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ventricular distribution of cardioplegia distal to coronary stenoses. Retrograde cardioplegia
infusion is usually delivered via a balloon-tipped catheter inserted through the right atrium
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Chapter 7: Myocardial protection and cardioplegia



and guided into the coronary sinus. The balloon is either inflated manually or is self-inflating
to prevent regurgitation of cardioplegia into the atrium. Retrograde infusion delivers cardio-
plegia uniformly throughout the left ventricle, but right ventricular coronary flow drains into
veins more proximal to the catheter tip in the coronary sinus and thus retrograde cardiople-
gia does not protect the right ventricle. Many surgeons, therefore, use a combined method
of antegrade and retrograde cardioplegia in most cardiac operations. In cases in which aortic
regurgitation is manifest, cardioplegia may be infused directly into the coronary ostia by
hand-held devices. A similar approach is used in other types of operations requiring opening
of the aortic root for surgical access, e.g., for operations on the aorta.

Antegrade delivery
Typically, a cannula for antegrade cardioplegia is placed high and slightly to the right side of
the ascending aorta, secured with a purse-string suture, which is tied at the end of the opera-
tion. The cannula may include a pressure line and a vent port to suction air and blood between
infusions. Antegrade infusion pressure during delivery of cardioplegia must be monitored.
High pressures (>80 mmHg) may cause endothelial damage and myocardial edema. Monitor-
ing pressure in the cardioplegia delivery system allows detection of inadvertent line occlusion
by clamping or kinking. However, using the delivery system line pressure alone to estimate
aortic or coronary sinus pressure is inaccurate. Accurate infusion pressure is obtained through
a line directly attached to the infusion port. Such systems are widely available commercially.
Antegrade infusion pressure should be kept between 60 and 80 mmHg. High pressure
during infusion is most likely to be due to extensive coronary stenotic lesions; the rate of infu-
sion should be slowed to permit infusion of the required volume (usually 300 ml/minute for 2
minutes). If there is mild aortic insufficiency, antegrade cardioplegia will be infused partially
into the left ventricle and will not be distributed into the myocardium very effectively. Light
manual pressure applied to the right ventricle will often help close the left ventricular out-
flow tract. The perfusionist can confirm that cardioplegia is flowing into the myocardium by
checking aortic root pressure and observing myocardial temperature change. Alternatively,
the aortic root can be partially opened and cardioplegia directly infused into the coronary
ostia using hand-held or self-inflating balloon catheters.
Further antegrade infusions of cardioplegia may be administered during CABG via the
proximal ends of vein grafts on completion of each distal anastamosis.

Retrograde delivery
A cannula for retrograde administration of cardioplegia is inserted through the lower part of
the right atrium into the coronary sinus, usually before cardiopulmonary bypass is started.
A cannula, designed for placement in the coronary sinus, with a malleable stylet and a self-
inflating, or manually inflated, balloon is commonly used. The retrograde cannula is directed
at a 45-degree angle towards the left shoulder in the path of the coronary sinus and posi-
tioned distally beneath the left atrial appendage. The cannula tip is palpated as it passes by the
junction of the inferior vena cava and right atrium into the coronary sinus. If the cannula is
directed into the posterior descending vein, it should be withdrawn slightly and reinserted. If
difficulty is encountered during placement, it is helpful to commence CPB and lift the apex of
the heart. The surgeon can then directly view and palpate the tip of the cannula making it eas-
ier to insert. In re-operations, if the posterior ventricular wall is adherent to the pericardium,
placement of the retrograde cannula may be attempted prior to CPB, but may prove difficult.
Alternatively, after CPB is instituted, adhesions can be dissected away from the heart and the
85
Chapter 7: Myocardial protection and cardioplegia



cannula positioned more readily. Failure to intubate the coronary sinus is rare (under 2% of
cases) and indicates a fenestrated thebesian valve or a flap over the coronary sinus ostium.
When this occurs, bicaval cannulation may be used, permitting opening of the right atrium
and direct insertion of the retrograde cannula into the ostium of the coronary sinus. During
infusion of retrograde cardioplegia, the perfusionist should monitor the infusion pressure
and reduce flow, if needed, so as not to exceed a pressure of about 40 mmHg. High pressures
usually indicate that the catheter is advanced too far and should be withdrawn slightly.
The coronary sinus can be injured by forceful cannulation or continued infusion of cardio-
plegia with coronary sinus pressures exceeding 40 mmHg. Perforation of the sinus is mani-
fest if an initially high coronary sinus pressure is followed by sudden low pressure, or by the
surgeon noting blood within the pericardial well during cardioplegia infusions. Perforation
can be directly repaired with a 5“0 suture or with pericardial pledgets if the tear site is not dis-
tinct. If a hematoma is noted, retrograde infusions should be discontinued. No further action
is needed because low venous pressure allows self-containment after heparin reversal.
Coronary sinus pressure <20 mmHg infers that the balloon is not inflated or not occlud-
ing the coronary sinus. The catheter may have migrated out of the coronary sinus into the
right atrium. The cannula tip and balloon should then be palpated and repositioned. Added
maneuvers to improve retrograde infusion include finger compression of the junction of the
coronary sinus and right atrium or placement of a snared suture around the coronary sinus,
thus fixing it in place and preventing regurgitation of cardioplegia into the atrium. A rare
cause of low retrograde infusion pressure is the presence of a left superior vena cava. This is
usually determined before cardiopulmonary bypass and the vessel occluded with a tourniquet
only if an intact innominate vein is present. If the innominate vein is absent, only antegrade
cardioplegia is used.

Cardioplegia temperature
Crystalloid cardioplegia solutions are usually delivered at 4°C, cold blood solutions at 10“16°C
and warm blood solutions at 37°C.
Adequacy of cardioplegia distribution can be confirmed by monitoring myocardial tem-
perature. The temperature probe can be placed in the septum first, the most vulnerable area,
and then moved according to the surgeon™s preferences to other regions of the heart. Tempera-
ture is generally kept below 15°C. Sometimes more cardioplegia needs to be infused to reach
low temperatures, e.g., in the face of severe left ventricular hypertrophy commonly seen in
hypertensive patients or in the setting of severe aortic stenosis. Inadequate cooling is some-
times seen if the two-staged venous cannula indirectly distorts the non-coronary cusp of the
aortic valve, resulting in aortic regurgitation during cardioplegia infusion. Simply reposition-
ing the cannula in the field will correct this problem.
Excessive blood accumulating in the heart during cardioplegic arrest leads to inadvertent
myocardial re-warming and can be prevented by judicious use of vent suckers to drain the
ventricles.

Alternatives to cardioplegia
There are certain circumstances in which cardioplegia is not used in cardiac surgery. Fibril-
latory arrest has been used for years and, though it is not advocated as a first-line method of
myocardial protection, it is useful in special situations. One of the limitations of fibrillatory
arrest is compression of the coronary vessels by the intensity of contraction of the fibrillat-
ing myocardium, which significantly impairs coronary blood flow. Systemic hypothermia to
86
Chapter 7: Myocardial protection and cardioplegia



about 24°C reduces myocardial activity, and in association with maintaining systemic aortic
pressure above 70 mmHg, may improve transmural perfusion pressure. Fibrillation, in con-
junction with hypothermia and maintenance of a physiological level of perfusion pressure, can
provide myocardial protection for periods of about an hour or more with reasonable recovery
of global function. Utilization of this method of cold ventricular fibrillation is particularly
useful during mitral valve repair or replacement in patients who have undergone prior coro-
nary bypass grafting, in whom the risk of injury to patent grafts is to be avoided. CPB is insti-
tuted via femoral arterial and venous cannulation. The core temperature is reduced and the
heart fibrillates at temperatures below 28°C. The left atrium can be entered via a limited right
thoracotomy, providing the surgeon with an excellent view of the mitral valve. Aortic valve
competence is necessary to prevent flooding of the operative field with blood. This method
has been extensively reported and is commonly used during re-operative surgery.

Optimum cardioplegic technique
Surgeons have advocated the merits of various manifestations of cardioplegia. There is ongo-
ing controversy regarding the ideal composition, temperature (cold vs. warm), frequency of
dosing and the route of administration (antegrade vs. retrograde) of cardioplegia.
The “integrated method” of cardioplegia administration is a technique that combines
the advantages of many strategies while addressing the immediate needs of the myocardium
during a cardiac operation. It hastens the recovery of the myocardium while not interfering
with visualization during the cardiac operation. Coronary artery bypass is the most common
cardiac operation, and so is used here to illustrate this example of the integrated method.
Cardiopulmonary bypass is first initiated with cannulation of the aorta and right atrium and
the core temperature is moderately reduced to about 34°C. The aorta is cross-clamped and the
heart arrested with a cold cardioplegic mixture containing high-dose potassium (20 mEq/l)
infused antegrade into the aortic root at a flow rate of 300 ml/minute for 2 minutes, followed
by retrograde coronary sinus infusion at a flow rate of 200 ml/minute for 2 minutes. A dia-
gram of a system used to deliver cold and warm cardioplegia via antegrade and retrograde
routes and at low or high potassium strengths is shown in Figure 7.3.
Septal temperature is monitored with a temperature probe and usually falls to below
15°C. Topical hypothermia of the right ventricle may be supplemented with cold saline or
iced saline slush with protection of the phrenic nerves to prevent postoperative palsy. This is
not, however, mandatory. The right coronary is first grafted with saphenous vein. “Mainten-
ance” low-dose cold potassium (8“10 mEq/l) blood cardioplegia is then infused simultane-
ously into the vein graft and coronary sinus at a flow rate of 200 ml/minute for 1 minute. The
vein graft is then sewn onto the aorta while a continuous non-cardioplegic solution of modi-
fied cold blood is infused at 200 ml/minute. This “modified cold blood solution” (10°C) con-
tains CPD, THAM, magnesium and mannitol and has been shown to provide better recovery
than cold blood alone. The aorta is actively vented with suction applied to the cardioplegia
catheter. The vent is discontinued and maintenance cardioplegia (low-dose cold potassium
(8“10 mEq/l) blood cardioplegia) is infused into the aortic root at a flow of 200 ml/minute for
1 minute. After residual air is displaced from the aorta and as the cardioplegia blood emerges,
the surgeon completes the anastamosis of the proximal end of the vein graft. The above pro-
cedure is repeated until all vein graft anastomoses, except one, are complete. After the last
distal anastomosis is completed, the “hot shot” of warm substrate-enhanced cardioplegia is
delivered, first antegrade into the ascending aorta at 150 ml/minute for 2 minutes, then retro-
grade through the coronary sinus and simultaneously through the last unattached saphenous
87
Chapter 7: Myocardial protection and cardioplegia




