Complication
% of cases
Right heart failure
10–39%; up to 50% when LVAD emergently placed
Respiratory failure
6–40%
Cerebral vascular accident
10–15%
Transient ischemic attack
4–12%
Delirium
10%
Renal failure
3–33%
Hepatic failure
2–8%
Arrhythmia
30–60%
Atrial
25%
Ventricular
22–52%
Thromboembolism
6% pulmonary or systemic vasculature
Hemolysis
3–5%
Infection
Up to 42% of index hospitalizations
Bleeding requiring transfusion
31–81%
Bleeding requiring reoperation
31%
Tamponade
15–28%
This chapter will focus on the perioperative management of patients who have received one of the two prevalent and FDA-approved CF-LVADs : the HeartMate II (HM2), which was approved for bridge to transplantation in 2008 and for destination therapy in 2010, and the HeartWare HVAD (HW HVAD), which was approved for bridge to transplantation in 2012.
Preoperative Management of LVAD Patients
The perioperative management of an LVAD recipient begins with preoperative optimization of the patient’s clinical status. Clear risk factors for poor outcomes after LVAD implantation have emerged over the past decade or so [1, 2, 5]. These are discussed in detail in Chap. 2. However, several of these adverse conditions are often, at least to some degree, remedial. Effective interventions for such conditions can sometimes allow for positive outcomes after LVAD placement . The recently published guidelines for mechanical circulatory support (MCS ) from the International Society for Heart and Lung Transplantation provide a helpful summary of these preoperative treatment strategies [5]. Optimization of cardiac status, particularly addressing RHF , is a major focus of preoperative care. Right heart failure is discussed in separate chapters, but we discuss remediation strategies for other conditions below.
A substantial percentage of patients considered for LVAD implantation are malnourished or at risk for malnourishment through the pathophysiology of cardiac cachexia [6]. Indeed, only 10% of patients being evaluated for heart transplantation or LVAD implantation are considered to be “well nourished” [7], and insufficient nutritional status is associated with poor LVAD implantation outcomes [8]. Therefore, preoperative nutritional assessment of LVAD candidates is recommended, including at least a prealbumin screening and possibly more advanced measures of nutritional status, such as caloric expenditure, along with specific, nutritionist-directed interventions [6–9].
All unnecessary lines and catheters should be removed from patients who are to undergo LVAD implantation. A dental evaluation and treatment of any active or potential infections is also recommended before LVAD placement. In addition, any other active infections should be fully treated preoperatively [5, 10]. The administration of prophylactic antibiotics within 60 min of the incision and continued use for 48 h postoperatively has become standard practice [5, 11]. The most recent guidelines suggest that antibiotic regimens include coverage for both gram-positive and gram-negative organisms [5]. The most aggressive regimens, which we favor, include preoperative administration of vancomycin, a broad-spectrum cephalosporin, and fluconazole, followed by a 2-day course of vancomycin in combination with cephalosporin. Patients with a high preoperative risk for or who had a preoperative nasal swab positive for methicillin-resistant Staphylococcus aureus should be given rifampin and nasal topical mupirocin preoperatively and for 7 days postoperatively [4]. Standard topical skin preps should include the use of chlorhexidine solution [3, 12].
The function of major nonheart organs, including the kidneys, liver, and lungs, should be optimized preoperatively. Renal failure , depending on degree, is a major risk factor for poor LVAD outcomes [13–16]. In fact, end-stage renal disease requiring hemodialysis is currently considered a contraindication for LVAD implantation [5]. Therefore, it is generally recommended that renal function be optimized before device implantation [5]. In the case of advanced congestive heart failure (CHF ) , renal perfusion is often compromised. In this circumstance, it is recommended that renal function be supported by optimizing the patient’s hemodynamics with pharmacologic therapies and, perhaps, temporary MCS [5]. The evolving practice of using temporary MCS as a bridge to LVAD implantation in patients with MSOF is covered in another chapter, but early studies have suggested that such strategies are very promising [5, 17]. However, studies are needed to assess the specific strategy of targeting preoperative renal function to improve LVAD implantation outcomes. Volume overload, usually demonstrated by a central venous pressure (CVP) of ≥16, has been shown to increase the risk of poor LVAD implantation outcomes [18], and it has generally been agreed that CVP should be controlled preoperatively by using diuretics or hemodialysis techniques [5]. However, it is sometimes difficult to separate outright RHF and volume overload from renal dysfunction when conducting a study. Interestingly, volume overload has also been shown to increase the risk of acute kidney injury after LVAD implantation [13, 19].
