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Physiology of Continuous‐Flow Left Ventricular Assist Device Therapy

Andrew N. Rosenbaum, James F. Antaki, Atta Behfar, Mauricio A. Villavicencio, John Stulak, Sudhir S. Kushwaha

10.1002/cphy.c210016

Source: Volume 12, Issue 1, January 2022

Published online: December 2021

Full Article on Wiley Online Library



Abstract

The expanding use of continuous‐flow left ventricular assist devices (CF‐LVADs) for end‐stage heart failure warrants familiarity with the physiologic interaction of the device with the native circulation. Contemporary devices utilize predominantly centrifugal flow and, to a lesser extent, axial flow rotors that vary with respect to their intrinsic flow characteristics. Flow can be manipulated with adjustments to preload and afterload as in the native heart, and ascertainment of the predicted effects is provided by differential pressure‐flow (H‐Q) curves or loops. Valvular heart disease, especially aortic regurgitation, may significantly affect adequacy of mechanical support. In contrast, atrioventricular and ventriculoventricular timing is of less certain significance. Although beneficial effects of device therapy are typically seen due to enhanced distal perfusion, unloading of the left ventricle and atrium, and amelioration of secondary pulmonary hypertension, negative effects of CF‐LVAD therapy on right ventricular filling and function, through right‐sided loading and septal interaction, can make optimization challenging. Additionally, a lack of pulsatile energy provided by CF‐LVAD therapy has physiologic consequences for end‐organ function and may be responsible for a series of adverse effects. Rheological effects of intravascular pumps, especially shear stress exposure, result in platelet activation and hemolysis, which may result in both thrombotic and hemorrhagic consequences. Development of novel solutions for untoward device‐circulatory interactions will facilitate hemodynamic support while mitigating adverse events. © 2021 American Physiological Society. Compr Physiol 12:1‐37, 2021.

