ity because these hearts are operating on the flat has proven refractory to maximal medical therapy.
portion of the Frank-Starling curve.5 In contrast, For this reason, the first question that needs to be
the failing heart is particularly sensitive to changes addressed in the perioperative evaluation is, ‘‘Why
in afterload.6 Moreover, ventricular dilation is now?’’ The common precipitants of end-stage
frequently associated with annular dilatation cardiac decompensation include infectious pro-
and mitral incompetence7; mitral regurgitation cesses such as sepsis and pneumonia, and cardiac
amplifies the afterload sensitivity of ventricu- events such as ischemia and arrhythmias. The
lar function. In other words, as afterload is re- degree of hemodynamic instability and respira-
duced, cardiac output is enhanced by greater tory compromise must be assessed with the focus
fiber shortening, as well as a smaller regurgitant on ensuring an uneventful transport to the op-
fraction. erating room. Seemingly small details, such as
These normal compensatory responses out- the maintenance of adequate positive end-
lined earlier lead to harmful changes over time.8 expiratory pressure (PEEP) during transport of
Chronic elevations of circulating catecholamines the intubated patient may mean the difference
lead to down-regulation of expression and func- between routine cannulation versus crashing on
tion of -adrenoceptors and ␣2 receptors.9 As a to bypass.
result, the responsiveness to beta-adrenergic ago- The remaining preoperative evaluation is
nists is reduced and myocardial catecholamines similar to the evaluation performed for any
are depleted.10 Moreover, chronic elevations in patient with heart failure. Special attention
left atrial pressure lead to changes in pulmonary must be paid to the airway, vascular access, the
vascular function and the development of in- potential for ischemia on induction, and end-
creased pulmonary vascular resistance.11 The re- organ involvement. Important points in the
sultant pulmonary hypertension poses a consider- clinical history include cause of heart failure,
able afterload stress to the RV, with the ultimate previous anesthetic experiences, previous cardiac
development of signs of right-sided failure (jugu- surgery, presence of angina, the ability to lie
lar distension, peripheral edema, hepatic conges- flat, current medications, and allergies. On physi-
tion). Hepatic congestion may lead to decreased cal examination, it is important to establish
synthetic function and coagulopathy. Symptoms baseline cognitive function, and to identify any
of congestive heart failure (reduced exercise toler- pre-existing neuromuscular impairment; addition-
ance, dyspnea, orthopnea), are primarily attribut- ally, physical examination may reveal jugular
able to pulmonary venous congestion. venous distention, hepatojugular reflex (reflect-
How does this complex pathophysiology im- ing degree of right heart failure), an S3 gallop,
pact the intraoperative management of pa- laterally displaced point of maximal impulse
tients with LVADs? The most important im- (reflecting left ventricular failure and cardio-
plications of congestive heart failure (CHF) are megaly). Important heart catheterization data
elevated pulmonary vascular resistance (PVR), include the transpulmonary gradient, PVR, the
impaired RV function, coagulopathy, renal insuffi- pulmonary vascular response to vasodilators (in
ciency, and abnormal responsiveness to catechol- patients with pulmonary hypertension), cardiac
amines. These considerations are discussed in the output, valvular function, and left ventricular
following section, which describes the stages of filling pressure. Serum creatinine and liver
anesthetic management of LVAD placement. 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
Preoperative Assessment
gauging the need for perioperative transfusion of
The decision to implant an LVAD is usually made blood and coagulation factors. Serum electrolytes
because a patient on a heart transplant waiting list are often abnormal as a consequence of either
has begun the final stage of decompensation, and alterations in the reninangiotensin system or
PERIOPERATIVE MANAGEMENT 49
aggressive diuretic therapy. Moderate renal tension and further decrease left ventricular
insufficiency is often present and it impacts filling. For this reason, rapid sequence induc-
on pharmacological management and the need tions are avoided despite the fact that many of
for postoperative hemofiltration and hemo- these patients are considered to have full stom-
dyalisis. 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
Lining/Induction slowly titrated and their hemodynamic effects
accommodated.
The induction of anesthesia may be associated Typically, anesthesia is induced after placement
with hemodynamic instability as a result of nega- of a large bore intravenous and a radial arterial
tive inotropic actions, negative chronotropic ac- line. Immediately after induction, a transesopha-
tions, and vasodilatory effects of induction agents, geal echocardiograph probe is passed, and the
the release of resting sympathetic tone, and the right internal jugular vein is cannulated for place-
transition from spontaneous ventilation to posi- ment of a Swan-Ganz catheter. Often, echocardi-
tive pressure ventilation. Patients treated with ography is helpful in directing the Swan-Ganz
angiotensin converting enzyme inhibitors have a catheter into the RV, especially in patients with
higher risk of hypotension on induction. More- dilated RV and significant tricuspid regurgitation.