Figure 7.3 Diagram of cardioplegia delivery circuit for “integrated myocardial protection.”


vein graft proximal end at 150 ml/minute for 2 minutes. There is sometimes transient mild
vasodilation due to the added amino acids and this is easily treated with neosynephrine
(0.5 “1 μg/kg/minute). The final distal anastomosis is that of the internal mammary to the left
anterior coronary artery. At this point the body and cardioplegia are re-warmed. As the last
vein graft is sewn to the aorta, the cardioplegia is washed out of the myocardium by retrograde
infusion of plain warm blood at a flow of 300 ml/minute. The heart begins contracting, slowly
at first, then more rapidly and vigorously. The cardioplegia delivery system is turned to the
antegrade mode of delivery and warm blood is infused into the aortic root while the aorta is
still clamped for another 3“5 minutes. During this time, the perfusionist adjusts the flow to
maintain an aortic root pressure of about 80 mmHg. Air is purged from the coronary grafts
with a fine needle. The aortic clamp is then removed and the patient weaned off bypass, usu-
ally within 5 minutes with minimal (dopamine 2.5 μg/kg/minute) or no inotropic support in
spite of lengthy aortic clamp times. Defibrillation is very rarely needed.
Note that the integrated method of protection involves a single period of aortic cross-
clamping, which serves to limit atheroembolic events. Ischemic times are actually shortened
in spite of longer clamp times and morbidity and cost have been shown to be reduced with
this technique.
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Chapter 7: Myocardial protection and cardioplegia




Septal function
Impairment of the coordinated contraction of the interventricular septum is often apparent
after cardiac operations. The “surgical septum” is a term echocardiographers use in describ-
ing the paradoxical movement of the septum seen in this context. A recent study of over 3000
cardiac surgical cases reported an incidence of approximately 40%. Interestingly, the septal
dysfunction recovers with time in the majority of cases, but not all. Some believe the phe-
nomenon of the “surgical septum” is normal after the pericardium is opened and is related to
dissipation of the cardiac impulse in the absence of the tension provided by the closed pericar-
dium. Alternatively, septal dysfunction may be viewed as a form of injury, either permanent
or transient (stunning). Review of over 100 consecutive cardiac surgical procedures, includ-
ing coronary bypass grafting and valve procedures with 2D echocardiography, has shown
that septal dysfunction was absent in patients receiving “integrated myocardial protection.”
Protection of the septum may thus be a further advantage of the integrated technique. Preven-
tion of septal dysfunction is crucial since the septum constitutes approximately one-third of
the weight, and therefore structure, of the heart. Patients with reduced systolic function are
particularly hemodynamically compromised immediately at the termination of CPB if septal
contractility is also impaired.

Cardioplegia in particular conditions
Under certain circumstances the technique of cardioplegia used ideally requires slight modi-
fications based on the same general principles of protection. These circumstances include
acute myocardial infarction and thoracic aortic aneurysms and examples of modifications
that may be of benefit are described below.

Evolving myocardial infarction
In patients with acute ischemia, or evolving myocardial infarction, the ventricle is ischemic
and energy depleted because of lack of perfusion. The goal is to restore the depleted substrates
and reverse ischemia by restoring flow with coronary grafts, while also preventing reperfusion
injury to the myocardium. A substrate-enhanced low-potassium cardioplegia is used during
these procedures, “acute MI/arrest” cardioplegia. This is a formulation that contains potas-
sium to keep the heart arrested, a calcium channel blocker to prevent intracellular calcium
influx and amino acid substrates to promote regeneration of high-energy phosphates. This
solution is infused over a prolonged time (20 minutes). The normothermic arrested heart is
replenished with the amino acid substrates aspartate and glutamate, which are rapidly assimi-
lated into the myocardium to generate ATP needed for contractility.
Leukocyte depletion by adding filters to the cardioplegia in cases of acute infarction has
also been shown to attenuate reperfusion injury.

Myocardial protection during aortic root replacement
The myocardium must be carefully protected during aortic root replacement for dissection
or aneurysmal disease. The coronary ostia are often surgically dissected and isolated for re-
implantation into a prosthetic graft. Intermittent cardioplegia can be administered directly
into these unattached ostia by hand-held cannulae or self-inflating balloon catheters, but care
must be taken to avoid injury, particularly if operation is indicated because of dissection. An
approach that has been found useful in cases of aortic dissection is first grafting the right coro-
nary artery with saphenous vein. The proximal right coronary artery is temporarily occluded
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Chapter 7: Myocardial protection and cardioplegia



with a silastic vascular loop or soft jaw clamp. Cardioplegia can then be administered inter-
mittently antegrade via the grafted right coronary artery for right ventricular protection and
simultaneously retrograde into the coronary sinus for left ventricular protection. This per-
mits excellent cardioplegia distribution throughout the myocardium and does not interfere
with visualization during the operative procedure. The aortic root and ascending aorta can be
replaced with ease in a dry field. After the root replacement, the saphenous vein graft is ligated
at the anastomosis to the right coronary artery, either with a running suture or with a large
hemoclip. The extra 5 minutes to execute this protective method ensures global myocardial
protection and avoids injury to the friable coronary ostia.

Conclusion
Blood cardioplegia is an effective and widely accepted method of myocardial protection. Ret-
rograde cardioplegic delivery has been found to be useful in enhancing even distribution of
cardioplegia, particularly distal to coronary stenoses in vessels supplying the left ventricu-
lar myocardium. Replenishment of substrates to the energy-depleted heart is a main focus
of development for cardioplegia formulations, designed to enhance recovery following the
ischemia required to carry out cardiac operations.
“Integrated myocardial management” is an easy and effective method of myocardial pro-
tection in adult cardiac procedures by expediting the operation and meeting the physiological
needs of the myocardium. The duration of cardiopulmonary bypass is shortened by this tech-
nique by eliminating the need for recovery time following unclamping of the aorta. Excellent
clinical outcomes have been reported and this method has been employed in many centers
for several years.
Ongoing studies are needed to develop additional cardioprotective strategies. These may
include the use of preconditioning agents, white blood cell filters, free radical scavengers and
endothelium-enhancing agents.

• Buckberg GD. Development of blood
Suggested Further Reading cardioplegia and retrograde techniques: the
• Allen BS, Okamoto F, Buckberg GD, et al. experimenter/observer complex. J Card
Immediate functional recovery after six Surg 1998; 13: 163“70.
hours of regional ischemia by careful
• Ihnken K, Morita K, Buckberg GD, et al.
control of conditions of reperfusion and
Simultaneous arterial and coronary sinus
composition of reperfusate. J Thorac
cardioplegic perfusion: an experimental and
Cardiovasc Surg 1986; 92: 621“35.
clinical study. J Thorac Cardiovasc Surg
• Athanasuleas C, Siler W, Buckberg G. 1994; 42: 141“7.
Myocardial protection during surgical
• Loop FD, Higgins TL, Panda R, Pearce G,
ventricular restoration. Eur J Cardiothorac
Estafanous FG. Myocardial protection
Surg 2006; 29 (Suppl 1): S231“7.
during cardiac operations: decreased
• Beyersdorf F, Acar C, Buckberg GD, et al. morbidity and lower cost with blood
Studies on prolonged acute regional cardioplegia and coronary sinus perfusion. J
ischemia. III. Early natural history of Thorac Cardiovasc Surg 1992; 104: 608“18.
simulated single and multivessel disease
• Noyez L, van Son JA, van der Werf T, et al.
with emphasis on remote myocardium. J
Retrograde versus antegrade delivery of
Thorac Cardiovasc Surg 1989; 98: 368“80.
cardioplegic solution in myocardial
• Buckberg GD, Beyersdorf F, Allen BS, revascularization: a clinical trial in patients
Robertson JM. Integrated myocardial with three-vessel coronary artery disease
management: background and initial who underwent myocardial
application. J Card Surg 1995; 10: 68“89. revascularization with extensive use of the

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Chapter 7: Myocardial protection and cardioplegia



internal mammary artery. J Thorac jeopardized myocardium. J Thorac
Cardiovasc Surg 1993; 105: 854“63. Cardiovasc Surg 1989; 97: 613“22.
• Partington MT, Acar C, Buckberg GD, Julia • Teoh KH, Christakis GT, Weisel RD, et al.
PL. Studies of retrograde cardioplegia. II. Accelerated myocardial metabolic recovery
Advantages of antegrade/retrograde with terminal warm blood cardioplegia. J
cardioplegia to optimize distribution in Thorac Cardiovasc Surg 1986; 91: 888“95.




