Left Ventricular Contributions to Right Ventricular Systolic Function During LVAD Support

Transcription

1 Left Ventrcular Contrbutons to Rght Ventrcular Systolc Functon Durng LVAD Support Wllam P. Santamore, PhD, and Laman A. Gray, Jr, MD Dvson of Thoracc and Cardovascular Surgery, Unversty of Lousvlle, Lousvlle, Kentucky Background. In patents wth postcardotomy low cardac output syndromes, rght ventrcular (RV) falure develops n approxmately 25% of patents recevng left ventrcular (LV) assst devce suppmt. Depresaed RV functon have been attrbuted to a b u ~ of the RV myocardum, excessve load ntpomed on the RV durng systole or dastole, or obstructon to llv nflow. However, recent studes also suggest that LV functon may sgnfcantly affect RV functon through ventrcular nterdependence. Methods. We revewed the data showng the mportance of systolc ventrcular nteractmt. We then related these observatons to the RV response durng LV assst devce support, and present our deas rekardn 8 the mechansms responsble for ths RV falure. Results. Usng an electrc.ally solated rght heart preparaton, Damano observed double-peaked waveforms for RV pressure, and pulmonary artery blood flow oc- he major cause of death after coronary revascularza- T ton s postoperatve low cardac output, usually resultng from acute, often reversble, peroperatve myocardal njury [1]. Between 4% and 7% of patents who undergo cardac procedures wth cardopulmonary bypass requre hemodynamc support wth ntraaortc balloon counterpulsaton; up to 2% of patents requre other forms of mechancal crculatory support [1, 2]. A survval rate of up to 50% has been reported wth the use of a left ventrcular assst devce (LVAD) n patents wth postcardotomy low cardac output syndromes. However, rght ventrcular falure wll develop n appro~nately 25% of patents recevng LVAD support [1-,3]. The major determnant of survval after LVAD placement s the ablty of the rght ventrcle to provde suffcent output to fll the LVAD tself. If severe rght ventrcular falure develops, cardovascular collapse wll occur and the patent wll not survve wthout bventrcular support. For example, Pennngton and assocates reported that n 26 patents wth bventrcular falure, 16 receved only LVAD support and none survved [2]. In the 10 patents who receved bventrcular support, 5 were weaned and 3 survved. Thus, although patents wth solated left ventrtcular alure do well wth an LVAD only, those wth bventrcular falure requre Presented at The Thrd Internatonal Conference on Crculatory Support Devces for Severe Cardac Falure, Pttsburgh, PA, Oct 28-30, 1994, Address reprnt requests to Dr Santamore, Dvson of Thoracc and Cardovascular Surgery, Unversty of Lousvlle, Lousvlle, KY curred over a wde range (0 to 300 ms) of pacng ntervals between the LV and RV. Numerc analyss ndcated that RV ~rstolc pressure and pulmonary artery blood flow were composed of both RV and LV components, wth the LV component domnatng (63.5% versus 36.5%). Concl~aons. The expermental studes ndcate a very consstent RV response durng LV assst devce support: a d~e~e n RV afterload, ncreased complance, and decreased contractlty. In normal hearts, the net effect s an ncrease or no change n cardac output. Wth a preexstng pathologc condton, the RV responses s qualtatvely the same, but anatomc ventrcular nteracton s accentuated, leadng to a greater decrease n RV contractlty. The net effect s a decrease n cardac output, whch may requre notropc or RV mechancal support. (Ann Thorac Surg 1996;61:350-6) bventrcular mechancal support for survval. Further, because delay n the decson to use an assst devce ncreases morbdty and mortalty, predctng whch patents are susceptble to rght ventrcular falure would mprove clncal outcome. Abnormaltes of rght ventrcular functon have been classcally attrbuted to prmary abnormaltes of the rght ventrcular myocardum, excessve load mposed on the rght ventrcular durng systole or dastole, or obstructon to rght ventrcular nflow. However, recent studes have also suggested that, n addton to the above mechansms, left ventrcular functon may sgnfcantly affect rght ventrcular functon. Ths so-called ventrcular nterdependence s