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disappear fi rst in sufentanil, then alfentanil, and fi nally, fentanyl; this effect is
mainly due to larger sufentanil volume of distribution. Of course, as discussed
later, the effects of remifentanil would disappear very much sooner than all the
other three compounds; vide infra (Kapila et al. 1995 ; Bosilkovska et al. 2012 ;
Jeleazcov et al. 2012 ).
Alfentanil
Alfentanil is another opioid compound similar to fentanyl but 5–10 times less
potent than fentanyl. Its clinical effects are presented very shortly, 1 min after IV
administration, mainly due to its very high lipid solubility which could bypass the
BBB very fast; its lipid solubility is even more than fentanyl. So, alfentanil phar-
macokinetics (like fentanyl and sufentanil) is not very much affected in patients
with renal disease; however, its effects are signifi cantly prolonged in patients with
hepatic disease due to impaired hepatic metabolism and the resulting drug accumu-
lation. As mentioned in the previous paragraph, its CSHL is shorter than fentanyl
and longer than sufentanil (Kapila et al. 1995 ; Bosilkovska et al. 2012 ; Jeleazcov
et al. 2012 ).
Remifentanil
Remifentanil is the newest version of synthetic opioids, being a potent mu agonist,
having an analgesic potency “equal to fentanyl and 20–30 times more potent than
alfentanil.” However, remifentanil has a very short start time lag (1 min); more
importantly, it has the shortest possible time (among all the opioids) for its effects
to be offset after discontinuation of drug infusion. The following are among the
most important pharmacologic and clinical features of remifentanil (Kapila et al.
1995 ; Hachenberg 2000 ; Servin 2003 ; Lotsch 2005 ; Murphy 2005 ; Scott and Perry
2005 ; Lahtinen et al. 2008 ; Servin and Billard 2008 ; Staahl et al. 2009 ; Olofsen
et al. 2010a , b ; Ing Lorenzini et al. 2012 ):
• Time interval from start of drug administration until presentation of its clinical
effects is about 1 min (i.e., very fast onset).
• Its CSHL being as short as 3–5 min irrespective of the duration of IV infusion
(the shortest CSHL among all the opioid compounds).
• The drug must be used as a continuous infusion as long as the patient has pain.
• The opioid effects of the drug, including respiratory depression, are offset in just
3–5 min after discontinuation of infusion irrespective of the duration of the
infusion.
• Acute postoperative pain management in patients under anesthesia using remi-
fentanil as the main opioid mandates considering an appropriate agent as soon as
the remifentanil infusion is set off, or remifentanil infusion with its analgesic
dose (and not the anesthetic dose) should be continued postoperatively.
• The main mechanism of remifentanil metabolism is rapid hydrolysis by nonspe-
cifi c esterase found in both tissue and plasma, which takes a very short time for
drug disappearance and leaves inactive drug metabolites.
• The drug metabolism mandates infusion of the drug as the main effective mecha-
nism of action; its bolus administration should be done very cautiously since
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bolus dose has the possibility for severe bradycardia, hypotension, decreased
cardiac output, and cardiac arrest.
• Its analgesic dose is 0.05–1 μg/kg/min based on ideal body mass.
• Only IV route is recommended; never use intrathecal or epidural routes for its
administration due to glycine added to drug combination.
• Remifentanil is the only opioid with no special consideration in patients with
either renal or hepatic regarding its metabolism.
11.8.2 Alpha 2 Agonists
α2 adrenergic agonists can cause analgesia, sedation, and sympatholysis. These
agents are primarily known in practice as clonidine (natural) and its synthetic ana-
log, dexmedetomidine, which is a pure α2 adrenergic agonist and has a half-life of
2–3 h. They could be administered orally, intrathecally, or through intravenous
administration. The mechanism of action in these agents is creation of sedation
through stimulation of α2-receptors in the locus ceruleus and creation of analgesia
through stimulation of α2-receptors within the locus ceruleus and the spinal cord;
also, these agents could enhance the analgesic effects of the opioids via an unknown
mechanism of action. Their clinical effects could be classifi ed after systemic admin-
istration (antinociception and sedation) and intrathecal administration (only antino-
ciception). There are reports that have mentioned tolerance to these agents after
their prolonged administration. Their perioperative effects include increased stabil-
ity of the hemodynamic parameters accompanied with decreased perioperative
myocardial ischemia; also, decreased need for analgesic agents is another potential
benefi t of these agents while these agents could decrease postoperative opioid con-
sumption, pain intensity, and nausea, accompanied with decreased use of analge-
sics, beta-blockers, antiemetics, epinephrine, and diuretics when used as sedative
for post-CABG patients. Also, they might have some protective effects in a number
of organs. However, overdose of these agents could induce excessive postoperative
sedation accompanied with postoperative hemodynamic instability, bradycardia,
and/or hypotension with bradycardia, at times mandating pharmacologic treatment
(Hogue et al. 2002 ; Herr et al. 2003 ; Buvanendran and Kroin 2009 ; Blaudszun et al.
