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18 Incidence and Management of Postoperative Low Cardiac Output Syndrome…
18.2 Low Cardiac Output Syndrome: Denition
andRecognition
Low cardiac output syndrome refers to the clinically signicant reduction in cardiac
output that may occur following either pericardiostomy for massive pericardial
effusion or pericardiectomy for chronic constrictive pericarditis. When occurred,
the consequences of low cardiac output syndrome are severe and life threatening. In
the absence of any stringent diagnostic criteria, an accepted constellation of haemodynamic and physiologic changes alert the cardiac intensivist to its presence [11–
19, 21, 37, 38, 61, 62, 71–73, 85, 102–115, 121, 133]
Low cardiac output syndrome is diagnosed if inotropic support of dopamine at
4-10 μg/[kg·min], dobutamine at 5–10 μg/[kg·min], epinephrine at 0.01–0.1 μg/
[kg·min], milrinone (50μg/kg intravenous bolus followed by 0.375–0.75μg.kg−1.
min−1), is required, either alone or in combination during operation or in intensive
care unit, to maintain stable haemodynamics in the absence of residual mechanical
constriction to cardiac chambers and intracardiac pathologies such as signicant
valvular lesions, after correction of electrolytes or blood gas abnormalities and,
after adjustment of preload to its optimal value. Despite inotropic support,need for
intra-aortic balloon counterpulsation therapy is also diagnostic of low-output syndrome. Patients who received only dopamine in a dose less than 4μg/kg/min to
increase renal perfusion were not considered to have low output syndrome [11–19,
21, 37, 38, 61, 62, 71–73, 85, 102–115, 121, 133].
A combination of relevant clinical, laboratory and bedside echocardiographic
criteria is used to diagnose low cardiac output syndrome. The criteria used for diagnosis include: cold extremities, reduced systolic pressure, absent pedal pulses,
impaired renal function and oliguria (<1.0 mL.kg−1.h−1), metabolic acidosis,
increased serum lactate levels ≥2.0mmol/L, ≥2h), low mixed venous oxygen satu-
ration (≤50%), and blunt sensorium [11–19, 21, 37, 38, 61, 62, 71–73, 85, 102–115,
121, 133].
18.2.1 Monitoring andDiagnostics
The key to mitigating low cardiac output syndrome in the postoperative period is
early recognition and timely intervention. The trend in change of the physiologic,
haemodynamic, and serologic variables are more valuable than any single-point
measurement. Serial non-invasive, semi-invasive and invasive monitoring strategies
are used routinely after cardiac surgery. It is important to understand that indirect
estimations of cardiac function, cardiac output and tissue oxygenation, based on
interpretation of clinical and haemodynamic parameters such as central venous
pressure, heart rate and blood pressure, are often discordant from measured values
[11–19, 21, 37, 38, 61, 62, 71–73, 85, 102–115, 121, 133]. Therefore the use of
adjunctive monitoring modalities is indispensable in making a timely and accurate
assessment of cardiac output and adequacy of tissue oxygenation [24]
18.2 Low Cardiac Output Syndrome: Denition andRecognition
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Assessment of cardiac performance is important in the management of patients
undergoing pericardiectomy for constrictive pericarditis [11–19, 21, 32, 33, 37, 38,
57–59, 61, 62, 71–73, 85, 102, 103, 121, 133]. Doppler myocardial imaging
enhances the diagnostic performance available from Doppler blood-ow indices.
However, TDI-derived mitral and tricuspid annular velocities are proven to be poor
predictors of operative outcome following pericardiectomy [11–18, 44–46, 63, 64].
Surgical manipulation of heart during pericardiectomy make thermodilution cal-
culation, pulmonary artery pressure monitoring, and transesophageal echocardiography unreliable as monitors on the operation table. However, Swan-Ganz catheter
helps in postoperative haemodynamic monitoring [11–18]. Thermodilution technique is invasive and there is no clear risk-benet advantage [47, 71, 86].
