. 7
( 8)


tive to dopamine. Unfortunately, a controlled trial among patients with chronic kidney disease
(CKD) undergoing CABG receiving presurgical angiography showed that the agent failed to
prevent AKI, nor did its use reduce 30-day mortality, dialysis requirements or decrease re-
hospitalization rates.
N-acetylcysteine has shown some promise in trials with respect to its ability to prevent
radiocontrast nephrotoxicity. However, a randomized, controlled trial of approximately 300 CKD
patients undergoing CABG at high risk for AKI revealed no benefit of N-acetylcysteine.

Chapter 13: Acute kidney injury (AKI)

Natriuretic peptides are also theoretically attractive as agents for the prevention of AKI.
Synthetic atrial natriuretic peptide (ANP), anaritide and a synthetic brain natriuretic pep-
tide, neseritide, have been studied in the context of AKI and congestive heart failure. The
ability of these agents to prevent AKI, decrease mortality rates and lessen the clinical severity
of AKI in multiple models (sepsis, ischemia, toxin exposure) has been demonstrated in ani-
mals. Unfortunately, a randomized, double-blind controlled human trial of patients under-
going CABG with or without mitral valve repair showed no clinically meaningful benefit.
Natriuretic peptides have also failed to prevent AKI among patients with congestive heart
Theophylline, dexamethasone, pentoxyphyline, clonidine and diltiazem have also been
evaluated as preventative agents. Unfortunately, none of these agents proved superior to
standard care/placebo therapy with respect to prevention of AKI.
Finally, prophylactic dialysis has been proposed for patients with pre-existing advanced
kidney disease. Mortality and prolonged requirement for dialysis was studied among a very
small, non-controlled cohort of patients treated with prophylactic dialysis (serum creatinine
preoperatively greater than 2.5 mg/dl). Mortality decreased from 30% to 5% and 30-day dialy-
sis requirement was less common in the interventional arm. This controversial approach has
yet to be duplicated/replicated.

Management of dialysis-dependent patients
Patients with CKD who are already dialysis dependent on presentation for cardiac surgery
should be dialysed close to the time of operation, generally this is best done in the 1“2 days
preceding surgery, to optimize their metabolic and circulatory volume status. Arrangements
should also be made for dialysis to re-commence in the early postoperative period. These
patients may benefit from intraoperative hemofiltration/ultrafiltration while on CPB to
maintain acid“base and electrolytes within normal limits, particularly to remove the potas-
sium load imposed by cardioplegia administration. Hemofiltration/ultrafiltration may be
required in the immediate postoperative period to manage fluid balance as well as biochemi-
cal parameters.
In the immediate postoperative period, hemofiltration/ultrafiltration provides a tempor-
izing measure in these patients until they are sufficiently stable to be re-established on their
usual dialysis regimen.

Management of patients with non-dialysis-dependent CKD
Patients with evidence of chronic renal impairment, but who do not have sufficiently advanced
renal disease to warrant dialysis, may benefit from intraoperative hemofiltration/ultrafiltra-
tion while on CPB to optimize acid“base and electrolyte status during surgery. Such patients,
as discussed above, have a high likelihood of developing AKI in the postoperative period and
may require renal replacement therapy postoperatively until their renal function returns to
a viable level.

Therapy for AKI
Supportive therapy for AKI includes avoidance of further nephrotoxins and optimization
of ventilation, perfusion and hemodynamic parameters. Timely management of acid“
base and electrolyte abnormalities and ensuring the adequacy of circulating volume are
Chapter 13: Acute kidney injury (AKI)

Hyperkalemia commonly complicates AKI and may be immediately life threatening. Emer-
gency treatment of hyperkalemia includes the myocyte membrane-stabilizing effects of calcium
chloride or gluconate initially, followed by attempts to shift potassium from the extracellular
space to the intracellular space. Infusion of insulin and dextrose, administration of bicarbonate
and perhaps the utilization of beta agonists are first-line approaches. Enhanced renal excretion
of potassium in AKI may be facilitated by loop diuretics after assurance of adequate intravas-
cular volume. Administration of colonic binding resins such as polystyrene sulfonate by enema
or orally with sorbitol has historically been an accepted clinical practice. Recently, documented
cases of colonic necrosis associated with the use of binding resins, as well as lack of relative clini-
cal efficacy, has dampened enthusiasm for its use. Failure of these measures to correct hyper-
kalemia, or its presence accompanying oliguria, require the institution of dialysis.
The metabolic acidosis associated with AKI is commonly due to decreased tissue per-
fusion and consequent lactic acidosis. Treatment of the underlying pathophysiology is the
preferred therapy. The acidosis associated with AKI may initially be exacerbated by accu-
mulation of phosphates, sulfates and other organic anions. Severe acidemia (pH <7.1) may
derange adrenergic receptor function, promote pulmonary vasoconstriction and dramatic-
ally increase minute ventilation requirements. Therapy specifically to correct severe acidemia
using sodium bicarbonate may thus be justified. Dialysis supplies massive amounts of bicar-
bonate via conductive means, i.e., transfer across the dialysis membrane, and is an extremely
efficient means of supplementing bicarbonate without sodium and volume overload.

Hyponatremia and hypernatremia
Management of hypo- or hypernatremia becomes nearly impossible without adequate renal
function. Severe dysnatremia with associated encephalopathy may require dialytic therapy
when complicating oliguric AKI. The rate of correction of plasma sodium disturbance needs
to be carefully considered, and often continuous dialysis modalities may be best. When medi-
cal management fails and/or volume overload occurs, dialysis/extracorporeal renal replace-
ment therapy may be required.

Use of high-dose diuretics has been advocated by some to convert oliguric to non-oliguric
renal failure. In general, these strategies have not been found to decrease mortality, hospi-
talization or requirements for long-term dialysis. In fact, patients treated with diuretics who
are successfully converted from oliguric to non-oliguric renal failure, but who subsequently
go on to require dialysis, have increased mortality risk as opposed to oliguric patients started
on dialysis within the first 48 hours of nephrology consultation. This calls into question the
“automatic” use of diuretics in oliguric AKI, an important shift in common clinical practice.
Whether “resting the kidney” occurs with the use of loop diuretics remains controversial.
Evaluation of effective circulating volume is critical in AKI, and use of diuretics without clini-
cal signs of volume overload should be questioned.

Renal replacement therapy
Renal replacement therapy is generally recommended when volume status cannot be medi-
cally managed and severe metabolic derangements are manifest (including hyperkalemia,

Chapter 13: Acute kidney injury (AKI)

severe hyper- or hyponatremia and severe metabolic acidosis). Additionally, severe azotemia/
uremia may be a relative indication for initiation of renal replacement therapy. Relative indi-
cations for initiation of dialysis, with respect to complicated azotemia, include pericardial
effusion, pleural rub, bleeding issues (uremic platelet defect) and encephalopathy, which can-
not be absolutely attributed to other etiologies. A BUN level of >100 mg/dl has been clinically
adopted as a point at which dialysis should be strongly entertained. The evidence to support
this practice is, however, not terribly rigorous by modern standards, and needs to be inter-
preted within the overall clinical context.
Timing of initiation of renal replacement therapy (continuous or intermittent) remains
somewhat empirical. Many experts recommend early intervention, citing decreased require-
ments for long-term dialysis and more rapid correction of azotemia/uremia and metabolic
derangements as sound rationale. However, accounting for whether improvement is the result
of early intervention with renal replacement therapy, or would have occurred spontaneously
with simpler supportive measures, becomes much more difficult as dialytic modalities are
initiated early in the clinical course of AKI.
The choice of intermittent versus continuous renal replacement modalities remains
very controversial. Hypothetically, continuous renal replacement therapy, which allows for
“online” volume management, solute control, potential management of “cytokinemia” and
easier titration of vasopressors, seems intuitively to be a better choice. However, randomized
trials have failed to demonstrate a benefit of continuous renal replacement therapy over inter-
mittent hemodialysis among all critically ill patients, particularly among those post cardio-
vascular surgery.

