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128 E. Kransdorf et al.
Norepinephrine is considered the first-line
•
agent for the treatment of vasoplegia, followed by vasopressin.
• Pulmonary vasodilators with minimal
effect on systemic arterial pressure, such as
inhaled nitric oxide or prostacyclin analogs,
should be considered in the management of
right ventricular dysfunction ± pulmonary
hypertension.
• Sinus node dysfunction is common posttransplant (especially in patients on amiodarone pre-transplant), resulting in
post-transplantation relative bradycardia that
resolves over 4 weeks; rarely, permanent pacing may be required.
• Renal dysfunction is common 24–48 h posttransplant; therefore, continuous assessment
of urine output in the early post-operative
period is important.
• Early mobilization of heart transplant recipients and involvement of physical therapy
with subsequent cardiac rehabilitation demonstrated to be beneficial.
Introduction
Monitoring and Management
of Hemodynamics in the Early Posttransplant Period
Recommended Hemodynamic Monitoring
As cardiac allograft dysfunction is common in
the early post-transplant period [2], adequate
hemodynamic monitoring of the post-transplant
patient is crucial. The 2023 International Society
for Heart and Lung Transplantation (ISHLT)
guidelines for the care of HTx recipients advised
that monitoring should include (a) invasive arterial pressure monitoring, (b) direct measurement
of right atrial pressure/central venous pressure
(CVP), (c) measurement of left atrial or pulmonary capillary wedge pressure, (d) intermittent
measurement of cardiac output, (e) intermittent
measurement of systemic vascular resistance, (f)
continuous measurement of arterial oxygen saturation, (g) intermittent measurement of mixed
venous saturation, (h) intraoperative transesophageal echocardiogram (TEE), and (i) continuous
assessment of urinary output [1].
The purpose of heart transplantation (HTx) is
to provide long-term survival and improve the
quality of life for patients with end-stage heart
disease [1]. The immediate post-operative period
is crucial in achieving this outcome. HTx clinicians should be familiar and comfortable with
treating multiple transplant-specific and medical issues in HTx recipients. This chapter aims
to provide an overview of the management in
the immediate post-transplant period, including
perioperative management strategies, frequently
encountered early morbidities, and short-term
complications. Although both induction and
maintenance immunosuppression are initiated in
the early post-transplant period, these regimens
will be discussed in depth in Chaps. 12 and 13,
respectively.
Causes of Cardiac Allograft Dysfunction
Numerous pre- and peri-transplant factors can
contribute to the development of cardiac allograft dysfunction early (days 0–7) after HTx.
These factors will be discussed here. Causes
of cardiac allograft dysfunction are generally
classified as primary, where the dysfunction
is intrinsic to the allograft, or due to a secondary cause, including rejection, intrathoracic
hemorrhage, cardiac tamponade, or pulmonary
hypertension [2]. The presence of early cardiac
allograft dysfunction is typically marked by
systemic arterial hypotension, abnormally low
cardiac output/index despite inotropic support
and/or abnormally high filling pressures. These
11 Immediate Post-operative Management After Heart Transplantation
129
abnormally high filling pressures include CVP
on the right ventricular (RV) side and left atrial/
pulmonary capillary wedge pressure on the left
ventricular side. In some cases, systemic arterial
pressure will be preserved, and disproportionately elevated pulmonary artery pressures will
be present. In either situation, hemodynamic
instability can contribute to the development of
renal dysfunction as marked by decreased urine
output and elevated laboratory makers such as
blood urea nitrogen/creatinine and/or hepatic
dysfunction as marked by coagulopathy and elevated laboratory markers such as total bilirubin.
When assessing a patient with cardiac allograft
dysfunction, the first step is to rule out secondary causes of cardiac allograft dysfunction.