Recently introduced, non-invasive and less invasive techniques include trans-
esophageal and transthoracic echocardiography, transthoracic bioimpedance, transonic (Nacl dilution), pulse dye densitometry, transpulmonary pulse contour cardiac
output (PiCCO, Pulsion, SG), transpulmonary lithium dilution method (LiDCO),
arterial pressure based cardiac output (Vigileo monitoring, Flotrac TM), and the
pulmonary artery catheter based continuous thermodilution methods (Vigilance,
Baxter, Opti-Q1 Abott, Trucco MS, AorTech). However, the validity, practicability,
and accuracy of these methods vary from one technique to another− [18, 39, 47,
94, 116].
New modalities of non-invasive haemodynamic monitoring have opened up the
prospects of evaluating patients without the risk of invasive cardiac catheterization
[6, 7, 31, 94]. The Flotrac™ sensor and Vigileo™ monitor system introduced by
Edwards Lifesciences allows continual measurement of cardiac output without
requiring dye or thermodilution. Its calculations are based on the characteristics of
the arterial waveform in conjunction with patient’s demographic data, without
external calibration [6, 7, 31, 39, 47–50, 74, 91, 116].
All data derived by calculation and extrapolation is accurate only if the patient’s
heart rate is stable and the pressures were recorded accurately at exactly the same time
that the thermodilution curve was done and time was spent in conrming the accuracy
of the transducer calibration.
In derived calculations, all mistakes in the initial data collection may be exagger-
ated. Concerns and limitations of arterial- based technologies revolve around the
obtainment of accurate arterial waveforms or the requirement for additional calibration. Blood lactate, pyruvate and lactate- pyruvate ratio, tonometry, tissue oxygen tension, near infra-red spectroscopy are the newer trends in hemodynamic monitoring.
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18.2.2 Management ofLow Cardiac Output Syndrome
It is difcult to spot a distinct factor for causing low cardiac output syndrome following pericardiectomy. High right atrial pressure and atrial brillation are associated with poor outcomes. However, in our practice we do not advocate an aggressive
surgical approach to treat tricuspid regurgitation or atrial brillation at the time of
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pericardiectomy. We prefer to digitalize these patients in the preoperative period to
control the heart rate and minimize/avoid perioperative supraventricular arrhythmias.
The effects of pericardiectomy on intra- and post-operative haemodynamics was
studied using a semi-invasive device (Vigileo™ monitor with FloTrac™ sensor,
Edwards Lifesciences, USA). It was demonstrated that despite a decrease in right
atrial pressure and systemic vascular resistance (SVR), and an improvement in cardiac output, the stroke volume did not increase proportionately on completion of
surgery. These parameters (i.e. stroke volume, stroke volume index) decreased from
the preoperative levels immediately following surgery. However, the indexed stroke
volume continued to improve in the postoperative period and returned to preoperative values by the time of discharge. This transient depression of stroke volume
could be due to impaired ventricular diastolic compliance [11–19, 21, 37, 38, 61,
62, 71–73, 85, 102–115, 121, 133]. There is always major uid shift from extravas-
cular to intravascular compartment following pericardiectomy for constrictive pericarditis. Also, repeated compression during pericardial mobilization causes
myocardial oedema which gradually subsides over time [11–19, 21, 37, 38, 61, 62,
71–73, 85, 102–115, 121, 133].
Therapeutic strategies that can support cardiac function and treat low cardiac
output syndrome are inotropic support, mechanical ventilation, afterload reducing
agents, and mechanical circulatory support. Therapeutic interventions for low cardiac output syndrome should be employed prior to the onset of end-organ ischemic
injury and organ failure. Serologic markers of anaerobic metabolism such as serum
lactate levels, while generally indicative of inadequate tissue oxygenation, are relatively late signs of cellular hypoxia. This emphasises the role of monitoring modalities such as venous and NIRS oximetry and Vigileo monitoring in the early detection
of low cardiac output. Low cardiac output syndrome is a clinical term used to
describe any set of conditions leading to an imbalance of oxygen supply and
demand. Once low cardiac output syndrome is detected, the next step is to evaluate
for the causative factor(s), and the impact of those factors on ventricular loading
condition, function as well as on heart rate and the conduction system. Strategies to
improve cardiac output and decrease oxygen demand will be discussed later [7,
11–18, 21, 29, 31, 33, 37, 39, 45–50, 57, 58, 61, 62, 73, 74, 85, 94, 95, 103–109,
114–116].
