Coronary Artery Disease and Anesthesia Management

Anesthesia Pharmacology Chapter 27: Adult Cardiac Procedures in Anesthesia

Regulation of coronary blood flow
- Normal physiologic regulation:
  - Autoregulation in response to myocardial metabolic requirements
  - Coronary flow increases with metabolic demand
- Abnormal physiological regulation in the presence of atherosclerotic coronary vessel disease
  - Atherosclerosis:
    - Physical obstruction of the coronary vasculature
    - Impairment of autoregulation
  - Consequences of an increase in myocardial oxygen demandspace for (or reduced myocardial oxygen supply) in the presence of atherosclerotic coronary vessel disease
    - Myocardial ischemia
- Major intraoperative goal for anesthesia providers:
  - Prevention/treatment of intraoperative cardiac ischemia -- method:
    - Minimize cardiac O₂ demand
    - Maximize cardiac O₂ supply
Myocardial Oxygen Demand: Major Determinants:
1. Myocardial wall tension
2. Cardiac contractility state
Intraoperative prevention of excessive myocardial O₂ demand:
- Before coronary revascularization, positive inotropic agents should be avoided (since the increase contractility thereby increasing O₂ demand)
- Excessive myocardial contractility may be reduced by anesthetics, which act by limiting sympathetic stimulation
- With adequate cardiac function ß-adrenoceptor blocking agents may be used to diminish contractility
Effects of anemia:
- Anemia increases myocardial O₂ demand while concurrently reducing myocardial O₂ supply
- Intervention: consider pre-bypass transfusion (given the transfusion will be required during bypass or post-bypass time frame)
Therapeutic intervention: Balancing myocardial O₂ supply and O₂ demand requirements--
- Example #1: ß-adrenoceptor blockade-- use of ß-blockers (e.g., propranolol (Inderal); metoprolol (Lopressor))
  - Reduces cardiac O₂ demand by attenuating contractility (negative inotropism) increases mediated by increased circulating catecholamines levels and sympathetic nervous system activity
  - Reduced heart rate (negative chronotropism) increases diastolic filling time, thereby increasing time available for coronary vascular perfusion
- Example #2: Blood pressure reduction
  - Advantage: reduced myocardial oxygen consumption (reduced afterload)
  - Disadvantage: reduced coronary blood flow through stenotic regions
- Overall objective -- both limitation in myocardial oxygen demand and maximization of supply: anesthetic should optimize this balance
Myocardial Oxygen Supply: Major Influences:
- Autoregulation: Constant flow despite significant blood-pressure variations
  - Anemia: blood flow increases to ensure adequate O₂ delivery to the myocardium
  - With maximal vasodilation, coronary blood flow is related linearly to blood pressure-- Definition "coronary vascular reserve" = blood flow beyond that which would normally occur with intact autoregulation.


Coronary Pressure-Flow Relationships

Coronary Pressure Flow relationships: Y axis= Flow (ml/min); X axis =mean pressure (mm Hg) Figure legend information: A= autoregulation D =maximal vasodilation R₁ and R₂ : coronary flow reserves at mean coronary perfusion pressure of 75 and 100 mm Hg -- with constant aortic pressure and heart rate With coronary stenosis: Coronary vascular reserve is used to counter stenotic flow effect Increasing coronary stenoses, associated with advancing coronary vascular disease, may use ultimately all vasodilator reserve. In this case coronary autoregulation is used to maintain the myocardial resting blood flow When this condition occurs, cornered blood flow will vary directly with blood pressure and therefore reduced blood pressure directly reduces coronary flow and causes myocardial ischemia Therefore: anesthesia major goal = In patients with significant coronary atherosclerosis: maintain arterial pressure adapted from Figure 68-1, Ross, AF, Gomez, MN. and Tinker, JH Anesthesia for Adult Cardiac Procedures in Principles and Practice of Anesthesiology (Longnecker, D.E., Tinker, J.H. Morgan, Jr., G. E., eds) Mosby, St. Louis, Mo., p. 1665, 1998.

Diastole: Importance in maintaining adequate myocardial oxygen supply

Reason: a significant percentage of epicardial and nearly all middle cardial and endocardial coronary flow occurs during diastole--this principle applies primarily to the left ventricle since significant right ventricular coronary flow occurs during systole

Consequence: diastole defines the time available for coronary blood flow

Tachycardia: detrimental secondary to diastolic interval reduction; ¯ ¯ reduced flow

Implication: significant coronary flow may be accomplished by reducing/avoiding conditions producing tachycardia (bradycardia however, is probably not desirable in terms of increasing epicardial coronary flow)

Diastolic Ventricular Filling Pressure-- a factor that opposes coronary blood flow

Blood flow through the myocardium is based on a pressure differential between (a) proximal coronary driving pressure and (b) distal opposing pressure

Definition:

proximal coronary driving pressure = considered to be the aortic pressure throughout diastole (note that the aortic pressure will be decreasing during diastole, therefore the driving force will not be constant)

Distal opposing pressure: measurement suggestions have included the ventricular wall pressure or LVEDP (left ventricular end diastolic pressure) or coronary sinus pressure

