With advances in medical therapy, patients with chronic heart failure, stable angina, and valvular disease are living longer. This means they are increasingly presenting for noncardiac surgery. As their perioperative presence grows, so does your responsibility to manage them safely through all phases of care. Thirty-day mortality risk, a key performance metric for hospitals and surgical centers, is heavily influenced by the management of cardiac risk factors. In many ways, this is your value proposition to the institution: delivering safe anesthesia care to patients with cardiovascular disease. A complete review of cardiac pathophysiology is beyond the scope of this section. Along with the “Myocardium at Risk” chapter, the goal here is to outline the core principles essential for safe perioperative cardiovascular management. These concepts are simple in theory, but demand vigilance in practice: A slow induction using propofol titrated alongside phenylephrine is a very effective induction strategy for a wide range of patients with cardiac failure. Whether the patient has chronic stable disease or is acutely decompensated, the strategy remains the same: optimize physiology and maintain an adequate mean arterial pressure (MAP). If you consistently optimize the fundamentals–volume status, blood pressure, oxygenation, ventilation–you are 99% of the way to delivering a safe cardiac anesthetic. Volume management in the context of cardiac disease is a nuanced and hotly debated topic in perioperative medicine. For cardiac and noncardiac patients alike, your primary responsibility is to avoid hypovolemia. Hypovolemia remains the most common and consequential perioperative volume status. As discussed earlier in this text, volume overload is rarely a relevant concern in the acute intraoperative setting, where your primary goals are maintaining perfusion and supporting end-organ function. While patients with chronic heart failure may be diuresed for total body volume overload in the outpatient setting, they are usually optimized and at their dry weight when presenting for elective surgery. In urgent or emergent cases, patients may be bleeding, septic, or NPO for extended periods. This takes precedent over any concerns for total body volume overload. Patients with significant cardiac disease will not only tolerate, but also benefit from fluid resuscitation if they are intravascularly dry. Many patients with advanced heart disease have persistent lower extremity edema or trace effusions, even after diuresis. These are markers of chronic fluid shifts and not necessarily representative of intravascular volume overload. Don’t let external edema mislead you into undertreating intravascular depletion. In the perioperative setting, precise cardiovascular language is essential. Vague terms like “CAD” or “low EF” are inadequate. Communicate like a doctor: These details directly inform intraoperative decisions and may become vital during complications. To level up your practice, go beyond labels: Having this information not only improves patient care, but it also establishes you as the clinical anchor when things go sideways. Patients with active myocardial ischemia should not undergo elective surgery, a principle covered in detail in Part 1 of this text. Outside of select circumstances, such as the urgent need for control of hemorrhage or evacuation of an infectious source, these patients should first be revascularized or medically optimized before proceeding to the OR. In the rare situations where emergent surgery cannot be delayed in a patient with active myocardial ischemia, anesthetic management must focus on preserving myocardial oxygen supply and demand balance. This includes maintaining hemodynamic stability, avoiding tachycardia, correcting any electrolyte disturbances, and ensuring acid–base homeostasis. These strategies are essential in minimizing ischemic burden during the physiologic stress of surgery. Patients with occult myocardial ischemia (CAD) that is not active should be managed with usual anesthetic precautions. They should ideally be on beta-blockers, assuming no contraindications. Beta blockade helps blunt sympathetic surges and reduces myocardial oxygen consumption during times of stress. The landscape of beta blockade is continuously changing, with some new studies suggesting that patients who are revascularized and otherwise compliant with lifestyle modifications may not need chronic beta-blocker therapy. Signs of intraoperative myocardial ischemia may include ST depressions or elevations on the ECG, the appearance of a new left bundle branch block, or the emergence of ventricular arrhythmias. These findings warrant immediate attention, as they may reflect a critical imbalance in coronary perfusion. Take steps to improve O2 supply, coronary perfusion, and limit exacerbating increased myocardial demand. Intraoperative myocardial ischemia should warrant a prompt discussion with the procedural team and cardiology consultation. Time from recognition to revascularization is critical. Beta-blockers should always be continued in the perioperative period, along with ACE inhibitors, ARBs, calcium channel blockers, and other antihypertensives. While intraoperative hypotension often draws the most attention, it is usually manageable. On the other hand, abrupt withdrawal of antihypertensives can lead to rebound hypertension, myocardial ischemia, or stroke, all of which are far more difficult to recover from postoperatively. Most surgical cases today are short-stay or ambulatory, with a premium placed on efficient throughput and safe discharge. It stands to reason that patients should be maintained on the medications that keep them optimized in daily life, especially when they are facing the physiologic stress of surgery. Consider this: “if they need a beta-blocker to watch TV, they need it for major surgery.” The concept of perioperative “vasoplegia” in patients on ACE inhibitors or ARBs has been revisited. It has repeatedly been established that while there may be a slightly increased risk of intraoperative hypotension, this does not clearly result in increased mortality or perioperative complications [10]. Most patients who are hypotensive under anesthesia are so because of vasodilation and hypovolemia, and not due to “vasoplegia.” First, rule out other causes of hypotension, and keep this as a diagnosis of last resort. Vasopressin always increases BP better than phenylephrine, so the fact that it improves BP in a patient on an ACEI does not confirm a diagnosis of ACEI vasoplegia. For perioperative hypotension, keep a broad differential, and don’t let the ACEI/ARB narrative dominate or anchor your reasoning. Finally, a special mention for SGLT-2 inhibitors, which are increasingly prescribed for patients with type 2 diabetes, cardiovascular disease, and chronic heart failure. These agents are associated with euglycemic diabetic ketoacidosis, a complication discussed further in the “Endocrine” section. For this reason, they are recommended to be held 3–4 days before an invasive procedure or a period of fasting.
Chapter 33
Cardiovascular
General Optimization Strategies
The Pillars of Cardiac Care
Induction: Safety Over Creativity
Intraoperative Management
Volume Optimization in Cardiac Disease
Use Specific Cardiac Terminology
“Chronic systolic heart failure from ischemic cardiomyopathy, compensated”
“Critical aortic stenosis with a valve area of 0.6 cm2”
“CAD with two RCA stents placed in March 2023”
Know the “Why,” Not Just the “What”
Myocardial Ischemia
Preoperative Medications
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