Perioperative Care of the Patient With the Total Artificial Heart : Anesthesia & Analgesia

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Cardiovascular Anesthesiology

Perioperative Care of the Patient With the Total Artificial Heart

Yaung, Jill MD*; Arabia, Francisco A. MD, MBA; Nurok, Michael MBChB, PhD*†

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Anesthesia & Analgesia 124(5):p 1412-1422, May 2017. | DOI: 10.1213/ANE.0000000000001851
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Advanced heart failure continues to be a leading cause of morbidity and mortality despite improvements in pharmacologic therapy. High demand for cardiac transplantation and shortage of donor organs have led to an increase in the utilization of mechanical circulatory support devices. The total artificial heart is an effective biventricular assist device that may be used as a bridge to transplant and that is being studied for destination therapy. This review discusses the history, indications, and perioperative management of the total artificial heart with emphasis on the postoperative concerns.

Cardiovascular disease is the leading cause of mortality worldwide. Accounting for 36% of deaths resulting from cardiovascular disease, heart failure affects over 5.7 million Americans1 and 23 million people globally.2 In the United States, an estimated 915,000 people are newly diagnosed with heart failure annually, and over 8 million people are projected to have heart failure by 2030.1,3 Although there has been improvement in survival after diagnosis, the 5-year mortality rate remains at approximately 50%.1,4,5 Although heart transplantation is the ideal treatment for patients with advanced heart failure, the number of transplant candidates unfortunately continues to exceed the number of suitable donors. Over the past decade, the adult transplant waiting list has increased by 34%, whereas the number of donors has remained the same.6 Because of this high demand and lack of supply, mechanical circulatory support has become more prevalent.

Indications for Total Artificial Heart Implantation

Mechanical circulatory support devices are used in patients with worsening advanced heart failure despite optimal pharmacologic therapy. A ventricular assist device is indicated for use as a bridge to transplantation, destination therapy, or a bridge to myocardial recovery. Most devices are implanted for left ventricular failure, but for some patients, right ventricular support may also be necessary, even if right ventricular function appears normal preoperatively. Right ventricular failure has previously been reported to occur on average between 10% and 40% of patients after left ventricular assist device (LVAD) placement and has been associated with higher morbidity and mortality, including a decreased rate of survival to transplantation.7–19 Several studies have identified varying risk factors for developing right ventricular failure after LVAD placement based on patient characteristics, hemodynamic factors, laboratory data, and echocardiographic imaging.7–23 There is no single consistent risk factor, but some recurring variables include elevated serum creatinine,16,18,23 elevated serum bilirubin,8,16 elevated serum hepatic function enzymes,16,18 decreased right ventricular stroke work index,8,12,17,19,23 elevated central venous pressure,8,9,14 preoperative use of an intra-aortic balloon pump,10,13 and severe tricuspid regurgitation.14,22 Patients being evaluated for mechanical circulatory support who appear to be at high risk of worsening right ventricular function after isolated LVAD insertion should be considered for planned biventricular support, because outcomes appear superior with primary biventricular device placement versus late conversion.24

Table 1.:
Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS®) Profiles25

The total artificial heart (TAH) offers biventricular support for patients with severe biventricular failure as a bridge to orthotopic cardiac transplantation. In the past 10 years, over 75% of patients receiving a TAH were categorized as Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS®) profiles 1 or 2,a corresponding with critical cardiogenic shock and progressive decline on inotropes, respectively (Table 1).25 These patients are at high risk for imminent death. Recent data from INTERMACS® suggest that survival outcomes are slightly better for patients implanted with a TAH compared with patients receiving other biventricular assist devices.26 Survival rates at 3 and 6 months after TAH implantation were 76% and 65%, respectively, and 45% of TAH patients in the last 10 years were transplanted by 6 months.a Applications for the TAH include use in patients with significant coexisting cardiac pathologies such as severe refractory arrhythmias, structural defects such as ischemic ventricular septal defect or ventricular wall rupture, intracardiac mass such as thrombus or aneurysm, infiltrative diseases such as amyloidosis or tumors, failed prior cardiac transplant, ventricular failure with presence of a mechanical valve prosthesis, and right ventricular failure in the presence of an LVAD.27–29