AKI complicating cardiovascular surgery portends a grave outcome both acutely and in
the long term. As non-remediable demography and pre-existing illnesses play such a large
role in the development of intra- and perioperative kidney injury, appropriate preopera-
tive counseling of patients and their families regarding these risks is critically important.
All efforts should be undertaken to prevent adverse outcomes by maximizing general sup-
portive measures and specifically avoiding nephrotoxins. Prompt initiation of medical and
extracorporeal therapy, coordination of care among the multiple care teams and avoidance
of further iatrogenic complications will maximize positive outcomes among these high-risk

• Chertow GM, Levy EM, Hammermeister
Suggested Further Reading KE, Grover F, Daley J. Independent
• Adabag AS, Ishani A, Koneswaran S, et al. association between acute renal failure and
Utility of N-acetylcysteine to prevent acute mortality following cardiac surgery.
kidney injury after cardiac surgery: Am J Med 1998; 104(4): 343“8.
a randomized controlled trial. Am Heart J
• Hilberman M, Myers BD, Carrie BJ,
2008; 155(6): 1143“9. Derby G, Jamison RL, Stinson EB.
Acute renal failure following cardiac
• Brown JR, Cochran RP, Dacey LJ, et al.
surgery. J Thorac Cardiovasc Surg 1979;
Northern New England Cardiovascular
77(6): 880“8.
Disease Study Group. Perioperative
increases in serum creatinine are predictive • Hix JK, Thakar CV, Katz EM, Yared JP,
of increased 90-day mortality after coronary Sabik J, Paganini EP. Effect of off-pump
artery bypass graft surgery. Circulation coronary artery bypass graft surgery on
2006; 114(1 Suppl): I409“13. postoperative acute kidney injury and

Chapter 13: Acute kidney injury (AKI)

mortality. Crit Care Med 2006; 34(12): • Schetz M, Bove T, Morelli A, Mankad S,
2979“83. Ronco C, Kellum JA. Prevention of cardiac
surgery-associated acute kidney injury.
• Lassnigg A, Donner E, Grubhofer G,
Int J Artificial Org 2008; 31(2): 179“89.
Presterl E, Druml W, Hiesmayr M. Lack of
renoprotective effects of dopamine and • Sirivella S. Gielchinsky I. Parsonnet V.
furosemide during cardiac surgery. J Am Mannitol, furosemide, and dopamine
Soc Nephrol 2000; 11(1):97“104. infusion in postoperative renal failure
complicating cardiac surgery. Ann Thorac
• Lombardi R, Ferreiro A, Servetto C. Renal
Surg 2000; 69(2): 501“6.
function after cardiac surgery: adverse effect
of furosemide. Renal Failure 2003; 25(5): • Smith MN, Best D, Sheppard SV, Smith DC.
775“86. The effect of mannitol on renal function
after cardiopulmonary bypass in patients
• Ranucci M, Ballotta A, Kunkl A, et al.
with established renal dysfunction.
Influence of the timing of cardiac
Anaesthesia 2008; 63(7): 701“4.
catheterization and the amount of contrast
media on acute renal failure after cardiac • Thakar CV, Worley S, Arrigain S, Yared JP,
surgery. Am J Cardiol 2008; 101(8): 1112“8. Paganini EP. Influence of renal dysfunction
on mortality after cardiac surgery:
• Rosner MH, Okusa MD. Acute kidney
modifying effect of preoperative renal
injury associated with cardiac surgery. Clin
function. Kidney Int 2005; 67(3): 1112“9.
J Am Soc Nephrol CJASN 2006; 1(1): 19“32.

Extracorporeal membrane

14 Ashish A. Bartakke and Giles J. Peek

Extracorporeal Membrane Oxygenation (ECMO) enables the technology associated with
cardiopulmonary bypass to be utilized in the setting of intensive care units. Although ECMO
is based on CPB there are fundamental differences (see Table 14.1).
ECMO provides a means of supporting blood gas exchange using a membrane oxygenator.
Venous blood is pumped through the oxygenator, where gas exchange occurs, and is actively
re-warmed before being returned to the patient, via either the venous or arterial circulation.
There are thus two types of ECMO (see Table 14.2):
• veno-venous (VV) ECMO, in which blood is returned to the patient via a vein; and
• veno-arterial (VA) ECMO, in which the blood is returned to an artery.
VA ECMO provides gas exchange as well as direct cardiac support, as arterial circula-
tory flow is augmented by the pump in the ECMO circuit. VV ECMO only provides gas

The first successful use of ECMO was reported by Hill for the treatment of posttraumatic
ARDS in an adult patient in 1972. Following this early success, in 1979 Zapol conducted
a randomized controlled trial of VA ECMO in adult patients in the USA. It showed no
benefit of VA ECMO compared to continued conventional treatment with approximately
10% survival in each group. However, this trial was fundamental to the development of a
number of treatment principles relating to ECMO:
• selecting patients before irreversible ventilator-associated lung injury has occurred;
• the use of lung protective ventilation;
• the use of low-range heparinization; and
• the use of veno-venous ECMO for respiratory support.
Following Zapol™s study, clinical ECMO use was largely confined to indications in the neo-
natal and pediatric age groups. Field and coworkers (Bennett et al. 2001) proved that ECMO
improves survival in neonates with severe respiratory failure (UK Collaborative ECMO Trial
Group) confirming the earlier work (Bartlett et al. 1985; O™Rourke et al. 1989). The use of
ECMO for the treatment of adult patients was taken up again in the late 1980s by a number of
groups using the lessons learnt from Zapol™s study and neonatal ECMO.

Because ECMO can potentially take over the function of both heart and lungs, it can be used
for the management of both cardiac and respiratory conditions. Veno-venous ECMO is usu-
ally used to support patients with respiratory dysfunction, whereas VA ECMO may be utilized
176 Cardiopulmonary Bypass, ed. S. Ghosh, F. Falter and D. J. Cook. Published by Cambridge University Press.
© Cambridge University Press 2009.
Chapter 14: Extracorporeal membrane oxygenation

Table 14.1. Differences between CPB and ECMO

Setup Operating room Intensive care unit
Venous reservoir Yes No
Arterial filter Yes No
Heparin dose High Low
ACT levels >400 seconds 160“180 seconds
Hypothermia Yes/No No
Anemia Yes No
Cardiac arrest induced Yes/No No

Table 14.2. Differences between veno-arterial and veno-venous ECMO

Veno-arterial ECMO Veno-venous ECMO
Cannulation site Vein: Vein:
“ internal jugular, “ internal jugular vein
“femoral “femoral vein
“right atrium “saphenous veins
Artery: “right atrium
“right common carotid
Systemic perfusion Circuit flow and cardiac output Cardiac output
Circulatory support Partial to complete No direct effect
“Preload “,
Cardiac effects No significant cardiac effects
“Afterload ‘,
“Pulse pressure “
Oxygen delivery capacity High Moderate
CVP monitoring Unreliable Reliable
Arterial PaO2 Unreliable Reliable
Indices of adequacy of perfusion “SvO2 “arterial blood gas,
“lactate levels “lactate levels
Recirculation No Yes
Decrease in ventilator “rest settings” Rapid Slow

to manage severe cardiac dysfunction with associated impairment of blood gas exchange. The
main indications for ECMO are summarized in Table 14.3.

Respiratory ECMO in adults
The current practice of ECMO for adults was pioneered by Bartlett and coworkers in 1988
at the University of Michigan, Ann Arbor. It is based on careful patient selection, the use of
Chapter 14: Extracorporeal membrane oxygenation

Table 14.3. Indications for ECMO

Neonatal and pediatric Adult
• Meconium aspiration syndrome • Severe pneumonia
• Persistent pulmonary hypertension of the newborn • ARDS
• Congenital diaphragmatic hernia • Severe bronchial asthma
• Severe pneumonia • Thoracic trauma involving lung contusion
• Smoke inhalation injury
• Cardiac arrest • Resuscitation:
• Failure to wean from cardiopulmonary bypass “cardiac arrest
• Treatment of fulminant myocarditis “cardiogenic shock
“cardiac trauma
“drug overdose
“pulmonary edema
“pulmonary embolism
“status asthmaticus
“smoke inhalation
• Procedural support:
“abdominal aortic graft replacement
“arrhythmia ablation
“tracheal surgery
“cerebral arterio-venous malformation resection
“donor organ preservation
“pulmonary embolectomy
“ventricular assist device placement

VV ECMO for CO2 removal and oxygenation, and a lung protective ventilatory strategy in
order to “rest” the lungs and provide optimal conditions for recovery of lung function. The
following criteria determine a patient™s suitability for adult ECMO:
• Potential reversibility of the disease “ only patients with acute and potentially reversible
processes are candidates for ECMO support. Chronic and irreversible pathology, such
as malignancy, systemic or interstitial diseases affecting the lungs, are not suitable for
management with ECMO.
• Premorbid condition of the patient “ even if a disease process may be reversible, in a
moribund patient the risks of ECMO are likely to outweigh the benefits.
• Etiology of respiratory failure.
• Duration of ventilation “ prolonged ventilation with high airway pressures and/or high
inspired oxygen concentrations (FiO2) may pose a contraindication to ECMO as the
Chapter 14: Extracorporeal membrane oxygenation

likelihood of ventilator-induced lung injury (VILI) becoming irreversible increases
with the duration of mechanical ventilation.