18 Incidence and Management of Postoperative Low Cardiac Output Syndrome…
18.2.3 Optimizing Preload
In order to determine optimal ventricular lling pressure (central venous or right
atrial and left atrial pressures), it is important to understand where the ventricles
reside on their pressure stroke volume curve. Moreover, a given atrial pressure may
not directly correlate with ventricular lling volume or stroke volume, due to
changes in the ventricular compliance. Additionally, the correlation between right
and left atrial pressures are absent in the setting of low cardiac output syndrome
18.2 Low Cardiac Output Syndrome: Denition andRecognition
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following pericardiostomy and pericardiectomy. This makes it even more challenging to determine the optimal lling pressure (preload) for the left ventricle. A solution for this dilemma is to administer volume and objectively assess the response.
This provides some information on where the ventricles reside on their pressure
stroke volume curve. Decrease in heart rate or increase in arterial blood pressure or
venous oxygen saturation immediately following volume administration indicates
that the ventricles are operating on the ascending portion of their pressure stroke
volume curve and therefore responds to increase in preload. The lack of a response
suggests that the ventricles are residing on the at portion of their pressure volume
curves. In that case rather than increase in preload, inotropic and/or afterload reducing agents are required to improve stroke volume and cardiac output [21]. However,
this method of assessment of preload reserve, is clinically useful in patients undergoing cardiac surgery for other pathologies, this may not be applicable in patients
undergoing pericardiostomy and pericardiectomy, due to the phenomenon of autotransfusion and cardiac dilation along with impaired ventricular compliance.
Therefore, in our practice, when patient is taken up for surgery, we insert a peritoneal dialysis catheter in the operation room and drain ascitic uid over the next
2–3h to prevent sudden autotransfusion, increased preload and failure of the FrankSterling mechanism after surgery. Massive ascites is a signicant factor for perioperative mortality according to multivariate analysis in previous investigations
[11–18].
Intravenous uid bolus challenge in these patients may actually prove deleteri-
ous and monitoring of central venous pressure alone (which is a static preload indicator) is not sufcient for haemodynamic assessment [11–18, 82, 97].
Beat-to-beat change in stroke volume around the mean in one respiratory cycle
is called stroke volume variation. It has been demonstrated that a stroke volume
variation >10% in a mechanically ventilated patient indicates that the patient is
likely to respond to uid administration [11–18, 21, 82, 95, 97, 115]. There is
marked elevation of stroke volume variation (stroke volume variation >10%) in
patients at presentation in operating room and during pericardiectomy. This can be
explained by the decreased compliance of both ventricles due to generalized pericardial compression, dissociation between intrathoracic and intracardiac pressures, and an interventricular “coupling” phenomenon, resulting in a septal shift
[11–18, 115]., Therefore, despite restricted uid administration, there was only
mild reduction of stroke volume variation throughout the postoperative period.
Once the constricting pericardium is excised, the stroke volume variation should
have immediately decreased and become more dependent on intravascular volume. This stroke volume variation could also be explained by signicant alterations in vasomotor tone as reected by a low systemic vascular resistance index
following pericardiectomy. The third possibility is the element of residual constrictive pericarditis posterior to the bilateral phrenic nerves in patients undergoing pericardiectomy via median sternotomy since the data shows borderline high
stroke volume variation values in some patients even after surgery [11–18, 21, 82,
95, 97, 98, 115].
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18 Incidence and Management of Postoperative Low Cardiac Output Syndrome…
18.2.4 Manipulating Systolic Function
Once the requirement is established and supplementation of preload is completed,
the next step in managing low cardiac output syndrome is to assess for the requirement of inotropic support. Many inotropic drugs are available with different adverse
effect proles and dose-dependent haemodynamic effects. Calcium ion, essential
for myobril contraction is another agent used in augmenting systolic function.
