Intraaortic Balloon Counterpulsation: A Review of Physiological Principles, Clinical Results, and Device Safety

COLLECTIVE REVIEW

Intraaortic Balloon Counterr>ulsation I

A Review of Physiological Principles, Clinical Results, and Device Safety Karl T. Weber, M.D., and Joseph S. Janicki, M.S. This article is dedicated to the memory of Frank W . Hastings, M.D. (1919-1971), whose insight, leadership, and contributions toward the advancement of improved and innovative methods of circulatory assistance and medical instrumentation have been an inspiration.

ABSTRACT The intraaortic balloon counterpulsation device (IAB) has been used in the treatment of several hundred patients with acute myocardial infarction shock and other conditions complicating the course of ischemic heart disease and characterized by low-output failure. With the balloon positioned in the thoracic aorta, synchronous inflation-deflation occurs during cardiac diastole and systole, respectively, thereby augmenting aortic diastolic or coronary perfusion pressure and reducing the impedance to ventricular ejection. The extent to which the fixed-volume IAB system can thus alter the circulatory physiology is a function of a number of mechanical and biological variables. In more than 80% of patients with infarction, the shock state may be reversed; however, the majority of these patients have been IAB-dependent. Complications during IAB support, while infrequent, have included aortic wall damage, femoral artery insufficiency, and thrombocytopenia. This review summarizes the major aspects and current status of this cardiocirculatory supportive device.

T

he high mortality in acute myocardial infarction shock and lowoutput failure following intracardiac surgery has prompted a search for more effective and aggressive therapeutic interventions, including cardiac assist devices. T h e majority of these devices employ the principles of counterpulsation, which include (1) augmentation of arterial diastolic or coronary perfusion pressure and (2) reduction in the impedance to

From the Division of Cardiology, Department of Medicine, and the Department of Physiology and Biophysics, University of Alabama School of Medicine, Birmingham, Ala. Supported by National Institutes of Health Subcontract No. 7125 and Grant HE 11,310 from the National Heart and Lung Institute. Address reprint requests to Dr. Weber, Cardiovascular Pulmonary Division, Department of Medicine, The University of Pennsylvania School of Medicine, 3400 Spruce St., Philadelphia, Pa. 19104.

602

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REVIEW:

Zntraaortic Balloon Counterpulsation

ventricular ejection and heart work. In addition, these devices maintain systemic perfusion to a variable degree. The primary aim of these additive effects on the ischemic heart is to reduce the metabolic demand-to-supply relationship of the ischemic parenchyma, thereby providing a favorable environment for the retrieval of as many of these cells as possible, thus minimizing infarct size. T o date, the intraaortic balloon counterpulsation device (IAB) has been the most frequently used assist unit in the treatment of low-output failure accompanying a variety of clinical disorders [6, 10, 16, 22, 551. Its hemodynamic performance, ease of application, and relative safety have made the IAB a useful emergency support system and valuable therapeutic tool. The ability to influence long-term mortality, however, is less certain and apparently dependent on a number of factors, including the underlying clinical disorder(s). The purpose of this report is to provide a review of the major aspects of the IAB device and to present both theoretical and practical information about its operation.

Historical Background Over the past two decades a number of significant contributions have made possible the successful clinical application of the counterpulsation concept. As early as 1953, Kantrowitz and Kantrowitz [29] found that augmenting arterial diastolic or coronary perfusion pressure by retardation of the systolic pressure pulse could increase coronary flow by 22 to 537& This was accomplished in dogs through a length of flexible tubing that had been used to cannulate and connect the femoral and left circumflex coronary arteries. In 1958 Kantrowitz and McKinnon [30], extending this concept further, mobilized the left hemidiaphragm around the distal thoracic aorta of the dog and, by synchronized electrical stimulation of the intact phrenic nerve, were able to augment aortic diastolic pressure. In 1961 Clauss and associates [131, using an external pumpactuator system and arterial cannulation, reduced systolic pressure and augmented diastolic arterial pressure in dogs by the synchronized withdrawal and infusion of blood. These investigators noted that the ability to induce these pressure changes was dependent on a number of important variables, including the volume of blood displaced, the pressure-volume relationship of the aorta, the position and size of the arterial cannula, and proper synchronization with the cardiac cycle. In an attempt to avoid the problems attendant upon blood-handling, Moulopoulos, Topaz, and Kolff [46] in 1962 constructed an inflatable latex tube resembling the present IAB device which they inserted into the descending thoracic aorta of the dog through the femoral artery. By pulsed inflation of the tube with carbon dioxide driving gas and ECG synchronization, they were able to augment arterial diastolic blood flow and reduce arterial end-diastolic pressure. Furthermore, their experiments in

VOL. 1 7 , NO.

6, JUNE, 1974

603

WEBER AND JANICKI

anesthetized dogs suggested that inflation-deflation duration or pump timing was an important hemodynamic consideration. With the founding of the Artificial Heart Program by the National Institutes of Health in 1964, a number of important research and development efforts in the area of cardiac assist devices were initiated and supported in both university and industrial laboratories. The director of this program, Dr. Frank W. Hastings, was instrumental in initiating studies relevant to device safety and optimum performance. The proceedings of the Artificial Heart Program Conference held in 1969 [26] reflect not only the commitment of Dr. Hastings and the N.I.H. but also the invaluable liaison of basic and applied scientists which had evolved. It was this latter force which has made possible the many continued advances in both circulatory supportive devices and general medical instrumentation. IAB counterpulsation was used clinically by Kantrowitz and coworkers [31] in 1967, and their results were presented in January, 1968. Two patients with infarction shock refractory to medical therapy were supported by the balloon assist device. In both patients it was apparent that intraaortic balloon pumping (IABP) had stabilized and reversed the hemodynamic shock state, although 1 patient died with irreversible ventricular fibrillation during interruption of assistance; the other patient recovered and was discharged from the hospital. Only minimal evidence of red cell destruction was found. Kantrowitz [32] followed this initial experience with a larger series of 16 patients who were supported with IABP during cardiogenic shock. IABP was able to reverse the shock state in all patients. Three of the 16 patients died during interruption of counterpulsation; of the 13 patients who recovered, 7 were long-term survivors (1 to 11 months). These results were suffitiently encouraging to stimulate others to apply the IAB in the treatment of medically refractory infarction shock. In 1969 Summers and coauthors [63] reported their experience with IABP in 3 similar patients. In addition to the hemodynamic stabilization which was possible with IABP, these investigators noted an improvement in myocardial metabolism. They further noted that it was possible to carry out emergency coronary angiography and left ventriculography during balloon support. Bregman, Kripke, and Goetz [7] and Buckley and associates [11] presented further evidence in 1970 that IABP was able to improve or correct the clinical shock state following acute myocardial infarction. While each group utilized a different model LAB system, hemodynamic performance appeared similar. Buckley and his colleagues, using a triple-segmented IAB in 8 patients, noted an average increase in cardiac output of 400 ml. per minute (3 to 16y0), a reduction in systolic pressure of 9.5 mm. Hg, and no significant change in mean arterial pressure. In 5 patients, Bregman and coworkers found a 12 to 50Y0 increase in cardiac output and a 12 to 25y0 reduction (9 to 15 mm. Hg) in systolic pressure when they used a unidirectional dual-chambered balloon device. 604

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REVIEW:

Zntruuortic Balloon Counterfiulsution

FIG. 1. Principles of intraaortic balloon counterpclsation. The intraaortic balloon (IAR) is positioned in the thoracic aorta and driven in synchrony with the electrocardiogram by an external console. Shown is the influence of intraaortic balloon pumping (IABP) on aortic root (PAo) and left ventricular (PLv) pressures, i.e., the respective augmentation of aortic diastolic pressure and reduction in ventricular systolic pressure.

From 1970 to the present, the counterpulsation concept, and the IAB device in particular, have emerged as valuable therapeutic tools. Clinical balloon assistance has been used in several hundred patients with low-output failure and hemodynamic collapse accompanying not only infarction shock but also a number of other clinical disorders. This collective experience is reviewed in detail in a subsequent section devoted to clinical results and indications.

P hy sio 1ogical Prin ci p 1es The IAB is inserted into the thoracic aorta through a Dacron graft anastomosed end-to-side to the femoral artery. The balloon is pulsed phasically in synchrony with the electrocardiogram by an external console with triggering circuitry and driving gas (Fig. 1). Balloon inflation is timed to begin at aortic valve closure and end sometime prior to valve opening. The performance characteristics and capabilities of the IAB as a counterpulsation device are dependent on a number of biological and physical variables. Because of their importance in optimizing clinical IAB performance, these factors are given in some detail below, presented according to their influence on diastolic pressure augmentation or impedance and work reduction. DIASTOLIC PRESSURE AUGMENTATION

Most coronary flow to the left ventricular myocardium occurs during cardiac diastole, when coronary vascular resistance is minimal. The objectives of using IABP in the ischemic heart are to elevate aortic root diastolic pressure, or more specifically coronary perfusion pressure, and VOL.

17, NO. 6, JUNE, 1974

605

WEBER AND JANICKI VARIABLES INFLUENCING IAB COUNTERPULSATION

Purpose of Counterpulsation Diastolic pressure augmentation

Impedance & work reduction

Physical (IAB) Position Volume Diameter Occlusivity Configuration Driving gas Timing Volume Occlusivity Inflation duration

Variables

Biological

Arterial pressure Heart rate Aortic pressure-volume relation

Arterial pressure Heart rate Aortic pressure-volume relation Afterload reduction Preload reduction Augmented shortening

consequently improve nutrient flow to the ischemic parenchyma. T h e magnitude and duration of augmentation of the mean aortic root diastolic pressure (MADP) with IABP have been shown to be related to several physical or balloon-dependent variables [ 17, 721: IAB position within the thoracic aorta, the volume displacement capabilities and dimensions of the IAB, the ratio of IAB to aortic diameters or occlusivity, balloon configuration, and balloon inflation-deflation duration or timing (Table). Optimum IAB position for MADP augmentation is that which creates the highest possible level of aortic compartmentalization [9, 17, 24, 721. In other words, the closer the balloon is to the aortic valve, the greater the elevation in MADP. In man, the risk of cerebral embolism appears to dictate that this position correspond to the junction of the left subclavian artery and thoracic aorta. T h e importance of balloon volume displacement on MADP has been determined experimentally [72]. In these studies balloons with volumes of 20, 30, or 40 cc. were tested in the thoracic aorta of the calf at varying mean arterial pressures (MAP). T h e calf is the most appropriate animal model and should be considered over dogs, sheep, or swine when evaluating human-sized balloons because of the similarity in aortic compliance and cardiovascular capacity in the calf and man [42, 671. T h e results are given in Figures 2 and 3 and indicate that a significant elevation in MADP (average 18 mm. Hg) was possible at all observed MAP levels, the degree being dependent on IAB volume. T h e 30 and 40 cc. balloons were able to increase MADP an additional amount (8 mm. Hg) above that seen with the smaller, 20 cc. IAB. It follows that the aortic diastolic volume displacement capabilities of the balloon will also determine its ability to reduce the systolic pressure developed during the subsequent contraction. To assess the influence of IAB diameter and occlusivity (e.g., the ratio of IAB and aortic diameters) on hemodynamic IAB performance, Weber and Janicki and their associates [73] used a distensible IAB and variable volume 606

THE ANNALS OF THORACIC SURGERY

Zntraaortic Balloon Counterfiulsation

COLLECTIVE REVIEW:

&

=

+

40302010-

F I G . 2. T h e percent augmentation in aortic root mean diastolic pressure (MADP) is given as a function of ZAB volume for four mean arterial pressure (MAP) levels.

