**4. Post-operative care and monitoring**

Immediate post-operative or perioperative care occurs in cardiac or cardiothoracic intensive care units. Optimizing volume status is extremely important in the initial phase as the right ventricle learns to manage the new preload it is exposed to. The LVAD speed is adjusted to optimize the patient's hemodynamics. Typically, the speed is changed with echocardiographic guidance to ensure adequate left ventricular unloading without overloading the right ventricle [25]. The aortic valve should open periodically and minimal mitral regurgitation should be evident.

When titrating the speed, visualization of the interventricular septum is required as the septum should be maintained midline to avoid right ventricular bowing, tricuspid regurgitation, and right ventricular failure. Typical speeds for the HeartMate III are 3000–9000 revolutions per minute (RPM), 6000–15,000 RPM for the HeartMate II, and 2400–3200 RPM for the HeartWare Ventricular Device [26, 27].

Due to mechanisms that are poorly understood, a significant proportion of LVAD patients develop RHF following implantation. Furthermore, RHF plays a pivotal role in the high mortality rates observed among LVAD patients who die from heart failure and multi-organ failure. As a result, in order to optimally manage patients in the postoperative period following surgical LVAD implantation, it is important to understand the pathophysiology of RHF, specifically as it presents in LVAD patients.

Each patient's physiology is monitored on the LVAD monitor via the power, flow, and pulsatility index (PI). Power is the amount of work the LVAD performs to maintain a set speed and typically ranges between 2.5 and 8.5 watts. The flow displayed


#### **Table 2.**

*Unexpected LVAD flows algorithm.*

is an estimation with normal values between 2 and 4 L/min. Changes in power and flow outside of the normal range raise concern for pump thrombosis or hypovolemia (**Table 2**). PI represents the strength of left ventricular unloading and is calculated as flow magnitude over 15 seconds with 1–10 being the expected range [25].

Shock in LVAD patients has a slightly different algorithm than in patients without LVADs since the LVAD controller is able to give live time reports. In events where the patient's MAP is less than 60 mmHg, the LVAD flow rate and power should be noted. Simultaneously, cardiac output should be calculated if hemodynamic monitoring is available and bedside echocardiography should be performed [26].

Having a high power with a low flow rate is a strong indicator of possible pump thrombosis. Treatment with thrombolysis, device exchange, or anticoagulation should be considered and implemented immediately. High flow indicator warrants evaluation of cardiac output. In a high flow state with high cardiac output, fluid resuscitation should be started and distributive shock due to infective, vasodilation, or adrenal insufficiency should be considered [26]. If the flow rate is high and the cardiac output is low, then aortic insufficiency (AI) should be evaluated urgently. Decreasing the pump speed would decrease the AI while increasing left ventricular volume. Increasing speed would improve end-organ perfusion while accelerating progression of AI. LVAD outflow cannula diastolic acceleration and systolic-to-diastolic peak velocity ratio correlates well with the true AI severity [28].

The optimal management of cardiac arrest in LVAD patients remains an area of ongoing debate, but a few general principles may be applied in this scenario. Physical exam should be performed promptly to verify the presence or absence of both an audible LVAD 'Hum,' as well as the presence or absence of an arterial pulse by doppler. In the absence of an audible hum or absence of a pulse by doppler examination, ACLS protocol should be

## *LVAD Continuing Care: A Comprehensive Guide to Long-Term Support and Management DOI: http://dx.doi.org/10.5772/intechopen.114271*

initiated immediately with establishment of an airway by intubation. As chest compressions are a relative contraindication, abdominal compressions have been attempted, but there is limited data to support the efficacy of this method. Postoperative cardiac arrest should be brought back to the operating room without delay [29].

Right ventricular function is thoroughly evaluated prior to LVAD placement (see additional details in 'Patient Selection for LVAD' section above). Postoperative RHF plays a pivotal role in the high mortality rates observed among LVAD patients who die from heart failure and multi-organ failure. As a result, in order to optimally manage patients in the post-operative period following surgical LVAD implantation, it is important to understand the pathology of right heart failure [14].

Favorable hemodynamic changes take place after LVAD implantation, including reductions in left ventricular (LV) and pulmonary artery (PA) pressures. With immediate reduction in LV filling pressures and more long-term remodeling of a longstanding pulmonary hypertension, pulmonary artery resistance goes down, leading to eventual improvement in RV afterload and systolic function. With improved cardiac output, comes increased preload for the RV to accommodate. Chronic right heart failure may result from chronic RV pressure and volume overload. This can occur in the setting of uncontrolled hypertension (excess afterload), excessive LVAD speed, hypervolemia, or any combination of these factors. Tricuspid regurgitation may also be exacerbated by leftward septal shift upon LV decompression which can cause tethering of the tricuspid valve leaflets. RV failure can be precipitated with hypoxemia and increased central venous pressure [14]. This should be evaluated with regular echocardiograms and cautious volume optimization with LVAD speed adjustments, diuresis, or ultrafiltration. Pulmonary hypertension should be treated with phosphodiesterase-5 inhibitors or inhaled nitric oxide [30].