These patients have myocardium extremely sensitive to changes in serum calcium
levels. Intravenous calcium supplementation contributes to increased contractility
as well as increased smooth muscle tone in peripheral vasculature. Therefore, prevention of hypocalcemia is essential in the management of patients following pericardiostomy and pericardiectomy.
Catecholamines are the rst choice as inotropic support. Dopamine and dobuta-
mine provide modest inotropic support, while pronounced inotropy is provided by
epinephrine and norepinephrine. Dobutamine and epinephrine in low doses
(<0.05–0.1mg/kg/min) are particularly attractive agents for systolic dysfunction as
they also decrease systemic vascular resistance and thereby decreases afterload. The
adverse effects of catecholamines are that they escalate the myocardial oxygen
demand and heart rate, thereby increasing the propensity for tachyarrhythmias.
18.2.5 Manipulating Afterload
When high, reducing afterload is a useful strategy to decrease myocardial oxygen
demand and improve cardiac output. The advantages of afterload reduction are
more pronounced as the severity of systolic dysfunction increase. Phosphodiesterase
(PDE) type III inhibitors, like Milrinone provide moderate inotropic support accompanied by reduction in pulmonary and systemic vascular resistances. Moreover,
they have lower chronotropicity, lesser arrhythmogenicity, and minor deleterious
effect on myocardial oxygen demand than catecholamines. They act by preventing
the breakdown of cyclic adenosine monophosphate (cAMP). The accumulation of
cAMP improves contractility in cardiomyocytes and relaxation of vascular smooth
muscle cells leading to peripheral vasodilation. In addition, since PDE type III
inhibitors do not rely on adrenergic receptors, they are immune to adrenergic receptor down regulation, which begins within hours of exposure to endogenous or exogenous catecholamines [21].
Milrinone is widely used in pediatric cardiac surgery to prevent or treat low car-
diac output syndrome. However use of milrinone has not been studied in patients
following pericardiostomy or pericardiectomy [9, 10, 21, 25, 51, 52, 88, 129]. In a
double-blind, placebo-controlled trial, Hoffman and colleagues showed a 64% relative risk reduction of low cardiac output syndrome in the rst 36hours following
cardiac surgery in infants randomized to high dose milrinone (0.75 mg/kg/min)
compared to placebo, low or moderate doses [53, 129].
18.2 Low Cardiac Output Syndrome: Denition andRecognition
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Other afterload reducing agents are nitric oxide donors such as nitroprusside and
nitroglycerin, and calcium channel blockers. Nitric oxide relaxes vascular smooth
muscle cell via cGMP.Nitroprusside is a potent nitric oxide donor which readily
increases venous capacitance and relaxes arterial resistance vessels in a dosedependent manner. Nitroglycerin is another drug which, in low doses vasodilates
venous capacitance vessels while causes vasodilation of arterial resistance vessels
in higher doses [21].
Levosimendan is an inotropic agent which functions by adenosine triphosphate
dependent potassium channel opening and calcium sensitization of contractile proteins. Additionally, it has mild phosphodiesterase inhibitory action. Levosimendan
does not activate the sympathetic nervous system [88]. It has been approved for
perioperative use in cardiac surgical patients with myocardial dysfunction and treatment of acutely decompensated cardiac failure [40, 122]. However, there are no
reports or studies on use of levosimendan for treatment of low cardiac output syndrome following pericardiectomy.
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18.2.6 Vasopressor Therapy
Vasoplegia or vasomotor paresis is marked by a pathologic decrease in vascular
tone, which results in increased venous capacitance and decreased systemic vascular resistance. Various intravenous agents are used to restore adequate vascular tone.