91
Weaning from cardiopulmonary
Chapter

bypass
8 James Keogh, Susanna Price and Brian Keogh




Weaning, the process of transition from cardiopulmonary bypass (CPB) to normal, physio-
logical circulation, requires excellent communication and teamwork between perfusionist,
surgeon and anesthetist. Numerous mechanical, physiological and pharmacological factors
need to be efficiently coordinated within an extremely short time frame. Weaning passes
smoothly in the majority of cases and, as such, is often viewed as a routine process. In patients
with pre-existing poor or borderline cardiac function, or in whom unexpected difficulties
are encountered, weaning from CPB may prove complex, but should not impede the patient™s
progression to recovery. By contrast, if the weaning process is poorly managed, or if warning
signs of deterioration are missed, complications encountered during the weaning phase may,
of themselves, contribute additional morbidity.


Preparation
Separation from CPB requires the heart to resume its function as the driving force of blood
flow, taking over from the mechanical pump in the CPB circuit. In order to achieve a smooth
transition, cardiac function must be optimized prior to weaning from CPB. Delays in inves-
tigating or treating abnormal parameters may lead to the heart failing, necessitating a return
to extracorporeal circulation. Consequently, anticipation of possible cardiac dysfunction and
thorough advance preparation are key elements of the weaning process. A checklist of physio-
logical parameters that should be optimized prior to weaning is given in Table 8.1 and dis-
cussed below.

Temperature
Re-warming to a core temperature above 36oC is the first step in weaning from CPB. In addi-
tion to multiple temperature monitoring sites on the bypass machine, which should include
blood temperature and the temperature of the heat exchanger, body temperature may be
monitored at a number of sites, for example nasopharyngeal, esophageal, intracardiac, blad-
der or rectum. It is important to appreciate that re-warming is not uniform and the deter-
mination of which site (or sites) best represents adequate re-warming will vary according to
how much the patient has been cooled, the duration of hypothermic bypass and patient con-
siderations, such as body surface area. A combination of bladder temperature and the tem-
perature of the venous blood returning to the bypass circuit is particularly valuable when CPB
temperature has been below 30°C. Active surface warming using a forced warm air device
should be combined with re-warming via the extracorporeal circuit to reduce redistribution
of heat from core to peripheral tissues. If re-warming is inadequate, or if the core-surface
gradient is greater than 7oC, significant further heat loss may occur during wound closure.
Shivering and increased peripheral vascular resistance in the recovery period will result in
92 Cardiopulmonary Bypass, ed. S. Ghosh, F. Falter and D. J. Cook. Published by Cambridge University Press.
© Cambridge University Press 2009.
Chapter 8: Weaning from cardiopulmonary bypass



Table 8.1. Preparation for weaning from cardiopulmonary bypass

Re-warm to target temperatures
Correct electrolytes and acid“base
Achieve target hemoglobin
Ensure access to blood and blood products
Establish vasoactive support infusions
Prepare anesthesia transition
Assess rate, rhythm and conduction
Control arrhythmias
Establish pacing as required
TOE functioning if employed
Additional techniques if difficulty predicted


an unwanted increase in oxygen consumption. Conversely, core temperature should not be
allowed to rise above 37oC as this will lead to tachycardia and may increase the risk of central
nervous system dysfunction.

Electrolytes and acid/base
Electrolyte abnormalities should be corrected before separation from CPB in order to opti-
mize myocyte function. In particular, potassium, magnesium and calcium should be kept
within the normal range.
• Potassium (4.0“5.5 mmol/l) “ Hypokalemia can cause arrhythmia and should be
treated if below 4 mmol/l. In many centers potassium is maintained at the “higher” end
of the normal range in order to suppress the development of arrhythmias, to which the
heart is particularly susceptible in the early post-CPB phase. Hyperkalemia can cause
conduction abnormalities and impair contractility. Values above 6.0 mmol/l should
serve as an alert to monitor biochemical parameters closely and levels above
6.5 mmol/l should be actively treated before weaning.
• Calcium (1.09“1.30 mmol/l) “ The concentration of calcium in the plasma may be
reduced by large volumes of citrated blood, leading to impaired contractility and
vasodilatation. Ionized calcium should be maintained above 1.0 mmol/l.
• Magnesium (0.80“1.40 mmol/l) “ Low levels of magnesium are associated with
dysrhythmia and should be corrected below 0.7 mmol/l. It is worth noting that some
point-of-care analyzers, notably the Nova Biomedical range, employ a lower range
measuring ionized magnesium, so it is important to check the nature of the measure-
ment and the device normal range before interpreting the result.
• Glucose (4.0“7.8 mmol/l) “ Tight glucose control in the postoperative period has
been shown by some investigators to improve outcome after cardiac surgery and
investigation of its impact in the perioperative phase is ongoing. Extrapolation
of the available evidence and majority practice suggest that significant hyperglycemia
(>12 mmol/l) should be treated with an insulin infusion, although treatment
thresholds remain varied. Hypoglycemia in association with CPB is extremely rare
in the absence of liver failure and, if encountered, should be judiciously treated and
its cause investigated.
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Chapter 8: Weaning from cardiopulmonary bypass



• Lactate (0.7“2.5 mmol/l) “ Elevated serum lactate levels are commonly encountered
during prolonged episodes of CPB, particularly if there have been periods of low pump
flow or if circulatory arrest has been employed. Treatment of lactic acidosis per se is
not usually instituted but the value should be noted and any progression seen as a
potential indicator of inadequate organ perfusion.
• Metabolic acidosis “ This is also commonly observed during CPB and there are
differing approaches to its correction. Some units very tightly correct base deficits to
baseline whereas the majority of units readily accept base deficits of up to “5 mmol/l.
Most teams would treat a base deficit in excess of “10 mmol/l. Between these values,
debate about treatment thresholds in this context continues.


Hemoglobin
For most patients, the hemoglobin concentration should be above 7.5 g/dl prior to termina-
tion of CPB. In situations where myocardial oxygen supply or whole body oxygen delivery are
expected to be impaired post-CPB, for example residual coronary stenosis or low cardiac output
states, it is preferable to aim for a higher hemoglobin concentration. Similarly, when bleeding is
expected to be an ongoing problem in the post-CPB period, hemoglobin should be maintained
at a higher level. Comorbid pathology, particularly coexisting respiratory disease, may also indi-
cate the need for a higher hemoglobin level at weaning. In patients with congenital heart disease
who remain cyanosed after surgery, a higher hemoglobin concentration is mandatory.
Stored, concentrated red blood cells should be immediately accessible for use in the post-
bypass period. In the majority of cases, cell salvaged blood should ideally become available
within 10“15 minutes of weaning from CPB, thus reducing the need for use of stored “bank”
blood in the first instance.


Coagulation
Due to the nature of cardiac surgery, particularly the anticoagulation required and the effects
of the extracorporeal circuit on the clotting cascade and platelet function, patients under-
going CPB are at significant risk of bleeding. Consequently, ready access to serum clotting
factors and platelets must be ensured. Following separation from CPB and reversal of anti-
coagulation, assessment of clotting and platelet function should be performed according to
unit protocols (laboratory-based clotting screen, activated clotting time, heparin assays or
thromboelastography (TEG)). Persistent surgical bleeding and the absence of visible clot for-
mation should initiate blood product support, informed by coagulation measurements. It is,
however, important to emphasize that abnormal clotting assessments alone should not initi-
ate blood product administration in the operating theater if the surgical field does not show
evidence of ongoing bleeding.

Volume
In addition to ready access to blood products, colloid and crystalloid solutions should be
immediately available to increase circulating volume when indicated.

Vasoactive drugs
Vasopressors, inotropes and vasodilators must be immediately to hand, if not already
prepared and loaded onto infusion pumps, primed for use. The choice of agents should be
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Chapter 8: Weaning from cardiopulmonary bypass



based on the patient™s circulation, nature of the surgery and local team protocols. The vasoac-
tive support strategy should be agreed by the team before weaning from CPB commences.

Anesthesia
Anesthesia, analgesia and neuromuscular blockade must be assessed and supplemented as
required. Weaning from CPB may instigate either a change in anesthetic technique (e.g.,
intravenous to volatile) or an adjustment to dose delivery. Regardless of the exact nature of
this change, it is vital that anesthesia is properly maintained and this should be confirmed by
the team members.

Cardiac function
Following unclamping of the aorta an adequate reperfusion period must be permitted. This
allows the heart to replenish metabolic substrates, specifically high-energy phosphates (ATP),
and “washes out” the products of anaerobic metabolism, before attempting to wean from CPB.
A commonly employed rule is 20 minutes of reperfusion for every hour of ischemic (aortic
cross-clamp) time, although practice is varied. Surgical sequence may facilitate this myocar-
dial resuscitative period “ for example, right-sided surgery (e.g., tricuspid annuloplasty) or
the aortic anastomoses of coronary revascularization grafts may be performed during the
reperfusion period.
Cardiac function should be assessed as far as possible prior to weaning from CPB. This
assessment should concentrate on three main areas: rate, rhythm and contractility. Follow-
ing CPB, the ventricles are generally less compliant and will not have the normal capacity to
increase stroke volume. Heart rate is therefore usually maintained at between 80 and 100 beats
per minute to partially compensate for this. Another result of a stiff ventricle is an increase in
the relative importance of the contribution of atrial contraction to stroke volume and conse-
quently sinus rhythm is always preferable if possible. Epicardial pacing leads and an external
pacemaker should always be immediately available, ideally with dual chamber function to
allow sequential atrio-ventricular pacing.
Contractility can be assessed by direct visualization of the right ventricle. If in use, trans-
esophageal echocardiography (TOE) enables a more detailed examination of all four cham-
bers. If any of the cardiac chambers have been opened during the procedure, for example in
valve replacement surgery, it is essential to evacuate any air from the heart prior to separation
from bypass.