defned heren as the forces that are transmtted from one ventrcle to the other ventrcle through the myocardum and percardum, ndependent of neural, humoral, or crculatory effects [4]. These ventrcular ndependent effects are mmedate as compared wth crculatory changes, whch requre several beats. Ventrcular nterdependence s a consequence of the close anatomc assocaton between the ventrcles: the ventrcles are encrcled by common muscle fbers, share a septal wall, and are enclosed wthn the percardum. In ths artcle, we wll frst brefly revew the mechansms for dastolc ventrcular nteracton, followed by a more n-depth revew of recent data showng the mportance of systolc ventrcular nteracton. We wll then relate these observatons to the rght ventrcular response durng LVAD support, and present our deas 1996 by The Socety of Thoracc Surgeons /96/$15.00 Publshed by Elsever Scence Inc SSDI (95)

2 Ann Thorac Surg CIRCULATORY SUPPORT SANTAMORE AND GRAY ;61:350-6 LVAD AND RIGHT VENTRICULAR FUNCTION ,o 80 t, o ' t f*~ k 201 o,,+ ~ r.r,+,,l 1,10 f 'O! lo! 10o so 1 4O L.\ f,+ lo 0 ~4)'t c 4S 40 o as 1SO 100 S0 I0 16 SO 10 S IOl ~ 401 m Fg 1. From an acute canne study. (A) Plot of le~ and rght ventrcular pressure. A partal constrcton of the pulmonary artery (or aorta n C) was released n daatole. On the subsequent sys~alc contracton, both left and rght ventrcular systolc decrease. (B) Le~ ventrcular pressure plotted before (sold lne) and after (dashed lne) pu/monary artery release. (D) Rght ventrcular pressure plotted before (sold lne) and a~er (dashed lne) aortc release. seoomls S regardng the mechansms responsble for ths rght ventrcular falure. Dastolc Ventrcular Interacton The evdence for dastolc ventrcular nteracton s ndsputable, and has been the source of n-depth revews [4, 5]. Brefly, the volume or pressure n one ventrcle can drectly nfluence the volume and pressure n the other ventrcle. Ths phenomenon, ventrcular nterdependence, was probably frst observed by Hendemon and Prnce n 1914 and later verfed n postmortem [6] and n solated heart preparatons [7, 8]. Increased dstenton of ether ventrcle durng dastole alters the complance and geometry of the opposte ventrcle. Taylor and assocates [6] n postmortem hearts and Santamore and colleagues [8] and Elznga and co-workers 7] n solated beatng hearts observed acute changes n ventrcular dstensblty caused by changng the volume of the opposte ventrcle. As left (or rght) ventrcular volume and pressure ncreased, the rght (or left) ventrcular pressurevolume curve shfted to the left and became steeper. Ths dastolc nteracton occurred even wth the percardum open, although the couplng was stronger wth t closed [91. Dastolc ventrcular nterdependence s present on a moment-to-moment, beat-to-beat bass; e, part of the measured dastolc ventrcular pressure s caused by the opposte ventrcle. Although always present, ventrcular nterdependence s most apparent wth sudden changes n ventrcular volume. For example, durng spontaneous nspraton, rght ventrcular dmensons and volume ncrease [10]. Concomtant wth these changes, left atral transmural pressure ncreases and the septum moves toward the left ventrcle n dastole [10]. Left ventrcular end-dastolc volume ether remans unaltered or decreases. Ths ncrease n fllng pressure wth a decrease n volume s consstent wth a change n left ventrcular dstensblty. Thus, dastolc nteracton s always present and the nteractons are large enough to be of physologc and pathophysologc mportance. Systolc Ventrcular Interacton In recent years, the evdence for systolc ventrcular nteracton s becomng ndsputable. In the sectons that follow, we revew the studes demonstratng the exstence, magntude, and mechansms of systolc ventrcular nterdependence. Exstence Fgure I shows a very smple way to demonstrate systolc ventrcular nterdependence. Left and rght ventrcular pressures are recorded, whle suddenly n dastole a partal constrcton of the aorta s released (Fg 1A, B). On the subsequent systole, not only does rght ventrcular systolc pressure decrease, but left ventrcular systolc pressure also decreases slghtly. Because preload was not altered, only systolc ventrcular nterdependence can explan ths decrease n left ventrcular pressure. Fgure 1 also shows the complementary study for the rght ventrcle. An aortc constrcton s released n dastole, lead-

