Terapie chirurgiche dell’Insufficienza Cardiaca Contropulsazione aortica

Intra Aortic Balloon Pump

IABP- History 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. 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. Then in the early 1960s Moulopoulus et al. 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. 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. This advance made it for even nonsurgical personnel possible, to perform an IAB insertion at the patient’s 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 patients’ 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.

Hemodynamic effects of IABP Therapy 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.

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.

Schematic representation of coronary blood flow, aortic and left ventricular pressure wave form with / without IABP TTI (= tension-time index ), is an important determinant of myocardial oxygen consumption. 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) Inflation of the balloon during diastole (= augmentation of the aortic diastolic pressure) increases coronary blood flow ( DPTI ). Deflation of the balloon occurs just prior to the onset of systole and reduces impedance to left ventricular ejection (TTI ). This results in less myocardial work, decreased myocardial oxygen consumption and increased cardiac output

Control of the IABP (1) TRIGGERING To achieve optimal effect of counterpulsation, inflation and deflation need to be correctly timed to the patient’s cardiac cycle. This is accomplished by either using the patient’s ECG signal, the patient’s arterial waveform or an intrinsic pump rate. The most common method of triggering the IAB is from the R wave of the patient’s 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.

Control of the IABP (2) TIMING and WEANING 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 patient’s 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 If the patient’s 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.

IABP Indications and Contraindications

Complications of IABP counterpulsation