Heart transplantation


Cardiac Transplantation

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Related Condition

Ventricular Assist Device

1. Description of the problem

Heart failure is a major public health problem in industrialized nations. Over 5 million Americans carry the diagnosis of heart failure with over a half a million new diagnoses annually. In the setting of acute, unanticipated heart failure, several options exist, including intra-aortic balloon pump (IABP) counterpulsation, extracorporeal membrane oxygenation, and emergent/urgent cardiopulmonary bypass.

These are temporary solutions that are primarily used until definite therapeutic options can be implemented. The two surgical options for refractory heart failure are heart transplantation and placement of a ventricular assist device. With less than 2500 available heart donors per year (in the United States), there has been significant interest in the development of increasingly sophisticated ventricular assist devices, some of which can now be implanted on a permanent basis.

Physiology of heart failure

Patients who present for heart transplant or placement of a ventricular assist device (either as a “bridge” to transplant or “destination” therapy) are universally in heart failure. Most will have some form of both systolic and diastolic heart failure. Pulmonary artery pressures will rise as intravascular volume shifts in the setting of left ventricular failure, eventually leading to increases in pulmonary vascular resistance. Chronic hypotension leads to vasoconstriction and retention of sodium (and free water), which, while intended to be compensatory, ultimately hastens demise.

Brief description of the surgical procedure(s)

Prior to the start of surgery, anesthesia providers will cannulate at least one central vein with a large-bore catheter (most commonly in the right internal jugular vein). If the operation is a “re-do” (i.e., the patient has had a prior median sternotomy), the surgical team will often prepare for emergency cardiopulmonary bypass by cannulating the femoral and artery veins prior to incision.

Heart transplantation

Orthotopic heart transplantation requires a median sternotomy approach. After the midline incision is complete and the pericardium is accessed, the surgeon will cannulate the aorta, inferior vena cava, and superior vena cava in preparation for cardiopulmonary bypass. After initiation of cardiopulmonary bypass and cross-clamping of the aorta, the heart is removed from the patient.

In the “classic” approach, a large atrial “cuff” is left in place to which the surgeon can suture the donor heart. In the “bicaval anastamotic technique” only a left atrial cuff is left in place, requiring that the native superior and vena cava be sutured directly to the donor superior and inferior vena cavae. Generally one large suture line is placed around the left atrium, with separate smaller suture lines around the vena cavae, followed by anastomosis of the pulmonary artery and aorta.

Following placement of the donor heart in the recipient chest and after the appropriate anastomoses are completed, the donor heart is “de-aired” with the aortic cross-clamp in place. Intravenous steroids are administered by the anesthesia provider while the cross-clamp is still in place. The cross-clamp is then removed and the donor heart allowed to function while still on cardiopulmonary bypass.

Ventricular assist device placement

Techniques are more variable than for cardiac transplantation, partly because of the variety of devices available for implantation. In general, the following steps are followed after pericardial access has been achieved – an outflow graft is sutured to the ascending aorta and the device is placed in the surgical field prior to initiating cardiopulmonary bypass (in order to minimize pump times).

After the outflow graft is in place and the device has been placed on the field, cardiopulmonary bypass is initiated. The inflow cannula is then placed (usually in the LV apex) and the device is de-aired and then activated.

End of operation(s)

Once hemodynamic and physiologic conditions are adequate, the patient is separated from cardiopulmonary bypass, temporary pacing wires are placed, hemostasis is achieved, the chest is closed, and preparations for transportation to the intensive care unit commence.

Immediate post-operative care

On admission to the intensive care unit, these patients will often require inotropic support (in the case of transplantation, the donor heart must withstand the double insult of cold ischemic time as well as reperfusion following cardiopulmonary bypass). Patients with elevated pulmonary vascular resistance will often require beta-agonists (e.g., dobutamine, low-dose epinephrine) and phosphodiesterase inhibitors (milrinone) to increase right ventricular function without increasing pulmonary vascular resistance. Inhaled prostaglandins (e.g., epoprostenol) or nitric oxide may be used in extreme cases.

Post-cardiac surgery bleeding

A general rule for excessive bleeding that may require operative intervention is 100 cc/hr for four hours, 200 cc/hr for two hours, or 400 cc in one hour. Coagulopathies should be sought and corrected. Important laboratory tests include platelet count, aPTT, INR, fibrinogen levels, and thromboelastography (if available). Unfortunately these laboratory tests are not always available in a timely fashion and products must sometimes be given empirically. Hypothermia can adversely affect the coagulation cascade and should be avoided.

Bleeding algorithm
  • Assess severity of bleeding and contact the surgical team. If there is greater than 400 mL chest tube output in four hours, strongly consider the possibility of “surgical” bleeding.

