an evaluation of hemodynamic instability during elective...
TRANSCRIPT
i
AN EVALUATION OF HEMODYNAMIC INSTABILITY
DURING ELECTIVE NEUROSURGERY
A TRANSESOPHAGEAL ECHO BASED STUDY
Thesis submitted for the partial fulfilment for the requirement of
the degree of DM Neuroanaesthesia
DR. NILIMA RAHAEL MUTHACHEN
DM NEUROANAESTHESIA RESIDENT
2014–2016
DIVISION OF NEUROANESTHESIA
DEPARTMENT OF ANAESTHESIOLOGY
SREE CHITRA TIRUNAL INSTITUTE FOR MEDICAL
SCIENCES AND TECHNOLOGY, TRIVANDRUM, KERALA 695011
v
ACKNOWLEDGEMENTS
I would like to place on record my sincere thanks to my guide Prof.
(Dr) Manikandan. S for his guidance, encouragement, teaching and constructive
criticism throughout the course of this study.
I am grateful to Prof. (Dr) Rupa Sreedhar, Head, Department of Anesthesiology and
Prof. (Dr) R. C. Rathod, Former Head, Department of Anesthesiology, for their
encouragement and valuable suggestions at all stages of this study.
I would like to thank Dr. Smita V and Dr Arulvelan for their suggestions, guidance
and help during this thesis. I am grateful to Dr Unnikrishnan and Dr Ajay Prasad
Hrishi for their cooperation during this study.
I would like to thank my colleagues at the Department of Anaesthesia for their help
and support while I undertook this thesis.
I would like to thank the Neurosurgery Department for their cooperation while I
undertook this study.
I would like to thank all the anesthesia technicians and the theatre sisters of the
Neurosurgery Theatre Complex
I would like to thank my parents for their constant encouragement during this
journey.
Last but not the least, I am grateful to the patients and their families who
participated in this study. I am humbled and honored by their willing participation in
this study.
vi
CONTENTS
1 INTRODUCTION 1
2 REVIEW OF LITERATURE 4
3 AIMS AND OBJECTIVES 13
4 MATERIALS AND METHODS 14
5 STATISTICS 31
6 RESULTS AND OBSERVATIONS 32
7 DISCUSSION 51
8 LIMITATIONS 58
9 CONCLUSION 59
10 BIBLIOGRAPHY 60
ANNEXURE
1. IEC APPROVAL LETTER
2. CONSENT FORM
3. PROFORMA
5. MASTER CHART
6. PLAGIARISM REPORT
vii
ABBREVIATIONS
ABP – Arterial Blood Pressure
ACC/AHA - American College of Cardiology/American Heart Association
ASA- American Society of Anesthesiologists
ASE-American Society of Echocardiography
AV- aortic valve
AVM- arterial venous malformation
BSA- body surface area
CO- Cardiac Output
CVP- central venous pressure
DEC- decrease
DTI- Doppler Tissue imaging
EAE-European Association of Echocardiography
EDV- end diastolic volume
EEG- Electroencephalogram
EF- ejection fraction
EF- Ejection Fraction
H/O – history of
HR- heart rate
IAS- inter atrial septum
IEC- Institutional Ethics Committee
INC- increase
IVC min- minimum diameter of IVC on inspiration
IVC-CI- Inferior Vene Cava Collapsibility Index
IVC-inferior vene cava
IVCmax- maximum diameter of IVC on expiration
LVEDV -left ventricular end diastolic volume
LVESV- left ventricular end systolic volume
LVIDD- left ventricular internal diameter end diastole
LVIDS- left ventricular internal diameter end systolic
LV-Left Ventricle
viii
LVOT- left ventricular outflow tract
MAP- Mean Arterial Pressure
ME 4C - Midesophageal Four Chamber View
ME Bicaval - Midesophageal Bicaval
ME LAX- Midesophageal Aortic Valve Long -Axis
ME- Mid Esophageal
NC- no change
NIBP- noninvasive blood pressure
PAC-Pulmonary Artery Catheter
PAOP- pulmonary artery occlusive pressure
PEEP- positive end expiratory pressure
PV- Pulmonary Valve
PW- pulse wave
PWD- pulse wave Doppler
RV -Right Ventricle
RWMA- regional wall motion abnormality
SBP- Systolic Blood Pressure
SV- stroke volume
SVC min- minimum diameter of SVC on inspiration
SVC-CI- Superior Vene Cava Collapsibility Index
SVCmax- maximum diameter of SVC on expiration
SVC-superior vene cava
SVR- Systemic vascular resistance
SVV- Stroke volume variation
TAPSE- Tricuspid Annular plane systolic excursion
TED -Transesophageal Doppler
TEE- Transesophageal Echocardiography
TMDF- Transmitral Doppler flow velocities
TV -Tricuspid Valve
VTI- velocity time integral
WNL- within normal limits
INTRODUCTION
1
Introduction
INTRODUCTION
Major neurosurgical procedures under anaesthesia can be associated with
hemodynamic changes that can affect the neurological and other systemic outcomes
of the patient.1,2
The human brain represents only 2% of the total body weight, but receives
12 to 15 % of the cardiac output. The functioning of the brain requires the constant
supply of oxygen and nutrients. It consumes 20% of the total body oxygen
consumption at the rate of 3 to 3. 5 ml/100gram /min (cerebral metabolic rate of
consumption of oxygen). This reflects its high metabolic rate. Global cerebral blood
flow is 50 – 55ml /100gm /minute with the grey matter receiving about 80% of this
and the white matter receiving about 20%. Sixty percent of the brains energy
consumption is directed towards electrophysiological activity and the remainder is
used for cellular homeostasis. Since most of the energy of the brain is supplied by
aerobic mechanisms, any fall in blood supply to brain is detrimental.
When cerebral perfusion decreases, the body extracts more oxygen from
hemoglobin, which can be detected by the arteriovenous oxygen difference. At 20 to
25 ml/100gm/min, changes in the electroencephalogram (EEG) and a fall in
conscious level occurs. As perfusion falls to 20 ml/100gm/min, the brain switches to
anaerobic metabolism with an increase in lactate and hydrogen ions. The EEG
becomes isoelectric. At 10-12 ml /100gram/min, neuroelectrical activity ceases.
Along with this, at the cellular level, the sodium-potassium pump fails and cytotoxic
edema occurs. At a perfusion of 6 to 10ml /100gm/min, death with calcium
glutamate imbalance at the cellular level occurs. This reiterates the importance of
maintaining adequate cerebral blood flow, which is supplied by the heart.3
Fluctuations in hemodynamics can occur during neurosurgery due to a
number of reasons- manipulation of the tumour, hypovolemia, blood loss, and
trigeminal/vagal stimulation, very deep anesthesia, inadequate anesthesia, analgesia,
2
Introduction
cardiac dysfunction, etc.4 Hypovolemia can be occurring due to preoperative
conditions such as the use of osmotic therapy e.g., mannitol in a bid to decrease
intracranial pressure. This may cause diuresis which can lead to hypovolemia and
hypotension.5 Patients with subarachnoid hemorrhage manifest hypovolemia due to
various reasons including supine diuresis and pooling in the peripheral vascular bed
as a result of bedrest, negative nitrogen balance, decreased erythropoiesis, iatrogenic
blood loss, osmotic agents (e.g., mannitol and glycerol), and hyponatremia.6
Sato K, et al. reported severe bradycardia during epilepsy surgery in patients
undergoing surgery for intractable epilepsy. It was hypothesized that stimulation of
parts of the limbic system like the amygdala, the insular cortex and the hippocampus
could lead to an increase in the parasympathetic response via the vagus nerve
leading to bradycardia and hypotension.7
Intravenous and inhalational anesthetic drugs can cause vasodilation and
lead to a fall in blood pressure. Patients with premorbid conditions like hypertension
and cardiac disease may be on various cardiac medications that make them
susceptible to swings in blood pressure under anaesthesia. For instance, the recent
ACC/AHA guidelines recommend continuing beta -blockers in patients undergoing
surgery who have chronically been on beta -blockers.8
They also give a class II A
recommendation for angiotensin converting enzyme inhibitors or angiotensin
receptor blockers, stating that continuation of these drugs in the perioperative period
is reasonable. However, the anesthetist has to manage any potential interactions that
occur during perioperative period and the ensuing hemodynamic alterations.9,10,11
The diabetic patient with autonomic neuropathy is also susceptible to profound
hypotension.12
Demographic shifts toward an increasingly aging population have resulted in
a large number of such patients presenting for non-cardiac surgery including
neurosurgery. The American Society of Anesthesiologist (ASA) Standards for basic
anaesthesia monitoring state that in order to ensure adequate monitoring of
circulatory function during all anaesthesia delivery, the anesthetist should ensure
that all patients are monitored by continuous electrocardiogram. Arterial blood
3
Introduction
pressure and heart rate should be monitored at least every five minutes. In addition,
circulatory function must be monitored by palpation of pulse, auscultation of heart
sounds, monitoring of intra-arterial pressure, ultrasound pulse pressure monitoring
or pulse plethysmography or oximetry.13
Apart from these standard monitors, there are a number of newer cardiac
output monitors such as estimation of cardiac output from carbon dioxide
rebreathing, pulse pressure, lithium dilution or transesophageal Doppler
measurements. The pulmonary artery catheter is the most accurate, but apart from
cardiac surgery, less invasive monitoring is used. With the advent of newer non-
invasive or minimally invasive modalities to assess cardiac output such as
echocardiography, the use of pulmonary artery catheters and its attendant
complications has declined.14
Vena caval collapsibility or distensability as assessed
by Doppler has been used to assess preload and fluid responsiveness in shock.15
In 2015, the Association of Anesthetists of Great Britain and Ireland
published guidelines for standards of monitoring during anaesthesia and recovery.
They state that echocardiography can be used to determine cardiac output and it also
allows the volume status and cardiac function to be observed. However, training and
experience is required.16
Utility of intraoperative Transesophageal echocardiography (TEE) has been
well established in major vascular and cardiac procedures.17,18,19,20,21
However,
limited literature is available on the utility of TEE during neurosurgical procedures.
