Treatment with intraaortic balloon counterpulsation has been used for more than 30 years. The intraaortic balloon pump (IABP) has emerged as the single most effective and widely used circulatory assist device for temporary mechanical assistance of the failing circulation. Although the initial indication for intraaortic balloon counterpulsation use was in patients with cardiogenic shock, encouraging clinical data extended its application to numerous other clinical situations such as preshock syndrome, threatening extension of myocardial infarction, unstable angina, intractable ventricular dysrrhythmias, septic shock, cardiac contusion, support during transport from community hospital, postsurgical myocardial dysfunction, prophylactic support during coronary interventions, and as a bridge for cardiac transplant.1
The concept of counterpulsation by mechanical means was initially described by Birtwell and Harken in 1958 and was reported by Clauss et al.2 in 1961. The beginning of the widespread use of counterpulsation in clinical practice was the result of the pioneering work of Moulopoulos et al.3 in 1962, who introduced the concept of counterpulsation by using an intraaortic balloon. The subsequent introduction of percutaneous insertion, usually through the femoral artery, improved the speed and ease of insertion, thereby providing an impetus for its expanded application. The first clinical data of IABP therapy in patients with cardiogenic shock were published by Kantrowitz et al.4,5 Thereafter, a great body of in vivo and in vitro experimental studies as well as clinical trials were performed, leading to development of technologically advanced balloons, pump driving systems, catheters, and software.
Basic Principles and Description of Intraaortic Balloon Pump Technique
A flexible catheter with a polyethylene balloon mounted on its end is inserted, usually through the femoral artery, and passed into the descending thoracic aorta, as depicted schematically in Figure 1. The proper balloon placement is confirmed by fluoroscopy or chest x-ray. Surgical insertion technique is reserved for alternate sites when severe disease of both femoral arteries is present. Optimally, the balloon should be placed 1–2 cm below the origin of the left subclavian artery and above the renal artery branches. Intraaortic balloon placement is critical for proper operation and avoidance of arterial tributary obstruction. If the catheter is placed too high, obstruction of the origin of the left subclavian or even the left carotid artery may occur, whereas if the balloon is positioned too low, the origin of the renal arteries could become obstructed, thereby counteracting normal renal perfusion. The central lumen of the balloon catheter is used to monitor the aortic blood pressure and the acutely induced pressor changes by the IABP. Balloon inflation is triggered according to the patient’s electrocardiogram, blood pressure waveform, a pacemaker (if there is one), or by a preset internal rate. The intraaortic balloon is inflated with an inert gas (helium) that is easily absorbed into the bloodstream in case of balloon rupture.
The hemodynamic consequences of IABP treatment are primarily associated with changes in preload, afterload, and aortic pressure, which are induced by an external force. However, the leading contribution of IABP treatment is from its metabolic effects, which tend to improve the cardiac energy balance a) by increasing oxygen supply to the ischemic myocardium and b) by reducing cardiac oxygen demand (consumption). The first objective is accomplished by the enhancement of coronary blood flow through an increase in aortic diastolic pressure, whereas the second is achieved by decreasing left ventricular (LV) afterload via a reduction in end diastolic and systolic aortic pressures.
Counterpulsation is realized by the rapid inflation and deflation of an intraaortic balloon into the thoracic aorta in synchronization with the cardiac function. The resulting volume displacement and pressure changes within the aorta exert the salutary IABP effects. The gas enters the balloon chamber occupying a space within the aorta almost equal to its volume. The usual adult balloon volume ranges from 30–50 cc, whereas in children, it varies from 2.5–25 cc. The sudden occupation of space inside the balloon by the gas during inflation causes the blood that surrounds the balloon to be moved from its original position superiorly and inferiorly to the balloon. Because the volume in the aorta is suddenly increased, the intraaortic pressure increases sharply. On the other hand, deflation of the intraaortic balloon induces reverse events. A rapid reduction in aortic volume leads to a sudden fall in aortic pressure within that localized aortic area. Displacement of blood volume, both away from the balloon upon inflation and toward the balloon upon deflation, is the principal mechanism by which the intraaortic balloon pump affects the hemodynamic state.
Timing of Intraaortic Balloon Pump
The balloon inflation and deflation must occur at optimal time points in the cardiac cycle to obtain the maximal IABP efficiency. Balloon inflation occurs during diastole, beginning with aortic valve closure. The balloon remains inflated during diastole, while its rapid deflation is set to be initiated a few milliseconds before the onset of left ventricular ejection. There is a great body of published studies investigating proper timing of balloon deflation. In general, optimal deflation time is considered when balloon volume is decreased to approximately one half of its fully inflated volume (i.e., 40 cc) before the end of LV diastole, while the deflation continues to occur into the next systole.6,7
The initiation of balloon inflation is timed to occur at the dicrotic notch of the aortic pressure waveform, which reflects the closure of the aortic valve. More specifically, inflation is set up approximately 40 msec earlier to compensate for the time delay, which is determined by the pulse wave velocity and the distance between the aortic root and the ascending aorta.