Predicting difficulty
Occasionally, despite careful preparation, weaning from CPB is difficult, and the identifica-
tion of patients who will present a particular challenge allows additional preparations to be
made in advance.
Commonly encountered risk factors for failure to wean from CPB include:
• poor preoperative ventricular function;
• urgent and emergency surgery;
• prolonged aortic cross-clamp time;
• inadequate myocardial protection; and
• incomplete surgical repair.
When faced with a high-risk patient there are several strategies that can be employed. An
intra-aortic balloon pump may be inserted before the start of surgery in patients with poor
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Chapter 8: Weaning from cardiopulmonary bypass



ventricular function. Inotropes and vasopressors can be commenced at re-warming, ensuring
they have cleared the dead-space of administration lines prior to weaning from CPB. If ino-
tropes require administration of a loading dose (e.g., milrinone, levosimendan), these should
ideally be given after aortic unclamping, during re-warming. Dilute solutions of adrenaline
(epinephrine) or noradrenaline (norepinephrine) can be prepared to allow delivery of small
boluses to aid evaluation of the response of the myocardium.
If sinus rhythm is not re-established, or supraventricular arrythmias or ventricular irrit-
ability is observed despite correction of metabolic parameters, anti-arrhythmic therapy
should be prepared and administered as necessary, well before weaning from CPB is attemp-
ted. Electrical cardioversion may be required in isolation, or in addition to anti-arrhythmic
agents.
Additional invasive monitoring lines may be prepared, permitting direct measurement of
cardiac chamber pressures and valve gradients. These lines may additionally be used later for
administration of protamine into the left side of the heart, thus attenuating the pulmonary
hypertensive response (see below).


Events immediately prior to initiating weaning
Mechanical ventilation
During CPB the lungs are allowed to deflate fully or to remain slightly inflated at low levels
of positive end expiratory pressure (PEEP). As a result there will be widespread alveolar col-
lapse. Prior to weaning from CPB full and effective expansion of the lungs should be ensured,
usually with manual hyperinflation. If one or both pleural cavities are open, visualization of
the lung is facilitated and the pleural cavities may be drained of any accumulated fluid. Once
expansion is achieved, mechanical ventilation is resumed, usually with PEEP. It is prudent to
apply tracheo-bronchial suction to the lungs to clear any excess respiratory secretions.
Effective mechanical ventilation of the lungs must be ensured prior to commencing
weaning from CPB. Ventilation should be initiated when it no longer interferes with surgical
maneuvers, and in any case when there are signs of significant left ventricular ejection; cardiac
ejection while on CPB in the presence of a competent aortic valve suggests re-establishment
of significant pulmonary blood flow. If the lungs remain unventilated, this pulmonary blood
flow will acts as a true right to left shunt, delivering deoxygenated blood to the left ventricle.
This deoxygenated blood will then be ejected and mixed with oxygenated blood from the
aortic cannula and, depending on the volume of ejected blood, may result in undesirable
systemic arterial hypoxia in the latter stages of CPB.
The perfusionist and anesthetist must confirm to each other that effective ventilation has
been resumed. The consequence of weaning from CPB without ventilation is the rapid onset
of hypoxia, followed by bradycardia, cardiac failure and organ damage.

Physiological alarms
Alarms settings for many parameters displayed on anesthetic monitors and ventilators are
greatly modified or even disabled during CPB. It is vital that physiological monitoring with
appropriate alarm settings is re-enabled prior to weaning from CPB. This should be seen as
a team responsibility rather than that of an individual, and the anesthetist and perfusion-
ist should specifically confirm that physiological and ventilation monitoring have been re-
enabled prior to commencing weaning.
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Chapter 8: Weaning from cardiopulmonary bypass




Arterial blood gases and electrolytes
Following re-warming, an arterial blood gas and electrolytes sample should be taken, reviewed
by the team and appropriate measures taken. In the majority of cases little or no corrective
action is required. The commonest adjustments that need to be made are to acid“base status
and potassium levels.
Metabolic acidosis may require treatment according to local protocols. Sodium bicar-
bonate (NaHCO3) is commonly administered to correct the acidosis. Administration of
sodium bicarbonate solution, usually into the cardiotomy reservoir of the extracorporeal
circuit, generates a substantial amount of intracellular carbon dioxide and is often asso-
ciated with a reduction in systemic vascular resistance. Although cardiac myocytes are
thought to have effective intracellular buffering mechanisms, the administration of a large
volume of sodium bicarbonate in a short period may generate paradoxical intracellular
acidosis. Clearance of this excess generated carbon dioxide via the oxygenator membrane
may take 5“10 minutes and can be monitored by a return to baseline of oxygenator exhaust
capnography levels or less obviously by in-line blood carbon dioxide tension. Most impor-
tantly, in patients with poor cardiac function, and in particular poor right ventricular
function, weaning from CPB should not be attempted until the risk of significant para-
doxical intracellular acidosis has passed and the majority of excess carbon dioxide has
been cleared.
As previously discussed, serum values of potassium and ionized calcium should be nor-
malized. Magnesium is increasingly popular as an anti-arrhythmic agent and may be admin-
istered following aortic de-clamping regardless of the baseline serum level. A bolus of MgSO4
can cause profound vasodilatation; the systemic vascular resistance should be allowed to
recover, or vasoconstrictors administered, prior to weaning from CPB. In general, magne-
sium is best administered soon after aortic unclamping.


De-airing of the heart
Any cardiac surgical procedure that requires opening of cardiac chambers will inevitably
allow introduction of air. Air in right-sided chambers is usually innocuous as long as its vol-
ume is not substantial enough to prevent forward flow and provided there are no breaches
in the atrial or ventricular septum. Air in the left side is dangerous and presents two major
risks:
• cerebral air embolus with postoperative morbidity, ranging from minimal transient
confusion to widespread neurological damage; and
• coronary air embolus, which may cause transient and possibly widespread regional
ventricular dysfunction and, in the extreme, irreversible myocardial damage.
It is therefore vital that meticulous attention to de-airing is applied. Direct cardiac mas-
sage and syringing of left-sided chambers and venting of the aorta or left-sided chambers is
best undertaken in a head down position, prior to, and after, aortic unclamping. It is custom-
ary to ventilate the lungs during the de-airing process in order to displace air that accumulates
in the pulmonary veins. Indeed, such air may arise from the pulmonary veins even if the
left-sided chambers are not opened, although its degree is usually limited in this context. The
introduction of TOE into cardiac practice has greatly improved the de-airing process, allow-
ing targeting of air “pockets” and de-airing until the amount of residual intracardiac air is
considered acceptable (Figure 8.1).
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Chapter 8: Weaning from cardiopulmonary bypass




Figure 8.1 Trans-esophageal echocardiogram (mid-esophageal, left ventricular outflow tract view) showing the
heart during de-airing following aortic valve surgery. Air is seen as white speckles throughout the left heart.
Of note, there is no air seen in the right heart. AA = ascending aorta; ECG = electrocardiogram; LA = left atrium;
LV = left ventricle; MV = mitral valve (arrowed); RVOT = right ventricular outflow tract.



Epicardial pacing
Epicardial pacing is commonly required in the immediate and early post-CPB period. Atrial
pacing may be used alone to increase heart rate in patients in sinus rhythm or in a junctional
rhythm in which atrio-ventricular (A-V) conduction is intact. When possible, atrial pacing
is preferable to A-V or ventricular pacing. Ventricular pacing may be employed in isolation
when there is no effective atrial contraction (e.g., in chronic atrial fibrillation). In cases in
which A-V synchronization is likely to be helpful and effective sinus rhythm is not estab-
lished, atrial and ventricular epicardial leads should be placed to facilitate sequential A-V pac-
ing. Sequential pacing, usually using atrial and right ventricular leads, may also be established
in atrio-left ventricular or atrio-biventricular (with right and left ventricular leads) fashion.
The latter is analogous to the application of cardiac re-synchronization therapy. This interven-
tion may result in a rapid increase in cardiac output of up to 30% and is increasingly employed
in patients with poor left ventricular function following, or as an aide to, weaning from CPB.
Epicardial pacing is usually established prior to weaning from CPB so that its benefits
can be harnessed during that process. Some surgeons, however, prefer to wean from CPB
with ventricular pacing alone and to secure atrial pacing leads after the venous cannulae have
been removed. The pacing system and pacing and sensing thresholds should be tested prior
to weaning.
Establishment of an appropriate mode of epicardial pacing is specifically intended
to improve cardiac performance. Commonly, pacing is usually set at around 80“90 bpm
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Chapter 8: Weaning from cardiopulmonary bypass



immediately post-CPB. However, the pacing rate should be determined by patient needs
and not strictly by protocol. When using dual chamber pacing, the standard preset atrio-
ventricular interval is usually 150 ms; however, where increased heart rates are required, the
A-V delay should be adjusted accordingly.
If cardiac function is adequate after weaning from CPB, pacing may not prove necessary.

