Symposium on a Physiologic Approach to Critical Care

External Counterpulsation in Low Cardiac Output States Martin 1. Broder, MD. *

Counterpulsation as a method of assisting the circulation is based on the principle of introducing energy into the vascular system during the diastolic phase of the cardiac cycle. The basic idea was first described by Kantrowitz 16 in 1953, whose experiments showed that "if it were possible to perfuse the coronary bed with peak systolic pressures during myocardial diastole, an increase of flow through the coronary bed could be expected." This cardinal feature of raising diastolic pressure in the aorta to increase coronary blood flow accounts for the term "diastolic augmentation" used by several investigators. 36 Reduction of peak systolic pressure generated by the left ventricle (so-called "systolic unloading") is the other major goal of all counterpulsation techniques. The physiologic rationale for this is the direct dependence of left ventricular work and myocardial oxygen consumption on peak left ventricular systolic pressure. 29 Alteration of the pressure waveform in the aorta so that diastolic pressure is raised and systolic pressure lowered thus has the theoretical possibility of simultaneously increasing coronary blood flow and reducing cardiac work. This inversion of the usual arterial pressure pulse contour (peak pressure during diastole, lowest pressure during systole) has prompted the term "counterpulsation."6

Counterpulsation Techniques Various techniques of producing counterpulsation have been experimentally tested and in some cases used clinically: (1) extra-aortic muscular compression; 17 (2) arterio-arterial pumping;6, 17, 35 (3) intra-aortic balloon pumping;23 (4) extra-aortic balloon compression;20 (5) an inseries mechanical auxiliary ventricle;18 (6) extremity cuff compression. 9, 27,32 Use of the diaphragm as an auxiliary ventricle did not produce sufficient reduction in left ventricular work and attention turned to the technique of withdrawing arterial blood through femoral arterial cannulas during systole with return to the circulation through the same cannulas during diastole. It soon became clear, however, that considerable hemolysis often resulted, with damage to platelets, plasma protein *Director, Cardiac Care Unit, Cleveland Metropolitan General Hospital; Assistant Professor of Medicine, Case Western Reserve University, School of Medicine, Cleveland, Ohio

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denaturation, and other adverse hematologic effects. In addition, bilateral femoral arterial cannulation was required and in some cases only a limited amount of blood could be withdrawn during a single cardiac cycle, thus attenuating the pressure change in the aorta and limiting the clinical usefulness of the technique.

The Intra-aortic Balloon Development of the intra-aortic balloon made it possible to alter aortic volume (and thereby pressure) by moving a gas (such as carbon dioxide or helium) in and out of the aorta rather than blood. The gas is contained in a balloon mounted at the end of a catheter inserted in the descending thoracic aorta. U sing the electrocardiogram for timing, the balloon is inflated during diastole and deflated during systole, correspondingly increasing and decreasing aortic volume and pressure. Damage to blood and its components is minimal, less arterial surgery is required than with arterio-arterial pumping, and the balloon catheter can be positioned closer to the heart to increase its pumping effectiveness. The insertion of the catheter, however, requires a femoral (or axillary) arteriotomy under local anesthesia in a sterile field. The patients requiring such mechanical cardiac assistance are seriously ill, usually following acute myocardial infarction or cardiac surgery, are often also being treated with mechanical respirators and pacemakers, and have indwelling central venous or pulmonary arterial catheters. In addition, assistance must be applied promptly to be of value and organizing the necessary vascular surgery may take several hours once the decision to begin pumping is made. This invasive and complex nature of balloon counterpulsation has tended to limit its application in medical patients to those with far-advanced shock or other cardiac problems that have been unresponsive to more conventional medical therapy, with understandable reluctance on the part of many internists and cardiologists to insert the balloon and begin pumping earlier in the course of these conditions. Its use in non emergency situations such as angina pectoris or acute myocardial infarction without shock is even more obviously limited by the surgery required. The application and effectiveness of balloon counterpulsation have thus been limited, and an alternative noninvasive method sought.