  • Ensure the patient is warm.

  • Consider lowering the systemic arterial blood pressure.

  • Consider adding positive end-expiratory pressure (up to 10 cm H2O).

  • Send labs (platelets, aPTT, INR, fibrinogen levels, thromboelastography).

  • Treat coagulopathy based on laboratory values when available; otherwise, treat empirically (fresh frozen plasma, cryoprecipitate, platelets, desmopressin).

Post-cardiac surgery arrhythmias

Arrhythmias are common after cardiac surgery and may be due to mechanical irritation (including volume overload, suture lines, etc.), inflammation, electrolyte abnormalities, and other causes. Many of these will resolve spontaneously over a period of one or two months. Hemodynamically unstable patients should be treated according to ACLS guidelines. Stable patients may receive rhythm or rate control (neither of which as been shown to be superior) after all potentially reversible causes have been addressed.


Tamponade should not occur if mediastinal chest tubes are functioning; however, if the mediastinal tubes clot or are otherwise obstructed, residual bleeding can accumulate in the thorax and impinge on the heart. At some point in the accumulation of fluid (around 250-300 ml with an intact pericardium, not the case post-surgically), maximal distention occurs and results in a phenomenon called pulsus paradoxus, in which any increase in right ventricular volume (increased venous return during spontaneous inspiration) causes the interatrial/ventricular septa to bulge leftwards. The opposite happens during spontaneous expiration.

Tamponade is defined by a drop in systolic blood pressure exceeding 10 mm Hg during inspiration). “Beck’s triad” of low blood pressure, increased JVP, and distant heart sounds may be present but is unreliable. A massive sympathetic response (tachycardia) may ensue. In the post-operative setting, management may require emergent re-opening of the sternotomy to relieve pressure. Initiation of positive-pressure ventilation in this setting may be detrimental.

Right ventricular failure

RV failure is common after both heart transplantation and placement of a left ventricular assist device. Patients with chronic left heart failure exhibit increased pulmonary artery pressures as intravascular volume shifts away from the systemic vascular beds (and pools in the pulmonic vascular beds), eventually leading to increases in pulmonary vascular resistance. The right ventricle can adapt by increasing wall thickness.

In the setting of heart transplantation, the donor heart has not had the chance to adapt to increased pulmonary vascular resistance and will not be prepared for increased afterload.

Initial signs of right ventricular failure include rising central venous pressure in conjunction with decreased cardiac output, which require echocardiographic confirmation. Echocardiography will reveal a dilated, hypocontractile right ventricle and decreased left ventricular end diastolic volume.

Treatment of right ventricular failure includes increased FiO2, mild hyperventilation (CO2 increases pulmonary vascular resistance), beta-agonists (e.g., dobutamine, low-dose epinephrine) and phosphodiesterase inhibitors (milrinone), inhaled prostaglandins (e.g., epoprostenol) and nitric oxide. Central venous pressures >20 mm Hg are unlikely to be helpful and may lead to hepatic congestion. In extreme cases, placement of a right ventricular assist device may be indicated.

Post-operative physiology and management
Heart transplant: post-operative

Due to the nature of the procedure, the donor organ is completely, and irreversibly, denervated. Unlike the native heart, which is directly innervated by sympathetic and parasympathetic efferent fibers, the donor heart relies completely on circulating hormones to adapt to changes in global oxygen demand. Indeed, the donor heart is almost completely reliant on stroke volume in order to maintain adequate cardiac output, emphasizing the importance of preload in this patient population.

Baseline heart rates are elevated and left ventricular compliance is reduced, leading to diastolic dysfunction, which further increases the importance of maintaining adequate preload.

The choice of pharmacologic agents may also be dictated by cardiac denervation. Direct-acting hemodynamic agents (such as epinephrine) are preferred. Drugs such as atropine (which is a competitive muscarinic antagonist) are ineffective as normal sympathetic and parasympathetic innervation is absent.

Drugs with both direct and indirect effects, such as ephedrine, may also behave differently and should preferentially be avoided. In addition to direct-acting inotropic agents, post-cardiac transplantation patients may require direct vasodilators in order to reduce left ventricular afterload (and thus decrease myocardial wall stress). In the rare instance that systemic vasoconstriction is indicated, vasopressin, which produces relatively less pulmonary vasoconstriction (as compared to systemic vasoconstriction) is preferred over alpha–agonists. Vasoactive agents may be required for up to four days post-operatively (or even longer).

Special cases in cardiac transplantation

Approximately 20% of patients presenting for heart transplantation will have previously received a left ventricular assist device as a “bridge to therapy” – these patients are generally more difficult to manage in the postoperative setting. The fact that a repeat sternotomy is required lengthens the duration of surgery and increases blood loss. These patients are coagulopathic at baseline and may bleed extensively following cessation of cardiopulmonary bypass.