Ramp testing is a formalized protocol that can be utilized to optimize speed and detect device thrombosis. Prior to ramp testing, ensure that the patient is therapeutically anticoagulated with an INR > 1.8 or PTT > 60 seconds. Opening arterial pressure via doppler should be >65 mmHg at baseline. The parasternal long axis view is the primary view used throughout the study. This is due to its optimal position in assessing the LVEDD and LVESD along with the frequency of opening of the aortic valve, any degree of AI or MR, and heart rate. Continuous-flow LVAD parameters are also monitored throughout the study including power, PI, and flow at each stage. Specific speed adjustments for the HMII, and HVAD are given as follows: testing speed range is 8000–12,000 rpm (HMII) and 2200–3200 rpm (HVAD). Start the test by decreasing the speed to 8000 rpm (HMII) and 2300 rpm (HVAD). Give it 2 minutes of washout time, and then evaluate for all the parameters listed above. Perform stepwise increases in speed at intervals of 400 rpm (HMII) and 100 rpm (HVAD) until the upper limit of speed is attained. This will be indicated by LVEDD <3 cm, a suction event or premature ventricular contraction (PVC) beats will occur. PVCs can indicate contact between the LVAD inflow cannula and the interventricular septum (IVS). As stated above, clinically the speed is adjusted to a midline interventricular septum, intermittent opening of the aortic valve as to prevent AI, and minimal MR. Other parameters such as high CVP, low RV stroke work index, elevated pulmonary vascular resistance (PVR), low pulmonary artery pulsatility index (PAPi), high CVP: PCWP ratio, and an elevated diastolic pulmonary gradient have been associated with RHF. The management of RHF can be a multimodal approach to therapy, but generally includes pulmonary artery catheter-guided therapy, aggressive volume optimization using diuretics or even renal replacement therapy when necessary, inotropes, pulmonary vasodilators, heart rate and/or rhythm control, and lastly mechanical RV support in the most severe cases [31].

Options for mechanical RV support include the Impella RP, Protek Duo, peripheral VA ECMO, Paracorporeal CentriMag RV assist device, and durable biventricular assist devices. The timing of when a mechanical RV support device is required varies among centers. One may find that certain centers even preemptively place RV mechanical support in high-risk patients. Others will only offer it once optimal medical therapy has failed. The choice of device also varies depending on the center's practice and experience levels [14].

Anticoagulation in the immediate postoperative period should entail the initiation of intravenous unfractionated heparin within 48 hours of implantation with goal aPTT titrated based on the particular LVAD manufacturer. For example, for the HMII, an aPTT of 40–45 seconds in the first 48 hours, followed by a titration up to an aPTT of 50–60 seconds by 96 hours. For HM III, start heparin 12–24 hours postimplantation with a goal aPTT of 45–50 seconds in the first 24 hours, 50–60 seconds in the subsequent 24 hours, and 55–65 seconds in the subsequent 24 hours. For the Heartware device, begin low-dose heparin at 10 units/kg/h on postoperative day one to target an aPTT of 40–50 seconds and gradually increase to a goal aPTT of 50–60 seconds. Close monitoring of chest tube drainage is key, and a goal aPTT should be adjusted with the quantity of chest drainage in consideration. Heparin is used as a bridge to anticoagulation with Warfarin (vitamin K antagonist therapy). Once a goal INR has been attained with warfarin therapy, heparin can be discontinued. For the HMII, start warfarin within 48 hours of implantation with a goal INR of 2–2.5 by postoperative day 5–7. For the HM III, start warfarin on postoperative day 3–5 once there is no evidence of bleeding and all chest tubes have been removed. A goal INR should be maintained between 2.0–3.0. For the Heartware device, Warfarin should be started within 4 days of implantation with a goal INR 2.0–3.0 [31].

Pump thrombosis is a dire complication and studies have shown increasing fibrous tissues on the LVAD surface due to thrombin generation [32]. As such, anticoagulation is initiated with low-dose heparin and aspirin on post operative day 1 with an aPTT goal 40–60 seconds which is later increased to 60–80 seconds. If no evidence of bleeding, warfarin is initiated after the removal of surgical chest tubes with a goal INR of 2.0–3.0 [33]. Post operative bleeding is an additional complication and management must be cautious as pump thrombosis can have fatal effects. Desmopressin and antifibrinolytics are used, however vitamin K or reversal of anticoagulation should not be considered lightly [34].

Ventricular arrhythmia is another factor that may worsen after LVAD implantation impacting mortality in the first 3 months. It is unclear whether arrhythmias are a sign of hemodynamic compromise rather than the primary cause of mortality [35]. ICD implantation is considered if all other causes of arrhythmias are ruled out and device therapy was not already in place prior to LVAD implantation [36].

Infections in LVAD patients remains one of the most common complications. While a significant proportion of patients developing postoperative infections unrelated to the LVAD had a higher observed mortality, infections of the driveline after 90 days contributes to significant morbidity and affects over 50% of patients at many institutions [37, 38]. In terms of prophylaxis, antibiotic protocols employed in these studies generally favor the use of vancomycin, a cephalosporin, a betalactam, and a quinolone. Many centers may also opt for fungal protection as well and add fluconazole. Some centers will even treat MRSA of the nares with mupirocin. Antibiotics prophylaxis is recommended to begin prior to implantation and continue throughout the peri and post operative periods. The major culprits of pocket and driveline infections are gram-positive Staphylococcus species and gram-negative

Pseudomonas species. There were eight retrospective studies and two prospective studies, including one randomized controlled trial (RCT), which describe the optimal antibiotic regimen, however large scale RCTs are needed to assess and validate the efficacy of each regimen [39].