Cardiac ECMO in adults
Cardiac arrest and shock are the most common indications for cardiac ECMO support in
adults. Survival rates with conventional cardiopulmonary resuscitation (CPR) are <5% in
cardiac arrests sustained outside a hospital and 5“15% for cardiac arrests within a hospital.
Furthermore, patients requiring CPR for more than 30 minutes have a lower incidence of sur-
vival, even if resuscitated within a hospital. Cardiac ECMO, usually conducted as VA ECMO,
involves passive drainage of blood via the venous cannula, which is then pumped through
the oxygenator into the arterial circulation. With VA ECMO survival may be increased to
30“40%, particularly when:
• patients have some return of spontaneous cardiac output; and
• ECMO can be instituted within 30“60 minutes.
VA ECMO is also used as mechanical circulatory support in patients who fail to wean
from cardiopulmonary bypass to allow the heart time to recover after cardiac surgery. The
advantages are provision of biventricular and pulmonary support and reduced cost compared
to ventricular assist devices (VAD) implantation.
A proportion of patients will not recover sufficient cardiac function to be successfully
weaned from ECMO. If appropriate, these patients can be supported with VADs and be
bridged to either recovery or transplantation (see also Chapter 9).

ECMO circuit
The basic ECMO circuit, as shown in Figure 14.1a“c, consists of:
• one or more draining (venous) cannulae;
• plastic tubing;
• a centrifugal or roller pump;
• an oxygenator with gas supplies;
• a heat exchanger; and
• an arterial cannula.
Blood flows via the venous cannula(e) to the pump, which pumps it through the oxygena-
tor where gas exchange takes place. A servo-regulation device may be incorporated in the
circuit to limit pump flow speed in the event of reduction in venous drainage. Many oxygena-
tors have an integral heat exchanger to re-warm the blood. From the oxygenator the blood
is returned to the patient, either into a large vein “ VV ECMO “ or an artery “ VA ECMO.
It is notable that in contrast to most cardiopulmonary bypass circuits the ECMO circuit is
“closed,” lacking a reservoir. This has important implications for patient management. In a
closed system, flow is dependent on venous return to the circuit at all times and related to
circulating volume and vascular resistance; consequently there is no reserve volume that can
be used to buffer changes in circulatory conditions.
• Cannulae “ Blood flow in the ECMO circuit is dependent on the size of the cannula.
It is directly proportional to the fourth power of the internal diameter of the cannula
and inversely proportional to the length of the cannula. Thus, a shorter cannula
with a greater internal diameter will provide higher flows through the ECMO circuit.
Chapter 14: Extracorporeal membrane oxygenation

Figure 14.1 (a) Diagram of ECMO circuit; (b) ECMO circuit; (c) patient (prone) supported on VV ECMO.

Chapter 14: Extracorporeal membrane oxygenation

Figure 14.1 Continued.

Cannulae are usually sized in French gauge (F), which is the circumference of the
cannula in millimeters. Typical sizes for adults are:
· arterial : 17“21 F
· venous: 21“28 F
· double lumen venous: 27“31 F
• Tubing “ This is usually made of PVC or silicon. If a roller pump is used (see below)
special super-durable tubing must be used in the raceway to prevent tubing rupture.
For adults, tubes of ½ inch internal diameter are used in the drainage line, 3/8 inch or ½
inch in the remainder of the circuit, according to institutional preference. The tubing
length is kept as short as possible to reduce surface area and priming volume.
• Pump “ The pump is the heart of the ECMO circuit. There are two types of pumps
currently available. These are the centrifugal pump and the roller pump:
· Centrifugal pumps “ These utilize the spinning action of cones to create a
constrained vortex, like a tornado, sucking blood into the pump head and expelling
it from its outer edge. Centrifugal pumps must be used with venous line pressure
monitoring to prevent excessive negative pressure and hemolysis. CentriMag
(Levitronix), RotaFlow (Maquet) and BioConsole 550 (Medtronic Perfusion) are
examples of centrifugal pumps commonly used for ECMO.
· Roller pumps “ These are positive displacement devices that compress the plastic
tubing and physically push blood forwards. Venous drainage is passive and can be
assisted by raising the height of the patient™s bed above the ECMO base. Roller
Chapter 14: Extracorporeal membrane oxygenation

pumps must be used with a servo-regulation device, such as a bladder box (OriGen),
Stockert pressure servo-regulator (SIII) or the Better-Bladder (CTI), otherwise
dangerously excessive negative pressure and cavitation can occur. Any air entering
the circuit or generated in the circuit as a result of cavitation may be pumped into
the patient. Because the risk of air entrainment is far greater with roller than
centrifugal pumps, centrifugal pumps are preferred for ECMO by most institutions.
• Oxygenators “ These are more correctly termed “membrane lungs” as their function is
gas exchange. Three types of oxygenators are commonly used:
· silicone spiral coil oxygenators;
· polypropylene oxygenators; and
· poly-methyl pentene (PMP) oxygenators.
The original silicone spiral coil oxygenator (Medtronic) has been largely superseded by
PMP hollow fiber oxygenators (Medos, Maquet & Dideco). They have a lower resistance, lower
priming volume and are more biocompatible. PMP oxygenators do not develop the plasma
leak seen with polypropylene devices.
• Heat exchanger “ This warms the blood before it is returned to the heart, thus allowing
patient temperature regulation through the ECMO circuit. Most adult oxygenators
have an integral heat exchanger.
• Bridge “ This is a connecting channel between the arterial and venous limbs of the
circuit. It is used as a bypass when it is necessary to isolate the patient from the circuit,
i.e., blood can be re-circulated within the ECMO circuit in order to prevent stagnation
and coagulation. Isolation of the patient from the circuit may be required during
circuit maintenance, or during a trial of weaning from VA ECMO. When not in use
the bridge is either not inserted (preferable) or kept clamped and flushed every 10“15
• Monitoring and safety devices “ Ultrasonic flow measurement devices are placed
around the ECMO circuit tubing and alarm limits are set to warn of low or high flows.
Drainage line pressure monitors are used to measure pressure in the venous draining
cannula, which is usually negative. When the line pressure becomes very negative (i.e.,
more than “70 mmHg in an adult), it can cause a non-wire wound cannula to collapse
and cause hemolysis. Increasingly, negative venous line pressure may indicate hypo-
volemia or mechanical obstruction, for example if the tip of the cannula abuts against
the vessel wall, leading to occlusion. Line pressure is also measured on the inflow and
outflow from the oxygenator to indicate oxygenator resistance. This may rise if clots are
collecting or developing in the oxygenator.
Blood gas analysis may be performed either by in-line monitoring or by intermittent
· In patients on VA ECMO venous line blood gas samples approximate to mixed
venous (SVO2) blood samples and are used to assess the adequacy of extracorporeal
support. A SVO2 <65% means that oxygen delivery to the patient is marginal and
should be increased by turning up the ECMO circuit flow rate if possible. Postoxy-
genator blood gas samples taken from the oxygenator outflow indicate the functional
status of the oxygenator: low PO2 values imply a poorly functioning oxygenator that
needs to be changed.
· During VV ECMO the arterial blood gas is used to adjust the level of support.
A reduced PaO2 (<6 kPa) prompts an increase in blood flow and a raised PaCO2
(>6 kPa) prompts an increase in sweep gas flow.
Chapter 14: Extracorporeal membrane oxygenation

• Anticoagulation “ Activated clotting time (ACT) analyzers are an important part of
the ECMO monitoring equipment. ACT is usually maintained in the 160“180 seconds
range and the rate of heparin infusion is titrated accordingly. This range ensures
prevention of clotting within the circuit without causing excessive bleeding. Thrombo-
elastography (TEG) may also be useful for monitoring anticoagulation during ECMO.

Inflammatory response to ECMO
The circuit tubing and oxygenator are primarily responsible for the inflammatory response
that is observed after putting patients on ECMO, as is evidenced by worsening of the chest
X-ray following initiation of ECMO. The inflammatory response may be reduced by using
albumin to coat the circuit during priming. The use of polymethyl pentene membrane oxy-
genators has further reduced the inflammatory response. Coating of the oxygenator mem-
brane with heparin may also contribute to the reduction in the inflammatory and coagulative
response. A variety of commercial circuit coatings exist “ these may be heparin or non-heparin
based. Other measures to reduce the inflammatory response may include the use of steroids
and hypothermia.