Vasopressin is an endogenous hormone produced in the hypothalamus which acts
on [123] receptors in the peripheral vasculature to cause vasoconstriction via activation of protein kinase C, leading to an inux of intracellular calcium. Landry and
colleagues, demonstrated that vasopressin levels were lower in adults with refractory vasodilatory septic shock [66]. Their ndings prompted the idea of using vasopressin for treatment of refractory hypotension. However, while augmenting
systemic vascular resistance, and improving mean arterial pressure, vasopressin
increases the afterload and may cause a reduction in stroke volume and cardiac
output, particularly in patients with systolic dysfunction [2, 9, 67, 75–77]. The vaso-
pressin has been documented to be useful in neonates with catecholamine-resistant
shock following cardiopulmonary bypass [2, 9, 67, 75–77]. Vasopressin has also
been demonstrated to be effective for treating systemic vasoparesis in post pericardiostomy and pericardiectomy cases where conventional doses of catecholamine
proved ineffective [11–18, 75–77].
Another important strategy to manage catecholamine-resistant shock following
pericardiostomy and pericardiectomy is administration of glucocorticoids for a
period of 24–72hours [11–18, 78, 117–119]. Glucocorticoids work through a number of different mechanisms, including an increase in expression of adrenoreceptors
[21]. It has also been noted that response to hydrocortisone does not appear to be
related to baseline cortisol level. There are few drawbacks with use of glucocorticoids. Administration of glucocorticoids in high doses may be associated with
increased morbidity. Although frequently administered, use of perioperative
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steroids have not demonstrated any mortality benet in multicenter trials [89, 124].
Recently, it has been demonstrated that cumulative steroid exposure (7 vs 4days,
p<0.001) is independently associated with occurrence of infection in postoperative
cardiac patients [26, 75, 76, 78, 88, 118, 119, 124, 125].
18 Incidence and Management of Postoperative Low Cardiac Output Syndrome…
18.2.7 Role ofPositive Pressure Ventilation inTreatment
ofLow Cardiac Output Syndrome
Positive pressure ventilation increases intrathoracic pressure and thereby decreases
systemic afterload, which is benecial in patients with ventricular systolic dysfunction. Another signicant advantage of positive pressure ventilation is the mechanical unloading of respiratory muscles. By unloading, the respiratory muscle perfusion
requirements decrease, so that the limited cardiac output is redistributed to other
vital organs, including the brain and myocardium [125].
18.2.8 Mechanical Circulatory Support
Intra-aortic balloon counterpulsation (IABC) is widely used in adults with acute left
ventricular dysfunction after myocardial infarction or cardiac surgery. However, it
is only used occasionally in patients undergoing pericardiectomy for chronic constrictive pericarditis [11–18, 44, 46, 59, 60, 81, 99, 130]. When all the available
medical management strategies fail to sustain the required cardiac output, the next
logical step is to assist the failing heart by mechanical circulatory assistance which
is discussed in detail in Chap. 19. Intra-aortic balloon counterpulsation facilitates
recovery of left ventricular function by reducing left ventricular end-diastolic and
left atrial pressure, thus mainly helping the systemic ventricle. However, the pulmonary ventricle also benets indirectly by the phenomenon of ventricular interdependence [18].
18.3 The Timing ofPericardiectomy, Surgical Approaches,
Adequacy ofPericardial Resection, andtheir
Relationship toLow Cardiac Output Syndrome
The clinical course of constrictive pericarditis is usually progressive, and it is
extremely difcult for the cardiologist to delineate the degree of pericardial and
myocardial restriction. The results of pericardiectomy are poor with dominant myocardial involvement, and better with dominant constrictive element [11–18]. Early
pericardiectomy is benecial for patients with central venous pressure or right atrial
18.3 The Timing of Pericardiectomy, Surgical Approaches, Adequacy of Pericardial…
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pressure between 12 to 15mm Hg, hepatorenal dysfunction, and massive ascites.
The survival of patients with chronic constrictive pericarditis following pericardiectomy is higher than without surgery [11–18].
