LVAD Hemodynamics — #1 When Pump Flow >100%

LVAD Hemodynamics — Interpreting “Flow >100%”

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What “>100% flow” actually means

The LVAD’s displayed flow is a computed value (speed–power–viscosity model). When the console persistently reads “>100%” of systemic cardiac output, the pump is delivering essentially all forward flow, and the native LV contribution is minimal. Under these conditions, small changes in preload, RV performance, afterload, or speed produce disproportionate shifts in left-sided filling (LAP/PCWP), right-sided pressures (RAP/CVP), and inlet pressure behavior. A pragmatic interpretation is to map three recurrent phenotypes—volume overload, excessive RPM/suction, and volume depletion—using RAP, LAP (or PCWP), and inlet pressure as the primary triad, then confirm with echo and a targeted ramp maneuver [1–4].

Pattern 1 — “Volume overload”

Signature: ↑RAP, ↑LAP (PCWP), ↑inlet pressure; high (often non-pulsatile) displayed flow.

Mechanism. The RV supplies generous preload; pulmonary venous return is robust; the LVAD drains a well-filled LV. If speed outstrips the vascular/valvular context (hypertension, MR), left-sided congestion persists even though total flow is high.

Bedside/echo clues.

  • Low arterial pulsatility with intermittent or absent AV opening despite enlarged LA/LV and elevated E/e′; MR may worsen.
  • High CVP from shared venous congestion and RV–pulmonary uncoupling as pulmonary edema raises PVR.

What to do. Treat the filling/afterload problem first: gentle diuresis or ultrafiltration, oxygenation/PEEP optimization, and BP control. If AV never opens and LAP/PCWP remains high after decongestion, consider a modest speed down-titration [3,4,11].

Pattern 2 — “Excessive RPM” (incipient suction)

Signature: ↑RAP, ↓LAP (PCWP), ↓inlet pressure; high but labile displayed flow with suction alarms.

Mechanism. Speed is too high for the available LV preload. Intermittent inflow “suck-down” collapses the LV cavity, lowers cannula pressure, and shifts the septum left→right, impairing RV geometry and raising RAP.

Bedside/echo clues.

  • Flattened/erratic arterial waveform synchronized with low-inlet-pressure alarms.
  • Echo: small, under-filled LV, septal bowing into the LV, cannula contact with septum/MV leaflet during respiration or position changes.

What to do. Reduce speed immediately, then correct substrate: treat hypovolemia if present; relieve RV afterload (optimize oxygenation/ventilation; consider pulmonary vasodilation); verify cannula position. Persistent events at appropriate speed suggest inflow obstruction/malposition or primary RV dysfunction masquerading as “high flow” [1,4].

Pattern 3 — “Volume depletion”

Signature: ↓RAP, ↓LAP (PCWP), ↓inlet pressure; high but fragile flow that collapses with minor perturbations.

Mechanism. Systemic under-filling (diuresis, bleeding, dialysis, vasodilation) allows the LVAD to over-drain a small LV; both atria are low-pressure and suction risk is high.

Bedside/echo clues.

  • Collapsed IVC, narrow pulse pressure, low MAP/orthostasis.
  • Echo: tiny LV with end-diastolic cavity obliteration; AV often closed; little or no MR.

What to do. Replete volume carefully (watch lungs/RV). If physiology is fragile, temporarily back off speed to avoid suction while restoring preload [1–3].

Practical algorithm (bedside)

  1. Corroborate the number: MAP, pulse pressure, SvO₂, lactate.
  2. Interrogate pressures: RAP/CVP, LAP (or PCWP) and the inlet pressure trend.
  3. Echo now: LV size, septal position, AV opening, MR, RV size/function, cannula–septum/MV relation.
  4. Act on the pattern:
    • Overload → decongest/afterload-reduce ± small speed down.
    • Excessive RPM/suction → speed down + fix RV/preload.
    • Depletion → judicious volume ± temporary speed down.
  5. Re-assess within minutes—cause and effect in LVAD physiology are immediate [1–4].