Figure 1. Figure 1. LVAD configuration. A standard configuration for durable CF‐LVAD support with near‐LV apical cannulation, rotor housing within the pericardium, and outflow cannula extending from the rotor housing to the right lateral ascending aorta. HeartMate III model shown. Reproduced, with permission, from Abbott Laboratories.
Figure 2. Figure 2. Bearing types utilized in contemporary continuous‐flow left ventricular assist devices. (A) Mechanical pivot bearing, (B) electromagnetic bearing, (C) hydrodynamic radial bearing, (D) hydrodynamic thrust bearing, and (E) hydrodynamic thrust and permanent magnet bearing combination. Reprinted, with permission, from Elsevier, Inc./Moazami N, et al., 2013 252.
Figure 3. Figure 3. Computational fluid dynamics modeling of HeartMate III. Reprinted, with permission, from John Wiley and Sons/Wiegmann L, et al., 2019 391.
Figure 4. Figure 4. Example of a benchtop mock circulatory setup with CF‐LVAD in situ. Reprinted via Creative Commons CC BY 4.0 license, with permission, from Bozkurt S, et al., 2016 49.
Figure 5. Figure 5. Hemodynamic assessment paradigm derived from left heart catheterization. (A) Relationship between transaortic gradient (TAG) and left ventricular end‐diastolic pressure in patients evaluated for hemodynamic optimization. (B) Relationship in patients evaluated for pump obstruction. (C) Relationship in patients evaluated for aortic insufficiency (D) Hemodynamics in one patient with severe aortic insufficiency demonstrating a rise in LVEDP with ramp. Reprinted via Creative Commons CC BY‐NC 3.0 license, with permission, from Rosenbaum AN, et al., 2019 310.
Figure 6. Figure 6. Simplified HQ curves for axial and centrifugal flow devices. Relationship between differential pressure (post‐pre rotor pressures, H) versus pump flow (Q) stratified by axial (blue) and centrifugal (red) flow devices. A flatter contour of the HQ curves in centrifugal flow devices results in greater sensitivity to the differential pressure and greater changes in flow based on loading conditions (ΔH vs. ΔQ). Across the cardiac cycle, this enhances pulsatility (top right inset) of centrifugal flow devices relative to axial flow (bottom left inset). Hemodynamic waveforms within insets represent continuous aortic pressure (light grey) and continuous left ventricular pressure (dark grey). RPM, revolutions per minute.
Figure 7. Figure 7. HQ loops in axial and centrifugal flow devices. Reprinted, with permission, from John Wiley and Sons/Noor MR, et al., 2016 274.
Figure 8. Figure 8. Clinical scenarios representing deviations in pump parameters. Top Left: A high power and high flow state with high pulsatility may reflect exercise and therefore enhanced contractility of the left ventricle with high flow. Myocardial recovery will similarly result in improved flow and high pulsatility index. Because significant aortic insufficiency will load the left ventricle, but if well tolerated, will increase contractility through a Frank‐Starling mechanism and result in higher pulsatility and flows. Top Right: A low flow situation with high pulsatility index may occur in the setting of relatively low speed, in which the LV ventricle is loaded to a greater degree and if able to compensate, may result in a high PI. Similarly, hypertension, because of the interaction with device flow will exaggerate the systolic and diastolic flows and therefore result in elevated pulsatility while flow may be low. Bottom Left: A high power situation with low PI may result from excessive unloading of the left ventricle due to high speed. However, if somewhat acute, may also represent rotor thrombus increasing power consumption while pulsatility is not well transmitted to the device. Excessive medication‐related vasodilation or sepsis may result in high flow, low pulsatility index due to low peripheral resistance. Bottom Right: A low flow, power, and PI situation may occur in hypovolemia from any cause as the ventricle is under‐filled resulting in low flows, pericardial tamponade, an effectively low filling state, right ventricular failure, where inadequate flow is provided to the LV, and ventricular dysrhythmias during which pulsatility index is low from lack of coordinated LV contraction, which also impairs flow through the device. Finally, both inflow or outflow obstruction will impair true device flow and shield the rotor from the normal variability in flow pulses resulting in a low pulsatility.
Figure 9. Figure 9. Myocardial stress distribution of the septum by CF‐LVAD speed. Reprinted via Creative Commons CC BY 4.0 license, with permission, from Sack KL, et al., 2018 318.
Figure 10. Figure 10. Immediate changes in longitudinal RV motion postpericardiotomy in patients undergoing traditional versus minimally invasive valve replacement. Reprinted, with permission, from Elsevier, Inc./Unsworth B, et al., 2013 369.
Figure 11. Figure 11. Invasive LV hemodynamics at rest and exercise in an LVAD‐supported patient. On the left, at baseline speed of 9000 RPM, the LV is unloaded, and aortic valve does not open owing to the high reverse pressure gradient across the aortic valve (A). Same patient at 7000 RPM simulating minimal support with consistent aortic valve opening resulting from high intrinsic LV contractility and aortic gradient (B).
Figure 12. Figure 12. Hemodynamic tracing before and after increase in pacing lower rate limit. (A) Hemodynamic tracings with simultaneous aortic, LV, and RA pressure waveforms and ECG are shown at 50 BPM. (B) The same tracing evaluated with a paced rhythm of 80 BPM.
Figure 13. Figure 13. Hemodynamic energy and pulsatility by pulse pressure. (A) Maximal dp/dy, (B) surplus hemodynamic energy (SHE), and (C) pulse power index (PPI) values over a range of pulse pressures (PP), stratified by modes of CF‐LVAD pulsation. Reprinted, with permission, from John Wiley and Sons/Kleinheyer M, et al., 2016 198.
Figure 14. Figure 14. Combined effects of shear stress and exposure time in relation to hemolysis. The relationship between the combined effects of shear stress exposure on blood cells and exposure time in the relevant vessel determines risk of hemolysis. The roughly cylindrical nature of LVAD blood flow pathways lends to higher exposure times. Reprinted, with permission, from Elsevier, Inc./Leverett LB, et al., 1972 221.
Figure 15. Figure 15. Diagrammatic representation of intravascular platelet aggregation using continuum modeling using two spatial scales. Reprinted, with permission, from Elsevier, Inc./Fogelson AL and Guy RD, 2008 109.
Figure 16. Figure 16. Outflow cannula pathologies leading to LVAD obstruction. (A) Kinking of the outflow cannula may occur due to surgical malpositioning or rotation within the thoracic cavity over time. (B) Outflow cannula stenosis may occur due to chronic thrombus accumulation and may be identified on cross‐sectional computed tomography. (C) Exudative thrombofibrotic material may accumulate between the outflow graft and proximal bend relief resulting in extrinsic compression and functional stenosis.