EXTERNAL COUNTERPULSATION Several groups of investigators9 • 27. 32 have shown that the legs can be used as a pumping chamber. Aortic diastolic pressure can be raised 40 to 50 per cent by application of a positive pressure pulse during diastole; release of this pressure or application of negative pressure during systole (the latter being more effective 26 ) lowers systolic aortic (and thus peak left ventricular) pressure. Compression of the legs also increases venous return to the heart, another way of increasing cardiac output. An external hindquarters sleeve 9 and half-body pressure suit27

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have been used experimentally in the dog. The result is a counterpulsated aortic waveform virtually identical to that produced by the intraaortic balloon. Technique Clinically, external counterpulsation':' is applied by encasing the legs from ankle to groin between two halves of a rigid case that are then fastened together (Fig. 1, A and B). A water-filled bladder surrounds the legs and completely fills the space between the legs and the outer case. The bladder and thus the legs are then pneumatically pressurized during the first part of diastole using the patient's electrocardiogram for timing. During the remainder of the cardiac cycle the pressure is lowered to about 25 mm Hg or to -50 mm Hg if a negative pressure phase is used. Proper delay and duration controls, oscilloscope display of the electrocardiogram and arterial pressure pulse (usually recorded from a finger plethysmograph), and a two-channel paper recorder are all provided on the control console (Fig. 1 C). The entire system does not take much more room than most modern mechanical ventilators and can be wheeled to the bedside in an ordinary hospital room or intensive care area and used there without difficulty. The electronic circuitry is adjusted to take into account the time needed to transmit a pressure wave along the aorta and makes possible precise phasing of the pump with cardiac action. Since adequate alteration of the aortic pressure waveform can be monitored in most cases from a finger pulse display, the procedure can be totally noninvasive and thus can be quickly begun once the decision is made to begin pumping. In the author's institution, pumping has usually been started within 15 minutes and the nurses and house staff have had no difficulty in operating and adjusting the leg unit and console, once initially instructed. Morbidity Patient acceptance of external counterpulsation has been excellent, and most conscious patients have been able to sleep during pumping with little or no sedation. Occasional patients complain of leg cramps or restlessness, and the only morbidity we have otherwise encountered has been skin irritation that can be avoided by careful positioning of the legs within the leg unit using adequate protective padding and full-length elastic stockings. The amount of pump pressure needed to produce significant elevation of aortic diastolic pressure is usually in the range of 150 to 200 mm Hg, which is well tolerated when applied in short bursts. The extent to which peak aortic (and therefore left ventricular) systolic pressure is reduced depends on whether negative pressure is applied to the legs during systole. More systolic unloading is produced by application of negative pressure rather than simply returning to the previous ambient leg pressure. No significant thrombotic, hemolytic, or embolic problems have been encountered. ':'Cardiassist, Medical Innovations, Inc., Waltham, Mass.

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Figure 1. A, The patient's legs are covered with either fulllength stockings or pajamas and are then positioned in the lower half of the leg unit. The empty water bladder is then fastened around the legs.

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Figure 1 Continued. B, The top half of the rigid outer case is then bolted into position, enclosing the water bladder. A finger plethysmograph is connected to the back of the control console, as are electrocardiograph leads from the patient's chest (not seen). The connecting hoses shown are used to fill the water bladder from storage tanks in the control console and to intermittently pressurize the bladder with compressed air. Bladder pressure is also transmitted to the control console. C, The control console has several sections. A twin-channel oscilloscope and paper recorder displays the EKG signal and arterial pressure pulse (obtained from either a transducer or finger plethysmograph). The system control module (lower righthand corner) permits precise control of the timing and amplitude of the cyclic pressure changes. The control console is mounted on wheels and can be positioned either at the foot or at the side of the patient's bed.

