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Ann Thorac Surg 1996;61:347-349
© 1996 The Society of Thoracic Surgeons

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Univentricular Versus Biventricular Support

Physiology of Univentricular Versus Biventricular Support

Department of Thoracic and Cardiovascular Surgery, La Pitie Hospital, Paris, France

Abstract

Right ventricular failure unresponsive to pharmacologic treatment occurs in approximately 20% to 30% of patients supported with a left ventricular assist device (LVAD). The effect of the assistance on right ventricular function is highly controversial. Increased venous return produced by an LVAD can affect right ventricular function by increasing preload. On the other hand, an LVAD can improve the filling of the right ventricle by unloading the left ventricle, reducing its chamber size and shifting the septum back to the left. Right ventricular function is highly afterload dependent, the ventricular function depending on the pulmonary vascular resistance. With a normal pulmonary vascular bed, the LVAD can improve right ventricular function by reducing right ventricular afterload. If there is a fixed high pulmonary pressure, however, the LVAD can increase right ventricular afterload and volume. We conclude that the right ventricle is dispensable if the pulmonary vascular bed is normal.

Right ventricular failure unresponsive to pharmacologic treatment occurs in approximately 20% to 30% of patients supported with a left ventricular assist device (LVAD) [1, 2]. Since the beginning of mechanical assistance this has been the major problem faced by medical teams with regard to recovery as well as bridge to transplantation. Today, with the lack of donors, patients require long-term support; therefore it is very important to know if they can be supported with only a wearable LVAD system, thus allowing increased mobility of the patient.

At the dawn of the chronic implantation phase, this problem is becoming more and more important with regard to better patient selection. Better knowledge of the physiology of univentricular or biventricular support is necessary. The effect of the assistance on the right ventricular function is highly controversial (Table 1). The physiology of this problem is not completely understood.

The right and left hearts have hemodynamic interactions: the two ventricles are in series, the left ventricular output becoming the input of the right. Mechanical interactions between the two ventricles exist because of anatomic coupling via the interventricular septum and common muscle fibers between the free wall of the right and the left ventricle.

Changes in Right Ventricular Preload

Several experimental studies have examined systolic and diastolic ventricular interactions in the setting of left ventricular assist. Increased venous return produced by an LVAD can affect right ventricular function by increasing preload. If the venous return is too great, right heart failure can result, thus leading to a subsequent reduction in right ventricular output, with a consequent reduction in LVAD filling and finally a reduction in systemic blood flow [1].

On the other hand, some studies have demonstrated an increased right ventricular free-wall-to-septum dimension corresponding to a decreased left ventricular free-wall-to-septum dimension during left ventricle unloading. An LVAD can improve the filling of the right ventricle by unloading the left ventricle, reducing its chamber size and shifting the septum back to the left (Fig 1).

View larger version (25K): [in this window] [in a new window]   Fig 1. . Improvement of right ventricular (RV) function by left ventricular (LV) assist device (LVAD). There is displacement of the septum back to the left. (PVR = pulmonary vascular resistance; SVR = systemic vascular resistance.)

Changes in Right Ventricular Afterload

Right ventricular function is highly afterload dependent. An LVAD can alter or improve the ventricular function depending on the pulmonary vascular resistance [4]. In patients with high pulmonary pressure due to left ventricular failure, but with a normal pulmonary vascular bed, the LVAD can improve right ventricular function by reducing right ventricular afterload [5]. Complete decompression of the left ventricle results in a significant reduction in left atrial pressure, which causes a decrease in pulmonary artery pressure, thereby reducing RV afterload. If there is a fixed high pulmonary pressure, however, the LVAD can increase right ventricular afterload and volume due to the increased blood flow through this high pulmonary vascular resistance [1].

Changes in Right Ventricular Contractility

The independent function of the right ventricle has been questioned since Starr and colleagues [6] demonstrated that severe damage to the right free wall does little to impair right ventricular pressure development. Some other studies have confirmed this hypothesis. For example, the destruction of the free wall of the right ventricle by cauterization or injection of vinyl acetate into the right coronary arteries has little effect on arterial and peripheral venous pressure and causes no observable decrease in the ability to exercise [7].

After electrical isolation of the right ventricular free wall, double peaked wave forms for right ventricular pressure and pulmonary arterial blood flow occur over a wide range of pacing intervals between the left and the right ventricles. One component of these wave forms could be directly related to right ventricular free wall contraction, whereas the second component is directly related to the left ventricular and septal contraction [8]. The results of all these studies indicate that left ventricular contraction is very important for right ventricular developed pressure and volume outflow.

When left ventricular pressure or volume is reduced, right ventricular developed pressure is also reduced [9]. Complete pressure unloading of the left ventricle with an LVAD shifts the interventricular septum to the left and reduces the contribution of the left ventricle to right ventricular contraction [10]. This phenomenon is especially important in cases of high flow. Left ventricular assist significantly reduced right ventricular E_max at a flow ratio of 75% or greater. This suggests that left cardiac assist can impair right ventricular contractility.

On the other hand, the aim of the LVAD is to increase the aortic pressure and therefore the coronary perfusion pressure. Right ventricular function can be improved by increasing myocardial blood flow.

Changes in Heart Rate

Changes in heart rate can be related to the tendency to restore to basal levels the neural and humoral reflexes that were activated by heart failure, due to improvement of the hemodynamic conditions. An increase in blood pressure activates the sinus and aortic arch baroreceptors, producing an inhibitory influence on sympathetic efferent outflow and a decrease in heart rate. At the same time, the unloading of the ventricle can reduce the size of the heart and thus activate the atrial and ventricular mechanoreceptors.

