LVAD Physiology in a Biventricular (BiV) Circulation

Core concept

A left-ventricular assist device (LVAD) augments systemic output by actively unloading the LV and delivering blood into the ascending aorta. In a biventricular circulation, forward flow through the LVAD is ultimately right-ventricle (RV) limited: the RV must provide preload to the lungs so that pulmonary venous return can fill the LV and LVAD. LVAD physiology is therefore a three-link chain—LV unloading and afterload, RV function and RV–pulmonary coupling, and pulmonary venous return—with the weakest link (often the RV) determining total flow [1–2].

Hemodynamic effects of LVAD support

1) LV unloading and left-sided pressures

Continuous-flow support lowers LV end-diastolic and left-atrial (LA) pressures, reducing pulmonary capillary hydrostatic pressure and edema; lung compliance and gas exchange improve (“lung protection”) [1].

2) Systemic perfusion and organ recovery

More stable cardiac output and mean arterial pressure restore end-organ perfusion and facilitate reversal of secondary organ dysfunction (renal, hepatic, neurologic) [1].

3) Afterload sensitivity

LVAD flow is afterload-dependent; higher systemic vascular resistance (SVR) depresses pump output at a given speed. Thoughtful vasodilator use can improve forward flow without provoking hypotension [1].

4) Ventricular interdependence

LV decompression shifts the septum rightward. At appropriate speeds this lowers RV afterload by decreasing LA/PA pressures; over-decompression can bow the septum into the RV and impair RV filling/contractility, precipitating RV failure [2].

The RV as the rate-limiting step (the central Elicit theme)

RV management is the critical hemodynamic challenge in LVAD support, especially in pediatrics/CHD. Early RV failure complicates ~20–40% of LVAD implants in contemporary series and powerfully worsens outcomes [2,5]. Pre- and intra-operative risk stratification (e.g., hemodynamics, end-organ status, echo-derived RV metrics, and validated risk scores) should be routine [2–3,9].

Determinants and targets

• Contractility: support with low-dose epinephrine or inodilators (e.g., milrinone) as needed.
• Afterload: reduce PVR via optimal oxygenation, avoidance of acidosis/hypercarbia, gentle ventilatory pressures, and selective pulmonary vasodilation (e.g., iNO) [4–5].
• Preload: maintain adequate intravascular volume while preventing RV over-distension and venous congestion; track CVP trends and end-organ signals [2,4].
• Rhythm/AV synchrony: promptly treat atrial arrhythmias; maintain adequate heart rate for RV stroke volume [2,4].

Clinical translation

LVAD implantation can unmask or exacerbate RV dysfunction (pre-existing RV myopathy, ischemia, significant TR, or elevated PVR). Anticipate and treat proactively; escalate to temporary RV support when the bundle above fails to restore LVAD inflow and systemic perfusion [2,4–5].

Pulmonary circulation and “lung protection”

Lower LA pressure reduces transcapillary filtration and improves lung mechanics, which enhances pulmonary venous return and stabilizes LVAD flow—creating a virtuous RV–lung–LVAD loop when RV–PA coupling is preserved [1–2]. Ventilation should avoid high mean airway pressures (raise RV afterload), maintain normal pH/PaCO₂, and correct hypoxemia swiftly to keep PVR low [4–5].

Failure modes and cautions

Aortic insufficiency (AI): the “closed loop”

With AI, blood recirculates aorta → LV → LVAD → aorta, diminishing net systemic output despite high displayed flows. Clinical signals include rising LV/LA pressures, reduced pulsatility, and hemolysis. Management: temper pump speed if over-decompressed, judicious afterload control, and definitive treatment of AI when moderate–severe or progressive [6–7,11,21].

RV dysfunction

Underfilled LVADs generate suction/low-flow events, hypotension, renal/hepatic congestion, and rising CVP. Use a protocolized bundle—inotropy/inodilation, pulmonary vasodilation, careful volume, rhythm control, ventilatory adjustments—and consider temporary RV support early if refractory [2,4–5,9–10].

Suction and inflow obstruction

Excessive speed or hypovolemia can collapse the LV around the inflow cannula, triggering alarms and arrhythmias. Reduce speed, correct volume/RV failure, and confirm cannula position and septal geometry by echocardiography [4,23].

Afterload/speed mismatch

High SVR depresses pump flow; very low SVR may cause excessive shear. Titrate vasoactive therapy and individualize speed to echo-guided goals (small but not “empty” LV, physiologic septal position, intermittent AV opening when desired) [1,17].

Arrhythmias and TR

Atrial tachyarrhythmias/AV block markedly reduce RV stroke volume; significant TR worsens venous congestion and RV inefficiency. Treat rhythm and consider TR management to optimize RV forward flow [2,4].