Heart failure adversely affects liver function and can lead to liver injury by inducing both hypoperfusion (ischemic hepatitis) and venous congestion (leading to cardiac cirrhosis) [20–22]. Of these two possibilities, it appears that RHF and passive venous congestion have a more profound adverse effect. Advanced liver dysfunction can cause coagulopathy and vasodilation [20, 22]. It has been well established that patients with liver cirrhosis or a high model for end-stage liver disease (MELD) score are at high risk for adverse outcomes after LVAD implantation [20, 23–25]. In fact, recent data from a single-center study suggest that significantly elevated levels of aspartate aminotransferase and alanine transaminase and the need for a preoperative liver biopsy are powerful independent predictors of survival for HM2 and HW HVAD recipients [26]. Therefore, patients with abnormal liver function tests are recommended to undergo ultrasound evaluation of the liver, hepatology consultation, and possibly biopsy of the liver [5, 20]. Cirrhosis and having a high MELD score are considered contraindications for LVAD implantation [5]. Patients with these contraindications are typically suggested to undergo combined heart and liver transplantation [5, 20]. However, for patients with hepatic dysfunction that is not severe enough to exclude them from consideration for LVAD implantation, the current recommendations suggest pharmacologic improvement of hepatic perfusion and treatment of RHF [20]. As suggested for patients with renal failure, one strategy that may be successful for improving outcomes of patients with liver dysfunction could be to use temporary mechanical right and left heart support to improve or normalize liver function before LVAD implantation [20, 26]. A recent publication from a German hospital reported excellent outcomes (75% survival at 1 year) in a large cohort of relatively young patients (mean age, 35 ± 12 years) with acute hepatic failure who underwent HM2 or HW HVAD implantation [27]. Interestingly, 85% were on pharmacological support, and 41% were on some form of MCS going into surgery. For any patient with a demonstrated liver abnormality, we recommend administering vitamin K (10 mg, intramuscular or intravenous, though it is worth noting the risk of rare but potentially dramatic anaphylaxis with such) preoperatively, as well as maintaining vigilance for coagulopathy both intraoperatively and postoperatively, because the liver makes many of the key coagulation factors.
Pulmonary function is often impaired in patients with advanced heart failure due to interstitial and alveolar edema, cardiomegaly, pleural effusions, and secondary pulmonary hypertension, which can cause restrictive and obstructive lung defects, impaired gas exchange, decreased lung compliance, increased work to breath [28–32], and in the case of cardiac cachexia, respiratory muscle dysfunction. Studies correlating preoperative pulmonary function test results to LVAD outcomes are lacking. A limited number of studies have suggested that pulmonary function may be reduced after LVAD implantation, in spite of otherwise controlled CHF, particularly in HM2 recipients [31, 32]. Limited data suggest that the HM2 device may affect diaphragm function [33], presumably because implantation requires transection of the left anterior hemidiaphragm and because the pump for the HM2 lies directly below the left hemidiaphragm, impairing its movement. However, there is substantial evidence correlating poor preoperative pulmonary function to adverse outcomes after cardiac surgery not involving ventricular assist device (VAD) implantation, and standard recommendations suggest optimizing pulmonary function before cardiac surgery [34, 35]. We recommend controlling pulmonary edema and any airway obstructions due to CHF or underlying obstructive lung disease as well as possible before the operation. However, again, no specific intervention studies have confirmed that this approach is beneficial. Additionally, preoperative respiratory muscle training may be beneficial for patients with advanced heart failure and respiratory muscle dysfunction, as has been shown for a high-risk cohort of patients undergoing general cardiac surgery [36].
Effects of Cardiopulmonary Bypass (CPB), Anesthesia, and Surgery on the Postoperative Course After LVAD Implantation
CPB
Immediately after CPB is initiated and the aortic cross clamp is placed, pulmonary capillary wedge pressure (PCWP) and pulmonary artery pressure (PAP) increase. This can cause pulmonary vascular endothelial dysfunction and result in pulmonary vasoconstriction and, ultimately, right heart strain when the patient is being weaned from CPB. However, a number of studies have demonstrated that pulmonary vascular resistance (PVR) actually declines immediately after CF-LVAD implantation and continues to decline over time [37].
Low cardiac output state, a well-recognized complication of CPB, is essentially characterized by poor ventricular performance [38]. The cause is thought to be multifactorial, including myocardial ischemia during cross-clamping, reperfusion injury, cardioplegia-induced myocardial dysfunction, and activation of inflammatory cascades, resulting in suppression of myocardial function. In our experience, patients who undergo LVAD implantation have the same complications, except that the LVAD, presumably, compensates for impaired left ventricular (LV) performance. The effects of LVAD implantation on the right heart are complex; these are discussed in Chap. 18 .
