Myocardial Oxygen Supply and Demand

Describe myocardial oxygen demand and supply, and the conditions that may alter each

  • Myocardial oxygen supply is a function of coronary blood flow
  • Myocardial oxygen demand is determined by myocardial work
  • Myocardial ischaemia occurs when demand exceeds supply

Myocardial Oxygen Supply

  • Myocardial oxygen supply is dependent on:
    • Coronary artery flow
    • Oxygen content of blood
    • Oxygen extraction
  • Functionally, coronary artery flow is the determinant. This is because:
    • Oxygen content in individuals without pulmonary disease is maximal
    • Resting myocardial oxygen extraction is near-maximal (~70%)
      This high ER makes the heart less tolerant of anaemia than organs with a low ER.
  • Therefore coronary blood flow is the limiting factor
    • Coronary blood flow is given by the equation:
      • Aortic root pressure is the driving pressure for coronary flow
      • Cavity (ventricular) pressure acts as a Starling resistor for coronary flow
        • Note that if RAP exceeds cavity pressure, RAP will be the pressure opposing coronary flow (due to downstream pressure at the coronary sinus)
      • Note that cavity and aortic root pressure change throughout the cardiac cycle, therefore:
        • The flow to each ventricle is different during the cardiac cycle
        • The left ventricle is best perfused in diastole
          Therefore heart rate is an important determinant of coronary blood flow, as tachycardia will decrease coronary blood flow
  • Flow to each ventricle is a function of how relationships change over the cardiac cycle

Left Ventricular Coronary Blood Flow:

Right Ventricular Coronary Blood Flow:

Myocardial Oxygen Demand

Normal myocardial oxygen consumption (MVO2) is 21-27ml.min-1. The three major determinants are:

  • Heart rate
    A change in heart rate will change the number of tension-generating cycles, causing a proportional change in MVO2.
  • Contractility
    Refers to the rate of tension development as well as its magnitude. Changing will change MVO2.
  • Ventricular wall tension
    Ventricular wall tension is pressure work, or the work done by the ventricle to generate pressure but not to eject volume.
    • Wall tension is given by the Law of LaPlace
      , where:
      • = Pressure during contraction
      • = Radius
    • Wall tension is therefore a function of:
      • Afterload
        Increasing afterload will increase the pressure during contraction.
      • Preload
        Increasing preload will increase radius, but to a lesser extent than increasing afterload.
        • This is because volume and radius are not directly proportional

Minor determinants of myocardial work are:

  • External work
    External work can also be thought of as volume work, or the energy expended to eject blood from the ventricle.
    • This is encompassed by the area enclosed by the pressure-volume loop
      • Conversely, internal work is defined as the work required to change the shape of the ventricle and prepare it for ejection
        On the pressure-volume loop internal work is represented by a triangle between the point of 0 pressure and volume, the end systolic point, and the beginning of rapid ventricular filling.
    • This is a minor determinant because the majority of ventricular work is generating the pressure required to eject blood, not actually move volume
    • External work is of greater importance at high CO
    • External work is used to calculate cardiac efficiency, given by the equation:
  • Basal oxygen consumption
    Basal oxygen consumption (~8ml.min-1.100g-1) comprises ~25% of MVO2.


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Last updated 2017-10-05

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