Perioperative Management of the Left
Ventricular Assist Device Recipient
Mark J.S. Heath and Marc L. Dickstein
An understanding of the unique preoperative, intra-
operative, and postoperative considerations of left
ventricular assist device implantation is essential
for the successful anesthetic management of
these challenging cases. This article discusses the
different stages of anesthetic care of the left ven-
tricular assist device recipient, including preop-
erative assessment, lining, induction, separation
from cardiopulmonary bypass, and the postbypass
period.
Copyright 娀 2000 by W.B. Saunders Company
S everal features distinguish left ventricular as-
sist device (LVAD) placement from other
procedures encountered by the cardiac anesthesi-
ologist. These include the extreme degree of heart
failure, the circulatory implications of LVAD
therapy, device complications, and the high inci-
dences of postbypass right ventricle (RV) failure
and bleeding. This article describes these and
other issues that arise during LVAD placement, as
well as discusses a range of scenarios that can be
encountered by the anesthesiologist in an active
LVAD program.
Pathophysiology of Heart Failure
The cardinal feature of the patient presenting for
LVAD implantation is the presence of decom-
pensated heart failure that is refractory to med-
ical management. Unlike the patient with heart
failure presenting for other procedures, these
patients typically display evidence of rapidly
progressing end-organ dysfunction and are likely
Progress in Cardiovascular Diseases, Vol. 43, No. 1 (July/August), 2000: pp 47-54
to be hemodynamically fragile or frankly un-
stable. An understanding of the physiology of
severe heart failure is therefore critical to the
successful anesthetic management of these pa-
tients.
Heart failure is a chronic condition character-
ized by the physiological consequences of im-
paired cardiac contractile function.1,2 Depressed
systolic function is evidenced by the Frank-
Starling relationship, which is shifted down and
to the right, and by ejection fraction, which is
markedly reduced. The reduction in cardiac out-
put and, hence, perfusion pressure initiate several
compensatory mechanisms that predominantly
serve to increase ventricular preload and blood
pressure. Sympathetic activity results in increased
circulating catecholamines, renin, angiotensin,
and vasopressin.3,4 Ventricular preload is in-
creased by venoconstriction, which redistributes
blood volume to central compartments, and by
renal fluid retention, which increases intravascu-
lar volume. Cardiac output is increased via the
Frank-Starling mechanism as well as by increased
resting heart rate.
Initially, increased preload stress is sufficient to
maintain normal cardiac output; however, severe
heart failure is characterized by preload insensitiv-
From the Department of Anesthesiology, Columbia Uni-
versity, New York, NY.
Address reprint requests to Mark J.S. Heath, MD,
Department of Anesthesiology, Columbia University, 630
W 168th St, New York, NY 10032.
Copyright 娀 2000 by W.B. Saunders Company
0033-0620/00/4301-0006$10.00/0
doi:10.1053/pcad.2000.7197
47
48
ity because these hearts are operating on the flat
portion of the Frank-Starling curve.5 In contrast,
the failing heart is particularly sensitive to changes
in afterload.6 Moreover, ventricular dilation is
frequently associated with annular dilatation
and mitral incompetence7; mitral regurgitation
amplifies the afterload sensitivity of ventricu-
lar function. In other words, as afterload is re-
duced, cardiac output is enhanced by greater
fiber shortening, as well as a smaller regurgitant
fraction.
These normal compensatory responses out-
lined earlier lead to harmful changes over time.8
Chronic elevations of circulating catecholamines
lead to down-regulation of expression and func-
tion of ␤-adrenoceptors and ␣2 receptors.9 As a
result, the responsiveness to beta-adrenergic ago-
nists is reduced and myocardial catecholamines
are depleted.10 Moreover, chronic elevations in
left atrial pressure lead to changes in pulmonary
vascular function and the development of in-
creased pulmonary vascular resistance.11 The re-
sultant pulmonary hypertension poses a consider-
able afterload stress to the RV, with the ultimate
development of signs of right-sided failure (jugu-
lar distension, peripheral edema, hepatic conges-
tion). Hepatic congestion may lead to decreased
synthetic function and coagulopathy. Symptoms
of congestive heart failure (reduced exercise toler-
ance, dyspnea, orthopnea), are primarily attribut-
able to pulmonary venous congestion.
How does this complex pathophysiology im-
pact the intraoperative management of pa-
tients with LVADs? The most important im-
plications of congestive heart failure (CHF) are
elevated pulmonary vascular resistance (PVR),
impaired RV function, coagulopathy, renal insuffi-
ciency, and abnormal responsiveness to catechol-
amines. These considerations are discussed in the
following section, which describes the stages of
anesthetic management of LVAD placement.