Brief History of the Total Artificial Heart

Research and development of the TAH started blossoming in the late 1950s and 1960s. Early leaders in the field included Dr Willem Kolff, Dr Tetsuzo Akutsu, Dr Michael DeBakey, and Dr Domingo Liotta. In 1957, Akutsu and Kolff at the Cleveland Clinic performed a TAH implant into a dog that survived for 90 minutes.30,31 Liotta at the National University of Córdoba, Argentina, started developing a TAH in 1958, which resulted in his recruitment to DeBakey’s team at Baylor College of Medicine in Texas in 1961. In a mission spearheaded by DeBakey in 1964, former U.S. President Lyndon B. Johnson approved financial support for the U.S. Artificial Heart Program with a goal of creating a TAH within 10 years.28,32

Dr Denton Cooley at the Texas Heart Institute performed the first TAH human implant in 1969 using a TAH designed by Liotta. Haskell Karp, a 47-year-old man with advanced heart failure, severe coronary artery disease, and postinfarction ventricular aneurysm, underwent ventricular remodeling surgery and aneurysm resection. He was implanted with the Liotta TAH when he failed weaning from cardiopulmonary bypass. He was extubated on the first postoperative day and was sustained on the TAH for 64 hours until he received a heart transplant. Unfortunately, he died 32 hours posttransplantation secondary to pneumonia and renal failure.33,34

Akutsu joined the team at the Texas Heart Institute in 1974, leading to the development of the Akutsu III TAH.35 This led to the second human TAH implantation in 1981 in a 36-year-old man with refractory ventricular fibrillation after coronary artery bypass surgery. The Akutsu III TAH supported him for 55 hours until he received a donor heart. He died approximately a week later secondary to multiorgan failure and sepsis.36 In the meantime, Akutsu’s former colleague, Kolff, had moved from the Cleveland Clinic to the University of Utah, where he and Dr Robert Jarvik developed the Jarvik-7 TAH. In 1982 at the University of Utah, Dr William DeVries implanted the first Jarvik-7 TAH in the third human TAH recipient, a 61-year-old retired dentist named Barney Clark. He was ineligible for a heart transplant and was supported by the Jarvik-7 for 112 days.37,38 By 1991, the Jarvik-7 TAH had been implanted in 198 patients.28 Secondary to changes in ownership, the Jarvik-7 TAH has been renamed multiple times to the Symbion Artificial Heart, the CardioWest™ TAH, and, since 2001, the SynCardia temporary TAH (TAH-t; SynCardia Systems, Inc, Tucson, AZ). The U.S. Food and Drug Administration (FDA) approved this device in 2004 for use as a bridge to transplant and granted approval in 2014 for an investigational study for use as destination therapy. The SynCardia TAH-t remains the only device to have full approval by the FDA, Health Canada, and European Union as a bridge to transplant. The only other TAH with FDA approval is the AbioCor® Implantable Replacement Heart (IRH; Abiomed, Inc, Danvers, MA), which received approval in 2006 as a Humanitarian Use Device. The CARMAT® TAH (CARMAT SA, Vélizy-Villacoublay, France) that has been developed in France has been implanted in 4 patients to date, completing a feasibility study, which was approved in 2013.39,40

SynCardia Temporary Total Artificial Heart

The SynCardia TAH-t is a pulsatile, pneumatically driven pump that is implanted orthotopically, replacing both native ventricles and all 4 valves (Figure 1). The 2 artificial ventricles are made with polyurethane, and each ventricle contains a 4-layer diaphragm that separates the air chambers from the blood chambers. SynCardia SynHall™ (SynCardia Systems, Inc, Tucson, AZ) mechanical valves, 27 mm inflow and 25 mm outflow, direct blood flow in each ventricle. Two tunneled drivelines deliver compressed air to the diaphragms in each ventricle. Maximum stroke volume is 70 mL, resulting in a cardiac output of 7 to 9 L/min. The drivelines are connected to an external console that provides diagnostic information and controls device settings.28,41–43 Device beat rate, duration of systole, and driving pressures may be manually configured, typically with ranges such as: (1) beat rate between 100 and 130 beats per minute; (2) systolic duration 50% to 60%; (3) right ventricular driving pressure 30 mm Hg above pulmonary artery pressure at approximately 50 to 70 mm Hg; and (4) left ventricular driving pressure 60 mm Hg above systemic pressure at approximately 180 to 200 mm Hg. Filling volumes of 50 to 60 mL per beat are ideal in the 70 mL TAH-t, allowing for a 10- to 20-mL safety window to accommodate episodes of increased venous return.41 A diastolic vacuum, usually set at approximately 10 mm Hg, may be applied to augment filling, but only when the chest is closed to avoid air entrainment.43 Normal pressure and flow waveforms should reflect the “partial fill/full eject” design of the TAH-t (Figures 2 and 3).

