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protection with plegic solutions, and total circulatory arrest that render this patient
population extremely susceptible to residual hemodynamic lability upon arrival in
the intensive care unit.
7.2.2.1 Low Cardiac Output
Afterload, preload, and myocardial contractility are the main determinants of heart
performance. Cardiac contraction cannot be considered independent from the vas-
cular system, and manipulation of both afterload and preload is necessary for opti-
mal cardiac function. Review of the Starling Curve is important in understanding
this relationship. Low cardiac output is the most critical complication after cardiac
surgery. It is defi ned as the need for inotropic infusion support (for longer than
30 min), IAPB, or both to achieve cardiac output >2.2 L/m
2
/min and preserve sys-
tolic blood pressure >90 mmHg despite afterload reduction, optimization of pre-
load, and correction of electrolytes and blood gases. Low cardiac output plays an
important role in morbidity and mortality after cardiac surgery.
Some causes of low cardiac output syndrome include incomplete myocardial
revascularization, insuffi cient myocardial protection during aortic cross clamp,
reperfusion injury, and systemic infl ammatory response. During aortic cross clamp,
myocardial perfusion is interrupted; a bloodless fi eld is provided at the expense of
potential myocardial ischemia. A cardioplegic solution is used to arrest the heart and
decrease the ischemic damage of myocardium during these intervals. Although
there is no consensus about type, time, temperature, route, and volume of cardiople-
gic solution, many studies had shown that inadequate myocardial preservation dur-
ing surgery leads to postoperative low cardiac output. Therefore, improved ways of
cardiac protection can minimize myocardial injury.
Studies have shown that there are multiple independent predictors of low cardiac
output after aortic valve and mitral valve replacement. These include:
• Preoperative renal disease
• Increasing age
• Female sex
• Redo surgery and small aortic valve
• Urgency of the operation and CPB time
The most important predictor of low cardiac output after CABG is preoperative
left ventricular dysfunction (EF < 20 %). Management of low cardiac output due to
left heart failure consists of increasing contractility, afterload reduction, and preload
limitation. For right heart failure, in addition to inotropic agents, adequate preload
status and reduction in pulmonary vascular resistance are recommended. In low
cardiac output states that do not respond to inotropic support and IABP, the use of a
ventricular assist device as a bridge to recovery or transplantation may be advised.
7.2.2.2 Diagnosis
The critical care team should accurately and effi ciently review the patient’s preop-
erative hemodynamic and intraoperative hemodynamic history as well as noting
signifi cant events which may have deviated from the usual and customary manage-
ment of a cardiothoracic surgical patient.
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Diagnosis should include assessment of systolic and diastolic blood pressure
trends as well as calculation of perfusion pressure, total peripheral resistance, and
possible cardiac output or cardiac index. Changes in the patient’s cardiac rhythm
and rate should also be conducted to determine if deviations from the intraoperative
status have occurred. Loss of circulating blood volume should also be determined
by assessing chest tube drainage or reductions in urinary output.
7.2.2.3 Management
The implementation of pressors, vasodilators, or inotropic agents may be necessary
based upon the specifi c hemodynamic disturbance. However, defi nitive therapy
should be aimed at determining the underlying etiology for the respective change
(i.e., hypovolemia causing hypotension). Persistent hypotension despite pressor
therapy may warrant further support such as administration of colloids or blood
products. Hypertension may denote inadequate pain relief or lack of adequate seda-
tion; therefore, opioids or sedatives may be warranted. Transesophageal echocar-
diography may be of assistance in delineating cardiac-specifi c pathology contributing
to hemodynamic compromise.
Implementation of inotropic support should be based upon more specifi c fi nd-
ings delineated by use of a pulmonary artery catheter or echocardiogram. Low car-
diac output states secondary to diminution of stroke volume can be augmented by
the use of fl uids or pharmacologic therapy (i.e., epinephrine, norepinephrine, dobu-
tamine, dopamine, or milrinone). The insertion of an intra-aortic balloon pump
should be reserved only for instances of refractory hemodynamic compromise unre-
sponsive to pharmacologic support (Mair and Hammerer-Lercher 2005 ; Noora
et al. 2005 ; Maganti et ak. 2010 ; Algarni et al. 2011 Hausenloy et al. 2012 ; Likosky
et al. 2012 ).