2012 ; Lin et al. 2012 ).
11.8.3 Nonsteroidal Anti-inflammatory Drugs (NSAIDs)
Having analgesic and anti-infl ammatory properties, a number of agents are catego-
rized in this class of analgesics. Their main mechanism of action is blockade of
cyclooxygenase (COX) enzyme leading to prostaglandin synthesis inhibition
described by Vane in 1971 for the fi rst time. Their analgesic mechanism is theoreti-
cally classifi ed as two main groups: traditional NSAIDs inhibiting COX in a nonse-
lective manner and relatively newer class of NSAIDs which inhibit COX-2 in a
selective manner. Selective COX-2 inhibitors were produced in order to decrease
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the unwanted effects of nonselective inhibition of COX-1 by traditional NSAIDs,
especially regarding the GI mucosa; however, their merit was not completely ful-
fi lled because of the deep concern of potential unwanted cardiac effects of COX-2
inhibitors. NSAIDs are used frequently in the perioperative period; however, they
are used usually in combination with other analgesic methods (mainly in combina-
tion with opioids, local anesthetics, or regional techniques) as a multimodal analge-
sic technique. NSAIDs are clinically effective in suppression of acute postoperative
pain; in decreasing the need for postoperative opioid use, an effect named as opioid-
sparing effect; and also, in improving the clinical outcome. If contraindications of
NSAIDs are considered logically, accompanied with close observation of their
potential side effects, these agents could be used cautiously and safely. Potential
contraindications of NSAIDs are elderly people, heart failure, hypovolemic states,
cirrhotic patients, renal failure, history of active GI tract disease and peptic ulcer
disease, active bleeding diathesis, and pregnant patients (Griffi n 1998 ; Tenenbaum
1999 ; Visser et al. 2002 ; Aldington et al. 2005 ; Brown et al. 2006 ; Langford and
Mehta 2006 ; Munir et al. 2007 ; Rainsford 2007 ; Dajani and Islam 2008 ; McCormack
2011 ; Moore et al. 2011 ; Barletta 2012 ; Derry and Moore 2012 ; Khan and Fraser
2012 ).
The most important adverse effects of NSAIDs are as follows:
1. Gastrointestinal complications which could lead to serious and life-threatening
hemorrhage, especially in postoperative period of cardiac surgery due to con-
comitant administration of anticoagulants.
2. Increased risk of bleeding which could be a potential complication in patients
receiving neuraxial block for postoperative pain suppression.
3. Acute renal ischemia, especially if administered concomitantly with diuretics,
angiotensin converting enzyme inhibitors (“ACE inhibitors”), and/or angioten-
sin receptor antagonists “ARA”; this drug combination is known as the “triple
whammy” (Loboz and Shenfi eld 2005 ) .
NSAIDs as adjuvant analgesics could reduce the dose of opioids needed for
acute pain suppression in postoperative period; the concomitant administration of
NSAIDs with opioids helps us to administer them, while this method of NSAID use
does not create clinically important renal impairments, though they might be able to
decrease renal function during the early postoperative period in a transient and
insignifi cant mode; meanwhile, these agents do not boost the risk of postoperative
renal failure in cardiac surgery patients would they be prescribed within a logical
dose range and avoiding their contraindications (Bainbridge et al. 2006a ; Ong et al.
2007 ; Buvanendran and Kroin 2009 ; Frampton and Quinlan 2009 ; Acharya and
Dunning 2010 ; Barletta 2012 ).