Figure 1.:
SynCardia temporary total artificial heart (TAH-t). Image courtesy:
Figure 2.:
TAH-t pressure waveforms reflecting full eject and partial eject. Blue and red waveforms reflect right and left ventricular pressures, respectively. The onset of systole causes a rapid increase in pressure as compressed air fills the air chamber in the ventricle and causes upward movement of the diaphragm. When driving pressure exceeds afterload pressure, the outflow valve opens. Subsequently, the waveform reflects a slower rate of pressure rise as blood is ejected from the ventricle. Completion of a normal systolic cycle results in a full eject flag (black arrow), indicating maximum upward position of the diaphragm and full emptying of the ventricle. Image adapted with permission from SynCardia. TAH-t indicates temporary total artificial heart.
Figure 3.:
TAH-t flow waveforms reflecting partial fill and full fill. Blue and red waveforms reflect right and left ventricular flows, respectively. The vertical lines indicate the opening of the inflow valve on each corresponding side. The initial steep descent before the opening of the inflow valve is as a result of the rapid release of pressure in the air chamber and closure of the outflow valve. As air pressure decreases, the diaphragm moves down and allows for diastolic filling. Integration of the area under the curve calculates total filling volume, which is equivalent to stroke volume in the presence of full systolic ejection. A waveform dropping to zero (black arrow) indicates full filling and should be investigated. Manipulating device beat rate, systolic duration, and diastolic vacuum may allow for optimization of ventricular filling. Image adapted with permission from SynCardia. TAH-t indicates temporary total artificial heart.
Figure 4.:
70 mL and 50 mL versions of the TAH-t. Image courtesy: TAH-t indicates temporary total artificial heart.

An important consideration is the size limitation of the SynCardia TAH-t, which displaces 400 mL of space. To minimize complications associated with improper fit, the TAH-t is generally restricted to patients with a body surface area of greater than 1.7 m2 or with an intrathoracic anteroposterior diameter of greater than 10 cm at the level of the tenth thoracic vertebra based on computed tomographic imaging.42 A smaller 50-mL version has been designed to address smaller adults and pediatric patients (Figure 4). Earlier in 2015, the FDA approved a clinical trial studying the 50 mL as a bridge to transplant.

AbioCor® Implantable Replacement Heart

The AbioCor® IRH developed by Abiomed and the Texas Heart Institute is a fully implantable device, omitting percutaneous external drivelines and maintaining skin barrier integrity. It uses electrohydraulic energy via a transcutaneous energy transmission system to produce pulsatile blood flow. All inner surfaces and all 4 valves of the IRH are made with a polyurethane plastic material (Angioflex®; Abiomed, Inc, Danvers, MA) resistant to calcification.44 The IRH weighs 1090 g and displaces 800 mL of space.45 It is able to produce a stroke volume of approximately 60 mL and generate a cardiac output of 4 to 8 L/min.46

Between 2001 and 2004, the AbioCor® IRH was implanted in 14 patients as destination therapy.28,44,47 Cerebrovascular accidents and device thrombi were common complications noted among the patients.47,48 In 2006, the FDA granted the AbioCor® IRH Humanitarian Device Exemption status for use in patients with severe biventricular failure who are not eligible for heart transplantation. Since approval, it has only been implanted once in 2009.