Mechanics of separation from CPB
On confirmation that cardiovascular, respiratory and metabolic parameters are within satis-
factory limits and that the patient is adequately re-warmed and ventilated, the perfusionist
commences weaning, initially by incrementally occluding venous return to the CPB circuit,
thus allowing cardiac filling. The arterial pump flow is gradually reduced. If cardiac ejection
progressively increases to a level considered suitable for maintenance of physiological circula-
tion, the venous return pipe is completely occluded, the arterial flow reduced to “off ” and the
transition from CPB to “normal” circulation completed.
At this stage, in an ideal situation, the heart should be relatively relaxed and empty, both left
and right atrial filling pressures low (2“5 mmHg). Ventricular filling can be further enhanced,
if required, by infusion of fluid via the aortic cannula (in adults, usually in 100 ml aliquots).
Conventional teaching is that the heart should be weaned from CPB with low filling pressures,
allowing both ventricles time to accommodate to working under the increasing ventricular
end-diastolic pressures associated with changes in pre- and afterload.
Weaning from CPB may take literally a few seconds in a patient with vigorous cardiac
action who might typically be taken to “half-flow” and then “off ” within moments. In patients
with less promising cardiac function, the weaning process may be considerably protracted,
necessitating a period of “partial bypass,” that is, low-flow CPB, during which time titration
of ventricular volume loading and optimization of inotropes, vasoconstrictors and cardiac
rhythm can be undertaken.

Assessment and adjustment of preload
Central venous pressure, in the context of the arterial pressures generated, guides the degree
of filling of the heart. Perfusionists rarely have the opportunity to inspect the external appear-
ance of the heart, which provides considerable information to surgeon and anesthetist. Nor-
mally, the right ventricle only is observed: a comfortable, relaxed and slightly underfilled right
ventricle typically displays inward dimpling of its anterior surface during systole. In patients
with impaired left ventricular function, or if weaning from CPB is proving difficult, direct left
atrial pressure or pulmonary artery/pulmonary capillary wedge pressure measurements are
helpful. In some centers, all patients presenting for cardiac surgery have both central venous
and pulmonary artery catheters placed perioperatively.
Surgeons typically also use pulmonary artery palpation, which reflects left atrial pres-
sure, to guide left ventricular filling. TOE, when available, helps to assess preload and may be
particularly useful in the presence of restrictive ventricular physiology, when higher filling
pressures may be encountered at lower ventricular cavity volumes.

Assessment of contractility and inotropic support
Considerable information about myocardial contractility can be gleaned from observing
the heart. Well-coordinated contraction generating an acceptable aortic pulsation to meet
desired arterial blood pressure targets suggests an acceptable inotropic state. Additionally,
a reasonably sharp upstroke in the monitored arterial wave (dp/dt) and wide area under the
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Chapter 8: Weaning from cardiopulmonary bypass



arterial waveform curve are also indicative of contractility, but are also dependent on pre-
and afterload. Quantitative measures of contractility include thermodilution or alternative
cardiac output evaluation techniques; these delineate values for stroke volume if the heart
rate is known. The information that TOE can provide about ventricular function is usually
qualitative, but technology is evolving to provide readily interpretable quantitative echocar-
diographic analyses of myocardial contractility.
Inotropic support should be adjusted using the best information available about the
patient™s cardiovascular status. The strategies employed are considered below and generally
guided by institutional and local team practice. Inotropic support should, if possible, be opti-
mized during the period of weaning from CPB, giving the patient with borderline cardiac
function the best conditions for a successful transition from CPB.

Assessment of afterload
Systemic vascular resistance (SVR) values are usually assumed to be low following CPB
because of the association between hemodilution and reduction in SVR and because of the
systemic inflammatory response accompanying CPB. Patients at risk of a profound inflam-
matory response include those with long CPB times, long aortic cross-clamp times, complex
surgery and previous exposure to CPB. It is therefore common for short-acting vasoconstric-
tors (e.g., metaraminol, phenylephrine) to be administered during CPB and in the wean-
ing phase. Similarly, infusions of noradrenaline (norepinephrine) or vasopressin (ADH) are
commonly administered to maintain SVR in the post-CPB period.
A reasonable estimate of systemic vascular resistance can be obtained while on CPB using
the equation:
[MAP (mmHg) RA (mmHg)]/pump flow (l/min) SVR (Wood Units)

This is accurate unless there is additional native cardiac output, in which case the equation
will overestimate the SVR, since the denominator will be falsely low. Wood units of vascular
resistance are converted to more commonly used international units (dyn.s/cm5) by multiply-
ing the Wood unit value by 80.
Normal values for SVR are 900“1200 dyn.s/cm5. Units of SVR are sometimes indexed to
body surface area.
As a wide range of conditions is encountered in cardiac surgical practice, optimal SVR
for weaning from CPB needs to be individually considered according to pathophysiology.
However, the following considerations generally apply:
• patients with dilated, poorly functioning left ventricles, exhibiting a low ejection
fraction (<30%), are thought to benefit from lower range SVR values;
• patients with coronary disease with residual, flow-limiting lesions or with left
ventricular hypertrophy with small cavity size, but normal cardiac outputs, are thought
to benefit from SVR values higher than normal; and
• coexisting disease in other organs, particularly cerebral or renal, may also dictate the
requirement for higher SVR in order to maintain adequate perfusion pressures to
these organs.
Consideration must also be given to the anesthetic protocol employed. Anesthesia based
on delivery of volatile agents, prior to and during extracorporeal circulation, typically results
in low SVR values (700“900 dyn.s/cm5) when the patient is fully re-warmed. Older, intrave-
nous agent-based protocols (e.g., high-dose opioids plus benzodiazepines) usually result in
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Chapter 8: Weaning from cardiopulmonary bypass



Table 8.2. Sequence of events prior to weaning from cardiopulmonary bypass

Confirm effective ventilation
Re-enable physiological alarms
Final check of electrolytes and acid“base status
Correct acidosis if required
Effective de-airing of heart
Confirm satisfactory pacing lead thresholds
Confirm vasoactive agent delivery
Engage all team members


Table 8.3. Key benefits of TOE when weaning from cardiopulmonary bypass

Confirm adequate de-airing
Guide filling and manipulation of preload
Confirm valve integrity and function
Identify para-prosthetic leaks
Confirm outflow tracts unobstructed
Display ventricular and septal movement
Identify regional wall abnormalities
Identify global ventricular dysfunction
Identify restrictive ventricular filling
Optimize pacing settings
Guide manipulation of contractility


values twice that level. The use of propofol infusions during CPB often result in lesser reduc-
tion in SVR than seen with volatile agents.
The steps to be taken immediately before attempting to wean a patient off CPB are sum-
marized in Table 8.2.

The role of TOE in weaning from CPB
Intraoperative TOE has an increasing role in cardiac surgical procedures. There is institu-
tional variation in the use of this tool in adult cardiac surgery, varying from its routine through
to highly selective application. If difficulties are encountered in weaning from CPB, and par-
ticularly if they are unexpected, TOE can be an extremely valuable tool in informed decision
making.
A detailed examination of the role of TOE is beyond the scope of this chapter. A limited
summary of key benefits specific to intraoperative weaning from CPB is given in Table 8.3.

Reversal of anticoagulation
To reverse heparinization, protamine is administered after successful transition from CPB to
physiological circulation. Practice of heparin reversal varies among centers:
• a fixed dose based on the patient™s weight (usually 3“4 mg/kg) can be given regardless
of the heparin dose; or
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Chapter 8: Weaning from cardiopulmonary bypass



• the protamine dose is titrated to the amount of heparin given, usually 1.0“1.3 mg
protamine for each 100 units of heparin administered.
The venous cannulae are removed prior to protamine administration and the arterial can-
nula is removed either prior to, during or after protamine is given, according to local practice.
Preload can be supported during protamine administration by titrated fluid administration
from the extracorporeal circuit whilst the arterial cannula is in situ.
Protamine administration may be associated with circulatory instability due to unwanted
vasoactive effects. They are usually limited to mild or moderate vasodilatation and mild
negative inotropic effects, which can normally be attenuated by slow administration of pro-
tamine over 5“15 minutes. More severe adverse reactions to protamine can be expected in
patients with existing pulmonary hypertension, due to its pulmonary vasoconstrictive effects.
In a small number of patients, and more likely following previous cardiac surgery, adverse
hemodynamic responses may be unexpectedly severe, some representing anaphylactoid or, in
extreme cases, anaphylactic responses to protamine or the protamine“heparin complex. These
rare but severe responses require escalation of inotropic and vasoconstrictor support. Use of
pulmonary vasodilators may be necessary and, in exceptional cases, return to CPB may be the
course of safety whilst measures to augment cardiovascular performance are instituted.

Failure to achieve satisfactory weaning from CPB
Reinstitution of CPB
Attempted weaning from CPB immediately resulting in unsatisfactory hemodynamic
parameters, or followed by a gradual decline in cardiovascular status, should prompt consid-
eration of a return to CPB, particularly if the hemodynamic deterioration is catastrophic or
unexpected.
Reinstitution of CPB should not necessarily be seen as an adverse event. Although it will
inevitably result in a prolongation of the total CPB time, it will allow:
• escalation of monitoring (e.g., left atrial line, pulmonary artery catheter);
• time for optimization of drug therapy and confirmation of drug delivery;
• fine tuning of hematocrit, acid“base and electrolyte status;
• checking the integrity of surgical intervention (e.g., eliminate kinked coronary bypass
grafts, paraprosthetic leaks); and
• identification of other reversible causes of myocardial failure.
It is occasionally necessary to return to CPB due to major bleeding, such as dehiscence of
a surgical anastamosis, correction of which might not be possible off-CPB.
An intra-aortic balloon pump may be inserted during this period and the team should
have a low threshold for employing this option if there is persistent myocardial failure not
readily reversible by less invasive measures.