11.8.3.1 Paracetamol
Paracetamol ( N -acetyl- p -aminophenol) is one of the most common analgesics used
worldwide, mainly acting through central blockade of acute pain pathways and cre-
ating mild to moderate analgesia and mild anti-infl ammatory effects. Its mechanism
is not fully elucidated yet; however, some clinicians consider paracetamol as one of
NSAIDs, though it does not have the same mechanism as classic drugs of this
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category. Its main toxicity could be after large doses to create hepatotoxicity, mani-
fested much earlier in alcoholics. Its analgesic properties are not so much consider-
able, especially in cardiac surgery patients and the drug is recommended just as part
of a multimodal analgesic regimen (Lahtinen et al. 2002 ; Fayaz et al. 2004 ;
Pettersson et al. 2005 ; McDaid et al. 2010 ; Maund et al. 2011 ; Tzortzopoulou et al.
2011 ).
11.8.4 Other Pharmaceutical Agents
Among the other pharmaceuticals used for acute pain suppression in cardiac sur-
gery patients, a number of other agents could be mentioned, including the
following:
11.8.4.1 Ketamine
This is an intravenous anesthetic, mainly acting through “N-methyl-D-aspartate
receptor” blockade; this drug could suppress acute pain effectively by a mechanism
completely different from opioids: it acts mainly through dissociative anesthesia,
“i.e., a combination of analgesia, hallucination, catalepsy, and some degrees of
amnesia”; so ketamine does not cause respiratory depression as much as opioids and
also does not perturb the hemodynamic status as much. However, due to unwanted
clinical experience of the patients (known as emergence reactions), it is strongly
recommended that ketamine should not be used solely unless preceded by an amnes-
tic agent (like one of the benzodiazepine family); otherwise, the patients would have
a very bad experience from the effects of the drug; however, a number of studies
have demonstrated fewer unwanted effects of ketamine when administered as the
S(+)-ketamine isomer. Currently, smaller doses of the drug are used as a part of a
multimodal analgesic regimen, especially for thoracic incisions, in such a way that
the needed amount of other analgesic drugs, especially opioids, is decreased, pos-
sibly improving the respiratory function. Ketamine could be used through many
different routes including intravenous or intravenous patient- controlled analgesia
(IV or IV-PCA). Some studies have claimed an anti- infl ammatory effect for ket-
amine in patients undergoing CPB, possibly through its mechanism of action:
NMDA antagonism (Lahtinen et al. 2004 ; Bell et al. 2006 ; Michelet et al. 2007 ;
Buvanendran and Kroin 2009 ; Suzuki 2009 ; Carstensen and Moller 2010 ; Mathews
et al. 2012 ).
11.8.4.2 Magnesium sulfate (MgSO
4
)
This ionic compound has gained frequent attention during recent years; its analgesic
mechanism is mainly through calcium channel antagonism and NMDA antagonism;
however, bolus doses of the drug could lead to asystole and accumulation of the
drug in the blood, “i.e., overdose” could lead to severe afterload reduction and,
hence, hypotension. Anti-infl ammatory effects of magnesium sulfate in patients
undergoing CPB have been observed in a number of studies (Ferasatkish et al. 2008 ;
Buvanendran and Kroin 2009 ; James 2009 ).
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11.8.4.3 Gabapentin or Pregabalin
This is mainly an anticonvulsant agent belonging to a class of drugs known as “alpha-
2-delta receptor modulators,” also used for management of chronic pain; its mecha-
nism of action is inhibition of glutamate release through NMDA antagonism.
Gabapentin has been used for treatment of acute pain as an adjuvant in the multi-
modal analgesia regimen (Ucak et al. 2011 ). Pregabalin is also an anticonvulsant
agent inhibiting the voltage-dependent calcium channel in CNS leading to inhibition
of release of a number of agents including glutamate. Its use as an analgesic for acute
pain suppression is off-label and as one of the agents in multimodal analgesia regi-
men (Buvanendran and Kroin 2009 ; Dauri et al. 2009 ; Graterol and Linter 2012 ).
11.8.5 Multimodal Analgesia
Multimodal or “balanced” analgesia is a method of analgesia which considers the
multistep nature of pain. In acute pain management, this method involves adminis-
tration of analgesics throughout the perioperative period; so pain management is
performed through administration of more than one single drug (opioids plus nono-
pioids), or even we can add non-pharmacologic analgesia methods to our list of
pharmacologic analgesics. Adjuvant analgesics (i.e., drugs which their primary
effect is not necessarily analgesia) and non-pharmacologic analgesia methods are
mainly added to our battery of opioid compounds and the wide range of opioid
administration. The main goals of multimodal analgesia are (Kehlet and Dahl 1993 ;
White 2008 ; Buvanendran and Kroin 2009 ; Gandhi et al. 2011 ):
• Create additive analgesia from administration of different classes of analgesic
methods.
