Ischemic Heart Disease

Cardiac Risk Assessment

• The Lee Revised Cardiac Risk Index assesses the risk of cardiac complications in high-risk surgery patients.
• High-risk surgery patients have:
  • Ischemic heart disease
  • Congestive heart failure
  • Cerebrovascular disease
  • Insulin-dependent diabetes
  • Preoperative serum creatinine > 2.0 mg/dl

Preoperative Cardiac Intervention

• Options for preoperative cardiac intervention:
  • Revascularization (CABG) - only if the risk of planned surgery exceeds the risk of cardiac cath + CABG + planned surgery
  • Percutaneous Coronary Intervention (PCI) - angioplasty + stenting
  • Optimizing medical management

Medical Therapy Intervention

• Recommendations for medical therapy intervention:
  • Perioperative beta-blockade: oral therapy initiated at least 30 days preop, IV therapy intraop and postop
  • Statin therapy: initiated at least 45 days preop, extended-release form on the day of surgery, and resumed postop
  • ACE inhibitors: Class I
  • Ca++ channel blockers: Class IIb, limited evidence for use in vascular surgery
  • Nitroglycerin: Not indicated for prophylaxis or initial treatment of myocardial ischemia

Intraoperative Management

• General principles:
  • Optimize the myocardial oxygen supply/demand ratio
  • Monitor for ischemia and treat aggressively
  • Maintain heart rate and blood pressure within 20% of baseline
• Induction and laryngoscopy:
  • Most any induction technique is acceptable if done properly
  • Avoid ketamine as the primary induction agent
  • Minimize the sympathetic pressor response
• Maintenance:
  • Volatile anesthetics: widely used, decrease myocardial oxygen requirements
  • Narcotic technique: may be used with nitrous oxide, benzodiazepines, and low-dose volatile or propofol infusion

Coronary Artery Disease

• Anatomy of the coronary circulation:
  • Coronary arterial system: origin, distribution, dominance, and collateral circulation
  • Coronary venous system: great cardiac vein, anterior cardiac vein, and middle cardiac vein
• Coronary blood flow:
  • Mechanical effects: coronary perfusion pressure, vascular resistance, and vessel length and blood viscosity
  • Regulation of coronary blood flow: metabolic control, neural control, and autoregulation
• Pathophysiology of ischemic heart disease:
  • Atherosclerosis: an inflammatory process, intimal lipid plaque, and acute coronary syndromes
  • Coronary steal: ischemic area distal to a high-grade stenosis, maximally dilated microvasculature, and redistribution of blood flow

Management of Ischemic Heart Disease

• ST elevation MI (STEMI):

  • Management goals: hemodynamic stability, increase O2 supply, decrease myocardial O2 demand, and reperfusion
  • Thrombolytic therapy, PCI, and CABG

• Unstable angina/NSTEMI:

  • Management goals: low risk patients managed medically, increase myocardial O2 supply, and prevent ongoing thrombus formation
  • High-risk patients considered for early invasive evaluation and intervention

• Predictors of long-term prognosis:

  • Degree of left ventricular dysfunction
  • Degree of residual ischemia
  • Potential for malignant ventricular dysrhythmias### Coronary Blood Flow and Metabolism

• Decreased capillary density in the interventricular septum and AV node, which may explain the vulnerability of these tissues to ischemia.

• The coronary venous system consists of the great cardiac vein, anterior cardiac vein, and middle cardiac vein, which terminate in the coronary sinus and empty into the right atrium.

• The coronary sinus receives approximately 75% of coronary venous blood, while the remainder empties directly into the atria and ventricles via thebesian veins.

Factors Affecting Left Ventricle Blood Flow

• Coronary perfusion pressure is determined by aortic pressure minus left ventricular end-diastolic pressure (LVEDP).
• Vascular resistance is related to the radius of the vessel to the fourth power, vessel length, and blood viscosity.

Regulation of Coronary Blood Flow

• Mechanical effects, metabolic control, and neural control regulate coronary blood flow.
• The Barash Guyton effect states that intense left ventricular muscular contraction limits systolic capillary blood flow, particularly to the subendocardial region.
• Large epicardial coronary vessels act as capacitors, and driving pressure for perfusion is essentially the average aortic root pressure during diastole.