7.2.3 Arrhythmias
Numerous rhythm disturbances may manifest themselves in patients’ status post-
cardiac surgery. Electrophysiologic cardiac abnormalities may be secondary to
manual manipulation of the heart, arrest with plegic solutions, anatomic/mechanical
disruption of electrical pathways, and/or impaired cardiac perfusion resulting in
ischemia. A more detailed discussion about arrhythmias could be found in this book
in the related chapter.
7.2.3.1 Diagnosis
The diagnosis of rhythm disturbances is most accurately assessed with a minimal of
two-lead electrocardiographic monitoring; however, more occult arrhythmias may
necessitate 12-lead electrocardiographic evaluation. Arrhythmias may include but
are not limited to bradyarrhythmias, tachyarrhythmias, malignant tachyarrhyth-
mias, and multiple degrees of heart block.
The most common arrhythmia occurring in both the acute and later phases of
postoperative recovery is the appearance of atrial fi brillation. A recent study of the
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STS database revealed an annual incidence of 20 % with the mean occurrence on
postoperative day three, but the range was from 0 to 21 days after surgery. Predictors
of atrial fi brillation during hospitalization include age greater than 65, history of
intermittent atrial fi brillation, atrial pacing, and chronic obstructive pulmonary dis-
ease. Predictors after discharge were atrial fi brillation during hospitalization, valve
surgery, and pulmonary hypertension. Patients with atrial fi brillation had almost
twice the hospital mortality of patients without atrial fi brillation.
7.2.3.2 Management
Sinus rhythm is the rhythm of choice with respect to optimizing cardiac perfor-
mance and ventricular fi lling. Electrical cardioversion or pharmacologic interven-
tion with pacing may be necessary to establish and maintain normal sinus rhythm.
Bradycardia can be treated with external or internal pacing and/or the administra-
tion of anticholinergics or catecholamines. Atropine (10–40 mcg/kg) and glycopyr-
rolate (10–20 mcg/kg) are two useful anticholinergics, but they are usually not
effective in the postoperative setting. Catecholamines such as epinephrine, norepi-
nephrine, isoproteronol, and ephedrine may also be used to treat symptomatic bra-
dycardia. Sinus bradycardia with an adequate stroke volume may respond to
anticholinergics; however, bradycardic patients with depressed ventricular perfor-
mance should likely receive a more potent catecholamine such as epinephrine.
More serious bradycardias (e.g., ventricular escape or idioventricular rhythms) will
require more aggressive therapy.
Perioperative tachycardia responds well to electroversion and pharmacologic
therapy. Post-electroversion pacing can also help to control dysrhythmias. In the
absence of electrolyte disturbances, new onset atrial fl utter and atrial fi brillation are
receptive to synchronized cardioversion. Beta-blockers (e.g., metoprolol and pro-
pranolol), calcium channel blockers (e.g., verapamil and diltiazem), and digoxin
can also be used to help control the rate. Ventricular tachycardia can be treated with
magnesium, lidocaine, bretylium, procainamide, and direct-current cardioversion.
The treatment of ventricular fi brillation is immediate asynchronous cardioversion.
Often times after initial rhythm correction maneuvers, intravenous medications
such as lidocaine (1–3 mg/kg), procainamide (250–500 mg load then 15–60 mcg/
kg/min), bretylium (5–10 mg/kg), and amiodarone (1–5 mg/kg) may need to be
started to help suppress further rhythm disturbance, and infusions of these medica-
tions are often necessary. The onset of atrial fi brillation may be mitigated by the use
of beta-blockers, angiotensin-converting enzyme (ACE) inhibitor, supplemental
potassium, or nonsteroidal anti-infl ammatory drug (Mathew et al. 2004 ; Bradley
et al. 2005 ; Bagshaw et al. 2006 ).