Cardiac vasoplegia syndrome (CVS) is a form of vasodilatory shock that occurs in up to 44% of CPB patients [37]. This syndrome is caused by blood exposure to the CPB circuit and the consequent neurohumoral factor and inflammatory mediator activation. The clinical picture of CVS is typical of a systemic inflammatory response, with a low systemic vascular resistance and hypotension, but it can potentially be characterized by its resistance to typical vasopressor dosing [39]. Patients who undergo LVAD implantation are at greater risk of developing CVS, and it appears that CVS may more significantly affect the outcomes of LVAD recipients than those of typical cardiac surgery patients. A recent study showed that norepinephrine-resistant CVS is associated with a 25% mortality rate in patients who have undergone LVAD implantation [39]. Cardiac vasoplegia syndrome should be treated with vasopressors, particularly vasopressin and norepinephrine. For refractory cases, methylene blue, cyanocobalamin, and steroids may be used [39].
Another factor to consider during the postoperative care of LVAD recipients is the fluid shifts associated with CPB and surgery. When patients are initially placed on bypass, the circuit priming volume adds to the intravascular volume. On the other hand, intraoperative bleeding may decrease intravascular volume during surgery. For these reasons, it is very difficult to predict intravascular volume and, hence, right ventricular (RV) loading at the end of CPB. This is among the reasons why it is standard to perform transesophageal echocardiography (TEE) at the termination of CPB and specifically important to view the right ventricle and intraventricular septum . The position of the septum and other aspects of the right ventricle are more fully discussed below, but essentially, a midline intraventricular septum is consistent with optimal intravascular volume and RV loading [40].
Anesthesia
Anesthetic agents and rewarming can compound the vasodilatory effects of CPB. Short-acting, less potent anesthetics are less likely to cause vasodilation. Some practitioners choose to avoid volatile agents altogether and use propofol instead. However, propofol can also significantly decrease systemic vascular resistance.
Surgery
Placement of the inflow cannula in the apical segments of the left ventricle causes increased LV dysfunction and loss of apical contractility. Analysis of LV tissue obtained up to a year after LVAD implantation showed persistent damage to myocytes and contractility derangements [41]. Because the majority of the LV contraction is based on twisting and untwisting of the apical portion to eject the blood, coring out the LV apex in order to place the inflow cannula invariably worsens LV contractility, compliance, and output. The loss of apical contractility adds to the decrease in inotropy seen once the LVAD is implanted [42], although LV function can certainly improve over time after LVAD implantation [43].
Coming Out of the Operating Room
Once the patient is stable and the LVAD speed has been set based on appropriate TEE imaging [40], it is time to transport the patient to the intensive care unit (ICU) and immediately begin cardiac intensive care management. All of our LVAD recipients leave the operating room with arterial and pulmonary artery catheters for monitoring pressure and measuring mixed venous oxygen saturation (MVO2) and cardiac output by thermodilution. The patients are also on inotropic support, often consisting of low doses of milrinone and a catecholamine (usually dobutamine or epinephrine). As discussed in detail below, the inotropes are primarily for supporting the right ventricle, which is at risk of stress and decompensating after LVAD placement [44]. In addition, the patients are usually on vasopressors to treat CVS; a combination of vasopressin and norepinephrine is standard at our institution .
Postoperative Course, Complications, and Management
The postoperative period is often characterized by labile hemodynamics (typically caused by volume shifts), vasoplegia, and RV dysfunction. Partly as a consequence of this, major organ function can change quickly in the postoperative period. Not surprisingly, postoperative complications occur frequently after LVAD implantation. The major postimplantation complications are listed in Table 8.1. Because of the possible complications, our care model is for the anesthesiologist and surgeon to directly hand off the care of the patient to a postanesthesia care unit (PACU )/ICU intensivist and nursing team at the bedside. Typically, the required nurse-to-patient ratio is either 1:1 or 2:1 for these patients. It is imperative that all team members are well trained and experienced. The complexity and dynamic nature of the immediate postoperative course requires the proximate presence of the ICU team and clear lines of communication to the cardiologist and surgical team for best outcomes.