CARMAT® Total Artificial Heart

The CARMAT® TAH created in France by Dr Alain Carpentier and his team is a pulsatile, electrohydraulically driven device that displaces approximately 750 mL of space. Pressure sensors embedded within the ventricles continuously measure preload and afterload. Internal electronics and microprocessors utilize a control algorithm to produce stroke volumes of 30 to 65 mL and flows of 2 to 9 L/min based on pressures. All blood-contacting surfaces and valves are made of bioprosthetic materials, and a single 8-mm percutaneous driveline provides power.39,40 The first 2 patients implanted with the C-TAH were supported for 74 and 270 days until they died from device failure and multiorgan failure, respectively. There were no thromboembolic complications, and no thrombus formation was noted on autopsy.40

Preoperative and Intraoperative Management of Total Artificial Heart Implantation

Management of TAH recipients during the preoperative and intraoperative periods has been previously discussed in detail27,43 and thus is only mentioned here in brief. Potential TAH recipients are all critically ill patients likely with multiorgan failure from decreased cardiac output and perfusion. These patients are typically already receiving some form of hemodynamic support, which may include inotropic agents or ventricular assist devices. Any inotropic or device support should be continued during the intraoperative period until the patient is placed on cardiopulmonary bypass.

Like most other major cardiac surgeries, intraoperative monitors and lines should include standard American Society of Anesthesiologists monitors, at least 1 arterial catheter, at least 1 central venous catheter, and transesophageal echocardiography. Many patients may already have indwelling central venous and arterial catheters, which may be used if there are no concerns for infection. If there is a pulmonary artery catheter present, it must be removed before cardiopulmonary bypass to avoid being in the surgical field. Induction of general anesthesia should take into account severe biventricular failure with likely multiorgan dysfunction.

Transesophageal echocardiography is performed before and after cardiopulmonary bypass (Figure 5) with emphasis on looking for TAH compression of the venae cavae (inferior more than superior) and pulmonary veins (left more than right). Compression of these vessels occurs especially when the chest is closed or whether the TAH is implanted in a smaller thoracic cavity.49,50 Echocardiographic findings indicative of caval compression include narrowing near the cavoatrial junction, turbulent flow distal to the narrowing or into the right atrium, flow acceleration across the stenosis, and decrease in right atrial size (Figure 6).49–52 Abnormal echocardiographic findings that may identify pulmonary vein obstruction include a turbulent flow pattern with loss of triphasic or quadriphasic pattern and high-flow systolic or diastolic velocities greater than 1.1 m/s (normal 0.4–0.7 m/s).50,53

Figure 5.:
Intraoperative transesophageal echocardiography from the midesophageal imaging window after implantation of the SynCardia (SynCardia Systems Inc, Tucson, AZ) total artificial heart demonstrates an intact RA and LA with prosthetic right (RIV) and left (LIV) single-tilting disk inlet valves (yellow arrows) in the (A) open and (B) closed positions. The prosthetic valves are anchored to ventricular rims and lead into their respective pneumatic pumping chambers (ventricles). Acoustic artifact from the pneumatic pumping chambers and prosthetic inlet valves obscure visualization of structures distal to the ventricular rims. The prosthetic right single-tilting disk inlet valve is shown in the (C) open position with color inflow into the RPV and in the (D) closed position. A mild regurgitant washing jet (yellow arrow) in the closed position is present with (D) normal prosthetic valve function. (E) The prosthetic left single-tilting disk outlet valve is shown (yellow arrow) in the (left image) short-axis and (right image) long-axis views. (F) The prosthetic right single-tilting disk outlet valve is more difficult to visualize (yellow arrow). Reprinted from Fine et al49 with permission from Elsevier. Ao indicates aorta; LA, left atrium; LPV, left pneumatic ventricle; PA, pulmonary artery; RA, right atrium; RPV, right pneumatic ventricle; TAH-t, temporary total artificial heart.
Figure 6.:
Intraoperative transesophageal echocardiography imaging of the IVC after implantation of a SynCardia (SynCardia Systems Inc, Tucson, AZ) TAH taken (A) immediately after device implantation, demonstrating a patent IVC (yellow arrow) with unobstructed flow and (B) immediately after chest closure, which resulted in shifting of the TAH in the chest cavity causing compression of the IVC (yellow arrow) and obstructed flow causing color aliasing. This subsequently resolved with device repositioning. In a different patient, the RA and LA are shown (C) after TAH implantation immediately after chest closure, demonstrating severe compression of the LA caused by shifting of the TAH in the chest cavity. This compression also resolved with device repositioning. Reprinted from Fine et al49 with permission from Elsevier. IVC indicates inferior vena cava; LA, left atrium; RA, right atrium; TAH, total artificial heart.