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7.3 Vasoplegic Syndrome
Vasoplegia is one form of vasodilatory shock occurring in up to 10 % of patients
after cardiac surgery. It is defi ned as profound hypotension associated with low
systemic vascular resistance (SVR), reduced fi lling pressure, and normal or high
cardiac output; vasoplegia may contribute to death in the perioperative period.
The cause of reduced vascular tone is a matter of controversy, but it is postu-
lated that endothelial dysregulation during CPB leading to an infl ammatory
response may play an important role. Known risk factors for developing
vasoplegia include preoperative use of certain drugs (β-blockers, ACE inhibi-
tors, calcium channel blockers, and amiodarone), valve surgery, low pre-CPB
mean arterial pressure, length of CPB, administration of pre-CPB vasopressors,
core temperature on CPB, and the intraoperative use of aprotinin.
Vasoplegia does not usually respond to volume expansion. Norepinephrine,
phenylephrine, high-dose dopamine, and vasopressin can increase systemic vascu-
lar resistance and maintain perfusion pressure after CPB. Whenever there is resis-
tance to vasoconstrictor agents, methylene blue is recommended (2 mg/kg
intravenously through a period of 20 min); an infusion may be necessary for refrac-
tory vasoplegia (Levin et al. 2004 ; Egi et al. 2007 ; Levin et al. 2009 ; Skuza et al.
2009 ; Langlet et al. 2011 ).
7.4 Postoperative Cardiac Tamponade (POCT)
POCT is a specifi c type of circulatory failure due to compression of right heart (and
sometimes left heart) chambers by blood accumulation in pericardial sac after car-
diac surgery; it is seen up to 8 % of cardiac surgeries. This accumulation of fl uid
leads to increased pressure in the pericardial cavity and a decreased systemic venous
return. It is typically secondary to either surgical bleeding (i.e., suture lines, can-
nulation site, and branches of internal mammary artery) or CPB-related coagulation
abnormalities.
The diagnosis of cardiac tamponade is based on clinical presentation, central
venous pressure monitoring, chest X-ray, and echocardiography. It should be sus-
pected in any patients with clinical hemodynamic instability (elevated central
venous pressure, decreased systemic blood pressure and urine output) in association
with increased need for inotropic agents in the setting of signifi cant chest tube
drainage. Echocardiograph fi nding may demonstrate diastolic collapse of right
atrium (and right ventricle) and lack of IVC collapse during inspiration. Diastolic
collapse of left heart chambers may occur in the presence of discrete localized fl uid
accumulation.
Independent risk factors for POCT are type of surgery (aortic aneurysm, heart
transplant, valve surgery in comparison with CABG alone), renal failure, prolonged
CPB time, pulmonary thromboembolism, and elevated BSA.
Some studies have shown that posterior pericardiotomy during cardiac surgery
prevents blood accumulation in posterior of left ventricular wall. Resternotomy and
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mediastinal re-exploration, clot removal, and search for the probable site(s) of
bleeding are the only effi cient treatment after cardiac surgery. Late pericardial effu-
sion and delay tamponade may occur after cardiac surgery. Diagnosis may be diffi -
cult. In this entity due to pericardial adhesion, effusion is localized often in posterior
portion of the heart. Transesophageal echocardiography is able to show the pres-
ence, size, and site of localized effusion and guide the approach to drainage. POCT
is seen especially in valve surgery where oral chronic anticoagulant agents were
usually utilized preoperatively (Kuvin et al. 2002 ; Mackay et al. 2002 ; Seferovi et al.
2006 ; Ashikhmina et al. 2010 ; Canadyova et al. 2012 ).
7.5 CPR After Cardiac Surgery
The incidence of cardiac arrest after cardiac surgery is less than 3 %. The outcome
is better than other causes of cardiac arrest due to its reversible causes and typically
witnessed arrest. The most common causes of perioperative cardiac arrest are ven-
tricular fi brillation, major bleeding, and tamponade; all of them are usually treated
immediately as they are recognized promptly in the ICU. As multiple hemodynamic
indices (i.e., arterial pressure, pulse oximetry, ECG monitoring, and central venous
pressure line) are observed continuously in the ICU, this allows for rapid identifi ca-
tion of a critical event and rapid response. Because of better outcome and survival
in these patients (if they are treated promptly), ICU staff must be trained to manage
cardiac arrest.