Preoperative Assessment
The decision to implant an LVAD is usually made
because a patient on a heart transplant waiting list
has begun the final stage of decompensation, and
HEATH AND DICKSTEIN
has proven refractory to maximal medical therapy.
For this reason, the first question that needs to be
addressed in the perioperative evaluation is, ‘‘Why
now?’’ The common precipitants of end-stage
cardiac decompensation include infectious pro-
cesses such as sepsis and pneumonia, and cardiac
events such as ischemia and arrhythmias. The
degree of hemodynamic instability and respira-
tory compromise must be assessed with the focus
on ensuring an uneventful transport to the op-
erating room. Seemingly small details, such as
the maintenance of adequate positive end-
expiratory pressure (PEEP) during transport of
the intubated patient may mean the difference
between routine cannulation versus crashing on
to bypass.
The remaining preoperative evaluation is
similar to the evaluation performed for any
patient with heart failure. Special attention
must be paid to the airway, vascular access, the
potential for ischemia on induction, and end-
organ involvement. Important points in the
clinical history include cause of heart failure,
previous anesthetic experiences, previous cardiac
surgery, presence of angina, the ability to lie
flat, current medications, and allergies. On physi-
cal examination, it is important to establish
baseline cognitive function, and to identify any
pre-existing neuromuscular impairment; addition-
ally, physical examination may reveal jugular
venous distention, hepatojugular reflex (reflect-
ing degree of right heart failure), an S3 gallop,
laterally displaced point of maximal impulse
(reflecting left ventricular failure and cardio-
megaly). Important heart catheterization data
include the transpulmonary gradient, PVR, the
pulmonary vascular response to vasodilators (in
patients with pulmonary hypertension), cardiac
output, valvular function, and left ventricular
filling pressure. Serum creatinine and liver
function tests, including coagulation profiles,
should be obtained to identify patients with
impaired renal and liver function. Evaluation of
the liver’s synthetic capacity is important for
gauging the need for perioperative transfusion of
blood and coagulation factors. Serum electrolytes
are often abnormal as a consequence of either
alterations in the reninangiotensin system or
PERIOPERATIVE MANAGEMENT
aggressive diuretic therapy. Moderate renal
insufficiency is often present and it impacts
on pharmacological management and the need
for postoperative hemofiltration and hemo-
dyalisis.
Lining/Induction
The induction of anesthesia may be associated
with hemodynamic instability as a result of nega-
tive inotropic actions, negative chronotropic ac-
tions, and vasodilatory effects of induction agents,
the release of resting sympathetic tone, and the
transition from spontaneous ventilation to posi-
tive pressure ventilation. Patients treated with
angiotensin converting enzyme inhibitors have a
higher risk of hypotension on induction. More-
over, bolus administration of vasoactive agents
used to counteract changes in vascular resistance
will take considerably longer to have their desired
effects because circulation time is more than
doubled in patients with congestive heart fail-
ure.12 In general, induction agents are selected
that are relatively devoid of negative inotropic or
chronotropic effects. The bradycardia that often
accompanies high-dose narcotic inductions may
be poorly tolerated because the increase in the
diastolic time period would not necessarily in-
crease stroke volume in the failing heart. Even in
the absence of inotropic or chronotropic changes,
systemic blood pressure may drop as a result of
vasodilation caused by release of resting sympa-
thetic tone during transition from the awake to
the anesthetized state. Although the concomitant
reduction in venous return is usually well toler-
ated in the failing heart operating on the flat
portion of the Starling curve, a reduction in left
ventricular preload may be poorly tolerated in
patients who have been subjected to aggressive
diuretic therapy. Left ventricular preload may
also be reduced as a result of the change from
spontaneous ventilation to positive pressure ven-
tilation; this increase in right ventricular after-
load will decrease right ventricular output and
decrease left ventricular filling. Furthermore, if
there is a prolonged period of hypoventilation,
hypercarbia may exacerbate pulmonary hyper-
49
tension and further decrease left ventricular
filling. For this reason, rapid sequence induc-
tions are avoided despite the fact that many of
these patients are considered to have full stom-
achs. Ventilation while maintaining cricoid
pressure allows for a slower induction process
than a true rapid sequence,13 hypercarbia may be
avoided, and induction agents may be more
slowly titrated and their hemodynamic effects
accommodated.
Typically, anesthesia is induced after placement
of a large bore intravenous and a radial arterial
line. Immediately after induction, a transesopha-
geal echocardiograph probe is passed, and the
right internal jugular vein is cannulated for place-
ment of a Swan-Ganz catheter. Often, echocardi-
ography is helpful in directing the Swan-Ganz
catheter into the RV, especially in patients with
dilated RV and significant tricuspid regurgitation.