Hyperacute rejection can manifest immediately
after allograft reperfusion and can be difficult to
identify since specific immunologic markers like
a crossmatch or donor-specific antibody testing
can take several days to return. Nevertheless,
hyperacute rejection should remain on the list of
possible causes of cardiac allograft dysfunction,
especially in recipients with a history of pretransplant allosensitization [3]. The presence of
intrathoracic hemorrhage can be identified based
on high chest tube output. Tamponade should be
suspected when refractory hypotension is present and can be confirmed with bedside echocardiography. Pulmonary hypertension often leads
to predominantly RV dysfunction and should
be suspected with pulmonary artery systolic
pressures ≥ 50 mmHg.
Primary Graft Dysfunction
If cardiac allograft dysfunction is present but
there is no apparent secondary cause of cardiac
allograft dysfunction present, primary graft dysfunction (PGD) should be suspected. PGD is
defined as allograft dysfunction within 24 h of
HTx unrelated to a secondary cause [2]. The
ISHLT has developed a classification system
for PGD based on the degree of ventricular dysfunction (i.e., mild, moderate, or severe) and the
ventricular function affected (i.e., RV versus
LV versus both) [2] (Table 11.1). According to
a recent meta-analysis by Buchan et al., pooled
incidences of mild, moderate, severe, and isolated RV-PGD were 3.5, 6.6, 7.7, and 1.6%, with
a 1-year mortality rate of 15, 21, 41, and 35%,
respectively [4]. The pathophysiology of PGD
is not fully understood, but numerous risk factors have been identified (Table 11.2). These risk
factors can be divided into donor, transplant, and
recipient factors and vary between studies [2, 4].
In terms of donor factors, increasing donor age
has been associated with an increased risk of
PGD in numerous studies. In terms of transplant
factors, increased allograft ischemic time [4] and
use of a donor undersized by donor-recipient
predicted heart mass ratio have been associated
with an increased risk of PGD [5]. In terms of
recipient factors, recipient mechanical circulatory support (MCS) [4], and treatment with amiodarone plus beta-blocker have been associated
with an increased risk of PGD [6]. Recently,
insights on the utility of recipients’ pre-transplant-microvesicle proteomics have expanded
our understanding of molecular pathways and
inflammatory biomarkers implied in the PGD
disease process and identified novel biomarkers
of PGD that can improve PGD prediction accuracy. Giangreco et al. studied 88 HTx recipients
who developed severe PGD post-HTx, incorporating pre-transplant data on 37 clinical characteristics and 181 protein markers; the authors
identified 16 proteins predictive of severe PGD
occurrence [7] and seven proteins predictive of
survival post-HTx in these patients [8]. Plasma
kallikrein, peroxiredoxin, tropomyosin alpha-4,
and myeloperoxidase were among the proteins
predictive of severe PGD occurrence [7].
Management of Cardiac Allograft Dysfunction
Inotropic and vasoactive pharmacologic support
is necessary to augment cardiac allograft function in the immediate post-cardiopulmonary