Arrhythmias and pacing

Bradycardia is the most common arrhythmia following heart transplantation, and many of these patients will require pacing (either with a pacemaker or direct-acting beta-agonists) in order to maintain adequate cardiac output in the immediate post-operative period. Up to 25% of heart transplant patients will require implantation of a permanent pacer. Calcium channel blockers should be avoided as they may interfere with immunosuppressant medications.

Renal function

Heart transplant patients are at increased risk for poor post-operative renal function following administration of nephrotoxic immunosuppressant agents (e.g., cyclosporine, tacrolimus). Additionally, many of them use furosemide chronically and require diuretics to produce urine. While no prospective, randomized data support one particular management strategy, to the extent that it is possible one should avoid all nephrotoxins.


While the initial immunosuppressive drugs are given intraoperatively, additional immunosuppressant agents will be administered shortly after arrival to the intensive care unit – commonly used agents include a steroid in combination with either azathioprine (purine analogue) and cyclosporine (calcineurin inhibitor) or tacrolimus (calcineurin inhibitor). Calcium channel blockers may interact with cyclosporine and tacrolimus and should be avoided whenever possible.

Polyclonal antilymphocyte antibodies are sometimes used and may lead to leucopenia and thrombocytopenia. 20% of patients will experience “cytokine release syndrome.” Daclizumab, an interleukin-2-binding monoclonal antibody, lowers the risk of acute cellular rejection but carries an increased risk of post-operative infections.

Organ rejection

Hyperacute rejection is rare, but may be seen in the setting of the post-operative intensive care unit. It is caused by preexisting antibodies to donor antigens, which activate the complement system, and is universally fatal. Acute rejection is T-cell mediated and occurs within the first six months of transplantation.


Heart transplant patients are significantly immunosuppressed and therefore at increased risk for post-operative infections. In the acute setting, bacterial pneumonia is the most likely cause. Vancomycin and piperacillin-tazobactam are commonly used for empiric bacterial prophylaxis, and is stopped after donor blood cultures have been assessed. Trimethoprim-sulfamethoxazole is often used for P.carinii prophylaxis and fluconazole for candidiasis prophylaxis while steroids are being administered. CMV patients receiving a CMV+ organ will receive CMV immune globulin (CytoGam) followed by valganciclovir.

VAD placement: post-operative

Low flows from the VAD may be due to inflow obstruction (either due to malposition or a collapsed left ventricle (RV failure, hypovolemia, etc.), problems with the outflow cannula, or tamponade (see above). Echocardiography should be used liberally to assess the volume status of the supported ventricle. Pulmonary vascular resistance should be managed (as discussed above). Mechanical problems may necessitate return to the operating room.

Special issues with VADs


A leading cause of mortality in this patient population. 50% of patients will develop sepsis within two years. As many as 25% of deaths in LVAD patients are due to sepsis. Often surgical intervention is required, with rare patients requiring VAD explantation and replacement with a transplanted heart.


Common following VAD placement due to preoperative illness (e.g., poor nutritional status, hepatic congestion, anticoagulation, etc.) and exacerbated by the artificial device surface and mechanical perturbation of blood product. Many devices require anti-platelet and/or anticoagulant medications; however, these medications are not generally started until practitioners can confidently exclude surgical bleeding. See “Post-Cardiac Surgery Bleeding” above.

Thromboembolic phenomena

Patients who receive ventricular assist devices are at increased risk for thromboembolism and neurologic deficit as compared to medically managed patients. Not all patients will require anticoagulation, although most will be on some form of anti-platelet agent.

Device failure

Device failure is the second leading cause of long-term mortality (after sepsis) in patients who receive a ventricular assist device. The most likely cause of failure is related to the type of device employed.

Types of ventricular assist devices

Ventricular assist devices were originally developed as a “bridge” to either myocardial recovery (in the setting of transient dysfunction [e.g., viral myocarditis]) or transplantation (in the setting of disabling dysfunction) and were not intended to be implanted permanently. As the technology has improved, ventricular assist devices have been safely used for increasing periods of time. In 2010, the United States Food and Drug Administration approved the Thoratec HeartMate II for “destination therapy” in which the ventricular assist device is implanted permanently, with no specific plans for removal.

Spectrum of ventricular assist devices

The spectrum of ventricular assist devices ranges in invasiveness from intra-aortic balloon pumps (IABPs), which are placed in the descending thoracic aorta via a femoral artery access point, to the more invasive and implantable ventricular assist devices (e.g. Thoratec HeartMate II), which require cannulation of both the heart and the aorta.