A well designed study is required regarding the benefits of transesophageal
echocardiographic parameters to evaluate hemodynamic fluctuations in heart rate
and blood pressure during the conduct of neuroanaesthesia. We evaluated
transesophageal echocardiographic derived measures of preload, myocardial
contractility and afterload along with heart rate and continuous arterial blood
pressure to better evaluate the causes of hemodynamic instability during
neurosurgery.
REVIEW OF LITERATURE
4
Review of Literature
REVIEW OF LITERATURE
In anaesthesia, hemodynamic monitoring is the cornerstone of perioperative
vigilance. In the perioperative anaesthetised patient, hemodynamic monitoring gives
us information about the patient’s cardiac output, volume status and tissue perfusion
as well as the depth of anaesthesia and adequacy of pain control. The various
devices available have their advantages and disadvantages.
In the perioperative period, the goal of hemodynamic monitoring is to ensure
adequate tissue perfusion and oxygen delivery, predict instability and be able to
direct therapy when this occurs. Neurosurgery can be associated with hemodynamic
instability at various points in the perioperative period. A hemodynamic monitor
which can visualise real time cardiac function as well as guide fluid administration
or pharmacotherapy in the form of inotropes or vasopressors is a valuable tool to the
perioperative physician.
Monitoring of the heart rate and arterial blood pressure are mandatory during
conduct of anaesthesia. (ASA guidelines). Blood pressure can be measured by
manual intermittent techniques as well as invasive arterial cannulation with
transduction of pressure.
Intermittent manual blood pressure monitoring has a number of drawbacks.
Any decrease in peripheral blood flow such as shock or intense vasoconstriction can
obscure the detection of Kortokoff sounds. Severe oedema, shivering and calcific
arteriosclerosis, inappropriate cuff size and excessively rapid cuff deflation can yield
inaccurate readings. Patients who have peripheral neuropathies, severe
coagulopathies, arterial or venous insufficiency, or recent use of thrombolytic
therapy may also be susceptible to complications from non-invasive methods of
blood pressure monitoring.3
The acceptable reference standard for arterial blood pressure monitoring is
cannulation of the artery with continuous transduction of pressure. It provides
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Review of Literature
crucial and timely information about the cardiovascular status of the patient. Factors
such as vasospastic disease, thrombocytosis, use of high dose vasopressors,
prolonged cannulation and infection can lead to vascular complications. Technical
requirements are also a consideration. An underdamped system can lead to arterial
waveform distortion and overshoot of systolic pressure. Pressure transducers have to
zeroed, calibrated and levelled to an appropriate position relative to the patient
otherwise it can lead to a fallacious value of blood pressure. As with any other
monitoring device, proper interpretation of wave form is also required. Dynamic
measures of preload such as Systolic Pressure variation and Pulse Pressure Variation
can be obtained from arterial pressure waveforms. However, parameters to assess
myocardial contractility and afterload are not available.3
Central venous cannulation is performed for patients undergoing major
operations. It is used to administer fluids or inotropic drugs, monitor central venous
pressure, transvenous cardiac pacing or for aspiration of entrained air or for giving
drugs that need to be given through a central vascular access such as hypertonic
saline.3
Central venous pressure is not a reliable indicator of volume status nor does
it help in the diagnosis of hemodynamic instability. Cannulation of a central vein is
associated with major complications, with more than 15% of patients experiencing
an adverse event.22
A whole gamut of complications can occur including arterial or
venous vascular injury, nerve injury including damage to phrenic nerve, stellate
ganglion or brachial plexus, pneumothorax, cardiac tamponade, infectious
complications and thromboembolism. Arrhythmias can occur if the catheter tip is in
an intracardiac location.3,23
The pulmonary artery catheter (PAC) is able to provide many important
hemodynamic parameters that help in assessment of cardiac output and volume
status. It has been considered the gold standard for the assessment of preload,
afterload contractility and tissue oxygenation. Measured variables like Pulmonary
artery wedge and diastolic pressure allows us to estimate left ventricular diastolic
pressure. This can be used as a surrogate for left ventricular end diastolic volume
6
Review of Literature
which is the left ventricular preload. Other physiological variables like systemic
vascular resistance, pulmonary vascular resistance and cardiac output can also be
derived. However, its use is not without controversy. Several studies have reported
that patients managed with PAC have similar outcomes to those without
PAC.24,25,26,27
Inouye et al studied the trends in the use of PAC in the aneurysmal
subarachnoid haemorrhage population and conclude that the use had decreased over
a ten-year period.28
Seifi et al also showed that use of PAC had declined in the
United States over the past two decade29
. Its use and insertion can be associated with
complications.30
The pulmonary artery catheter can be used to assess cardiac output via the
thermodilution method, but the presence of intracardiac shunts, tricuspid or
pulmonary regurgitant lesions, inadequate delivery of the thermal indicator,
thermistor malfunction, respiratory cycle influences and pulmonary artery
temperature can all affect it.31,32
The use of minimally invasive cardiac monitoring has been increasing.33
A
recent meta-analysis by Ripoll’s et al concluded that in non-cardiac surgery,
intraoperative goal directed hemodynamic therapy with minimally invasive cardiac
monitoring decreased postoperative complications significantly significant reduction
in complications for goal directed hemodynamic therapy was observed (RR: 0. 70,
95% CI: 0. 62---0. 79, p < 0. 001).34
Transoesophageal Doppler (TED) is a minimally invasive method of
evaluating cardiac parameters in the perioperative period. Valtier et al compared 136
paired cardiac output (CO) measurements using the thermodilution method and used
esophageal Doppler. A good correlation was found between the two methods for
cardiac output measurement. Variations in cardiac output between two consecutive
measures using either transoesophageal Doppler or thermodilution techniques were
similar in direction and magnitude (bias = 0 L/min; limits of agreement = +/-1. 7
L/min). They concluded that transoesophageal echocardiography provided a
clinically useful estimate of cardiac output noninvasively and could detect
hemodynamic changes in mechanically ventilated, critically ill patients.35
7
Review of Literature
Laupland KB et al reviewed the utility of transoesophageal Doppler as a
minimally invasive cardiac output monitor. They reviewed twenty-five publications
comparing transoesophageal Doppler and pulmonary artery catheter measurement of
cardiac output. They found a good correlation between CO determined by TED and
thermodilution (n = 18 studies, median R = 0. 89, range 0. 52 to 0. 98) and minimal
bias (n = 13, median -0. 01, range 1. 38 to 2 L x min (-1)). They concluded that TED
was a reliable, valid and practical device for the measure of cardiac output
monitoring.36
Perrino et al compared multiplane TEE with the thermodilution method for
the evaluation of cardiac output and reported that multiplane TEE can provide an
alternative for intraoperative measurement of cardiac output. The left ventricular
outflow tract was imaged in 32 of 33 patients (97%). Data analysis reveal a mean
difference between techniques of -0. 01 l/min, and a standard deviation of the
differences of 0. 56 l/min. Multiple regression showed a correlation of r = 0. 98
between intrasubject changes in CO. Multiplane TEE correctly tracked the direction
of 37 of 38 serial changes in thermodilution CO.37
Parra V et al compared intraoperative Doppler by transoesophageal
echocardiography and the thermodilution method. They assess intraoperative
changes in cardiac output in fifty cardiac surgical patients via these two methods.
They obtained Doppler reading in forty-four patients (88%). They found that Echo-
Doppler was accurate (92% sensitivity and 71% specificity, P = 0. 008 by receiver
operating characteristic curves) for detecting more than 10% of change in
thermodilution cardiac output.38
In mechanically ventilated patients, respiratory variations in the superior and
inferior vene cava and in left ventricular stroke volume variation have been
validated as parameters of fluid responsiveness. Transoesophageal derived
collapsibility index has been described as the most reliable of these parameters.39
Transoesophageal echocardiography can be used to assess left ventricular
systolic and diastolic function, cardiac output, presence of valvular pathology, right
8
Review of Literature
ventricular systolic and diastolic function and fluid responsiveness and assess
volume status in intraoperative patients.
The American society of Echocardiography (ASE) recommends that every
complete echocardiographic examination should include evaluation of chamber size
and function and reiterates the importance of these measurements for clinical
decision.
Assessment of ventricular size and function
The ME view can be used for the biplane Simpson’s method of disks for the
calculation of left ventricular volume and ejection fraction when the entire length of
the left ventricle (LV) can be imaged without foreshortening. The normal right
ventricle (RV) is similarly composed of an inlet portion containing the tricuspid
valve (TV) apparatus, an apical portion with characteristic muscle bundles and an
outlet portion proximal to the pulmonary valve (PV). For the right ventricle
however, the three portions do not lie in one plane, and the apical and outflow
portions of the ventricle wrap around the LV. The shape of the RV cannot be
distilled into a simple geometric shape, and thus volumes cannot be accurately
derived from linear measurement.
The mid esophageal (ME) level provides the following views; the four-
chamber (00–10
0), two-chamber (80
0–100
0), and apical LAX (long axis) (120
0–140
0)
views, as well as the five-chamber (00-10
0) and mitral commissural (50
0-70
0) views.
The sum of these views provide excellent and comprehensive coverage of the LV
endocardial motion for all segments, as previously described, allowing assessment
of regional wall motion abnormalities. Optimizing two dimensional images helps
improve the accuracy and reliability of ventricular function assessment. This
includes adjusting the depth to include the entire ventricle, manipulating the ante
flexion and retroflexion of the probe tip to avoid foreshortening the ventricle,
optimizing gain to best depict the endocardium.
9
Review of Literature
LV global systolic function40
LV systolic performance can be assessed qualitatively or quantitatively. The
most commonly used parameter to describe it is ejection fraction. Qualitative
estimation can be done by visual estimation of left ventricular ejection fraction by an
experienced echo cardiographer, however the ASE recommends that qualitative
measurements be crosschecked with calibrated measurements. Ejection fraction can
also be measured from the left ventricular end diastolic volume (LVEDV) and left
ventricular end systolic volume (LVESV), where
Ejection fraction= {(LVEDV-LVESV)/LVEDV} X100
Method of discs (Modified Simpsons rule) is used to calculate LV volume.
As Biplane planimetry (area acquired using both ME four- and Two- chamber
views) corrects for shape distortion and minimizes mathematical assumptions, the
method of discs is the recommended technique for volumetric measurements of the
left ventricle, particularly in those patients with regional wall motion abnormality.
