Efficiency is defined as the ratio of the energy delivered by a system to the energy supplied to it. Depending on the particular question being addressed, there exist a plethora of definitions of efficiency in medical texts, thus hampering their comparison. If only the ventricular work seen by the arterial system is under investigation, pressure-volume work will serve as a useful numerator. If, on the other hand, external and internal work together, i.e. the total mechanical work, is of interest, the pressure-volume area might be employed. Total myocardial oxygen consumption (MVO2) will be a useful denominator in the case of aerobic energy production. The MVO2 for the unloaded contraction must be assessed if, as in other energy transfer systems, net efficiency is to be addressed.
Whether the heart by itself employs mechanisms to improve its efficiency is still a matter of discussion: there is evidence that when oxygen supply decreases, the heart can switch from one substrate to a less costly one, or possibly can improve efficiency through better use of oxygen. Moreover, the heart seems to “sense” an even more decreased oxygen supply and reduce function in response. Myocardial stunning could be regarded as a protective mechanism as well, with function remaining depressed and the oxygen supply being normal or close to normal.
One may conclude from the decreased efficiency that the excess oxygen consumption is used up for repair processes. The improved efficiency found in hypertrophied hearts represents another adaptive process.
Effect of Potassium Ions. Excess potassium in the extracellular fluids causes the heart to become dilated and flaccid and also slows the heart rate. Large quantities also can block conduction of the cardiac impulse from the atria to the ventricles through the A-V bundle. Elevation of potassium concentration to only 8 to 12 mEq/L—two to three times the normal value—can cause such weakness of the heart and abnormal rhythm that this can cause death.
These effects result partially from the fact that a high potassium concentration in the extracellular fluids decreases the resting membrane potential in the cardiac muscle fiber.The membrane potential decreases, the intensity of the action potential also decreases, which makes contraction of the heart progressively weaker.
Effect of Calcium Ions. An excess of calcium ions causes effects almost exactly opposite to those of potassium ions, causing the heart to go toward spastic contraction. This is caused by a direct effect of calcium ions to initiate the cardiac contractile process, as explained earlier in the chapter.
Conversely, deficiency of calcium ions causes cardiac flaccidity, similar to the effect of high potassium. Fortunately, however, calcium ion levels in the blood normally are regulated within a very narrow range. Therefore, cardiac effects of abnormal calcium concentrations are seldom of clinical concern.
All cellular processes require ATP as a primary energy source. The heart requires ATP for the function of membrane transport systems (e.g., Na+/K+-ATPase) as well as for sarcomere contraction and relaxation, which involve myosin ATPase and ATP-dependent transport of calcium by the sarcoplasmic reticulum. Therefore, increasing the mechanical activity of the heart by increasing heart rate and contractility increases myocardial metabolism.
Cellular ATP pools depend on the balance between ATP utilization and ATP production. The heart has an absolute requirement for aerobic production of ATP to maintain adequate ATP concentrations because anaerobic capacity is limited in the heart. Cellular ATP levels will fall if there is insufficient O2 available to produce ATP aerobically, or if there is an increase in ATP utilization (increased ATP hydrolysis) that is not matched by a parallel increase in ATP synthesis..
The heart can use a variety of substrates to oxidatively regenerate ATP depending upon availability. In the postabsorptive state several hours after a meal, the heart utilizes fatty acids (60-70%) and carbohydrates (~30%). Following a high carbohydrate meal, the heart can adapt itself to utilize carbohydrates (primarily glucose) almost exclusively. Lactate can be used in place of glucose, and becomes a very important substrate during exercise.
The heart can also utilize amino acids and ketones instead of fatty acids. Ketone bodies (e.g., acetoacetate) are particularly important in diabetic acidosis. During ischemia and hypoxia, the coronary circulation is unable to deliver metabolic substrates to the heart to support aerobic metabolism. Under these conditions, the heart is able to utilize glycogen (a storage form of carbohydrate) as a substrate for anaerobic production of ATP and the formation of lactic acid.
However, the amount of ATP that the heart is able to produce by this pathway is very small compared to the amount of ATP that can be produced via aerobic metabolism. Furthermore, the heart has a limited supply of glycogen, which is rapidly depleted under severely hypoxic conditions.