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EXPERIMENTAL STUDIES USING EXTERNAL COUNTERPULSATION General Hemodynamics Early studies of external counterpulsation in dogs 9 • 27 showed that the tension-time index and left ventricular systolic pressure were reduced and aortic diastolic pressure elevated to the level of control systolic pressure. Cardiac output increased 30 per cent. Later studies confirmed these results and also showed cyclic changes in venous return, which decreased when pumping chamber pressure was lowered and increased when it was raised. Coronary Blood Flow Coronary blood flow data have been harder to obtain. An indirect assessment of the effects of external counterpulsation on coronary collateral circulation 19 showed that canine left ventricular myocardium recovered more rapidly from the ischemia produced by coronary artery ligation when external counterpulsation was started as soon as the artery was ligated. In another indirect study,14 epicardial ST segment mapping was used to define the zone of myocardial ischemia resulting from ligation of a coronary artery branch. External counterpulsation resulted in a 30 per cent decrease in the size of the ischemic area, with no alteration in hemodynamic parameters other than a consistent increase in peak aortic diastolic pressure. Two recent studies using direct techniques to measure coronary blood flow have shown opposite results. Watson and co-workers 34 measured both total and regional coronary flow, the latter using radioactive microspheres. When external counterpulsation was started immediately after the second of two serial coronary artery ligations, coronary collateral flow increased by almost 30 per cent. The most significant increase occurred in the subepicardium, with less clear increases in the subendocardial region. Blood flow to the papillary muscles increased significantly, but there was no change in flow to the nonischemic region, the ventricular septum, or total coronary blood flow. Peak aortic diastolic pressure increased significantly with no change in any other hemodynamic parameter. External and intraortic balloon counterpulsation produced changes of similar magnitude in collateral coronary flow. Silverstein and co-workers30 used radionuclide-tagged macroaggregated albumin to measure the distribution of coronary blood flow distal to a ligated left anterior descending coronary artery. Maximal external pressure diastolic augmentation begun immediately after ligation produced a slight increase in coronary collateral flow compared to that occurring spontaneously, but it was not statistically significant. Mean coronary flow increased 6 per cent. If pumping pressures were reduced to those reachable in man (peak diastolic pressure during pumping equal to peak systolic pressure before), or if the start of counterpulsation were delayed, even less collateral flow increase or none at all resulted. Further studies are needed to clarify these issues.

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CLINICAL USE OF EXTERNAL COUNTERPULSATION Acute Myocardial Infarction without Shock Mueller and co-workers 24 ,25 studied 13 patients with acute transmural myocardial infarction without shock within 6 to 8 hours of the clinical onset of infarction. Data were collected before pumping, after 90 minutes of pumping while still receiving assistance, and 1 hour after termination of pumping. Diastolic aortic pressure was significantly increased while systolic aortic pressure fell slightly. Resistance to left ventricular ejection decreased 24 per cent, with a corresponding rise in stroke index. Cardiac index increased and pulmonary wedge pressure fell. Those patients obtaining excellent diastolic augmentation had little decrease in left ventricular ejection resistance while those with poor augmentation had more striking decreases in resistance to ejection. These investigators felt that those patients with low cardiac outputs and peripheral vasoconstriction responded to external counterpulsation predominantly with systolic unloading and improvement in peripheral perfusion, with less prominent diastolic augmentation. Patients with relatively normal pre pumping hemodynamics responded mainly with diastolic pressure augmentation. Coronary blood flow increased significantly and abnormal lactate metabolism (present in nine of the 13 patients) reverted to normal. Coronary sinus oxygen tension also increased significantly. The improvements in coronary blood flow and lactate metabolism were still present 1 hour after termination of pumping, suggesting that the benefits of external counterpulsation (perhaps the opening of coronary collateral channels 13 ) persisted for longer than the actual pumping period. Generally, similar results have been reported by Parmley and coworkers 28 and AI-Sadir and co-workers.1 Diastolic pressure, stroke work index, and cardiac index rose significantly. Systolic aortic pressure did not change significantly, and in contrast to the previous study no change was observed in coronary sinus flow, myocardial lactate metabolism, or myocardial oxygen consumption. The addition of sodium nitroprusside 28 produced additional benefit in those patients receiving external counterpulsation by decreasing aortic and left ventricular systolic pressures. Recently, Gowda and co-workers12 compared estimated infarct size and frequency of premature ventricular contractions in 13 patients with acute myocardial infarction treated with external counterpulsation and 13 conventionally managed infarct patients. Infarct size was predicted from projected serum CPK levels and compared to observed infarct size calculated from actual serum CPK levels. Although pumping did not result in a clear reduction in calculated infarct size, the frequency of the arrhythmia decreased in the counterpulsation group.