3 352 CIRCULATORY SUPPORT SANTAMORE AND GRAY Ann Thorac Surg LVAD AND RIGHT VENTRICULAR FUNCTION 1996;61:350-6 Fg 2. The upper four tracngs are ventrcular assst devce pneumatc drve pressure CL DRIVE P), left and rght ventrcular pressure (LVP and RVP, respectvely), and pulmonary artery flow (Q PA). The lower three tracngs are the d~erences between each beat and the precedng beat (del). Durng left ventrcular unloadng, rght ventrcular pressure and ~low are markedly reduced as a result of systofc ventrcular nteracton. (Reprnted from Wvodard ]C, Chow E, Farrar D]. Isolated ventrcular systolc nteracton durng transent reductons n left ventrcular pressure. Crc Res 1992;70: Copyrght 1992, Amercan Heart Assocaton.)! UNLOAD l O,O ~ 4.8 ng on the subsequent systolc contracton to a decrease n left ventrcular systolc pressure and also, through ventrcular nterdependence, to a decrease n rght ventrcular systolc pressure. A number of studes have revealed smlar observatons [7, 8, 11, 12]. Intal studes employed solated heart preparatons to break the crculatory connectons and thus demonstrate ventrcular nterdel~enduence. These studes showed that ncreasng the pressure or volume n one ventrcle leads to an ncrease n both the dastolc and systolc pressure n the other ventrcle. Expermental studes have also shown that ths systolc nteracton s an mmedate effect: rapd wthdrawal or njectons nto the left ventrcle caused mmedate changes n rght ventrcular pressure and volume outflow [4, 13]. In whole anmal studes, Woodard and assocates [13] used a ventrcular assst devce to rapdly wthdraw blood from the left ventrcle. Ths wthdrawal occurred n systole durng a sngle cardac cycle. Fsure 2 show~ the typcal response. The wthdrawal of blood from the left ventrcle caused a rapd decrease n left ventrcular pressure. Rght ventrcular pressure and flow outflow also decreased, resultng n a large change n developed pressure and outflow. These studes show that systolc ventrcular nterdependence can have a purely systolc component. Injecton or wthdrawal of flud from the left ventrcle durng systole caused mmedate changes n rght ventrcular pressure. Magntude Although these studes proved the exstence of systolc ventrcular nterdependence, they dd not quantfy the magntude of systolc nterdependence on rght ventrcular functon. Are these observatons just nterestng phenomenon or are they physologcally mportant wth sgnfcant clncal mplcatons? Two studes addressed ths queston and quantfed the magntude of ths left ventncular assstance, usng an electrcally solated rght heart preparaton [14, 15]. The electrcally solated rght heart preparaton allowed for wde varatons n the tmng nterval between rght and left ventrcular contractons. Double-peaked waveforms for rght ventrcular pressure and pulmonary artery blood flow occurred over a wde range (0 to 300 ms) of pacng ntervals between the left and rght ventrcles (Fg 3). Numerc analyss ndcated that these pressures and volume waveforms were due to two components [14]. One component could be drectly related to rght ventrcular contracton, whereas the other component was drectly related to left ventrcular contracton. Rght ventrcular systolc pressure and pulmonary artery blood flow were composed of both rght ventrcular and left ventrcular components, wth the left ventrcular component domnatng. For rght ventroalar pressure, the left ventrcular component was sgnfcantly greater than the rght ventrcular compo- I.V RA-RV RA-RV RA-RV RA-I;fV lo luec 120 me{: IO0 Id$[ 240 IdS( Fg 3. Left ventrcular (LV) pressure, rght ventrcular (RV) pressure, and volume ou~iow are presented at 60-, 120-, 180-, and 240-ms delay between rght atral (RA) and RV pacng. At 60 ms delay, RV pressure and volume outflow are double-peaked waveforms wth one peak occurrng before L V pressure. At 240 ms delay, RV pressure and volume ou~ are agan double-peaked waveforms but wth one peak occurrng after LV pressure. (PA = pulmonary artery.) (From Damano et al [14], wth permsson.)