Pulmonary Considerations
As with any patient who has undergone cardiac surgery, the initial PACU assessment for LVAD recipients begins with an evaluation of gas exchange and pulmonary status ; however, for these patients, evaluation and management of mechanical ventilation, which virtually all LVAD recipients are on when they leave the operating room, is particularly important. Continuous-flow MCS, though not extensively studied, does not appear to affect the ventilation/perfusion relationships in the lungs or gas exchange [45]. Gas exchange is evaluated with hemoglobin oxygen saturation and arterial blood gas testing. However, the standard pulse oximetry test for assessing oxygen saturation of the blood may be unreliable in CF-LVAD recipients [46]. Obviously, the goal for the arterial hemoglobin oxygen saturation level is greater than 90% for optimal DO2. The goal for the carbon dioxide arterial tension is to be near but not over 40 mmHg in order to optimize the acid-base balance. But for LVAD recipients, these goals are particularly important because failure to meet them will result in increased PVR [47], which can add afterload burden to a right ventricle already burdened by an increased preload from the increased cardiac output of the new LVAD. As discussed below and elsewhere, RHF is an extremely important complication to avoid in hearts with a newly implanted LVAD.
Physical exams and chest x-rays are used to assess for atelectasis and pulmonary edema, both of which can affect gas exchange. Both should be aggressively treated, but we are particularly diligent about correcting any significant atelectasis because it is a frequent consequence of cardiac surgery and can significantly increase PVR [34, 36]. Usually, we treat atelectasis by increasing either the ventilator-delivered tidal volume (Vt) or the positive end-expiratory pressure (PEEP), although sometimes therapeutic bronchoscopy is required in cases of airway obstruction.
Mechanical ventilation can have three distinct effects on cardiac physiology through the effects of applied mean airway pressure (Paw) [34, 47]. First, increased Paw, via transmission of such pressure to the pleural space, can reduce the RV preload by discouraging venous inflow into the higher pressure chest cavity. Second, increased Paw can potentially cause the alveoli to overdistend, thereby causing compression of the pulmonary capillaries and increasing the PVR. Finally, increased Paw can decrease LV afterload via effects on LV wall tension. Our general approach is to assure a low peak airway pressure (<20 cmH2O), as concerns about PVR and RHF are paramount. Typically, high RV preload and high LV afterload are dealt with by using interventions other than mechanical ventilation manipulation. The best postoperative ventilator management involves using settings that promote gas exchange, prevent and/or treat atelectasis, and avoid a high Paw. As of yet, no studies have specifically sought to determine the optimal ventilator practice in the LVAD postimplantation setting [44], so we follow standard post-cardiac surgery guidelines for ventilation management. Our usual mechanical ventilation mode is volume cycled with a Vt of 6–8 mL/kg and a PEEP setting of 5 cmH2O. The respiratory rate is typically set at 10–12 breaths per minute, with a fraction of inspired oxygen (FiO2) of 50% or titrated to an O2 saturation level of >92%. Adaptive support ventilation, a newer mode of ventilatory support, has been used successfully to shorten the postoperative ventilator times of cardiac surgery patients [48]. Our preliminary experience with using adaptive support ventilation for LVAD patients has been good; however, close attention must be paid to gas exchange and the potential development of atelectasis and alveolar overdistension. As with other types of cardiac surgery patients, if LVAD patients demonstrate hemodynamic stability, rewarm properly, come out of anesthesia appropriately, and meet the basic mechanical ventilation weaning criteria, we aim to extubate the patient and remove the mechanical ventilation within 6–8 h of surgery. One caveat to note for the extubation of LVAD patients is that extubation may cause an increase in RV preload. That is, removal of the positive thoracic pressure of mechanical ventilation may increase venous return to the right ventricle, placing it at risk of decompensation. Therefore, it is important to monitor the CVP and RV function by echocardiography , along with other hemodynamic parameters, immediately after extubation of these patients. Prolonged postoperative respiratory failure (PPRF) (the definition for which varies but usually includes a mechanical ventilation requirement of at least 6 days) has been reported to occur in 9–40% of LVAD recipients postimplantation [3, 49–53]. However, the exact causes of prolonged ventilation have not been well delineated in the literature. In our experience, conditions/procedures often associated with PPRF include poor DO2 with MSOF, bleeding requiring reoperation, open chest, acute lung injury associated with MSOF, transfusions, and sepsis. Thus far, there have been no sophisticated studies evaluating the effects of CF-LVAD implantation on respiratory load and respiratory muscle power output in humans. Patients with PPRF should be cared for by following the same guidelines as above, but additionally, vigilance for ventilator-associated pneumonia should be increased, as these patients are at significant risk for this complication [3].
Hemodynamic and LVAD Function Considerations
As LVAD and total artificial heart technology progresses , there are likely to be significant advancements made in device auto adjustments to respond to the fluctuating hemodynamic states in the postoperative and other periods [54]. However, for now, the bedside hemodynamic assessments and interventions made by the care team during the immediate postoperative period are often critical to the outcomes of these patients. The initial postoperative assessment of hemodynamics consists of a review of the standard data presented in Table 8.2, including clinical parameters, catheter filling pressure, thermodilution cardiac output, and laboratory measurements (adequate and optimal values are provided). Additionally, the key LVAD operational parameters (displayed on the bedside inpatient LVAD monitors) and the important heart-LVAD interaction parameters (obtained by point-of-care echocardiography ) are reviewed immediately after the operation (expected values are provided in Table 8.3).