Cardiogenic Shock Following Acute Myocardial Infarction Soroff and co-workers 33 applied external counterpulsation using negative systolic pressure to 20 patients with cardiogenic shock following myocardial infarction. Nine patients (45 per cent) survived the shock state, a considerable improvement over the usual survival rate of 5 to 15

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per cent. All patients who responded did so within several hours and there seemed to be little benefit in applying the treatment for more than 6 hours. This surviv3.I rate was obtained despite a relatively long interval from the time of diagnosis of shock to the onset of treatment (10 hours for the deaths, 81f2 hours for the survivors). Singh and co-workers 31 compared the intra-aortic balloon method to external counterpulsation in 20 patients, ten treated with the balloon and ten with external compression. The two groups were similar in all major respects prior to treatment, and conformed to the rigorous definition of shock proposed by the Myocardial Infarction Research Units of the National Institutes of Health. Both forms of assistance increased diastolic aortic pressure and cardiac index, and decreased pulmonary wedge pressure and resistance to left ventricular ejection. In all cases, however, changes were of greater magnitude with the intra-aortic balloon than with external assist (negative pressure during cardiac systole was not used in these patients). Peak systolic aortic pressure decreased during balloon pumping but was unchanged with external assist. Right atrial pressure was elevated in both groups and did not change during either form of assistance. Coronary blood flow was increased by balloon pumping, while myocardial oxygen extraction and lactate utilization strikingly improved. The changes in these parameters were similar but less in magnitude with external counterpulsation. The most striking difference between the two types of cardiac assistance was the decrease in myocardial oxygen consumption seen with the balloon and the increase with external assist. In these patients external assist appeared to increase myocardial oxygen supply with less of an effect on cardiac work, resulting in a net increase in myocardial oxygen demand. The shock state could be reversed in all ten balloon-treated patients, but only two were long-term survivors. None of the externally assisted patients survived. The authors concluded that in profound shock following myocardial infarction, the balloon technique is superior to external counterpulsation. The extremely high mortality even in the balloon group, however, suggests that earlier institution of assistance may be necessary, and several patients in earlier stages of shock in their unit did very well following external counterpulsation (Mueller, H.: Personal communication). Beckman and co-workers 3 studied 22 patients with shock refractory to steroids and divided into three groups: postcardiotomy low-output syndrome (5 patients); acute myocardial infarction with shock (9 patients); and failure to come off cardiopulmonary bypass (8 patients). Diastolic augmentation was achieved in both groups, as was a rise in cardiac index. Systolic arterial pressure and tension-time index were decreased by the balloon, but not by external assist. Two patients with cardiac tamponade were strikingly improved by external pumping but not helped at all by the balloon (perhaps related to the slight increase in central blood volume seen with external assistance). Studies to date would therefore seem to indicate that in far advanced cardiogenic shock following myocardial infarction, the intra-aortic balloon is somewhat more effective hemodynamically than external

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counterpulsation, although in most cases the mortality is still extremely high. The striking success of Soroff's group33 is an exception, perhaps related to differences in patient selection but also to their use of a negative pressure phase during systole, providing more effective systolic unloading of the left ventricle. An alternative approach is the combined use of a vasodilator (such as nitroprusside) to lower aortic and left ventricular systolic pressure and external counterpulsation to raise diastolic aortic and coronary perfusion pressure. Further work is in progress 8 to see whether early and aggressive use of a noninvasive method of assistance such as external counterpulsation in patients with myocardial infarction without shock can reduce the incidence of progression to shock and/or reduce the morbidity and mortality of acute myocardial infarction in other respects. Additional studies of external counterpulsation are also needed in patients in the earliest stages of cardiogenic shock, rather than waiting for failure to respond to conventional medical therapy. The noninvasive nature of external assistance and its conspicuous lack of morbidity and ease of application make it an ideal therapeutic intervention if efficacy can be established.