0

4/ .

20

30

40

i

50

I A B VOLUME (cc)

limiter+ in the calf at varying MAP. Occlusivity was determined from the simultaneous measurement of aortic root and abdominal aorta diastolic pressures and the pressure-volume-diameter relation of the distensible IAB. It was observed that for any arterial pressure or aorta size, the greatest augmentation in MADP was seen with complete occlusion. Indirect evidence in support of these findings is also seen in Figure 2, which shows that the greatest percent augmentation in MADP for all fixed volume IABs occurred at a MAP of 50 mm. Hg. Because of the potential aortic wall and red cell damage at 1 0 0 ~ occlusion, o the estimated optimum occlusivity was judged to be 90 to 9574, although this may be an overestimation; further efforts in this area are required. The choice of appropriate balloon diameter will vary not only from UOr

I A D P mm Hh?

41 /

20

0

Lo

40

M A D P mm

, 80

4

;".

lA8P (120~)

80

100

no 100 -

w60-

40

-

PI-

*

IPO

MAP mm Hg

FIG. 3. Mean aortic diastolic pressure (MADP) during the basal state and its augmentation with ZABP at varying mean arterial pressures (MAP). Regression lines 2 1 SD are presented for ( A ) dogs (volume, 12 cc. ZAB) and ( B ) calves (volume, 20 and 40 cc. ZAB). (From K. T. Weber, J. S. Janicki, A . A . Walker, and J. W . Kirklin, A n assessment o f intra-aortic balloon pumping in hypovolemic and ischemic heart preparations. J . Thorac. Cardiovasc. Surg. 64:869-877, 1972.) *Tecna Corp., Emeryville, Calif. VOL.

17,

NO.

6, JUNE, 1974

607

WEBER AND JANICKI

patient to patient, but also with MAP within any given aorta. Therefore, determining the correct IAB size for a particular patient is somewhat uncertain and to date has been based on such indirect information as estimating aorta size from the caliber of the femoral artery [7, 101 or from body weight [32]. Weikel and associates [76] reviewed a large series of aortograms from 169 patients and found that 90% of the patients had a midthoracic aorta diameter in excess of 19 mm. (16 to 30 mm.). All balloons currently available fall within this range. The actual choice of IAB size therefore becomes the decision of the responsible physician. It is our opinion, one shared by Feola and colleagues [17], that since the maximum hemodynamic gains for any IAB counterpulsation unit require that optimal occlusivity be maintained at any arterial pressure and aorta size, this could best be controlled and titrated for all conditions by a variable volume system. We further believe that such an approach could most easily be accomplished with a distensible balloon. At present such a unit is not commercially available. Another physical or balloon-dependent variable that affects diastolic pressure augmentation is that of configuration. It has been stated that cylindrical or sausage-shaped balloons are susceptible to the development of a large lateral wall pressure. This would lead to preferential inflation of the balloon ends, trapping of blood in the central segment, and ineffective volume displacement and pressure augmentation. This phenomenon has been termed bubble-blowing [37]. To circumvent this potential clinical problem the IAB has undergone several alterations in design. The triplesegmented IAB is an outgrowth of these efforts. Recently, however, Bleifeld and co-workers [4] have questioned the occurrence of such a phenomenon in vivo except when the IAB diameter substantially exceeds that of the aorta. These investigators found that in dogs a hydrostatic pressure gradient of about 20 mm. Hg exists from the proximal (tip closest to the aortic valve) to the distal end of the balloon and that this gradient was associated with a preferential inflation pattern that began at the proximal tip and progressed distally. The reverse was true during deflation. On the other hand, they were able to recreate the bubble-blowing phenomenon, although only in vitro, after encasing a mock aorta in a rigid cylinder and placing the test apparatus in a horizontal position, duplicating the conditions of the original study. Without the rigid casing, no central trapping was observed. Others [6] have reasoned that additional considerations of performance would necessitate the use of still another configuration, namely the dual-chambered balloon. The triple-segmented and dual-chambered balloons and all other models which are commercially available are pictured in Figure 4. It is not the purpose or intent of this review to recommend or endorse any particular IAB. For a detailed analysis of the performance characteristics, safety, and biocompatibility features of these systems, the interested reader is referred to the N.1.H.608

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REVIEW:

Intraaorlic Balloon Counterpulsation

FIG. 4 . T h e five commercially available IAB models: ( A ) the Avco triple-segmented model, the ( B ) the single- and dual-chambered Datascope IABs, (C) the Milton-Roy balloon, (0) SMEC model IAB, and (E) the fusiform Tecna IAB.

sponsored comparative evaluation carried out by Kaye and associates [33] at the Test and Evaluation Facility of the IIT Research Institute. Carbon dioxide and helium have each been used as the driving gas for the balloon device. T h e choice of gas has been based on the consideration of response time and therefore gas density and viscosity. Lightweight helium has been chosen by some [16, 551 because of minimum delays in transport and rapid inflation capabilities, particularly during tachyarrhythmias. Others [6, 711 have preferred the heavier but more soluble carbon dioxide because of a lesser risk of gas embolism in the event of leakage; they found that the response characteristics of their systems were not severely curtailed. Gas embolism is discussed further in subsequent sections. Finally, the timing or duration of balloon inflation and deflation likewise determine MADP. Mechanical balloon inflation should begin at end-ejection with the closure of the aortic valve. T h e inflation rate and pressure vary with each system and driving gas and therefore are not discussed here. Premature inflation to close the aortic valve and increase the

VOL. 17, NO.

6, JUNE,1974

609

WEBER AND JANICKI

EC6 2

pLv

m m Hg

200

P

A0

m m Hg

0

AOQ

FIG. 5 . T h e experimental results of premature IAB inflation prior to aortic valve closure are shown for a conscious calf preparation following left circumflex coronary artery occlusion. Aortic (PAo) and ventricular (PLv) pressures and aortic root flow (AoQ) are shown for the basal (off) and IABP (on) states. Note the late rise in PLV, the diminished diastolic augmentation in PAO,and the reduction in stroke volume and abbreviation in ventricular ejection time (LVET); concerning LVET, the solid and dotted lines in the right-hand panel represent the duration of ejection during basal and IABP states, respectively.

duration of diastole only serves to impede and prematurely terminate ventricular ejection and dissipate diastolic pressure (Fig. 5). Early inflation would also cause a reduction in stroke volume, an increase in end-systolic and end-diastolic ventricular volumes, and therefore an augmentation rather than a reduction in ventricular preload. This is clearly less than the desired end-point of unloading the already enlarged and failing heart. Because of inherent electrical and mechanical delays in any IAB system, the onset of balloon inflation which best coincides with aortic valve closure should therefore be referenced against either the dicrotic notch of the arterial pressure pulse or the electrocardiogram. This has been done for the Westinghouse carbon dioxide-driven IAB unit (not commercially available) and was found to correspond to the latter half of the T wave [72]. Inflation is continued and terminated at a time prior to aortic valve opening. Prolonged inflation beyond valve opening imposes on ejection, creates a large intraventricular wall stress which is hazardous in a weakened, infarcted ventricle because of the potential for free wall or septa1 rupture, and retards the amount of ventricular shortening or stroke volume [70]. Opinion on the exact point in the cardiac cycle at which to terminate balloon inflation likewise requires comment. Balloon inflation could be terminated with the R wave corresponding to the end of ventricular diastole. T h e trigger circuitry can easily distinguish the R wave and under most circumstances-except that of severe hypotension, when the isovolumetric contraction time is quite short-guard against the possibility of partial inflation during ejection. In addition, premature ventricular contractions 610

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REVIEW:

lntraaortic Balloon Counterpulsation

would automatically deflate the device. Deflation here would also reduce arterial end-diastolic pressure. Alternatively, using an adjustable delay, balloon deflation could be timed to occur just prior to aortic valve opening. Experimental observations [71, 721 during normotension or moderate hypotension indicate that this more prolonged or late inflation to valve opening (corresponding to the J junction of the electrocardiogram) is the more effective hemodynamic maneuver. While peak systolic pressure was reduced to an equivalent amount with R wave (early) or J junction (late) timing patterns, an additional reduction in pressure and augmentation in stroke volume during the first third of the ejection period was seen with the late deflection sequence and was reflected in maximum reductions in tension time index per beat and mean impedance to ejection. Concomitant measurements of coronary and brachiocephalic arterial flow demonstrated that retrograde flow from these vessels occurred as arterial end-diastolic pressure was reduced with balloon deflation; however, the amount of retrograde flow could be minimized with late timing. Clearly, then, the duration of inflation-deflation is critical to the balloon’s ability to maximize coronary perfusion pressure and reduce myocardial work requirements. Inflation that begins at aortic valve closure and is extended to valve opening has been found to be the most effective hemodynamic pattern for several reasons. Retrograde coronary and brachiocephalic flow into the aortic root at end-inflation is minimized. This is desirable not only from a flow delivery standpoint but also because it serves to maximize the reduction in afterload. Second, active balloon deflation by vacuum imparts to the aortic root blood column a momentum which will approximate the ventricular ejection rate over about one-third of the ejection period until the peripheral bed and its resistance retard aortic flow. This momentum serves to reduce the instantaneous and mean impedance to ejection beyond that obtained purely by blood displacement accompanying balloon inflation alone and thereby further aids in ventricular unloading. T h e critical qualification to the non-R-wave sensing mode, however, is the dependence on a regular and stable rhythm. Furthermore, the patient with an IAB unit would have to be continuously attended by a physician or appropriately trained personnel so that in the event of dysrhythmias the triggering circuitry could be adjusted to prevent prolonged inflation. These constraints dictate that the inflation-deflation time should be chosen by the responsible physician and based on hemodynamic performance and patient safety. Regardless of which mode is used to end inflation, the appropriate inflation-deflation period for any given situation must also be derived from careful observation o f not only the existent heart rate but also the mean arterial pressure level. As we have suggested, MAP will influence IAB timing and can best be emphasized by giving the electrocardiographic correlates of the non-R-wave sensing modality that were found for various heart rates and VOL.

17,

NO.