There is a high likelihood of intraoperative blood product transfusion. Major risk factors for bleeding include preoperative anticoagulation, hepatic dysfunction, renal failure, and redo sternotomy. Postoperative mediastinal bleeding requiring surgical re-exploration is reported in 20% to 39% of TAH patients.42,45,54,55 Bleeding resulting in repeat surgery mostly occurs within the first postoperative month with the highest incidence reported during the first week.42,45,54 Delayed bleeding after the first postoperative month is rare but has been reported.56 If intraoperative hemostasis is inadequate, the chest may be left open for delayed sternal closure to decrease risk of tamponade. This technique has been shown to be beneficial in major cardiac surgery,57 including implant surgery for ventricular assist devices58 and TAH.59 There does not appear to be an increased risk for infection associated with delayed sternal closure in the device population.58,59

Postoperative Management in the Intensive Care Unit

Hemodynamic Monitoring and Considerations.

Monitoring for the postoperative TAH patient includes pulse oximetry, arterial blood pressure monitoring, central venous pressure monitoring, and temperature. Electrocardiography is not necessary because the patient will no longer have electrical activity. Typically the arterial pressure is measured invasively via a radial arterial catheter or, less frequently, a femoral arterial catheter. Because the TAH is a pulsatile device, there should be an arterial waveform. The patient will also have central venous access usually by means of a central line in the right or left internal jugular vein. It is crucial to confirm appropriate positioning of the central line to prevent TAH inflow valve interference and device malfunction.42,60,61 The central line should not enter the right atrium, because the catheter may become trapped in the tricuspid valve and cause pump arrest leading to death.42,54,60 If the patient requires replacement of central access (including peripherally inserted central catheters), ideally the line should not go beyond the junction of the innominate vein and the superior vena cava, and placement is best done with fluoroscopic guidance to prevent the catastrophic complication of wire or line interference with the TAH. A chest radiograph obtained on intensive care unit (ICU) admission may be used to confirm optimal central line and endotracheal tube positioning.

The TAH is sensitive to preload, and thus maintenance of venous tone and intravascular volume is important. TAH patients generally will be hypertensive secondary to vasomotor dysregulation and will require vasodilators such as nicardipine, nitroprusside, or nitroglycerin. The nitrovasodilators have rapid onsets of action and short half-lives, allowing for easy titration; however, both have a risk of tachyphylaxis and increased shunt from inhibition of hypoxic pulmonary vasoconstriction. Nitroprusside also has the risk of cyanide toxicity with prolonged treatment, especially in patients with renal failure. Nitroglycerin produces greater venodilation and may cause too much of a decrease in preload, which the TAH cannot tolerate. Nicardipine, a dihydropyridine calcium channel blocker, is a good alternative to the nitrovasodilators, but it cannot be as rapidly titrated secondary to its slower onset time and longer elimination half-life. If there is vasoplegia after weaning from cardiopulmonary bypass, vasopressors such as vasopressin62–66 or low-dose norepinephrine67–70 are preferred, because these tend to have less effect than other vasoconstrictors such as phenylephrine or epinephrine on pulmonary vascular pressures. Inotropic and chronotropic support will be ineffective given the lack of myocardium, although TAH settings can be adjusted to improve cardiac output and oxygen delivery.

Overall volume status of the patient with a TAH can be deceptive because the device settings can be manipulated to provide a normal cardiac output even in the setting of hypovolemia. Signs of hypovolemia include decreased mean arterial pressure, low fill volumes, and decreased central venous pressure. If prolonged, hypovolemia and decreased fill volumes may lead to poor organ perfusion and result in altered mental status, delayed capillary refill, clammy or diaphoretic skin, and decreased urine output. Laboratory findings of decreased organ perfusion may include an elevated serum lactate, elevated base deficit, and metabolic acidosis. On the other hand, acute volume overload may result in hypertension, elevated central venous pressure, and pulmonary edema.