Figure 1. LVAD configuration. A standard configuration for durable CF‐LVAD support with near‐LV apical cannulation, rotor housing within the pericardium, and outflow cannula extending from the rotor housing to the right lateral ascending aorta. HeartMate III model shown. Reproduced, with permission, from Abbott Laboratories.


Figure 2. Bearing types utilized in contemporary continuous‐flow left ventricular assist devices. (A) Mechanical pivot bearing, (B) electromagnetic bearing, (C) hydrodynamic radial bearing, (D) hydrodynamic thrust bearing, and (E) hydrodynamic thrust and permanent magnet bearing combination. Reprinted, with permission, from Elsevier, Inc./Moazami N, et al., 2013 252.


Figure 3. Computational fluid dynamics modeling of HeartMate III. Reprinted, with permission, from John Wiley and Sons/Wiegmann L, et al., 2019 391.


Figure 4. Example of a benchtop mock circulatory setup with CF‐LVAD in situ. Reprinted via Creative Commons CC BY 4.0 license, with permission, from Bozkurt S, et al., 2016 49.


Figure 5. Hemodynamic assessment paradigm derived from left heart catheterization. (A) Relationship between transaortic gradient (TAG) and left ventricular end‐diastolic pressure in patients evaluated for hemodynamic optimization. (B) Relationship in patients evaluated for pump obstruction. (C) Relationship in patients evaluated for aortic insufficiency (D) Hemodynamics in one patient with severe aortic insufficiency demonstrating a rise in LVEDP with ramp. Reprinted via Creative Commons CC BY‐NC 3.0 license, with permission, from Rosenbaum AN, et al., 2019 310.


Figure 6. Simplified HQ curves for axial and centrifugal flow devices. Relationship between differential pressure (post‐pre rotor pressures, H) versus pump flow (Q) stratified by axial (blue) and centrifugal (red) flow devices. A flatter contour of the HQ curves in centrifugal flow devices results in greater sensitivity to the differential pressure and greater changes in flow based on loading conditions (ΔH vs. ΔQ). Across the cardiac cycle, this enhances pulsatility (top right inset) of centrifugal flow devices relative to axial flow (bottom left inset). Hemodynamic waveforms within insets represent continuous aortic pressure (light grey) and continuous left ventricular pressure (dark grey). RPM, revolutions per minute.


Figure 7. HQ loops in axial and centrifugal flow devices. Reprinted, with permission, from John Wiley and Sons/Noor MR, et al., 2016 274.