Echocardiographic evaluation of left ventricular diastolic function
When we consider pulmonary artery catheterization, it is useful to assess
global cardiac function. However, since it cannot directly measure LV pressure,
volume or transmitral flow, its ability to measure diastolic function is limited. In
contrast, echocardiography provides a safe, practical and non-invasive means to
evaluate diastolic function.
Doppler Echocardiographic evaluation of left ventricular filling utilises
Transmitral Doppler flow velocities (TMDF)to assess diastolic function. The TMDF
profile is obtained by placing a pulse wave Doppler sample volume at the tips of the
mitral valve. The initial rapid phase of early left ventricular filling gives the E wave.
This is followed by a period of minimal flow (diastasis)and finally late diastolic
filling due to atrial contraction.
Mitral annular motion assessed with Doppler Tissue imaging (DTI), is a
technique which utilises a low velocity high amplitude signal to eliminate high
10
Review of Literature
velocities associated with blood flow, and provides a signal with high temporal and
velocity range resolution.41
The mitral annular DTI profile has a systolic component, which is shown to
correlate with ejection fraction. It has a biphasic diastolic component that appears to
be the mirror image of TMDF profile except that the velocities are much lower in
magnitude. The initial, early diastolic tissue velocity wave, E’, begins
simultaneously with mitral inflow. E’ indicates tissue velocities associated with
changes in LV volume and is primarily influenced by the rate of myocardial
relaxation and elastic recoil. The later diastolic tissue velocity wave is A’ which
reflects LA systolic function. E’ is a relatively preload insensitive measure of
diastolic function that may be particularly useful in the perioperative period when
loading conditions vary.
Tissue Doppler imaging of the mitral annulus (E’) combined with transmitral
E wave inflow pattern can predict left ventricular mean diastolic pressures. A
compliant ventricle has an E/E’ value of 8. Ventricles with high mean filling
pressures and poor compliance will have an E/E’ greater than 15.37,42,43
Evaluation of RV Global and Regional Function
During the evaluation of a critically ill patient, assessment of RV size and
function may shed light on the presence or physiologic consequences of pathology,
such as RV infarction, pulmonary embolus, loculated pericardial effusion, and
extracardiac pathology such as masses that may be impinging on the right ventricle.
RV size on TEE is often assessed visually and considered normal if less than two
thirds the diameter of the LV.44
Assessment of preload
Pulmonary artery catheters measure a pressure, which is an indirect
assessment of preload. In addition, in a ventilated critically ill patient, the correlation
between pressures and volumes is unreliable. TEE however gives an assessment of
left ventricular volume which is a direct measure of preload. Left ventricular volume
on TEE can be assessed as a one time -measure or as a continuous monitor to assess
11
Review of Literature
fluid responsiveness. The various measures used include left ventricular end -
diastolic volume, left ventricular end diastolic area, superior vene caval collapsibilty,
inferior vene caval size and fluid responsiveness.42,45,46,47
Guidelines for indications of TEE
The 2010 practice guidelines for perioperative transoesophageal
echocardiography by the American Society of Anaesthesiologists and the Society of
Cardiovascular Anaesthesiologist Task Force recommended that TEE be used in
non-cardiac surgery when the nature of the planned surgery or the patient’s known
or suspected cardiovascular pathology might result in severe hemodynamic,
pulmonary, or neurologic compromise. If equipment and expertise are available,
TEE should be used when unexplained life-threatening circulatory instability
persists despite corrective therapy. For critical care patients, TEE should be used
when diagnostic information that is expected to alter management cannot be
obtained by transthoracic echocardiography or other modalities in a timely manner.
Regarding contraindications for TEE, they recommended the TEE may be used for
patients with oral, esophageal, or gastric disease, if the expected benefit outweighs
the potential risk, provided the appropriate precautions are applied. These
precautions may include the following: considering other imaging modalities (e.g.,
epicardial echocardiography), obtaining a gastroenterology consultation using a
smaller probe, limiting the examination, avoiding unnecessary probe manipulation,
and using the most experienced operator.48
The European Association of Echocardiography updated their
recommendations for use of transoesophageal Echocardiography in 2010 to state
that TEE may be used in patients undergoing specific types of major surgery where
its value has been repeatedly documented. These include neurosurgery at risk from
venous thromboembolism liver transplantation, lung transplantation, and major
vascular surgery, including vascular trauma. It also recommended that TEE may be
used may be used in patients undergoing major non-cardiac surgery in whom severe
or life-threatening haemodynamic disturbance is either present or threatened. TEE
may be used in major non-cardiac surgery in patients who are at a high cardiac risk,
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Review of Literature
including severe cardiac valve disease, severe coronary heart disease, or heart
failure. They also noted that major complications of TEE, including esophageal
trauma were rare.49
Role of TEE in non-cardiac surgery
TEE has become a standard intraoperative monitor in patients undergoing
cardiac surgery.50,51
It is now being used increasingly in non-cardiac surgery as
well.52
It has been used to visualise intracaval thrombus in surgery for renal
carcinoma with vene caval thrombus.53
It has been used in lung transplant
surgery54,55
and in liver transplant surgery.56
AIMS AND OBJECTIVES
13
Aims and Objectives
AIMS AND OBJECTIVES
The present study has the following aims and objectives;
1. To assess the utility of transesophageal echocardiography in detecting causes
of hemodynamic instability that may occur during neurosurgical operations.
2. To identify the common TEE findings that may be associated with the
hemodynamic disturbances.
3. To identify the causes of hemodynamic instability that occur during
neurosurgical procedures.
MATERIALS AND METHODS
14
Materials and Methods
MATERIALS AND METHODS
The study was designed as a prospective pilot observational study in patients
undergoing craniotomy for major neurosurgical interventions. The primary objective
was to study the various causes of hemodynamic instability that may occur in
elective neurosurgical patients using Transesophageal Echocardiography parameters.
It was conducted over a period of one year from June 2015 to May 2016.
This study was approved by the Institutional Ethics Committee (IEC) and
written informed consent was obtained from all the participants of the study. The
total number of patients recruited was sixty-three.
The following were the inclusion and exclusion criteria.
Inclusion criteria
Patients planned for major neurosurgical interventions (surgery lasting more
than 4 hours, where hemodynamic fluctuations are anticipated)
Age > 18 years
Male and female patients
Exclusion criteria
Patient refusal
Patient incompetent to give consent
Emergency surgery
Abnormal neck flexion and abnormal neck rotation. (less than 3 finger
breadth between mentum and upper end of sternum and less than 3 finger breadths
between lower border of body of mandible and ipsilateral clavicle)
Any contraindication for insertion of the TEE probe (history of (H/O)
dysphagia, odynophagia, H/O active upper gastro intestinal bleed, documented cases
15
Materials and Methods
of esophageal stricture, esophageal mass, tracheoesophageal fistula, perforated
viscus, H/O esophageal surgery, abnormal coagulation parameters, cervical spine
disease)
Pregnant and nursing women
Detailed description of the study protocol
Written informed consent was taken by the principle investigator during the
preoperative visit the day before the surgical procedure.
Fasting consists of 8 hours for all foods as per our hospital protocol.
Premedication consists of only the anti-epileptic drugs, steroids, cardiac
medications, and thyroid replacement medications the patient already was receiving
in the morning at 6 AM with sips of water. No other drugs were administered.
On arrival in the operating suite, standard monitors like electrocardiogram,
noninvasive blood pressure cuff, pulse oximetry (SpO2) were attached and baseline
heart rate (HR), non-invasive blood pressure (NIBP) and SpO2 were noted. (Philips
Intellivue, MX700, Philips Medizin systems, Germany) An 18-gauge intravenous
cannula was placed after infiltration of local anaesthesia (2% lignocaine) and an
infusion of 2ml/kg of Ringer Lactate was started. An arterial line was placed in the
radial artery and arterial blood pressure (ABP) was transduced and continuously
monitored.
General anaesthesia was then induced using a standard protocol. The patient
was preoxygenated with oxygen at 6L/min for three minutes. The patient was then
induced with fentanyl 2 mcg/kg, propofol 1-2mg/kg and then paralyzed with an
intermediate acting muscle relaxant (vecuronium) dosed at 0. 1 mg/kg. After oral
intubation with an appropriate sized tube (8. 5 cuffed for males and 7. 5 cuffed for
females), the patient was connected to the ventilator (Aestiva /5, Datex -Ohmeda).
Mechanical ventilation was instituted in volume-controlled mode with a square
wave (constant inspiratory flow) adjusted to obtain a PaCO2 of 35- 40 mm Hg
during surgery and a minimum PEEP (positive end expiratory pressure) of 5 cm of
H2O. The patient was maintained on an oxygen to air ratio of 1:1 and a minimum
16
Materials and Methods
alveolar concentration (MAC) of sevoflurane of 0. 8 -1. An infusion of fentanyl with
vecuronium was started with an infusion rate of 1mcg/kg /hr of fentanyl and 0. 01 to
0. 02 mg/kg /hr of vecuronium.
An arterial line was placed in the radial artery and invasive arterial blood
pressure was continuously monitored. Additional monitoring after endotracheal
intubation consisted of end tidal carbon-dioxide (EtCO2), end tidal anesthetic gas
concentration, ventilator parameters like tidal volume, airway pressure, arterial
blood gas analysis, blood loss, total fluids administered and hourly urine output.
The transesophageal probe was then placed after adequate lubrication with
lubricant jelly and application of a bite block. (GE Vivid 7 with 9T 4. 0-10. 0 MHz
multiplane TEE probe, GE Healthcare, Wauwatosa, WI 53226, USA) The patient
was then positioned for surgery and skull pinning. Fentanyl 1mcg /kg and propofol
0. 5 mg /kg were given for pinning of the skull. A blanket and warming system (Bair
Hugger Warming system, Augustine Medical, USA) were placed to avoid
hypothermia.
Baseline hemodynamic variables measured were heart rate, systolic blood
pressure and mean arterial pressure. Baseline recording of TEE derived variables
were recorded as per standard ASA/ASE guidelines. Transesophageal
Echocardiography derived readings of left ventricular internal diameter end systolic
(LVIDS) and left ventricular internal diameter end diastole (LVIDD), left ventricular
end diastolic volume (LVEDV) and left ventricular end systolic volume (LVESV),
ejection fraction (EF), stroke volume (SV), cardiac output (CO), presence of
regional wall motion abnormality (RWMA), E/A, E’/A’ and E/E’, presence of
tricuspid or mitral regurgitation , patent foramen ovale or Atrial Septal defect, and
Superior and Inferior vene cava diameter were noted using the echo machine.