• Veno-venous “ Cannulae used for VV ECMO are either single or double lumen.
Cannulation sites for single lumen cannulae include the right or left internal jugular
vein, or the right or left femoral veins. The right internal jugular vein is used for
cannulation with a double lumen cannula. The double lumen cannula is placed in such
a way that the distal end of the cannula is in the inferior vena cava, the proximal
drainage port is in the superior vena cava and the re-infusion port is in the low right
atrium directed at the tricuspid valve. Cannulation is a percutaneous procedure
performed under full surgical asepsis. Preventing air embolism is essential. Prophylactic
antibiotics are given. Heparin 50“100 U/kg is administered prior to cannulation. For
larger patients (weight >90 kg) additional drainage cannulae may be used to ensure
adequate flows. The position of the cannulae is confirmed by a plain chest X-ray.
• Veno-arterial “ In addition to single lumen venous cannulation as described above, an
artery is instrumented. The femoral artery is the usual site in adults due to its ease of
access. Cannulation will typically be percutaneously; however, in some cases an open
dissection may become necessary to place the cannula under direct vision. If the
cannulated leg becomes ischemic, distal perfusion must be restored either by moving
the cannula or by inserting an antegrade or retrograde distal perfusion cannula.

Prior to accepting a patient for ECMO a detailed medical history should be obtained. Ideally,
a discussion of the patient™s current condition and any comorbid disease should take place
between members of a multidisciplinary ECMO team. It is helpful to have standardized docu-
mentation available for ECMO patients to record observations, results and progress.
An emergency cart, containing items required for cannulation and connection to the ECMO
circuit, should also be available. The typical contents of an ECMO cart are listed in Table 14.4.
On arrival of the patient in the accepting ECMO center, baseline investigations, as out-
lined in Table 14.5, should be performed. Underlying disease, patient condition and institu-
tional protocol may make any number of additional investigations necessary.
Chapter 14: Extracorporeal membrane oxygenation

Table 14.4. Contents of an ECMO cart

• Cable tie-gun
• Sterile scissors
• 500 ml bag of 0.9% sodium chloride
• Rapid access intravenous giving set
• Adult bridge
• 50 ml Luer lock syringe
• Connectors appropriate to tubing used
• Antiseptic (e.g., chlorhexidine) spray
• Tie-straps
• Spare pigtails (three-way taps with 3”extension tubing “ used within the ECMO circuitry mainly as ports for
blood sampling, drug injections and infusions)
• High-flow taps
• Sterile gloves
• Antiseptic (e.g., Betadine) solution

Table 14.5. Baseline investigations

• Full blood count
• Coagulation profile “ platelet count, INR, aPTT ratio, serum fibrinogen
• Liver function tests
• Renal function tests
• Blood sugar
• Infection screening “ blood, urine and sputum culture; wound swabs

Once the circuit is established, the day-to-day management of patients on ECMO is gen-
erally protocol driven. Specialist ECMO nurses or perfusionists, who can make adjustments
or repair the circuit, conduct hourly checks for loose connections, bleeding from cannula-
tion sites and clots within the circuit. They also manage anticoagulation by measuring hourly
ACTs to titrate the heparin infusion. A typical infusion dose to maintain adequate antico-
agulation is 20“60 IU/kg/hour. Usually the ACT is maintained between 160 and 180 seconds.
Blood gases should be monitored continuously or by regular intermittent sampling. Circuit
blood flow and sweep gas are adjusted to maintain the desired blood gas parameters.
In addition to careful maintenance of the circuit, the management of the ECMO patient
should include:
• Daily laboratory routine
· hematological investigations “ full blood count, platelets;
· biochemistry “ urea, electrolytes, creatinine, liver function tests, plasma-free Hb; and
· coagulation profile “ INR, serum fibrinogen, aPTT, APR.
• Ventilation “ settings should be adjusted to provide lung protective ventilation, i.e.
· airway pressures should be restricted to <30 cmH2O irrespective of tidal volumes to
avoid barotrauma or volutrauma;
· PEEP of 10“15 cmH2O should be used to prevent further atelectasis;
· respiratory rate should be limited to 8“10 breaths per minute; and
Chapter 14: Extracorporeal membrane oxygenation

· FiO2 is reduced to the lowest possible setting to avoid further damage through
generation of free oxygen radicals.
If the lungs are “stiff ” due to poor compliance, high-frequency oscillatory ventilation
(HFOV) can be initiated on ECMO. Ventilation in the prone position has been found to
improve gas exchange by allowing adequate aeration of the posterior segments of the lungs.
However, turning the ECMO patient should be undertaken with extreme care to avoid dis-
lodgement of ECMO cannulae, other vascular lines and the endotracheal tube.
• Steroids “ These may be helpful in treating the inflammatory processes during ECMO
and ARDS. Methyl prednisolone can be used for this purpose as per the Meduri
protocol. A loading dose of 1 mg/kg of methyl prednisolone is administered as a bolus,
followed by an infusion of 1 mg/kg from day 1 to day 14, 0.5 mg/kg from day 15 to day
21, 0.25 mg/kg from day 22 to day 25 and 0.125 mg/kg from day 26 to day 28. If the
patient is extubated within the first 14 days, they are advanced to day 15 of therapy and
then tapered off according to the schedule.
• Transfusion “ This is a regular occurrence while patients are treated with ECMO.
Sepsis, the inflammatory response to foreign surfaces and the mechanical stress caused
by ECMO pumps, will cause damage to red blood cells and platelets. In addition
anticoagulation may lead to bleeding complications. Blood and platelets are transfused
to maintain a platelet count above 80 000 and hematocrit between 40 and 45%. Coagu-
lation is optimized by transfusion of fresh frozen plasma and cryoprecipitate as
indicated by clotting study results.
• Nutrition, antibiotic therapy and sedation as well as other daily routine should be
managed in accordance with institutional protocols.
• It is advisable to have protocols for other situations, ranging from changing the
three-way taps in the circuit to major situations, such as the emergency management of
air entrainment into the circuit, in order to ensure these situations are safely handled.

Weaning and decannulation
Weaning is commenced when the function of the heart and the lungs improve.
• VV ECMO “ Improvements are seen clinically in lung compliance, chest X-ray
appearance and a reduction in the amount of extracorporeal support required. The
ECMO flow is gradually reduced; once it is down to approximately 1 l/minute, a “trial
off ECMO” can be attempted. This involves increasing the ventilatory support and
disconnecting the ECMO sweep gas flow. Following that native gas exchange is assessed
by arterial blood gas sampling. Usually, a PaO2 of >8.0 kPa and PaCO2 of 4.5“6.5 kPa
during the “trial off ECMO” with lung protective ventilator settings while keeping the
FiO2 <60% and respiratory rate <15 breaths/minute indicate sufficiently good gas
exchange to allow decannulation.
• VA ECMO “ Once the heart is deemed to have recovered suitably, flows are reduced
and pulse pressure and arterial waveform are assessed. Achieving a mean blood
pressure of 60 mmHg without using excessive amounts of inotropes and evidence of
adequate tissue perfusion, using indices such as blood gases, acid“base status, serum
lactate and SvO2, on 1 l/minute of ECMO flow, is adequate to begin a “trial off ECMO.”
A 2D echocardiogram is useful to assess the contractility of the heart and any structural
and functional cardiac abnormalities. The actual “trial off ” proceeds with clamping the
patient limb of the ECMO circuit and allowing the blood to circulate through the
bridge as described earlier. The patient™s response to this maneuver is assessed in terms
Chapter 14: Extracorporeal membrane oxygenation

of ability to maintain satisfactory cardiovascular parameters and adequate tissue
oxygenation. Provided that cardiac function is within acceptable limits on the 2D
echocardiogram the patient is decannulated. Percutaneously placed venous cannulae
are removed as for VV ECMO using a horizontal mattress suture to close the cannula-
tion site. Decannulation of the artery is usually done by surgical cut-down and usually
involves reconstruction of the vessel.

Extracorporeal membrane oxygenation in adults is an established therapy for treatment
of severe respiratory dysfunction where conventional methods are insufficient to treat
the patient. The Conventional Ventilation or ECMO for Severe Adult Respiratory Failure
(CESAR) trial is a national, randomized, controlled trial conducted in the UK (http://cesar-
trial.org), comparing 180 patients treated either with ventilation only or ECMO. The results,
when available, will further define the usefulness of ECMO in this situation. The use of cardiac
ECMO in adults is very challenging but it is certainly a useful adjunct to the use of VAD
and transplantation. ECMO is a complex therapy that is reliant on a skilled multidisciplinary
team. As there undoubtedly is a correlation between case load and competence of the team,
it is almost always safer to refer the patient to an established ECMO center than to try and
extemporize from scratch.