6,

JUNE,

1974

611

WEBER AND JANJCKI

MAP. For heart rates < 120 beats per minute and MAP > 60 mm. Hg, the late inflation duration pattern (onset to cessation) best coincides with the latter one-half of the T wave (0.5 T ) to J junction period. At MAP < 60 mm. Hg, however, the isovolumic contraction time is abbreviated, and in this situation late timing corresponds to the 0.5 T to R wave period. Non-R-wave sensing in this latter setting would lead to an abnormally prolonged inflation and an imposition on ventricular qjection. T h e 0.5 T to R wave period likewise is appropriate for heart rates > 120 beats per minute. With MAP < 40 mm. Hg, however, the 0.5 T to PR interval is most appropriate. It should again be pointed out that these electrocardiographic correlates are representative for the Westinghouse IAB system and not those commercially available. Certainly this information needs to be determined for each unit. Deflation rate and duration are the final timing considerations based on rapid response requirements during tachyarrhythmias and severe hypotension. Nonactive balloon deflation, which is dependent only on lateral aortic wall pressure for collapse, will more than likely be incomplete at MAP < 40 mm. Hg. T h e resultant partial IAB inflation would impose on the next ejection; and if intraventricular stress were sufficient and applied over a prolonged period, the potential for rupture of the infarcted segment would be substantial. T h e biological factors which influence the balloon’s ability to augment mean arterial diastolic pressure (MADP) include mean arterial pressure, the aortic pressure-volume relationship, and heart rate. While it is difficult to separate these effects from the purely mechanical variables such as occlusivity, a few words would appear appropriate. Figure 3 demonstrates the ability of IABP to elevate MADP over a wide range of mean arterial pressures (MAP 24 to 122 mm. Hg). In the dog, using a sausage-shaped IAB, significant ( p < 0.01) elevations in MADP (average, 8 mm. Hg) were obtained only when MAP was greater than 40 mm. Hg. Whenever the aortic end-systolic volume is severely reduced, IABP while on the lower end of the aortic pressurevolume relation will result in limited increments in MADP. Furthermore, with MAP < 40 mm. Hg and the aortic diameter severely reduced, the decreased diastolic augmentation observed was probably due to bubble-blowing. Observations in calves with a fusiform IAB demonstrate a significant elevation in MADP (average, 18 mm. Hg) at all observed MAP levels, the degree being dependent on IAB volume. Included in these observations are the influence of the larger-capacitance aorta of the calf and heart rate. As MAP declines, compensatory reflex increments in heart rate occur which also serve to shorten the diastolic interval. Consequently there is less time for peripheral dissipation of the augmented diastolic pressure wave form. This effect is reflected in the divergence of the regression lines in Figure 2 at MAP < 60 mm. Hg for calves. In addition, balloon occlusivity was greater as MAP declined, further retarding peripheral run-off. In general these 612

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REVIEW:

Zntraaortic Balloon Counterpulsation

observations on the extent of diastolic augmentation are in agreement with the clinical and experimental observations of others [6, 11, 16, 551. With Enfarction shock, the aorta is on the flat portion of the pressurevolume curve. Coronary perfusion pressure must be maintained or augmented since the myocardium is the major priority. In addition to balloon assistance, concomitant pharmacological support in the form of a peripheral vasoconstrictor is indicated [19]. For a review of a detailed protocol and the pharmacological agents used to support the patient in shock following acute infarction, the interested reader is referred to the recent report of Gunnar and Loeb [25]. T h e aforementioned physical and biological variables are all directed at maximizing MADP augmentation. While diastolic pressure may be elevated some 15 to 20 mm. Hg by IABP, this does not assure that coronary flow, or more specifically nutrient collateral flow, to the ischemic area will be improved. T h e delivery of collateral flow is dependent on a number of biological factors in addition to perfusion pressure, including the vasomotor or autoregulatory tone of the coronary circulation, the size of the ischemic area, the degree of collateral formation, and the extent of significant obstructive atherosclerotic disease in the major coronary vessels. A consideration of these factors may explain the wide discrepancy in the results of IABP on the coronary circulation which have appeared in the current 1iterature. A number of investigators have measured flow in another major patent vessel after a major coronary vessel was acutely ligated and have found a 7 to 50% increase with IABP [12, 14, 17, 771, whereas others [9] have reported n o change or a decline in flow. In yet another series of reports, in which coronary sinus efflux was monitored [7, 35, 47, 64, 651, a 5 to 1 0 0 ~ o increase in flow was observed with IABP. Powell and his colleagues [51] were the first to shed any light on this variability. Using a right heart bypass preparation, they found that not until total coronary flow had been significantly reduced (< 50 ml./min./100 gm. of left ventricle) during hypotension could IABP augment coronary sinus flow. These findings demonstrate the influence of coronary autoregulatory tone on flow augmentation by IABP. We have recently documented the influence of autoregulation on collateral flow delivery with IABP by measuring the pressure-flow response for the ischemic and collateral beds in calves during normotensive and hypotensive conditions [68]. It was found that collateral flow could be increased 21 -+ 9% above basal levels during balloon assistance but only at MAP < 9 0 mm. Hg. For normotensive conditions collateral flow was unchanged. Shaw and co-workers [59], using radioactive microspheres to measure the regional distribution of coronary flow within the ischemic and nonischemic myocardium, have also found recently that nutrient flow to the ischemic border zone was not augmented by IABP in normotensive dogs. VOL.

17, NO. 6, JUNE,1974

613

WEBER AND JANICKI

Gundel, Brown, and Gott [24], on the other hand, found that retrograde or collateral flow was augmented an average of 35% by IABP, irrespective of the existing arterial pressure. In their canine heart preparation, however, the aortic arch vessels were either ligated or occluded by the IAB, and aortic compartmentalization was therefore more pronounced. In addition, the range of retrograde flows which they observed was quite small (0.3 to 4.1 ml./min.) and a 20 to 30y0 augmentation for flows less than 2 ml. per minute could be of limited significance to the ischemic parenchypa. We have purposely chosen not to present information on collateral flow delivery observed for counterpulsation techniques other than the IAB because of difficulties in equating variable-volume systems such as arterioarterial counterpulsation with the fixed-volume balloon device. We conclude, then, that the ischemic portion of the coronary circulation is maximally dilated and acts as a pressure sink. Flow into this sink is dependent on the size of the ischemic area, the resistance of the major coronary vessels, and surrounding collective collateral bed. In the case of a small infarct without hemodynamic collapse, IABP may reduce the metabolic requirements of the remaining viable myocardium sufficiently for autoregulation to occur, preventing a significant amount of collateral flow from reaching the ischemic area. With a large infarction or low MAP, on the other hand, this autoregulation is lost, and IABP would increase collateral flow. Aside from autoregulation and the size of the ischemic area, the extent and caliber of the collateral network will also determine the amount of flow that IABP could deliver. T h e major stimulus to collateral growth and development is persistent ischemia [54]. In the acutely ischemic heart it is unlikely that a collateral network of sufficient caliber would exist. Although this requires more detailed study, indirect evidence has been presented [74] that the amount of IABP-induced collateral flow into the ischemic area of an acutely ligated coronary artery may not be sufficient to prevent the appearance of lethal arrhythmias. On the other hand, a well-formed collateral bed of a chronically ischemic heart may permit a more substantial collateral flow with IABP. Schaper [54] has shown that the pressure-flow responses of the collateral vasculature in the chronically ischemic myocardium (coronary arteries constricted for 8 weeks or more), unlike the acutely ischemic bed, are more dependent on perfusion pressure and indicative of collateral enlargement. Finally, collateral flow delivery will depend on the resistance of the major coronary vessels or the extent of obstructive atherosclerotic disease. Evidence has been presented that significant disease exists in several major coronary vessels of hearts in which the shock state ensued fallowing acute infarction [40, 751. Such disease in association with hypotensian may lead to a self-perpetuating process of ischemia and a significant amount of injury (often estimated at greater than 40y0 of the left ventricle). T h e task of reversing such injury by IABP would be an extremely difficult one. 614

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REVIEW:

Intraaortic Balloon Counlerpulsation

IMPEDANCE AND WORK REDUCTION

It should be clear from the foregoing discussion that IABP-induced reductions in mean ejection impedance are likewise dependent on many of the same balloon-related variables. T h e most important of these are the volume displacement capabilities and occlusivity of the balloon and the inflation duration utilized. T h e blood displaced by IABP into the peripheral circulation will reduce the aortic end-diastolic volume and thereby decrease the impedance to ejection during the subsequent contraction. Most reports indicate that IABP is capable of reducing left ventricular systolic pressure by 4 to 20% [6, 9, 11, 12, 14, 16, 17, 45, 47, 63-65] with the majority finding a 15% reduction. Urschel and associates [66] and Weber and co-workers [72] have calculated the change in mean ejection impedance and reported a 10 to 21yo reduction with IABP. Mueller and colleagues [47] were able to reduce ejection resistance by approximately 46y0. Like MADP augmentation, systolic pressure and impedance reduction are directly related to IAB displacement volume; however, for any given IAB, occlusivity within the aorta will also influence these results. It appears that for any MAP, the reduction in impedance is greatest with total or neartotal occlusion [73]. T h e explanation for these findings, while not entirely clear, may be related to minimizing dissipation of the augmented diastolic pressure and augmenting peripheral flow. Finally, inflation duration also affects the reduction in impedance for reasons previously presented. In brief, active balloon deflation (by vacuum) just prior to aortic valve opening imparts a momentum to the aortic root column of blood. This column is moving away from the valve as the ventricle begins its ejection, so instantaneous and mean impedance are reduced to a greater extent with this timing pattern than with diastolic volume displacement alone. Furthermore, retrograde flow from the aortic arch vessels and coronary arteries into the aortic root is reduced by prolonged inflation. By inference, mechanical heart work should be less with the reduction in aortic impedance. T h e calculation of external stroke work or product of stroke volume and the difference in mean ejection and filling pressures reflects this notion. A more complete assessment of heart work and accompanying metabolic expenditures, however, would necessarily have to consider the loading conditions of the ventricle and how they are affected by IABP [5]. T h e intraventricular mural force, whether developed (afterload) or passive (preload), may be determined from the product of intraventricular pressure (ventricular systolic and end-diastolic pressures, respectively) and cross-sectional chamber area. It foIlows that with the reduction in mean impedance and developed systolic pressure, afterload would be reduced; indeed, when Urschel and co-workers [66] calculated peak wall stress during IABP, they found a 14% decrease. Our group has recently measured the response in ventricular internal diameter and pressure during IABP (Fig. 6). Assuming a thick-walled spherical model for the ventricle, we found a VOL.

17,

NO.

