Low cardiac output syndrome is defined as inadequate perfusion as a result of impaired pumping function and a cardiac index of <2.2 L/min/m². Clinical manifestations of hypoperfusion are listed in Table 93.1. Management of low cardiac output is characterized by optimization of hemodynamic parameters, which include heart rate, rhythm, preload, afterload, and contractility. All of these parameters play a significant role in the balance of oxygen supply and demand of the myocardium. Mechanical circulatory support must be considered to optimize these parameters, especially when there is ongoing ischemia.

The intra-aortic balloon pump (IABP) is a device that can support these hemodynamic goals. It is designed to augment coronary blood flow and can reduce the vascular impedance seen by ejecting myocardium during systole. In its capacity to optimize myocardial oxygen supply and demand and to improve cardiac output, distal perfusion generally improves as well.

The indications for placement of an IABP include complications of a myocardial infarction (including mitral regurgitation); ongoing ischemia or chest pain despite maximal medical therapy for myocardial ischemia; prophylactic support in patients scheduled for cardiac surgery with a high-grade left main coronary artery stenosis; and post– cardiac surgery in a low cardiac output state. The contraindications include aortic insufficiency, aortoiliac disease, and irreversiblemyocardial disease. The first, aortic insufficiency, is an absolute contraindication because inflation of the balloon during diastole will cause an increase in regurgitant flow, adding significantly to preload and increasing myocardial oxygen demand and risk of injury to the aortic valve. The other contraindications are relative. Many patients have some degree of aortoiliac disease and if the patient is suffering an acute decompensation that is reversible, then there may be a role for the IABP, even if he or she is not a candidate for revascularization, ventricular assist placement, or transplant.

The catheter part of the IABP is made up of a nonthrombogenic balloon that inflates and deflates in synchrony with the cardiac cycle. The IABP produces its desired effect through counterpulsation; the
balloon inflates during diastole and deflates during systole, or counter to what the intra-aortic blood volume and pressures are. The inflation during diastole increases the intra-aortic pressure during the portion of the cardiac cycle in which the coronary arteries are perfused, thus augmenting flow, especially through ischemic vessels that may have lost their autoregulation. The IABP deflates prior to opening of the aortic valve to decrease afterload and optimize ejection.