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dened. Additionally, “radical pericardiectomy” is impossible since it calls for the
removal of all three layers of the pericardium, which are “brous” and “serous”
with two components—“parietal and visceral epicardium”; this is impossible in real
life [12, 13].
Secondly, the signicance of unrecognized constricting epicardial peel was
described by Harrington in 1944 [28]. Successful pericardiectomy requires removal
of all constricting layers including decortication of the ventricular epicardium [4–
13, 28].
10 Denitions of The Extent of Pericardiectomy, Echocardiographic Variables,…
10.1 Echocardiographic andTissue Doppler Imaging Studies
Patients who exhibit symptoms and signs of constrictive pericarditis undergo comprehensive evaluation with M-mode, two-dimensional (2-D) and pulsed-wave
Doppler echocardiography with a respirometer recording and tissue Doppler imaging (TDI) before and after pericardiectomy using a Phillips iE33 with 2.0 to 5.0
MHZ transducer or HP Sonos 5500, a Hewlett Packard, Andover, MA machine [4–12].
Mitral, tricuspid, superior caval vein, hepatic vein and pulmonary ow velocities
are measured using transthoracic two-dimensional, colour-ow Doppler echocardiographic studies before and after the operation [1, 4–12, 35–37].
Left ventricular ejection fraction (LVEF) is calculated by two-dimensional echocardiography with a modied method of Quinones and colleagues [53, 54]. The
modied biplane area-length method is used to calculate the left atrial volume [31,
95]. Right ventricular systolic function is visually assessed [1, 14, 35–37].
On Doppler, two ow velocity envelopes can be seen during diastole in patients
with sinus rhythm: the E-wave, representing the early, passive lling of the ventricle, and the A-wave occurring in late diastole, which represents the atrial contraction [1, 7, 13, 14, 19, 24, 28, 32, 35–38, 45, 61–63, 69, 95, 96].
By using pulsed wave Doppler echocardiography, the following variables are
measured: trans-mitral and trans-tricuspid peak velocities of early (E) and late lling (A), and E wave deceleration time.
For both the mitral and tricuspid valve, E and A waves are measured. Mitral or
tricuspid regurgitation is semi-quantitatively assessed as grade 1+ to 4+. A constrictive pattern is dened as an increase in mitral E-velocity during expiration as compared with inspiration by more than 25%, and an augmented (25% or more) diastolic
ow reversal in the hepatic vein after the onset of expiration compared with inspiration [1, 7, 13, 14, 19, 20, 24, 28, 35–38, 45, 48, 61–63, 69, 95, 96].
On tissue Doppler imaging, peak annular velocities are measured from the apical
four-chamber view at systole (s’), early (e’) and late (a’) diastole, with a 2–5mm
tissue Doppler sample volume placed at the septal corner and at the mitral and tricuspid lateral annuli. In patients with atrial brillation, average of ve consecutive
signals are taken. Inferior caval venous diameter is assessed in the subcostal sagittal
view [1, 7, 13, 14, 19, 20, 24, 28, 35–38, 45, 48, 56, 57, 61–63, 68, 95, 96].
10.2 Strain by Speckle Tracking
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On tissue Doppler imaging, lateral mitral e’ represents early diastolic myocardial
relaxation velocity below the baseline as the annulus ascends away from the apex
with cursor at lateral annulus; medial mitral e’ and lateral tricuspid e’ are the same
velocities measured at the mitral medial annulus and tricuspid lateral annulus
respectively. The mitral lateral s’ velocity represents the systolic myocardial velocity at the lateral mitral annulus. The medial mitral s’ and lateral tricuspid s’ are the
same velocities measured at the mitral medial annulus and tricuspid lateral annulus
respectively [19, 20, 32, 39, 40, 45, 46, 55–57, 61, 62, 64].
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10.2 Strain by Speckle Tracking
Speckle tracking is a post-processing computer algorithm that uses routine grey
scale digital images [20, 36, 46, 47, 50, 51, 65–69, 96]. Briey, routine grey scale
digital images of the myocardium contain unique speckle patterns.