A sudden drop in flow, fill volume, or cardiac output may indicate driveline or inflow obstruction. Inspection of the drivelines may reveal a mechanical obstruction such as a kink. Serious device malfunctions are rare, but there have been a few cases of diaphragm ruptures and driveline tears.42,61,71,72 Inflow obstruction may be caused by atrial tamponade or venae cavae compression, resulting in a potentially fatal drop in ventricular preload. Atrial tamponade causes a decrease in fill volumes, a decrease in cardiac output, and an increase in central venous pressure. The mediastinal silhouette on chest radiograph may have an altered contour or bulge, which may indicate fluid accumulation.73 As previously mentioned, the pulmonary veins are also susceptible to compression, which may lead to hemodynamic collapse. Pulmonary vein obstruction is often first noted by an increase in pulmonary venous congestion with a concomitant increase in oxygen requirement and opacification of the chest radiograph. If left unidentified or untreated, any venous inflow obstruction may lead to cardiac arrest. Transesophageal echocardiography should be used to exclude compression of the venae cavae or pulmonary veins as well as evaluate for atrial tamponade. Treatment involves immediate surgical re-exploration and evacuation of the pericardial effusion. Standard Advanced Cardiovascular Life Support interventions and chest compressions will not help, because the plastic ventricles are incompressible. Furthermore, vasoconstrictor medications such as epinephrine may actually be dangerous because they may worsen the decreased return to the right ventricle.

Mechanical Ventilatory Support

All postoperative TAH patients will be transported to the ICU intubated and sedated. In some high-volume centers, patients are routinely left with an open chest given the high risk of postoperative bleeding. The oscillations from the TAH may cause autocycling, or inappropriate ventilator triggering, if a flow trigger setting is used. Autocycling may be resolved by using a pressure trigger setting.74 Like with other cardiac surgical patients, the goal is early extubation to prevent ventilator-associated complications such as atelectasis and pneumonia. Patients are extubated once the chest is closed and hemodynamic parameters are stable. For patients requiring a longer period of ventilatory support, standard measures such as head of bed elevation, daily sedation vacations, and chlorhexidine oral care should be utilized to improve outcomes.75

Renal Considerations

Patients with advanced heart failure have increased levels of brain natriuretic peptide secondary to chronic ventricular myocyte stretching. Brain natriuretic peptide is a potent vasodilatory hormone produced primarily by the ventricles that aids in volume homeostasis and blood pressure regulation.76–78 With worsening heart failure, there is a decrease in renal responsiveness to this hormone. Some proposed explanations include downregulation of natriuretic peptide renal receptors, decreased natriuretic peptide availability, and altered signaling.79 A patient with a newly implanted TAH no longer has the main endogenous source of brain natriuretic peptide and may develop acute kidney injury even if renal function was normal preoperatively.61 INTERMACS® data from the past decade reveal that approximately one-third of TAH patients experienced renal dysfunction.a An infusion of nesiritide, a recombinant form of human brain natriuretic peptide, may be beneficial to maintain urine output and renal function until levels normalize.80–82 At the authors’ institution, patients who do require nesiritide generally need a very slow wean.

Hematologic Concerns

Patients with any mechanical circulatory support device are at risk for thrombosis and adverse sequelae such as embolic stroke caused by platelet interactions with the device. Pump thrombosis is a major fatal complication that has an average incidence of 2% to 11% in patients with HeartMate II® (Thoratec Corporation, Pleasanton, CA) LVADs.83–87 Device thrombosis around the atrial struts in the AbioCor® IRH was a major complication resulting in stroke and device modification.47,48 However, there have been rare reports of nonfatal thrombi forming within the TAH-t, including 1 mitral valve thrombus88 and 1 thrombus caused by a diaphragm rupture.61 Both patients survived and eventually received heart transplants. Incidence rates of stroke are low and comparable in TAH-t patients and HeartMate II® patients at on average approximately 0.06 to 0.08 events per patient-year.45,54,89–94 In 1 study comparing biventricular assist devices, stroke rates were significantly lower in the TAH-t group at 16% versus 61% in the implantable biventricular assist device group and 57% in the paracorporeal biventricular assist device group.95 Neurologic dysfunction was reported in 25% of TAH patients in recent INTERMACS® data.a

