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Intra Aortic Balloon Pump (IABP) Counterpulsation

The Internet Journal of Thoracic and Cardiovascular Surgery TM ISSN: 1524-0274

P. J Overwalder, M.D.
Department of Surgery I
Division of Cardiac Surgery
University Hospital Graz

P. J Overwalder: Intra Aortic Balloon Pump (IABP) Counterpulsation . The Internet Journal of Thoracic and Cardiovascular Surgery. 1999. Volume 2 Number 2.

Table of Contents

Physiologic Effects of IABP Therapy
Control of the IABP
Insertion Techniques
Experience at a Single Center


In 1958 Harken described for the first time a method to treat left ventricular failure by using counterpulsation or diastolic augmentation. He suggested removing a certain blood volume from the femoral artery during systole and replacing this volume rapidly during diastole. By increasing coronary perfusion pressure this concept would therefore augment cardiac output and unload the functioning heart simultaneously 1 , 2 . This method of treatment was limited because of problems with access (need for arteriotomies of both femoral arteries), turbulence and development of massive hemolysis by the pumping apparatus. Even experimental data showed that no augmentation of coronary blood flow was obtained 3 .

Then in the early 1960s Moulopoulus et al. 4 , 5 from the Cleveland Clinic developed an experimental prototype of the intra-aortic balloon (IAB) whose inflation and deflation were timed to the cardiac cycle. In 1968 the initial use in clinical practice of the IABP and it`s further improvement was realized resp. continued by A. Kantrowiz`s group 6 , 7 .

In its first years, the IABP required surgical insertion and surgical removal with a balloons size of 15 French. In 1979 after subsequent development in IABP technology a dramatic headway with the introduction of a percutaneous IAB with a size of 8,5 to 9,5 French was achieved 8 , 9. This advance made it for even nonsurgical personnel possible, to perform an IAB insertion at the patientís bedside. In 1985 the first prefolded IAB was developed.

Today continued improvements in IABP technology permit safer use and earlier intervention to provide hemodynamic support. All these progresses have made the IABP a mainstay in the management of ischemic and dysfunctional myocardium.

Physiologic Effects of IABP Therapy

After correct placement of the IAB in the descending aorta with it`s tip at the distal aortic arch (below the origin of the left subclavian artery) the balloon is connected to a drive console. The console itself consists of a pressurized gas reservoir, a monitor for ECG and pressure wave recording, adjustments for inflation/deflation timing, triggering selection switches and battery back-up power sources. The gases used for inflation are either helium or carbon dioxide . The advantage of helium is its lower density and therefore a better rapid diffusion coefficient. Whereas carbon dioxide has an increased solubility in blood and thereby reduces the potential consequences of gas embolization following a balloon rupture.

Inflation and deflation are synchronized to the patientsí cardiac cycle. Inflation at the onset of diastole results in proximal and distal displacement of blood volume in the aorta. Deflation occurs just prior to the onset of systole (Fig. 152-a) .

Figure 152-a

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Intra aortic balloon (IAB) during systole and diastole

The primary goals of IABP treatment are to increase myocardial oxygen supply and decrease myocardial oxygen demand. Secondary, improvement of cardiac output (CO), ejection fraction (EF), an increase of coronary perfusion pressure, systemic perfusion and a decrease of heart rate, pulmonary capillary wedge pressure and systemic vascular resistance occur 10 , 11 , 12 (Tab.1 goals of IABP)

There are several determinants of oxygen supply and demand (Tab.2 Determinants of O2 Supply and Demand).

Table 1: Hemodynamic effects of IABP Therapy

Table 2: Determinants of Myocardial Oxygen Supply and Demand

In particular systolic wall tension uses approximately 30% of myocardial oxygen demand. Wall tension itself is affected by intraventricular pressure, afterload, end-diastolic volume and myocardial wall thickness. Regarding to the studies of Sarnoff et al. the area under the left ventricular pressure curve, TTI (= tension-time index ), is an important determinant of myocardial oxygen consumption 13. On the other hand, the integrated pressure difference between the aorta and left ventricle during diastole (DPTI = diastolic pressure time index) represents the myocardial oxygen supply (i.e. hemodynamic correlate of coronary blood flow) 14 , 15 .