A 9-F introducer is recommended because smaller
catheters are inadequate for volume rescucitation.
Although oxymetric pulmonary artery catheters
provide important data regarding the adequacy of
oxygen delivery, the monitoring of continuous
LVAD flows postimplant may decrease the use of
continuous pulmonary oxymetry. Continuous car-
diac output catheters are particularly useless
given the availability of monitoring LVAD flow.
Right ejection fraction catheters (equipped with
a rapid-response thermistor) in theory provide
useful physiological information; however, the
accuracy of this technique is questionable and
is therefore of little practical benefit.14 Often, a
second central line is placed and connected
to a rapid infuser and used as a dedicated vol-
ume infusion line; this is especially important
because patients are at risk for massive hemor-
rhage.
Transesophageal
Echocardiography
There are several aspects of the transesophageal
echocardiography (TEE) examination that are
particularly important during LVAD implanta-
tion. The competence of the aortic valve must be
assessed in the prebypass period. Because regurgi-
tant flow across the aortic valve causes recircula-
50
tion through the LVAD (device to outflow can-
nula, retrograde into the LV, back into the device
via the inflow cannula), the incompetent aortic
valve must be either replaced or oversewn.
In view of the high incidence of postimplanta-
tion RV failure, it is important to evaluate the
baseline RV size, wall motion, and tricuspid valve
function. Additionally, because dilated cardio-
myopathy predisposes to left atrial and ventricu-
lar mural thrombi, their presence and mobility
should also be assessed so they can, if necessary,
be removed.
The presence of intracardiac shunts such as
patent foramen ovale (PFO) and ventricular sep-
tal defect (VSD) should be investigated by a
bubble study (agitiated blood or saline injected
into the right atrium). In these patients, left atrial
pressure usually exceeds right atrial pressure
throughout the entire cardiac cycle; hence, a
PFO would not be evident under normal condi-
tions. An important maneuver to reverse the
atrial transseptal gradient is the sudden re-
lease of sustained airway pressure. This maneuver
increases increased airway pressures and de-
creases blood flow across the lungs, thus, reduc-
ing left atrial (LA) pressure; release of sustained
intrathoracic pressure also allows the sudden
return of blood to the right atrium and further
shifts the transseptal gradient. However, it is
important to appreciate that the LA de-
compression associated with LVAD operation
coupled with the often elevated right atrial (RA)
pressures causes considerable bowing of the intra-
atrial septum to the left; therefore, a PFO may not
be shown until separation from bypass is insti-
tuted.
Additionally, the TEE is extremely useful for
determining the adequacy of chamber deairing.
This is of critical importance at the end of the
bypass period when filling and ejection of the
LVAD often results in air entering the aortic
root, coronary arteries, and systemic circulation.
The right coronary circulation is particularly
prone to air embolism because bubbles rise to-
ward the right coronary ostium, leading to arrhyth-
mias and right ventricular failure. Air tends to
collect in the LV apex, along the interventri-
cular septum, and in the pulmonary veins; the
device is also a major source of air bubbles.
HEATH AND DICKSTEIN
Because the anastamosis of the outflow conduit
to the ascending aorta may be difficult to visualize
with the TEE, it is useful to gauge the severity of
intravascular air by interrogating the descending
aorta.
Separation From Cardiopulmonary
Bypass
After the completion of the inflow and outflow
conduit anastamoses, preparations are made to
separate from cardiopulmonary bypass. The
pharmacological management of these patients
is directed toward providing inotropic support
for the RV, RV afterload reduction, and adequate
systemic perfusion pressure. The combination
of milrinone and dobutamine provides effective
inotropic support, and also is effective in reduc-
ing PVR.15 In situations requiring further reduc-
tions in PVR, inhaled nitric oxide is likely to
be the most effective therapy.16,17 In contrast to
intravenous pulmonary vasodilators, inhaled
nitric oxide has the important benefit of limiting
pulmonary vasodilation to areas of ventilation
and thus improves ventilation/perfusion (V/Q)
matching and hence PAO2.18 Further, avid
binding of nitric oxide by hemoglobin permits
pulmonary vasodilation without negative ino-
tropic effects or dilation of the systemic vascula-
ture.19 The expected hemodynamic responses
in patients that benefit from this therapy include
an increase in LVAD flow and a reduction in
central venous pressure (CVP); pulmonary artery
(PA) pressures may remain unchanged even in
the presence of a positive response. However,
dependency on nitric oxide may occur within
hours owing to suppression of nitric oxide syn-
thase expression; it is thus important to discon-
tinue therapy in patients who fail to respond.
