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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3715_Библиотеки_им_академика_М_И_Перельмана
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17.1 Surgical Management
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293
Fig. 17.7 (a–f) A new
cleavage plane is being
developed between the
diaphragmatic pericardium
and diaphragm. The
inferior half of the calcic
pericardium is divided
using a bone cutter
avoiding injury to the left
phrenic nerve and apex of
the left ventricle
a
b
c
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17 The Operation: Total Pericardiectomy for Calcic Constrictive Pericarditis…
Fig. 17.7 (continued)
d
e
f
17.1 Surgical Management
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295
Fig. 17.8 (a, b) The left
half of the diaphragmatic
pericardium is
subsequently mobilized
and excised
a
b
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17 The Operation: Total Pericardiectomy for Calcic Constrictive Pericarditis…
Fig. 17.9 (a–d) The right
phrenic neurovascular
pedicle is identied and the
pericardial ap on the right
side is divided in two
halves. The calcic
pericardial ap is
mobilized from the
underlying right atrium till
the superior cavoatrial
junction superiorly and the
inferior cavoatrial junction
inferiorly. Use of a No.15
scalpel blade is helpful in
facilitating the dissection
process. The surgeon
should be more cautious on
the right side due to
thinness and dilation of the
right atrium
a
b
c
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297
Fig. 17.9 (continued)
Fig. 17.10 (a, b) The
right-sided diaphragmatic
pericardium is carefully
dissected off the dilated
and thinned inferior caval
vein and excised
d
a
b
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17 The Operation: Total Pericardiectomy for Calcic Constrictive Pericarditis…
Fig. 17.11 (a–c)
Following placement of
two ventricular pacing
wires, the pericardial
cavity is being irrigated
using dilute betadine and
normal saline
a
b
c
References
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299
References
1. Chowdhury UK, Subramaniam G, Kumar AS, Airan B, Singh R, Talwar S, etal. Pericardiectomy
for constrictive pericarditis: clinical, echocardiographic and haemodynamic evaluation of two
surgical techniques. Ann Thorac Surg. 2006;81:522–30.
2. Chowdhury UK, Narang R, Malhotra P, Choudhury M, Choudhury A, Singh SP.Indications,
timing and techniques of radical pericardiectomy via modied left anterolateral thoracotomy
(UKC’s modication) and total pericardiectomy via median sternotomy (Holman and Willett)
without cardiopulmonary bypass. J Prac Cardiovasc Sci. 2016;2:17–27.
3. Chowdhury UK, Kumari LS, Hasija S.Surgery for chronic constrictive pericarditis, tuberculous pericarditis and effusive-constrictive pericarditis. Cardiological Society of India, 2018.
Essentials of Postgraduate Cardiology, Evangel Publishers, Invited Chapter 64, pages 1-10.
4. Chowdhury UK, George N, Kumari LS, Singh S, Chauhan AS, Gupta A, Chowdhury S.Total
pericardiectomy via median sternotomy (Holman and Willett): a video presentation. Int Med.
2019;1(4):244–5.
Chapter 18
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Incidence andManagement
ofPostoperative Low Cardiac Output
Syndrome After Pericardiectomy
Over past 100years there have been tremendous progress in diagnostic accuracy of
constrictive pericarditis and principles regarding treatment of chronic constrictive
pericarditis have evolved over time. However, there remain several unsubstantiated
approaches in the medical and surgical management of massive pericardial effusion
and chronic constrictive pericarditis. Also there is no infallible method to decide on
the optimal surgical approach for a given patient [1, 3, 4, 11–20, 34, 35, 41, 42, 54,
61, 62, 68–70, 81, 83, 100, 101, 120, 121, 132].
Low cardiac output syndrome was rst described by Parr etal. in 1975 [84].
They measured the cardiac index (CI) by dye dilution method and discovered that
25% of children after cardiac surgery had a cardiac index of less than 2.0L/min/m2
[41, 42, 84]. Twenty years later, Wernovsky and colleagues also demonstrated low
cardiac output syndrome in children after arterial switch operation [126]. In 1983,
Vandyke and colleagues described low cardiac output syndrome for the rst time
following pericardiostomy for cardiac tamponade [123].
Despite scientic advances, there remain several myths and controversies in the
management of acute and chronic pericardial diseases.
18.1 Unresolved Issues andControversies
1. Ascitic and pleural uid drainage after pericardiostomy and pericardiectomy can
cause hypovolemic shock.
2. Digoxin should be used routinely in the preoperative period.
3. There is no difference between median sternotomy or left anterolateral thora-
cotomy approaches in achieving total pericardiectomy.
4. Cardiopulmonary bypass is necessary to achieve complete pericardiectomy.
Ltd. 2023
U. K. Chowdhury, L. K. Sankhyan, Surgical Treatment of Chronic Constrictive
Pericarditis, https://doi.org/10.1007/978-981-99-5808-5_18
301© The Author(s), under exclusive license to Springer Nature Singapore Pte
302
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18 Incidence and Management of Postoperative Low Cardiac Output Syndrome…
5. The recommended sequence of excision of pericardium starts from left ventricle,
then aorta followed by right ventricle, pulmonary artery, left atrium in that order
and lastly right atrium.
6. Ideal investigative modality for early recognition and timely intervention of low
cardiac output syndrome: Doppler echocardiography/ transesophageal echocardiographic monitoring / tissue Doppler imaging/thermodilution catheter /pulmonary artery catheter/ vigileo™ FloTrac™ device/IKON?
7. Assessment and timely institution of inotropes for management of perioperative
low cardiac output syndrome.