Figure 8. Clinical scenarios representing deviations in pump parameters. Top Left: A high power and high flow state with high pulsatility may reflect exercise and therefore enhanced contractility of the left ventricle with high flow. Myocardial recovery will similarly result in improved flow and high pulsatility index. Because significant aortic insufficiency will load the left ventricle, but if well tolerated, will increase contractility through a Frank‐Starling mechanism and result in higher pulsatility and flows. Top Right: A low flow situation with high pulsatility index may occur in the setting of relatively low speed, in which the LV ventricle is loaded to a greater degree and if able to compensate, may result in a high PI. Similarly, hypertension, because of the interaction with device flow will exaggerate the systolic and diastolic flows and therefore result in elevated pulsatility while flow may be low. Bottom Left: A high power situation with low PI may result from excessive unloading of the left ventricle due to high speed. However, if somewhat acute, may also represent rotor thrombus increasing power consumption while pulsatility is not well transmitted to the device. Excessive medication‐related vasodilation or sepsis may result in high flow, low pulsatility index due to low peripheral resistance. Bottom Right: A low flow, power, and PI situation may occur in hypovolemia from any cause as the ventricle is under‐filled resulting in low flows, pericardial tamponade, an effectively low filling state, right ventricular failure, where inadequate flow is provided to the LV, and ventricular dysrhythmias during which pulsatility index is low from lack of coordinated LV contraction, which also impairs flow through the device. Finally, both inflow or outflow obstruction will impair true device flow and shield the rotor from the normal variability in flow pulses resulting in a low pulsatility.


Figure 9. Myocardial stress distribution of the septum by CF‐LVAD speed. Reprinted via Creative Commons CC BY 4.0 license, with permission, from Sack KL, et al., 2018 318.


Figure 10. Immediate changes in longitudinal RV motion postpericardiotomy in patients undergoing traditional versus minimally invasive valve replacement. Reprinted, with permission, from Elsevier, Inc./Unsworth B, et al., 2013 369.


Figure 11. Invasive LV hemodynamics at rest and exercise in an LVAD‐supported patient. On the left, at baseline speed of 9000 RPM, the LV is unloaded, and aortic valve does not open owing to the high reverse pressure gradient across the aortic valve (A). Same patient at 7000 RPM simulating minimal support with consistent aortic valve opening resulting from high intrinsic LV contractility and aortic gradient (B).


Figure 12. Hemodynamic tracing before and after increase in pacing lower rate limit. (A) Hemodynamic tracings with simultaneous aortic, LV, and RA pressure waveforms and ECG are shown at 50 BPM. (B) The same tracing evaluated with a paced rhythm of 80 BPM.


Figure 13. Hemodynamic energy and pulsatility by pulse pressure. (A) Maximal dp/dy, (B) surplus hemodynamic energy (SHE), and (C) pulse power index (PPI) values over a range of pulse pressures (PP), stratified by modes of CF‐LVAD pulsation. Reprinted, with permission, from John Wiley and Sons/Kleinheyer M, et al., 2016 198.


Figure 14. Combined effects of shear stress and exposure time in relation to hemolysis. The relationship between the combined effects of shear stress exposure on blood cells and exposure time in the relevant vessel determines risk of hemolysis. The roughly cylindrical nature of LVAD blood flow pathways lends to higher exposure times. Reprinted, with permission, from Elsevier, Inc./Leverett LB, et al., 1972 221.


Figure 15. Diagrammatic representation of intravascular platelet aggregation using continuum modeling using two spatial scales. Reprinted, with permission, from Elsevier, Inc./Fogelson AL and Guy RD, 2008 109.


Figure 16. Outflow cannula pathologies leading to LVAD obstruction. (A) Kinking of the outflow cannula may occur due to surgical malpositioning or rotation within the thoracic cavity over time. (B) Outflow cannula stenosis may occur due to chronic thrombus accumulation and may be identified on cross‐sectional computed tomography. (C) Exudative thrombofibrotic material may accumulate between the outflow graft and proximal bend relief resulting in extrinsic compression and functional stenosis.
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Article Title: Physiology of Continuous‐Flow Left Ventricular Assist Device Therapy
 

How to Cite

Andrew N. Rosenbaum, James F. Antaki, Atta Behfar, Mauricio A. Villavicencio, John Stulak, Sudhir S. Kushwaha. Physiology of Continuous‐Flow Left Ventricular Assist Device Therapy. Compr Physiol 2021, 12: 2731-2767. doi: 10.1002/cphy.c210016