The IABP decreases myocardial oxygen consumption by decreasing the mean left ventricular ejection pressure, and by decreasing the duration of isovolumetric contraction.
The left ventricle, in its valiant struggle against its end-diastolic volume, has several variables to overcome as it attempts to eject some blood into the systemic circulation. One of these is the mass of blood itself, in a brutally Newtonian sense (force being the product of mass and acceleration). Another is the aortic end-diastolic pressure: this is the pressure that must be overcome in order for the aortic valve to open.
The mass of the blood you cant do much about. There is the liquid mass (the water content) which is pretty much invariable, and there is the hematocrit (which you cant decrease too much, lest you imperil the oxygen-carrying capacity of the blood).
However you can do something about the aortic end-diastolic pressure.
The deflation of the balloon assists the left ventricle by decreasing the aortic end-diastolic pressure, by suddenly decreasing the aortic fluid volume. The aortic end-diastolic pressure is determined in part by the elastic recoil of the encircling aortic walls on the effective volume of blood within the aorta; if that volume suddenly decreases by 40cc, the walls of the aorta relax slightly, and put a lower pressure on the remaining volume.
The result is a lower pressure required for aortic valve opening.
How does this translate into a benefit for the myocardium?
Well. What is one trying to achieve? It is to decrease the left ventricular oxygen consumption. The oxygen consumption, in turn, is related to left ventricular workload. And a major determinant of left ventricular workload is the area under the LV systolic pressure curve.
This area, termed TTI (tension time index) is directly related to myocardial oxygen consumption. The more time the LV spends struggling against aortic pressure, the more oxygen it consumes.
Now, let us reduce the aortic end-diastolic pressure. If the ventricle has a lower pressure to overcome when it opens the aortic valve, it generates a proportionally lower ejection pressure.
From the TTI equation it follows that for any given heart rate and systolic ejection time, a lower LV mean ejection pressure will result in a lower TTI value, and thus a decrease in myocardial oxygen consumption.
However, the mean ejection pressure is actually not the most important player in this game. By the time the aortic valve opens, most of the myocardial work has already been done. As far as myocardial oxygen consumption goes, the chief benefit from IABP counterpulsation is actually from reducing the amount of time spent in isovolumetric contraction.
After the mitral valve closing, and prior to the aortic valve opening, the left ventricle performs an isovolumetric contraction.
Let us take a closer look at the events during this tiny few-millisecond-long interval in the cardiac cycle:
This is a period of significant oxygen consumption by the left ventricle; it contracts against a static intraventricular volume, and it seems about 90% of myocardial oxygen consumption occurs during this period. Additionally, during this time the self-inflicted pressure increase in the left ventricular walls squeezes the precious oxygenated blood out of the subendocardium.
Obviously, anything that causes the aortic valve to open earlier reduces the duration of this period.
Decreased myocardial oxygen consumption is your reward.
Additionally, there seems to be a hemodynamic performance gain to be made from this. Early dog studies demonstrated that the decrease in the impedance to LV ejection translates into some real measurable benefits. Peak aortic flow, stroke volume and cardiac output increased by 15 percent.
Additionally, there are situations when a decreased aortic end-diastolic pressure can mimic the effects of a vasodilator without dropping the mean arterial pressure too much. This is an advantage in situations where there is some benefit in decreasing the pressure gradient between the ventricular-arterial circulation and the pulmonary-atrial circulation.
Two such examples are severe mitral regurgitation and ventricular septal defects. In both cases, the left ventricle ejects blood both into the systemic circulation and into some other chamber, be it the left atrium with MR or the right ventricle with VSD. The amount of blood ejected into these useless receptacles is proportional to the pressure gradient between the aortic end-diastolic pressure and the pressure inside said receptacles. In short, if the aortic pressure increases, the left ventricle will eject less blood into the aorta, and more blood into the regurgitant valve or septal defect.
This is counterproductive. But, the IABP comes to the rescue. By decreasing the aortic end-diastolic pressure, the deflation of the balloon decreases the abovementioned pressure gradient, and increases the amount of blood ejected into the systemic circulation.