The two surgical approaches used for treatment of chronic constrictive pericardi-
tis include median sternotomy and conventional left anterolateral thoracotomy. The
median sternotomy approach is preferred in following conditions: (i) calcic pericardial patch compressing the right atrium and right ventricular outow tract; (ii)
annular chronic constrictive pericarditis; (iii) presence of gradient at the superior or
inferior cavoatrial junction of 2mmHg or greater; (iv) extracardiac intrapericardial
mass; (v) previous open heart surgery; (vi) circumferential ‘cocoon’ calcication of
the pericardium; and (vii) recurrent chronic constrictive pericarditis after partial
pericardiectomy. It has been demonstrated that maximum benet occurs after total
pericardiectomy, which is best achieved through a median sternotomy and is very
difcult through conventional left anterolateral thoracotomy [11–18].
However, left anterolateral thoracotomy is a preferred approach in cases of puru-
lent pericarditis and effusive-constrictive pericarditis, because of the presence of
concomitant pyothorax and concerns of sternal infection [11–18].
Studies comparing the outcomes after total versus partial pericardiectomy dem-
onstrated that total pericardiectomy was associated with lower perioperative mortality and low cardiac output syndrome, abbreviated hospitalization, and better
long-term survival than partial pericardiectomy. Ascites, renal dysfunction, hyperbilirubinaemia, elevated preoperative right atrial pressure (>24 mm Hg), atrial
brillation, low ejection fraction (0.40 or less), pericardial calcication, tricuspid
regurgitation, mitral regurgitation, partial pericardiectomy, thoracotomy approach
and postoperative low cardiac output syndrome negatively affected survival.
Patients undergoing partial pericardiectomy had 4.5 times higher risk of death
(95% CI: 2.05–9.75) compared to patients undergoing total pericardiectomy
[11–18].
Despite total pericardiectomy, the operative mortality rate was 7.6% in our series
and 6% to 19% in several other studies published after 1985 [1, 3, 4, 11–27, 29, 41,
42, 54, 61, 62, 69–73, 84, 85, 100, 101, 104–109, 120, 132, 133]. Unlike pointed out
in other studies, we could not nd correlation with age, tuberculous aetiology and
advanced NYHA symptoms on late survival. We presume this is because of comparatively younger population in our study group and timely institution of anti
tuberculous treatment and surgery [1, 3, 4, 11–27, 29, 41, 42, 54, 61, 62, 69–73, 84,
85, 100, 101, 104–109, 120, 132, 133].
Median sternotomy approach allowed a more radical clearance of pericardium
overlying the right atrium and caval veins including the cavo-atrial junctions.
However, these areas usually are of little haemodynamic signicance in a majority
of patients. Another drawback of this approach is the inability to excise the portion
of pericardium posterior to the phrenic nerve [1, 3, 4, 11–27, 29, 41, 42, 54, 61, 62,
69–73, 84, 85, 100, 101, 104–109, 120, 132, 133].
In an effort to decrease hospital mortality rates and postoperative low cardiac
output syndrome, the author proceeded to perform several technical modications
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18 Incidence and Management of Postoperative Low Cardiac Output Syndrome…
of the conventional left anterolateral thoracotomy approach to achieve further radical excision of pericardium posterior to the phrenic nerve and diaphragmatic pericardium without utilizing cardiopulmonary bypass [13, 14, 82].
The step-by-step technical details of median sternotomy (n=55) and the author’s
modication of left anterolateral thoracotomy (n=67) to achieve radical pericardiectomy without utilizing cardiopulmonary bypass have been alluded to in our previous publications, and have been addressed in Chapters 13, 14, 15, 17, 22, 23, 24,
and 25 [11–18].
By employing these modications, radical pericardiectomy was associated with
further reduction of hospital mortality from 7.6 to 2.9% (total pericardiectomy) and
reduction of postoperative low cardiac output syndrome from 69% (total pericardiectomy) to 26.8% (radical pericardiectomy) [11–18].
On the basis of published literature, the following recommendations are made
for the management of low cardiac output syndrome following pericardiostomy and
pericardiectomy:
• Irrespective of the pathologic mechanism, slow pericardiocentesis should
be considered to facilitate gradual myocardial adaptation. After attaining
stable haemodynamics, complete decompression of pericardium can be
done safely.