4 Ann Thorac Surg CIRCULATORY SUPPORT SANTAMORE AND GRAY ;61:350-6 LVAD AND RIGHT VENTRICULAR FUNCTION [ RV Free Wall drectly affects all three walls; e, a drect transfer of forces between the left and rght ventrcular free walls and septum occurs. Thus, changng left ventrcular volume not only alters the left ventrcular free wall and septum, but also alters the dmensons of the fght ventrcular free wall [19]. y A Tr! LV Free Wall Fg 4. Balance of forces at the nterventrcular sulcus. The top panel shows cross-secton of heart. The summaton of the forces at the sulcus s zero. The bottom panel shows how the stress or tenson (T 1) n the left ventrcular CLV) free wall s balanced by the tenson n both the septum (T~) and the rght ventrcular (CRV) free wall (T~). (Reprnted wth permsson from Santamore WP, Gray L Jr. Sgnfcant left ventrcular contrbutons to fght ventrcular systolc functon: mechansm and clncal mplcatons. Chest 1995;107: ) nent (63.5% versus 36.5% peak-to-peak value; 65.2% versus 34.8% root-mean-square value). Smlarly, for pulmonary artery blood flow, the left ventrcular component was sgnfcantly greater than the rght ventrcular component (67.5% versus 32.5% peak-to-peak value; 68.3% versus 31.8% root-mean-square value). Ths study shows that left ventrcular contracton s very mportant and may be the prmary source for rght ventrcular developed pressure and volume outflow [14]. Mechansm The above studes have clearly shown that ventrcular nterdependence exsts, that a sgnfcant porton of rght ventrcular developed pressure and volume outflow depends on left ventrcular functon, and that systolc nteracton s mmedate: rapd left ventrcular volume changes result n mmedate changes n fght ventrcular pressure and volume outflow [4, 13]. Many nvestgators have attrbuted ventrcular nterdependence to transseptal pressure gradents, septal moton, ventrcular wall characterstcs, and other factors [7, 10, 16-18]. However, ventrcular pressures and volumes are really a consequence of the stress n the ventrcular walls. Thus, we beleve that ventrcular nterdependence should be vewed as the balance of forces at the nterventrcular sulcus [18] (Fg 4). At ths juncton, the force n the left ventrcular free wall s balanced by forces n the rght ventrcular free wall and nterventrcular septum. Ths vew mples that changng one wall Hemodynamc Consequences of Systolc Ventrcular Interdependence Left Ventrcular Assst Devces The expermental studes ndcate a very consstent rght ventrcular response to left ventrcular unloadng by cardac assst devces (LVADs): a decrease n rght ventrcular afterload, ncreased complance, and decreased contractlty [20-24]. In normal hearts, the net effect s an ncrease or no change n cardac output. In an eloquent canne study, Moon and colleagues [20] mplanted tantalum markers nto the left and rght ventrcular walls for computaton of bventrcular volumes and geometry. Wth full LVAD support, left ventrcular end-dastolc volume decreased and pulmonary artery nput mpedance decreased. Rght ventrcular end-dastolc volume ncreased, whle rght ventrcular end-dastolc pressure decreased. A sgnfcant leftward septal shft occurred. The rght ventrcular pressure, volume, and dmenson changes showed an ncrease n rght ventrcular complance. Global rght ventrcular end-systolc elastance and preload recrutable stroke work decreased; however, rght ventrcular power output dd not change sgnfcantly due to smultaneous changes n rght ventrcular preload and afterload. Other expermental studes have shown smlar changes n rght ventrcular afterload, complance, and contractlty. In normal dogs, Farrar and assocates [21] observed sgnfcant reductons n rght ventrcular peak systolc pressure and mean pulmonary arteral pressure ndcatng a reduced afterload. No sgnfcant changes n cardac output or rght ventrcular stroke volume oc -~ curred durng left ventrcular bypass. However, enddastolc volume, stroke volume, and ejecton fracton were unchanged n response to the reduced afterload. Further, the maxmum and mnmum rates of change n rght ventrcular pressure and the maxmum rate of change n pulmonary arteral flow were reduced, suggestng reductons n fght ventrcular contractlty. In dogs, Fukamach