• Decrease the dose of each analgesic modality.
• Experience less unwanted side effects of each drug or non-drug method.
• Counteract pain at different levels, i.e., at the level of CNS, spinal cord, periph-
eral nerves, wound site, etc.
• Decrease time duration of recovery from surgery.
11.8.6 Patient-Controlled Analgesia
During the last decades, patient-controlled analgesia (PCA) has been proposed to
replace the conventional method of analgesia prescription, in order to increase the
effi cacy of analgesic methods. Among its benefi ts, increased patient autonomy,
decreased time from pain sensation until receiving analgesics, more matching of
analgesics with patient demands, and decreased frequency of some complications
of opioids like nausea and vomiting have been mentioned; however, the effi cacy of
the method is not yet proved. Compared with intramuscular analgesics, PCA is
more effective; however, compared with nurse-administered intravenous (IV) anal-
gesia or epidural PCA, it is not yet determined which method is more effective.
Anyway, in order to have a successful PCA, some studies suggest (Dolin et al. 2002 ;
Bainbridge et al. 2006b ; Hudcova et al. 2006 ; Mota et al. 2010 ) the following:
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• Using a baseline analgesic infusion added by PCA which could prevent unwanted
effects of delayed analgesia administration with concomitant effective
analgesia.
• Baseline opioids added to other analgesics could increase the effi cacy of pain
management.
• Respiratory depression should always be considered as a potential risk.
• Usually, a baseline appropriate PCA dose accompanied with lockout interval
should be adjusted for each patient.
• If there is no suffi cient patient cooperation, the method would not work effec-
tively, and so its use should be discouraged.
11.9 Regional Anesthetic Techniques for Acute
Pain Suppression in Cardiac Surgeries
There are a number of regional anesthetic techniques used for acute pain suppression
in cardiac surgery patients, each having their benefi ts and drawbacks. These tech-
niques include the following; however, they are not limited just to the
following list:
• Infi ltration of local anesthetic in wound
• Intercostal nerve block
• Intrapleural infi ltration of local anesthetics
• Neuraxial analgesia (paravertebral, intrathecal, thoracic epidural)
11.9.1 Infiltration of Local Anesthetics in Wound
This is an effective method in cardiac surgery patients especially when used as an
adjunct to other analgesic methods for controlling acute postoperative pain and
administered as parasternal approach or, possibly, directly into the surgical wound;
we could control sternotomy-related acute pain and also pain related to chest tubes
and thoracic pain. This method has two characteristics in order to be effective for
pain control:
• It is better to use this technique as “post-incision infi ltration method” of local
anesthetic; however, pre-incision local anesthetic infi ltration is “equivocal” since
acute postoperative pain in cardiac surgery patients is originated mainly from
sternotomy.
• It should be used primarily in patients after sternotomy.
Infusion of local anesthetic directly into the surgical wound is another possible
method, with tissue necrosis being the most common potential complication; how-
ever, cellulitis, infection, and tissue necrosis of the wound are very rare after cardiac
surgery. In cardiac surgery patients, it is possible that the use of bilateral catheters
for continuous infusion of local anesthetics could be even more effective, when
used as a part of multimodal analgesia technique (Dowling et al. 2003 ; White et al.
2003 ; Chaney 2005b ; McDonald et al. 2005 ; Kocabas et al. 2008 ; Buvanendran and
Kroin 2009 ; Eljezi et al. 2012 ).
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11.9.2 Intercostals Nerve Block
This is a simple and effi cient method for administration of local anesthetic agents
into the intercostals neurovascular bundle, which could be as an effective adjuvant
analgesic method for acute postoperative pain suppression, causing pain temporal
blockade; however, it would last between 6 and 12 h unless an indwelling catheter
is placed adjacent to the intercostal nerves or repeated injections are needed. The
block is better to be performed under direct vision, i.e., before chest closure by the
surgeon or after the operation by injecting the local anesthetics into intercostal
nerves through the subcostal approach for each of the nerves. However, prophylac-
tic administration (i.e., before surgical incision) is equivocal. Ropivacaine (0.5–
0.75 %) or bupivacaine (0.25–0.5 %) is usually used for this purpose (Barr et al.
2007 ; Chaudhary et al. 2012 ).