over, bolus administration of vasoactive agents A 9-F introducer is recommended because smaller
used to counteract changes in vascular resistance catheters are inadequate for volume rescucitation.
will take considerably longer to have their desired Although oxymetric pulmonary artery catheters
effects because circulation time is more than provide important data regarding the adequacy of
doubled in patients with congestive heart fail- oxygen delivery, the monitoring of continuous
ure.12 In general, induction agents are selected LVAD flows postimplant may decrease the use of
that are relatively devoid of negative inotropic or continuous pulmonary oxymetry. Continuous car-
chronotropic effects. The bradycardia that often diac output catheters are particularly useless
accompanies high-dose narcotic inductions may given the availability of monitoring LVAD flow.
be poorly tolerated because the increase in the Right ejection fraction catheters (equipped with
diastolic time period would not necessarily in- a rapid-response thermistor) in theory provide
crease stroke volume in the failing heart. Even in useful physiological information; however, the
the absence of inotropic or chronotropic changes, accuracy of this technique is questionable and
systemic blood pressure may drop as a result of is therefore of little practical benefit.14 Often, a
vasodilation caused by release of resting sympa- second central line is placed and connected
thetic tone during transition from the awake to to a rapid infuser and used as a dedicated vol-
the anesthetized state. Although the concomitant ume infusion line; this is especially important
reduction in venous return is usually well toler- because patients are at risk for massive hemor-
ated in the failing heart operating on the flat rhage.
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 Transesophageal
also be reduced as a result of the change from
Echocardiography
spontaneous ventilation to positive pressure ven- There are several aspects of the transesophageal
tilation; this increase in right ventricular after- echocardiography (TEE) examination that are
load will decrease right ventricular output and particularly important during LVAD implanta-
decrease left ventricular filling. Furthermore, if tion. The competence of the aortic valve must be
there is a prolonged period of hypoventilation, assessed in the prebypass period. Because regurgi-
hypercarbia may exacerbate pulmonary hyper- tant flow across the aortic valve causes recircula-
50 HEATH AND DICKSTEIN
tion through the LVAD (device to outflow can- Because the anastamosis of the outflow conduit
nula, retrograde into the LV, back into the device to the ascending aorta may be difficult to visualize
via the inflow cannula), the incompetent aortic with the TEE, it is useful to gauge the severity of
valve must be either replaced or oversewn. intravascular air by interrogating the descending
In view of the high incidence of postimplanta- aorta.
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- Separation From Cardiopulmonary
lar mural thrombi, their presence and mobility Bypass
should also be assessed so they can, if necessary, After the completion of the inflow and outflow
be removed. conduit anastamoses, preparations are made to
The presence of intracardiac shunts such as separate from cardiopulmonary bypass. The
patent foramen ovale (PFO) and ventricular sep- pharmacological management of these patients
tal defect (VSD) should be investigated by a is directed toward providing inotropic support
bubble study (agitiated blood or saline injected for the RV, RV afterload reduction, and adequate
into the right atrium). In these patients, left atrial systemic perfusion pressure. The combination
pressure usually exceeds right atrial pressure of milrinone and dobutamine provides effective
throughout the entire cardiac cycle; hence, a inotropic support, and also is effective in reduc-
PFO would not be evident under normal condi- ing PVR.15 In situations requiring further reduc-
tions. An important maneuver to reverse the tions in PVR, inhaled nitric oxide is likely to
atrial transseptal gradient is the sudden re- be the most effective therapy.16,17 In contrast to
lease of sustained airway pressure. This maneuver intravenous pulmonary vasodilators, inhaled
increases increased airway pressures and de- nitric oxide has the important benefit of limiting
creases blood flow across the lungs, thus, reduc- pulmonary vasodilation to areas of ventilation
ing left atrial (LA) pressure; release of sustained and thus improves ventilation/perfusion (V/Q)
intrathoracic pressure also allows the sudden matching and hence PAO2.18 Further, avid
return of blood to the right atrium and further binding of nitric oxide by hemoglobin permits
shifts the transseptal gradient. However, it is pulmonary vasodilation without negative ino-
important to appreciate that the LA de- tropic effects or dilation of the systemic vascula-
compression associated with LVAD operation ture.19 The expected hemodynamic responses
coupled with the often elevated right atrial (RA) in patients that benefit from this therapy include
pressures causes considerable bowing of the intra- an increase in LVAD flow and a reduction in
atrial septum to the left; therefore, a PFO may not central venous pressure (CVP); pulmonary artery
be shown until separation from bypass is insti- (PA) pressures may remain unchanged even in
tuted. the presence of a positive response. However,
Additionally, the TEE is extremely useful for dependency on nitric oxide may occur within
determining the adequacy of chamber deairing. hours owing to suppression of nitric oxide syn-
This is of critical importance at the end of the thase expression; it is thus important to discon-
bypass period when filling and ejection of the tinue therapy in patients who fail to respond.