and co-workers [22] observed that left heart bypass decreased pulmonary arteral resstance (-15%), ncreased rght ventrcular chamber complance (38%), and decreased the slope of the rght ventrcular end-dastolc pressure versus cardac output relatonshp. The net effect of the left heart bypass was an ncrease n cardac output (20%) for any gven rght ventrcular end-dastolc pressure. Elbeery and assocates [23] showed that durng full support, left ventrcular end-dastolc volume decreased by 31%, left ventrcular septal-free wall dameter decreased by 7%, and the rate of rse of rght ventrcular pressure declned by 13%. Analyss of fght ventrcular end-dastolc pressurevolume relatonshps suggested mproved fght ventrcular chamber complance. In dogs, Myamoto and colleagues [24] observed that ncremental ncreases n the

5 354 CIRCULATORY SUPPORT SANTAMORE AND GRAY Ann Thorac Surg LVAD AND RIGHT VENTRICULAR FUNCTION 1996;61:350-6 level of left ventrcular unloadng resulted n ncremental decreases n the rate of rght ventrcular pressure change. Therefore, durng LVAD support, global rght ventrcular contractlty s mpared wth leftward septal shftng, but rght ventrcular myocardal effcency and power output are mantaned through a decrease n rght ventrcular afterload and an ncrease n rght ventrcular preload. However, not all the studes have observed a decrease n rght ventrcular contractlty. In pgs, Chow and assocates [25] calculated rght ventrcular maxmal systolc elastance as the slope between an sovolumc beat and a seres of transently occluded beats. Durng LVAD support, there were no sgnfcant changes n cardac output, mean systemc arteral pressure, or n maxmum rate of change of rght ventrcular pressure. Most mportant, rght ventrcular maxmal systolc elastance durng LVAD unloadng was unchanged from control. Wth a preexstng pathologc condton, such as regonal myocardal schema, the rght ventrcular response s qualtatvely the same: a decrease n rght ventrcular afterload, ncreased complance, and decreased contractlty. However, because of the preexstng condton, anatomc ventrcular nteracton s accentuated, leadng to a greater decrease n rght ventrcular contractlty. The net effect s ether no change or a decrease n cardac output. For example, n pgs, LVAD support resulted n a leftward septal and a 13% ncrease n rght ventrcular septal-to-free wall dmenson, wth no changes n rght ventrcular cardac output or stroke work [26]. In contrast, rght coronary artery occluson alone produced rght heart falure wth a 50 /0 reducton n rght ventrcular global stroke work and 26% and 27% reductons n cardac output and rght ventrcular peak systolc pressure, respectvely. Durng LVAD support, rght heart falure perssted, whch resulted n further leftward septal shftng and unchanged but stll depressed stroke work and flow output. Chow and Farrar [27] produced congestve heart falure n pgs by rapd ventrcular pacng. Wth congestve heart falure, left ventrcular unloadng by assst devce led to a further mparment n cardac output (-14%), mean arteral pressure (-15%), and the slope of the rght ventrcular global stroke-work curve (-50%). Based on analyss of the rght ventrcular pressure and free wallto-septum dmenson data, left ventrcular pressure unloadng resulted n a 48% reducton n the slope and 20% ncrease n the dmenson ntercept of the preload recrutable stroke-work relatonshp. There was also a 45% reducton n the slope and 16% ncrease n the dmenson ntercept of the end-systolc pressure-dmenson relaton. These slope changes plus reductons n cardac output and global stroke work, whch are ndcatve of mpared rght ventrcular functon durng left ventrcular pressure unloadng n the congestve heart falure pgs, were not seen n normal hearts. In calves, when ventrcular functon was normal, establshment of left heart bypass dd not sgnfcantly affect rght ventrcular functon [28]. Septal schema durng support caused a rapd and remarkable ncreased n rght ventrcular short-axs dmenson n every experment. Rght ventrcular end-dastolc area ncreased durng septal schema by 275% and rght ventrcular fractonal area change decreased from 82% to 28%. Rght ventrcular developed pressure decreased and a further decrease n ntraventrcular