LVAD implantation advantages/disadvantages
Total CPB
MECC
Off-pump
VA ECMO
Hemodilution – priming
+++
+
−
++
Heparin and anticoagulation level
+++
++
+
++
Inflammatory response syndrome
+++
+
−
++
Reactive vasoplegia
++
+
−
++
Increased PVR
++
+
−
+
Platelets activation
++
+
−
++
Impaired renal function
++
+
−
++
Feasibility of concomitant open-heart procedures
Yes
Yes
No
No
Feasibility in middle sternotomy
Yes
Yes
No
Yes
Risk of intraprocedural hemodynamic instabilization
No
No
Yes
No
Risk of postoperative bleeding
++
+
−
+++
Risk of blood transfusion
++
+
−
+++
Accurate visual inspection of LV cavity
+++
+
−
+
19.2.5 De-airing Procedure
De-airing of the LVAD and the native ventricle is crucial before weaning from the CPB. It prevents air embolism, reducing the risk of RV transitory dysfunction. The most common locations for air embolism are the right coronary artery and the innominate artery. This may produce RV dysfunction or contribute to postoperative neurocognitive impairment [11, 12].
Initially, the components of the LVAD are flushed with saline and prepared for implantation at the temperature of 37°. The left ventricular vent has to be clamped and removed just after the inflow cannula insertion and before starting the LVAD pump. This cannula is removed underwater to avoid potential entry of air.
After positioning the inflow cannula, the clamp occluding the outflow graft is rapidly removed in order to avoid the increase of the LV filling pressure and air embolization across the opening aortic valve. Additional de-airing is accomplished by passively filling the heart and pump and elevating the apex and gently shaking the ventricle while lungs are ventilated.
In case of left mini-thoracotomy LVAD implantation, CO2 flooding of the operative field is mandatory, since with this approach the elevation and shaking of left ventricular apex is almost impossible.
After outflow-graft anastomosis, additional needles can be placed into the graft between the cross clamp and the aorta. The patient is then placed in the Trendelenburg position and ventilation is resumed.
The ascending aortic vent should remain open until all visible air is removed. A sufficient quantity of air entering the right coronary artery causes RV ischemia and manifest as RV dysfunction. The treatment consists of further de-airing, an adequate coronary perfusion pressure, assisting the heart on CPB until RV contractility recovers.
19.3 Weaning from CPB
Low-dose inotrope infusion should be started to support the RV function at least 10 min before the weaning from CPB.
Norepinephrine may therefore be beneficial in patients with hypotension and tachycardia who do not tolerate dobutamine, but it must be carefully used in case of pulmonary hypertension and acute RVF without significant hypotension or vasoplegia.
Adrenaline and IABP should be considered only in case of severe RV failure.
Inhalatory nitric oxide (iNO) has not been clearly showed to be effective despite it is frequently used in many center at this stage. Levosimendan also plays a debated role in this crucial phase.
Ventilation should be started as soon as possible after de-airing to decrease pulmonary vascular resistances. Higher tidal volume (VT) and positive end-expiratory pressure may increase pulmonary artery pressure and right atrial pressure, worsen tricuspid regurgitation, and increase RV afterload [16].
The lowest VT, plateau pressure, and positive end-expiratory pressure needed to provide adequate ventilation and oxygenation should be used [16, 17].
Hypoxic pulmonary vasoconstriction should be avoided. During CPB alveolar nutritive flow relies solely on bronchial circulation which is less than 10% of total pulmonary flow [18].
Reperfusion and restoration of pulmonary flow at the end of CPB contributes to ischemia-reperfusion injury. CPB is also associated with interstitial edema, disruption of gas-capillary exchange, decreased compliance, and increased pulmonary vascular resistance. These effects could impact on the RV function during the weaning from CPB [18, 19].
Recent reports suggest to maintain continuous pulmonary ventilation and perfusion through the main pulmonary artery during CPB thus reducing ischemia-reperfusion injury and minimizing the risk of post-implant RV failure [19].
19.3.1 Pump Speed
Cardiopulmonary bypass (CPB) flow should be gradually reduced to allow filling of the left ventricle. Prior to start LVAD pump the LV should be full. After reducing CPB flow to 2 l per minute, the cross clamp is removed, and the pump started at the minimum speed (HVAD at 1800 rpm; HM II at 6000 rpm; Jarvik 2000 at 8000 rpm; Incor I at 5000 rpm).
RV function is greatly affected by pump speed. It is important to avoid setting the pump speed so high that it causes an abnormal RV geometry, which can adversely affect RV function. Pump speed has to be increased slowly to avoid suction events. Suction events can lead to the ingestion of tissue/clot from inside the LV and may also lead to episodes of ectopy and arrhythmias such as atrial fibrillation or ventricular fibrillation.
Pump speed should be maintained as low as possible at the same flow rate delivered. The pump flow is not exactly the cardiac output which is influenced by the combination of the device flow and the stroke volume of the heart.
When adjusting pump speed, the aortic valve should open every second or third beat. This low pump speed policy reduces the risk of aortic valve thrombosis, and it assures that the LV is reasonably loaded. In some cases even at low pump speed, the aortic valve will not open due to poor LV function.
19.3.2 Ventricular Interdependence: Changes in LVAD Setting
LVAD decompresses the LV and reduces LV end-diastolic pressure and pulmonary artery pressure, and it may improve right ventricular (RV) function. However the increased LVAD output increases venous return to the RV and can potentially worsen pre-existing RVF.
An aggressive LV unloading can cause an excessive leftward shift of the septum decreasing septal contribution to RV contraction.
LV unloading frequently reduces tricuspid regurgitation (TR) reducing RV afterload. However increased RV volume and tethering of valve leaflets to a leftward shifted septum can increase TR. Prolonged CPB and cardioplegic arrest are significant risk factors for early postoperative RV failure.
19.3.3 Intraoperative Transesophageal Echocardiographic Findings
Immediately after CPB, the positions of the inflow and outflow conduit, the blood flow velocity and direction are assessed using color and spectral Doppler. LVAD should have a consistent phasic, slightly pulsatile, low-velocity inflow and outflow patterns [20].
LV decompression and septum position should be monitored. A neutral position of the interventricular septum indicates adequate LV filling (◘ Fig. 19.1). If the LV is not adequately decompressed, a rightward septum shift can be seen (◘ Fig. 19.2). A leftward septal shift may indicate excessive decompression due to high pump speed or RV dysfunction (◘ Fig. 19.3). An increase in RV size, a reduction in RV systolic function, and the presence of significant TR may be demonstrated on TEE [21].
Fig. 19.1
Neutral position of the interventricular septum indicates adequate LV filling (Illustration by Ilaria Bondi’s Peppermint Advertising)
Fig. 19.2
Rightward shift of interventricular septum indicates non-adequate LV unloading (Illustration by Ilaria Bondi’s Peppermint Advertising)