A multitargeted antithrombotic approach that includes both anticoagulation and antiplatelet therapies has been recommended.94,96 Regimens may vary based on institution, but most commonly anticoagulation is achieved with unfractionated heparin with an eventual transition to warfarin, and antiplatelet therapy consists of either aspirin or dipyridamole.94,96,97 When the chest is closed and chest tube output is less than 30 mL/h for 4 hours, then anticoagulation with IV heparin may be started at 2 to 5 units/kg/h.43,45,94 Therapeutic goals may include heparin levels between 0.11 and 0.27 units/mL or an activated partial thromboplastin time of 40 to 60 seconds. Thrombelastograph® or TEG® (Haemonetics Corp, Braintree, MA) can be useful in identifying which parts of the coagulation cascade require therapeutic manipulation. Within the next 1 to 2 weeks, transition to warfarin may be initiated once renal and hepatic functions have recovered.45 Starting doses may range from 2 to 7.5 mg/day.43,45,96 Therapeutic international normalized ratio goals are between 2.0 and 3.0. Both heparin and warfarin dosing should be titrated to normocoagulability based on whole blood TEG® to ensure adequate bridging.45

A potential risk of heparin use is heparin-induced thrombocytopenia, an immune-mediated reaction caused by antibodies formed against heparin–platelet factor 4 complexes. The immune complexes subsequently bind and activate platelets, causing a prothrombotic state. Up to 50% of cardiac surgical patients may have antibodies present, but only 1% to 3% will develop heparin-induced thrombocytopenia.98,99 In patients with ventricular assist devices including the TAH, the incidence has been reported to be approximately 8% to 10%.98–101 Higher levels of antibodies have been associated with higher rates of thrombotic events including stroke.98–101 If the patient develops heparin-induced thrombocytopenia, direct thrombin inhibitors such as bivalirudin and argatroban are a reasonable alternative. The starting dosage of bivalirudin is 0.005 mg/kg/h and is adjusted to normocoagulability based on TEG®, typically falling between the range of 0.01 and 0.02 mg/kg/h.102 Argatroban has been successfully used in patients with ventricular assist devices103,104 with starting doses of 0.02 to 0.42 µg/kg/min and up to 1.5-µg/kg/min maintenance doses.104 Plasmapheresis to reduce antibody load may also be considered, but currently data remain limited.

Antiplatelet therapy with aspirin and/or dipyridamole is promptly started postoperatively as long as platelet count is over 100,000 × 106/L and there are no bleeding complications. Aspirin, usually at 81 mg/day and titrated up to 325 mg/day, may be started when chest tube output is less than 30 mL/h for 4 hours. The aspirin dose may be increased as long as TEG® platelet mapping indicates a maximum amplitude greater than 50 mm. Dipyridamole, at 50 mg every 8 hours and up to 400 mg every 6 hours, may be started immediately on arrival to the ICU. Some protocols additionally recommend the use of pentoxifylline at 200 mg to 400 mg every 8 or 12 hours to help decrease blood viscosity, especially if there is a high amount of hemolysis. It may also be started immediately postimplantation.94,96,97

Postoperative anemia is common in TAH patients and is multifactorial in nature. Bleeding, reported in 47% of all TAH patients in the last 10 years,a is a common adverse event that is likely the main cause of acute anemia. As previously mentioned, mediastinal bleeding usually occurs during the first few postoperative days and may require surgical re-exploration. Gastrointestinal bleeding is another concern, especially when anticoagulation and antiplatelet therapies are initiated. Hemolysis occurs in mechanical devices as a result of wall shear stress and flow acceleration105 and contributes to both acute and chronic anemia. The majority of TAH patients will have laboratory evidence of hemolysis, including decreased haptoglobin, increased plasma-free hemoglobin, increased lactate dehydrogenase, and elevated reticulocyte counts.106 TAH patients also exhibit abnormal hematopoiesis secondary to increased inflammatory markers impairing normal bone marrow response to anemia.106 However, because TAH patients are being bridged to transplant, it is recommended to avoid transfusing blood products as much as possible to avoid foreign antigen exposure. TAH patients may be able to tolerate anemia even as low as a hemoglobin level of 6 g/dL, the transfusion threshold used at the authors’ institution. Chronic anemia associated with the TAH appears to resolve after TAH removal and heart transplantation.106