Airway pressure at the time of the readings was also noted.
.
HEMODYNAMIC PARAMETERS
1. Heart rate (HR)
2. Systolic Blood Pressure (SBP)
17
Materials and Methods
3. Mean Arterial Pressure (MAP)
TRANSESOPHAGEAL ECHOCARDIOGRAPHIC PARAMETERS
1. Right ventricular preload
1. Superior Vene Cava Collapsibility Index (SVC-CI)
A collapsibilty index above 36% could predict a significant increase
in cardiac output after blood volume expansion with a sensitivity of
90% and a specificity of 100%.57
2. Inferior Vene Cava Collapsibility Index (IVC-CI)
More than 50% collapse implies significant low preload
2. Left ventricular preload
1. Left ventricular end diastolic volume (LVEDV)
(men- 67-155ml, women -56-104ml)58
2. E/E’- a ratio of less than 8 is associated with normal filling pressures,
whereas a ratio of greater than 15 is associated with increased filling
pressures. 59
3. Stroke volume variation (SVV)-
Normal range is 10-15%.
3. Right ventricular contractility
Tricuspid Annular plane systolic excursion (TAPSE)
Normal values- 1. 5 to 2cms
4. Left ventricular contractility
1. Cardiac Output (normal value- 4 to 8 l/min)
2. Stroke Volume (normal value -60 to 100ml/beat)
3. Ejection Fraction (EF) (normal value-55 to 70%)
5. Left ventricular afterload
Systemic vascular resistance. (SVR) (normal value- 800 to 1200
dynes/sec/cm-5
18
Materials and Methods
Echocardiographic (TEE) based evaluation and measurements
1. Midesophageal Four Chamber View (ME 4C)
Figure 1: Midesophageal Four Chamber View (ME 4C)
With the imaging angle at 0 to 10 degrees, the sector depth at 12-14 cms and
with the TEE probe in neutral, the four chamber view was obtained. The probe was
advanced to a depth of 30 to 35cm until it was immediately posterior to the left
atrium. The probe was turned to the left (counter clockwise rotation of the probe) to
center the mitral valve (MV). Clockwise rotation of the probe (turning it to the right)
would center the left ventricle in the sector display. The multiplane angle was
adjusted to 10 to 20 degrees until the aortic valve (AV) or the left ventricular
outflow tract (LVOT) was not visualized and the tricuspid annular dimension was
maximized. The key structures observed here were the left atrium, the left ventricle,
19
Materials and Methods
the right atrium, right ventricle, tricuspid and mitral valves, and the septal and lateral
walls of the myocardium.
In this view we measured left ventricular end diastolic volume (LVEDV),
left ventricular end systolic volume (LVESV), left ventricular internal diameter end
diastolic (LVIDD) and left ventricular internal diameter end systolic (LVIDS). In the
ME four chamber view, short loops were saved and end -systolic and end diastolic
frames were identified. End-diastole was defined as the largest left ventricular cross-
sectional area immediately after R-wave peak in the echocardiogram. End-systole
was defined as the smallest left ventricular cross-sectional area immediately after the
end of the T wave. The endocardial borders were traced, starting at the medial or
anterior mitral annulus and finishing at the lateral or posterior mitral annulus. We
obtained non foreshortened views of the left ventricle so as to visualize the true apex
and prevent underestimation of volumes. Left ventricular volume was calculated
using Simpsons method. In this method, the LV is described as a series of 20 discs
from the base to the apex of the left ventricle, like a stack of coins with decreasing
size. The computer software package calculated the volume of each disc as area
multiplied by height and the volumes were summated to give total left ventricular
volume.
20
Materials and Methods
Figure 2: Calculation of LV volume using Simpsons Method
Ejection fraction
is the proportional change in LV volume during systole, expressed in %.
EF = (SV/LVEDV) X 100 where,
SV = (LVEDV- LVESV)/LVEDV
Normal ranges: LVEDV 80 to 180 ml, LVESV 30 to 90 ml, EF 55 to 75%
This view was also used to evaluate left ventricular filling Transmitral
Doppler Flow (TMDF) which provides information about diastolic function. The
sample volume was placed at the mitral valve leaflets to obtain pulse wave Doppler
(PWD) recordings of TMDF velocities. During early diastolic filling, an initial peak
flow velocity (E wave) occurs: a later peak flow velocity (A wave) occurs during
atrial systole. Normal values of E/A are 1 -3 in patients less than 30 years and 0. 7-1.
3 in patients greater than 60 years.
Tissue Doppler imaging (TDI) also was used to assess diastolic filling. This
measures the velocity of the myocardium which is displayed as a spectral pulse
wave (PW) signal or as a color map. In the four chamber view, a PW Doppler
sample volume is positioned on the lateral corner of the mitral annulus. It should be
aligned as parallel as possible to the longitudinal axial motion of the LV.
The mitral annular DTI profile has a biphasic diastolic component wherein
the initial early diastolic tissue velocity (E’) begins simultaneously with mitral
inflow and reflects tissue velocities associated with changes in left ventricular
volume. The later Diastolic tissue velocity A’ tends to reflect Left atrial systolic
function. In this way, we calculated E’/A’ and E/E’.
Presence of a regurgitant jet across the mitral or tricuspid valve was assessed
by Colour flow Doppler.
21
Materials and Methods
Figure 3: Assessment of E/A ratio
Figure 4: Assessment of E’/A’ and E/E’
22
Materials and Methods
Tricuspid annular plane systolic excursion (TAPSE)
When the right ventricle contracts during systole, it decreases in both its
short and long axis dimensions. The magnitude of shortening of the long axis of the
right ventricle is termed TAPSE. This is a useful measure of global RV systolic
function. In the ME four chamber view, long axis shortening is normally more than
25 mm. Clinically, this is seen as descent of the tricuspid annulus.
Figure 5: Showing TAPSE assessment
2. Midesophageal Aortic Valve Long -Axis (ME LAX) view.
This view was obtained by rotating the imaging angle to approximately 110
to 130 degrees and a sector depth of 8 to 10 cm with the probe in neutral position.
The important structures seen here are the left ventricular outflow tract (LVOT),
aortic valve (AV) and the ascending aorta. The stroke volume (SV), cardiac output
(CO) and stroke volume variation are measured at the LVOT. The aortic valve
diameter was recorded in this view.
23
Materials and Methods
Figure 6: Midesophageal Aortic Valve Long Axis View
3. Deep Transgastric aortic long axis view:
The probe was pushed into the deep Transgastric position and the angle was
rotated to 80-90 degrees to bring the aortic long axis view. The pulse wave Doppler
cursor was placed 5 mm below the level of aortic valve. The Doppler recordings
were obtained with low speed (16 mm /sec) to depict both the high and low height of
the wave tracing in the same respiratory cycle. The stroke volume was calculated
from multiplying the aortic valve cross sectional area with the velocity time integral
(VTI) by tracing the systolic flow both at the high and low waves.
The pulsed wave Doppler sample is positioned in the LVOT immediately
proximal to the aortic valve to calculate the stroke volume and cardiac output using
the software provided in the ECHO machine.
Cardiac output= Stroke volume x Heart rate.
24
Materials and Methods
Figure 7: Showing Deep Transgastric aortic long axis view
Calculation of stroke volume variation (SVV)
SVV is the variation of beat-to-beat SV from the mean value during a single
respiratory cycle and is calculated as
SVV = (SVmax - SVmin)/SVmean
We also assessed presence /absence of aortic regurgitation by Colour flow
Doppler.
25
Materials and Methods
Figure 8 Showing calculation of stroke volume
Figure 9 Showing stroke volume variation
26
Materials and Methods
Calculation of Systemic Vascular resistance (SVR)
Systemic vascular resistance refers to resistance offered to blood flow by the
systemic vasculature.
SVR= {(Mean arterial pressure- central venous pressure)/cardiac output} X 80
3. Midesophageal Bicaval View
This view was obtained by turning the probe further to the patients right at an
angle of 105 to 120 degrees and a sector depth of 8 to 10 cms with the probe in
neutral. Structures visualized in this view include the left atrium, the right atrium,
right atrial appendage and the inter atrial septum (IAS), superior vene cava and
inferior vene cava. Colour Doppler of the IAS can be used to detect an inter-atrial
shunt or a patent foramen ovale.
Using the Colour Doppler flow across the IAS, we were able to detect presence
/absence of patent foramen ovale or atrial septal defect. We also used this view if we
suspected venous air embolism in any patient.
Anatomical M-mode was used to measure the diameters of the superior vene
cava (SVC) and the inferior vena cava (IVC) by adjusting the probe position
cranially or caudally. The SVC diameters measured were the maximum diameter on
expiration (SVCmax) and minimum diameter on inspiration (SVC min). The
measurements were done during the same respiratory cycle. Average of two values
were used for statistical purposes.
27
Materials and Methods
Figure 10 Showing ME Bicaval View
Superior vena cava collapsibility index (SVCCI)
Calculation of SVC collapsibility index is done by using the formula:
SVC collapsibility index = [(SVCmax – SVCmin)/ (SVCmax)] X 100%
Figure 11 Showing SVC Collapsibility index
28
Materials and Methods
Inferior vena cava collapsibility index (IVCCI)
The IVC diameters measured were the maximum diameter on expiration
(IVCmax) and the minimum diameter on inspiration (IVC min). The measurements
were done during the same respiratory cycle. Average of two values were used for
statistical purposes.
Inferior vena cava collapsibility index (IVCCI)
Calculation of IVC collapsibility index is done by using the formula:
IVC collapsibility index = [(IVCmax – IVCmin)/ (IVCmax)] X 100%
Figure 12 Showing IVC collapsibility index
5. Trans gastric Basal short axis view
This view is with the probe at an angle of 0 degrees and a sector depth of 12
cm with the probe neutral to ante flexed. The structure seen are the mitral leaflets,
29
Materials and Methods
the mitral subvalvular apparatus and the left ventricle (basal segments). This view
was used to detect left ventricular systolic dysfunction in the basal segments or any
mitral valve pathology.