Factors Compromising Subendocardial Blood Flow

• Coronary artery disease, left ventricular hypertrophy, tachycardia, decreased aortic-intraventricular pressure gradient, decreased aortic diastolic pressure, and increased LVEDP can compromise subendocardial blood flow.

Myocardial Oxygen Consumption

• Heart rate, myocardial contractility, and wall stress are major determinants of myocardial oxygen consumption.
• The Kaplan DPTI/SPTI ratio provides a more accurate picture of myocardial oxygen consumption in normal animal models.

Regulation of Coronary Blood Flow

• Myocardial blood flow is primarily under metabolic control, which is tightly linked to myocardial oxygen consumption.
• The exact mechanism or mediator of metabolic control has not been identified, but it is likely dependent on local mechanisms such as depletion of oxygen or accumulation of products of metabolism.

Neural Control

• Direct effects of neural control on coronary blood flow are minimal, but indirect effects are more significant, particularly changes in heart rate and contractility.
• The sympathetic nervous system has a greater influence on coronary blood flow than the parasympathetic nervous system.

Autoregulation and Failure

• Increasing occlusion results in dilation of capillary beds to maintain flow, but when coronary flow reserve is exhausted, autoregulation fails, and coronary blood flow becomes dependent on pressure gradients.
• Tachycardia markedly increases the mean arterial pressure at which autoregulation fails due to increased myocardial oxygen consumption and decreased diastolic perfusion time.

Pathophysiology of Ischemic Heart Disease

• Atherosclerosis is an inflammatory process that produces chronic stenosis and episodic thrombosis, often occurring in epicardial arteries.
• Characteristics of a vulnerable plaque include high lipid content, thin fibrous cap, decreased number of smooth muscle cells, and increased macrophage activity.
• Acute coronary syndromes result from sudden decreases in coronary blood flow, nearly always caused by thrombosis of a coronary artery.
• The degree of stenosis is less important than the extent of plaque rupture.

Management of Ischemic Heart Disease

• Management goals for ST-elevation myocardial infarction (STEMI) include hemodynamic stability, increasing oxygen supply, decreasing myocardial oxygen demand, and reperfusion.
• Management goals for unstable angina/non-ST-elevation myocardial infarction (UA/NSTEMI) include decreasing myocardial oxygen demand, increasing oxygen supply, and preventing ongoing thrombus formation.
• Predictors of long-term prognosis include the degree of left ventricular dysfunction, degree of residual ischemia, and potential for malignant ventricular dysrhythmias.

Arrhythmias and Ischemia

• Ventricular arrhythmias are most likely to occur in the first 10 minutes following acute occlusion.
• Three primary mechanisms of ventricular arrhythmias include failure of repolarization of ischemic myocytes, activation of the sympathetic nervous system, and left ventricular dilatation or aneurysm formation.

Coronary Steal and Silent Ischemia

• Coronary steal occurs when blood flow is redistributed away from an ischemic area via collateral vessels.
• Silent ischemia is often associated with elevations in heart rate or blood pressure and is closely related to circadian sleep-wake cycles.

Preoperative Assessment and Management

• Preoperative assessment should include a cardiac history, physical exam, preoperative testing, and risk stratification algorithms.
• Preoperative intervention may include revascularization, percutaneous coronary intervention, and optimizing medical management.

Intraoperative Management

• General principles of intraoperative management include optimizing the myocardial oxygen supply/demand ratio, monitoring for ischemia, and treating aggressively.
• Induction and laryngoscopy should be performed carefully to minimize the sympathetic pressor response.
• Maintenance anesthesia should focus on decreasing myocardial oxygen requirements, and muscle relaxants should have minimal effects on heart rate and blood pressure.

Postoperative Management

• Postoperative management should focus on increasing the potential for myocardial ischemia, particularly in the first 6-12 hours after surgery.
• Particular concerns include hypothermia, pain, inadequate ventilation, infection, and unreplaced or ongoing blood loss.

The Transplanted Heart

• The transplanted heart lacks parasympathetic, sympathetic, or sensory innervation for the first 6-12 months.
• After 6-12 months, partial reinnervation may occur, but results in a higher than normal resting heart rate and an inability to detect anginal pain.
• The transplanted heart is dependent on preload and the Frank-Starling mechanism to maintain cardiac output.