Performance and Hemodynamic Effects of Intraaortic Balloon Pump
The efficiency and the beneficial effects of IABP can be evaluated by three main aspects: 1) the acute hemodynamic changes induced by IABP, by comparing the assisted to the unassisted hemodynamics; 2) the medium-term hemodynamic and clinical status a few hours or days after mechanical assistance by IABP; and 3) the successful weaning from IABP and survival.
Intraaortic balloon counterpulsation produces both hemodynamic and metabolic changes. The extent and the degree of these effects are influenced by the severity of cardiac dysfunction at the time of IABP use.
Major Hemodynamic Changes
Augmentation of diastolic aortic pressure is induced by the rapid inflation of the intra aortic balloon during cardiac diastole. As a result, a second pressure wave is introduced in the diastolic part of the aortic pressure waveform (Figure 2). Also, mean diastolic pressure increases as expressed by the area under the diastolic part of the aortic waveform. A maximal augmentation of diastolic aortic pressure by approximately 30–70% (compared with the unassisted end diastolic aortic pressure) has been observed.8,9
Systolic aortic pressure is reduced during balloon deflation as a result of the induced reduction of left ventricular afterload (end diastolic aortic pressure). Peak systolic aortic pressure usually declines by 5–15% during assistance with IABP. Mean systolic pressure is also decreased, leading to an additional reduction in left ventricular systolic work.1,8 End diastolic aortic pressure decreases as a consequence of balloon deflation at the end of cardiac diastole. The decrease in end diastolic aortic pressure varies from 5–30%.1,8 Cardiac output and stroke volume have been found to be increased by IABP up to 20%,9,10 while no change has been also observed. The change in cardiac output, however, may be caused by either an enhancement of left ventricular pumping performance during assistance or to the pumping efficiency of intraaortic balloon per se. Left ventricular end diastolic pressure and volume may decrease by 10–15%.11 The degree of this effect strongly depends upon the contractility of myocardium and the severity of heart failure. Heart rate is slightly influenced by IABP. A decrease by approximately 10% may be observed, explaining in part the increase in stroke volume and cardiac output. Arterial distensibility and wave reflections may also be favorably affected by IABP. It has been reported that during IABP, arterial stiffness and wave reflections are reduced, providing evidence that these effects may be important mechanisms by which IABP improves the circulatory function.12
Various other hemodynamic effects have been observed during treatment by IABP (Table 1). It should be noted that the degree and significance of some changes induced by IABP are controversial because there is a strong dependence upon the severity of myocardial ischemia and LV dysfunction during assistance.1
Major Metabolic Effects
Myocardial oxygen balance is determined by the oxygen supplied by the coronary circulation to the myocardium and by the factors that determine the oxygen demand. As mentioned before, IABP induces favorable effects in oxygen balance through an increase in oxygen supply and a reduction in oxygen consumption by the myocardium.
Coronary blood flow is very low during cardiac systole because of the contraction of coronary arteries but increases markedly during diastole. Coronary blood flow is mainly adjusted by resistance changes of coronary vessels, whereas changes in aortic diastolic blood pressure play a minor role in coronary flow regulation in physiologic conditions. In contrast, in pathologic situations (e.g., severe hypotension, coronary artery stenoses, or heart failure), diastolic aortic pressure affects the coronary blood flow to a greater degree. Intraaortic balloon inflation during diastole tends to enhance coronary blood flow via the increase in mean diastolic aortic pressure. An increase in coronary blood flow during IABP operation by more than 100% has been reported in previous studies,13 whereas in others, no significant change14 or even a decrease15 has been found. It seems that the cardinal factor that determines the change of blood flow in the coronary circulation during intraaortic balloon counterpulsation is the presence and severity of coronary artery stenoses.
Cerebral, renal, mesenteric, and pulmonary blood flow have been reported to be increased by IABP,16–18 whereas no change may also be observed.
Other metabolic beneficial effects of intraaortic counterpulsation are reflected, for example, by an increase in urine output, decrease in lactic acidosis, increase in lactate use, and enhancement of venous oxygen saturation.
The induced hemodynamic and metabolic effects of the IABP are listed in Table 1. It should be noted that the increase (+) or decrease (−) indicated in Table 1 represents the desirable, expected effects during IABP treatment or the observed ones in the majority of published studies. The reverse changes or no change may also be observed, depending upon various other clinical or technical factors that influence IABP performance.
Indices of Acute Intraaortic Balloon Pump Hemodynamic Efficacy
A great number of indices and formulas have been described to assess the acute hemodynamic performance of IABP.19,20 However, there is no single index that could be used to evaluate the overall performance of IABP. In clinical practice, the direct evaluation of IABP hemodynamic performance is often performed by calculating changes acutely induced in aortic pressure characteristics during intraaortic balloon pump operation. Such indices are directly estimated by comparing aortic pressure waveforms with IABP on and off. Three main indices reflect the acute hemodynamic performance of IABP and are widely used in clinical practice: 1) the decrease in peak systolic aortic pressure, 2) the reduction in end diastolic aortic pressure, and 3) the peak increase in diastolic aortic pressure (Figure 2). Of course, various other hemodynamic changes could be used either separately or in combination to characterize the acute IABP efficiency more globally.