• Landis C. Pharmacologic strategies
Suggested Further Reading for combating the inflammatory response.
• Bartlett RH, Gazzaniga AB, Jefferies MR, J Extra Corpor Technol 2007; 39(4):
Huxtable RF, Haiduc NJ, Fong SW. 291“5.
Extracorporeal membrane oxygenation
• Meduri GU, Golden E, Freire AX, et al.
(ECMO) cardiopulmonary support in
Methylprednisolone infusion in early severe
infancy. Trans Am Soc Artif Intern Organs
ARDS: results of a randomized controlled
1976; 22: 80“93.
trial. Chest 2007; 131: 954“63.
• Bennett C, Johnson A, Field D, Elbourne D.
• Pagani FD, Lynch W, Swaniker F, et al.
UK collaborative randomised trial of
Extracorporeal life support to left
neonatal extracorporeal membrane
ventricular assist device bridge to heart
oxygenation: follow-up to age 4 years. The
transplant: a strategy to optimize survival
Lancet 2001; 357(9262): 1094“1096.
and resource utilization. Circulation 1999
• Conventional Ventilation or ECMO for
100(19 Suppl.): II206“10.
Severe Adult Respiratory Failure. The
• Peek GJ, Moore HM, Moore N, Sosnowski
CESAR Trial. http://cesar-trial.org
AW, Firmin RK. Extracorporeal membrane
• Hill JD, O™Brien TG, Murray JJ, et al.
oxygenation for adult respiratory failure.
Prolonged extracorporeal oxygenation for
Chest 1997; 112: 759“64.
acute post-traumatic respiratory failure
• Younger JG, Schreiner RJ, Swaniker F, et al.
(shock-lung syndrome). Use of the Bramson
Extracorporeal resuscitation of cardiac
membrane lung. N Engl J Med 1972; 286:
arrest. Acad Emerg Med 1999; 6(7):
• Khoshbin E, Roberts N, Harvey C, et al.
• Zapol WM, Snider MT, Hill JD, et al.
Poly-methyl pentene oxygenators have
Extracorporeal membrane oxygenation in
improved gas exchange capability and
severe acute respiratory failure:
reduced transfusion requirements in adult
a randomized prospective study. JAMA
extracorporeal membrane oxygenation.
1979; 242: 2193“6.
ASAIO J 2005; 51(3): 281“7.

Cardiopulmonary bypass in

non-cardiac procedures
15 Sukumaran Nair

Since its first successful use in 1953 by John Gibbon, cardiopulmonary bypass (CPB) has
evolved to such an extent that it has become an indispensable tool for cardiac surgeons. The
majority of cardiac operations performed use CPB, but CPB can be an essential adjunct in
certain non-cardiac procedures. This chapter discusses the various indications to resort to
CPB in clinical circumstances outside of the routine cardiac surgical arena.

CPB in thoracic aortic surgery
Operations on the aorta present a particular challenge because of the unique function of the
aorta as the primary conduit for blood flow to the body. Surgical procedures on the aorta can
thus only be undertaken by either disrupting flow to some organs completely or by supporting
organ perfusion using cardiopulmonary bypass (CPB). Of particular concern are maintenance
of blood flow to the brain, kidneys and spinal cord; if blood supply is to be necessarily compro-
mised during the procedure then strategies to protect these organs should be adopted.
Techniques for maintaining effective blood flow to vital organs are dictated by the nature
of the underlying pathology and the anatomical site requiring surgical correction.
This chapter summarizes commonly encountered aortic pathology, the surgical
approaches used and requirements for perfusion.
The most commonly encountered pathologies are dissection, aneurysmal dilatation and
transection of the aorta.
Thoracic aortic disease is classified as follows:
1. Dissection “ intimal tear/hematoma in media creating a “false” lumen.
2. Aneurysm “ dilation; atheromatous or associated with Marfan™s syndrome.
3. Transection/tear “ following major trauma.
4. Coarctation “ congenital narrowing.

Thoracic aortic dissection
Degeneration of the inner layers of the aortic wall, usually as a result of atheromatous disease,
ageing or in association with hypertension, results in a sudden transverse tear of the intima;
blood is forced under pressure into a false lumen created by destruction of the substance of the
media and stripping of part of the media from the adventitia. Blood flow to organs and limbs
may be compromised, depending on the site of the dissection, and the dissection flap may
retrogradely extend to the aortic root and/or coronary ostia, giving rise to aortic regurgitation
and myocardial ischemia.
Thoracic aortic dissections are classified as per the Stanford classification into:
Type A “ involving the ascending aorta; and
Type B “ involving the aorta distal to the left subclavian artery.
Cardiopulmonary Bypass, ed. S. Ghosh, F. Falter and D. J. Cook. Published by Cambridge University Press.
© Cambridge University Press 2009.
Chapter 15: CPB in non-cardiac procedures

Management is aimed at stopping progression of the dissection. Type A generally requires
urgent surgery to limit progression of the dissection into the ascending aorta, prevent aortic
regurgitation, intrapericardial rupture and coronary ischemia. Type B is usually managed
conservatively using vasodilators and beta blockers.
Type A dissections that do not involve the aortic arch, aortic valve or coronary ostia can
be surgically corrected by interposition of a tubular dacron graft to re-establish circulation
through the true lumen; stagnation of blood in the false lumen leads to thrombosis and even-
tually fibrosis. If the aortic valve or coronaries are involved then additionally valve replace-
ment and/or coronary re-vascularization may be necessary. If the aortic arch is involved then
more complex surgery is undertaken under deep hypothermic circulatory arrest (DHCA) as
discussed later.
In most centers, current surgical practice is to establish CPB, with core cooling, via femoral
arterial and venous cannulation before attempting sternotomy. This technique provides “con-
trolled” conditions in the event that the aorta is damaged during chest opening or exposure of
the mediastinum; aortic dissections are often associated with fragility and gross anatomical
distortion of the mediastinal contents leading to the potential for catastrophic hemorrhage.
Commencing cooling early affords protection against neurological damage accompanying
sudden, inadvertent hypotension.
Commonly, venous drainage may be poor via the femoral venous cannula; options
to improve drainage include using the largest diameter venous cannula that the vein
can accommodate, using vacuum-assisted venous drainage, using a long venous
cannula that can be passed up the inferior vena cava into the right atrium or placing an
additional venous cannula in the right atrium, once the heart has been safely exposed,
and connecting the femoral and venous cannula together with a Y-connector to the CPB
Femoral arterial cannulation may be complicated by the fact that many of these patients
also have peripheral vascular disease; cannulation of the vessel may lead to lower limb
ischemia. An alternative approach when cannulating peripheral arteries for CPB is to first
connect a prosthetic graft, using an end to side anastomosis, to the artery and then placing
the cannula in this prosthetic limb rather than directly in the vessel. If the femoral arteries
are grossly diseased or too small to accommodate a reasonably sized arterial cannula then
the iliac artery may be used instead. A further disadvantage of using the femoral artery for
CPB is that perfusion is retrograde and thus, in the face of aortic dissection, may result in
blood flowing up the false lumen, compromising rather than improving organ perfusion. At
the onset of femoro-femoral CPB particular attention needs to be paid to line pressures, flow
rates and the monitored systemic arterial pressure to ensure adequacy of perfusion via the
true aortic lumen. The arterial cannula can be transferred to the right axillary artery follow-
ing sternotomy; this has the advantage of providing antegrade perfusion and may provide
better cerebral perfusion than perfusion via the femoral artery. Many surgeons will cannu-
late the aortic graft as soon as it is in place and use this as the route for arterial return from
the CPB machine.
Operative mortality is said to be about 5“10%, with 70% surviving beyond 5 years with
good control of hypertension. If the arch is involved then mortality is higher.