Lastly, adequate systemic vascular tone may be
achieved by the combination of norepinephrine
and vasopressin infusions. This combination, com-
pared with norepinephrine alone, increases renal
perfusion and decreases pulmonary vascular resis-
tance.20
Immediately before separation from cardiopul-
monary bypass, one should look for the presence
of a PFO, aortic insufficency, and LV decompres-
PERIOPERATIVE MANAGEMENT
sion. To avoid unnecessary reheparinization, it is
important to identify a PFO before protamine
administration. If present, the PFO can be re-
paired by inserting the venous cannula down the
inferior vena cava (IVC) and by using the pump
sucker to drain the superior vena cava (SVC), this
preserves the venae cavae for bicaval cannu-
lation during subsequent heart transplantation.
Aortic insufficiency may be identified by color
flow Doppler; if present, the magnitude of the
recirculation may be appreciated by the discrep-
ancy between LVAD flow and thermodilution
cardiac output. The adequacy of LV decom-
pression must be frequently verified because the
lack of LV decompression suggests a mechani-
cal problem either with the LVAD inflow conduit
(eg, malposition or graft kinking) or the device
itself.
RV failure is a common and incompletely
understood complication of LVAD implanta-
tion.21 The cardinal features are low LVAD flows
in the setting of elevated CVP and a decom-
pressed LV. A sudden decompensation shortly
after separation from cardiopulmonary bypass is
likely to be the result of intracoronary air emoboli.
Corroborative signs include a sudden loss of
rhythm, ST elevations, and the presence of air on
TEE examination. The treatment strategy is to
maintain a high coronary perfusion pressure
while resting the heart on cardiopulmonary by-
pass. Another cause of RV failure may be owing to
impaired contracile function. It is widely thought
that the inflammatory responses to cardiopulmo-
nary bypass, major surgery, and massive blood
product infusion can produce negative inotropic
effects on the right ventricle. Even in the absence
of depressed myocyte function, RV pump func-
tion may also be impaired by ventricular interac-
tions. Because the 2 ventricles share a common
wall, it is not altogether surprising that the
emptying of LV by the LVAD impacts RV perfor-
mance; in fact, direct ventricular interactions are
more prominent in the dilated22 and the failing
heart.23
RV failure may also be caused by increased
afterload. Two important determinants of RV
afterload are PVR and left atrial pressure. PVR
may be elevated owing to a variety of factors,
most notably hypoxia, hypercarbia, airway pres-
51
sure, acidosis, inflammatory agents, and the ef-
fects of massive blood product transfusion. PVR
may be acutely elevated, thus, negating the benefi-
cial effects of the reduction in LA pressures
achieved by the LVAD. Because of its thin wall,
the normal RV is highly sensitive to increases in
its afterload; the failing RV exhibits even more
afterload sensitivity. For this reason, nitric oxide
therapy may be highly efficacious in restoring
adequate RV output and avoiding the need for RV
mechanical assistance (RVAD).
In addition to RV failure, a major concern of
the anesthesiologist during LVAD placement is
the potential for severe hemorrhage. In the major-
ity of patients, platelets and fresh frozen plasma
(FFP) transfusions are required to restore coagu-
lation; it is important to aggressively infuse prod-
ucts soon after bypass to prevent dilutional coag-
ulopathy. The magnitude of surgical dissection
(both intrathoracic and abdominal), and the large
amount of blood products and other fluids admin-
istered, place the patient at risk for hypothermia
and its inherent complications. Adequate fluid
warming equipment is required, and it is often
helpful to have a dedicated central line for
rapid administration of volume. LVAD recipi-
ents have a high rate of re-exploration for bleed-
ing, and are sometimes brought to the intensive
care unit (ICU) with the chest open. As with all
major cardiac patients, aprotinin is infused from
the time immediately before cardiopulmonary
bypass (CPB) until bleeding has subsided in the
ICU.
Intraoperative arrhythmias are common after
LVAD placement; their hemodynamic effects are
dependent on the effect on PVR. LVAD flow is
entirely dependent on the output of the right
heart, which is in turn a function of RV function
and RV afterload. In the setting of normal PVR
and decompressed left atrium, a moderate CVP is
sufficient to generate adequate blood flow through
the lungs without any contribution from the RV
(Fontan physiology). As a result, some LVAD
patients may tolerate severe arrhythmias, includ-
ing ventricular fibrillation, without significant
hemodynamic instability. However, LVAD recipi-
ents with high PVR are dependent on the RV to
drive blood through the pulmonary circulation,
and even a slight rhythm abnormality may signifi-
cantly impair RV function and, thus, LVAD flow.