For clinical applications: LVEDP is used because it may be readily estimated and it is related directly to the myocardial region most susceptible to ischemia, the subendocardium

Complicating Factor: critical effects of coronary stenoses on flow-- a significant pressure drop occurs in blood is forced through a stenotic region: Consequence--

The actual driving pressure therefore is not the aortic diastolic pressure but rather whatever residual pressure is present, distal to stenotic region

In patients with coronary vascular disease, the pressure gradient which drives coronary blood flow may be small in influence significantly by LVEDP (wedge pressure)

Clinical consequence: anesthesia providers must carefully monitor ventricular filling pressures using the pulmonary artery catheter

Nitroglycerin may be used to maintain optimal filling pressures

Optimization of coronary perfusion pressure gradients involved typically:

Raising the diastolic arterial pressure

Decreasing LVEDP (left ventricular and diastolic pressure)

Special Clinical Considerations

Patient exhibits both elevated filling pressures and hypotension

Question: Can nitroglycerin be administered safely/appropriately?

Answer: Yes, however the arterial pressure must be protected

Judgment Issues with respect to myocardial contractility

Left ventricular function is very poor: use epinephrine or norepinephrine (Levophed) \to provide inotropic support before nitroglycerin is administered

Left ventricular function is satisfactory: increase arterial pressure using a pure vasoconstrictor, then add nitroglycerin

Avoid: Do not add fluids -- BP will probably remain unchanged but increased filling pressure is likely to worsen coronary blood flow, particularly to the left ventricular subendocardium

Concern: nitroglycerin reduces preloaded come the causing the decrease in cardiac output

Response: The primary objective is to improve/increase coronary blood flow, not cardiac output

Interventions which both decrease filling pressures (vasodilators, e.g. nitroglycerin) and increase BP (a-adrenergic receptor agonists) may increase cardiac output, secondary to reduced myocardial ischemia

Other ways of improving myocardial O₂ delivery:

Increased inspired O₂concentration

Correction of preoperative anemia

Summary
- Anesthetic protocol should:
  - Improve/facilitate myocardial oxygen delivery
  - Block sympathetic responses that would tend to increase myocardial oxygen requirements
- Primary goal: Enhance oxygen delivered to the heart (not to increase cardiac output)
  - Administering fluids to increase cardiac output is likely inappropriate as long as sufficient systemic perfusion avoids metabolic acidosis [increase filling pressures may readily degraded coronary perfusion pressure gradients]
  - Positive inotropic drugs should not be used unless needed to increase contractility sense these agents increase myocardial oxygen demand and thus might promote an ischemic state

Hemodynamics and Coronary Artery Disease
Hemodynamic event	Pharmacological intervention
Surgical stress induces: Autonomic, sympathetic stimulation which increases myocardial oxygen demand by both positive chronotropic (increased heart rate) and positive inotropic (increased contractility) Increased circulating catecholamines and direct cardiac stimulation by norepinephrine release from sympathetic endings	Properly chosen anesthetic agents block the stress response; β-adrenergic receptor blockers also only used to avoid increased contractility/rate
Ventricular dilatation associated with congestive heart failure, with increasing ventricular wall stress and LVEDP (left ventricular end diastolic pressure)	With left ventricular heart failure, inotropic support may improve the relationship between oxygen supply and demand
Increased BP increases oxygen demand and coronary blood flow; decreased BP may promote reduced coronary flow	Optimize coronary flow by maintaining blood-pressure at or slightly above normal (may require α-adrenoceptor agonist administration)
Tachycardia shortens available time between heart beats for diastolic coronary blood flow.	prevent increased heart rate using anesthetic agents initially and β-receptor blockade as needed
Increased ventricular filling pressures reduce coronary blood flow, particularly subendocardial flow.	Maintain reduced filling pressures using nitroglycerin
Provide optimal oxygenation	Important considerations: Adequate title volume Positive end expiratory pressure (PEEP) Insure high inspired oxygen Treat anemia with blood transfusion

Primary Reference: Ross, AF, Gomez, MN. and Tinker, JH Anesthesia for Adult Cardiac Procedures in Principles and Practice of Anesthesiology (Longnecker, D.E., Tinker, J.H. Morgan, Jr., G. E., eds) Mosby, St. Louis, Mo., pp. 1659-1698, 1998.
Primary Reference: Shanewise, JS and Hug, Jr., CC, Anesthesia for Adult Cardiac Surgery, in Anesthesia, 5th edition,vol 2, (Miller, R.D, editor; consulting editors, Cucchiara, RF, Miller, Jr.,ED, Reves, JG, Roizen, MF and Savarese, JJ) Churchill Livingston, a Division of Harcourt Brace and Company, Philadelphia, pp. 1753-1799, 2000.
Primary Reference: Wray Roth, DL, Rothstein, P and Thomas, SJ Anesthesia for Cardiac Surgery, in Clinical Anesthesia, third edition (Barash, PG, Cullen, BF, Stoelting, R.K, eds), Lippincott-Raven Publishers, Philadelphia, pp. 835-865, 1997