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Schematic representation of coronary blood flow, aortic and left ventricular pressure wave form with / without IABP. (Effects on DPTI and TTI . Balloon inflation during diastole augments diastolic pressure and increases coronary perfusion pressure as well as improving the relationship between myocardial oxygen supply and demand (DPTI:TTI ratio)

Control of the IABP


To achieve optimal effect of counterpulsation, inflation and deflation need to be correctly timed to the patientís cardiac cycle. This is accomplished by either using the patientís ECG signal, the patientís arterial waveform or an intrinsic pump rate. The most common method of triggering the IAB is from the R wave of the patientís ECG signal. Mainly balloon inflation is set automatically to start in the middle of the T wave and to deflate prior to the ending QRS complex. Tachyarrhythmias, cardiac pacemaker function and poor ECG signals may cause difficulties in obtaining synchronization when the ECG mode is used. In such cases the arterial waveform for triggering may be used.


It is important that the inflation of the IAB occurs at the beginning of diastole, noted on the dicrotic notch on the arterial waveform. Deflation of the balloon should occur immediately prior to the arterial upstroke. Balloon synchronization starts usually at a beat ratio of 1:2. This ratio facilitates comparison between the patientís own ventricular beats and augmented beats to determine ideal IABP timing. Errors in timing of the IABP may result in different waveform characteristics and a various number of physiologic effects (Fig. 152-c).

Figure 152-c: Arterial pressure wave form alterations associated with inflation and deflation of the IAB

If the patientís cardiac performance improves, weaning from the IABP may begin by gradually decreasing the balloon augmentation ratio (from 1:1 to 1:2 to 1:4 to 1:8) under control of hemodynamic stability . After appropriate observation at 1:8 counterpulsation the balloon pump is removed.

Indications and Contraindications

Early purposed indications for intraaortic balloon pumping have included cardiogenic shock or left ventricular failure, unstable angina, failure to separate a patient from cardiopulmonary bypass and prophylactic applications, including stabilization of preoperative cardiac patients as well as stabilization of preoperative noncardiac surgical patients 10, 17 , 18 , 19 , 20 , 21 . Today more extending indications are: Cardiac patients requiring procedural support during coronary angiography and PTCA, or as a bridge to heart transplantation. Further on in pediatric cardiac patients and as well as in patients with stunned myocardium, myocardial contusion, septic shock and drug induced cardiovascular failure the IABP can be life-saving 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31

IABP therapy should only be considered only for use in patients who have the potential for left ventricular recovery, or to support patients who are awaiting cardiac transplantation. Absolute contraindications of IABP are relatively few (Tab.3 Contraindications of IABP). There are successful reports of its usage in patients with aortic insufficiency 32 , 33 and in patients with acute trauma to the descending aorta 34 .

Table 3: IABP Counterpulsation Indications and Contraindications

Insertion Techniques

In the early years of IABP - therapy, insertion of the balloon was performed by surgical cut down to the femoral vessels. After a longitudinal incision in the groin, the femoral arteries were identified and controlled. A vascular graft was then sewn to the common femoral artery in an end-to-side fashion. The balloon was introduced into the artery via the graft and properly positioned in the thoracic aorta and the graft tightly secured to the distal portion of the balloon catheter. Finally the skin incision was closed. Removal of the balloon required a second operation.

Since 1979, a percutaneous placement of the IAB via the femoral artery using a modified Seldinger technique allows an easy and rapid insertion in the majority of situations. After puncture of the femoral artery a J-shaped guide wire is inserted to the level of the aortic arch and then the needle is removed. The arterial puncture side is enlarged with the successive placement of an 8 to 10,5Fr dilator/sheath combination. Only the dilator needs to be removed.

Continuing, the balloon is threaded over the guide wire into the descending aorta just below the left subclavian artery. The sheath is gently pulled back to connect with the leak-proof cuff on the balloon hub, ideally so that the entire sheath is out of the arterial lumen to minimize risk of ischemic complications to the distal extremity. Recently sheathless insertion kits are available. Removal of a percutaneously placed IAB may either be via surgical removal or closed technique. There are alternative routes for balloon insertion. In patients with extremely severe peripheral vascular disease or in pediatric patients the ascending aorta or the aortic arch may be entered for balloon insertion 35 , 36 . Other routes of access include subclavian, axillary or iliac arteries 37 , 38 , 39 .


Although the incidence of complications has decreased significantly as experience with the device has increased, IABP therapy in todayís patients` population does still hold a risk for complications (Tab. 4). Because todayís patient population is elderly (68 - 80 years), very often female and may suffer from severe peripheral vascular disease and hypertension or diabetes. The most common vascular complication is limb ischemia. It may occur in 14-45% of patients receiving IABP therapy 40 , 41. Therefore the patient must be consistently observed for any symptoms of ischemia during IABP counterpulsation. If signs of ischemia appear the balloon should be removed. In general, vascular injuries should be dealt with directly by surgical interventions and repair. Balloon related problems and infection require removal and / or replacement of the IAB .