52
Atrial fibrillation, junctional rhythm, and ventricu-
lar ectopy are common arrhythmias that may, in
the pulmonary hypertensive, be very poorly toler-
ated.24 Placement of AV sequential pacing wires
can be highly valuable in these patients, and
careful attention to pacemaker programming can
lead to rewarding increases in RV performance
and, hence, LVAD flow.
Management in the ICU
The ICU management of the LVAD recipient in
many regards represents a continuation of the
intraoperative care. Initially, the major problem is
likely to be hemorrhage, and large amounts of
platelets, FFP, packed red blood cells may be
required. Coagulation studies, including acti-
vated clotting time (ACT), hepcon, prothrombin
time (PT), partial thromboplastin time (PTT),
fibrinogen, and ionized calcium should be per-
formed at frequent intervals to guide therapy.
Aprotinin infusion should be continued while
bleeding persists, and normothermia should be
maintained.25 In some instances the coagulapothy
may be a result of a poorly understood response
to the internal surface of the device, resulting in
delayed bleeding seen in the ICU in the patient
who had good clot formation in the operating
room.
As is the case in the operating room, the
LVAD flow is a key indicator of overall status,
and the LVAD console/display should be situ-
ated where it can easily be monitored. Low
LVAD flows can be corroborated by thermodilu-
tion cardiac output and mixed venous oxygen-
ation measurement. Occasionally a patient will
display signs of hypoperfusion, (such as low
blood pressure, low urine output, low mixed
venous PO2) despite robust flows as reported by
the LVAD monitor. In this setting it is important
to perform an independent measurement of
cardiac output (eg, by thermodilution) to rule
out the possibility of recirculation through an
incompetent aortic valve. Alternatively, color
flow Doppler during TEE examination may be
used to directly assess the competence of the
aortic valve.
Hypovolemia (usually associated with hemor-
rhage) and RV dysfunction remain principle causes
HEATH AND DICKSTEIN
of low LVAD flow. As in the operating room,
improvement of RV performance may require
volume, increased inotropic support, or reduction
of PVR. Again, the combination of milrinone/
dobutamine for inotropy, and vasopressin/levo-
phed for support of SVR, is highly effective in
supporting LVAD circulation. It is critical to
maintain sufficient aortic pressure to adequately
perfuse the right coronary artery. Nitric oxide is
used if necessary, but should be weaned as soon as
possible. In general, it is preferable to wean nitric
oxide before inotropic support, thus, accelerating
extubation. When weaning nitric oxide the param-
eters to monitor are LVAD flow and CVP; tran-
sient shifts in other parameters are unlikely to be
problematic.
Relative hypoxemia is frequently encountered
postoperatively; acute respiratory distress syn-
drome (ARDS) and pulmonary edema, associated
with the administration of large amounts of blood
products, are common culprits. It may be prudent
to repeat interrogation for a PFO because increas-
ing PEEP will exacerbate shunt flow and paradoxi-
cally worsen hypoxemia. Otherwise, continuous
veno-venous hemofiltration (CVVH) may be use-
ful in accelerating fluid removal and, thus, reduce
the time to extubation. Patients are also at risk for
postoperative acute tubular necrosis (ATN) and
CVVHD may be required.
If the major hurdles of RV failure and hemor-
rhage can be avoided, it is often possible to
extubate the LVAD recipient within 24 hours.
Patients with more prolonged courses are likely
to require intravenous sedation; this can be ac-
complished with infusions of agents such as
propofol, midazolam, and fentanyl. Muscle relax-
ation with nondepolarizing agents should be
avoided because the prolonged ICU course and
severity of illness places these patients at risk
for critical illness polyneuropathy/myopathy.26
This poorly understood entity, characterized
by peripheral motor axon conduction deficits
and muscle atrophy, has been associated with
steroid administration, nondepolarizing muscle
relaxants, prolonged immobility, sepsis, and mul-
tiple organ failure.27 The diagnosis is usually
suggested when a patient is hemodynamically
robust but is unable to be weaned from respira-
tory support.
PERIOPERATIVE MANAGEMENT
Summary
The complexities of end-stage heart failure and
assisted circulation render LVAD implantation
one of the most challenging procedures encoun-
tered by the adult cardiac anesthesiologist. At
this point, much of what has been learned about
these procedures is in the form of anecdotal
experience and extrapolation from other types
of cases. The completion of scientific studies
and well-designed outcome trials should provide
further insight and guidance on the successful
perioperative anesthetic care of LVAD implanta-
tion.
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