Figure 13 Showing Trans gastric Basal short axis view
6. Trans gastric mid-papillary short axis view
This view is with the probe of the TEE at an angle of 0 degrees and a sector
depth of 12 cm with the probe in the ante flexed position. This view shows the left
ventricular walls, the left ventricular cavity and the papillary muscles. It can be used
to diagnose left ventricular hypertrophy, left ventricular enlargement systolic
dysfunction and mid segment left ventricular regional wall motion abnormality.
The TEE derived values were used to ascertain the cause of the
hemodynamic instability as well as the need for management of the episodes. If
there was reduction in the preload, fluids/blood were administered as appropriate, if
there was increase in LV preload or reduced myocardial contractility, inotrope
support was planned. If there was reduction in the after load, vasopressors and if any
30
Materials and Methods
increase in after load increasing inhalational anesthetic concentrations/analgesics
were planned, as administration of vasodilators can increase the intracranial
pressure. We noted the surgical step (pinning, positioning, skin to dura, dissection of
tumor, or closure) and anesthetic step (induction, maintenance and emergence) at the
time of each reading. Any untoward event like venous air embolism or paradoxical
air embolism was also noted. We averaged two readings per patient. The probe was
removed at the end of the surgery before extubation of the patient.
We defined hemodynamic instability as a change of + 20% of heart rate or
blood pressure from the baseline. These episodes were defined as hypotension or
hypertension when the change in systolic blood pressure or mean arterial pressure
was 20% less than baseline or 20% more than baseline respectively. Bradycardia
was defined as an episode where the heart rate decreased to 20% below baseline. An
episode where heart rate increased to 20% or more from the baseline was defined as
tachycardia. For occurrence of each episode of hemodynamic instability, TEE was
used immediately to identify the changes and to ascertain the cause of hemodynamic
instability. TEE derived variables were classified to focus on the changes in preload
of the heart, myocardial contractility and after load.
STATISTICAL ANALYSIS
31
Statistical Analysis
STATISTICAL ANALYSIS
Power of the Study: This is a prospective pilot observational study involving the
patients who are scheduled to undergo major neurosurgical procedures. Literature
search did not show similar studies and the true incidence of significant
hemodynamic changes occurring intraoperatively could not be obtained. Hence
sample size could not be calculated. We have designed the study as a pilot study to
include patients who met the inclusion and exclusion criteria during the period 2015-
16 in our hospital.
Statistical analysis was done using SPSS software version 21 (IBM SPSS
statistics, Chicago USA) The demographic data like age, weight, body surface area
etc was analyzed using descriptive statistics and the results were expressed as mean+
standard deviation (SD). The changes in hemodynamic variables like heart rate,
systolic blood pressure and mean arterial pressures were calculated for % deviation
from baseline. Episodes with more than+ 20% change were considered significant
and were grouped separately for HR, SBP and MAP. Episodes without significant
change were grouped separately. For each variable (HR, SBP and MAP) chi square
test was used to test the significant changes in each of the TEE variables measured
between those who had significant change versus no significant change. A ‘p’ value
of <0. 05 was taken as statistically significant.
RESULTS AND OBSERVATION
32
Results and Observations
RESULTS AND OBSERVATIONS
This prospective pilot observational study was conducted over a period of
one year from June 2015- May 2016.
During this period, we recruited 63 eligible patients. In all the patients TEE
examination could be done successfully. There were no intraoperative and
postoperative complications related to TEE.
The baseline measurements in each patient included age, gender, weight,
height, body surface area, diagnosis and surgery, intraoperative position,
preoperative medication, preoperative echocardiography findings, baseline heart rate
and blood pressure and baseline TEE recordings.
Out of the 63 patients, a total of 137 episodes of significant hemodynamic
changes in heart rate and blood pressure occurred. There was a mean of two
episodes per patient (ranging from zero episodes to seven episodes per patient)
We defined hemodynamic changes in heart rate and blood pressure as follows
1. Group 0- change in heart rate or blood pressure within 20% from baseline.
2. Group 1- change in heart rate or blood pressure were below 20% from baseline
3. Group 2- change in heart rate or blood pressure were above 20% from baseline
Changes in TEE parameters were defined as follows:
1. WNL- changes in parameter within 10% from baseline.
2. DEC- changes in parameter below 10% from baseline.
3. INC- changes in parameter above 10% from baseline
We compared each group of changes in hemodynamic parameters (Group 0, Group
1, Group 2) with changes in transoesophageal parameters.
33
Results and Observations
TABLE 1: DEMOGRAPHICS
TABLE 2: ETIOLOGY
ETIOLOGY NUMBER %
Tumour 43 68. 3
Epilepsy 8 12. 7
Aneurysm 8 12. 7
AVM 3 4. 7
Abscess 1 1. 6
TABLE 3: PREOPERATIVE ECHOCARDIOGRAPHY DATA
(TRANSTHORACIC)
SL NO PREOP ECHO NUMBER %
1 NORMAL 28 44. 44
2 ABNORMAL 16 25. 39
3 NOT DONE 18 28. 57
DEMOGRAPHIC MEAN +/- SD
Age (years) 42+/- 11
Weight (kg) 61+/-8
Height cms) 161+/-7
BSA (m2)
1. 64+/-0. 14
Male: Female 34:29
34
Results and Observations
TABLE 1 shows the demographic data of the patients who were part of our study.
The mean age was 42+/- 11years, weight was 61 +/- 8 kg and height was 161+/- 7
cms and body surface area was 1. 64+/- 0. 14 m2. There were 34 males and 29
females.
Table 2 shows the etiology for which the patients were operated. The majority of
the patents were operated for tumour (68. 3%). There were eight patients each
operated for epilepsy and aneurysm surgery, three patients for AVM and one patient
for brain abscess.
POSITION
Out of 63 patients, 82. 5% (n=52), were operated in the supine position. 12. 6%
(n=8) were operated in the lateral position. One patient was operated in the prone
position and two patients in the sitting position.
Table 3 shows the preoperative echocardiographic data. Twenty eight patients had
normal echocardiograms, and sixteen patients had abnormal echocardiograms
35
Results and Observations
FIGURE 14: PREOPERATIVE ECHOCARDIOGRAPHY DATA
(TRANSTHORACIC)
TABLE 4: BASELINE HEMODYNAMIC DATA
.
TABLE 5: NUMBER OF PATIENTS WITH HEMODYNAMIC CHANGES
Variable +20% increase -20% decrease No change
HR 27 5 105
SBP 10 20 107
MAP 19 21 97
PARAMETER MEAN +/- SD
MEAN HR 69. 71+/-11. 2
MEAN SBP 121. 16+/-10. 24
MEAN MAP 86. 4+/-9. 76
PREOPERATIVE ECHO
NORMAL
NOT AVAILABLE
VALVULAR DYSFUNCTION
GRADE 1 DIASTOLICDYSFUNCTION
CONCENTRIC LVH
36
Results and Observations
Figure 14 shows the preoperative echocardiograms with the reasons for the
abnormal echocardiograms. There were 16 subjects with abnormal preoperative
transthoracic echocardiography. Of them, 14 had valvular dysfunction, 8 had grade 1
diastolic dysfunction, and one patient each had Takotsubo cardiomyopathy and mild
concentric left ventricular hypertrophy.
Baseline hemodynamic data is shown in Table 4. The mean baseline heart rate was
69. 7+/-11. 2 . Beats /min, mean SBP was 121. 16+/-10. 24 mm Hg and mean MAP
was 86. 4+/- 9. 76 mm Hg.
Table 5 shows the number of patients with hemodynamic changes.
Each one of the variables (HR, SBP, MAP) were analysed for corresponding
changes in echocardiographic parameters. Out of 137 episodes, there were 27
episodes of tachycardia and 5 episodes of bradycardia. In 105 episodes, there was
less than 20% change from the baseline heart rate.
10 episodes showed an increase in systolic blood pressure and there were 20
episodes of decreased systolic blood pressure.
There were 19 episodes of increase in mean arterial pressure and 21 episodes of
decrease in mean arterial pressure.
37
Res
ult
s an
d O
bse
rvati
on
s
TA
BL
E 6
: S
HO
WIN
G D
EC
RE
AS
E I
N H
EA
RT
RA
TE
WIT
H P
RE
LO
AD
PA
RA
ME
TE
RS
HR
N
um
ber
(%)
SV
CC
I
- in
c
SV
CC
I-
dec
SV
CC
I
NC
IVC
CI
-in
c
IVC
CI
-dec
IVC
CI-
no
cha
ng
e
ED
V-
inc
ED
V-
dec
ED
V-n
o
cha
ng
e
E/E’-
inc
E/E’-
dec
E/E’-
no
cha
ng
e
SV
V-
INC
SV
V
-DE
C
SV
V N
O
CH
AN
GE
NC
1
05
(9
5.
5)
42
(40
)
47
(45
)
15
(14
)
34
(32
.
4)
48
(46
)
17
(16
. 2)
27
(25
. 7
)
51
(48
. 6
)
23
(22
)
41
(39
) 3
5
(33
)
25
(24
)
26
(25
)
44
(42
)
29
(26
. 7
)
dec
5
(4.
5)
1
(0.
9)
2
(1.
8)
2
(1.
8)
0
5
(4.
5)
0
1
(0.
9)
2
(1.
8)
2
(1.
8)
2
(1.
8)
2
(1.
8)
1
(0.
9)
1
(20
)
3
(60
)
1
(20
)
P
0
. 4
5
0.
13
0.
8
0.
9
0.
8
TA
BL
E 7
: S
HO
WIN
G D
EC
RE
AS
E I
N H
EA
RT
RA
TE
WIT
H C
ON
TR
AC
TIL
ITY
AN
D A
FT
ER
LO
AD
HR
N
um
ber
(%)
TA
PS
E
PR
ES
E
NT
TA
PS
E
AB
SE
NT
CO
-
inc
CO
-
dec
CO
-NC
S
V-i
nc
SV
-dec
S
V-
NC
EF
-in
c
EF
-dec
E
F-N
C
RW
MA
pre
sen
t
RW
MA
ab
sen
t
SV
R
inc
SV
R
dec
SV
R-
NC
NC
1
05
(9
5.