Thoracic aortic aneurysms
Fusiform or saccular dilatation of the aorta as a result of atherosclerosis, cystic medial necro-
sis or more rarely infection, gives rise to an “aneurysm.” The aortic wall in the region of the
Chapter 15: CPB in non-cardiac procedures

aneurysm is weakened and prone to rupture, with risk of rupture increasing as the diameter of
the aneurysm begins to exceed 5 cm. Aortic aneurysms are classified according to their loca-
tion into ascending, arch or descending.
1. Ascending “ proximal to innominate artery.
2. Arch “ between innominate and left subclavian.
3. Descending “ distal to left subclavian.
Ascending aneurysms may be treated with an interposition graft, sometimes also requir-
ing aortic valve replacement and coronary ostial re-implantation or coronary bypass grafting.
Cannulation for CPB is as described above for aortic dissection.
Arch aneurysms are more complex to correct, requiring replacement of the arch from
the innominate artery to the left subclavian artery and anastomosis of the prosthesis to the
great vessels. DHCA is required and in addition selective antegrade cerebral perfusion or
retrograde cerebral perfusion may be used to try to protect the brain from ischemia. These
techniques are discussed in more detail in Chapter 10.
Descending aneurysms require replacement of the aorta from below the left subclavian
artery to the diaphragm. A particular hazard is spinal cord ischemia because of the variable
origin from the posterior aspect of the aorta of the Radicularis Magna, the principal blood
supply of the spinal cord. There are two approaches to descending aortic aneurysm surgery:
the older approach is to clamp the aorta proximal to the aneurysm and sew in the graft as
rapidly as possible. Alternatively, partial femoro-femoral bypass can be established to main-
tain perfusion to the lower part of the body. The aorta is clamped proximal and distal to the
lesion. Endogenous cardiac output sustains perfusion to the upper half of the body above the
proximal aortic clamp. Hypertension in the upper body commonly develops after application
of the proximal cross-clamp and needs to be controlled using short-acting vasodilators, or if
partial femoral bypass is used by increasing venous drainage into the bypass reservoir and
so reducing circulating volume. On completion of the surgical repair, removal of the cross-
clamp should be preceded by measures to allow blood pressure and circulating volume to
rise, in anticipation of hypotension, and metabolic parameters fully corrected. With regard
to the latter, metabolic acidosis is a particular issue following reperfusion of the lower body;
if femoral bypass is used a hemofilter can be incorporated in the circuit to assist in metabolic

Reducing spinal cord ischemia during
descending aneurysm surgery
As mentioned earlier the blood supply to the spinal cord is particularly vulnerable dur-
ing descending aortic aneurysm surgery; up to 30% of patients sustain severe neurologi-
cal injury. The best method of protecting the spinal cord from ischemia is to keep the
cross-clamp time short (<30 minutes). Maintaining distal aortic perfusion pressure using
partial femoral bypass may help in some cases, but the evidence of significant benefit in
preserving neurological function is equivocal. Mild hypothermia may have a role, but
again evidence of distinct benefit is lacking. Drainage of cerebrospinal fluid (CSF) to
reduce the compression of vessels supplying the spinal cord by rising CSF pressure may be
beneficial in maintaining blood flow and is gaining increasing popularity as a protective
strategy. Avoidance of hyperglycemia may reduce the damage sustained from ischemia.
The role of specific pharmacological agents such as calcium channel blockers remains
Chapter 15: CPB in non-cardiac procedures

Blunt thoracic aortic injury
Transection of the aorta occurs as a result of blunt thoracic injury, most commonly road traffic
accidents and 80“90% of patients die at the scene. Ninety percent of survivors die within 10
weeks. Survivors have an intact adventitia and the most common site of injury is near the liga-
mentum arteriosum, distal to the left subclavian artery. Those who reach hospital alive usually
have multiple injuries, which may include splenic rupture and head injury. Once adequate
assessment and stabilization have been instituted surgical repair of the transection may be
appropriate and depends on the site and extent of the tear. Cardiopulmonary bypass may be
particularly hazardous because of the need for heparinization in the face of multiple trauma.
Use of heparin-bonded circuitry with only partial heparinization has been advocated. Can-
nulation for CPB depends on the site of the tear and follows the principles discussed above for
management of dissections or aneurysms. Use of left heart bypass for emergency aortic repair
is described in the section on “CPB in Trauma Care” later in this chapter. With the recent
advances made in interventional radiology, percutaneous stenting across the transected aorta
has been successfully performed in many instances. Vascular access is achieved through the
left common femoral artery and a covered stent is deployed across the transection line under
radiological guidance. Long-term performance data of this intervention is awaited.
In conclusion, management of operations on the aorta requires detailed preoperative plan-
ning of the choice of initial cannulation site and strategy for improving CPB flow and quality
of perfusion with additional cannulation if required, adaptability intraoperatively to resort
to DHCA and ability to conduct full or partial CPB. Preoperative “work up” of the patient is
crucial, but time may not always be available as many of these procedures are emergent. Intra-
operatively key factors in successful outcome are limiting ischemic times, rigorous correction
of metabolic parameters and skilled imaging using TOE, not only to define the lesion, but also
to assess perfusion within the true lumen of the aorta, valvular competence and cardiac func-
tion. Thoracic aortic surgery still carries a high rate of morbidity and mortality.

Re-warming from severe hypothermia
Every year, approximately 4 out of 1 000 000 people in the USA die as a result of hypother-
mia. Between 1999 and 2002, 4607 death certificates identified hypothermia or related com-
plications as the underlying cause of death in the USA. Accidental hypothermia is defined
as an unintentional decrease in core temperature below 35°C due to hypothermic exposure
in individuals without intrinsic thermoregulatory dysfunction. Depending on the degree of
core cooling, accidental hypothermia can be mild (32.2“35°C), moderate (28“32.2°C) or deep
(below 28°C). Deep accidental hypothermia (DAH) usually follows accidental exposure to
extreme cold, resulting in suspension of all signs of life and mimicking death, particularly if an
“after drop” in temperature occurs. “After drop” is a phenomenon of conductive heat loss that is
usually associated with immersion hypothermia following accidental drowning.
The most important differential diagnosis of severe hypothermia is death. Hyperkalemia
may be a useful diagnostic tool to differentiate between these two states. Mair and coworkers
in a retrospective study involving 22 hypothermic patients re-warmed with the aid of CPB,
suggested that the following were indicative of the inability to restore spontaneous circulation
due to irreversible cell death:
• hyperkalemia exceeding 9 mmol/l:
• pH ¤6.5: or
• ACT >400 seconds in a venous blood sample.
Chapter 15: CPB in non-cardiac procedures

Patients with such severely deranged metabolic parameters did not regain spontaneous
circulation despite full re-warming on CPB.
Severe hypothermia is a medical emergency. Core re-warming may be required in a short
space of time to prevent resistant cardiac arrhythmias and death. There are many ways of re-
warming, broadly divided into invasive and non-invasive methods. In the emergency room
re-warming techniques are usually limited to administration of warmed intravenous fluids,
warming blankets and gastric and bladder lavage. These methods are relatively slow and inef-
fective. The only reliable way of safely and reliably restoring normothermia relatively quickly
is to use CPB.
Other non-invasive techniques for re-warming include:
• warming inspired gases;
• microwave therapy;
• warm water immersion; and
• body cavity lavage, which involves the repeated instillation of up to 2.5 l of normal
saline into the peritoneal cavity, and leaving it for 20 minutes before draining
again “ this sequence is repeated until a core temperature of 37°C is achieved.
More recently arterio-venous anastomosis (AVA) warming has been promoted. This
involves the application of heat in the form of circulating warm air, with or without negative
pressure to distal extremities in an effort to increase AVA blood flow.
In 1996, Kornberger and colleagues published the results of a study where 55 patients who
had suffered severe accidental hypothermia were treated using three different methods of
re-warming, namely:
• airway re-warming, warmed fluids and insulation in patients in a stable hemodynamic
• peritoneal dialysis in patients in an unstable hemodynamic state; and
• extracorporeal circulation in patients who had circulatory arrest.
Survival rates were 100%, 72% and 13%, respectively, in these three groups. This study
concluded that the method used to re-warm a patient with severe accidental hypothermia
should be adjusted to the hemodynamic status of the patient in order to achieve best results.
Prognosis seemed to be excellent in patients with no hypoxic event preceding hypothermia
and with non-serious underlying disease.
Whenever possible, re-warming should be attempted with invasive methods. Patients
with a cardiac output and systolic pressure over 80 mmHg might benefit from continuous
arterio-venous re-warming (CAVR) alone. This entails establishing peripheral arterial and
venous access to maintain low flow rates through an extracorporeal circuit incorporating
a heat exchanger for re-warming. The commonest route of arterial access is via the femoral
artery, while venous access is normally established via the femoral or internal jugular vein.
The arterial and venous cannulae can be either introduced percutaneously or after a vascular
cut down. Arrested and hemodynamically unstable patients should be treated with full CPB
using a circuit incorporating an oxygenator. Formal full-dose heparinization is required. The
use of pharmacological means of vasodilatation with agents such as sodium nitroprusside
during the re-warming phase of CPB has been shown to improve peripheral re-warming;
vasodilators enhance the distribution of blood to peripheral vessels and so help to “even out”
the core“peripheral temperature difference.
Controlled studies comparing the efficacy of CPB and alternative warming techniques
have not been performed so far. In a literature review published by Vretenar et al. in 1994, it
Chapter 15: CPB in non-cardiac procedures

was shown that femoro-femoral bypass was used as a means to re-warm 72% of profoundly
hypothermic patients. The overall survival was 60% in this series with 80% of the survivors
suffering no long-term organ dysfunction.