Table 8.2
Postoperative hemodynamic parameters
Adequate | Optimal | |
|---|---|---|
Cardiac index | 2.2 L/min/m2 | ≥2.5 L/min/m2 |
Mean arterial pressure | 60–90 mmHg | 70–80 mmHg |
Mixed venous oxygen | >50% | >70% |
Central venous pressure | ≤15 mmHg | 5–10 mmHga |
Pulmonary artery occlusion pressure | ≤15 mmHg | 8–12 mmHg |
Cardiac rhythm | – | Normal sinus rhythm |
Lactate | <4 mmol/L | – |
Hemoglobin | – | ≥10 g/dL |
Table 8.3
Expected left ventricular assist device (LVAD) and echocardiography parameters after device implantation
Clinical screen of LVAD monitor | HM2 | HW HVAD |
|---|---|---|
LVAD speed | 8000–10,000 rpm | 2400–3200 rpm |
LVAD flow | 2.5–7 L/min | 2.5–7 L/min |
LVAD power | 4–9 W | 2.5–8.5 W |
Pulsatility index | 3.5–5.5 | – |
Pulsatility waveform | – | ∆ flow >2–4 L/min |
Bedside point-of-care TTE | HM2 and HW HVAD |
|---|---|
Interventricular septum | Midline |
Left ventricular size | Reduction of LVID by 20–30% |
Right ventricular size | Variable effects on right ventricular size |
Right ventricular function | Normal RV EFXN >45% |
Inflow cannula | Directed at mitral valve |
Doppler: Turbulence minimal or less | |
Aortic valve opening | Every 2–3 beats |
Aortic valve | Doppler: Regurgitation minimal or less |
Mitral valve | Doppler: Regurgitation minimal or less |
Tricuspid valve | Doppler: Regurgitation minimal or less |
Pericardial effusion | Minimal and no evidence of right ventricular or right atrial collapse (a sign of tamponade) |
The bedside inpatient LVAD monitors for the HM2 and HW HVAD are connected to the device controllers, which operate the pumps and serve as the user interfaces [55, 56]. The inpatient monitors are specifically designed to provide bedside clinicians with a real-time, optimized data display from the controllers. The LVAD speed, which refers to the revolutions per minute (RPMs) of the device’s impellers, is the only set operational parameter for the devices. The HM2 is an axial-flow device that “pushes” blood through the pump casing, moving it from the inflow cannula through to the outflow cannula with a turning propeller. The propeller is turned by magnets and supported by mechanical bearings. In contrast, the HW HVAD is a centrifugal-flow device that “throws” blood from the pump. Specifically, this device takes in blood from the inflow cannula, pushes it between the blades of a rotating disk that is housed in the pump casing and levitated with magnets and hydrodynamic forces, and then throws it tangentially out the outflow cannula. The HW HVAD acts much like a discus thrower, who releases the disk after generating energy through a spinning motion [44, 55–57]. The HM2 operates at a set speed between 6000 and 15,000 RPMs, but the speed is usually set between 8000 and 10,000 RPMs. The HW HVAD can operate at a speed between 1800 and 4000 RPMs, but the usual setting is between 2200 and 3200 RPM. These speeds result in the typical optimal blood flow of between 2.5 and 6 L/min, but both devices can provide up to 10 L/min of flow. The power input to the pump is measured and displayed in wattage and varies according to the pump speed and volume or flow through the pump. For both devices, the flow displayed is an estimate that is calculated using an algorithm based on the speed and measured power of the device and is not directly measured [55, 56]. The only way to directly measure LVAD output is via Doppler TEE determination of flow at the outflow cannula. This data, together with the diameter of the outflow cannula, allows the output from the device to be calculated [58, 59]. The HW HVAD also uses hematocrit, a measure of blood viscosity (which is manually entered), to estimate flow. The default hematocrit is 30. Generally, the calculated flow is quite accurate for the HW HVAD over the usual range of speeds [57, 60]. However, flow estimation is much less accurate for the HM2, which shows substantial variability between patients [61, 62]. In the usual range of flows (i.e., 2.5–6 L/min), the calculated flow is typically 15–20% below the actual flow rate. However, for both devices, the accuracy of the calculated flows cannot be assured at high or low LVAD speeds or when there is an obstruction at the inflow or outflow cannula or within the pump [55, 56]. This is key to understanding and troubleshooting the devices. Both the HM2 and HW HVAD have a measure of pulsatility or variability in flow. It is important to understand that flow through these devices, like that through the heart, is determined, in part, by preload and afterload, as well as by the pump speed [3, 44, 55–58, 63]. Or to put it another way, the flow rate partly depends upon the differential pressure (or “head pressure”) between the inflow and outflow cannulae. The pressure at the inflow cannula is equal to the pressure in the left ventricle, and the pressure at the outflow cannula is equal to the pressure in the proximal aorta. The equation for differential pressure (Diff P) is as follows:
where Pa = pressure in the aorta, Pv = pressure in the left ventricle, and delta P pump is the change in pressure as blood flows through the pump (typically, this is negligible).