5)
0
(0)
10
5
(10
0)
39
(37
)
39
(37
)
25
(24
)
34
(32
. 4
)
35
(33
. 3
)
34
(32
.
4)
22
(21
)
41
(39
)
40
(38
)
0
(0)
10
5
(10
0)
34
(32
)
46
(44
)
22
(21
)
DE
C
5
(4.
5)
0
(0)
5
(10
0)
2
(2.
7)
2
(2.
7)
1
(0.
9)
1
(0.
9)
3
(2.
7)
1
(0.
9)
1
(0.
9)
2
(1.
8)
2
(1.
8)
0
(0)
5
(10
0)
1
(0.
9)
3 (
2.
7)
1 (
0.
9)
P
0.
9
0.
6
0.
9
0
. 8
8
KE
Y:
INC
- IN
CR
EA
SE
, D
EC
- D
EC
RE
AS
E,
NC
-NO
CH
AN
GE
38
Results and Observations
DECREASE IN HEART RATE COMPARED WITH PRELOAD (TABLE 6)
Table 6 shows episodes with change in heart rate with preload compared with
episodes where there was no change in heart rate with preload. Episodes with a
decrease in heart rate were more likely to show a decrease in preload
echocardiographic values. 60% of episodes with decreased heart rate had decreased
stroke volume variation (SVV)compared to 20% with increase or no change in SVV.
1. 8% of episodes showed decrease in E/E’ compared to 0. 9% of episodes with no
change in E/E’. All episodes showed a decrease in IVC-CI with bradycardia. 1. 8%
of episodes of bradycardia were associated with decrease in SVC-CI compared to 0.
9% of episode with increase SVC-CI. However, the numbers were too small to be
statistically significant.
DECREASE IN HEART RATE WITH CONTRACTILITY AND
AFTERLOAD (TABLE 7)
Table 7 shows that episodes with decrease in heart rate were more likely to have a
decrease in cardiac output than no change in cardiac output. (2. 7% versus 1. 9%)
They were also more likely to have a decreased or normal ejection fraction n than an
increased ejection fraction. (1. 8% versus 0. 9%).
Interestingly, patients with no change in heart rate also were more likely to show a
decrease or normal ejection fraction than an increased ejection fraction.
Episodes with a decrease in heart rate were more likely to show a decrease in
systemic vascular resistance (2. 7%) than an increase or no change in SVR. (0. 9%)
Patients with no change in heart rate were also more likely to have a decrease in
systemic vascular resistance than no change in SVR. (44% versus 21%). However,
the results were not statistically significant.
39
Res
ult
s an
d O
bse
rvati
on
s
TA
BL
E 8
: S
HO
WIN
G I
NC
RE
AS
E I
N H
EA
RT
RA
TE
WIT
H P
RE
LO
AD
PA
RA
ME
TE
RS
HR
N
um
ber
(%)
SV
CC
I-
inc
SV
CC
I-
dec
SV
CC
I
NC
IVC
CI-
inc
IVC
CI-
dec
IVC
CI-
no
cha
ng
e
ED
V-
inc
ED
V-
dec
ED
V-
no
cha
ng
e
E/E’-
inc
E/E’-
dec
E/E’-
no
cha
ng
e
SV
V-
INC
SV
V -
DE
C
SV
V N
O
CH
AN
GE
NC
1
05
(79
. 5
)
42
(40
)
47
(45
)
15
(14
)
34
(32
)
48
(45
. 7
)
17
(16
. 2
)
27
(26
)
51
(48
. 6
)
23
(22
)
41
(39
)
35
(33
. 3
)
25
(24
)
26
(25
)
44
(42
)
29
(26
. 7
)
INC
2
7
(20
. 5
)
15
(55
. 6
)
10
(37
)
2
(7.
4)
9
(33
. 3
)
11
(40
)
6
(22
. 2
)
7
(26
)
16
(59
)
4
(15
)
9
(33
)
15
(56
)
3
(11
)
10
(38
. 5
)
4
(15
)
10
(38
. 5
)
P
0
. 4
0.
8
0.
5
0.
1
0.
09
TA
BL
E 9
: S
HO
WIN
G I
NC
RE
AS
E I
N H
EA
RT
RA
TE
WIT
H C
ON
TR
AC
TIL
ITY
AN
D A
FT
ER
LO
AD
HR
N
um
ber
(%)
TA
PS
E
PR
ES
E
NT
TA
PS
E
AB
SE
N
T
CO
-
inc
CO
-
dec
CO
-
NC
SV
-in
c
SV
-dec
S
V-
NC
EF
-
inc
EF
-
dec
EF
-NC
R
WM
A
pre
sen
t
RW
MA
ab
sen
t
SV
R
inc
SV
R
dec
SV
R-
NC
NC
1
05
(95
. 5
)
0
(0)
10
5
(10
0)
39
(37
)
39
(37
)
25
(24
)
34
(32
. 4
)
35
(33
. 3
)
34
(32
. 4
)
22
(21
)
41
(39
)
40
(38
)
0
(0)
10
5
(10
0)
34
(32
)
46
(44
)
22
(21
)
IN C
27
(20
. 5
)
0
(0)
27
(10
0)
12
(45
)
8
(30
)
7
(26
)
4
(15
)
13
(48
)
10
(37
)
11
(40
)
11
(40
)
5
(18
. 5
)
0
(0)
27
(10
0)
11
(40
. 7
)
11
(40
. 7
)
5
(18
. 5
)
P
0.
7
0.
2
0.
09
0
. 7
40
Results and Observations
INCREASE IN HEART RATE COMPARED WITH PRELOAD (TABLE 8)
Table 8 shows that more episodes of tachycardia had an increase in SVV (38. 5%)
compared to decrease in SVV (15%). 55. 6% of episodes with increased heart rate
had an increase in SVC-CI compare to 37% with decrease in SVC-CI and 7. 4%
with no change in SVC-CI.
INCREASE IN HEART RATE COMPARED WITH CONTRACTILITY AND
AFTERLOAD (TABLE 9)
Table 9 shows that episodes with an increase in heart rate were more likely to have
an increase in cardiac output (45%) but a normal or decrease in stroke volume. 37 %
of the episodes had no change in stroke volume while only 15% had an increase in
SV.
41
Results and Observations
TABLE 10: SHOWING DECREASE IN SBP WITH PRELOAD PARAMETERS
SBP NUMBER
(%)
SVCCI-
INC
SVCCI-
DEC
SVCCI
NC
IVCCI-
INC
IVCCI-
DEC
IVCCI-
NO
CHANGE
EDV-
INC
EDV-
DEC
EDV-NO
CHANGE
E/E’-
INC
E/E’-
DEC
E/E’-NO
CHANGE
SVV-
INC
SVV
-DEC
SVV NO
CHANGE
NC 107 (84. 3)
47 (44)
47 (44)
12 (11)
33 (31)
47 (44)
20 (18. 5)
26
(24. 3)
51
(47. 7)
26 (24. 3)
46
(43)
37
(35)
20 (18)
26
(24. 3)
44
(41)
29 (27)
DEC 20 (15. 7) 4 (20) 11 (55) 5 (25) 5 (25) 14 (70) 1 (5) 5 (25) 13
(65)
2 (10) 5
(25)
9
(45)
6 (30) 6 (30) 5 (25) 9 (45)
P 0. 1 0. 1 0. 34 0. 3 0. 2
TABLE 11: SHOWING DECREASE IN SBP WITH CONTRACTILITY AND AFTERLOAD PARAMETERS
SBP Number
(%)
TAPSE
PRESENT
TAPSE
ABSENT
CO-inc CO
-
dec
CO-
NC
SV-inc SV-dec SV- NC EF-inc EF-dec EF-
NC
RWMA
present
RWMA
absent
SVR
inc
SVR
dec
SVR-
NC
NC 107
(84. 3)
0
(0)
107 (100) 38
(35. 5)
42
(39)
25
(23. 4)
27
(25)
38
(35. 5)
40
(37. 4)
29
(27)
38
(35. 5)
38
(35. 5)
0
(0)
107
(100)
37
(34. 6)
39
(36. 4)
28
(26)
DEC 20
(15. 7)
0
(0)
20
(100)
11
(55)
4
(20)
5
(25)
8
(40)
8
(40)
4
(20)
2
(10)
13
(65)
5
(25)
0
(0)
20
(100)
0 20
(100)
0
P 0. 28 0. 35 0. 86 0
42
Results and Observations
DECREASE IN SYSTOLIC BLOOD PRESSURE WITH PRELOAD (TABLE
10)
Most of the preload parameters showed a decrease with fall in systolic blood
pressure. 55% of the episodes showed a decrease in SVC-CI compared to only 20%
increase in SVC-CI. 70% of episodes showed a fall in IVC-CI compared to 25%
episodes with increase in IVC-CI. End diastolic volume showed a fall in 65% of
episodes compared to 10% of episodes where there was no change in EDV. There
was a fall in E/E’ in 45% of episodes of hypotension. In 41% of episodes with no
change in SBP, there was a decrease in Stroke volume variation.
SYSTOLIC BLOOD PRESSURE DECREASE WITH CONTRACTILITY
AND AFTERLOAD PARAMETERS (TABLE 11)
With decrease in systolic blood pressure, there was a statistically significant
decrease noted in systemic vascular resistance. There were no episodes of regional
wall motion abnormality. 65% of episodes showed a decrease in ejection fraction,
compared to 25% of episodes with no change in ejection fraction in spite of
hypotension.