Among the predisposing factors leading to cardiac arrest, myocardial infarction
has the worst prognosis. Hence it is rational that the guideline of CPR after cardiac
surgery is different from cardiac arrest in other settings. The last guideline protocol
for resuscitation after cardiac surgery was in 2009 and recommended for use in ICU
for all patients with sternotomy. Its brief summary follows:
(a) Diagnosis of cardiac arrest
• Because of full monitoring of intubated patients in ICU, observation of any
“fl at line” in monitors must be checked by central pulse palpation (femoral,
carotid) for 10 s.
• As a clinical point, ECG lead displacement will not imitate VF or asystole
pattern; it causes “fl at line” with preserved pressure lines.
(b) Defi brillation attempts
• A precordial thump may be recommended within 10 s of VT/VF onset, but
does not replace defi brillation. As VF is recognized, three consecutive
biphasic defi brillation shocks (between 150 and 360 J) are recommended to
restore cardiac output. It must be done consecutively without intervening
CPR. Its time sequence is emphasized before starting external cardiac
massage.
• If defi brillation fails, a bolus of intravenous amiodarone (300 mg) is recom-
mended. If amiodarone is not available, 1 mg/kg of lidocaine may be given.
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• If the patient had severe bradycardia or asystole and cannot be treated by
cardioversion, a single dose of 3 mg of atropine is recommended. Epicardial
pacing should be instituted at 90 beats/min.
• If adequate cardiac output is not achieved, CPR should be started. In pulse-
less electrical activity, the pacemaker must be set off to rule out VF.
(c) Timing of external cardiac massage
• With VF or VT, if defi brillation either was not accessible or was unsuccessful
(after three failed attempts), external cardiac massage must be started.
Techniques should apply pressure in the middle of sternum 100 beats/min and
press down 4–5 cm in depth. The effi cacy of cardiac massage can be assessed
by arterial trace on monitor; systolic impulse must be over 60 mmHg.
• In the presence of a balloon-expandable valve stent (i.e., TAVR), there is the
risk of valve damage during external cardiac massage.
(d) Airway control
• The second person to attend during a cardiac arrest is responsible for respira-
tory state. In intubated patient, oxygen on ventilator is raised to 100 % and
PEEP is omitted. If the patient is not intubated, 100 % oxygen with a bag/
valve mask should be initiated, 2 breaths for every 30 chest compressions.
Bilateral and equal lung expansion must be checked.
• Capnography confi rms position of endotracheal tube and quality of CPR.
A rough way to assess lung compliance is disconnection from the ventilator
and to continue with bag/valve ventilation; if there is adequate ventilation,
reconnect to the ventilator.
• Occlusion or malposition of endotracheal tube must be ruled out whenever
lung infl ation is not easy; in this condition the endotracheal tube should be
removed, and bag/valve ventilation with airway is continued.
• If tension pneumothorax is suspected, a large-bore angiocath catheter is
placed in second intercostal space at anterior-midclavicular line with imme-
diate insertion of a chest tube.
(e) Emergent sternotomy
• After failed defi brillation or pacemaker activation, there is proven benefi t for
resternotomy in the ICU. If the pressure generated by compression is not
enough, the cause of arrest may be massive bleeding, tamponade, or tension
pneumothorax, and emergent resternotomy should be accelerated. It is a
common belief among cardiac surgeons that if initial resuscitation is not suc-
cessful, resternotomy should be performed.
• Location of internal mammary artery and other grafts should be considered
before internal massage.
• Resternotomy could be considered in the most common causes of cardiac
arrest (i.e., tension pneumothorax, cardiac tamponade, hypothermia, hyper-/
hypokalemia).
• Internal cardiac massage can improve coronary and cerebral perfusion pres-
sure more than doubling of external massage. Return of spontaneous circula-
tion may be increased as well.