bypass period. Furthermore, the catecholamine
stores of the newly transplanted heart are often
130 E. Kransdorf et al.
Table 11.1 Definition of severity scale for primary graft dysfunction (PGD)
Category Severity/Grade Criteria
Left ventricle (LV) Mild PGD–LV: One of the following criteria must
be met
Moderate PGD-LV: Must meet one criterion from I
and another criterion from II
Severe PGD-LV Dependence on left or biventricu-
Right ventricle (RV) Diagnosis requires either both i and ii, or iii alone
LVEF ≤ 40% by echo
-ORHemodynamics with
RAP > 15 mmHg, PCWP > 20 mmHg,
CI < 2.0 L/min/m2 (lasting > 1 h)
requiring low-dose inotropes
I. One criteria from the following:
i. LVEF ≤ 40% by echo
-ORii. Hemodynamics with
RAP > 15 mmHg, PCWP > 20 mmHg,
CI < 2.0 L/min/m2, hypotension with
MAP < 70 mmHg (lasting > 1 h)
II. One criteria from the following:
i. High-dose inotropes − inotrope
score > 10
-ORii. Newly placed IABP (regardless of
inotropes)
lar mechanical support including
ECMO, LVAD, BiVAD, or percutaneous LVAD. Excludes requirement
for IABP
i. Hemodynamics with RAP > 15 mm
Hg, PCWP < 15 mm Hg, CI < 2.0 L/
2
min/m
ii. TPG < 15 mm Hg and/or pulmonary artery systolic pressure < 50 mm
Hg,
or
iii. Need for RVAD
Abbreviations BiVAD = biventricular assist device; CI = cardiac index; ECMO = extracorporeal membrane oxyge-
nation; IABP = intra-aortic balloon pump; LVAD = left ventricular assist device; LVEF = left ventricular ejection
fraction; PCWP = pulmonary capillary wedge pressure; RAP = right atrial pressure; RVAD = right ventricular assist
device; TPG = transpulmonary pressure gradient. Reprinted from The Journal of Heart and Lung Transplantation,
33(4), Jon Kobashigawa, Andreas Zuckermann, Peter Macdonald, Pascal Leprince, Fardad Esmailian, Minh Luu,
Donna Mancini, Jignesh Patel, Rabia Razi, Hermann Reichenspurner, Stuart Russell, Javier Segovia, Nicolas Smedira, Josef Stehlik, Florian Wagner, Report from a consensus conference on primary graft dysfunction after cardiac
transplantation, 327–340, Copyright (2014), with permission from Elsevier
depleted, requiring exogenous supplementation
[9]. The 2023 ISHLT guidelines for the care of
HTx recipients recommend that continuous infusion of an inotropic agent or a combination of
agents should be used to maintain hemodynamic
stability post-operatively and be weaned as tolerated over the first three to five days. As far as
agent choice, the guidelines recommend the following agents: (a) isoproterenol, 1–10 μg/min,
or (b) dobutamine, 1–10 μg/kg/min ± dopamine
1–10 μg/kg/min, or (c) isoproterenol, 1–10 μg/
min ± dopamine 1–10 μg/kg/min, or (d) mil-
rinone, 0.375–0.75 μg/kg/min, or (e) milrinone,
0.375–0.75 μg/kg/min ± epinephrine 0.01–
0.1 μg/kg/min [1]. If pharmacologic treatment
alone is insufficient to support allograft function, MCS is required. According to the ISHLT
guidelines [1], MCS should be considered as
11 Immediate Post-operative Management After Heart Transplantation
Table 11.2 Risk factors for primary graft dysfunction
Donor risk factors Recipient risk factors Surgical procedu-
Age Age Ischemic time
Cause of death Weight Donor-recipient
Trauma Mechanical support Weight mismatch
Cardiac dysfunction Congenital heart disease as etiology
of heart failure
Inotropic support Multiple reoperations Experience of
Comorbidities: diabetes, hypertension LVAD explant Cardioplegia
Downtime of cardiac arrest Comorbidities: renal dysfunction,
liver dysfunction (high MELD), DM
Drug abuse: alcohol, cocaine, amphetamines Ventilator dependent Elective versus
Left ventricular hypertrophy Multiorgan transplant
Valvular disease Elevated PVR
Hormone treatment Allosensitization
CAD/wall motion abnormalities on TTE Infection
Sepsis Retransplant
Alternate list/marginal donor allocation—not increased
risk
Troponin trend
Hypernatremia
ral risk factors
size mismatch
Non-cardiac organ
donation
procurement team
and center volume
solution
Increased blood
transfusions
emergency transplant
131
CAD, coronary artery disease; DM, diabetes mellitus; LVAD, left ventricular assist device; MELD, Model for
End-stage Liver Disease; PGD, primary graft dysfunction; PVR, peripheral vascular resistance; TTE, transthoracic
echocardiogram; UNOS, United Network for Organ Sharing. Reprinted from The Journal of Heart and Lung Transplantation, 33(4), Jon Kobashigawa, Andreas Zuckermann, Peter Macdonald, Pascal Leprince, Fardad Esmailian,
Minh Luu, Donna Mancini, Jignesh Patel, Rabia Razi, Hermann Reichenspurner, Stuart Russell, Javier Segovia, Nicolas Smedira, Josef Stehlik, Florian Wagner, Report from a consensus conference on primary graft dysfunction after
cardiac transplantation, 327–340, Copyright (2014), with permission from Elsevier
early as during the operation if there is a failure
to wean from cardiopulmonary bypass (CPB).