Vasopressors and inotropes “ choices in weaning from CPB
Hypotension caused by reduction in SVR post-CPB may result in impaired coronary
blood flow and myocardial ischemia. In this situation, a vasopressor such as noradrenaline
(norepinephrine), vasopressin or phenylephrine is indicated.
Low cardiac output syndrome after cardiopulmonary bypass is multifactorial, but poten-
tial causes include pre-existing ventricular dysfunction, residual myocardial ischemia,
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Chapter 8: Weaning from cardiopulmonary bypass



inadequate myocardial protection, prolonged cross-clamp time with reperfusion injury,
arrhythmia, activation of inflammatory cascades and imperfect surgical repair. Reversible
causes for cardiac failure should be identified, treated appropriately and inotropic support
instituted as necessary.
Inotropic drugs improve ventricular performance at the cost of increasing myocardial
oxygen demand. Their use in the early post-CPB period should ideally be guided by objective
measurements of cardiac performance such as left atrial pressure (reflecting left ventricular
end-diastolic pressure, in the absence of mitral valve disease), cardiac output monitoring,
pulmonary capillary wedge pressure measurement or TOE.
There are considerable variations in pharmacological strategies employed by cardiotho-
racic teams in weaning from CPB. As yet there is no clear evidence for the use of any one
inotropic drug or combination of drugs over any other.
The main options for acute inotropic support during weaning from CPB are:
• Adrenaline (epinephrine) “ A naturally occurring catecholamine with both alpha and
beta receptor activity leading to increased intracellular cyclic AMP and protein kinase
C activity. Adrenaline increases cardiac output by increasing contractility and heart
rate, and is frequently employed in moderately to severely impaired contractility. It
may be administered during weaning as a bolus injection to rapidly stimulate
increased ventricular contractility. At high continuous infusion doses it may cause
considerable vasoconstriction and raised serum lactate.
• Dopamine “ A naturally occurring catecholamine that binds to both alpha and beta
adrenergic receptors. Beta effects tend to predominate at low doses with alpha effects
more prominent at high doses. Dopamine increases cardiac output by increasing heart
rate and contractility; however, at higher doses blood pressure may be increased by
raising systemic vascular resistance with no increase in cardiac output. Dopamine is
generally used in more mild impairment of hemodynamics. There is no evidence to
confirm the role of dopamine as a “renal protective drug.”
• Dobutamine “ A synthetic catecholamine and derivative of isoprenaline, dobutamine
possesses strong affinity to beta receptors with little alpha activity. Contractility and
heart rate are increased along with a reduction in systemic vascular resistance, leading
to a rise in cardiac output. At higher doses the effects on heart rate tend to predomi-
nate and may limit its use in moderate cardiac failure. Its use in weaning from CPB
appears to have waned with the availability of phosphodiesterase inhibitors.
• Milrinone, enoximone “ Often referred to as “inodilators,” these are bipyridine
phosphodiesterase-III (PDE III) inhibitors, which exert their effects by inhibiting the
breakdown of intracellular cyclic AMP and thus increasing stores of the high-energy
phosphate, ATP. PDE III inhibitors improve contractility, increase heart rate and cause
systemic and pulmonary vasodilatation. PDE III inhibitors appear to be associated
with a lower incidence of tachycardia and arrhythmia than beta-agonists and tolerance
is not a feature, but they may need to be administered with a vasoconstrictor. There
is some evidence that prophylactic use of PDE III inhibitors prior to separation from
cardiopulmonary bypass improves the chances of successful weaning and reduces the
incidence of low cardiac output syndrome postoperatively.
• Levosimendan “ This is another class of inodilator, which binds to cardiac troponin
C, enhancing the myofilament responsiveness to calcium. Early studies suggest
levosimendan is more effective at improving cardiac performance than dobutamine,
but experience and information available in the literature remain limited.

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Chapter 8: Weaning from cardiopulmonary bypass




Functional mitral regurgitation
Acute mitral regurgitation in a patient with a morphologically normal mitral valve is occa-
sionally encountered during and after weaning from CPB. Although infrequent, it usually
occurs in patients undergoing coronary revascularization. This phenomenon, functional
mitral regurgitation, is readily treatable with an excellent outcome, but can be surprisingly
difficult to identify. Failure to recognize and treat it appropriately may lead to considerable
morbidity.
As mentioned previously, weaning from CPB should be accomplished with a low
ventricular filling volume and pressure, allowing the heart time to accommodate to the
changing loading conditions. If CPB is terminated rapidly with high venous pressures
and ventricular volumes, the left ventricle may become relatively ischemic and dilate.
As a result the mitral valve annulus will be stretched, rendering the mitral valve acutely
incompetent; the right ventricle faces acute left atrial hypertension and will appear char-
acteristically dilated and domed, with limited contraction and no effective dimpling of its
anterior surface. More commonly than this sudden scenario, the development of func-
tional mitral regurgitation is insidious and the result of overzealous fluid infusion to treat
low systemic arterial pressures. A further fluid challenge in this state characteristically
results in a fall in systemic pressure. Adrenaline administration may increase the systemic
diastolic pressure through vasoconstriction, but usually makes both the mitral regurgitant
fraction and oxygen demand of the left ventricle much worse. Typically, even in a patient
with previously preserved left ventricular function, systemic hypotension intractably per-
sists and the condition rapidly becomes a medical emergency. The diagnosis is confirmed
by TOE, if available, but the condition occurs typically in patients with low-grade indica-
tion for TOE. In the absence of TOE in situ, it is confirmed by direct left atrial pressure
measurement, characteristically displaying a peak mitral regurgitant systolic wave of the
order of 50“70 mmHg.
The treatment for functional mitral regurgitation is venodilatation, using nitroglycerine
(GTN) or sodium nitroprusside, to rapidly reduce the left ventricular end-diastolic volume.
Venodilatation is inevitably accompanied by arteriolar vasodilatation and, as effective
coronary blood flow must be restored, aggressive venodilatation should be followed by a
short-acting vasoconstrictor. The administration of a venodilator to a patient with a mean
arterial pressure of 40“50 mmHg may appear counterintuitive, and brave, but is supported
by an understanding of the pathophysiology. It is necessary to first reduce ventricular volume
and shrink the mitral valve annulus and then support coronary perfusion to the ventricle by
raising systemic pressure.
Alternative surgical approaches to the management of functional mitral regurgitation may
include rapidly returning to cardiopulmonary bypass, performing an atriotomy or draining
blood via the CPB cannulae, if still in situ, allowing rapid reduction in circulating volume and
left ventricular preload.

Mechanical support
Occasionally, despite an optimal circulating volume, epicardial pacing and appropriate
inotropic therapy, ventricular function is insufficient to maintain adequate organ perfusion.
Under these circumstances mechanical strategies may improve myocardial performance
sufficiently to allow separation from CPB. These are discussed briefly here and are dealt with
in greater detail in Chapters 9 and 14.
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Chapter 8: Weaning from cardiopulmonary bypass



Chest splinting
Closure of the chest increases intrathoracic pressure and may adversely affect hemodynam-
ics, particularly in right ventricular dysfunction. The chest wound can be left open with the
sternum splinted and covered with a dressing, pending closure at a later date when myocardial
edema has subsided and cardiac function has improved.

Intra-aortic balloon counterpulsation
The intra-aortic balloon pump (IABP) consists of a balloon-tipped catheter, usually inserted
via the femoral artery to a point in the aorta just distal to the origin of the left subclavian artery.
Inflation of the balloon is timed to coincide with the dichrotic notch of the arterial waveform,
thus increasing pressure in the aorta during diastole and consequently improving coronary
perfusion. The balloon deflates just prior to systole, reducing afterload, left ventricular wall
tension and, as a result, myocardial oxygen demand.
IABPs are preferably inserted percutaneously. In high-risk cardiac surgical patients, it is
prudent to insert a femoral arterial line prior to CPB, either pre or post induction of anesthe-
sia, when the femoral pulses can be felt. This line can then be used to facilitate percutaneous
insertion of IABP if required. The percutaneous approach obviates the need for a surgical
“cutdown” and dissection to locate the femoral artery, and importantly avoids the need for
surgical removal when the IABP is no longer required.

Ventricular assist devices (VADs)
Mechanical pumps can be used to assist left, right or biventricular function. These devices
are inserted in parallel to one or both ventricles, reducing myocardial work and buying time
for the ventricle to recover. VADs should be inserted only when other reasonable options of
enhanced cardiac support in the weaning process have been explored.