Flow rate is inversely related to the differential pressure. If the LV volume (and hence the pressure in the left ventricle and at the inflow cannula) increases, then the flow though the pump will increase. Similarly, if the LV volume decreases, then the flow will drop. If the LV contractile force (and hence the pressure at the inflow cannula) increases, then the flow through the pump increases. If the pressure in the aorta (and hence at the outflow cannula) decreases due to low vasotone, then the flow will increase. If the aortic vasotone increases, then the flow will decrease. So, normally, although the speed is set, flow through the device is somewhat pulsatile, and the pulsatility is driven primarily by cyclical differences in LV pressure. It is important to note here that the HW HVAD and all the centrifugal-flow pumps are, by design, more sensitive to head pressure and usually demonstrate greater pulsatility. The design of these devices also makes them particularly sensitive to afterload. The HM2 provides a pulsatility index, whereas the HW HVAD displays a pulsatility waveform as a marker of pulsatility. The pulsatility index (PI) for the HM2 is calculated as follows (note that the value has no units):
where the flow max and flow min are the averaged peak and valley flows over a 10- to 15-s interval and the flow average is the total averaged flow over this interval (refer to the device manual for the expected ranges).
The HW HVAD displays flow pulsatility as a continual waveform on the bedside monitor (refer to the device manual for ranges) [55, 56]. Pulsatility measures are used, along with other measures, to identify disturbances in preload and afterload conditions that affect flow of CF-LVADs.
Standard echocardiography windows (parasternal and four-chamber views) are usually adequate for the initial bedside point-of-care assessment by the intensivist [58, 59, 64]. The first and key echocardiography parameter to assess is the position of the interventricular septum. Fig. 8.1 demonstrates the optimal change in septal position after LVAD implantation (i.e., midline between both ventricles) [58]. When the septum is midline, the LVAD speed and flow are generally within the desired ranges, and the LV preload and afterload conditions are appropriate for the settings [44, 57–59, 64–66]. Septal midline position is consistent with an LVAD flow adequate enough to appropriately decompress the failing, distended left ventricle but not so high as to empty the left ventricle to the point where the inflow cannula is at risk of coming up against the LV wall and causing dynamic inflow obstruction. Furthermore, when the septum is at midline, the speed and flow are typically appropriate for optimal RV function. If the LVAD flow is too high, the septum is pulled leftward toward the over-emptied and small left ventricle, causing the septal contribution of the RV contraction to be impaired. A leftward-shifted septum can also compromise tricuspid valve geometry (annular dilatation and chordae tendineae tension) and function (papillary muscle). If the LVAD flow is too low, the left ventricle is inadequately emptied, thus causing the left ventricle to enlarge and the septum to bulge rightward, similarly impairing the septal contribution to RV contraction. A leftward shift of the septum may also signal volume overload of the right ventricle. An overdistended right ventricle essentially “pushes” the septum leftward. An LVAD-driven increase in circulatory flow may cause the blood to be delivered at a higher pressure and volume than the right ventricle can pump through and into the pulmonary circulation. This may be due, in part, to a high PVR or poor RV function , as is common in patients with advanced heart failure before they undergo LVAD implantation, or to incompletely understood negative effects of LVAD implantation on RV function . Overdistention of the right ventricle can lead to a cycle of progressive RHF, which is among the most common and feared complications of LVAD implantation. Overdistension can force the right ventricle to operate on the descending limb of the Starling curve, producing RV wall stress and injury and a decrease in RV wall perfusion, creating conditions for ischemic injury. A midline septum also typically insures that the inflow cannula is appropriately aligned with the mitral valve to allow for unobstructed flow into the pump.