On the myocardial wall, a user-dened zone of interest is positioned. The imageprocessing method automatically splits regions into blocks of pixels while monitoring steady patterns of speckles inside this region of interest. Subsequent frames are
then automatically analysed by searching for the new location of the speckle patterns within each of the blocks, using correlation criteria and the sum of absolute
differences. The location shift of these acoustic markers from frame to frame depicts
tissue movement provides the spatial and temporal data used to calculate velocity
vectors. Temporal alterations in these stable speckle patterns are identied as moving farther apart or closer together creating a series of regional strain vectors.
Because strain information is independent of the Doppler angle of incidence like
tissue Doppler imaging strain, several more strain analyses are possible, including
longitudinal, circumferential, radial, and rotational [20, 36, 47, 50, 51, 65–68, 96].
This recently developed technique for characterization and quantication of myocardial deformation provided data noninvasively for better assessment of the efcacy of pericardiectomy. (i.e. in chronic constrictive pericarditis, the epicardial
dysfunction leads to depressed Global Circumferential Strain (GCS) and Left
Ventricular Torsion (LVT), whereas Global Longitudinal Strain (GLS) and Global
Radial Strain (GRS) are preserved).
Perioperative mortality is dened as death that occurs within 30days of surgery.
Cardiac-related death is dened as death due to cardiac causes, such as progressive
congestive cardiac failure [2, 4–12]. Hypoproteinemia is dened as serum albumin
level less than 3.5g/dl. Renal dysfunction is dened as serum creatinine more than
2.0g/dl [2, 4–17, 94].
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10 Denitions of The Extent of Pericardiectomy, Echocardiographic Variables,…
10.3 Low Cardiac Output Syndrome: Denition
andRecognition
The term “low cardiac output syndrome” refers to the decrease in cardiac output
that may happen after pericardiostomy for massive pericardial effusion or pericardiectomy for persistent constrictive pericarditis. It is a well-recognized postoperative
phenomenon that is quite commonly encountered following the above-mentioned
surgical interventions, with dreaded consequences. Although no stringent diagnostic criteria exist, an accepted constellation of physiologic and haemodynamic alterations occurs which alerts the cardiac intensivist to its presence [2, 4–12, 15–18, 21,
22, 25–27, 33, 34, 39, 41–43, 52, 70–94, 97].
Low cardiac output syndrome following pericardiotomy or pericardiectomy was
diagnosed if the patient required inotropic support (dopamine at 4–10 μg/
[kg−1·min−1]), dobutamine at 5–10 μg/[kg−1·min−1], epinephrine at 0.01–0.1 μg/
[kg−1·min−1], milrinone (50 μg/kg intravenous bolus followed by 0.375–0.75 μg.
kg−1.min−1), either isolated or in combination in the operating room or in the intensive care unit, to maintain stable haemodynamics in the absence of residual mechanical cardiac constriction, residual structural lesions such as signicant valvular
lesions, and mechanical external compression after correction of all electrolytes or
blood gas abnormalities and after adjustment of the preload to its optimal value.
Low-output syndrome was also diagnosed if there was an increasing requirement of
the above-mentioned inotropes with or without intra-aortic balloon counterpulsation along with afterload reduction with sodium nitroprusside. Patients who received
less than 4μg.kg−1.min−1 dopamine to increase renal perfusion were not considered
to have low output syndrome [2, 4–12, 15–18, 21, 22, 25–27, 33, 34, 39, 41, 42, 52,
70–94, 97].
Accordingly, under the denition of low output syndrome after pericardiostomy
and pericardiectomy, an integration of pertinent clinical, laboratory and bedside
echocardiographic criteria was used. The criteria for diagnosis were as follows: cold
extremities, absent pedal pulses, decreased toe temperature, reduced systolic pressure, impaired renal function and oliguria (<1.0mL.kg−1.h−1), metabolic acidosis,
increased serum lactate levels ≥2.0mmol/L, ≥2hours), low mixed venous oxygen
saturation (≤50%), and blunt sensorium [2, 4–12, 15–17, 21, 22, 26, 27, 33, 34, 39,
41, 42, 52, 70–94, 97].