11.9.3 Intrapleural Infiltration of Local Anesthetics
This method involves administration of local anesthetics between the visceral and
parietal pleura. The main origin of pain is parietal pleura; however, the proposed
mechanism of analgesia in this method is diffusion of local anesthetics in the poten-
tial space between the two pleural layers leading to diffusion of a very thin layer of
local anesthetics distributed between the two pleura layers and, fi nally, blocking
pain, though some studies are controversial regarding its clinical outcome. Local
anesthetics may be administered as a single shot or continuous infusion through a
catheter. The method has a number of limitations:
• Intact anatomy and physiology of the pleural layers.
• If the patient has chest tubes, it may lead to leakage of local anesthetics into the
chest bottle.
• The lung is not damaged (e.g., after lung surgery).
• There is the possibility for systemic absorption of local anesthetics (Chaney
2005b ; May and Bartram 2007 ; Ogus et al. 2007 ; Mansouri et al. 2011 ; Esme
et al. 2012 ) .
11.9.4 Neuraxial Blocks (Paravertebral, Intrathecal,
Thoracic Epidural)
11.9.4.1 Thoracic Paravertebral Block
Thoracic paravertebral block is considered as one of the neuraxial analgesia tech-
niques by some authors; being considered an old technique, it was reappraised just in
the last two to three decades used for local anesthetic blockade through the paraver-
tebral spaces, so to some clinicians it is not as much familiar as intrathecal and epi-
dural techniques. Paravertebral spaces are located bilaterally, in each side; they are
anatomically located lateral to the spine, where the nerve endings pass through them
to go from spine to end in their related nerve fi bers (Fig. 11.1 ). Thoracic epidural
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analgesia usually considered as the gold standard of care for acute postoperative pain
management, namely, in some procedures like thoracic and cardiac surgeries, espe-
cially regarding cardiovascular and pulmonary outcomes; however, thoracic paraver-
tebral block could be a good potential alternative when performed appropriately. The
interested reader is referred to study the related referenced for the classic approach of
Eason and Wyatt in performing thoracic paravertebral block; however, a summary of
the technique is described and includes a step-by-step process:
• Placing the patient in sitting position with the spine being curved as a “C” letter
or in lateral decubitus position, i.e., “fetal position”
• Using strict aseptic technique
• Finding and localizing the 6th cervical vertebra (C6)
• Localization of the spinous process at the level of 4th thoracic vertebra (T4)
• Going 3–6 cm laterally in horizontal direction
• Creating a local wheal by local anesthetics in awake patients
• Inserting the needle in a perpendicular direction
• Reaching the transverse process (Fig. 11.1 )
• Walking downward and lateral until a sense of “loss of resistance” is reached
• Injection of local anesthetic slowly
The main benefi ts of thoracic paravertebral block compared with thoracic epi-
dural could be considered as the following:
• Being less invasive
• Very lower risk for epidural hematoma formation
• Less hemodynamic derangement (albeit some degrees of sympathetic block
exist)
• Fewer contraindications
Fig. 11.1 A schematic
representation of thoracic
paravertebral block,
demonstrating the spine body
and other parts of the spine,
spinal cord, and its nerve
roots and the location where
paravertebral needle is
introduced ( on right )
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• Easier technique
• Lower incidence of complications (especially neurologic complications)
• Very few reports of postoperative complications like nausea, vomiting, and uri-
nary retention
• Very rare reports of systemic toxicity due to local anesthetics, though very high
doses are used in this technique
Some clinicians believe that bilateral thoracic paravertebral block is not as effec-
tive as thoracic epidural analgesia in suppressing acute pain-induced stress response,
especially in major procedures like cardiac surgery, while there are others who
believe exactly vice versa and consider thoracic paravertebral block as effective as
and even at times more effective than thoracic epidural analgesia improving clinical
outcomes with reduced rate of complications (Eason and Wyatt 1979 ; Davies et al.
2006 ; Daly and Myles 2009 ; Scarci et al. 2010 ; Thavaneswaran et al. 2010 ;
Richardson et al. 2011 ; Rawal 2012 ).