septal wall thckenng occurred. The nterventrcular septum became thn wth flattenng of ts normal contour. Septal reperfuson resulted n rght ventrcular recovery wth sgnfcant mprovement n all factors. Nshgak and assocates [29] compared a control group wth groups wth schemc njures to the rght ventrcular free wall and nterventrcular septum. Wth LVAD support, septal schema shfted the rght ventrcular pressure-volume ponts to the rght, ndcatng sgnfcant depresson of functon. The response n human hearts s smlar to the expermental studes: decreased rght ventrcular afterload, ncreased rght ventrcular fllng, and an ncrease n cardac output wthout regonal schema. Farrar and co-workers [30] smulated an LVAD n the operatng room by bypassng and unloadng the left ventrcle wth the heart-lung machne before a routne open heart operaton. Durng bypass, n patents wth normal left ventrcular functon, mean pulmonary arteral pressure decreased from 17 to 10 mm Hg, whch resulted n a decrease n rght ventrcular end-dastolc pressure (from 8 to 6 nun Hg) wth no change n cardac output. However, n patents wth poor left ventrcular functon, durng bypass, pulmonary arteral pressure decreased from 27 to 12 mm Hg and rght ventrcular end-dastolc pressure decreased from 13 to 8 mm Hg. Ths caused an ncrease n cardac output durng left ventrcular bypass from 4.5 to 5.3 L/mn. Mechansm for Rght Ventrcular Falure Durng Left Ventrcular Assst Devce Support The seres crculatory connectons and ventrcular nterdependence help to explan the observed rght ventrcular responses to LVAD support. Va the crculatory connectons, decreasng left ventxcular preload wll decrease pulmonary artery pressure. Ths passve decrease n pulmonary pressures s caused by the reductons n left ventrcular fllng pressure durng left ventrcular bypass. Wth hgher ntal left ventrcular end-dastolc pressures, greater reductons n left ventrcular fllng pressures wll occur. Ths wll result n greater decreases n pulmonary artery pressure. Rght ventrcular fllng s ncreased by the ncreased left ventrcular output wth LVAD support (the seres crculatory component). Rght ventrcular fllng s further asssted by the decrease n left ventrcular dastolc volume (the ventrcular nterdependence component). The decrease n left ventrcular dastolc volume alters rght ventrcular complance, makng t easer to fll the rght ventrcle. The observed changes n rght ventrcular shape and septal poston and the observed ncreases n rght ventrcular volume wth rght ventrcular fllng pressure decreases reflect ths altered complance. Wthout ventrcular nterdependence, the reduced pulmonary artery pressure and ncreased rght ventrcular fllng would ncrease rght ventrcular stroke volume. Knoshta and colleagues [31] examned ths queston n calves wth artfcal hearts. The total artfcal heart

6 Ann Thorac Surg CIRCULATORY SUPPORT SANTAMORE AND GRAY ;61:350-6 LVAD AND RIGHT VENTRICULAR FUNCTION NORMAL LVAD SUPPORT A B C LVAD + SEPTAL ISCHEMIA Fg 5. Possble mechansm for rght ventrcular falure wth left ventrcular assst devce (LVAD) support. CLV = left ventrcle; RVFW = rght ventrcular free wall.) elmnated ventrcular nterdependence because the ventrcle dd not have anatomc or mechancal nteractons. Bventrcular falure was smulated by reducng both ventrcular drve pressures of the total artfcal heart. In the smulated condton, LVAD support decreased pulmonary artery pressure and ncreased cardac output. These postve effects have to compensate for the reduced left ventrcular systolc assstance, whch leads to a decrease n rght ventrcular systolc functon. Va ventrcular nterdependence, the decrease n left ventrcular systolc functon decreases left ven~cular assatance to rght ventrcular functon. Ths sets up a postve feedback mechansm: the decreased left ventrcular assstance decreases rght ventrcular systolc pressure and stroke volume, whch decrease left ventrcular fllng. Agan, ths depressed rght ventrcular functon va ventrcular nterdependence s reflected n the observed changes n rght ventrcular septal poston that persst throughout systole and the decreases n rght ventrcular elastance and maxmal rate of change of rght ventrcular pressure. As mentoned before, ventrcular