging in patients with recent coronary stent placement. It should be stopped 6 hours preoperatively.

5. Direct oral anticoagulants (DOACs) such as factor Xa inhibitors apixaban, rivaroxaban and edoxaban, and thrombin inhibitor dabigatran should be stopped 3 to 5 days before cardiac surgery. Andexanet Alfa is approved for emergency reversal of rivaroxaban and apixaban. Idarucizumab is approved for emergency reversal of dabigatran. Use of these DOAC reversal agents must be weighed against the risk of thrombotic events in consultation with Hematology. Off-label use of prothrombin complex concentrates may also be considered for refractory hemorrhage during cardiac surgery for patients on a DOAC.

6. Warfarin is held 3 to 5 days preoperatively to allow normalization of the international normalization ratio. IV vitamin K (5 to 10 mg) or

   fresh–frozen plasma (FFP) may be used emergently to correct coagulopathy. However, FFP will only transiently correct a warfarin-induced coagulopathy due to the relatively longer half-life of warfarin compared with the vitamin K–dependent cofactors (factors II, VII, IX, and X), thus putting the patient at risk for rebound coagulopathy. Emergent reversal requires the administration of four-component prothrombin complex concentrates.

7. Heparin infusions initiated for unstable angina or left main CAD are continued preoperatively. The anticoagulant effects of unfractionated heparin are reversible with IV protamine administration. In contrast, the anticoagulant effects of low–molecular-weight heparin (LMWH) preparations are not fully reversible with protamine. LMWH has been associated with increased perioperative hemorrhage in cardiac surgical patients.