10.4 Monitoring andDiagnostics
Recently introduced, non-invasive and less invasive techniques include transesophageal and transthoracic echocardiography, transthoracic bioimpedance, transpulmonary pulse contour cardiac output (PiCCO, Pulsion, SG), transonic (NaCl dilution),
pulse dye densitometry, transpulmonary lithium dilution method (LiDCO), arterial
pressure based cardiac output (Vigileo monitoring, Flotrac TM), and the pulmonary
10.7 FloTrac™ Sensor, Vigileo™ Monitor: Edwards Lifesciences, Irvine, CA, USA
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artery catheter based continuous thermodilution methods (Vigilance, Baxter,
Opti-Q1 Abbott, Trucco MS, AorTech). However, the validity, practicability and
accuracy of these techniques vary [4–13, 27, 30, 58, 93].
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10.5 Haemodynamics Variables
Stroke volume is the amount of blood pumped per heart beat. The variation in beatto- beat stroke volume around the mean during a respiratory cycle is known as stroke
volume variance (SVV).
The normal acceptable range of measured variables includes cardiac index (CI):
2.5–4.2l/min/m2; stroke volume index (SVI): 30–65ml/beat/m2; systemic vascular
resistance index (SVRI): 1500–2500 dynes/cm5/m2; oxygen delivery index (DO2I):
450–600ml/min/m2; stroke volume variation (SVV): less than 10%; central venous
pressure (CVP): 6–8 mmHg; blood lactate levels: 5 mmoles/L; systemic arterial
oxygen saturation>95%; arterial blood gas analysis (ABG): pH: 7.35–7.45; partial
arterial oxygen tension (PaO2): ≥100mmHg; partial arterial carbon dioxide tension
(PaCO2): 35–45mmHg [3, 10, 23, 29, 30, 44, 49, 58–60, 93].
10.6 Serial Semi-Invasive Haemodynamic Monitoring
In the author’s institution, a FloTrac™ sensor and Vigileo™monitor (Edwards
Lifesciences, Irvine, CA, USA) were used to monitor haemodynamics semi- invasively starting from the time radial arterial and internal jugular venous lines were
inserted in the operating theatre through the procedure till the time when the patient
was shifted to the cardiac intensive care unit, at 12hours, 24hours, 48hours, and
72hours postoperatively [10].
10.7 FloTrac™ Sensor, Vigileo™ Monitor: Edwards
Lifesciences, Irvine, CA, USA
The system consists of a FloTrac™ sensor and a processing/display unit (Vigileo,
Edwards LLC). The sensor is a transducer that preprocesses and transmits a signal
to both the cardiovascular monitor (for real time waveform display) and Vigileo
monitor [10]. The Vigileo is a small instrument, weighing 2.1 kg, and can be
mounted on an intravenous pole. The processing unit applies a proprietary algorithm to the digitized arterial pressure wave, and reports cardiac output (CO), cardiac index (CI), stroke volume (SV), stroke volume index (SVI) and stroke volume
variation (SVV). The Vigileo can interface with a central venous pressure catheter’s
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10 Denitions of The Extent of Pericardiectomy, Echocardiographic Variables,…
signal to calculate systemic vascular resistance (SVR) and systemic vascular resistance index (SVRI). When used with a central venous oximetry catheter, the Vigileo
also provides continuous central venous oxygen saturation. The rear panel of the
Vigileo allows interfacing with central venous pressure (CVP) and oximetry, external video and a printer (USB). The Vigileo reports haemodynamic parameters at
20 seconds intervals, performing its calculations on the most recent 20seconds
of data.
The system calculates the arterial pressure using arterial pulsatility, resistance
and compliance, according to the following equation: Stroke volume=K×Pulsatility.
Where K is a constant quantifying arterial compliance and vascular resistance, and
pulsatility is proportional to the SD of the arterial pressure wave over a 20-s interval. K is derived from patient characteristics (gender, age, height and weight), as
well as waveform characteristics. This calibration constant is recalculated every
10minutes.
This cutting-edge technology can be used in the operating room, medical/surgical ICU, and emergency department because it evaluates all hemodynamic factors
without requiring external calibration. Additionally, it reports the variance in beatto- beat stroke volume around the mean throughout a respiratory cycle, or stroke
volume variation (SVV). Hypovolemic patients exhibit an exaggerated SVV (>
10%). However, SVV may be affected by other factors, such as vasodilator therapy,
lung disease and mechanical ventilation [10, 44, 49, 58–60].
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