CPB in management of acute respiratory failure
Institution of urgent CPB is of value in patients with sustained respiratory arrest or obstruc-
tion in whom endotracheal intubation is not possible. This approach can be life-saving in
young patients with treatable pathology such as mediastinal lymphadenopathy due to hem-
atological malignancies causing superior vena caval and tracheal obstruction. Mediastinal
tumors can compress major airways to such an extent that the occurrence of even mild supra-
glottic edema can result in complete airway obstruction. This may occur following minimal
handling of the airway during attempted endotracheal intubation, or following upper respi-
ratory tract infections. Initiation of femoro-femoral CPB is the only safe interim procedure
prior to controlled tracheotomy to secure an airway. This approach provides a safe solution
for airway control when intubation or a surgically created airway is either unsuccessful or too
hazardous to attempt.

Management of acute pulmonary embolism
The majority of cardiothoracic surgeons would agree that pulmonary embolectomy is cur-
rently rarely indicated as acute pulmonary embolism can be treated effectively and safely with
thrombolytic agents, delivered either intravenously or via a pulmonary artery catheter loc-
ally. Emergency cardiopulmonary support by CPB in massive pulmonary thromboembolism
can be helpful in increasing the efficiency of thrombolytic agents by establishing circulation.
A few instances where institution of percutaneous CPB in patients with acute pulmonary
embolism was life-saving have been reported. Cardiopulmonary bypass was of use particularly
when cardiogenic shock was evident and helped in the immediate resuscitation and stabiliza-
tion of cardiopulmonary function, allowing for subsequent successful emergency pulmonary
embolectomy. Pulmonary embolectomy can also be achieved by pulmonary arteriotomy and
retrograde flushing of the pulmonary circulation via the pulmonary veins after establishment
of CPB. With the ubiquitous availability of effective thrombolytic agents, surgical pulmonary
embolectomy is an infrequently performed procedure in the current era.

CPB in single and sequential double lung transplantation
CPB has been frequently used for single and double lung transplantation. Certain transplan-
tation centers have been reluctant to resort to CPB during lung transplantation due to poten-
tial side effects, including hemorrhage and triggering of the systemic inflammatory response
syndrome (SIRS) associated with CPB, leading to sequestration of neutrophils and platelets
in the pulmonary capillary bed, endothelial damage, increased capillary permeability and
subsequent pulmonary edema. A study from a major center involving 74 patients over 4 years
compared patients who had their lung transplant with or without CPB. It failed to demonstrate
any significant difference in the short- or long-term outcome of the grafts between the groups,
thereby refuting the argument of the adverse effects of CPB-induced SIRS. Most commonly,
however, the decision to establish partial or complete CPB is made after hemodynamic assess-
ment of the patient following occlusion of the pulmonary artery during surgery. Criteria for
the establishment of CPB include a mean pulmonary artery pressure of more than 50 mmHg,
hypoxia, hypercapnea or hemodynamic instability. Prior to surgery it is also possible to get an
Chapter 15: CPB in non-cardiac procedures

indication of the need for CPB support by eliminating ventilation to the operative lung. If the
non-operative lung is ineffective for maintaining ventilation on its own, the patient is unlikely
to tolerate the period of lung isolation during explant and implant of the operative lung and
CPB will be required.
As yet, there are no reliable preoperative predictors for the need for CPB in lung transplanta-
tion. In a study involving 109 lung transplant recipients, however, the following parameters:
• preoperative right ventricular ejection fraction <40%,
• a 6-minute walk test result of less than 250 m and
• a drop in arterial oxygen saturation on exercise to <94% on room air
were positive predictive factors for resorting to CPB.

Extracorporeal circulation in liver transplantation
Occasionally extracorporeal circulation is used to assist liver transplantation. In general terms,
extracorporeal circulation provides a means of decompressing the hepatoportal circulation
and reducing the risk of bleeding when operating on patients with portal hypertension. It also
reduces the risk of post-transplantation renal failure and of intestinal venous congestion with
subsequent hepatic dysfunction. The femoral vein is cannulated at the groin for venous return
using a standard short venous cannula. The venous blood thus drained is passed through a
centrifugal pump to be returned to the systemic venous circulation by cannulae inserted into
the internal jugular or subclavian vein. The circuit is constituted of heparin-bonded material
and full systemic heparinization is avoided if possible.
Systemic venous return is often impaired by surgical manipulation during both excision
of the native liver and implantation of the transplant organ. Employing an extracorporeal per-
fusion technique allows the portal circulation to be decompressed as well as systemic venous
return to be maintained at adequate levels to optimize systemic cardiac output. Furthermore,
it allows extravasated blood to be salvaged and returned to the circulation. If portal hyperten-
sion persists despite inferior vena cava drainage via the femoral vein, an extra-venous drain-
age cannula can be inserted directly into the portal vein. It should be noted that the circuit
described here is not a cardiopulmonary bypass circuit as it does not include a gas exchanger,
there is no arterial cannulation and the cardiac output is maintained by the heart.

CPB in resection of tumors
The commonest indication to resort to cardiopulmonary bypass is the excision of a liver or
renal malignancy growing into the inferior vena cava and occasionally into the right atrium.
Selective cannulation and snaring of the venae cavae, along with a generous right atriotomy
after establishment of CPB, helps the surgeon to extract tumors extending into the inferior
vena cava and right atrium under direct vision (see Figure 15.1). With tumors extending into
the right atrium, or in exceptional circumstances even into the pulmonary artery, complete
excision of the tumor might require deep hypothermic circulatory arrest DHCA.
Cardiopulmonary bypass permits maintenance of systemic perfusion at a low pressure,
cessation of pulmonary artery inflow into the lungs and, if required, drainage of the whole cir-
culating volume into the venous reservoir, thereby allowing total circulatory arrest. The risk
of stroke and other neurological complications is minimal if DHCA is employed and does not
exceed 30 minutes. Cardiopulmonary bypass thus enables safe resection of vascular tumors
and tumors occupying anatomical locations that are difficult to access. The risk of hemor-
rhage and organ damage is reduced by lowering the systemic pressure on CPB, cooling down
Chapter 15: CPB in non-cardiac procedures

Figure 15.1 Cardiac-gated
MRI scan demonstrating uterine
benign leiomyoma extending
from pelvis through the inferior
vena cava into the right atrium,
right ventricle and subsequently
into the main pulmonary artery.
(Courtesy: Mr Ray George and
Mr Jon Anderson, Department
of Cardiothoracic Surgery,
Hammersmith Hospital.)

the patient and, if required, stopping the circulation completely for a finite period of time to
allow surgical dissection in a bloodless field. Mediastinal tumors that are diffuse or infiltrat-
ing the heart and great vessels are best excised after institution of CPB. Though infiltration of
major vascular structures of the mediastinum can be a contraindication for attempting cura-
tive resection of advanced lung cancer, there are studies that have shown a survival benefit
when performed in selected patients with advanced T4 lung tumors assisted by CPB.

CPB in other elective procedures
Resection or decompression of complex arterio-venous malformations of the retroperito-
neum, mediastinum, limbs and brain using endovascular embolization with, or without, open
surgical techniques will benefit from low-flow CPB or DHCA; CPB and DHCA have been of
particular value in converting otherwise inoperable tumors or vascular malformations of the
brain or spinal cord to those amenable to a relatively safe surgical procedure.
Profound hypothermia, circulatory arrest and exsanguination is a common approach
in certain high-risk neurosurgical interventions to remove intracranial aneurysms, glomus
jugulare tumors and hemangioblastoma of the brain. In such instances, DHCA provides a
bloodless surgical field and protection of the brain, which make precise clipping of the vas-
cular malformation possible. The disadvantages of this technique include cardiac distension
and arrhythmia during CPB, hemorrhage from systemic anticoagulation and central nervous
system injury due to inadequate cerebral protection.