Factors Affecting Intraaortic Balloon Pump Acute Performance
Besides the baseline clinical conditions that exist before IABP initiation, there are also other technical and biologic factors that affect IABP acute performance.
Major Technical Factors
Synchronization of balloon inflation and deflation within the cardiac cycle is one of the most essential technical factors that influence the hemodynamic effects of IABP. Speed of balloon inflation and deflation also affects counterpulsation effects; the higher the balloon inflation and deflation speed, the better the hemodynamic performance of the IABP.21 Balloon volume determines the “counterpulsation” volume displaced during inflation and deflation. It has been demonstrated that balloon volume should be as high as possible,22,23 without however letting the balloon walls occlude the lumen of the aorta at its full inflation. Balloon position within the aorta should be 1–2 cm below the origin of the left subclavian artery and above the renal artery branches.
Major Biologic Factors
Biologic factors are likely the more crucial determinants of IABP performance. Several pathologic conditions have been reported where IABP remains ineffective.24
Aortic blood pressure.
IABP is known to be ineffective in patients with systolic aortic pressures less than 60–70 mm Hg. Animal studies have supported this evidence, showing a markedly decreased diastolic augmentation during IABP at mean aortic pressure less than 40 mm Hg.25 IABP becomes more effective as blood pressure increases. However, it is likely that IABP hemodynamic performance is not affected by low blood pressure per se but rather by the arterial compliance, which is usually increased at low blood pressure levels.26
Left ventricular stroke volume.
It has been demonstrated that the optimal left ventricular stroke volume that results in maximal IABP effects should be equal to the counterpulsation volume, almost 30 cc for a 40 cc balloon.27 In cardiogenic shock or severe heart failure, LV stroke volume is approximately 20–30 ml, whereas in physiologic situations, it is much higher (65–75 ml). As the stroke volume approximates normal values, the performance of IABP is reduced.28
Heart rate influences the acute performance of IABP, although in a nonlinear way.29 The increase of heart rate to more than 120 beats per minute (bpm) results in a significant decline in the hemodynamic changes induced by IABP, mainly because of the inadequate time that is required for complete inflation and deflation of the intraaortic balloon. Commercially available driving systems have been developed, achieving rapid balloon inflation and deflation and thus allowing a satisfactory balloon function from a mechanical point of view, even at increased pumping rates (∼140 bpm). However, the development of intraaortic balloon driving systems does not necessarily mean that the hemodynamic response to intraaortic balloon counterpulsation is equivalently improved. In conclusion, heart rates between 80–110 bpm seem to provide optimal IABP hemodynamic effects, whereas the efficacy of IABP diminishes when operating at rates lower than 80 or greater than 110 bpm.29,30
The mechanical properties of the aorta directly affect the hemodynamic response to intraaortic balloon function. Studies in mock circulatory systems, animals and patients with cardiogenic shock, have demonstrated that the greater the arterial compliance the lower the changes in arterial pressures induced by IABP.31–33 Arterial compliance levels seem to be predictive of IABP efficiency regardless of heart rate or blood pressure level.32 Development of noninvasive techniques that may be easily used to estimate arterial stiffness indices at the bedside would add a further criterion to management of IABP treatment.26,34
It is now clear that IABP effectiveness depends upon both the extent and severity of heart failure and upon the hemodynamic conditions, which can be further affected by pharmaceutical interventions, in the short and long term. Therefore, drugs usually administered simultaneously with IABP treatment also affect its effectiveness, rendering the issue of IABP performance even more multifactorial. For example, pressor agents, either via a- or b-adrenergic stimulation, are routinely used in patients with cardiogenic shock (Classes III and IV), aiming for an elevation of mean arterial blood pressure to satisfactory levels, which is also favorable for an increased IABP performance. Specifically, drugs stimulating a-receptors may increase blood pressure levels through vasoconstriction with a possible further decline in arterial compliance, which also provides an advantage for the enhancement of IABP efficiency. Also, drugs used to control cardiac arrhythmias or tachycardia are also beneficial, not only for the patients’ critical conditions but also to the operation and performance of IABP. In many cases, combinations of different pharmaceutical agents are administered during IABP treatment. Their synergistic effects upon acute IABP hemodynamic performance are difficult to distinguish; however, a beneficial effect upon overall clinical outcome is often evident.
The intraaortic balloon pump, to date, remains the single most effective and widely used device for temporary mechanical assistance of the failing heart. Even though the principles underlying IABP function are simple and widely scrutable, the mechanisms altering its performance are particularly complex. In various clinical situations, IABP remains ineffective, requiring further research. To overcome the shortcomings presented by intraaortic balloon counterpulsation in specific situations, researchers have developed alternative techniques of counterpulsation, such as juxtaaortic counterpulsation,35,36 enhanced external counterpulsation,37 and paraaortic pump.38,39 The integrated effort by cardiologists, surgeons, physiologists, biomedical engineers, critical care nurses, and technicians has resulted in great progress in the field of mechanical assistance of the failing heart.
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