LVAD often results in air entering the aortic Lastly, adequate systemic vascular tone may be
root, coronary arteries, and systemic circulation. achieved by the combination of norepinephrine
The right coronary circulation is particularly and vasopressin infusions. This combination, com-
prone to air embolism because bubbles rise to- pared with norepinephrine alone, increases renal
ward the right coronary ostium, leading to arrhyth- perfusion and decreases pulmonary vascular resis-
mias and right ventricular failure. Air tends to tance.20
collect in the LV apex, along the interventri- Immediately before separation from cardiopul-
cular septum, and in the pulmonary veins; the monary bypass, one should look for the presence
device is also a major source of air bubbles. of a PFO, aortic insufficency, and LV decompres-
PERIOPERATIVE MANAGEMENT 51
sion. To avoid unnecessary reheparinization, it is sure, acidosis, inflammatory agents, and the ef-
important to identify a PFO before protamine fects of massive blood product transfusion. PVR
administration. If present, the PFO can be re- may be acutely elevated, thus, negating the benefi-
paired by inserting the venous cannula down the cial effects of the reduction in LA pressures
inferior vena cava (IVC) and by using the pump achieved by the LVAD. Because of its thin wall,
sucker to drain the superior vena cava (SVC), this the normal RV is highly sensitive to increases in
preserves the venae cavae for bicaval cannu- its afterload; the failing RV exhibits even more
lation during subsequent heart transplantation. afterload sensitivity. For this reason, nitric oxide
Aortic insufficiency may be identified by color therapy may be highly efficacious in restoring
flow Doppler; if present, the magnitude of the adequate RV output and avoiding the need for RV
recirculation may be appreciated by the discrep- mechanical assistance (RVAD).
ancy between LVAD flow and thermodilution In addition to RV failure, a major concern of
cardiac output. The adequacy of LV decom- the anesthesiologist during LVAD placement is
pression must be frequently verified because the the potential for severe hemorrhage. In the major-
lack of LV decompression suggests a mechani- ity of patients, platelets and fresh frozen plasma
cal problem either with the LVAD inflow conduit (FFP) transfusions are required to restore coagu-
(eg, malposition or graft kinking) or the device lation; it is important to aggressively infuse prod-
ucts soon after bypass to prevent dilutional coag-
itself.
ulopathy. The magnitude of surgical dissection
RV failure is a common and incompletely
(both intrathoracic and abdominal), and the large
understood complication of LVAD implanta-
amount of blood products and other fluids admin-
tion.21 The cardinal features are low LVAD flows
istered, place the patient at risk for hypothermia
in the setting of elevated CVP and a decom-
and its inherent complications. Adequate fluid
pressed LV. A sudden decompensation shortly
warming equipment is required, and it is often
after separation from cardiopulmonary bypass is
helpful to have a dedicated central line for
likely to be the result of intracoronary air emoboli.
rapid administration of volume. LVAD recipi-
Corroborative signs include a sudden loss of ents have a high rate of re-exploration for bleed-
rhythm, ST elevations, and the presence of air on ing, and are sometimes brought to the intensive
TEE examination. The treatment strategy is to care unit (ICU) with the chest open. As with all
maintain a high coronary perfusion pressure major cardiac patients, aprotinin is infused from
while resting the heart on cardiopulmonary by- the time immediately before cardiopulmonary
pass. Another cause of RV failure may be owing to bypass (CPB) until bleeding has subsided in the
impaired contracile function. It is widely thought ICU.
that the inflammatory responses to cardiopulmo- Intraoperative arrhythmias are common after
nary bypass, major surgery, and massive blood LVAD placement; their hemodynamic effects are
product infusion can produce negative inotropic dependent on the effect on PVR. LVAD flow is
effects on the right ventricle. Even in the absence entirely dependent on the output of the right
of depressed myocyte function, RV pump func- heart, which is in turn a function of RV function
tion may also be impaired by ventricular interac- and RV afterload. In the setting of normal PVR
tions. Because the 2 ventricles share a common and decompressed left atrium, a moderate CVP is
wall, it is not altogether surprising that the sufficient to generate adequate blood flow through
emptying of LV by the LVAD impacts RV perfor- the lungs without any contribution from the RV
mance; in fact, direct ventricular interactions are (Fontan physiology). As a result, some LVAD
more prominent in the dilated22 and the failing patients may tolerate severe arrhythmias, includ-
heart.23 ing ventricular fibrillation, without significant
RV failure may also be caused by increased hemodynamic instability. However, LVAD recipi-
afterload. Two important determinants of RV ents with high PVR are dependent on the RV to
afterload are PVR and left atrial pressure. PVR drive blood through the pulmonary circulation,
may be elevated owing to a variety of factors, and even a slight rhythm abnormality may signifi-
most notably hypoxia, hypercarbia, airway pres- cantly impair RV function and, thus, LVAD flow.
