Indications for IABP placement include patients with acute myocardial infarction (MI) and cardiogenic shock secondary to continued ischemia or myocardial stunning. Without revascularization, survival rates in patients with cardiogenic shock supported with IABP and medical therapy are quite poor. The IABP provides temporary hemodynamic stabilization until definitive revascularization can be performed. The IABP might also be used to support patients with shock due to mechanical complications of MI—e.g. ventricular septal rupture – until corrective surgery can be performed. Additionally, it has been shown to be an effective temporary therapeutic option in patients with shock due to non-ischemic reversible causes, such as myocarditis or drug toxicity. IABP support is often used in patients who are difficult to wean off bypass after cardiac surgery due to severe LV dysfunction or secondary to myocardial stunning from prolonged cardioplegia. Patients with refractory heart failure and those with end-stage cardiomyopathy awaiting cardiac transplantation–i.e., “bridge to transplantation” — might also gain benefit from IABP support. Furthermore, the IABP can contribute to the management of patients with medically intractable ventricular arrhythmias, including ventricular tachycardia and ventricular fibrillation [1, 2].

The IABP is often used to alleviate medically refractory unstable angina in patients awaiting definitive revascularization — e.g., a patient with severe triple vessel coronary artery disease awaiting bypass surgery. Prophylactic placement is employed in patients with severe left main coronary obstruction or decompensated aortic stenosis awaiting surgery. The IABP might also be placed to mitigate continued ischemia following complex/complicated percutaneous coronary intervention (PCI) or to support patients with failed PCI. In addition, the prophylactic placement of IABP is occasionally employed during high-risk PCI [1]

After the leg is shaved and prepped with anti-septic solution, the femoral artery is accessed and J-tipped guide wire is passed through a needle to the aortic arch. After an introducer sheath is inserted, the balloon is advanced over the guide wire with the radiopaque tip positioned in the descending aorta just distal to the origin of the left subclavian artery (generally at the level of the carina). When available, fluoroscopic guidance should always be employed for IABP placement. If fluoroscopic guidance is not available, the distance from the angle of Louis (or between the second and third intercostal spaces) to the umbilicus and then obliquely over to the femoral insertion site can be measured to determine the approximate distance the balloon should be advanced. After positioning of the IABP is confirmed, the helium gas line extending from the console is connected. Balloon counterpulsation is then initiated at 1:2 setting (balloon inflation with every other beat) and fluoroscopy again is used to confirm uniform expansion. Sheathless insertion is sometimes performed in patients with peripheral vascular disease in an attempt to reduce the incidence of lower limb ischemia. However, sheathless insertion does not allow for repositioning once the balloon is placed, and is associated with higher rates of infection [1].

Inflation and deflation of the balloon are usually timed and triggered by the surface electrocardiogram. Triggering can also be initiated by the arterial pressure waveform or set to a fixed asynchronous cycle for patients with significant arrhythmias—e.g., ventricular fibrillation – or patients on bypass. Pacing spikes should be used to trigger the balloon in patients with 100 % paced rhythms. Adjustments to timing are performed with initial pump triggering set at 1:2, thereby allowing comparison of the arterial tracing with and without counterpulsation (Fig. 36.2). Timing of inflation is delayed after the R wave on the surface ECG such as to begin on the downslope of the systolic pressure waveform, just before the dicrotic notch (when the aortic valve closes). Deflation should be timed just before the opening of the aortic valve to allow for the maximum reduction in aortic systolic pressure compared with an unassisted beat. After timing of inflation and deflation is adjusted, the balloon counterpulsation is then set at 1:1 (Fig. 36.3) [1].

When the patient is returned to the appropriate unit, a chest x-ray should be immediately obtained to again verify balloon position and check for any possible migration during transfer. To prevent thrombus formation, the patient is heparinized, the activated partial thromboplastin time being carefully maintained at 50–70 s. The patient must be kept at bedrest and the head of the bed should not be elevated more than 30°. Daily chest x-ray should be obtained to evaluate balloon position and migration. During counterpulsation, evaluation of circulation should take place on every nursing shift (or at least Q8h). Daily monitoring for evidence of sepsis, bleeding, hemolysis, and embolus should also be performed [1].

Before the IABP is removed, the patient is progressively weaned from its support. Under close hemodynamic supervision the counterpulsation mode is decreased step-wise from 1:1 to 1:2, and then to 1:3. The patient should be monitored for 2–3 h at each downgraded level to ensure tolerance to reduced support. When safety of withdrawal is established, the balloon is set back to 1:1 and the heparin drip is discontinued for at least 4 h. The activated clotting time is checked until it falls below 160 s. The balloon and sheath are then removed as a single unit to prevent any tearing of the balloon membrane. Manual pressure is then applied proximal to the insertion site for 30–60 min until hemostasis is achieved. After removal the patient is kept at strict bed rest avoiding hip flexion on the affected side for the next 6–12 h [1].