An IABP is a device used to improve the function of a failing heart. It is an 8.5 to 9.5 French dual-lumen catheter with a 40- to 60-mL helium-filled balloon attached at its tip. The IABP provides counterpulsation, whereby the systolic afterload to cardiac ejection is reduced and the perfusion of the coronaries and proximal aortic arteries is augmented.

The IABP is placed either percutaneously or under surgical exposure into a peripheral large artery (primarily femoral) and directed retrograde into the thoracic aorta. The size of the balloon used is dictated by the height of the patient (50 mL balloon being most common). The optimal position is with the balloon tip positioned just distal to the origin of left subclavian artery and the proximal end of the balloon before the orifice of the renal arteries. The positioning of an IABP is done either blindly, with subsequent verification of the depth of position with fluoroscopy or x-ray, or under the guidance of transesophageal echocardiography (TEE) in the anesthetized patient. The incorrect placement may cause obstruction of the head or visceral vessels. This may result in possible cerebral or visceral organ ischemia and an ineffective counterpulsation. During IABP support, the patient is anticoagulated.

The balloon is connected to a control console that is regulating the inflation and deflation of the balloon at the tip of the IABP. The IABP balloon is inflated in diastole and deflated in systole. The triggers for balloon inflation are (1) the electrocardiogram (ECG) T wave; (2) the dicrotic notch on the arterial waveform, which is recorded from the tip of the IABP; and (3) an internal, predetermined ratio. The balloon deflation is timed to occur prior to the ECG Q wave or the upstroke of the arterial line waveform.

The balloon is timed to inflate in diastole causing an augmented diastolic pressure with resultant increase in blood flow to the coronary arteries, great vessels, and visceral organs. The balloon deflates in systole (just prior to the opening of the aortic valve) causing a “void” or “potential” space in the aorta that reduces left ventricular afterload, which in turn facilitates ventricular systolic ejection and an increase in stroke volume. The decreased systolic afterload reduces the left ventricular wall tension, decreases the myocardial oxygen demand, and ameliorates the effects of coronary ischemia. The IABP counterpulsation is at variable intervals, regulated by the operator, from 1:1 ratio to 1:3 ratio (each beat, to every third beat, respectively). In a properly functioning IABP, the operator looks for (1) the counterpulsation to create a diastolic pressure wave, which is usually higher than the preceding systolic wave, that is, the “assisted” diastolic aortic pressure, with a diastolic pressure value lower than the unassisted diastolic pressure; and (2) for the following systolic pressure wave that is lower than the unassisted systolic pressure.

In the majority of the cases, the patient is already on maximal vasoactive support without significant improvement in symptoms and/or signs of cardiac failure.

The contraindications to IABP placement include the following:

The most common complication of IABP placement is injury at the vascular entry site, especially in the face of severe peripheral vascular disease. Other complications include ischemia to the ipsilateral limb and bleeding at the insertion site.

Correct diastolic inflation and systolic deflation are critical to optimize the benefits of IABP counterpulsation. Early diastolic inflation of the IABP balloon (inflation is initiated during late systole) will result in increased left ventricular afterload and increased myocardial oxygen consumption. Late diastolic inflation will result in suboptimal coronary perfusion and diastolic augmentation. Early deflation of the IABP will cause suboptimal diastolic augmentation, and the assisted aortic end-diastolic pressure may be equal to or less than the unassisted aortic end-diastolic pressure. In late deflation, the assisted aortic end-diastolic pressure may be equal to the unassisted aortic end-diastolic pressure, resulting in a prolonged isovolumetric contraction phase and increased left ventricular afterload and increased myocardial oxygen consumption.

Weaning from IABP support is initiated once the patient’s requirement for inotropic support is reduced. The IABP weaning is done in the presence of vasoactive support, so should cardiac output or overall hemodynamics worsen, inotropic support may be increased. Weaning is gradually undertaken over the course or 6 to 12 hours. During this time, the ratio of augmented to nonaugmented beats is decreased gradually from 1:1 to 1:2 to 1:3. At any time, if there are any hemodynamic derangements, the weaning process is halted and the vasoactive medications are adjusted to achieve a stable cardiac output (or mixed venous oxygen saturation). Following a successful weaning period, the IABP device is removed. Weaning from an
IABP may be also performed by sequentially reducing the volume of the balloon inflation during diastole.