Bypass: Principles and Practice, 3rd ed.
Suggested Further Reading Philadelphia: Lippincott Williams &
• Gillies M, Bellomo R, Doolan L, Buxton B. Wilkins; 2008: 614“31.
Inotropic drug therapy after adult cardiac
• Shanewise JS, Cheung AT, Aronson S, et al.
surgery: a systematic literature review.
ASE/SCA guidelines for performing a
Critical Care 2005; 9: 266“79.
comprehensive intraoperative multiplane
• Hogue CW, Palin CA, Arrowsmith JE. transesophageal echocardiography
Cardiopulmonary bypass management and examination: recommendations of the
neurological outcomes: an evidence-based American Society of Echocardiography
appraisal of current practices. Anesth Analg Council for Intraoperative
2006; 103: 21“37. Echocardiography and the Society of
Cardiovascular Anesthesiologists Task
• Royster RL, Thomas SJ, Davis RF.
Force for Certification in Perioperative
Termination of cardiopulmonary bypass. In
Transesophageal Echocardiography. Anesth
Gravlee GP, Davis RF, Stammers AH,
Analg 1999; 89: 870“84.
Ungerleider RM, eds. Cardiopulmonary




105
Mechanical circulatory support
Chapter
Kirsty Dempster and Steven Tsui


9
The successful introduction of cardiopulmonary bypass in 1953 for closure of an atrial septal
defect was an important milestone in the history of circulatory support. Whilst incremental
refinements to cardiopulmonary bypass were being made during the ensuing decade, devel-
opmental work had already begun with other forms of mechanical circulatory support (MCS).
In 1966, a patient who failed to wean from cardiopulmonary bypass due to postcardiotomy
shock was successfully bridged-to-recovery with a left ventricular assist device (LVAD). Two
years later, a patient with cardiogenic shock was salvaged with an intra-aortic balloon pump.
Research on the total artificial heart (TAH) also commenced in the late 1960s.
There are now a wide range of options available for circulatory support (see Table 9.1).
This chapter will focus on two of these options: the intra-aortic balloon pump and ventricu-
lar assist devices. The decision of whether to proceed to MCS depends on the aetiology of
the heart failure and on the likely long-term treatment strategy. Which method of MCS is
deployed depends on the acuteness of onset of heart failure, its potential reversibility, its
severity and the anticipated duration of support required.

Intra-aortic balloon counterpulsation
The intra-aortic balloon pump (IABP) is the most commonly used device for circulatory sup-
port (see Table 9.2). The balloon catheter has two channels: one for the passage of helium gas
used to inflate and deflate the balloon, the other for direct monitoring of intra-aortic blood
pressure. It is usually inserted in a retrograde fashion via the femoral artery, with a sheath-
less insertion technique, causing less obstruction to distal limb perfusion than if the IABP
catheter is inserted via a large-bore sheath in the artery. Occasionally, in surgical patients with
severe aorto-iliac disease, it is inserted antegrade via the ascending aorta. The IABP catheter
is positioned in the descending thoracic aorta, the balloon segment of the catheter lying distal
to the origin of the left subclavian artery.
The balloon is rapidly inflated at the end of ventricular systole, just as the aortic valve
closes, generating a surge in aortic pressure during ventricular diastole. Just before ventricu-
lar systole, the balloon is rapidly deflated, reducing the aortic pressure against which the left
ventricle has to eject. The timing of balloon inflation and deflation can be triggered auto-
matically by the patient™s ECG or arterial waveform. The combined effects on cardiovascular
physiology are listed in Table 9.3.


Management of the IABP patient
The frequency and degree of balloon augmentation can be controlled via the balloon pump
console. The inflation ratio refers to the number of balloon inflations to the number of QRS
complexes and can be set at 1:1, 1:2 or 1:3 (see Figure 9.1a“c). The degree of augmentation
106 Cardiopulmonary Bypass, ed. S. Ghosh, F. Falter and D. J. Cook. Published by Cambridge University Press.
© Cambridge University Press 2009.
Chapter 9: Mechanical circulatory support



Table 9.1. Types of mechanical circulatory support

Cardiopulmonary bypass (CPB)
Extracorporeal membrane oxygenation (ECMO)
Intra-aortic balloon pump (IABP)
Ventricular assist devices (VAD)
Total artificial hearts
Cardiac compression devices
Aortic compression devices


Table 9.2. Indications for IABP

Ischemic myocardium
• Unstable angina despite maximal medical therapy
• Ischemia-induced ventricular arrhythmia
• Elective support in high-risk percutaneous coronary interventions
Structural complications of acute myocardial infarction
• Ventricular septal defect
• Acute mitral valve regurgitation
Cardiogenic shock
• Post myocardial infarction
• Acute myocarditis
• Acute deterioration of chronic heart failure
• Post cardiotomy
• Acute donor organ failure



can range from 10% to 100%. During normal use, IABP support is initiated with a 1:1 inflation
ratio at 100% augmentation. The timing of the inflation/deflation triggers should be checked
regularly and adjusted when required to optimize the support provided. To reduce throm-
boembolic risks associated with an IABP, systemic anticoagulation with heparin infusion is
advised, aiming for an activated partial thromboplastin time ratio (APR) of 1.5 to 2.0. Distal
limb perfusion must be examined regularly and distal pulses checked either by palpation or
with a hand-held Doppler probe.
The effectiveness of IABP augmentation is diminished when there is excessive tachycardia
(>120 bpm) or when the cardiac rhythm becomes irregular, e.g., atrial fibrillation (see Figure
9.1e & f ). Therefore, inotropic support should be moderated to minimize the occurrence of
such rhythm disturbances. Invasive hemodynamic monitoring is indispensable and provides
the best assessment of the adequacy of circulatory support. A Swan-Ganz pulmonary artery
catheter can provide important information, including left ventricular preload (pulmonary
capillary wedge pressure), left ventricular afterload (systemic vascular resistance), right ven-
tricular afterload (pulmonary vascular resistance) and cardiac output as well as providing
information on the adequacy of systemic oxygen delivery (mixed venous oxygen saturation).
When cardiac function begins to recover, the inotrope dose should be reduced before IABP
support is weaned. If cardiac index is maintained above 2.2 l/minute/m2 with acceptable
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Table 9.3. Beneficial effects of IABP

Balloon deflation during ventricular systole
• Reduces left ventricular afterload
• Reduces peak LV wall stress and LV stroke work
• Decreases myocardial oxygen demand
• Reduces mitral valve regurgitation
• Increases LV ejection
Balloon inflation during ventricular diastole
• Increases coronary perfusion pressure
• Augments coronary blood flow
• Improves myocardial oxygen delivery
Overall effects
• Augments cardiac output
• Reduces pulmonary capillary wedge pressure
• Relieves pulmonary congestion




preload (pulmonary capillary wedge pressure <15 mmHg), attempts can be made to wean
the IABP. Firstly, the IABP augmentation can be reduced to 50% for 2“4 hours. The inflation
ratio is then progressively reduced from 1:1 to 1:2 for another 2“4 hours and then to1:3 before
the balloon catheter is removed. The IABP must be switched off and the catheter completely
deflated just prior to removal. Heparin should be discontinued at the start of IABP weaning so
that coagulation is normalized by the time the IABP catheter is removed.

Complications of IABP use
Major vascular complications can occur in up to 15% of patients treated with an IABP. Femo-
ral insertion of an IABP catheter may not be possible in 5% of patients, because of a tortuous
or diseased ilio-femoral system. During insertion, vascular injury can lead to dissection, rup-
ture and hemorrhage. Once in situ, distal limb ischemia can result from thromboembolism or
a combination of peripheral vasoconstriction and low cardiac output state. Malpositioning of
an IABP catheter may result in obstruction of visceral or renal arteries, making a visual check
on catheter position via chest radiography essential.
In the operating room, placement is usually facilitated with the use of transesophageal
echocardiography, which is also instrumental in assessing the potential risks of IABP place-
ment from atherosclerotic disease in the thoracic aorta.
Other complications can include infection, thrombocytopenia and rupture of the IABP
catheter. Helium is used as the driving gas for IABP inflation because of its high blood solu-
bility, so reducing the risks from gaseous emboli. If the IABP ruptures, blood is seen to track
down the gas channel of the balloon driveline. Whenever this is observed, the IABP must be
immediately stopped and the catheter removed.

Ventricular assist devices
Severe heart failure refractory to medical management and IABP support has an appalling
prognosis. Inadequate forward perfusion gives rise to end-organ dysfunction and metabolic
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Figure 9.1 Intra-aortic balloon console tracings. The screen displays ECG at the top, aortic pressure waveform in
the center and balloon inflation/deflation at the bottom. (a) Full IABP augmentation with inflation 1:1 and inflation
interval highlighted showing correct balloon inflation at the dicrotic notch of the arterial pressure trace. (b & c) Full
augmentation with inflation interval 1:2 and 1:3, respectively. (d) Balloon augmentation set at 50%. (e) IABP on full
support but showing diminished effectiveness due to tachycardia. (f) Auto R-wave deflate mode for a patient in AF.



acidosis, whilst excessive back-pressure results in pulmonary edema and systemic venous
congestion. Ventricular assist devices (VADs) can be used to augment perfusion and relieve
congestion, potentially reversing the damaging effects of severe heart failure.
VADs are mechanical blood pumps that can provide either left, right or biventricular support
(see Figure 9.2). A left ventricular assist device (LVAD) withdraws oxygenated blood from the left
atrium or left ventricle, and returns it to the aorta; a right ventricular assist device (RVAD) draws
venous blood from the right atrium or right ventricle, and returns it to the pulmonary artery. In
general, it is preferable to cannulate the ventricle for VAD inflow as this provides superior ven-
tricular decompression, avoids ventricular stasis and affords higher VAD flow rates.
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Figure 9.2 Thoratec Paracorporeal Ventricular Assist Device showing examples of cannulation for LVAD and
RVAD. (a) LVAD with cannulation of left atrium (LA) and aorta (Ao). (b) RVAD with cannulation of right atrium (RA)
and pulmonary artery (PA) and LVAD with cannulation of left ventricular apex (Apex) and aorta. (c) RVAD with
cannulation of right atrium and pulmonary artery and LVAD with cannulation of left atrial inflow (LAG) and aorta.


