Myocardial Oxygen Demand

Myocardial oxygen demand is determined mainly by three important factors such as heart rate, intra myocardial wall tension and the contractile state of the myocardium. With an increase in heart rate, the number of contractions and the number of ATP consumed per minute increases and oxygen requirements rise. Conversely, slowing the heart rate decreases the ATP utilization and oxygen consumption.

Wall stress is directly proportional to systolic ventricular pressure. Conditions with greater pressure development is associated with increased wall stress and myocardial oxygen consumption. It is also proportional to radius of left ventricle, so conditions which augment left ventricular filling raise myocardial oxygen consumption. Increase in myocardial contractility is associated with greater oxygen consumption.

Myocardial oxygen demand has constant relationship to the cardiac work. Cardiac work is composed of external and internal cardiac work. External cardiac work refers to work done during the ejection phase of the cardiac cycle. Internal work refers to the work done during isovolemetric contraction. Even though the external cardiac work is less than half of the total cardiac work it has a constant relationship with the oxygen demand. The Oxygen demand increases with increase in external work done.

The three major determinants of myocardial oxygen demand are:  ventricular wall stress, heart rate and contractility. If the heart rate increases the number of contractions and the amount of ATP consumed per minute increases and the oxygen requirement rises.

A, B, C  i.e. Preload, Afterload, Intramyocardial tension, Myocardial muscle mass > Blood Hb concentration

Anemia, anxiety, arterio-venous fistula (AVF), beriberi, hyperthyroidism, paget’s disease, pregnancy, and pulmonary disease commonly cause high cardiac output due to reduced total peripheral resistane.

Anemia decreases total peripheral resistance by reducing viscosity of blood (d/t decreased RBC concentation) and causing local vasodilation (d/t diminished delivery of O₂ to tissue).

Long term increased work load (but not so much excess that damages the heart) causes the heart muscle to increase in mass and contractile strength in the same way that heavy exercise causes skeletal muscle to hypertrophy.