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(f) Administration of drugs
• During CPR all medication infusions must be stopped. Although concern
about severe hypertension and major bleeding after adrenaline use is justifi -
able, adrenaline is nonetheless recommended when reversible causes of car-
diac arrest are excluded; 1 mg of adrenaline should be administered for
asystole/pulseless electrical activity and after the second failed cardiover-
sion in VT/VF is used.
• All drugs should be administered via the central line when available.
(g) Cardiac arrest in the setting of IABP
• When pacemaker is activated, cardiac arrest may be identifi ed by changes in
pressure trace of CVP, pulse oximetry on monitor. Pressure trigger of IABP
is turned on during cardiac massage with maximum augmentation with 1:1
counter pulsation to increase cardiac massage effect. Internal trigger must be
set up whenever there is a period without cardiac massage.
(h) Mechanical circulatory support after cardiac arrest
• Mechanical circulatory support (CPB, extracorporeal membrane oxygen-
ation) may be effective when spontaneous circulation has not been started by
internal massage (Twomeya et al. 2008 ; Dunning et al. 2009 ; Ngaage and
Cowen 2009 ; Segesser 2009 ) .
7.6 Assist Devices
7.6.1 Intra-Aortic Balloon Pump (IABP)
The intra-aortic balloon pump (IABP) is the most commonly utilized mechanical
circulatory assist device in cardiac surgery and has been used since the late 1960s.
It is used after cardiac surgery, coronary angioplasty, myocardial infarction, and
other low output conditions, as the fi rst step in the treatment of cardiogenic shock.
IABP increases coronary artery perfusion pressure (and thus improves oxygen sup-
ply) during diastole by infl ation and decreases the metabolic demand of myocar-
dium (afterload reduction) in systole by defl ating. The drive mechanism is pneumatic
(helium). This volume replacement during cardiac cycles may increase cardiac out-
put by 20 %, but it cannot provide complete mechanical support.
IABP is used to facilitate CPB weaning intraoperatively when hemodynamic
stabilization is not adequate despite adequate preload and afterload and use of ino-
tropic agents. It provides a protective method against hemodynamic deterioration
during the early postoperative period in the ICU. It is believed that use of preopera-
tive IABP has better outcomes compared to later insertion in the intraoperative or
postoperative period. Studies had suggested that prophylactic IABP (instead of res-
cue therapy for cardiovascular instability) may decrease mortality and morbidity
and improve outcome in high-risk cardiac surgery patients who have at least two of
following conditions: unstable angina at the time of surgery, redo operations,
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congestive heart failure in spite of full-dose medical treatment, EF <30 %, and left
main artery stenosis >75 %.
There is controversy that levosimendan can be as effective as IABP in high-risk car-
diac surgery patients. Levosimendan is the only inotropic agent that increases the sensi-
tivity of myocardial contractile protein to calcium (others act by raising intracellular
calcium). It decreases myocardial demand and afterload and increases cardiac index.
The insertion technique for IABP is either percutaneously or insertion under
direct visualization by surgical exposure of femoral artery (retrograde approach).
When there is no access through femoral artery (due to aortic occlusion or previous
surgery), transthoracic arch, axillary, subclavian, and iliac arteries are suggested
(antegrade approach). The complication rate for IABP is low, and distal embolic
event (and limb ischemia) is the most common complication with frequent need for
vascular intervention (Fogarty arterial embolectomy catheter). Size of balloon pump
catheter, female sex, presence of peripheral arterial diseases, and duration of IABP
use are predictors of IABP-related complications. Limitations of IABP are small
body size, right ventricular failure, profound heart failure, and tachyarrhythmia
(Baskett et al. 2002 ; Christenson et al. 2007 ; Lorusso et al. 2010 ; Lomivorotov et al.
2011 ; Litton and Delaney 2012 ).