Evidence-based targets and ramp testing (Elicit integration)

  • Hemodynamic goals during optimization: several programs target CVP <12–15 mmHg, PCWP <18–20 mmHg, CI >2.2 L·min⁻¹·m⁻², and MAP ~70–90 mmHg, individualized to RV status and end-organ perfusion [2,3,8].
  • Ramp testing provides an objective, reproducible way to reach those goals. In a landmark hemodynamic-echo ramp study, each speed step increased cardiac output by ~0.16 ± 0.19 L/min and reduced PCWP by ~1.23 ± 0.85 mmHg, while exposing occult inflow/outflow issues and guiding speed and medication adjustments [1]. A randomized pilot confirmed feasibility of standardized hemodynamic ramp-guided care across centers [7].
  • Right-sided vulnerability matters. Early or late RV failure remains common in continuous-flow LVAD cohorts (~20–40%, depending on case-mix and definitions), so every speed or volume change must be viewed through RV–pulmonary coupling and LVAD preload delivery [5,6]. Practical clues include RAP disproportionately high relative to PCWP, rising hepatic/renal congestion, and loss of LVAD pulsatility with septal shift on echo [4–6].

Teaching pearls

  • Right-heart limited system. Without RV preload, LVAD flow cannot be sustained—speed alone is not a solution [4–6].
  • Aortic valve strategy. Chronic operation with a persistently closed AV is associated with leaflet fusion/thrombus risk; many centers favor intermittent AV opening when feasible while maintaining adequate unloading and end-organ perfusion [3,11].
  • Numbers in context. Always interpret targets in the context of oxygenation/ventilation (PVR), rhythm, vasoactives, and afterload. Optimize the patient first; then fine-tune speed (often via a short ramp) to land on your hemodynamic goals [1–3].

References

[1] Uriel N, Sayer G, Addetia K, et al. Hemodynamic ramp tests in patients with left ventricular assist devices. JACC Heart Fail. 2016;4(3):208-217.

[2] Imamura T, Nguyen A, Chung B, et al. Optimal hemodynamics during left ventricular assist device support are associated with reduced readmission. Circ Heart Fail. 2019;12(1):e005094.

[3] Ben Gal T, Burkhoff D, Estep JD, et al. Guidance on the management of left ventricular assist device supported patients for the non-LVAD specialist. ESC Heart Fail. 2021;8(8):4424-4443.

[4] Stainback RF, Estep JD, Agler DA, et al. Echocardiography in the management of patients with left ventricular assist devices: Recommendations from the American Society of Echocardiography. J Am Soc Echocardiogr. 2015;28(8):853-909.

[5] Ródenas-Alesina E, Cediel-García P, Garcia-Gonzalez P, et al. Prediction, prevention, and management of right ventricular failure after LVAD implantation. Front Cardiovasc Med. 2022;9:1040251.

[6] Kormos RL, Teuteberg JJ, Pagani FD, et al. Right ventricular failure in patients with the HeartMate II continuous-flow LVAD. J Thorac Cardiovasc Surg. 2010;139(5):1316-1324.

[7] Uriel N, Adatya S, Malý J, et al. Impact of hemodynamic ramp test–guided HVAD speed optimization on clinical outcomes: the Ramp-It-Up study. J Heart Lung Transplant. 2019;38(5):552-559.

[8] Bernhardt AM, Garan AR, Burkhoff D, et al. 2023 International Society for Heart and Lung Transplantation consensus statement on mechanical circulatory support. J Heart Lung Transplant. 2023;42(7):e1-e67.

[9] Gonzalez J, Estevez-Loureiro R, Lopez-Vilela R, et al. Invasive haemodynamic assessment before and after LVAD implantation. Interv Cardiol Rev. 2021;16:e06.

[10] Uriel N, Colombo PC, Cleveland JC Jr, et al. Clinical hemodynamic evaluation of patients implanted with the HeartMate 3 LVAD. J Heart Lung Transplant. 2017;36(6):660-666.

[11] Mancini D, Colombo PC. Left ventricular assist devices: a rapidly evolving alternative to transplant. J Am Coll Cardiol. 2015;65(24):2542-2555.