Medical Pharmacology Chapter 43:  Adult Cardiac Procedures

Coronary Artery Disease and 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

•  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

• 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 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