The intra-aortic balloon is constructed of a biocompatible, nonthrombogenic material and mounted on a catheter constructed of the same material. An opening at the catheter-balloon connection allows pressurized gas (usually helium) to move in and out of the balloon, causing inflation and deflation to occur. Most catheters have two lumens: an inner lumen for central pressure monitoring at the catheter tip and a second lumen for the gas. Properly positioned, the distal tip of the balloon catheter rests just distal to the origin of the left subclavian artery and the proximal end of the balloon is positioned proximal to the renal arteries. Figure 26-1 illustrates proper anatomic position of the IABP catheter. (See Figure 12-3 in Chapter 12.) The tip of the catheter is radio-opaque so that its position can be verified with a chest x-ray. The catheter is inserted via a direct femoral or iliac arteriotomy or by percutaneous insertion using the Seldinger technique with or without a sheath. Although a direct arteriotomy approach is rarely used today, prior designs made it mandatory, and it may still be the optimal choice for a patient with severe peripheral vascular disease (when direct visualization is desired) or for pediatric patients. The approach requires an incision in the groin for access to the femoral or iliac artery. This technique is more invasive and time consuming, and requires surgical removal. The percutaneous technique is faster, less
invasive and allows for easy bedside removal. In all catheters, the balloon is wrapped tightly around its own guide wire so that it slides easily through a sheath or directly into the artery. Once in proper position, the balloon is inflated, resulting in unwrapping of the balloon, allowing inflation and deflation to commence. This catheter is secured to the skin by sutures. Figure 26-2 illustrates the percutaneous insertion technique utilizing an introducer sheath.

A newer design (SupraCor) has recently been introduced. This device can be placed in the ascending aorta for use after cardiac surgery. In an animal model, the device was shown to increase blood flow in saphenous vein and internal mammary bypass grafts, when a standardly placed IABP did not.⁸

The two goals of IABP therapy are to increase coronary artery perfusion pressure and thus coronary artery blood flow, and to decrease LV workload by lowering LV afterload. These goals are achieved by displacement of volume in the aorta during systole and diastole with alternating inflation and deflation of the balloon. A typical adult-sized balloon contains 40 mL of gas or volume. For smaller adult patients, a 35-mL balloon is available; for larger patients, a 50-mL balloon is available. Placing a smallersized balloon (shorter) in smaller patients is important because a larger (longer) balloon could extend into the abdominal aorta, potentially compromising blood flow to the renal vasculature or even the lower extremities and exposes the balloon to abrasion (and even rupture) from calcified abdominal aortic atherosclerotic plaques.

The size of the catheters range from 7 to 9.5 French. When the balloon is rapidly inflated at the onset of diastole, an additional 35 to 50 mL (depending on the balloon size) of volume is suddenly added to the aorta. This acute increase in volume creates an early diastolic pressure rise in the aortic root (where the coronary ostia lie), increasing coronary artery perfusion pressure. Figure 26-3 illustrates this effect. Because ischemic coronary beds are maximally vasodilated, no further autoregulatory increases in flow are possible, and flow is pressure dependent.⁹, ¹⁰, ¹¹ IABP inflation provides this enhanced pressure. The early diastolic pressure increase is referred to as the diastolic augmentation. Diastolic augmentation increases coronary perfusion pressure and in addition, by increasing overall mean arterial pressure, also contributes to enhanced flow to other organs.

This augmented diastolic pressure gradually falls, as diastolic pressure normally does when diastolic run-off occurs. Rapid evacuation of gas out of the balloon during deflation removes 35 to 50 mL of volume (the same amount used in inflation) out of the aorta. This sudden drop in aortic volume rapidly decreases pressure. Deflation is timed to occur at the end of diastole, just before the patient’s next systole. Effective deflation, which decreases end-diastolic pressure, decreases the impedance or afterload that the ventricle must contract against to open the aortic valve and sustain ejection during systole. The lower the impedance, the lower the wall stress, and, therefore, the lower the LV workload. In cardiogenic shock, high systemic vascular resistance contributes to greater impedance, resulting in a greater workload for the failing
left ventricle. With properly timed deflation, which lowers end-diastolic pressure and impedance to ejection, the LV workload is reduced. Figure 26-4 illustrates this effect. Systolic pressure is decreased when deflation of the balloon is timed properly. As a result of decreased afterload, there is more effective forward flow during systole. Improved forward flow contributes to decreased endsystolic volume in the ventricle. Improved emptying leads to decreased subsequent preload, which also contributes to decreasing LV workload. Cardiac output is increased and so is the mean arterial pressure. The need for compensatory tachycardia is reduced and heart rate is expected to fall, further decreasing myocardial oxygen demand. Better systemic perfusion helps to reverse the acidosis often seen in shock and improves secondary organ dysfunction related to the previous hypoperfused state. Although there is significant patient-to-patient variability, the expected beneficial outcomes of IABP therapy are listed in Displays 26-2 and 26-3.¹⁰,¹²