Fig. 8.1
Right ventricular size and function . Two perpendicular sections of a 3D transesophageal echocardiography reconstruction of the right ventricle from tricuspid valve (TV) to pulmonary (PV) valve are shown. The cross section (a) demonstrates the crescent shape and the sagittal section (b) the triangular shape of the right ventricle (RV). Ventricular interdependence between the left ventricle (LV) and RV during systole relies on interventricular septum position as shown in cross section for different clinical scenarios. Used with permission from Meineri et al. [58]
When determining the appropriateness of LVAD flow, other factors to assess, besides septal position, are the gross sizes of the left and right ventricles, especially in relationship to the preload and afterload of the heart-LVAD system. An enlarged left ventricle may signal that the LVAD flow is too low to decompress the left ventricle or, alternatively, it may indicate a volume overload state with adequate DO2 from the LVAD flow. In both of these circumstances, the right ventricle may be distended, as well, but it certainly would not be expected to decrease in size. An underfilled left ventricle may signify an LVAD speed too high for the volume state or RHF with an inability to deliver adequate preload to the left ventricle. In the latter case, the right ventricle would be expected to be distended.
On gross inspection, the LVAD inflow cannula should be directed at the mitral valve to allow for the most linear flow through the ventricle into the pump. Additionally, Doppler signals should show minimal turbulence at the inflow cannula, ruling out significant anatomic or thrombotic obstruction of the inflow cannula. The outflow cannula is usually difficult to visualize on a standard transthoracic echocardiogram (TTE).
Initial echocardiographic inspection by the intensivist should include visualization of the aortic and mitral valves, both by two-dimensional and Doppler imaging. Though somewhat controversial, it is generally recommended that the LVAD speed be adjusted to allow the aortic valve to open every two to three beats, if the DO2 is otherwise adequate after LVAD implantation [59, 67]. When the LVAD speed is sufficiently low, enough blood is allowed to build up in the ventricle to be ejected through the valve, creating a parallel flow to the devices. This can help to minimize the risk of thrombus formation at or immediately above the valve and to decrease the chance of valve fusion due to disuse [67]. A fused aortic valve may eventually degenerate, and under pressure from LVAD flow into the proximal aorta, become incompetent, eventually leading to aortic valve regurgitation. Left ventricular assist devices may also exacerbate pre-existing aortic valve regurgitation. After LVAD implantation, proximal aortic flow and pressure increase, typically along with a decrease in LV diastolic pressure due to LV unloading. The change in pressure gradient across the aortic valve can promote an increase in aortic valve regurgitation. Severe aortic valve regurgitation can lead to continuous recirculation of blood from the proximal aorta to the left ventricle and back to the proximal aorta again, thereby decreasing systemic DO2 [59, 67]. As such, severe aortic valve regurgitation after LVAD implantation may prompt the need for surgical correction of the valve.
Moderate-to-severe mitral valve regurgitation is common in patients with dilated cardiomyopathy, occurring in 76% of the patients in one study [67, 68]. Mitral valve regurgitation is a function of annular dilation and LV end-diastolic pressure [67]. Left ventricular assist device implantation typically mitigates mitral valve regurgitation via LV unloading. Failure to do so may suggest that the LVAD inflow cannula is interfering with the mitral valve apparatus and that it may be necessary to decrease the LVAD speed or even surgically intervene .
Tricuspid valve regurgitation is also very common in patients with dilated cardiomyopathy (30–60% of cases, depending upon the series). This is due to the elevated PAP resulting from LV failure and a dilated right ventricle [67]. Typically, LVAD implantation would be expected to decrease PAP via LV unloading. However, persistent pulmonary vascular bed remodeling and pulmonary vasoconstriction from CPB may cause PVR to increase after the operation. This may contribute to RHF during the postoperative period. Significant tricuspid valve regurgitation should prompt at least pharmacologic treatment of pulmonary hypertension and possibly surgical correction of the valve.
Finally, after LVAD implantation, echocardiography should be performed to ensure that there is only a minimal amount of pericardial fluid. If pericardial effusion is significant, then the possibility of developing cardiac tamponade should become a concern. Tamponade is much more common in patients who have undergone LVAD implantation (occurring in 15–28% of patients) than in those who have undergone most other types of cardiac surgery. It is usually caused by postoperative bleeding into the pericardium or by a mediastinal hematoma extrinsic to the pericardial space. With either pathophysiology, the echocardiogram almost always shows collapse of the right atrium and right ventricle. Occasionally, the echocardiography signs of tamponade are atypical in this patient population [69], and other signs are used to diagnose tamponade (see discussion below).