• Autotransfusion results in major uid shifts from extravascular to intravascular
compartment following pericardiectomy. Massive ascites is a signicant factor
for periprocedure mortality. Sudden autotransfusion after pericardiectomy can
be prevented by slow drainage of ascitic uid via a peritoneal dialysis catheter
inserted during surgical procedure. Drainage of ascitic uid over 2–3hours prevents sudden auto-transfusion related increased preload and failure of Frank
Sterling mechanism after surgery.
• Semi invasive cardiac output monitoring devices like FloTrac™/Vigileo™
device should be employed for routine serial measurement of hemodynamic
parameters. This will help in early detection and treatment of low cardiac output
syndrome before signicant end organ damage.
• One should not rely completely on central venous pressure as a measure of preload since it is a static indicator and also it may not reect the preload status of
ventricle due to altercations in ventricular compliance. It is safer to start inotropes like dopamine and dobutamine in moderate doses, immediately on completion of pericardiectomy than instituting late in the postoperative period. Trial
administration of intravenous uid or blood in these patients should be done with
caution and may actually be deleterious.
• Total pericardiectomy through median sternotomy is associated with enhanced
safety, decreased mortality, reduced postoperative low cardiac output syndrome,
abbreviated hospitalization, and better long-term survival than that obtained via
conventional thoracotomy. In case of an emergency, median sternotomy approach
allows to establish cardiopulmonary bypass easily.
• The surgical approach of choice is median sternotomy for chronic constrictive
pericarditis, calcic patches, pericardial masses, and redo-pericardiectomy.
18.4 Conclusions
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• Left anterolateral thoracotomy should be reserved for surgery for pyogenic and
effusive pericardial diseases.
• Although routine use of cardiopulmonary bypass is not necessary, one should not
be reluctant to utilize cardiopulmonary bypass if needed to facilitate a complete
resection to improve survival. When cardiopulmonary bypass is used, ultraltration can be done to reduce effects of autotransfusion.
• Radical pericardiectomy via modied left anterolateral thoracotomy without
using cardiopulmonary bypass, as developed by the author recently, is associated
with a further reduction of operative mortality as compared to total pericardiectomy (2.9% vs. 7.6%), and a further reduction of postoperative low cardiac output syndrome from 69% (total pericardiectomy) to 26.8% (radical
pericardiectomy).
• Successful pericardiectomy requires removal of pericardium as described under
total and radical pericardiectomy including decortication of the ventricular epicardial peel as described by Harrington.
• In order to decrease postoperative myocardial oedema, cardiac manipulation and
intermittent prolonged hypotension during pericardiectomy should be minimised.
• In select instances where medical management is inadequate to maintain cardiac
output, intra-aortic balloon counterpulsation facilitates the recovery of ventricular function. The key is to identify and timely institute intra-aortic balloon counterpulsation in patients with sudden or progressive deterioration of ventricular
function, not responding to optimal inotropic doses.
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18.4 Conclusions
Diagnosis and treatment of low cardiac output syndrome is a common challenge
following pericardiostomy and pericardiectomy. It requires knowledge of underlying pathophysiological mechanisms, diligent monitoring and thoughtful intervention. The goals of treatment are to augment cardiac output, decrease oxygen demand,
and improve the relationship between oxygen supply and demand. These goals are
achieved by use of inotropes, steroids, inodilators, afterload reducing agents, and
mechanical ventilation. When medical interventions fail, transition to intra-aortic
balloon counterpulsation should be pursued to support end organ function, allowing
for myocardial recovery.
We advocate caution against widespread use of intraaortic balloon counterpulsa-
tion therapy after pericardiectomy. There must be an exhaustive search for adequacy
of pericardiectomy, and exclusion of any other surgically correctable cause(s) like
signicant mitral and/or tricuspid regurgitation or signicant coronary artery disease. The timing of initiation of intraaortic balloon counterpulsation support remains
difcult since its use as an absolute “last resort” decreases the possibility of success.
Although not easy in clinical setting, if possible, randomized studies are required to
dene specic indications, proper time of intervention, and factors that can predict
a successful outcome.
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