43
Results and Observations
TABLE 12: SHOWING INCREASE IN SBP WITH PRELOAD PARAMETERS
SBP Number
(%)
SVCCI-
inc
SVCCI-
dec
SVCCI
NC
IVCCI-
inc
IVCCI-
dec
IVCCI-
no
change
EDV-
inc
EDV-
dec
EDV-no
change
E/E’-
inc
E/E’-
dec
E/E’-no
change
SVV-
INC
SVV -
DEC
SVV NO
CHANGE
NC 107
(84. 3)
47
(43. 9)
47
(43. 9)
12
(11)
33
(31)
47
(44)
20
(18. 7)
26
(24. 3)
51
(47. 7)
26
(24. 3)
46
(43)
37
(35)
20
(18. 7)
26
(24. 3)
44
(41)
29
(27)
INC 10
(8. 5)
7
(70)
1
(10)
1
(10)
5
(50)
3
(30)
2
(20)
4
(40)
5
(50)
1
(10)
1
(10)
6
(60)
3
(30)
2
(20)
5
(50)
2
(20)
P 0. 2 0. 5 0. 5 0. 1 0. 3
TABLE 13: SHOWING INCREASE IN SBP WITH CONTRACTILITY AND AFTERLOAD PARAMETERS
SBP Number
(%)
TAPSE
PRESEN
T
TAPSE
ABSEN
T
CO-inc CO-
dec
CO-
NC
SV-
inc
SV-dec SV-
NC
EF-
inc
EF-dec EF-NC RWMA
present
RWMA
absent
SVR
inc
SVR
dec
SV
R-
NC
NC 107
(84. 3)
0
(0)
107
(100)
38
(35. 5)
42
(39)
25
(23. 4)
27
(25)
38
(35. 5)
40
(37. 4)
29
(27)
38
(35. 5)
38
(35. 5)
0
(0)
107
(100)
37
(34. 6)
39
(36. 4)
28
(26)
INC 20
(15. 7)
0
(0)
20
(100)
4
(40)
3
(30)
3
(30)
4
(40)
5
(50)
1
(10)
3
(30)
3
(30)
4
(40)
0
(0)
20
(100)
9
(90)
1
(10)
0
P 0. 89 0. 3 0. 9 0. 008
44
Results and Observations
INCREASE IN SYSTOLIC BLOOD PRESSURE WITH PRELOAD
PARAMETERS (TABLE 12)
There were more episodes of increase in SVC-CI with increase in SBP compared to
decrease or no change. Patients with no change in SBP had equal episodes of
increase or decrease in SVC-CI. IVC-CI was also increased in 50% of episode with
increase in SBP compared to 20% of episodes where there was no change in IVC-CI
despite increase in SBP. However it did not attain statistical significance.
INCREASE IN SYSTOLIC BLOOD PRESSURE COMPARED WITH
AFTERLOAD AND CONTRACTILITY (TABLE 13)
There was a statistically significant increase in systemic vascular resistance (p =0.
008) with increase in systemic blood pressure.
45
Res
ult
s an
d O
bse
rvati
on
s
TA
BL
E 1
4:
SH
OW
ING
DE
CR
EA
SE
IN
MA
P W
ITH
PR
EL
OA
D P
AR
AM
ET
ER
S
MA
P
Nu
mb
er
(%)
SV
CC
I-
inc
SV
CC
I-
dec
SV
CC
I
NC
IVC
CI-
inc
IVC
CI-
dec
IVC
CI-
no
cha
ng
e
ED
V-
inc
ED
V-
dec
ED
V-n
o
cha
ng
e
E/E’-
inc
E/E’-
dec
E/E’-
no
cha
ng
e
SV
V-
INC
SV
V -
DE
C
SV
V N
O
CH
AN
GE
NC
9
7
(82
)
38
(39
)
49
(50
)
9
(9.
3)
30
(31
)
43
(44
. 3
)
17
(17
. 5
)
24
(24
. 7
)
47
(48
. 5
)
22
(22
. 7
)
45
(46
. 4
)
34
(35
)
14
(14
. 4
)
24
(24
)
40
(40
)
28
(28
)
DE
C
21
(17
. 8
)
7
(33
)
7
(33
)
7 (
33)
5
(24
)
16
(76
)
0
5
(24
)
12
(57
)
4
(19
)
4
(19
)
8
(38
)
9
(43
)
6
(28
. 6
)
6
(28
. 6
)
8
(38
)
P
0
. 0
3
0.
02
0.
7
0.
01
0.
6
TA
BL
E 1
5:
SH
OW
ING
DE
CR
EA
SE
IN
MA
P W
ITH
CO
NT
RA
CT
ILIT
Y A
ND
AF
TE
RL
OA
D P
AR
AM
ET
ER
S
MA
P
Nu
mb
er
(%)
TA
PS
E
PR
ES
EN
T
TA
PS
E
AB
SE
NT
CO
-
inc
CO
-
dec
CO
-
NC
SV
-
inc
SV
-
dec
SV
-
NC
EF
-in
c
EF
-
dec
EF
-NC
R
WM
A
pre
sen
t
RW
MA
ab
sen
t
SV
R
inc
SV
R
dec
SV
R-
NC
NC
9
7
(82
)
0
97
(10
0)
35
(36
)
35
(36
)
25
(26
)
24
(24
. 7
)
34
(35
)
37
(38
)
27
(27
. 8
)
34
(35
)
34
(35
)
0
97
(10
0)
32
(33
)
39
(40
. 2
)
23
(23
. 7
)
DE
C
21
(17
. 8
)
0
21
(10
0)
8
(38
)
9
(43
)
4
(19
)
8
(38
)
9
(43
)
4
(19
)
2
(9.
5)
13
(62
)
6
(28
)
0
21
(10
0)
2
(9.
5)
17
(81
)
2
(9.
5)
P
0.
8
0.
3
0.
1
0
. 0
09
46
Results and Observations
MEAN ARTERIAL PRESSURE DECREASE WITH PRELOAD
PARAMETERS (TABLE 14)
There was a statistically significant decrease in the IVC-CI in episodes with
decreased mean arterial pressure. In 57% of episodes there was a decrease in End
diastolic volume compared to 24% of episodes where there was an increase in end
diastolic volume.
MEAN ARTERIAL PRESSURE DECREASE WITH CONTRACTILITYAND
AFTERLOAD PARAMETERS (TABLE 15)
There was a statistically significant decrease in systemic vascular resistance
associated with fall in mean arterial pressure. There were more episodes of
hypotension associated with a fall in cardiac output (43%), fall in stroke volume
(43%) and fall in ejection fraction (62%).
47
Res
ult
s an
d O
bse
rvati
on
s
TA
BL
E 1
6:
SH
OW
ING
IN
CR
EA
SE
IN
MA
P W
ITH
PR
EL
OA
D P
AR
AM
ET
ER
S
MA
P
Nu
mb
er
(%)
SV
CC
I-
inc
SV
CC
I-
dec
SV
CC
I
NC
IVC
CI-
inc
IVC
CI-
dec
IVC
CI-
no
cha
ng
e
ED
V-
inc
ED
V-
dec
ED
V-
no
cha
ng
e
E/E’-
inc
E/E’-
dec
E/E’-
no
cha
ng
e
SV
V-
INC
SV
V
-
DE
C
SV
V N
O
CH
AN
GE
NC
9
7
(83
. 6
)
38
(39
)
49
(50
. 5
)
9
(9.
3)
30
(31
)
43
(44
. 3
)
17
(17
. 5
)
24
(24
. 7
)
47
(48
. 5
)
22
(22
. 7
)
45
(46
. 4
)
34
(35
)
14
(14
. 4
)
24
(24
)
40
(40
)
28
(28
)
INC
1
9
(16
. 4
)
13
(69
)
3
(16
)
3
(16
)
8
(42
)
5
(26
)
6
(31
)
6
(31
. 6
)
10
(53
)
3
(16
)
3
(16
)
10
(53
)
6
(31
. 6
)
8
(42
)
5
(26
)
4
(21
)
P
0
. 0
4
0.
2
0.
7
0.
03
0.
3
TA
BL
E 1
7 S
HO
WIN
G I
NC
RE
AS
E I
N M
AP
WIT
H C
ON
TR
AC
TIL
ITY
AN
D A
FT
ER
LO
AD
PA
RA
ME
TE
RS
MA
P
Nu
mb
er
(%)
TA
PS
E
PR
ES
EN
T
TA
PS
E
AB
SE
N
T
CO
-
inc
CO
-dec
C
O-
NC
SV
-in
c
SV
-
dec
SV
-
NC
EF
-in
c
EF
-
dec
EF
-
NC
RW
MA
pre
sen
t
RW
MA
ab
sen
t
SV
R
inc
SV
R
dec
SV
R-
NC
NC
9
7
(83
. 6
)
0
97
(10
0)
35
(36
)
35
(36
)
25
(26
)
24
(24
. 7
)
34
(35
)
37
(38
)
27
(27
. 8
)
34
(35
)
34
(35
)
0
97
(10
0)
32
(33
)
39
(40
. 2
)
23
(23
.
7)
INC
1
9
(16
. 4
)
0
19
(10
0)
10
(52
)
5
(26
)
4
(21
)
7
(37
)
8
(42
)
4
(21
)
5
(26
)
7
(37
)
7
(37
)
0
19
(10
0)
12
(63
)
4
(21
)
3
(16
)
P
0.
5
0.
4
0.
9
0
. 0
9
48
Results and Observations
INCREASE IN MEAN ARTERIAL PRESSURE WITH PRELOAD
PARAMETERS (TABLE 16)
There were more episodes of increase in MAP associated with increase in SVC-CI
(69%) and this was statistically significant. 42% of episodes showed an increase in
IVC-CI compared to 26% episodes showing a decrease in IVC-CI . Fall in mean
arterial pressure was more likely to be associated with decrease in end diastolic
volume (53%) compared to increase in end diastolic volume (31. 6%). More
episodes of hypotension were associated with a fall in E/E’ (53%),than an increase
or no change in E/E’. This finding was statistically significant.
INCREASE MEAN ARTERIAL PRESSURE WITH AFTERLOAD AND
CONTRACTILITY PARAMETERS (TABLE 17)
There was a statistically significant increase in systemic vascular resistance
associated with an increase in mean arterial pressure. There were more episodes of
increase in cardiac output (52%) associated with increase in MAP.
49
Res
ult
s an
d O
bse
rvati
on
s
TA
BL
E 1
8:
SH
OW
ING
CH
AN
GE
IN
HE
MO
DY
NA
MIC
S W
ITH
PR
EL
OA
D P
AR
AM
ET
ER
S
HD
N
um
ber
(%)
SV
CC
I-in
c
SV
CC
I-d
ec
SV
C
CIN
C
IVC
CI
-in
c
IVC
C
I-d
ec
IVC
C
I-n
o
cha
ng
e
ED
V-
inc
ED
V-
dec
ED
V-
no
cha
ng
e
E/E’-
inc
E/E’-
dec
E/E’-
no
cha
ng
e
SV
V-
INC
SV
V -
DE
C
SV
V N
O
CH
AN
GE
NC
7
4
(54
%)
29
(39
)
37
(50
)
7
(9.