52 HEATH AND DICKSTEIN
Atrial fibrillation, junctional rhythm, and ventricu- of low LVAD flow. As in the operating room,
lar ectopy are common arrhythmias that may, in improvement of RV performance may require
the pulmonary hypertensive, be very poorly toler- volume, increased inotropic support, or reduction
ated.24 Placement of AV sequential pacing wires of PVR. Again, the combination of milrinone/
can be highly valuable in these patients, and dobutamine for inotropy, and vasopressin/levo-
careful attention to pacemaker programming can phed for support of SVR, is highly effective in
lead to rewarding increases in RV performance supporting LVAD circulation. It is critical to
and, hence, LVAD flow. 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
Management in the ICU
oxide before inotropic support, thus, accelerating
The ICU management of the LVAD recipient in extubation. When weaning nitric oxide the param-
many regards represents a continuation of the eters to monitor are LVAD flow and CVP; tran-
intraoperative care. Initially, the major problem is sient shifts in other parameters are unlikely to be
likely to be hemorrhage, and large amounts of problematic.
platelets, FFP, packed red blood cells may be Relative hypoxemia is frequently encountered
required. Coagulation studies, including acti- postoperatively; acute respiratory distress syn-
vated clotting time (ACT), hepcon, prothrombin drome (ARDS) and pulmonary edema, associated
time (PT), partial thromboplastin time (PTT), with the administration of large amounts of blood
fibrinogen, and ionized calcium should be per- products, are common culprits. It may be prudent
formed at frequent intervals to guide therapy. to repeat interrogation for a PFO because increas-
Aprotinin infusion should be continued while ing PEEP will exacerbate shunt flow and paradoxi-
bleeding persists, and normothermia should be cally worsen hypoxemia. Otherwise, continuous
maintained.25 In some instances the coagulapothy veno-venous hemofiltration (CVVH) may be use-
may be a result of a poorly understood response
ful in accelerating fluid removal and, thus, reduce
to the internal surface of the device, resulting in
the time to extubation. Patients are also at risk for
delayed bleeding seen in the ICU in the patient
postoperative acute tubular necrosis (ATN) and
who had good clot formation in the operating
CVVHD may be required.
room.
If the major hurdles of RV failure and hemor-
As is the case in the operating room, the
rhage can be avoided, it is often possible to
LVAD flow is a key indicator of overall status,
and the LVAD console/display should be situ- extubate the LVAD recipient within 24 hours.
ated where it can easily be monitored. Low Patients with more prolonged courses are likely
LVAD flows can be corroborated by thermodilu- to require intravenous sedation; this can be ac-
tion cardiac output and mixed venous oxygen- complished with infusions of agents such as
ation measurement. Occasionally a patient will propofol, midazolam, and fentanyl. Muscle relax-
display signs of hypoperfusion, (such as low ation with nondepolarizing agents should be
blood pressure, low urine output, low mixed avoided because the prolonged ICU course and
venous PO2) despite robust flows as reported by severity of illness places these patients at risk
the LVAD monitor. In this setting it is important for critical illness polyneuropathy/myopathy.26
to perform an independent measurement of This poorly understood entity, characterized
cardiac output (eg, by thermodilution) to rule by peripheral motor axon conduction deficits
out the possibility of recirculation through an and muscle atrophy, has been associated with
incompetent aortic valve. Alternatively, color steroid administration, nondepolarizing muscle
flow Doppler during TEE examination may be relaxants, prolonged immobility, sepsis, and mul-
used to directly assess the competence of the tiple organ failure.27 The diagnosis is usually
aortic valve. suggested when a patient is hemodynamically
Hypovolemia (usually associated with hemor- robust but is unable to be weaned from respira-
rhage) and RV dysfunction remain principle causes tory support.
PERIOPERATIVE MANAGEMENT 53
25. Goldstein DJ, Seldomridge JA, Chen JM, et al: Use of drome after cardiac surgery? Eur J Cardiothorac Surg
aprotinin in LVAD recipients reduces blood loss, blood 12:826-835, 1997
use, and perioperative mortality. Ann Thorac Surg 27. Nauwynck M, Huyghens L: Neurological complica-
59:1063-1067, 1995 tions in critically ill patients; Septic encephalopathy,
26. Thiele RI, Jakob H, Hund E, et al: Critical illness critical illness polyneuropathy. Acta Clin Belg 53:92-
polyneuropathy: A new iatrogenically induced syn- 97, 1998