The output of an LVAD is dependent on adequate right ventricular function to deliver
sufficient blood flow across the lungs into the left heart chambers for the LVAD to pump.
Likewise, an RVAD can only provide benefit if the native left ventricle can generate enough
stroke work to cope with the pulmonary blood flow produced by the RVAD. If both native
ventricles are failing, two VADs are required in order to provide biventricular assistance to
support the circulation.
In its simplest form, emergency short-term VAD support can be provided by any blood
pump (e.g., a Biomedicus centrifugal pump) and a couple of vascular cannulae: one for inflow
from the heart to the VAD; the other for outflow return from the VAD to the aorta. In the
absence of specialist VAD equipment, such a setup can be lifesaving and maintain the circula-
tion for hours or days.
There is, however, a growing number of pump systems specifically intended for use as a
VAD. These systems consist of blood pumps that are less traumatic to the blood components,
and have cannulae that are designed to provide more secure attachment to the heart cham-
bers with superior flow characteristics. Temporary VAD systems are intended for short-term
circulatory support in the intensive care unit for days or weeks. Long-term VAD systems
are designed to provide circulatory support for months or years. Continual improvements
in long-term VADs are enabling patients to be discharged from hospital and treated as out-
patients, often with a relatively normal quality of life.
The fate of patients receiving a VAD depends on the underlying cause of the cardiac
dysfunction and its reversibility. In some cases of postcardiotomy shock and fulminant
myocarditis, cardiac function recovers after a period of circulatory support and the VAD can
be weaned and removed, a process known as “bridge to recovery.” Unfortunately, in the major-
ity of cases of chronic heart failure, e.g., ischemic or dilated cardiomyopathies, the myocardial
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dysfunction is unlikely to be reversible. Occasionally, a VAD is required for these patients,
who are usually already waiting for a heart transplant because of deteriorating cardiac status.
Here the VAD is used to buy time for the patient until a suitable donor heart can be found,
a process called “bridge to transplant” or BTT. For a selected few patients with advanced
heart failure who are not transplant candidates, VAD support can be offered as a permanent
implant, a process called “destination therapy” or DT.

Ventricular assist devices: decision making process
The key decisions of which patient to support with a VAD, when to insert a VAD, whether the
patient requires LVAD alone or BiVAD and which VAD system to use are often difficult ones
to make. They are influenced by a number of factors including patient comorbidities, trans-
plant waiting times, resource availability, institutional experience and device availability. In
general, patients who are considered for VAD support can be divided into the following four
categories (see Table 9.4).
• Group I “ This consists of transplant-eligible patients with precarious hemodynamics
who are managed on the intensive care unit. They are the most challenging group of
patients to make a decision on because a rush to implant a VAD too early may “deny”
them a more straightforward course of heart transplantation without mechanical
bridging, whereas waiting too long for a donor heart may result in end-organ failure
or, worse still, cardiac arrest and death. In these cases, it is important to monitor the
trends in hemodynamics as well as inotrope requirements. Adequacy of end-organ
function is best assessed by monitoring hourly urine output, arterial oxygenation,
prothrombin time and acid“base balance. In the United Kingdom, where the median
waiting time for an “urgent” donor heart is 2 or 3 weeks, most of these patients can be
transplanted without needing VAD support. In other countries, where the minimum
waiting time for an “urgent” heart runs into many months, most of these patients are
treated with a VAD. Ventricular tachy-arrhythmia is an ominous sign and should
prompt an earlier decision for VAD insertion. Since the “bridging” period to a
transplant can range from months to sometimes over a year, these patients should be
implanted with a long-term VAD so that they can be discharged home. Currently,
there are several wearable or portable VAD systems that allow patients independent
mobility during VAD support with reasonable quality of life. Patients in this category
have an 80“90% chance of being successfully bridged to a heart transplant if treated
with a VAD.



Table 9.4. Categories of patients considered for VAD insertion

Group Description
I Precarious Severe heart failure with borderline hemodynamics
requiring inotropic therapy +/’ IABP
II Decompensated Untransplantable due to acute end-organ failure or
chronically raised pulmonary vascular resistance
(>6 Wood units)
III Failure to wean from CPB Postcardiotomy shock or acute donor organ failure after
heart transplant
IV Salvage Cardiac arrest refractory to CPR

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• Group II “ This consists of patients who are transplant candidates except for one or
more serious, but potentially reversible, complications of advanced heart failure, e.g.,
acute end-organ failure or pulmonary hypertension. Unless such complication(s)
can be reversed, these patients are not transplantable and they will invariably die
from their heart failure. Acute end-organ failure secondary to a low cardiac output
state sometimes recovers when the systemic circulation is mechanically augmented;
elevated pulmonary vascular resistance due to left ventricular failure and pulmo-
nary venous congestion often decreases with mechanical unloading of the left
ventricle. This category of patients are sick and those who survive the surgery of
VAD implant often require weeks or months of VAD support to reverse their
end-organ failure before they are acceptable for a heart transplant. It is therefore
most appropriate to consider a long-term VAD system in these cases. Operative
risks are higher in this decompensated group and only 60“70% of them will survive
to a heart transplant.
• Group III “ This consists of patients who could not be weaned from cardiopulmonary
bypass despite maximal inotropic therapy and IABP support. This includes patients
with postcardiotomy shock and those with acute donor organ failure following heart
transplantation. In the absence of contraindications (see Table 9.5), a short-term VAD
may be considered to enable weaning from CPB. Alternatively, a veno-arterial ECMO
circuit may be used to support the circulation. Injured hearts that are likely to recover
tend to do so within 5“7 days. If weaning from MCS cannot be accomplished after this
period because of ongoing poor ventricular function, a decision has to be made
between device removal and death, or continued support and bridging to transplanta-
tion (or re-transplantation). Occasionally, it may be felt appropriate to switch over to a
long-term device to wait for a suitable donor heart. Overall survival rate for the
postcardiotomy group is poor at 30“40%.
• Group IV “ This consists of patients with catastrophic heart failure/cardiac arrest who
have been put onto CPB or ECMO for resuscitation under cardiopulmonary resuscita-
tion (CPR) conditions. These patients tend to be young, previously fit and would
normally be good candidates for heart transplantation. The main uncertainty that exists
concerns the patient™s neurological status following a period of cardiopulmonary
resuscitation. Again, a short-term VAD or veno-arterial ECMO may be used to support

Table 9.5. Contraindications to use of VADs postcardiotomy

Age >65 years
Uncontrollable bleeding
Intractable metabolic acidosis
Other comorbidities
• Pre-existing neurological impairment
• Severe cerebral vascular disease
• Severe peripheral vascular disease
• Advanced chronic pulmonary disease
• Chronic renal failure
• Chronic liver disease
• Recent malignancy

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the circulation until neurological assessment can be conducted. Severe neurological
injury usually becomes obvious within 48 hours of circulatory support, permitting
withdrawal of treatment. Otherwise, consideration may have to be given to bridging to
transplantation or switching to a longer term device.


Types of ventricular assist devices
Technical developments in mechanical circulatory support have progressed rapidly over the
last 10 years. There is now a large range of systems available for clinical use. These can be
classified into temporary systems and long-term systems. Within each group, they can be
subdivided into volume displacement devices (pulsatile devices) and continuous flow devices
(see Table 9.6). There has been much debate over pulsatile versus continuous flow pumps, but
recent studies have shown no differences in end-organ function and patient survival between
the two types of devices. A full description of all available devices is beyond the scope of this
book. A few selected examples of commonly available VADs that are in clinical use are briefly
described below.

Table 9.6. Classification and examples of VAD systems

A. Temporary devices:
• Volume displacement
· Abiomed BVS 5000 and AB5000
· Medos
• Continuous flow
· Impella
· CardiacAssist TandemHeart
· Levitronix CentriMag*
B. Longer term devices:
• Volume displacement
· Abiomed AB5000
· Berlin Excor
· Thoratec HeartMate XVE
· Novacor
· Thoratec PVAD
· Thoratec IVAD
• Continuous flow
· Micromed DeBakey
· Jarvik 2000 Flowmaker
· Thoratec HeartMate II
· Berlin Incor*
· Ventracor VentrAssist*
· Terumo Duraheart*
· HeartWare HVAD*
* The latest bearing-less designs.

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Levitronix CentriMag
The Levitronix CentriMag is a continuous flow extracorporeal system comprising a single-
use polycarbonate centrifugal pump, a motor and a primary drive console (see Figures 9.3
and 9.4). It is intended for short-term left, right or biventricular support of up to 30 days™
duration. Compared to other short-term devices, the Levitronix CentriMag is unique in that
it is designed to operate without mechanical bearings or seals, which are components known
to contribute to hemolysis and thrombus formation. The magnetically suspended impeller
achieves rotation with no friction or wear at speeds of 1500“5500 rpm, providing flow rates of
up to 9.9 l/minute in vitro. In vivo, flows of 4.0“5.0 l/minute are often observed.
The inflow and outflow cannulae can be rapidly inserted into the heart and great vessels
with or without cardiopulmonary bypass (see Figure 9.5). Other clinical equipment such as

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