CPB in trauma care
In complex traumatic injuries of intrathoracic organs, institution of CPB can be life-saving.
This enables the surgeon to work in a bloodless field with non-ventilated, collapsed lungs.
More importantly, CPB ensures that the rest of the body is adequately perfused during the
operation and allows salvaging of shed blood.
Chapter 15: CPB in non-cardiac procedures

Aortic injury is the commonest and most serious intrathoracic injury. Total CPB, as men-
tioned earlier, or at least left heart bypass, should be resorted to before attempting repair of
an aortic tear or rupture. The technique of left heart bypass may be used for repair of the
descending aorta: after thoracotomy the left atrium is typically cannulated via a pulmonary
vein, and oxygenated blood is drained to a pump which is used to return the oxygenated
blood via a femoral arterial cannula. This provides perfusion to organs below the distal aortic
cross-clamp. The left ventricle is partially decompressed and ejects the remainder of the left
atrial volume into the aorta to supply the head and neck vessels. This allows cross-clamping
of the injured aorta above and below the site requiring repair or replacement, while circu-
lation is maintained to all vital organs. The lungs continue to function as the means of gas
CPB is also essential in the emergency repair of multiple or single chamber heart
injury. In 1990, Reichman and coworkers published their results of using CPB for the treat-
ment of cardiac arrest after trauma. Of the 38 patients in their series, 95% were success-
fully resuscitated and 50% weaned from bypass, although the overall survival rate was only
16%. The main reason attributed to account for this poor outcome was the need for full
heparinization, which resulted in high rates of bleeding complications. Far better results
were reported by Perchinsky and coworkers in 1995 using heparin-bonded circuits. They
demonstrated a survival rate of 50% in six patients with severe pulmonary injuries and
profuse hemorrhage.

CPB for emergency cardiopulmonary support (ECPS)
The use of a portable CPB device in the emergency room to resuscitate patients with severe
hypothermia or thoracic trauma is controversial. The need for systemic anticoagulation with
heparin, and the subsequent bleeding complications in the setting of trauma, generally result
in an increased demand for transfusion, which has limited widespread application of the
technique. Moreover, initial experience showed disappointing results for trauma patients.
The introduction of heparin-bonded circuitry in the ECPS system has improved survival

Portable ECPS device
The development of a portable ECPS system soon followed the first successful use of CPB.
In 1954, its usage was limited to the operating theater and to the field of cardiac surgery. In
the 1970s, ECPS became an evolving therapeutic option for treating medical emergencies.
In 1972, Hill and coworkers reported the first successful application of extracorporeal mem-
brane oxygenation in a patient with traumatic respiratory failure. Later, cardiologists started
using portable ECPS for supporting patients after high-risk angioplasties and other interven-
tional procedures following myocardial infarction.

Concept of ECPS
The system consists of a pump, an oxygenator, tubing and percutaneous venous and arterial
cannulae. Cannula sizes vary from 17 to 19 Fr for the arterial cannula and 19 to 21 Fr size for
the venous cannula. The vessels are cannulated either percutaneously or by direct cut down.
Full heparinization monitored by serial ACT measurements is required. Blood is drained
from a large-bore central vein, usually the femoral vein, and perfused back, after oxygenation,
via the femoral artery. A heat exchanger included in the circuit helps to control temperature.
Chapter 15: CPB in non-cardiac procedures

Figure 15.2 Lifebridge B2T is one of the first fully
portable emergency life support systems for patients
suffering cardiogenic shock. First introduced in 2005,
currently it has a CE mark for use all over Europe. It
measures 61 — 45 — 37 cm and weighs 17.5 kg with an
ability to generate up to 6 l/minute flow with peripheral
or central arterio-venous cannulation.

Table 15.1. Main indications for ECPS, National Registry of Cardiopulmonary Support for Emergency

Indications Percentage of patients
Cardiogenic arrest post cardiotomy 55
Cardiogenic shock 9
Cardiogenic shock post cardiotomy 18
Hypothermia 5
Pulmonary insufficiency 6
Others 7

Currently, portable ECPS devices are available commercially for emergency cardiopulmo-
nary support (see Figure 15.2).
The National Registry of Cardiopulmonary Support for Emergency Applications details
the main indications for ECPS (see Table 15.1). It reflects the large experience of using ECPS
in the operating theater and cardiology catheter laboratories. In this database, 63% of all
patients died while on a ECPS system. Ten percent of patients lived for less than 30 days while
25% survived for more than 30 days. Unwitnessed cardiac arrest resulted in a high mortality
even after resorting to ECPS.
Though the success of survival in witnessed cardiac arrest patients supported with
ECPS was better than in the unwitnessed group, mortality was still over 70%. Patients
who survived had more therapeutic procedures undertaken than the non-survivors, sug-
gesting that complete correction of precipitating medical factors is important for a suc-
cessful outcome. Though severely compromised patients can be resuscitated effectively
for a period of up to 6 hours with the ECPS, further therapeutic or diagnostic steps need
to be undertaken in order to save the patient™s life. While ECPS is not a therapy by itself,
it has been proven to buy time, potentially allowing for the correction of underlying dis-
ease processes. New heparin-bonded circuitry avoids the need for full dose heparin, thus
allowing ECPS to be used in patients with acute hemorrhage or other contraindications
for extracorporeal circulation.
Definitive criteria for defining the patients who will benefit most from treatment with
ECPS are still lacking, and future research should be directed to provide more information
regarding this issue.
Chapter 15: CPB in non-cardiac procedures

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138“48 (Review).
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• Perchinsky M, Long W, Hill J, Parsons J,
1999“2002 and 2005. MMWR 2006; 55:
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• De Perrot M, Fadel E, Mussot S, De Palma in the resuscitation of massively injured
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• Pocar M, Rossi V, Addis A, et al. Spinal cord
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• Hill JD, O™Brien TG, Murray JJ, et al.
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J Card Surg 2007; 22(2): 124“8 (Review).
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• Reichman R, Joyo C, Dembitsky W, et al.
(shock-lung syndrome): use of the Bramson
Improved patient survival after cardiac
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• Hlozek C, Smedira N, Kirby T, Patel A, Perl
• Vogel R, Shawl F, Tommaso C, et al. Initial
M. Cardiopulmonary bypass (CPB) for lung
report of the National Registry of Elective
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Coronary Angioplasty. J Am Coll Cardiol
• Hoyos A, Demajo W, Snell G, et al.
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• Vretenar D, Urschel J, Parrott J, Unruh H.
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Cardiopulmonary bypass resuscitation for
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• Kornberger E, Mair P. Important aspects in
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J Neurosurg Anesthesiol 1996; 8(1): 83“7. Am Surg 2008; 74(5): 364“80 (Review).


antifibrinolytic agents, 50“1,
CPB monitoring, 20
re-enabling before weaning
acid-base management
aorta. See thoracic aorta
from CPB, 96
DHCA, 132“3
aortic root replacement
albumin, 39
acid-base status during CPB,
cardioplegia, 89“90
aprotinin, 51, 131
metabolic, 74“5
acidosis. See metabolic acidosis;
ARDS (acute respiratory
respiratory, 75
respiratory acidosis
distress syndrome)
alpha-stat management of
activated clotting time (ACT),
post-CPB, 150“1
blood gas, 75, 132“3
43, 47, 61
argatroban, 45
”-aminocaproic acid (EACA),
acute ischemia during CPB, 89
50“1, 131 arterial blood analysis, 78“9
acute kidney injury (AKI),
anesthesia arterial blood gases
for DHCA, 126“8 weaning from CPB, 97
acute tubular necrosis (ATN),
weaning from CPB, 95 arterial cannulae, 3“5
analgesia arterial cannulation, 54“7
definitions, 167“8
weaning from CPB, 95 ascending aorta, 55
effects of endotoxins, 171
antegrade cerebral perfusion axillary artery, 57
effects of SIRS, 171
(ACP), 74 cannula types, 54“5
etiology, 170“1
antegrade delivery of complications of aortic root
hyperkalemia therapy,
cardioplegia, 84“5 cannulation, 55“6
anti-thrombin III (AT-III) connection to the patient, 55
hypo- and hypernatremia
deficiency, 43, 61 femoral artery, 55“6
therapy, 173
anticoagulation during CPB, innominate artery, 55
hypoxia and renal damage,
41“52 performance index of an
activated clotting time arterial cannula, 54
incidence, 167
(ACT), 47 peripheral arterial
management of dialysis-
argatroban, 45 cannulation, 56“7
dependent patients, 172
bivalrudin, 45 presence of atherosclerosis,
management of patients with
coagulation cascade, 41 55
danaproid, 44“5
CKD, 172 subclavian artery, 55
dangers of clot formation, 41
oliguria therapy, 173 arterial line filters, 13“4, 23
direct thrombin inhibitors,
outcomes associated with, ascending aorta
168 arterial cannulation, 3“5
fibrinolytics, 45
prevention strategies, autologous priming of the CPB
heparin, 42“4
171“2 circuit, 37, 71
heparin neutralization,
renal replacement therapy, AVR surgery, 58
lepirudin, 45
risk factors for, 169“70 B
therapy for AKI, 172“4
bicarbonate buffer system, 74
heparin (LMWH), 44
acute pulmonary embolism
bicaval cannulation, 6, 58
monitoring anticoagulation


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