6,

JUNE,

1974

615

WEBER AND JANICKI

IABP Basal

160

Lv Wall

120

Stress gm/cm2 80

40

FIG. 6. T h e hemodynamic responses to ZABP (on), including that of left ventricular internal diameter (LVID) observed in a dog, are shown in the upper portion of the figure. Below is the plot of intraventricular wall stress for basal and IABP states. Indicated also (arrows) are the end of diastole (ED) and left ventricular ejection time (LVET).

decline in end-diastolic diameter and volume together with an observed decline in systolic pressure. This amounted to a 19 and lSyo reduction, respectively, in peak and developed wall stress as shown in Figure 6. 616

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REVIEW:

Zntraaortic Balloon Counterfiulsation

Furthermore, it is predictable from the force-shortening relationship of the left ventricle [70] that as afterload is reduced, shortening or stroke volume is increased. This was confirmed in the studies in which ventricular diameter and shortening were monitored and is shown in Figure 6, where stroke volume and stroke diameter were increased by 6 to 7y0 during assistance. T h e augmentation in shortening leads to more complete emptying, a decline in end-systolic and end-diastolic volumes and pressure, and thereby a reduction in preload (19yo). Therefore IABP, if properly used, is capable of partially unloading the left ventricle by reducing both preload and afterload, a desirable end-point in the failing heart. This partial unloading of the left ventricle reduces myocardial metabolic expenditures. Such an attenuation in demand alone or in combination with an increase in coronary collateral flow may serve to minimize infarct size. Several recent clinical and experimental observations indicate that such may be possible. In 1969 Summers and colleagues [63] first noted the reversal of anaerobic myocardial metabolism and lactate production to lactate utilization in 3 patients with infarction shock who were treated by IABP. Mueller and associates [47] had similar success with 21 patients when balloon counterpulsation was applied during the postinfarction shock state. When myocardial metabolism was assessed in 10 patients who had partially recovered from shock and whose condition was stabilizing, Leinbach and co-workers [39] could not demonstrate a consistent response in lactate metabolism. Rather, a variable pattern of response in oxygen consumption and coronary flow was observed, indicating in part coronary autoregulation. Maroko and colleagues [44], using an epicardial mapping technique to estimate infarct size, were able to reduce the magnitude and extent of ischemic myocardial injury by utilizing IABP in 2 patients with hemodynamic shock following acute infarction and in 19 dogs with coronary occlusion. While these observations are encouraging, overall mortality in these clinical series was not significantly altered, and the question therefore remains whether the IABP-induced alterations in metabolic demand and supply are of sufficient magnitude. Other factors may be influential in this regard. A further discussion of the overall clinical response to IABP is presented in a subsequent section. SYSTEMIC PERFUSION

Aside from the favorable influence on cardiac dynamics, IABP also displaces blood from the aorta as an auxiliary in-series ventricle. T h e influence of IABP on peripheral perfusion has been estimated by measuring renal, carotid, and femoral artery flow. Although most investigators have found some change in flow with IABP, net flow was not significantly altered. Specifically, Brown and associates [9] reported a decrease of approximately 5% in renal flow and a 5% increase in carotid flow while femoral artery flow was unaltered during 5 minutes of IABP. Chatterjee and Rosensweig [12] VOL. 17, NO.

6, JUNE, 1974

617

WEBER AND JANICKI

were able to maintain renal artery flow, provided the catheter did not encroach on the renal artery ostia, and increase carotid flow by 6%. Both Corday [ 141 and Feola [20] and their co-workers found that in normotensive animals renal flow remained the same or increased slightly during IABP. In dogs with graded degrees of ventricular failure following acute coronary artery ligation, however, the influence of IABP on renal and carotid artery flows was more variable and dependent on the degree of failure. T h e specific influence of IAB timing and induced retrograde flow on organ perfusion remains to be determined. To date, specific estimates of organ perfusion during IABP have not been carried out in man; by all indirect clinical evidence available, however, it must be assumed that perfusion is adequate. Stabilization or improvement of the shock state has been observed in more than 89% of the patients in each of three series [7, 16, 551 as evidenced by the maintenance of adequate hourly urine output, improved mentation, and defervescence of peripheral vasoconstriction and cyanosis. Femoral artery flow in the catheterized limb, however, may not be as adequate. Vascular insufficiency of variable severity distal to the arteriotomy site has been observed with some frequency and is disciissed further in the section on clinical findings. Another influence of IABP on the systemic circuit is its effect on aortic baroreceptor output and resultant changes in reflex neurohumoral circulatory control, specifically in peripheral vascular resistance. Several investigators have measured the output from these receptors during IABP and found them to be dramatically altered. Diastolic pressure augmentation produced a diphasic output and accentuated diastolic output volley (normally absent), resulting in a net increase in baroreceptor output [ZO, 491. It was also observed that the magnitude of the baroreceptor output was responsive to balloon inflation pressure and inflation-deflation timing. Although Normann and Kennedy [49] postulated that these IABP-induced neurohumoral responses may be significant, their influence on the overall biological system response to IABP remains unknown. In this regard, Feola and colleagues [18] were able to demonstrate a decrease in heart rate and hind limb vascular resistance but only in normotensive or hypertensive animals and not those in shock.

Clinical Results and Indications T o date the balloon has been used in the treatment of several hundred patients with low-output failure accompanying two major clinical disorders: (1) acute myocardial infarction shock due solely to either myocardial injury and dysfunction, ventricular septa1 perforation, or papillary muscle rupture; and (2) postoperative heart failure following intracardiac surgery often characterized by the inability to discontinue venoarterial bypass support. Because of several considerations relevant to the clinical setting in which 618

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REVIEW:

Zntraaortic Balloon Counterpulsation

IABP has been used, the results of these clinical observations are presented according to each specific disease state. Detailed observations relevant to clinical hemodynamic IAB performance have been presented in the foregoing discussion and will be repeated only when necessary for emphasis. Part of the overall management program for infarction shock at a number of medical centers has included IABP. While many of the resultant observations have been fragmented into numerous earlier reports, the collective experience with IABP in 127 patients with cardiogenic shock has recently been presented [16, 551. Following Buckley’s [ l l ] initial report on the balloon assist device, Massachusetts General Hospital (MGH) has accumulated an extensive experience which was reviewed by Dunkman and colleagues [16]. In 40 patients with cardiogenic shock following acute infarction in which the secondary causes of shock, such as hypoxia, dysrhythmias, and hypovolemia, had been discounted, the hemodynamic response to IABP and the cessation of assist could be characterized in the following manner. With the institution of IABP, improvement in the clinical shock state occurred within 1 to 2 hours. Reversal of the shock state and the peak hemodynamic response noted in 31 of the 40 patients were present after approximately 25 hours (range, 1 to 90 hr.) of assistance. This delayed peak effect was documented as an increase in cardiac index (CI) from a mean base-line level of 1.7 liters per minute per square meter of body surface area to 2.5 L./min.,/m.2 and a reduction in left ventricular filling pressure (LVFP) as indicated by the pulmonary capillary wedge pressure (22 to 18 mm. Hg). In the 9 patients who did not respond to IABP, it was not possible to augment CI to 2.0 L./min./m.2, and 8 of these patients died within 48 hours of IAB assistance. Another set of patients (20 of the Sl), while stabilized out of shock with IABP, could not be weaned off the device and were termed IAB-dependent. Dependence was established when CI could not be maintained above 2.0 L./min./m.*, MAP fell below 60 mm. Hg, and LVFP rose above 20 mm. Hg when the pump was turned off or after IABP was used at a reduced level of support. This lower level of IABP was created by using a reduced inflation volume or frequency of inflation, Dependence in many cases was most pronounced only after 12 to 24 hours. T h e observation that some of the IABdependent patients had electrocardiographic evidence of persistent or recurrent ischemia or angina while off IABP suggested that perhaps revascularization may be of value in this group. Clearly some additional intervention was necessary if there was to be any chance of survival for the dependent and nonresponsive patients. Selective coronary angiography and left ventriculography for identifying correctable diseases plus bypass grafting alone or in combination with infarctectomy appeared the most appropriate route. T h e criteria for

VOL. 17, NO.

6, JUNE, 1974

619

WEBER AND JANICKI

angiography which evolved from earlier observations when IABP was the only mode of therapy were based on the likelihood of in-hospital mortality and included the patient’s dependence on the pump after 12 to 24 hours, failure to respond to IABP, increasing vasopressor (levarterenol) requirements, and refractory pump failure one week after myocardial infarction. Fifteen patients underwent emergency operation. Six of the 15 patients were long-term survivors, with 4 of the 6 still alive at 8 to 16 months. Of these 6 survivors, 1 (a nonresponder with recurrent ventricular arrhythmias) had infarctectomy alone and 5 had single or double bypass grafts with or without infarctectomy. It was noted that several of the survivors who were discharged in an asymptomatic condition and without cardiomegaly were in the ischemic-IAB-dependent subset. Furthermore, it should be pointed out that all in the nonresponsive group died, even with the additional operation. T h e third response pattern to IABP, observed in 9 patients, was one in which assist could be successfully discontinued and an operation was not considered necessary. Five of this latter group, however, died before discharge at a mean of 30 days after removal of the device. Two of the 4 who were discharged were alive at 21 and 30 months, whereas the other 2 had recurrent infarction and died despite IABP and operation. T h e results of a cooperative study on balloon assistance involving 10 institutions and 87 patients with refractory cardiogenic shock was recently presented by Scheidt and other collaborating investigators [55]. Criteria in patient selection included not only the confirmed presence of hemodynamic shock (systolic arterial pressure < 80 mm. Hg) but also a tested lack or minimal response in arterial pressure, urine output, and mental status to various inotropic agents and vasopressors. Of those patients totally refractory to medical therapy, 12% survived with IABP. T h e patients with a partial or limited response to various pharmacological agents had a 32y0 survival rate. As expected, a high incidence (52 of 87 patients) of IAB-dependence was observed in these patients with refractory shock. Furthermore, all patients who required more than 48 hours of support died. Discontinuation of circulatory support was not uniform but was based on the preferences of the attending physicians and included either abruptly stopping IABP after 24 to 48 hours of assistance and resuming support only if shock reappeared, or using intermittent IABP with variable on-off periods. T h e range in duration of IABP prior to successful discontinuation was 2 to 209 hours. Thirty-five patients were weaned off the device, and of these, 15 were discharged from the hospital (17Q/,)with 8 living more than 1 year (9yo). Historical, clinical, and hemodynamic data did not identify potential survivors in this series except for the finding of a persistent increase in urine output following withdrawal of IABP which was significantly higher than that observed in nonsurvivors (85 vs. 61 ml./hr.). This collective experience with 127 patients suffering infarction shock indicates that three patterns of response to IABP may be identified. Pattern 620

THE ANNALS OF THORACIC SURGERY

CoLLEcTivE

REviEw:

Intraaortic Balloon Counterpulsation

one is seen in a small number of patients and consists of hemodynamic stabilization and survival with IAB support and medical therapy alone. Pattern two is also observed in a limited number of patients and is characterized by nonresponsiveness, and in fact often uncontrolled deterioration, in the face of IAB support. T h e third response pattern, which occurs in the majority, is that of the IAB-dependent circulatory state. T h e course and survival in this third group of patients is an uncertain issue and may be favorably influenced by the addition of bypass grafting or infarctectomy or both. T h e meaning of these responses may seem unclear; however, a review of the clinicopathological and hemodynamic aspects of infarction shock may shed some valuable light. Approximately 15y0 of patients with acute myocardial infarction develop circulatory collapse and shock. T h e attendant mortality once shock has appeared is substantial. Recent evidence suggests, however, that not all patients with acute myocardial infarction shock are at equal risk. In a review of 41 patients with acute myocardial infarction shock observed from January, 1970, to June, 1972, at the University of Alabama in Birmingham Myocardial Infarction Research Unit, we found that 35 patients had shock due solely to muscle damage while 6 others had circulatory collapse associated with rupture of papillary muscle, ventricular septum, or free ventricular wall [75]. Overall mortality for the 35 patients was 77y0;however, a high-risk subset could be identified consisting of 24 patients, all of whom died. This high-risk group was not characterized by historical or clinical information but was distinguishable solely on the basis of hemodynamic data, as follows: CI < 2.0 L./min./m.2 and LVFP > 15 mm. Hg (Fig. 7A). Cardiomegaly shown roentgenographically, increased heart weight, and significant obstructive double or triple coronary vessel disease associated with a mean left ventricular muscle loss of > 45y0 was noted at postmortem examination. It would appear that in these patients compensatory responses in ventricular volume and mass had been exhausted and a critical contractile mass of the left ventricle was lost. Other patients with infarction shock were at lesser risk. Four patients with a CI of < 2.0 L./min./m.2 but an LVFP of < 15 mm. Hg had a 25y0 mortality; all 5 patients with a CI of > 2.0 L./min./m.2 regardless of LVFP survived. Heart size as shown roentgenographically was normal in 50% of the survivors of these latter two subsets. These subsets, however, are derived from a limited number of patients. A more recent version of these various subsets has been presented [69], based on personal estimates and a review of the literature on shock, and consists of the following (Fig. 7B): (1) high-risk subset with 1 0 0 ~ omortality, CI < 2.0 L./min./m.2 and LVFP > 15 mm. Hg; (2) two subsets at lesser risk (i.e., estimated survival 50y0)including one in which patients have a CI < 2.0 L./min./m.2 and LVFP < 15 mm. Hg and one in which CI > 2.0 L./min./m.2 and LVFP > 15 mm. Hg; and (3) the subset with the most favorable prognosis with infarction shock, i.e., patients with a VOL.