Angina Pectoris Because of its ability to increase coronary perfusion pressure, external counterpulsation has been evaluated under several experimental conditions in patients with angina pectoris due to obstructive coronary disease. Banas and co-workers2 treated 21 patients with angina pectoris, 20 of whom had frequent and incapacitating pain, with 1 hour of pumping for 5 days. Significant aortic diastolic pressure augmentation was produced in 18 patients, of whom 17 were free of pain by the 4th day of treatment. One month later most of the patients had less frequent pain than was present before pumping. The three patients whose diastolic pressure had not been raised showed no change in their pain pattern. Repeat coronary arteriography 4 to 8 weeks after counterpulsation was inconclusive. In four patients whose angina recurred 4 to 6 months after pumping, repeat counterpulsation again relieved the pain. These workers 5 then compared sham and true counterpulsation in another group of 18 patients with severe angina pectoris, using bicycle ergometry, nitroglycerin usage, and functional class before and after treatment as parameters for evaluation. Sham counterpulsation was performed 2 hours daily for 5 days, producing no diastolic pressure augmentation. Pumping was then done in identical fashion, significantly elevating aortic diastolic pressure. No change in functional class, nitroglycerin usage, or heart rate-systolic pressure product with exercise followed sham pumping, but 11 of the 18 patients showed significant improvement in these parameters after true pumping. The coronary arteriograms of the improved patients showed somewhat less extensive disease than those of the seven nonimproved patients, although both groups had significant symptoms and were being treated with nitrates and propranolol. Thus the anatomy of the coronary vascular obstruction may be an important determinant of the response of the coronary bed to aortic diastolic pressure elevation. These results could not be corroborated by

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Loeb and co-workers,2!' 22 who used atrial pacing to produce either angina or a heart rate of 150 per minute. These workers 15 did, however, document a modest improvement in exercise tolerance in 14 patients with angina pumped for five I-hour sessions.

Sequenced External Counterpulsation A modification of external assist in which the legs are compressed sequentially (first distally and then proximally), rather than all at once, has also been tested. 7 Although peak diastolic augmentation was equal in both forms of external assist, cardiac output was greater when sequenced pumping was performed, perhaps because of enhanced venous return resulting from the "milking" action exerted on the legs.

SUMMARY External counterpulsation represents a rational extension of the basic principles of counterpulsation as developed over the past 20 years. Its unique properties of being totally noninvasive, free of significant morbidity, and easily and quickly instituted clinically suggest that it may have a significant therapeutic role in the prevention and treatment of cardiogenic shock following acute myocardial infarction as well as being helpful in other cardiac disorders. Continuing evaluation is necessary, and it should be thought of as one of several useful mechanical circulatory assist devices now available to the internist, cardiologist, and surgeon caring for the critically ill patient. 4