Post-operatively, MCS should be considered if
there is persistent hemodynamic instability due
to cardiac allograft dysfunction that is resistant
to treatment with upward titration of vasoactive agents. A variety of MCS devices may be
used. The ISHLT guidelines recommend that an
intra-aortic balloon pump (IABP) is attempted
prior to other forms of MCS. The IABP is often
effective in establishing sufficient pulsatility to
improve coronary perfusion and cardiac performance to separate from cardiopulmonary
bypass. Extracorporeal membrane oxygenation
(ECMO) is a frequently used short-term MCS
device for recipients with cardiac allograft dysfunction unresponsive to vasoactive agents and/
or IABP. Patients with severe PGD requiring
VA-ECMO appear to benefit from plasmapheresis in the immediate post-transplant period,
132 E. Kransdorf et al.
potentially by alleviating the inflammatory
milieu contributing to its development [10].
Approximately 50% of patients with severe
PGD requiring ECMO will have normalization
of allograft function and consequently will be
able to be weaned off of ECMO [6]. Patients
who are placed on ECMO post-transplant and
are subsequently able to be weaned off ECMO
have a similar survival to those who did not
require ECMO at 1-year post-transplant but have
a lower number of days alive out of the hospital
[11].
Management of Vasoplegia
Vasoplegia is a hemodynamic complication
that can occur post-transplant that can overlap
in presentation with cardiac allograft dysfunction in that severe systemic arterial hypotension
is present but distinct in that cardiac allograft
function is preserved. Vasoplegia is more common after HTx in recipients with older age,
longer cardiopulmonary bypass time, higher
pre-transplant creatinine, chronic liver disease
and pre-transplant durable MCS [12]. However,
unlike recipients with severe PGD, patients with
vasoplegia did not exhibit a higher risk of mortality 1-year post-transplant. The 2023 ISHLT
guidelines for the care of HTx recipients recommend that norepinephrine is considered the
first-line agent for the treatment of vasoplegia,
followed by vasopressin [1]. Additional vasoactive agents that can be utilized include epinephrine, norepinephrine, dopamine, and angiotensin
II. Adjunctive medications, including methylene
blue, ascorbic acid, and hydrocortisone, may
also play a supportive role [13].
bind to the cardiac allograft and fix complement, resulting in severe allograft dysfunction.
It typically presents immediately following reperfusion of the allograft. This phenomenon is
covered in more detail in Chap. 19. The development and use of the prospective cytotoxic
crossmatch, and subsequently the virtual crossmatch, has greatly reduced the frequency of
this complication [14]. Treatment for hyperacute rejection should be initiated as soon as the
diagnosis is suspected. In addition to standard
management for cardiac allograft dysfunction, aggressive immunosuppression consisting of high-dose intravenous corticosteroids,
plasmapheresis, intravenous immunoglobulin,
anti-thymocyte globulin cytolytic agents, and
eculizumab, as well as immediate initiation of
intensified maintenance immunosuppression
including a calcineurin inhibitor and metabolic
cycle inhibitors or mammalian target of rapamycin (mTOR) inhibitors [1].
Intrathoracic Hemorrhage and Cardiac Tamponade
In the immediate post-operative period in the
intensive care unit, output from chest tubes is
to be expected. However, output of 1500 mL
within an hour or 200 mL/h over four hours suggests active intrathoracic bleeding and may be
accompanied by hemodynamic compromise.
Likewise, the sudden appearance of systemic
arterial hypotension accompanied by cardiac
allograft dysfunction may indicate the accumulation of blood in the pericardium. Cardiac tamponade should be excluded as a possible cause
by bedside echocardiography. If intrathoracic
hemorrhage or cardiac tamponade is present,
direct surgical exploration is indicated to prevent
further hemodynamic decompensation.