17,

NO.

6, JUNE, 1974

621

WEBER AND JANICKI

(WwIA)

35-

30.

-4wk * t i * ; D

did

mWrrt*l;uin

.i i l a r k ikrthdid

0 .

inhtia ilmtlan: din

25'

c,

(L/min/rn*)

..

20.--------------,----------------------------0

15.

1.0-

05. 0

.

I I I I.

0

i

=

:

I

I' I* I

I

1

.

.. . . .

.

I I

d

CI of > 2.0 L./min./m.2 and LVFP < 15 mm. Hg. A patient's position within this spectrum of hemodynamic dysfunction following infarction would be determined by the size of the present and previous infarctions; the compensatory responses in volume, mass, and heart rate; the imposed hemodynamic demands; and the state of the coronary circulation. It would appear that IABP in the high-risk subset, in whom there is muscle loss of greater than 40Q/,, is useful only for emergency circulatory support and that a more complete form of assistance or allograft replacement is needed for survival. With IABP alone, either the condition of these patients would deteriorate or they would be totally pumpdependent. T h e other subsets at lesser risk may benefit, in terms of survival, from IABP alone or with corrective operation. A large experience with these latter subsets is not currently available, primarily because of the initial hesitancy to utilize the balloon device except in those most gravely ill. With current evidence indicating that the IAB device is a reasonably safe and effective clinical tool, this experience should be accumulated. T h e limited current experience with IABP would also indicate that those with normal heart size and a CI of > 2.0 L./min./m.2 have a far better prognosis. T h e clinicopathological features and hemodynamic grouping of patients which we have suggested appear similar to the observations made at MGH of IABP in infarction shock. 622

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REVIEW:

Intraaortic Balloon Counterpulsation

Leinbach [4 13 noted that when roentgenographic evidence showed more than 40% of the left ventricular myocardium to be avascular and akinetic, it was predictable and substantiated at postmortem examination that 40% or more myocardial necrosis was present. T h e nonsurvivors had very limited contractile performance of the left ventricle. Seven of the 11 patients in his series had bypass operations, and 3 survived. Two of these patients were discharged asymptomatic without cardiomegaly and presumably with only small infarctions. T h e third patient died with congestive failure following a large anterior infarctectomy. Dunkman [16] extended this series: in 21 of 30 patients who came to postmortem examination, 17 had necrosis of 40y0 or more of the left ventricle. T h e patients unresponsive to IABP in Dunkman’s series could not achieve a CI of 2.0 L./min./m.* During IAB withdrawal and diminished circulatory assistance, those who eventually survived were able to augment CI to 2.1 L./min./m.2 or greater and to reduce LVFP to < 20 mm. Hg. It should be noted that LVFP was purposely maintained at 17 to 19 mm. Hg with albumin or fluid infusions to maximize the fiber length-shortening relationship previously demonstrated in the postinfarction patient by Russell and co-workers [53]. Scheidt [MI,on the other hand, was not able to identify survivors on hemodynamic or clinical grounds except for the previously mentioned hourly urine flow measurement. It appeared that heart rate in his series was less in the survivors (96 vs. 108 beats/min.), although this could not be substantiated statistically. Our own experimental observations [74], those of Hood and co-workers [27] on the heart rate response to IABP following partial circumflex occlusion in the presence of healed anterior infarction, and our clinical findings [75] that heart rate was significantly higher ( p < 0.05) in nonsurvivors of the shock state (104 vs. 86 heats/min.) suggest that this higher heart rate may have real prognostic significance. T h e impact of IABP on the overall mortality accompanying infarction shock should therefore be considered in light of these various subsets. It would appear that the course of patients in the high-risk subset is not significantly influenced by circulatory assistance, albeit the shock state may be stabilized for a varying period. T h e overall survival rate of 16y0 (4 patients) and 17% (15 patients) reported by Dunkman [16] and Scheidt [55], respectively, in all likelihood reflects the predominance of high-risk patients in their series. Furthermore, it did not appear that the time from the onset of postinfarction shock to the institution of IABP had any influence on survival, which further indicates the profound pathology of the myocardium. Whether or not it would be possible to control or even minimize ischemic injury in the lesser-risks subsets is not known, since methods to quantify infarct size [44, 601 are in their infancy and only a few such patients have been supported with IABP. It is apparent, however, that once hypotension is present, a self-perpetuating process of injury will be in effect, and control of VOL.

17,

NO.

6,

JUNE,

1974

623

WEBER AND JANICKI

injury and improvement in survival require early reversal of the shock state. In addition, if it is indeed possible to reduce the ischemic marginal zone of the infarct with IABP, a significant contribution in survival may be realized, not only during the time of the acute infarction but also with subsequent infarctions when larger amounts of functioning myocardium would be available to maintain the circulatory state. The question of whether or not all patients with acute myocardial infarction (with or without evidence of failure) should have IABP is an intriguing one. This discussion has been limited so far to shock accompanying acute myocardial infarction that is solely a result of muscle injury and necrosis. Clearly, other well-known cardiogenic causes of shock exist such as dysrhythmias, hypovolemia, and the vasovagal response. It is assumed that the individual physician would rule out these possibilities prior to considering the institution of circulatory assistance. Ventricular septal or papillary muscle rupture (or dysfunction) is also seen following infarction. Classically these complications are said to occur several days after the infarction and are heralded by the onset of a systolic murmur and vascular collapse and failure. Appropriate oxygen sampling and right-sided pressure and wave form analysis will make the diagnosis. In those patients in whom shock is present, the rapid institution of effective therapy is critical. Physiologically speaking, any therapeutic maneuver that reduces systemic impedance should favorably influence the abnormal ventricular hemodynamics, whether it be the left-to-right shunt of a ventricular septal defect or the mitral regurgitation of papillary muscle dysfunction. The counterpulsation concept, involving reduction of aortic impedance and augmentation of diastolic pressure while maintaining systemic perfusion and pressure, would appear to be an ideal form of therapy in such a setting. Laniado and coworkers [38] have in fact shown this to be the case in experimentally induced mitral regurgitation. These investigators found that forward or effective stroke volume is improved 51% and regurgitant flow reduced 2Oy0 by IABP. These observations likewise have been clinically demonstrated recently by Gold and colleagues [22]. In 11 patients with either interventricular septal rupture or mitral regurgitation accompanying acute myocardial infarction, left ventricular hemodynamics could be favorably influenced and the circulatory state stabilized with IABP. In 5 patients with ventricular septal defects, LVFP or wedge pressure was reduced from 17 to 13 mm. Hg, the pulmonary-to-systemic flow ratio improved with a reduction in the systemic arteriovenous oxygen difference from 9.7 to 8.1 vol. per 100 ml., and MAP increased from 68 to 73 mm. Hg. In the 6 patients with mitral valve incompetence, LVFP fell from 30 to 25 mm. Hg and the regurgitant “v” wave was reduced in amplitude. Cardiac output in these patients was raised 600 ml. per minute from the initial mean level of 3.1 liters per minute. Furthermore, it was possible to safely carry out emergency angiography which indicated that all patients had 624

THE ANNALS OF THORACIC SURGERY

COILECTIVE REVIEW:

Zntrnaorlic Balloon Counterpulsation

significant proximal obstructive disease in both the left anterior descending and right coronary arteries. Cardiac failure and shock are also observed following intracardiac surgery. Buckley and co-authors [lo] have utilized IABP in 27 patients in whom it was not possible to discontinue venoarterial bypass subsequent to mitral or aortic valve replacement alone or in combination with bypass grafting. Twenty-three patients were supported with the IAB for periods of 36 to 120 hours; of these, 18 were weaned from the balloon with 13 long-term survivors. Four patients remained pump-dependent in the face of IABP support and could not come off bypass. It appeared that IABP was most effective in those patients in whom acute ischemia occurred either during operation or in the preoperative period. Because the counterpulsation concept is ideal for the treatment of ischemic heart disease and its complications, it appears safe to assume that a number of new applications for the IAB system will be found. T h e possibilities are numerous and include the adjunctive treatment of persistent dysrhythmias following infarction; the control or reduction of infarct size and as an aid in the delivery of metabolic substrates such as glucose, insulin, and potassium; the conversion to pulsatile bypass during coronary revascularization and shock [I]; and the control or reversal of recurrent ischemia or angina. In fact, in 11 patients with recurrent (preinfarction) or accelerated (postinfarction) angina at rest, Gold and associates [23] found that when routine medical methods failed to control the number of angina attacks, the institution of IABP could decrease the frequency or abolish the number of attacks in both groups. During temporary cessation of IABP, pain and failure recurred within 5 to 10 minutes. On the average, resumption of IABP could reduce the accompanying elevation in LVFP and heart rate within 3 minutes. Furthermore, IABP provided hemodynamic support for these patients during coronary angiography and ventriculography as well as during anesthesia induction for bypass procedures and postoperatively. It is also possible that IABP could be used to reverse the left ventricular overload and failure without shock which may accompany acute coronary occlusion. That such is possible has been amply demonstrated experimentally [20,27, 45, 741 and clinically [40] by observations of IABP in patients who developed sudden left ventricular failure during angina or following ven triculograph y. Another possible use of IABP might be in the treatment of massive pulmonary embolism with the accompanying limited state of coronary flow and right ventricular overload. Talpins and associates [64] in 1968 noted that IABP not only favors left ventricular hemodynamics, but that right ventricular minute work and tension-time index could be reduced 51y0and 29yo,respectively. Spotnitz, Berman, and Epstein [62] indicated that the right ventricular failure, systemic hypotension, and reduced cardiac output following acute pulmonary embolism in dogs could be reversed by elevation VOL.

17,

NO.

6,

JUNE,

1974

625

WEBER AND JANICKI

of central aortic pressure with an occlusive spherical intraaortic balloon. In a separate set of experiments these investigators counterpulsed the pulmonary artery using a reciprocating pump and found similar results. T h e limited state of coronary flow seen with prolonged and severe hemorrhagic shock might similarly benefit from both IABP and volume restoration. T h e IAB has also been used in situations other than low-output failure. Bregman and Wolinsky [S] have reported that when a balloon is implanted subcutaneously in dogs and pulsed, a durable autogenous fibrocellular conduit is induced which could be used for reconstructive vascular surgery. For the interested reader, it should be noted that a number of other counterpulsation techniques are available and have been used clinically. These include the external synchronous assist suit [6 13 and arterioarterial counterpulsation with a reciprocating pump [ZS]. An implantable, in-series pump (left ventricle to aorta) [2]may be a future consideration.

