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 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
- Coronary blood flow is given by the equation:
- 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
- Afterload
- Wall tension is given by the Law of LaPlace
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.
- Conversely, internal work is defined as the work required to change the shape of the ventricle and prepare it for ejection
- 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:
- This is encompassed by the area enclosed by the pressure-volume loop
- Basal oxygen consumption
Basal oxygen consumption (~8ml.min-1.100g-1) comprises ~25% of MVO2.
References
- Grossman W, Baim DS. Grossman's Cardiac Catheterization, Angiography, and Intervention. 7th Ed (revised). 2006. Lippincott Williams and Wilkins.
- Leslie RA, Johnson EK, Goodwin APL. Dr Podcast Scripts for the Primary FRCA. Cambridge University Press. 2011.
- Kam P, Power I. Principles of Physiology for the Anaesthetist. 3rd Ed. Hodder Education. 2012.
- Miller RD, Eriksson LI, Fleisher LA, Weiner-Kronish JP, Cohen NH, Young WL. Miller's Anaesthesia. 8th Ed (Revised). Elsevier Health Sciences.