Table 4: Complications of IABP counterpulsation

Experience at a Single Center

Treatment of low cardiac output syndrome using IABP counterpulsation has been used at our institution since 1983. Till December 1993 a total number of 440 patients (pts) (9,95%) out of 4420 patients, who underwent cardiac surgery procedures with the use of cardiopulmonary bypass, were supported with an IABP. (Age distribution : Tab. 6) There were 294 male and 146 female patients. Overall survival rate after implantation of the IABP was 75% (n=330 pts) .

Table 5: Diagnosis prior to IABP implantation

Table 6: Age Distribution of IABP patients

In the early years (1983-1989) as method of choice, implantation of the balloon was performed via a surgical cut down of the femoral artery. Complications were observed in 20 pts (8.4%) : In 9 pts (3.7%) positioning of the balloon was impossible due to severe vascular disease, 5 pts (2.1%) developed a thrombosis of the femoral artery and 1 patient (0.4%) died because of untreatable thrombosis of the mesenteric artery. Hospital mortality in this group was 36% (survival rate of 64%). Mean pumping time was 3 days (1 - 15).

Since 1990 we prefer the percutaneous insertion of the device. After a learning curve more than 90% of 202 patients received an IABP using this technique. Complication rate was less than 8% (mainly leg ischemia with amputation of the leg in 1 patient, 3 infections of the puncture point and 4 cases of impossible positioning of the balloon ). Survival rate was 68.5% (hospital mortality of 31.5%) . 278 pts (63%) received the balloon pump at the operating theater - mainly because of failure to wean from cardiopulmonary bypass -151 pts (34,3%) at an intensive care unit and 11 pts (2,5%) as a bridge to transplant. Table 6 shows a detailed list of all various diagnoses prior to IABP therapy .


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There are numerous respiratory complications of obesity, including an increased breathing workload, respiratory muscle inefficiency, decreased functional reserve capacity and expiratory reserve volume, and closure of peripheral lung units.These complications often result in a ventilation-perfusion mismatch, especially in the supine position. Obesity is a classic cause of alveolar hypoventilation. Historically, the obesity-hypoventilation syndrome has been described as the "pickwickian" syndrome, and obstructive apnea was first observed in patients with severe obesity. Sleep apnea is defined as repeated episodes of obstructive apnea and hypopnea during sleep, together with daytime somnolence and/or altered cardiopulmonary function. The prevalence of sleep-disordered breathing and sleep disturbances rises dramatically in obese subjects and obesity is by far the most important modifiable risk factor in sleep-disordered breathing. It has been estimated that 40 million Americans suffer from sleep disorders and that the vast majority of these patients remain undiagnosed.

Despite careful screening by history and physical examination, sleep apnea is revealed only by polysomnography in most patients. Although, some clinical features could be useful in screening for sleep apnea, the diagnostic accuracy is inadequate.
Patients with sleep apnea have an increased risk of diurnal hypertension, nocturnal dysrhythmias, pulmonary hypertension, right and left ventricular failure, myocardial infarction, stroke, and mortality. The prevalence of pulmonary hypertension in subjects with obstructive sleep apnea is 15 to 20 percent; however, pulmonary hypertension rarely is observed in the absence of daytime hypoxemia. According to Kessler and colleagues the extent of pulmonary hypertension in patients with obstructive sleep apnea is generally mild to moderate (pulmonary artery pressures ranging between 20 and 35 mmHg) and does not necessitate specific treatment.

Although there is a link between sleep apnea and systemic hypertension, the association of obesity with both disorders confounds the relationship. A physician who evaluates an obese patient who has been referred for hypertension should address related symptoms such as habitual snoring, nocturnal gasping or choking, witnessed episodes of apnea, and daytime sleepiness. It is important to remember, however, that the clinical and ECG signs of cor pulmonale appear later than do those of pulmonary hypertension (assessed by right heart catheterization). Numerous treatments are available for sleep apnea, but weight loss in obese patients should always be advocated.

Severe untreated sleep-disordered breathing can further impair LV function, leading to arterial oxyhemoglobin desaturation and arrhythmias.Central sleep apnea may occur in as many as 40% of patients with heart failure, and 10% suffer from obstructive sleep apnea. Obstructive sleep apnea increases afterload and heart rate during sleep but is responsive to continuous positive airway pressure.