Device Safety While the performance characteristics of any cardiac assist device are extremely important, the associated concern for biocompatibility and device safety is far greater. T o date, a great deal of experimental work has been carried out to determine whether or not the IAB is safe for human use. T h e question of biocompatibility has been investigated from several vantage points, including aortic wall damage, blood element destruction, thrombus formation, and the potential for embolism. In addition, the number of patients who have undergone IABP is in excess of 200, so a thorough review of both clinical and experimental results can be made at this time. We will not, however, evaluate each commercial unit and each specific aspect of IAB biocompatibility, since we do not wish to suggest the superiority or inferiority of any one unit based solely on evidence available in the medical literature. Furthermore, the detailed, objective comparison made by Kaye and associates [33] presents much of this information. These complications have been observed in patients on IAB support: Aortic damage (rare) Dissection of wall Laceration Subadventitial hematoma Platelet reduction Red cell destruction (minimal) Embolic phenomena (rare) Renal Testicular Ventricular rupture (not proved) Vascular insufficiency of catheterized limb Balloon rupture and gas embolus (rare) 626

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REVIEW:

Intraaortic Balloon Counterpulsation

Difficulties in balloon insertion in some patients because of severe aortoiliac atherosclerosis have been reported by several investigators [6, 16, 551. Dissection of the common iliac artery at the site of a plaque has also been observed [ 161. Alternative insertion sites when ileofemoral disease was severe have proved unsatisfactory. Clinical evidence of gross damage to the thoracic aorta has not been reported with any frequency. In 1 patient it was determined at postmortem examination that the balloon had dissected into the aortic wall and created a false lumen for 3 to 4 cm. in the descending thoracic aorta, after which it reentered the aorta [16]. At postmortem examination O’Rourke and Shepherd [50] noted a laceration in the wall of the aortic arch adjoining the origin of the subclavian artery and a small dissecting aneurysm extending from the tear about 10 cm. down the thoracic aorta, even though the tip of the IAB was 2 to 3 cm. distal to the tear. In another patient left subclavian artery obstruction by the IAB was evident when the patient sat forward. This prompted these investigators to perform an examination of IAB movement within the aorta of 6 cadavers. They found that the tip of the IAB moved between 1 and 4.5 cm. cephalad when the thigh was flexed or the body bent forward. Such movement could result in aortic arch damage or subclavian obstruction and therefore must be considered when the patient’s position is changed. Finally, an aortic subadventitial hematoma with dissecting fusiform aneurysm has been observed in 1 patient [55]. Microscopical evidence of endothelial damage with clinical IABP has not been reported. In animal experiments, however, a variable degree of IAB-induced aortic damage has been observed and appears related to the duration of assistance. In dogs, Brown and colleagues [9] found no microscopically visible damage to aortas after 2 hours of IABP and only slight adventitial hemorrhage in one aortic section after 1% days of assistance. After 7 days of IABP in pigs, Madras and colleagues [43]found barely visible fibrin deposition on gross examination of the aortic endothelium in the region of the balloon in 2 animals and damage to the aortic arch where the balloon tip came in contact with the aortic wall in 3. In every case this damaged area was found to have a platelet-fibrin deposit attached to the aortic endothelium. Schneider and co-workers [57] performed scanning electron microscopical studies (SEM) of selected regions of the calf aorta following 3 days of IABP with anticoagulation; these demonstrated both extensive deformation and patchy losses of the luminal endothelium adjacent to the balloon with mural thrombus formation firmly attached to the exposed subendothelium. In addition, renal emboli and infarctions, presumably from these mural thrombi, were noted. T h e influence of IAB occlusivity in this regard remains unknown. A consistent hematological complication of IABP is a reduction in platelet count, which occurs within the first 24 hours of assistance. In patients with acute infarction shock, Dunkman [16] found a 50% reduction

WEBER AND JANICKI

from prepumping levels during the first 60 hours of IABP. T h e count remained suppressed in approximately one-half of those who demonstrated an initial decline, despite the administration of heparin and dextran. While the influence of shock on microcirculatory platelet rheology is uncertain, both DeLaria [15] and Madras [43] found that the number of platelets was decreased during the first 24 hours of IABP in normotensive, conscious swine and calves. Furthermore, the return to normal levels has been variable. Schneider [56] found only minimal physical changes in circulating platelet structure; however, numerous irregularly shaped platelet microaggregates were attached to a fibrin network on the IAB surface and catheter after either several days of discontinuous pumping or 7 days of continuous assist, despite systemic anticoagulation. This was particularly apparent in areas of diminished blood flow such as along that portion of the IAB catheter which was in the lower abdominal aorta and ileofemoral system. Schoen and associates [58] conducted SEM studies of balloon surfaces that had been counterpulsed both experimentally (calves) and clinically. Comparable volumes of dextran or saline were given to the calves, and all patients received heparin and, to a variable extent, dextran. These investigators noted similar thrombotic patches approximately 2 mm. in diameter. T h e extent of these patches appeared related to the duration of implantation. Aside from these areas the balloon surface was clean, and the only difference noted between dextran-, heparin-, or saline-treated subjects was the presence of subcellular particles less than 1 p in size on the balloon surface in those receiving dextran. Red cell damage and hemolysis have not been significant with IABP. A minimal rise in plasma hemoglobin has been observed clinically and experimentally [3, 6, 9, 16, 431 but always remained less than 56 mg. per 100 ml. (0.5 to 56 mg. per 100 ml.) for recorded periods of IABP as long as 7 days. Alterations in white cell structure or function have not been reported. Embolic phenomena as a result of balloon-induced thrombosis appear to be rare in humans. Scheidt and co-workers [55] reported 1 death attributable to renal emboli associated with a balloon thrombus. This patient had not been anticoagulated, and there had been a period of time when the balloon was motionless. Dunkman and co-workers [16] did not observe any clinical evidence of peripheral embolization but noted the presence of two small emboli, one testicular and one renal, at postmortem examination. T h e incidence of embolic infarctions has been higher in pigs and calves with extended periods of IABP (> 2 days). Madras [43] found a solitary renal infarct of less than 5% of the kidney mass in 2 of 7 swine. Renal and occasionally splenic infarcts in calves were noted by Schneider [56]. Chatterjee and associates [12], on the other hand, found no evidence of embolic phenomena or organ abnormality in a series of dogs that had undergone 4 hours of IABP. One patient also was reported to have had coincidental renal atheromatous emboli [55]. 628

THE ANNALS OF THORACIC

SURGERY

COLLECTIVE REVIEW:

Zntraaortic Balloon Counterpulsation

T h e differences in the incidence of peripheral embolism and aortic injury between clinical and experimental series may be related simply to the duration of assistance or to species differences in the hematological system, aortic anatomy, or some as yet undetermined variable(s). It appears clear, however-and this has been confirmed by the observations of Bernstein and Murphy [3]-that to leave the IAB motionless or nonpulsatile is not safe and that thrombosis may be expected in the folds of the collapsed balloon. Synchronous or slow asynchronous pumping can retard thrombosis of the IAB and catheter. Therefore, when establishing IAB dependence or weaning a patient off the assist, a method of intermittent pulsation is mandatory. This could be accomplished by either on-off periods of assistance, diminished inflation pressures, or decreased frequency of synchronous or asynchronous assistance. T h e choice of the most appropriate is left to the responsible physician. It is our opinion that systemic anticoagulation with heparin during assistance is the safest procedure. In those patients for whom the institution or continuation of heparin therapy is contraindicated, dextran may be a suitable alternative. T h e total duration of IABP which is clinically safe is not entirely certain and must be determined by the particular clinical setting; it should be noted, however, that Rubenfire and co-workers [52] supported 2 patients with infarction shock for periods of 34 and 35 days, respectively, without untoward effects. Interestingly, the most frequently cited complication [16, 551 related to clinical IABP-namely, vascular insufficiency distal to the arteriotomy site of the catheterized limb-was never documented in related research in conscious animals. This only serves to emphasize the difficulties in equating healthy young animals with humans who have extensive atherosclerosis. Fortunately this complication has never been severe enough to result in the loss of a limb. Dunkman and co-workers [16] now routinely explore catheterized vessels with a Fogarty catheter at the time of balloon removal. I n their experience recovery of clots has reduced the incidence and severity of vascular insufficiency. Scheidt and co-workers [55] reported femoral artery insufficiency in 13 patients. Six died, and it is not possible to discuss their course. Of the remaining 7, 1 had permanent insufficiency; 2 required ileofemoral bypass and are presently asymptomatic; 2 experienced no problems after balloon removal; and the remaining 2 developed leg neuropathies without obvious arterial insufficiency. One of these last 2 patients is currently asymptomatic, and the other is improving. In the cooperative study on IABP in 87 patients, Scheidt and co-workers [55] reported the occurrence of left ventricular rupture in 5 patients (10%) who died with infarction shock. This represents a slight increase above the incidence of rupture reported for patients with acute infarction without assistance [48, 751. These investigators suggest-and indeed, such may be the case-that IABP maintained life several hours beyond the usual course, thus permitting continued myocardial destruction and eventual rupture to occur. VOL.

17,

NO.

6, JUNE, 1974

629

WEBER AND JANICKI

T h e role of the systemic steroids used in some patients in this series is uncertain. Furthermore, it must be restated that slight imperfections in inflation duration increase the potential risk of rupture by creating excessive levels of intraventricular wall stress. We raise this note of caution not to reflect on these results, but to reemphasize an important aspect of IABP. Such improper timing need not be true for the entire ejection period, but only during that portion of the cycle when stress is greatest, i.e., immediately at and slightly beyond aortic valve opening (see Fig. 6). Moreover, such imperfections would not be reflected in estimates of systolic pressure reduction since it may only be represented by a pressure spike at the onset of ejection. Such delays in inflation are possible when the timing is inappropriate for both the given heart rate and MAP or when the rate of balloon deflation is not sufficiently rapid, as in the case of nonvacuum deflation during which collapse is dependent on the surrounding intraaortic pressure-a hazardous situation during shock. Finally, an ever-present danger of IABP is that of balloon rupture and gas embolism. T o date, only 1 death has been reported as a result of balloon rupture [55], which in this case was thought to be secondary to improper insertion. Helium was the driving gas at the time of rupture. Imperfections or discontinuities in the balloon surface may be small, resulting in gas diffusion through the IAB material or through pinhole leaks, or they may consist of large rents. T h e quality-control aspects of commercial balloon fabrication appear acceptable in view of the low incidence of this complication, and these are briefly discussed in the paragraphs that follow; first, a few words are in order concerning the risk of gas embolism. T o date the choice of driving gas for the IAB system has been based on considerations of response time or safety. Helium is lightweight and offers a greater advantage when short inflation times with heart rates in excess of 140 beats per minute are required. However, Bregman [6] and Weber [72] have not encountered any difficulty using carbon dioxide at similar rates. Moreover, tachyarrhythmias in excess of 140 beats per minute should be considered contributory to the shock state and need to be controlled. In the event of pinhole leaks, carbon dioxide clearly has the safety advantage. Even though one would insist on the highest quality-control standards possible to negate this possibility and certainly would not permit such imperfections to lead to larger tears, one cannot always control the unforeseen tear induced by a calcific, atherosclerotic plaque. In such an event a large bolus of gas will enter the patient’s system. Here neither carbon dioxide nor helium is favorable in this situation, although a small margin of safety may exist with carbon dioxide as evidenced by its use in roentgenographic procedures involving the cardiac chambers; also, Kinkler and King [MI found that dogs could tolerate an intraventricular injection of 20 to 40 cc. of carbon dioxide with the thoracic aorta clamped without developing evidence of cardiac failure or nervous system damage. 630