REFERENCES 1. AI-Sadir, J., Zimmet, L., Brooks, H., King, S., and Resnekov, L.: Hemodynamic evaluation of external counterpulsation in acute myocardial infarction. Clin. Res., 21 :396 (abst.), 1973. 2. Banas, J. S., Brilla, A., and Levine, H. J.: Evaluation of external counterpulsation for the treatment of angina pectoris. Am. J. Card., 31 :118 (abst.), 1973. 3. Beckman, C. B., Romero., L. H., Shatney, C. H., Nicoloff, D. M., Lillehei, R C., and Dietzman, R H.: Clinical comparison of the intra-aortic balloon pump and external counterpulsation for cardiogenic shock. Trans. Am. Soc. Artif. Int. Organs, 19:414, 1973. 4. Broder, M. I.: Circulatory assistance with external counterpulsation. In Berk, J. L. (ed.): Manual of Critical Care. Boston, Little, Brown and Co., in press. 5. Clapp, J. C., Banas, J. S., Stickley, L. P., Salem, D. N., Pollak, R. H., and Levine, H. J.: Evaluation of sham and true external counterpulsation in patients with angina pectoris. Circulation, 49-50 (SuppL 111):111-108 (abst.), 1974. 6. Clauss, R H., Birtwell, W. C., Albertal, G., Lunzer, S., Taylor,.W. J., Fosberg, A. M., and Harken, D.' E.: Assisted circulation. I. The arterial counterpulsator. J. Thorac. Cardiovasc. Surg., 41 :447, 1961. 7. Cohen, L. S., Langou, R, Wolfson, S., Porterfield, D., and Mitchell, J. H.: Hemodynamic studies of sequenced and non-sequenced external counterpulsation. Am. J. Card., 33: 131 (abst.), 1974. 8. Co-operative study: Assessment of the capability of external pressure circulatory assist to reduce the morbidity and mortality of left ventricular failure secondary to acute myocardial infarction. Sponsored by Medical Innovations. Inc., Waltham, Mass. 9. Dennis, C., Moreno, J. R., Hall, D. P., Grosz, C., Ross, S. M., Wesolowski, S., and Senning, A.: Studies on external counterpulsation as a potential measure for acute left heart failure. Trans. Am. Soc. Artif. Int. Organs, 9:186, 1963.