Management of Specic Causes
of Cardiac Allograft Dysfunction
Hyperacute Rejection
Hyperacute rejection is a very rare complication that occurs early post-transplant when
pre-formed anti-ABO or anti-HLA antibodies
Pulmonary Hypertension
Elevated recipient pre-transplant pulmonary
vascular resistance (PVR) is known to be a significant risk factor for early post-transplant RV
dysfunction and subsequent mortality [1, 15,
16]. The risk of RV failure is as high as 75%,
with a 15% mortality risk among patients with
11 Immediate Post-operative Management After Heart Transplantation
133
pre-transplant PVRi (indexed to body surface
area) > 6 Wood units x m2. In contrast, patients
without increased pre-transplant PVR only demonstrate a 20% risk of RV failure [17, 18]. The
mechanism of RV failure in the immediate posttransplant period is thought to be multifactorial.
The donor’s RV is particularly vulnerable to
peri-procedural myocardial strain, ischemia, cardioplegia, and surgical trauma. When exposed
to elevated recipient PVR, factoring in complications from transitional pulmonary vascular
hyper-reactivity resulting from cardiopulmonary
bypass [19], the sudden and dramatic increase
in PVR can cause RV failure. This situation is
exacerbated by a donor heart that is too small
for a larger recipient [20]. Thus, in all patients,
particular attention should be given to continuous monitoring of the post-operative pulmonary
artery pressures. An invasive pulmonary arterial
line, as per ISHLT recommendations [1], permits continuous post-operative pulmonary arterial pressure monitoring and facilitates treatment
when elevated to prevent subsequent RV failure.
Broadly speaking, management of pulmonary
hypertension-induced RV dysfunction can be
approached on four fronts: (a) preload optimization with CVP maintained at 5–12 mmHg,
(b) maintenance of sinus rhythm and atrioventricular synchrony, (c) ventilatory support, and
(d) appropriate pharmacologic and/or mechanical support to stabilize hemodynamic function.
For preload optimization, diuretics should be
utilized to achieve CVP goals. If diuretics are
not able to achieve CVP goals, then ultrafiltration/renal replacement therapy may be needed.
Ventilatory parameters that may help improve
pulmonary hypertension include avoiding
hypercapnia or hypoxia. Pharmacologic support
for RV dysfunction is the same as that for left
ventricular dysfunction: inotropic agents such
as isoproterenol, milrinone, dobutamine, and
epinephrine [1]. However, to specifically target pulmonary arterial hypertension (high pulmonary artery pressure and normal pulmonary
capillary wedge pressure), as compared to pulmonary venous hypertension (high pulmonary
artery pressure and high pulmonary capillary
wedge pressure), selective pulmonary vasodilating agents may be beneficial. Examples of selective vasodilators include epoprostenol (inhaled),
iloprost (inhaled), nitric oxide (inhaled), and
sildenafil (oral). All of the aforementioned
agents have proven effective at decreasing PVR
and improving pulmonary artery pressures in a
small series of adult post-transplant recipients
[21–24].
Monitoring and Management
of Arrhythmias in the Early PostTransplant Period
Electrical Monitoring
In the immediate postoperative period, the
ISHLT guidelines recommend the use of both
continuous electrocardiographic monitoring and
post-operative 12-lead electrocardiography [1].
Furthermore, it is recommended that both atrial
and ventricular temporary epicardial pacing
wires be placed at the time of the HTx surgery,
even if the initial rhythm is sinus.