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REVIEW:

Intraaortic Balloon Counterpulsation

On the other hand, Furman and associates [21] have shown that similar volumes of helium injected into the thoracic aorta are lethal within 2 to 3 minutes. Furthermore, the helium was distributed to the coronary and cerebral vessels despite its having been injected into the descending thoracic aorta. Lesser volumes of helium did not reduce the risk. Consequently it is our considered opinion that helium poses an unnecessary risk and should not be used as the driving gas. T h e fact that IAB quality has been satisfactory to date does not sway our opinion. Furthermore, a safety chamber that would prohibit more than one balloon volume of gas from escaping should be a mandatory component of all present consoles. Future improvements in design should aim at minimizing the escaped volume of gas even further. Finally, any discussion of device safety and utility would of necessity include some of the following: (1) the quality-control features of the balloon (surface defects, film thickness, and life testing with dimensions before and following usage) and drive console (supportive electronics, the pneumatic drive system, an alarm system for operational failures, and electrical safety): (2) the performance characteristics and capabilities of the console, such as ECG triggering (wave discrimination) and arrhythmia tracking: inflationdeflation delays and response times; fail-safe system features for balloon deflation, loss of driving gas, and driving pressures: accompanying monitoring capabilities of ECG and systemic and arterial pressures, with appropriate displays: (3) the need for simplicity to facilitate easy operation since the physician’s engineering background is limited: this also requires that system documentation, orientation, and precautions be readily available, appropriate, and easily understood; and finally, (4) the need for system costs to be priced in a range commensurate with widespread availability and reasonable operational and maintenance costs. This description is only a partial listing of the many aspects of device safety and availability of which the responsible physician and his appropriately manned cross-disciplinary team should be aware. At present, four different drive consoles and five balloons are commercially available in the United States. T h e reader is referred to the detailed government-sponsored investigation and report of Kaye and associates [33] in which the aforementioned considerations of quality control, performance, documentation, and the like are thoroughly and objectively presented for each commercial unit and balloon. No recommendations are given; rather, and we concur with this, the final choice is left to the individual clinician, who is best able to assess his own particular needs.

R ererences 1. Berger, R. L., and Saini, V. K.

Conversion of nonpulsatile cardiopulmonary bypass to pulsatile flow by intraaortic balloon pumping during myocardial revascularization for cardiogenic shock (abstract). Circulation 46 (Suppl. 11):130, 1972. VOL. 17, NO.

6,

JUNE,

1974

631

WEBER AND JANICKI 2. Bernhard, W. F., LaFarge, C. G., Husain, M., Yamamura, N., and Robinson, T. C. Physiologic observations during partial and total left heart bypass. J. Thorac. Cardiovasc. Surg. 60:807, 1970. 3. Bernstein, E. F., and Murphy, A. E. T h e importance of pulsation in preventing thrombosis from intraaortic balloons: A note of caution. J. Thorac. Cardiovasc. Surg. 62:950, 1971. 4. Bleifeld, W., Meyer-Hartwig, K., Irnich, W., Bussmann, W. D., and Meyer, J . Dynamics of balloons in intraaortic counterpulsation. A m . J. Roentgenol. Radium Ther. Nucl. Med. 116: 155, 1972. 5. Braunwald, E. Control of myocardial oxygen consumption: Physiologic and clinical considerations. Am. J. Cardiol. 27:416, 1971. 6. Bregman, D., and Goetz, R. H. Clinical experience with a new cardiac assist device: T h e dual-chambered intraaortic balloon assist. J. Thorac. Cardiovasc. Surg. 62:577, 1971. 7. Bregman, D., Kripke, D. C., and Goetz, R. H. T h e effect of synchronous unidirectional intraaortic balloon pumping on hemodynamics and coronary blood flow in cardiogenic shock. Trans. Am. SOC. Artif. Intern. Organs 16:439, 1970. 8. Bregman, D., and Wolinsky, H. Use of a subcutaneous pulsatile system to induce formation of autogenous vascular prostheses. Clin. Re;. 2 1 :406, 1973. 9. Brown, B. G., Goldfarb, D., Topaz, S. R., and Gott, V. L. Diastolic augmentation by intraaortic balloon: Circulatory hemodynamics and treatment of severe, acute left ventricular failure in dogs. J. Thorac. Cardiovasc. Surg. 53:789, 1967. 10. Buckley, M. I., Craver, ,I. M., Gold, H. K., Mundth, E. D., Daggett, W. M., and Austen, W. G. Intra-aortic balloon pump assist for cardiogenic shock after cardiopulmonary bypass. Circulation 46 (Suppl. 11):76, 1972. 11. Buckley, M. J., Leinbach, R. C., Kastor, J. A., Laird, J. D., Kantrowitz, A. R., Madras, P. N., Sanders, C. A., and Austen, W. G. Hemodynamic evaluation of intra-aortic balloon pumping in man. Circulation 46 (Suppl. 11):130, 1970. 12. Chatterjee, S., and Rosensweig, J . Evaluation of intraaortic balloon counterpulsation. J. Thorac. Cardiovasc. Surg. 61 :405, 1971. 13. Clauss, R. H., Birtwell, W. C., Alberta], G., Lunzer, S., Taylor, W. J., Fosberg, A. M., and Harken, D. E. Assisted circulation: I. T h e arterial counterpulsator. J. Thorac. Cardiovasc. Surg. 41:447, 1961. 14. Corday, E., Swan, H. 1. C., Lang, T., Goldman, A., Matloff, J. M., Gold, H., and Meerbaum, S. Physiologic principles in the application of circulatory assist for the failing heart: Intraaortic balloon circulatory assist and venoarterial phased partial bypass. Am. J. Cardiol. 26:595, 1970. 15. DeLaria, G. A., Nyilas, E., and Bernstein, E. F. Intraaortic balloon pumping without heparin. Trans. A m . SOC. Artif. Intern. Organs 18:501, 1972. 16. Dunkman, W. B., Leinbach, R. C., Buckley, M. J., Mundth, E. D., Kantrowitz, A. R., Austen, W. G., and Sanders, C. A. Clinical and hemodynamic results of intraaortic balloon pumping and surgery for cardiogenic shock. Circulation 46:465, 1972. 17. Feola, M., Adachi, M., Akers, W. W., Ross, I . N., Wieting, D. W., and Kennedy, J. H. Intraaortic balloon pumping in the experimental animal. A m . J. Cardiol. 27:129, 1971. 18. Feola, M., Limet, R. R., and Glick, G. Direct and reflex vascular effects of intraaortic balloon counterpulsation (IABC) in dogs at four levels of aortic pressure. Clin. Res. 19:313, 1971. 19. Feola, M., Limet, R. R., and Glick, G. T h e beneficial effects of the

632

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REVIEW:

20.

21. 22.

23. 24. 25. 26. 27.

28. 29.

30. 31. 32. 33.

34. 35.

36.

Intraaortic Balloon Counterpulsation

combined use of vasoconstrictors and intraaortic balloon counterpulsation in the therapy of cardiogenic shock (abstract). A m . J . Cardiol. 29:261, 1972. Feola, M., Normann, N. A., Haiderer, O., a n d Kennedy, J . H. Assisted Circulation: Experimental Intraaortic Balloon Pump. I n F. W. Hastings and L. T. Harmison (Eds.), Proceedings of the Artificial Heart Program Conference. Washington, D.C.: Government Printing Office, 1969. P. 637. Furman, S., Vijaynagar, R., Rosenbaum, R., McMullen, M., a n d Escher, D. J. W. Lethal sequelae of intraaortic balloon rupture. Surgery 69:121, 1971. Gold, H. K., Leinbach, R. C., Sanders, C. A., Buckley, M. J., Mundth, E. D., and Austen, W. G. Intraaortic balloon pumping for ventricular septa1 defect or mitral regurgitation complicating acute myocardial infarction. Circulation 47: 1191, 1973. Gold, H. K., Leinbach, R. C., Sanders, C. A., Buckley, M. J., Mundth, E. D., and Austen, W. G. Intraaortic balloon pumping for control of recurrent myocardial ischemia. Circulation 47: 1 197, 1973. Gundel, W. D., Brown, B. G., and Gott, V. L. Coronary collateral flow studies during variable aortic root pressure waveforms. J . Apfil. Physiol. 29:579, 1970. Gunnar, R. M., and Loeb, H. S. Use of drugs in cardiogenic shock due to acute myocardial infarction. circulation 45: 11 11, 1972. Hastings, F. W., a n d Harmison, L. T. (Eds.) . Proceedings of the Artificial Heart Program Conference. Washington, D. C.: Government Printing Office, 1969. Hood, W. B., Jr., Joison, J., Kumar, R., Norman, J. C., Tyberg, 1. V., and Urschel, C. W. Experimental myocardial infarction: VII. Effects of intraaortic balloon pump counterpulsation on cardiac performance in intact conscious dogs with left ventricular failure due to coronary insufficiency. Cardiovusc. Res. 5: 103, 1971. Jacobey, J. A. Results of counterpulsation in patients with coronary artery disease. A m . J . Cardiol. 27:137, 1971. Kantrowitz, A., and Kantrowitz, A. Experimental augmentation of coronary flow by retardation of arterial pressure pulse. Surgery 34:678, 1953. Kantrowitz, A., and McKinnon, W. M. P. Experimental use of diaphragm as auxiliary myocardium. Surg. Forum 9:266, 1958. Kantrowitz, A., Tjmneland, S., Freed, P. S., Phillips, S. J., Butner, A. N., and Sherman, J. L., Jr. Initial clinical experience with intraaortic balloon pumping in cardiogenic shock. J.A.M.A. 203: 135, 1968. Kantrowitz, A., Tjmneland, S., Krakauer, J . S., Phillips, S. J., Freed, P. S., and Butner, A. N. Mechanical intraaortic cardiac assistance in cardiogenic shock: Hemodynamic effects. Arch. Surg. 97: 1000, 1968. Kaye, M. P., Tobin, H. G., Simonaitis, D. F., and Giuffre, V. W. Comparative Evaluation of Commercial IAB Systems (Report Number N7308TR1, Vols. 1-111, in preparation, 1974.) Springfield, Va. : National Technical Information Service. Krakauer, J. S., Rosenbaum, A., Freed, P. S., Jaron, D., and Kantrowitz, A. Clinical management ancillary to phase-shift balloon pumping in cardiogenic shock: Preliminary comments. Am. J . Cardiol. 27: 123, 1971. Kuhn, L. A., Unger, A. H., Novick, S. A., Marano, A. J., and Rosenberg. A. S. Hemodynamic and cardiac metabolic effects of diastolic intraaortic balloon obstruction combined with distal aortic “booster” occlusion in experimental acute myocardial infarction with shock. A m . J . Cardiol. 25: 111, 1970. Kunkler, A., and King, H. Comparison of air, oxygen and carbon dioxide embolization. Ann. Surg. 149:95, 1959. VOL.