11.9.4.2 Spinal (Intrathecal) Analgesia
Postoperative analgesia through intrathecal (IT) administration of drugs is a very
popular method among clinicians for noncardiac surgeries of the abdominal and
pelvic area and/or lower extremities used for more than 100 years. However, in
cardiac surgeries, the idea of IT analgesia was fi rst described in 1980 which included
IT morphine administration (Mathews and Abrams 1980 ). Later, IT administration
of local anesthetics was also used which was performed through lumbar interspaces
accompanied with downward positioning of the patient (usually after induction of
general anesthesia) to deliberately create a high level of spinal block. Theoretically,
this method appeared effective, since spinal receptors of pain are located in substan-
tia gelatinosa of Rolando, posterior horn of the spinal cord (Wu et al. 1999 ; Furue
et al. 2004 ; Fujita and Kumamoto 2006 ); hence, the drug could attach the receptors
with much easier access and higher effi cacy than the intravenous route of drug
administration of analgesics. Potential benefi ts of this method would be possibly the
following:
• Improved postoperative analgesia with better quality of pain control
• Fewer postoperative respiratory problems
• Decreased level of postoperative stress response
• Improved clinical outcome
The fi rst studies favored IT morphine usage for cardiac surgery, and even during
the recent years, some studies approved it. These studies have usually administered
a wide range of IT opioid “from 0.3 to 10 mg IT morphine as single shot” adminis-
tered just before induction of general anesthesia, just after induction of anesthesia,
or, even, during the early postoperative period; however, further studies have dem-
onstrated that IT opioid for cardiac surgery could not suppress the level of stress
response. Also, improved postoperative analgesia and decreased respiratory prob-
lems are gained at the expense of unwanted opioid effects in the postoperative
period including pruritus, respiratory depression (early or delayed), urinary reten-
tion, nausea and vomiting, and delayed extubation. To the above should be added
the fact that shorter-acting opioids are possibly less effective during the
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postoperative period, shifting the choice for IT opioids to opioid compounds like
morphine with a longer time profi le in order to have adequate postoperative analge-
sia which at the same time would result in increased chance for postoperative opioid
complications, especially delayed postoperative respiratory depression (which is
usually due to delayed or cephalad migration of water-soluble opioids like mor-
phine) and delayed extubation; also, we should add to the above items that the
unwanted respiratory depression and delayed extubation are aggravated by con-
comitant use of other sedatives and anesthetics; besides, some other factors like
underlying age could not be neglected; elderly people are at increased risk for
unwanted postoperative respiratory depression of IT opioids (Stoelting 1989 ;
Chaney et al. 1997 , 1999 ; Boulanger et al. 2002 ; Liu et al. 2004 ; Jacobsohn et al.
2005 ; Parlow et al. 2005 ; Chaney 2006 ; Meylan et al. 2009 ; Sultan et al. 2011 ).
On the other hand, IT administration of local anesthetics in a way to create high
spinal levels of block covering the spinal thoracic nerve roots could create a suffi -
cient sensory block to decrease the level of stress response; however, simultaneous
widespread sympathetic block associated with this method leads to repeated epi-
sodes of hypotension and hemodynamic instability mandating administration of
vasopressors and inotropes. Finally, most studies have claimed that benefi ts of IT
local anesthetics could not clearly outweigh its risks. Besides, the effects of IT local
anesthetics usually last shorter duration and often disappear or vanish during the
early postoperative hours.
Finally, though the risk of neurologic complications (including epidural hema-
toma) is much lower in spinal technique compared to thoracic epidural technique, it
is not negligible and could be as high as 1:1,500 up to 1:220,000. Detailed discus-
sion about prevention and management of this complication is presented just in the
next pages, and the reader is addressed to refer there (Horlocker et al. 2010 ).
In summary, creating analgesia through administration of IT opioids or IT local
anesthetics in cardiac surgery patients could not improve the clinical outcome
sharply and is not usually considered as a main analgesic method in such patients.
11.9.4.3 Thoracic Epidural Analgesia
Thoracic epidural analgesia (TEA) is considered by many as the gold standard of
care for acute postoperative pain management in adult cardiac surgery mainly for
nearly two decades, because of the following features:
• Adequate and qualitative analgesia (both intraoperative and postoperative).
• Effi cient suppression of stress response (induced by CPB and the surgery).
• Thoracic sympathectomy which is relatively selective in TEA and does not
involve total sympathetic block as seen in total spinal anesthesia.
• Improved myocardial blood fl ow (mainly due to thoracic sympathetic block
which covers cardiac sympathetic nerves, T1–T5) is associated with increased
diameter of the coronary arteries (especially the stenotic epicardial coronary
arteries).
• Improved left ventricular function due to the previous item.
• Decreased level of myocardial ischemia mainly due to cardiac sympathetic block
(T1–T5).
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