Because inflation of the balloon during diastole increases pressure in the aortic root, significant aortic regurgitation is a contraindication to IABP therapy. Inflation would otherwise increase regurgitation and thus LV workload. The presence of an aortic aneurysm is also a contraindication to IABP therapy. Trauma or rupture of the aneurysm can occur during IABP insertion. Dislodgement of adjacent thrombus can occur during insertion or from balloon inflation resulting in embolization. These risks are all unacceptable. Severe peripheral vascular occlusive disease in the femorial or iliac artery contraindicates IABP therapy. Catheter insertion may be difficult or impossible, and occlusion of the affected vessel, dissection, and dislodgement of plaque from the vessel wall are all possibilities as well. These potential problems can be avoided by selecting an alternate method of insertion. In the cardiac surgery patient, the catheter may be inserted directly into the thoracic aorta, although this method requires reopening the sternotomy incision to remove the catheter. The catheter can also be placed antegrade in the aorta via the right subclavian/axillary artery.¹³ This approach requires a subperiosteal clavicular resection to access the artery, but is less invasive than a sternotomy incision. Newer catheters of smaller diameter minimize the risk of occluding distal blood flow. In addition, the ascending aorta device described above (SupraCor) could be considered. Uncontrolled sepsis and coagulopathy are other contraindications. Lastly, if invasive therapies are contrary to the goals of care (e.g., comfort care in a patient who is very unlikely to survive despite even heroic measures), IABP therapy should not be utilized.

Proper timing of IABP therapy is crucial to achieving the beneficial hemodynamic changes described above. Proper timing requires coordination of inflation and deflation of the balloon with the patient’s cardiac cycle. To evaluate balloon timing properly, the assist ratio is set at 1:2, meaning the balloon is assisting every other cardiac cycle. In this way, the observer can compare the effect of balloon inflation and deflation with unassisted beats. Most patients tolerate this ratio well, at least for a brief period. The R wave from the ECG, pacemaker spikes on the ECG, or the arterial systolic pressure can be used to identify individual cardiac cycles. Each can act as signals for the IABP console to discriminate systole from diastole. The R wave signals the onset of electrical depolarization, which immediately precedes mechanical systole. A ventricular pacemaker spike essentially represents the same event. Arterial systolic pressure signals the onset of mechanical systole. Any of these reference points can be used to determine when deflation of the balloon should optimally occur. An arterial waveform is necessary to determine the onset of mechanical diastole and systole and to verify timing. Diastole has begun when the dicrotic notch (which results from aortic valve closure) appears on the arterial waveform. Balloon inflation is timed to occur at this point in the cardiac cycle. The deflation point can be optimally adjusted by observing the end-diastolic drop in pressure created by balloon deflation. The goal is to create the greatest pressure drop possible. Ideally, there would be at least a 10 mm Hg difference between end-diastolic pressure without the balloon effect and the end-diastolic pressure created by balloon deflation. Evidence that afterload reduction has occurred is seen in the following systolic pressure. With afterload reduction, the next systolic pressure after balloon deflation is lower than the systolic pressure with no balloon effect, which is evidence that LV workload has been decreased. Five criteria can be used to determine the effectiveness of IABP timing, as illustrated on the arterial pressure tracing (Fig. 26-5) and detailed below.

IABP therapy carries a relatively low risk of additional morbidity in a generally sick population. In the series of nearly 17,000 patients with IABPs placed (from 1996 to 2000) mentioned above, the incidence of any complication was 7% and major complications (i.e., severe bleeding, major acute limb ischemia, death from IABP insertion, or failure) was 2.6%.⁷ Vascular complications have been reported to range from 6% to 25% of cases depending on the report.¹⁴, ¹⁵, ¹⁶ Vascular injuries include plaque dislodgement, dissection, laceration, and compromise of the circulation to the distal extremity. Peripheral nerve injury is another possible complication of insertion (particularly if a cut down approach is used). Compromised circulation can occur any time during IABP therapy as a result of the presence of the indwelling catheter, compartment syndrome, or embolus from thrombus formation along the catheter or on the balloon.¹⁷ The incidence of limb ischemia ranges from 5% to 35%.¹⁷,¹⁸ Although intravenous heparin is generally used with IABP, there is little evidence that heparin reduces limb ischemia, and one randomized trial of 153 patients did not find a difference in such events.¹⁹

Complications are more common in patients with peripheral vascular occlusive disease, in women, those who are smaller (body surface area [BSA] <1.8 m²), and in patients with a history of stroke, transient ischemic attacks, and diabetes.⁷,¹⁷,²⁰, ²¹, ²², ²³ Risk is decreased with sheathless insertion and with smaller balloon sizes.²²,²⁴,²⁵ In addition, operator’s and hospital-staff’s experience likely play a part.²⁶ Nurses monitor for and prevent compromised circulation by carefully assessing peripheral perfusion; preventing the patient from flexing the hip of the affected extremity, which may compromise blood flow; and maintaining coagulation times within prescribed parameters by careful titration of any prescribed anticoagulants. The nurse should be aware that multiple or prolonged attempts at insertion increase the risk of vascular injury and thrombus formation. Infection at the insertion site is reported to occur in less than 5% of patients, with an increase risk after 7 days of therapy. Insertion site infections may dictate the removal of the IABP catheter. Careful efforts must be made to maintain the sterility of insertion site dressings. Other problems that may be encountered include thrombocytopenia; compromised circulation to the left subclavian, renal, or mesenteric arteries because of balloon malposition; and bleeding from the insertion site or other line insertion sites. Mechanical problems related to the balloon include improper timing or a leak or perforation in the balloon, necessitating its removal. A leak in the balloon becomes evident as augmentation becomes less effective. Eventually, blood backs up in the catheter and can be detected. When a leak has occurred, the balloon must be removed immediately to avoid the possibility of gas embolus or balloon entrapment. Entrapment occurs when blood enters the balloon and becomes a large, hardened mass. The size makes it difficult to remove without a surgical intervention.