17,

NO.

6, JUNE,1974

633

WEBER AND JANICKI 37. Laird, J. D., Madras, P. N., Jones, R. T., Kantrowitz, A. R., Kothari, M. L., Buckley, M. J., and Austen, W. G. Theoretical and experimental analysis of the intraaortic balloon pump. Trans. Am. SOC. Artif. Intern. Organs 14: 338, 1968. 38. Laniado, S., Miller, H., Yellin, E., Barlow, B., Goetz, R. H., and Frater, R. M. Favorable effect of intra-aortic balloon pumping (IABP) on the distribution of total stroke volume in acute mitral regurgitation. Circulation 46 (Suppl. 11):118, 1972. 39. Leinbach, R. C., Buckley, M. J., Austen, W. G., Petschek, H. E., Kantrowitz, A. R., and Sanders, C. A. Effects of intra-aortic balloon pumping on coronary flow and metabolism in man. Circulation 43 (Suppl. I):77, 1971. 40. Leinbach, R. C., Dinsmore, R. E., Mundth, E. D., Buckley, M. J., Dunkman, W. B., Austen, W. G., and Sanders, C. A. Selective coronary and left ventricular cineangiography during intraaortic balloon pumping for cardiogenic shock. Circulation 45:845, 1972. 41. Leinbach, R. C., Nyilas, E., Caulfield, J. B., Buckley, M. J., and Austen, W. G. Evaluation of hematologic effects of intraaortic balloon assistance i n man. Trans. Am. SOC. Artif. Intern. Organs 18:493, 1972. 42. Lin, C.-Y., Galysh, F. T., Ho, J., and Patel, A. S. Response to intraaortic balloon pumping as related to aortic compliance. Ann. Thorac. Surg. 13:468, 1972. 43. Madras, P. N., Laird, 1. D., Iatridis, E., Kantrowitz, A. R., Buckley, M. J., and Austen, W. G. ‘Effects of prolonged intraaortic balloon pumping. Trans. Am. SOC.Artif. Intern. Organs 15:400, 1969. 44. Maroko, P. R., Bernstein, E. F., Libby, P., DeLaria, G. A., Covell, J . W., Ross, J., Jr., and Braunwald, E. Effects of intraaortic balloon counterpulsation on the severity of myocardial ischemic injury following acute coronary occlusion: Counterpulsation and myocardial injury. Circulation 45: 1150, 1972. 45. Matloff, J. M., Parmley, W. W., Manchester, J.. H., Berkovits, B., Sonnenblick, E. H., and Harken, D. E. Hemodynamic effects of glucagon and intraaortic balloon counterpulsation in canine myocardial infarction. A m . J. Cardiol. 25:675, 1970. 46. M O L I ~ O ~ O U O STopaz, , S. ~D., S., and Kolff, W. J . Diastolic balloon pumping (with carbon dioxide) in the aorta-a mechanical assistance to the failing circulation. Am. Heart J. 63:669, 1962. 47. Mueller, H., Ayres, S. A., Giannelli, S., Conklin, E. F., Mazzara, 1. T., and Grace, W. J. Effect of isoproterenol, 1-norepinephrine and intraaortic counterpulsation on hemodynamics and myocardial metabolism in shock following acute myocardial infarction. Ciwzrlation 45:335, 1972. 48. Naeim, F., de la Maza, L. M., and Robbins, S. L. Cardiac rupture during myocardial infarction: A review of 44 cases. Circulation 45: 1231, 1972. 49. Normann, N. A., and Kennedy, J. H. Arterial baroreceptor responses to intraaortic balloon assistance. J. Szirg. Rcs. 1 I :396, 1971. 50. O’Rourke, M. F., and Shepherd, K. M. Protection of the aortic arch and subclavian artery during intraaortic balloon pumping. J. Thorac. Cardiovasc. Surg. 65:543, 1973. 51. Powell, W. J., Daggett, W. M., Magro, A. E., Bianco, J. A., Buckley, M. J., Sanders, C. A., Kantrowitz, A. R., and Austen, W. G. Effects of intraaortic balloon counterpulsation on cardiac performance, oxygen consumption and coronary blood flow in dogs. Circ.Res. 26:753, 1970. 52. Rubenfire, M., Krakauer, I., Ciborski, A4., Wajszczuk, W., Malinowski, E., Jaron, D., Freed, P., and Kantrowitz, A. Prolonged circulatory support by intraaortic balloon pumping (abstract). Circulation 46 (Suppl. 11):214, 1973. 53. Russell, R. O., Rackley, C. E., Pombo, J., Hunt, D., Potanin, C., and Dodge,

634

THE ANNALS OF THORACIC SURGERY

COLLECTIVE REviEw:

54. 55.

56.

57. 58.

59. 60. 61.

62. 63.

64. 65. 66. 67. 68. 69.

Intraaortic Balloon Counterpulsation

H. T. Effects of increasing left ventricular filling pressure in patients with acute myocardial infarction. J. Clin. Invest. 49: 1539, 1970. Schaper, W. T h e Collateral Circulation of the Heart. New York: American Elsevier, 1971. Scheidt, S., Wilner, G., Mueller, H., Summers, D., Lesch, M., Wolff, G., Krakauer, J., Rubenfire, M., Fleming, P., Noon, G., Oldham, H., Killip, T., a n d Kantrowitz, A. Intraaortic balloon counterpulsation in cardiogenic shock: Report of a co-operative clinical trial. N. Engl. J. Med. 288:979, 1973. Schneider, M. D., Blatt, S. J., and Kaye, M. P. Compatibility study of blood/intraaortic balloon surfaces in living calf aortas. (Accession Number PV210749.) Springfield, Va.: National Technical Information Service, 1972. Schneider, M. D., and Eckner, F. A. 0. Surface Effects of Intraaortic Balloon Counterpulsation. I n Scanning Electron Microscopy/l973. Chicago, Ill.: I I T Research Institute, 1973. Pp. 451-458. Schoen, F. J., DeLaria, G. A., and Bernstein, E. F. Morpholo of bloodsurface interaction on intraaortic balloons: An analysis of c inical and experimental specimens by scanning electron microscopy. J. Thorac. Cardiovasc. Surg. 65:304, 1973. Shaw, J., Taylor, D., and Pitt, B. Effects of diastolic augmentation on regional myocardial blood flow in dogs with acute myocardial infarction. Clin. Res. 21:450, 1973. Shell, W. E., and Sobel, B. E. Prediction of infarct size from serum CPK changes early after myocardial infarction (abstract). Am. J. Cardiol. 3 1:157, 1973. Soroff, H. S., Cloutier, C. T., Birtwell, W. C., Banas, J. S., Brilla, A. H., Begley, L. A., and Messer, 1. V. Clinical evaluation of external counterpulsation in cardiogenic shock (abstract). Circulation 46 (Suppl. 11): 75, 1972. Spotnitz, H. M., Berman, M. A., and Epstein, S. E. Pathophysiology and experimental treatment of acute pulmonary embolism. A m . Heart J. 82:511, 1971. Summers, D. N., Kaplitt, M., Norris, J., Rubin, R., Nacht, R., Arieff, A., Lee, M., Wechsler, B., and Sawyer, P. N. Intraaortic balloon pumping: Hemodynamic and metabolic effects during cardiogenic shock in patients with triple coronary artery obstructive disease. Arch. Surg. 99:733, 1969. Talpins, N. L., Kripke, D. C., and Goetz, R. H. Counterpulsation and intraaortic balloon pumping in cardiogenic shock: Circulatory dynamics. Arch. Surg. 97:991, 1968. Tyberg, J. V.. Keon, W. J., Sonnenblick, E. H., and Urschel, C. W. Effectiveness of intraaortic balloon counterpulsation in the experimental low output state. A m . Heart J. 80:89, 1970. Urschel, C. W., Eber, L., Forrester, ,I., Matloff, J., Carpenter, R., and Sonnenblick, E. Alteration of mechanical performance of the ventricle by intraaortic balloon counterpulsation. Am. J . Cardiol. 25:546, 1970. Weber, K. T., Dennison, B. H., Fuqua, J . M., Speaker, D. M., and Hastings, F. W. Hemodynamic measurements in unanesthetized calves. J. Surg. Res. 11:383, 1971. Weber, K. T., and Janicki, 1. S. Coronary collateral flow and intraaortic balloon counterpulsation. Trans. Am. Soc. Artif. Intern. Organs 19:395, 1973. Weber, K. T., Janicki, J . S., Ratshin, R. A., Rackley, C. E., and Russell, R. 0. Acute Myocardial Infarction Shock: T h e Identification of the High Risk Subset. I n T. I. Malinin, R. Zeppa, W. B. Drucker, and A. B. Callahan

7

VOL. 17, NO.

6, JUNE,1974

635

WEBER AND JANICKI

70. 71. 72. 73. 74.

75.

76.

77.

636

(Eds.), Acute Fluid Replacement in the Therapy of Shock. New York: Intercontinental Medical Book Corp., 1974. Weber, K. T., Janicki, J. S., Reeves, R. C., and Hefner, L. L. Factors influencing stroke volume and ejection fraction in the isolated canine heart. Fed. Proc. 32:331, 1973. Weber, K. T., Janicki, J. S., and Walker, A. A. An assessment of intraaortic balloon pumping in hypovolemic and ischemic heart preparations. J . Thorac. Cardiovasc. Surg. 64:869, 1972. Weber, K. T., Janicki, J . S., and Walker, A. A. Intraaortic balloon pumping: An analysis of several variables affecting balloon performance. Trans. Am. SOC. Artif. Intern. Organs 18:486, 1972. Weber, K. T., Janicki, J. S., and Walker, A. A. The influence of balloon volume and diameter on optimal intraaortic balloon assist (abstract). Trans. Am. SOC. Artif. Intern. Organs 2:71, 1973. Weber, K. T., Malinin, T. I., Heck, F. J., Dennison, B. H., and Hastings, F. W. Experimental Production of Vascular and Microvascular Ischemia and Infarction: T h e Effects of Different Rates and Degrees of Coronary Flow Reduction in Calves. In T. I. Malinin, R. Zeppa, F. Gollan, and A. B. Callahan (Eds.), Reversibility of Cellular Injury Due to Inadequate Perfusion. Springfield, Ill.: Thomas, 1972. Pp. 266-287. Weber, K. T., Ratshin, R. A., Janicki, J. S., Rackley, C. E., and Russell, R. 0. Left ventricular dysfunction following acute myocardial infarction: A clinicopathologic and hemodynamic profile of shock and failure. Am. J. Med. 54:697. 1973. Weikel, A. M., Jones, R. T., Dinsmore, R., and Petschek, H. E. Size limits and pumping effectiveness of intraaortic balloons. Ann. Thorac. Surg. 12345, 1971. Yahr, W. Z., Butner, A. N., Krakauer, J. S., Tomecek, J., TjZnneland, S., and Kantrowitz, A. Cardiogenic shock: Dynamics of coronary blood flow with intraaortic phase-shift balloon pumping. Surg. Forum 19: 122, 1968.

THE ANNALS OF THORACIC SURGERY