Antimicrobial Therapy

Patients are routinely started on broad-spectrum antibiotic prophylaxis during the perioperative period. Infections are common in the TAH population with reported rates of up to 53% to 83%.42,54,71,88 The respiratory tract, urinary tract, and drivelines are the most frequent sites of infection.54,72,88,107 Mediastinitis has been reported in 3% to 14% of TAH patients, but rarely has been secondary to ascending driveline infection.45,55,61,71,88 Although rates of infection are high, mortality secondary to infectious causes is on average less than 20%.45,55,72,88

Medications used should cover both Gram-positive and Gram-negative organisms. A common regimen is vancomycin and piperacillin–tazobactam or levofloxacin. There should be at least 1 dose given within 1 hour before surgical incision. Antibiotics are continued for at least 48 hours postoperatively and may be discontinued if there is no concern for infection. If the chest is not closed, adding an antifungal agent such as fluconazole should be considered, and the duration of microbial coverage should be extended. Early extubation, pulmonary toilet, mobilization, and invasive line removal may reduce infection risk. Discussion with an infectious disease specialist is recommended.

Transition Out of the Intensive Care Unit

Figure 7.:
External pneumatic drivers for the TAH-t. The Companion 2 (C2) Hospital Driver provides the power supply for the TAH-t while the patient is in the hospital. It may be docked into the C2 Hospital Cart or into the C2 Driver Caddy when the patient is ambulatory. The Freedom® portable driver allows eligible patients to be discharged home while waiting for heart transplantation. Image courtesy: TAH-t indicates temporary total artificial heart.
Figure 8.:
Freedom® portable driver. Image courtesy:

When the TAH patient has stabilized and no longer needs to be in the ICU, the patient is transferred to a step-down unit. Certain SynCardia TAH-t patients may be considered for transition to the Freedom® portable driver system (SynCardia Systems, Inc, Tucson, AZ), which was designed to allow TAH-t patients to be discharged home. It has approval from the FDA, Health Canada, and European Union. Weighing approximately 6 kg and packaged in a wearable backpack or bag, the Freedom® portable driver liberates the patient from being tethered to a larger pneumatic console (Figures 7 and 8). The Freedom® portable driver display shows beat rate, left ventricular fill volume, and cardiac output, but only the beat rate may be adjusted.108,109 Preliminary experiences have shown that it is possible to safely discharge a TAH-t patient home with a portable driver, allowing for improved quality of life and potential reduction in medical costs while awaiting heart transplantation.109–111


Despite advancements in the medical management of heart failure, the demand for heart transplantation continues to be a growing burden worldwide. The use of mechanical circulatory support has become more prevalent, and clinician familiarity with devices has become more significant. Several TAHs have been developed over the past 60 years, but currently the SynCardia TAH-t is the only 1 being used. The SynCardia TAH-t has shown that it can be an effective bridge to heart transplantation in patients with biventricular failure. With the Freedom® portable driver, certain TAH-t patients may even be discharged home to wait for a transplant offer as an outpatient. TAH technology will continue to evolve with hope that it may offer a more definitive treatment for patients with heart failure in the near future.


Name: Jill Yaung, MD.

Contribution: This author helped write and edit the manuscript.

Conflicts of Interest: None.

Name: Francisco A. Arabia, MD, MBA.

Contribution: This author helped write and edit the manuscript.

Conflicts of Interest: Francisco Arabia is a consultant for BiVACOR®, HeartWare®, and SynCardia Systems, Inc.

Name: Michael Nurok, MBChB, PhD.

Contribution: This author helped write and edit the manuscript.

Conflicts of Interest: None.

This manuscript was handled by: W. Scott Beattie, PhD, MD, FRCPC.


aArabia F, Gregoric I, Kasirajan V, et al. Total Artificial Heart (TAH): Survival Outcomes, Risk Factors, Adverse Events in Intermacs. Abstract presented at: International Society for Heart and Lung Transplantation 36th Annual Meeting and Scientific Sessions; April 27–30, 2016; Washington, DC. Manuscript in preparation.


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