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Ventricular Assist Device

Last modified: 02 June 2021, 1:30:27 PM AEST

Gems1 / 8

optimal pump function

adequate preload
not excessive afterload

Types2 / 8

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pulsatile VAD = Gen 1 VAD
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continuous flow VAD = Gen 2/3
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https://youtu.be/liPKnrlduLk
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rotary pumps = centrifugal
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axial pumps, along long axis = similar to jet engine
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Heartmate 3 (Abbott) = fully magnetically levitated flow technology
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- with artificial pulse
- https://www.youtube.com/watch?v=T37WrT-lDhQ
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HeartWare (Medtronic)
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- https://www.youtube.com/watch?v=k6rs1pRM6lg
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Mechanism3 / 8

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1:pump
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- outflow anastomosed to ascending aorta
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2:driveline
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- lead connecting pump to controller and power source
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3:controller
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- modify pump parameters
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response to preload
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no Starling response to preload
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⬆preload = no increase in output
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response to afterload
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⬆AL = ⬇output of pump
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Contraindications4 / 8

active malignancy
complicated DM\n
- HbA1c > 7.5
- established microvascular complications
- extensive PVD
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morbid obesity BMI > 30
uncontrolled infection
other infections\n
- HIV / HCV / HBV
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inability to comply with complex medical therapy\n
- neuropsychiatric
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active substance ause\n
- alcohol / cigs / illicit
- 6/12 abstinence required
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irreversible end organ damage\n
- renal GFR < 40 mL/min
- bili > 50
- intractable ascites / ⬇alb
- advanced neurodegenerative
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Risks / disadvantages5 / 8

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ventricular suction
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inadequate blood in ventricle
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ventricle muscle sucked against pump inlet, causing obstruction to flow
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pump thrombus
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abrupt increases in power consumption > 2 watts
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Technique / description6 / 8

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bleeding
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- bleeding + risk of thromboembolism
- early postop bleeding = likely tamponade
- late bleeding often GIT
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shear stress + altered rheology
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acquired von willebrand syndrome
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- shear stresses in VAD support causes conformational change in vWF protein
- loss of multimers = bleeding diathesis
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GI haemorrhage
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- 10x more in VAD
- angiodysplasia may develop from non-pulsatile flow, high shear stress, avWS
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thrombosis
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ACT + APT required for lifetime of device
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risk = 8%
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inlet cannula thrombosis = low flow alarms + low pump power
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pump thrombosis = ⬆power consumption
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outflow cannula thrombosis
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neurological events
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- primary cause of death post VAD
- 18% deaths
- annual risk of stroke = 15%
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infection = major RF for thrombosis / stroke
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physiology of LVAD and RV
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in-series ventricular interdependence
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- the RV and LV outputs must match over a short number of cardiac ycles
- otherwise = APO / liver congestion
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in-parallel ventricular interdependence
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- mechanical nature of shared pericardial space
- intraventricular septum contributes to both RV and LV
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infection
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cardiovascular
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- arrhythmias
- RHF
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newer
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aortic valve dysfunction
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- lack of aortic valve opening
- thickening and commissural fusion after VAD
- AS and AR
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angiodysplasia GI bleeding = non-pulsatile flow
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device malfunction
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driveline failure
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pump thrombosis
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Periop management7 / 8

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anticoagulation planning
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MDT = surgeon, anaesthetist, ICU, cardiac surgeon, cardiologist, haematology
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usually
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- heparin stopped
- warfarin reversed
- re-institute 24 hours postop
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assess / changing VAD settings
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support from VAD centre
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VAD energy
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spare batteries
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personnel
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VAD nurse
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VAD coordinator
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perfusion specialist
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careful positioning
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avoid traction of driveline / pressure on abdomen
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monitoring
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very low pulse pressure
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automated NIBP likely inaccurate
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pulse oximetry maybe inaccurate
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NIRS = near-infra red spectroscopy useful
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- does not rely on pulsatility
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use IAL
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TOE for all but the briefest of procedures
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introp goals
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avoid ⬆PVR
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maintain adequate MAP = RV perfusion pressure
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maintain sinus rhythm
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inotropic support of RV
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selective pulmonary vasoD
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- inhaled NO
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Cardiac arrest8 / 8

set VAD to lowest speeding setting
allow LV filling
prevent regurgitation of blood retrograde through VAD
defib = AP pads
pulse detection difficult = use TTE to determine pseudo PEA from true PEA

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