Intra-aortic balloon pump

IABPs differ from implantable ventricular assist devices in that rather than augmenting cardiac output throughout the cardiac cycle, the focus of the IABP is to simultaneously increase cardiac output while at the same time decreasing myocardial oxygen consumption and improving myocardial blood flow. When functioning optimally, IABPs can increase cardiac output no more than 30%, and much of their benefit is due to their favorable effect on myocardial oxygen supply and demand matching – the ability to decrease ventricular afterload (by deflating during systole) while at the same time increasing coronary perfusion (by inflating during diastole) provides a highly artificial but advantageous hemodynamic state that can, in the setting of cardiogenic shock, help preserve myocardial viability.

Short-term ventricular assist devices

The TandemHeart pVAD is a centrifugal pump designed to be placed percutaneously.This allows the practitioner to place a pVAD much more rapidly than other ventricular assist devices (with the exception of IABPs). Although placement of a pVAD requires access to the femoral arteries and veins, pVADs can be placed outside of the operating room environment.

To ensure perfusion of oxygenated blood, the 21 French venous cannula must be advanced across the intra-atrial septum and into the left atrium – because pVAD inflow is generally less than with implantable VADs (which derive their inflow from the ventricle itself), pVADs are often unable to decompress the failing left ventricle and thus are not able to reduce myocardial oxygen consumption to the same extent as some of the implantable VADs.

pVADs may produce up to 5 L/min of non-pulsatile cardiac output and do require systemic heparinization (goal activated clotting time of approximately 180-200 seconds). Large studies comparing pVADs to IABPs have not been completed.

Other ventricular assist devices designed for short term use include the Impella pump system by Abiomed, and the Lifebridge by Lifebridge AG.

Long-term ventricular assist devices

The Heartmate XVE (Thoractec) is one of only two VADs approved for destination therapy by the FDA. It is a pulsatile flow device implanted in a preperitoneal pocket or within the peritoneum itself. It has a textured titanium inner surface, which reduces thrombogenicity. The inflow cannula is placed in the left ventricular apex and the outflow cannula in the ascending aorta. The device is not very durable (less than 5% last to two years) and requires frequent reoperation.

The Heartmate II (Thoratec), the other VAD approved for destination therapy by the FDA, is newer than the XVE. The Heartmate II is less pulsatile (which may improve outcomes) and compared to the XVE is smaller, more durable, and easier to implant. As in the XVE, the inflow cannula is placed in the left ventricular apex and the outflow cannula in the ascending aorta.

VAD physiology

Ventricular assist devices do not obey the Frank-Starling Law. Their output depends on both preload and afterload. As afterload increases, output decreases. VADs can only pump the volume provided, which is why right ventricular output is so critical for LVADs. If ventricular volumes decrease significantly, a “suck down event” may occur in which the ventricular walls collapse on the VAD inflow cannula, leading to hemodynamic embarrassment and potentially death.

Many newer VADs are “low-pulsatile.” The amount of pulsatility in VADs is dependent on their outflow relative to cardiac output. A native heart that has completely failed will often not produce any pressure, leading to a flat arterial pressure tracing. A native heart that continues to beat (either because the VAD RPMs are too low or due to recovery) will eject some blood through the aortic valve, leading to pulsatile blood flow.

VADs do not measure their own output; rather, they estimate it based on RPMs and the amount of power they consume. This relationship is especially inaccurate at outputs < 3 L/min.

Near-term outcomes
Heart transplantation

The most common causes of death in the near term (30 days) are graft failure (40% of deaths), multiorgan failure (14% of deaths), and non-CMV infection (13%). Pneumonia is the most common infectious presentation and carries a mortality risk of up to 31%. One year mortality rates are approximately 85% following cardiac transplantation.

Ventricular assist devices

According to the International Society for Heart and Lung Transplantation (ISHLT) Mechanical Circulatory Support Device database, overall one-month survival is 83%. Overall survival at one year is 50%. These data are based primarily on patients who received VADs as a bridge to transplantation, and thus more recent patients (e.g., who receive VADs for destination therapy) may have improved survival.

2. Emergency Management


3. Diagnosis






Special considerations for nursing and allied health professionals.


What's the evidence?

Rose, EA. “Long-term use of a left ventricular assist device for end-stage heart failure”. New England Journal of Medicine. vol. 345. 2001. pp. 1435

Lietz, K. “Outcomes of left ventricular assist device implantation as destination therapy in the post-REMATCH era: implications for patient selection”. Circulation. vol. 116. 2007. pp. 497

Slaughter, MS. “Advanced heart failure treated with continuous-flow left ventricular assist device”. New England Journal of Medicine. vol. 361. pp. 2241-2251.