7.6.2 Ventricular Assist Device (VAD)
While the IABP is very helpful for hemodynamic instability, it only increases car-
diac output by 10–20 %, the only way to survive in severe decompensated condi-
tions is the use of ventricular assist device. Circulatory assist devices have been
designed and utilized to support the heart by providing forward fl ow, bridge to
recovery, heart transplant, or destination therapy; they have been shown to improve
quality of life and outcome. VADs may be used for short- and long-term support,
without removal of the native heart. VADs are commonly labeled as LVAD (left),
RVAD (right), BiVAD (biventricular), and TAH (total artifi cial heart). VADs may be
implantable intracardiac or externally (abdominal wall or intraperitoneal); a mid-
sternotomy and aid of CPB are necessary for insertion of inlet tube from the heart
to device and outlet tube from device to the aorta. The device power source may be
electrical or pneumatic; forward fl ow may be pulsatile or continuous. VADs require
long-term anticoagulation; however, patients have nearly unlimited mobility. Newer
generation of assist devices are smaller, require less complex surgical implantation,
have less blood-surface contact, and provide longer durability.
In cardiac surgery, VADs are used in reversible ventricular dysfunction. It was
shown that patients who underwent elective assist device had better outcomes than
when inserted in emergent or urgent situations. VADs are not recommended in
patients with terminal severe comorbidities (severe hepatic or pulmonary dysfunc-
tion, chronic dialysis), sepsis, and metastatic cancer. The most common complica-
tions are bleeding, infection, and thromboembolic events.
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7.6.3 Extracorporeal Membrane Oxygenation (ECMO)
Extracorporeal membrane oxygenation (ECMO) is used instead of conventional
cardiopulmonary bypass for reversible respiratory or cardiac failure, whenever
there is no response to usual therapies (optimized preload state, use of inotropic
agents, and ventilator support). The sole ECMO advantage is its application in
emergency situation (at the bedside and operating room) and as a satisfactory partial
cardiopulmonary support for both heart (left and right) and lung for severe, acute,
and reversible dysfunction.
In less than 1 % of patients after routine cardiac surgery operations, there is failure
to wean off CPB in spite of high-dose inotropic agents, pressors, and IABP.
Emergency surgery, redo surgeries, severe LV dysfunction, renal failure, and younger
age are predictors of postcardiotomy pump failure and need for ECMO support. The
cause of this low cardiac output syndrome may be the systemic infl ammatory
response during CPB, myocardial ischemia, and reperfusion injury. Other indica-
tions for implementing ECMO include cardiogenic shock with correctable pathol-
ogy, bridge to transplantation, myocarditis, postpartum cardiomyopathy, and cardiac
arrest. ECMO is not suggested in the presence of sepsis, multiorgan failure, and
severe neurologic defi cit and absolutely contraindicated in active bleeding and when-
ever recovery of cardiac function due to severe underlying disease is not expected.
The ECMO circuit is composed of a blood-pumping device (roller/centrifugal
pump), infl ow and outfl ow cannula, membrane oxygenator, hemofi lter, heparin-
coated circuit, and heat exchanger. There are two methods of cannula insertion:
peripheral and central (transthoracic). Peripheral arterial and venous cannulations
are performed percutaneously (by Seldinger technique), cut-down, or both. Central
cannulation can be accomplished by sternotomy or thoracotomy. Whenever there is
lung dysfunction with normal circulatory state, venovenous type of ECMO is
applied. Venoarterial ECMO is recommended in acute heart failure or needed to
both heart and lung. The adequacy of perfusion is determined by serum lactate level,
mixed venous oxygen saturation, and arterial base defi cit.
Activated clotting time must be kept around 180–200 s during use of ECMO in
order to prevent thrombosis and hemorrhagic events. Other described complications
and causes of inhospital death with ECMO include ischemia of lower limbs, organ
system dysfunction (lung, renal, and neurologic), sepsis, DIC, myocardial failure,
and oxygenation failure. Vascular complications with venovenous cannulation are
less than arterial cannulation. Open vascular exposure, use of antegrade catheter to
increase limb perfusion, rapid clinical diagnosis, and intervention to remove can-
nula and replace vascular access reduce ischemic events (Hirsch and Cooper 2003 ;
Doll et al. 2004 ; Wilhelm et al. 2005 ; Wagner et al. 2007 ; Luo et al. 2009 ; Formica
et al. 2010 ; Lund et al. 2010 ; Dalton 2011 ; Peura et al. 2012 ) .
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