nterdependence s best vewed as the balance of forces at the ntraventrcular sulcus. What s not obvous s that the stress n the left ventrcular wall s not zero, even when left ventrcular cavty pressure s zero: even wth no left ventrcular cavty pressure, stress s stll present n left ventrcular walls. For example, Kresh and assocates [32] measured left ventrcular ntramyocardal pressure. They demonstrated that despte total left ventrcular decompresson tenson-tme ndex less than zero the systolc pressuretme ntegral estmated usng ntramyocardal pressure was only slghtly reduced from 2,340 n a beatng ejectng heart to 2,080 n a beatng empty left ventrcular bypass. Further, the systolc pressure-tme ntegral could be ncreased by epnephrne nfuson despte the absence of left ventrcular tenson-tme changes. In a nonworkng cat heart preparaton, Mhalescu and Abel [33] measured sgnfcant ntramyocardal pressure although left ventrcular cavty pressure was zero. Although the heart s not performng pressure or volume work, t contnues to generate ntramyocardal stresses. Fgure 5 s a cartoon that summarzes the possble mechansms for rght ventrcular falure wth LVAD support. The rght ventrcle ejects blood through a unform reducton n ts free wall area and a decrease n the septal-to-free wall dstance [34]. Wth ts large surface area-to-volume rato, small decreases n septal-to-free wall dstance cause large volume dsplacements. Ths bellows effect was frst proposed by Rushmer and assocates [35], who consdered the rght ventrcular free wall and septum to be the hands holdng the bellows. Based on ventrcular nterdependence, we propose that one hand s the rght ventrcular free wall, whereas the other hand s the whole left ventrcle. Durng normal contractons (see Fg 5A), both contrbute to rght ventrcular ejecton. Wth LVAD support (see Fg 5B), rght ventrcular afterload s decreased. The rght ventrcular free wall moves more and contrbutes more (decreased afterload), whle the left ventrcle contrbutes less (due to the decrease n ventrcular nterdependence). Wth septal schema, the left ventrcle moves away from the rght ventrcle, a negatve contrbuton. The rght ventrcular free wall cannot compensate, and rght ventrcular falure occurs wth a decrease n cardac output. We would speculate that ths movement of the septum away from the rght ventrcular cavty and toward the left ventrcle probably occurs wth rght ventrcular falure. Durng systole, the change n the nterventrcular septum from ts normal shape to a flattened or nverted shape would result n a net moton of the septum away from the rght ventrcular cavty. Agan, gven the bellows-lke contracton of the rght ventrcle, ths septal moton wll greatly decrease rght ventrcular output, and may explan the observed rght ventrcular falure. What separates mld from severe rght ventrcular depresson wth LVAD support? Frst, underlyng rght ventrcular dysfuncton appears necessary. Second, the degree of rght ventrcular afterload reducton s mportant. Thrd, regonal schema s probably worse than global dysfuncton, especally of the septum. Kawa and assocates [36] evaluated the dfferental performance of the rght ventrcular free wall and septum to dentfy the need for addtonal rght ventrcular support. Cross-

7 356 CIRCULATORY SUPPORT SANTAMORE AND GRAY Ann Thorac Surg LVAD AND RIGHT VENTRICULAR FUNCTION 1996;61:350-6 sectonal vews of the rght ventrcle were obtaned mmedately before and 1 hour after Novacor LVAD (Novacor Dvson, Baxter Healthcare Corp, Irvne, CA) mplantaton n 12 consecutve patents usng transesophageal echocardography. Percentage change between premplantaton and po6tmplantaton rght ventrcular ejecton fracton, fractonal area change for the rght ventrcular free wall and the septum, and the fractonal shortenng of the free wau-to-septum dstance were reported for patents based on the need for rght ventrcular support: mnmal or maxmal. Wth LVAD support, patents showed a reducton n septal fractonal area change. However, ths reducton was most pronounced n patents requrng maxmal rght ventrcular support. The degree of septal mparment may explan the mechansm of rght ventrcular falure n patents on an LVAD. 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