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10. Furman, S., Whitman, R., Stewart, J., Parker, B., and McMullen, M.: Proximity to aortic valve and unidirectionality as prime factors in counterpulsation effectiveness. Trans. Am. Soc. Artif. Organs, 17:153, 1971. 11. Giron, F., Birtwell, W. C., Soroff, H. S., Ruiz, U., Collins, J. A., and Deterling, R. A. Jr.: Assisted circulation by synchronous pulsation of extramural pressure. Surgery, 60:894, 1966. . 12. Gowda, K. S., Roberts, R., Ambos, H. D., and Sobel, B. E.: Salutary effects of external counterpulsation in patients with acute myocardial infarction. Am. J. Card., 35:140 (abst.), 1975. 13. Jacobey, J. A., Taylor, W. J., Smith, G. T., Godin, R., and Harken, D. E.: A new therapeutic approach to acute coronary occlusion. II. Opening dormant coronary collateral channels by counterpulsation. Am. J. Card., 11 :218, 1963. 14. Johansen, K. H., DeLaria, G. A., and Bernstein, E. F.: Effect of external counterpulsation in reduction of the myocardial ischemia following coronary artery occlusion. Trans. Am. Soc. Artif. Int. Organs, 19:419, 1973. 15. Johnson, S., Loeb., H. S., Kahn, M., Towne, W., and Gunnar, R. M.: Clinical response in patients with coronary artery disease to external counterpulsation. Circulation, 47-48 (Suppl. IV): IV-59, (abst.), 1973. 16. Kantrowitz, A., and Kantrowitz, A.: Experimental augmentation of coronary flow by retardation of the arterial pressure pulse. Surgery, 34:678, 1953. 17. Kantrowitz, A., and McKinnon, W. M. P.: The experimental use of the diaphragm as an auxiliary myocardium. Surg. Forum, 9:266, 1958. 18. Kantrowitz, A., Sherman, J. L., Jr., and Krakauer, J.: Clinical experience with permanent mechanical circulatory assistance. Prog. Cardiovasc. Dis., 10:134, 1967. 19. Kataoka, K., Birtwell, W. C., Norton, R. L., and Soroff, H. S.: Experimental evaluation of coronary collateral enhancement by external counterpulsation. Trans. Am. Soc. Artif. Int. Organs, 19:408, 1973. 20. Liotta, D., Hall, C. W., Henley, W. S., Beall, A. C., Jr., Cooley, D. A., and DeBakey, M. E.: Prolonged assisted circulation during and after heart or aortic surgery. Trans. Am. Soc. Artif. Int. Organs, 9:182,1963. 21. Loeb, H. S., Khan, M., Towne, W., and Gunnar, R. M.: Effects of external counterpulsation on myocardial ischemia induced by atrial pacing. Circulation, 49-50 (Suppl. 11):11-255, 1974. 22. Loeb, H. S., Khan, M., Towne, W., and Gunnar, R. M.: Acute effects of external counterpulsation on the relationship between myocardial oxygen delivery and requirement in patients with coronary artery disease. Am. J. Card., 33:153, (abst.), 1974. 23. Moulopoulos, S. D., Topaz, 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. 24. Mueller, H., Ayres, S. M., and Grace, W. J.: Hemodynamic and myocardial metabolic response to external counterpulsation in acute myocardial infarction in man. Am. J. Card., 31: 149 (abst.), 1973. 25. Mueller, H., Evans, R., and Ayres, S.: External counterpulsation-a non-invasive form of cardiac assistance. Am. J. Card., 33:158 (abst.), 1974. 26. Norton, R. L., Kataoka, K., Birtwell, W. C., and Soroff, H. S.: Effects of change of ambient pressure differential on the effectiveness of peripheral external assist. Trans. Am. Soc. Artif. Int. Organs, 17:169, 1971. 27. Osborn, J., Main, F. B., and Gerbode, E. L.: Circulatory support by leg or airway pulses in experimental mitral insufficiency. Circulation, 28:781 (abst.), 1963. 28. Parmley, W. W., Chatterjee, K., Charuzi, T., and Swan, H. J. C.: Hemodynamic effects of noninvasive systolic unloading (nitroprusside) and diastolic augmentation (external counterpulsation) in patients with acute myocardial infarction. Am. J. Card., 33:819, 1974. 29. Sarnoff, S. J., Braunwald, E., Welch, G. H., Jr., Case, R. B., Stainsby, W. N., and Macruz, R.: Hemodynamic determinants of oxygen consumption of the heart with special reference to the tension-time index. Am. J. Physiol., 192:148, 1958. 30. Silverstein, D. M., Hamilton, G. W., and Hammermeister, K. E.: The effect of external pressure diastolic augmentation on the perfusion of the acutely ischemic myocardium. Circulation, 49-50 (Suppl. III): 111-140 (abst.), 1974. 31. Singh, J., Mueller, H., and Ayres, S.: Invasive versus noninvasive cardiac assistance in myocardial infarction shock in man. Circulation, 49-50 (Suppl. 111):111-108 (abst.), 1974. 32. Soroff, H. S., Birtwell, W. C., Giron, F., Collins, J. A., and Deterling, R. A., Jr.: Support of the systemic circulation and left ventricular assist by synchronous pulsation of extramural pressure. Surg. Forum, 16:148, 1965. 33. Soroff, H. S., Cloutier, C. T., Birtwell, W. C., Begley, L. A., and Messer, J. V.: External counterpulsation. Management of cardiogenic shock after myocardial infarction. J.A.M.A., 229:1441,1974.

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34. Sugg, W. L., Watson, J. T., Platt, M. R, and Willerson, J. T.: Similarities between external counterpulsation and intra-aortic balloon pumping: Influence on collateral coronary blood flow in ischemic myocardium. Circulation, 49-50 (SuppI. III): III-69 (abst.), 1974. 35. Watkins, D. H., and Duchesne, E. R: Postsystolic myocardial augmentation: 1. Effect upon an induced shock state. Proc. Soc. Exper. BioI. Med., 107:659, 1961. 36. Willman, V. L., Cooper, T., Riberi, A., and Hanlon, C. R: Cardiac assistance by diastolic augmentation: Hemodynamic evaluation in dogs with complete heart block. Trans. Am. Soc. Artif. Int. Organs, 7:198, 1961. Cardiac Care Unit Cleveland Metropolitan General Hospital 3395 Scranton Road Cleveland, Ohio 44109

External counterpulsation in low cardiac output states.

External counterpulsation represents a rational extension of the basic principles of counterpulsation as developed over the past 20 years. Its unique ...
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