8. Dening the role of intra-aortic balloon counterpulsation therapy in manage-
ment of low cardiac output syndrome after pericardiectomy/pericardiostomy.
In order to bring clarity in these issues, we searched for all published literature
which discussed low cardiac output syndrome and their management after pericardiostomy for pericardial effusion and pericardiectomy for chronic constrictive pericarditis. The search engines employed were PubMed, Google Scholar, Cochrane
Database for Systematic Reviews, Cochrane Central Register of Controlled Trials,
Ovid MEDLINE, ACP Journal Club, Ovid EMBASE, and Database of Abstracts of
Review of Effectiveness in all languages. We found 97 publications related to these
topics. The knowledge from these investigations was collated and analyzed to outline the pathophysiology of this paradoxical response, issues of concern, and various surgical, non-surgical, and myocardial supportive strategies which can be
employed to achieve an improved clinical outcome.
Incidence of low cardiac output syndrome following pericardial decompression
is 4.1–7.5% in patients with cardiac tamponade, and 24–28% following pericardiectomy. Hospital mortality secondary to low cardiac output syndrome, but not directly
related to surgical procedure ranges between 24% and 28% in both groups of
patients, following either pericardiostomy or pericardiectomy [1, 3, 4, 11–29, 41,
42, 54, 61, 62, 69–73, 84, 85, 100, 101, 104–109, 120, 132, 133].
Thorough understanding of the pathophysiologic changes that may impair car-
diac function following pericardiostomy or pericardiectomy is required to determine the factors contributing to low cardiac output syndrome. The aetiology of low
cardiac output syndrome is generally multifactorial [1, 3, 4, 11–27, 29, 41, 42, 54,
61, 62, 69–73, 84, 85, 100, 101, 104–109, 120, 132, 133].
Impaired ventricular diastolic compliance is the haemodynamic hallmark of
chronic constrictive pericarditis. After a successful pericardiectomy, there are major
uid shifts from extravascular to intravascular compartments. This auto transfusion
results in failure of the Frank-Starling mechanism, causing acute cardiac dilation
mimicking acute left ventricular dysfunction from volume overload. The volume
overload and ventricular dysfunction lead to acute stretching of the annulus resulting in functional regurgitation. Massive ascites is a signicant predictor of mortality
[11–18]. Another important factor is the myocardial oedema due to the repeated
mechanical compression during pericardial mobilization. A paradoxical response
with severe biventricular dysfunction is noted in some patients after pericardial
decompression, despite improved cardiac lling and stroke volume [5, 11–18].
18.1 Unresolved Issues andControversies
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Patients with constrictive pathology have more diastolic and systolic dysfunction
than patients with non-constrictive pathology like myocardial ischemia, stunning,
atrophy or over-dilation [1, 6, 8, 22, 30, 43–49, 55, 63–65, 79, 80, 86, 87, 110–112].
However, clinical outcomes of these patients have not been studied in post- pericardiectomy periods [11–17].
The offending pathophysiological mechanisms responsible for low cardiac out-
put syndrome following pericardiostomy/pericardiectomy are not well understood.
Various theories that have been proposed to explain it are:
• Occult systolic dysfunction. Preexisting systolic dysfunction masked by reduced
chamber size and tachycardia is brought out by pericardial decompression.
Vandyke and associates postulated that the acute haemodynamic changes due to
change of intraventricular volume in setting of dilated ventricles and changing
systemic vascular resistance could be the reason for cardiac dysfunction following tamponade decompression [123]. Release of constrictive pericarditis causes
improvement of right ventricular ejection fraction according to Frank-Starling
mechanism. However, continued increase in intraventricular volume causes
increased systolic wall stress, a reduction in stroke volume, and fall in cardiac
output [123]. Left ventricular systolic dysfunction has also been noted following
pericardiocentesis in two patients of cardiac tamponade by Wolfe and Edelman
[127]. Two factors important in predicting low cardiac output noted in this study
were abrupt increase in myocardial wall stress and chronicity of tamponade [127].
• Pericardial decompression attenuate the increased sympathetic tone and endogenous catecholamines due to tamponade. This could result in unmasking of preexisting myocardial dysfunction. This was hypothesized by Chamoun and
colleagues in 2003 [23].
• Pericardiostomy or pericardiectomy, may result in rapid over dilation of the heart
resulting in postoperative low cardiac output syndrome. This response is related
to the magnitude and velocity at which the load develops [36, 69, 90–92,
102, 103].
• According to Hamaya and colleagues, changing intramyocardial blood distribution during operative management of tamponade results in myocardial stunning
and low cardiac output [43].
• Another theory put forward by Wechsler and colleagues incriminates subendocardial hemorrhage during surgery for tamponade for causing myocardial stunning and necrosis [128]. Transient biventricular dysfunction after pericardiectomy
without any coronary artery disease was demonstrated by Ligero and colleagues
[65, 66, 128].
• Various other factors implicated in low cardiac output syndrome after pericardiectomy are myocardial involvement by same pathology, immobilisation myocardial atrophy, incomplete or ineffective decortication, ventricular remodelling,
worsening tricuspid regurgitation, abnormal diastolic lling, and postoperative
mitral regurgitation secondary to papillary muscle elongation [3, 30, 31, 37, 38,
50, 54, 56, 57, 63, 64, 92–96, 130, 131]. It has been observed that, regardless of
the extent of pericardial resection or operative technique, a subset of patients
with chronic constrictive pericarditis developed postoperative low cardiac output
syndrome [3, 11–18, 54].
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