Coronary Artery Disease & Anesthesia Management

• 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

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•  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)*

* 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.

Figure legend information: A= autoregulation D =maximal vasodilation R1 & R2  : coronary flow reserves at mean coronary perfusion pressure of 75 & 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

• 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:

        1. Raising the diastolic arterial pressure

        2. 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 O₂ concentration

  •  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

• 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 & 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

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