Sinus Node Dysfunction
While most cardiac allografts return to sinus
rhythm after reperfusion in the operating room,
dysfunction of the sinus node is very common,
with prevalence as high as 50% [25]. The electrophysiologic parameters affected may include
prolonged sinus node recovery time, prolonged
corrected sinus node recovery time, and abnormal sinoatrial conduction time. Post-transplant
sinus node dysfunction is believed to be multifactorial in origin, including surgical trauma,
cardiac denervation, and ischemia–reperfusion
injury [26]. Sinus bradycardia is also common for recipients who received amiodarone
prior to transplant, as amiodarone has a very
long half-life (average 60 days), and so will
remain in the recipient’s system for a prolonged
period after HTx. Recipients who receive amiodarone prior to a HTx are at an increased risk
of needing a pacemaker after HTx [27]. In the
134 E. Kransdorf et al.
immediate postoperative period, the cardiac
allograft exhibits a restrictive hemodynamics
[28], and consequently, a high heart rate needs
to be maintained to support adequate cardiac
output (due to smaller stroke volume). The 2023
ISHLT guidelines for the care of HTx recipients
recommend pharmacologic treatment or temporary pacing to maintain a minimum heart rate of
at least 90 bpm [1]. Such pharmacologic agents
may include isoproterenol while awaiting the
return of normal sinus node function. Although
sinus node dysfunction is typically transient
[29], a few patients display permanent sinus
node dysfunction and require permanent pacing.
Recommendations suggest delaying pacemaker
implantation until at least three weeks after
HTx. A 2–10% prevalence of pacemaker placement during the transplant hospitalization has
been reported [30, 31].
Atrial Fibrillation
Atrial fibrillation is common in the early postoperative period after a HTx, affecting approximately 14% of patients in one cohort study [32].
Its frequency is not surprising, given that atrial
fibrillation is a common complication of cardiac surgery. However, in HTx recipients, older
studies suggest that atrial fibrillation can be a
sign of rejection, and as such, it is also prudent
to rule out rejection in HTx patients presenting
with atrial fibrillation [33]. The use of vasoactive agents, as well as the lack of cardiac innervation, lead to high ventricular rates when HTx
patients have atrial fibrillation early after HTx.
Thus, hemodynamic instability may develop,
and emergent restoration of sinus rhythm via
synchronized cardioversion may be needed. In
the absence of hemodynamic instability, amiodarone can be used to control ventricular rate
urgently and potentially restore sinus rhythm.
Beta-blockers or calcium channel blockers can
be used if the patient has sufficient systemic
blood pressure for the addition of these agents.
Digoxin is not recommended as it is not effective in HTx recipients, given the lack of parasympathetic innervation [34]. If atrial fibrillation
is recurrent, anticoagulation may be needed
to reduce the risk of stroke. Given the need for
procedures such as endomyocardial biopsy early
after HTx, direct oral anticoagulants have been
used successfully [35].
Ventricular Tachycardia
Non-sustained ventricular tachycardia is very
common in the early postoperative period due
to the use of vasoactive agents and electrolyte
abnormalities. In contrast, sustained ventricular
tachycardia is rare and should prompt consideration for causes of allograft dysfunction, such as
hyperacute rejection or PGD.
Non-cardiac Medical Issues After Heart Transplant
Renal Dysfunction
Renal reserves are often impaired prior to HTx
due to the prolonged low cardiac output and
chronic administration of diuretics that occurs in
end-stage heart failure. This vulnerability combines with the renal effects of cardiopulmonary
bypass, post-transplant hemodynamic complications, and initiation of calcineurin inhibitor immunosuppression to cause acute kidney
injury (AKI) in about 40% of HTx recipients
[36]. Specific complications associated with an
increased risk of AKI include tamponade, hemorrhage, and RV failure. In patients with AKI
and oliguria (urine output < 0.5 mL/kg/h), highdose diuretics, potentially including the use
of both loop and thiazide diuretics, should be
undertaken. If the patient fails to respond and
CVP continues to increase, the ISHLT guidelines recommend renal replacement therapy
[1]. For patients with pre-existing renal insufficiency, the use of induction immunosuppression
with delayed initiation of calcineurin inhibitor
may be helpful to mitigate worsening kidney
function [37]. Thus, early involvement and consultation of Nephrology is essential. Subsequent
to the changes to the heart allocation system in
13511 Immediate Post-operative Management After Heart Transplantation
the United States in 2018, about 13% of posttransplant patients required de novo hemodialysis [38]. Patients who required hemodialysis had
decreased survival at 1- and 2 years post-transplant. Pre-transplant renal function (as measured
by the glomerular filtration rate) and pre-transplant ECMO were strong predictors of the need
for post-transplant hemodialysis.