Role of Peripheral Vascular Resistances

The relationship between the right and left ventricle during assist is essential as we have seen, but peripheral vascular resistances also have a main role in the hemodynamic evolution. Venet and associates [11, 12] performed some experiments in our laboratory at La Pitie using a mock circulation to illustrate the importance of this.

It is possible, with few modifications, to regulate the aortic and pulmonary water gates, which represent the systemic and pulmonary vascular resistances (Fig 2). In a stable state, the inflow (q1) and the outflow of the left ventricle (q2) are the same. The difference between the mean aortic pressure (AP) and the central venous pressure (right atrial pressure) determines the flow of the venous return, according to the law of Torricelli: q1 = q2 = Q = S H = AP - PR, where Q = cardiac flow, S = section diameter, H = difference between mean aortic pressure and central venous pressure, and PR = pulmonary resistance.

View larger version (23K): [in this window] [in a new window]   Fig 2. . Hydraulic mock circulation model. (AP = aortic pressure; H = differences between mean aortic pressure and central venous pressure; LA = left atrium; LV = left ventricle; PP = pulmonary pressure; PR = pulmonary water gate representing pulmonary resistances; Q = cardiac flow; q1 = inflow; q2 = outflow; RA = right atrium; RV = right ventricle; S = diameter of section; SR = aortic water gate representing systemic resistance.)

View larger version (19K): [in this window] [in a new window]   Fig 3. . Evolution of venous return with systemic vascular resistance. (AR = systemic vascular resistance; H = differences between mean aortic pressure [AP] and central venous pressure [CVP = right atrial pressure]; Q = cardiac flow.)

View larger version (20K): [in this window] [in a new window]   Fig 4. . Evolution of venous return with pulmonary vascular resistance. (AR = systemic vascular resistance; H = differences between mean aortic pressure [AP] and central venous pressure [CVP = right atrial pressure]; PuR = pulmonary vascular resistance; Q = cardiac flow.)

Conclusions

We conclude that the right ventricle is dispensable if the pulmonary vascular bed is normal. However, in all circumstances where right ventricular function or the pulmonary vascular bed has deteriorated, biventricular support is needed. In such a case, the only problem with device use is to respect the flow balance between the right and left sides.

Footnotes

Presented at The Third International Conference on Circulatory Support Devices for Severe Cardiac Failure, Pittsburgh, PA, Oct 28-30, 1994.

Address reprint requests to Dr Pavie, Hôpital de la Pitie, 83 Blvd de l'Hôpital, 75013, Paris, France.

References

1. Farrar DJ, Compton PG, Hershon JJ, Fonger JD, Hill JD. Right heart interaction with the mechanically assisted left heart. World J Surg 1985;9:89–102.[Medline]
2. Elbeery JR, Owen CH, Savitt MA, et al. Effects of the left ventricular assist device on right ventricular function. J Thorac Cardiovasc Surg 1990;99:809–16.[Abstract]
3. Fukamachi K, Asou T, Nakamura Y, et al. Effects of left heart bypass on right ventricular performance. Evaluation of the right ventricular end-systolic and end-diastolic pressure-volume relation in the in situ normal canine heart. J Thorac Cardiovasc Surg 1990;99:725–34.[Abstract]
4. Farrar DJ, Compton PG, Hershon JJ, Hill JD. Right ventricular function in an operating room model of mechanical left ventricular assistance and its effects in patients with depressed left ventricular function. Circulation 1985;72: 1279–85.[Abstract/Free Full Text]
5. Farrar DJ, Compton PG, Dajee H, Fonger JD, Hill JD. Right heart function during left heart assist and its effects of volume loading in a canine preparation. Circulation. 1984;70:708–16.[Abstract/Free Full Text]
6. Starr I, Jeffers GW, Meade RH. The absence of conspicuous increments in venous pressure after severe damage to the right ventricle of the dog, with a discussion of the relation between clinical congestive failure and heart disease. Am Heart J 1943;26:291–301.
7. Feneley MP, Gavaghan TP, Baron DW, Branson JA, Roy PR, Morgan JJ. Contribution of left ventricular contraction to the generation of right ventricular systolic pressure in human heart. Circulation 1985;71:473–80.[Abstract/Free Full Text]
8. Damiano RJ, La Folette P, Cox JL, Lowe JE, Santamore WP. Significant left ventricular contribution to right ventricular systolic function. Am J Physiol 1991;261:H1514–24.[Abstract/Free Full Text]
9. Chow E, Farrar DJ. Effects of left ventricular pressure reductions on right ventricular systolic performance. Am J Physiol 1989;257:H1878–85.[Abstract/Free Full Text]
10. Woodard JC, Chow E, Farrar DJ. Isolated ventricular systolic interaction during transient reductions in left ventricular pressure. Circ Res 1992;70:944–51.[Abstract/Free Full Text]
11. Venet R, Venet A, Pavie A, et al. Bases hydrauliques de l' assistance ventriculaire gauche. Act Méd Int Angiol 1992;162:3237–47.
12. Venet R, Pavie A, Venet A, Cabrol C, Gandjbakhch I. Relation between pressure and outflow in the carotid arterial system. Cah CECEC 1993;39:17–38.
13. Guyton A, Abernathy B, Langston J, Kaufman B, Fairchild H. Relative importance of venous and arterial resistances in controlling venous return and cardiac output. Am J Physiol 1965;959:1008–14.

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Alain Pavie Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pavie, A. Articles by Leger, P. Search for Related Content PubMed PubMed Citation Articles by Pavie, A. Articles by Leger, P.