Practical monitoring and bedside targets

• Clinical: perfusion, mentation, UOP, lactate, hepatic/renal indices [1–2].
• Device: pump flow/power/speed/pulsatility; beware low-flow/suction alarms [1].
• Invasive hemodynamics (as available): goal MAP tailored to age; falling CVP/RA (often <10–12 mmHg in larger children/adults) with stable PA pressures and improving wedge/LA surrogates [2].
• Echocardiography:
• LV small but not empty; no inflow obstruction.
• Aortic valve: periodic opening if strategy permits; track AI severity serially [6–7,17].
• RV: size/function, TR, septal position; estimate PA pressures [2,4].
• Respiratory: avoid high PEEP/plateau; maintain normal pH/PaCO₂ and good oxygenation (PVR control) [4–5].

Pediatric/CHD-specific considerations

Children have small LV cavities and highly compliant lungs, making speed selection and suction avoidance particularly delicate; small volume shifts can cause large hemodynamic swings. CHD anatomy (systemic RV, prior repairs, elevated PVR) amplifies RV dependence—keep a low threshold for inodilators and iNO and coordinate closely with perfusion/ICU teams. Contemporary pediatric data (e.g., Berlin Heart EXCOR) underscore that outcomes depend on vigilant RV surveillance and tailored critical care strategies [4–5,8,16].

Take-home synthesis

LVAD support in a BiV circulation protects the lungs by lowering LA pressure and stabilizes systemic perfusion, but effectiveness is limited by RV performance. Optimal outcomes require the triad of (1) appropriate speed and afterload, (2) preserved RV function with low PVR, and (3) vigilant avoidance/correction of AI and suction—treating the LVAD as one element of an RV–lung–LVAD continuum [1–2,5–7].

References

[1] Slaughter MS, Rogers JG, Milano CA, Russell SD, Conte JV, Feldman D, et al. Advanced heart failure treated with continuous-flow left ventricular assist device. N Engl J Med. 2009;361(23):2241-2251. PubMed

[2] Kormos RL, Teuteberg JJ, Pagani FD, Russell SD, John R, Miller LW, et al. Right ventricular failure in patients with the HeartMate II continuous-flow left ventricular assist device: incidence, risk factors, and effect on outcomes. J Thorac Cardiovasc Surg. 2010;139(5):1316-1324. PubMed+1

[3] Matthews JC, Koelling TM, Pagani FD, Aaronson KD. The right ventricular failure risk score: a pre-operative tool for assessing the risk of right ventricular failure in left ventricular assist device candidates. J Am Coll Cardiol. 2008;51(22):2163-2172. scirp.org

[4] Lampert BC, Teuteberg JJ. Right ventricular failure after left ventricular assist devices. J Heart Lung Transplant. 2015;34(9):1123-1130. PubMed+1

[5] Rodenas-Alesina E, Hernandez-Montfort J, Rivas-Lasarte M, Arrigo M. Prediction, prevention, and management of right ventricular failure after left ventricular assist device implantation. Front Cardiovasc Med. 2022;9:1040251. Frontiers

[6] Cowger J, Pagani FD, Haft JW, Romano MA, Aaronson KD. The development of aortic insufficiency in left ventricular assist device-supported patients. Circ Heart Fail. 2010;3(6):668-674. ahajournals.org

[7] Grinstein J, Kruse E, Sayer G, Fedson S, Kim GH, Sarswat N, et al. Novel echocardiographic parameters of aortic insufficiency in continuous-flow LVADs and their clinical implications. Circ Heart Fail. 2016;9(7):e003907. PubMed+1

[8] Fraser CD Jr, Jaquiss RDB, Rosenthal DN, Humpl T, Canter CE, Chrisant MR, et al. Prospective trial of a pediatric ventricular assist device. N Engl J Med. 2012;367(6):532-541. nejm.org

[9] Soliman OII, Akin S, Muslem R, Boersma E, Manintveld OC, Krabatsch T, et al. Derivation and validation of the EUROMACS right-sided heart failure risk score after LVAD implantation. Circulation. 2018;137(9):891-906. ahajournals.org

[10] Bellavia D, Iacovoni A, Scardulla C, Pilato M, Bertani A, Liccaro M, et al. Prediction of right ventricular failure after LVAD: systematic review and meta-analysis. Eur J Heart Fail. 2017;19(7):926-946. onlinelibrary.wiley.com

[11] Cowger JA, Aaronson KD, Romano MA, Haft JW, Pagani FD. Consequences of aortic insufficiency during long-term axial-flow LVAD support. J Heart Lung Transplant. 2014;33(12):1233-1240. PubMed

[12] Estep JD, Vivo RP, Krim SR, Cordero-Reyes AM, Bhimaraj A, Trachtenberg BH, et al. A simplified echocardiographic technique for detecting continuous-flow LVAD malfunction due to pump thrombosis. J Heart Lung Transplant. 2014;33(6):575-586. jhltonline.org

[13] Almond CS, Morales DL, Blackstone EH, Turrentine MW, Imamura M, Massicotte MP, et al. Berlin Heart EXCOR pediatric ventricular assist device for bridge to transplant: North American experience. Circulation. 2013;127(16):1702-1711. ahajournals.org