Neurological Dysfunction
Neurological dysfunction in the early posttransplant period may present in several forms:
focal neurological deficit (e.g., unilateral upper
and/or lower extremity motor deficits), seizures, or encephalopathy. These differing
presentations may arise from several causes:
hypotension associated with cardiac allograft
dysfunction, stroke from systemic embolus,
metabolic derangements, or side effects of calcineurin inhibitors [1]. With regards to the latter, tacrolimus in the presence of low lipid levels
has been associated with an increased risk of
encephalopathy, as low lipids result in higher
amounts of free tacrolimus, which can more
easily translocate across the blood–brain barrier [39]. In this situation, switching from tacrolimus to cyclosporine has been helpful. Both
stroke and seizures require the involvement of
neurology care, and thus, early consultation is
imperative.
Gastrointestinal Dysfunction
HTx recipients are at increased risk of intraabdominal complications in the early postoperative
period, affecting 20% or more of HTx recipients in older cohort series [40, 41]. The most
common events include ischemic bowel, viscus
perforation, cholecystitis, and gastrointestinal
hemorrhage. These complications can be difficult to identify in the setting of HTx recipients with multiple ongoing medical issues, and
thus, clinicians should maintain a high index of
suspicion.
Antibiotic Use for Prophylaxis of Infection
In the first month post-transplant, infections are
most commonly bacterial and typically related
to indwelling catheters and wound infections.
Coagulase-negative Staphylococci and S. aureus
(MRSA and MSSA) are the most common pathogens causing surgical site infections in HTx
recipients; other encountered pathogens include
gram negatives and Candida spp. For prophylactic purposes, broad-spectrum antibiotics such as
first/third-generation cephalosporin with/without
vancomycin are commonly used [1]. For prophylaxis against Pneumocystis jiroveci, the preferred agent is trimethoprim-sulfamethoxazole.
For cytomegalovirus (CMV) prevention, the
ISHLT recommended that the CMV serologic
status of the donor and recipient should be used
to risk stratify patients for post-transplant CMV
infection. Acyclovir (if low risk) or valganciclovir (if high risk) are being used. For prophylaxis
against mucocutaneous candidiasis, nystatin or
clotrimazole are used.
Nutritional Insuciency
Nutritional insufficiency and cachexia are common in patients with end-stage heart failure [42],
and thus, returning to an adequate nutritional
state is an important endpoint for HTx recipients. For transplant recipients with a delay in
extubation or inability to swallow safely, enteral
nutritional supplementation should be initiated.
Once the recipient has been extubated or can
swallow safely, enteral nutritional supplementation can be discontinued. However, clinicians
should continue to monitor the patient’s oral
intake to ensure that caloric needs are being met.
Debility
Patients with end-stage heart failure who
undergo HTx are likely to have been ill for a
prolonged period of time. As a result of this,
136 E. Kransdorf et al.
as well as immobility related to the HTx surgery, HTx recipients are likely to have debility that varies in severity from mild to severe.
Early involvement of physical, occupational, and
speech therapy (when needed) is important. For
patients with severe debility, transfer to inpatient
rehabilitation has been shown to improve functional status [43]. For patients with more mild
debility, discharge with home therapy is appropriate. When the patient is ready (6–12 weeks
post-procedure), completion of cardiac rehabilitation has been shown to improve functional status [44].
Conclusions
Mortality in the first year after a HTx remains
significant, ranging between 6% and 10% in
most HTx programs in the United States. Thus,
the events that occur immediately after surgery
are critically important for the long-term survival of HTx recipients. Each HTx center uses
its own set of protocols with regard to early
post-transplant care in the intensive care unit
and hospital, but here, we have outlined general
principles and highlighted complications clinicians should be aware of to ensure optimal outcomes for HTx recipients.
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