The principal concern regarding hemodynamics during the postoperative period is poor DO2, which is generally defined as having a thermodilution cardiac index of <2.5 (certainly when <2.2) [5] or otherwise is suggested by having a MVO2 level of <70% (certainly when <50%) or a lactic acid level of 4 mmol or greater. Our algorithm for assessing poor DO2 is presented in Table 8.4. This algorithm follows several recently published guides for assessing hypotension and low DO2 in patients immediately after LVAD implantation [3, 5, 44, 58, 63, 64]. Essentially, our algorithm follows standard hemodynamic evaluation protocols by looking at cardiac preload and afterload (arterial vasotone), as well as “central” (cardiac equivalent in normal physiology) LVAD output or flow. The LVAD flow is key to our algorithmic assessment.
Table 8.4
Decreased oxygen delivery : assessment and treatment
↓CO, ↓MVO2, ↑LA | ||||||
|---|---|---|---|---|---|---|
Low |  | LVAD flow |  | High | ||
Volume depletion | Severe aortic regurgitation | |||||
Hemodynamics | Differential diagnosis: − Hypovolemia − Bleeding Treatment: Volume − RBCs for Hgb ≥10 − Bolus 250 mL 5% albumin and reassess Surgical − Possible surgery for bleeding | Hemodynamics | Differential diagnosis: − Severe AR Treatment: Device − Trial ↓ speed Surgical − Aortic valve repair Medications − Nicardipine − Nitroprusside | |||
MAP | ↓ | MAP | ↓ | |||
PCWP | ↓ | PCWP | ↑ | |||
CVP | ↓ | CVP | ↑ or no change | |||
Echo findings | Echo findings | |||||
IVC | ↓ | IVC | ↑ or no change | |||
LV | ↓ | LV | ↑ or no change | |||
RV | ↓ | RV | ↑ or no change | |||
Septum | Midline or left shifted | Septum | Right shifted | |||
LVAD | LVAD | |||||
PI | ↓ | PI | ↑ | |||
PP | ↓ | PP | ↑ | |||
RHF or PE | Vasodilation | |||||
Hemodynamics | Differential diagnosis: − PHTN (SPAP ≥ 40) − RHF − TR − PE (massive or submassive) Treatment (for RHF/PHTN): Device − Trial ↓ speed Pulmonary vasodilators − NO/inhaled epoprostenol − Sildenafil − Milrinone Inotropes for RHF − Epinephrine − Dopamine − Dobutamine Pulmonary embolism − AC/possible catheter-directed therapy Surgical − Possible surgery for TR | Hemodynamics | Differential diagnosis: − Cardiac vasoplegia − Sepsis − Systemic inflammatory response syndrome Treatment: Volume − 250 mL 5% albumin or crystalloid and reassess Medications − Vasopressin − Levophed Suspected sepsis − Culture and use empiric broad-spectrum antibiotics | |||
MAP | ↓ | MAP | ↓ | |||
PCWP | ↓ | PCWP | ↓ or no change | |||
CVP | ↑ | CVP | ↓ or no change | |||
Echo findings | Echo findings | |||||
IVC | ↑ | IVC | ↓ or no change | |||
LV | ↓ | LV | ↓ or no change | |||
RV | ↑ | RV | ↓ or no change | |||
Septum | Left shifted | Septum | No change or left shifted | |||
LVAD | LVAD | |||||
PI | ↓ | PI | ↓ | |||
PP | ↓ | PP | ↑ | |||
Cardiac Tamponade | Pump dysfunction (flow erroneously high) | |||||
Hemodynamics | Differential diagnosis: − Pericardial effusion − Mediastinal hematoma − Tension pneumothorax Treatment: Surgical − Pericardial window − Hematoma evacuation Tension PTX treatment − Tube thoracostamy *Note: PCWP may be ↓ early due to LV unloading, ↑ PCWP is a late finding | Hemodynamics | Differential diagnosis: − Rotor thrombosis − Mechanical failure of rotor Treatment: Medication − AC or thrombolytics Surgical − Pump replacement | |||
MAP | ↓ | MAP | ↓ | |||
PCWP | ↑* | PCWP | ↑ | |||
CVP | ↑ | CVP | ↑ | |||
Echo findings | Echo findings | |||||
IVC | ↑ | IVC | ↑ | |||
LV | ↓ | LV | ↑ | |||
RV | Collapsed | RV | ↑ | |||
RA | Collapsed | RA | ↑ | |||
Septum | N/A | Septum | Right shifted | |||
LVAD | LVAD | |||||
PI | ↓ | PI | ↓ | |||
PP | ↓ | PP | ↑ | |||
Increased LV afterload | ||||||
Hemodynamics | Differential diagnosis: − Hypertension − Vasopressors Treatment: − Stop or reduce vasopressors and/or start nicardipine or nitroprusside | |||||
MAP | ↑ | |||||
PCWP
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