5)
24
(32
. 4
)
31
(42
)
13
(17
. 6
)
18
(24
)
33
(45
)
19
(26
)
36
(48
. 6
)
21
(28
. 4
)
13
(17
. 6
)
16
(1.
6)
35
(47
)
18
(24
)
CH
A
NG
E
63
(46
%)
29
(46
)
22
(35
)
12
(19
)
19
(30
)
33
(52
)
10
(16
)
17
(27
)
36
(57
)
10
(16
)
16
(25
. 4
)
31
(49
. 2
)
16
(25
. 4
)
21
(33
. 3
)
16
(25
. 4
)
22
(35
)
P
0
. 1
5
0.
16
0.
2
0.
004
0.
06
TA
BL
E 1
9:
SH
OW
ING
CH
AN
GE
IN
HE
MO
DY
NA
MIC
S W
ITH
CO
NT
RA
CT
ILIT
Y A
ND
AF
TE
RL
OA
D P
AR
AM
ET
ER
S
HD
N
um
ber
(%)
TA
PS
E
PR
ES
E
NT
TA
PS
E
AB
SE
N
T
CO
-
inc
CO
-
dec
CO
-NC
S
V-i
nc
SV
-dec
S
V-
NC
EF
-
inc
EF
-
dec
EF
-NC
R
WM
A
pre
sen
t
RW
MA
ab
sen
t
SV
R
inc
SV
R
dec
SV
R-
NC
NC
7
4
(54
%)
0
74
(10
0)
24
(32
. 4
)
30
(40
. 5
)
18
(24
. 3
)
19
(25
. 7
)
25
(33
. 8
)
28
(37
. 8
)
17
(23
)
26
(35
)
29
(39
. 2
)
0
74
(10
0)
26
(35
)
26
(35
)
19
(25
. 7
)
C
63
(46
%)
0
63
(10
0)
29
(46
)
19
(30
)
15
(23
. 8
)
20
(31
. 7
)
26
(41
. 3
)
17
(27
)
17
(27
)
28
(44
)
18
(28
. 6
)
0
63
(10
0)
20
(31
. 7
)
34
(54
)
9
(14
. 3
)
P
0.
2
0.
2
0.
2
0
. 0
5
50
Results and Observations
CHANGE IN HEMODYNAMICS WITH PRELOAD PARAMETERS
(TABLE 18)
There was a statistically significant change in E/E’ with change in hemodynamics.
(p=0. 004). Even in patients with no change in hemodynamics, there were changes
in preload parameters. 47% of the episodes showed a decrease in stroke volume
variation, despite no change in hemodynamics. This could be compared to 24% of
episodes where there was no change in hemodynamics or SVV which was not
statistically significant however.
CHANGE IN HEMODYNAMICS WITH AFTERLOAD PARAMETERS
(TABLE 19)
There was a statistically significant decrease in systemic vascular resistance with a
change in hemodynamics (p=0. 05) Ejection fraction was decreased in 44% of
episodes and stroke volume was decreased in 41. 3% of episodes where there was
change in hemodynamics, but these were not statistically significant. In 40. 5% of
episodes with no change in hemodynamics, a fall in cardiac output was seen.
DISCUSSION
51
Discussion
DISCUSSION
Hemodynamic changes occurring intraoperatively are generally managed
with conventional monitoring and most of the episodes that occur are believed to be
caused by preload changes, inadequate anesthesia/analgesia or due to excess action
of anesthetic agents and treatment is instituted based on the timing of the occurrence
like incision, blood loss and use of agent monitors. However, such management can
lead to error in management of these patients.
In the present study, we have tried to evaluate the changes in the
echocardiographic indices during significant hemodynamic disturbances that can
happen in non-cardiac surgeries like neurosurgery using TEE. Echocardiography can
give a wealth of information, provides comprehensive monitoring regarding
intraoperative hemodynamic status, gives the etiology of disturbance and helps in
the management compared to traditional routine monitors used in the operation
theaters today. However, there are limited studies in non-cardiac environment due to
limited availability as well as lack of trained anesthesiologists in echo in non-cardiac
surgery. None of the studies have tried to analyze comprehensively the echo based
hemodynamic management in non-cardiac surgery. We have compared the changes
in echo derived values between those patients who had significant changes with
those patients who did not have significant changes. We grouped the different
variables with representation for cardiac preload, after load and myocardial
contractility and tried to analyze our findings.
Of the 63 patients recruited, we had 137 episodes of major intraoperative
hemodynamic disturbances (defined as more than 20% changes in HR, SBP and
Mean BP). Even though some patients had combination of the HR and blood
pressure changes, in order to identify the effects of these changes in TEE derived
values, we analyzed each variable independently. We analyzed changes in HR, MBP
and SBP independently with TEE parameters to identify specific changes and its
etiology in TEE parameters.
52
Discussion
With regard to heart rate changes (for both bradycardia and tachycardia)
there were no statistically significant changes in the TEE derived variables. Our
study patients had more tachycardia (20. 5%) than bradycardia (4. 5%). The
common recognized causes of tachycardia under anesthesia are hypovolemia, blood
loss, lighter plane of anesthesia /pain, increased sympathetic stimulation etc. The
expected TEE changes in hypovolemia would be reduction in preload, decreased
filling of ventricles, low stroke volume, cardiac output and a compensatory increase
in SVR. In contrast increased sympathetic discharge can cause increased cardiac
output and increased SVR. This could be compensation for hypovolemia or lighter
plane or inadequate anesthesia. Without recognizing the cause of tachycardia,
increasing the depth of anesthesia or administering analgesics in tachycardia can
lead to worsening in a hypovolemic patient. On analysis, we found that in
tachycardia, there were more patients with increased SVC collapsibility, increased
stroke volume variation, low left ventricular EDV, low E/E’, more increased SVR,
and decreased stroke volume compared to no change patients. The preserved SVR
and cardiac output could be due to increased sympathetic activity. Hence our study
showed that patients with tachycardia showed echo features of reduced right
ventricular and left ventricular preload with compensation in cardiac output and
SVR. The myocardial contractility was well preserved.
In our study, patients who had bradycardia did not show major changes in
TEE derived variables compared to patients with no change in heart rate due to the
fact the bradycardia is transient and the numbers are too small to get a trend in
changes.
Similar to HR changes, blood pressure also varies intra operatively with
preload, myocardial contractility and after load. With regards to decrease and
increase in SBP and MAP, the most significant change we observed was
corresponding decrease and increase in systemic vascular resistance. The EF, stroke
volume, and cardiac output were either maintained or increased compared to patients
without blood pressure changes.
53
Discussion
In patients with low SBP who would have been thought to have hypovolemia
otherwise, did not show significant differences in preload indices like SVC, IVC
collapsibility, SVV and E/E’ nor there were there any features of myocardial
dysfunction. In patients whom MAP was low intraoperatively, in addition to low
SVR, we observed that except for decreased IVC collapsibility, they had preserved
SVC collapsibility, SVV and E/E’ compared to patients without a decrease in MAP
indicating that these patients had significantly low after load and a well preserved
preload as a cause of low MAP.
Regarding the increase in SBP, we observed that the only change was
increased SVR. Other variables were not significantly different from the patients
without change. Similarly, in patients with increased MAP, SVR and cardiac output
increased with preservation of preload and contractility compare to those who did
not show a significant change.
Increased heart rate during neurosurgery can be due to a number of factors
like pain, anxiety and depleted volume status. Hypovolemic patients generally
manifest tachycardia, however the use of beta blockers, and the effect of anaesthetic
drugs can confound the assessment of preload. Adequate urine output may be
misleading as mannitol and loop diuretics may be part of the treatment in
neurosurgical patients. The use of central venous pressure (CVP) and pulmonary
artery occlusive pressure (PAOP) may also not be indicative of hypovolemia as
these values can be affected by mechanical ventilation, high airway pressures,
technical issues like insertion time, complications associated with invasive devices
etc.60, 61
The use of SVV was found to be a good predictor of preload. Berkenstadt et
al performed graded volume loading on fifteen patients undergoing neurosurgery.
Responders and nonresponders did not differ in their pre-volume loading values of
HR and CVP, but did differ in SVV. They found that a SVV of 9. 5% or more
predicts an increase in stoke volume of 5% or more in response to a 100ml load. The
specificity was 93% and sensitivity was 75%.62
In our study, we found that episodes
with increased heart rate were associated with parameters of decreased preload like
increase in SVV and increase in SVC-CI ,but it did not attain statistical significance.
54
Discussion
Cannesson et al also studied SVV in 25 patients undergoing coronary artery
bypass grafting using the VigeloFloTrac system. SVV was significantly higher in
the responders than the non-responders. (15+/-5% vs 7+/- 4% respectively; P < 0.
01). Another study on SVV in non-cardiac surgery, done on patients undergoing
liver transplantation, showed that SVV is able to predict fluid responsiveness.63
Collapsibility of the vene cava has been studied as a measure of assessing the
volume status of a patient. Feissel et al studied the response of cardiac output and
respiratory variation in IVC diameter (IVC collapsibilty index) to a standardised
volume load in thirty-nine mechanically ventilated critically ill patients. They found
an increase in cardiac output (5. 7+/-2. 0 to 6. 4+/-1. 9 L/min (P<0. 001) and a
decrease in respiratory variation in IVC diameter (from 13. 8+/-13. 6 vs 5. 2+/-5. 8%
(P<0. 001 ) in responders.64
The patients who responded to volume loading by an
increase in cardiac output had a greater collapsibilty index at baseline (25% to 6%)
compared to the patents who did not respond. Weeks et al reported that the majority
of the patients in their study had a decrease in vene caval index and rapid IVC
filling. In their study on hypotensive emergency department patients,65
Sefidbakht et
al demonstrated a higher vene caval collapsibilty index in vene cava in patients in
shock.66
They studied 88 trauma patients divided into two groups- shock and
control. They found that the mean collapsibilty index was higher in the shock group
than the control group (27% vs 20%, p<0. 001). These studies highlight how vene
cava collapsibilty index can be used to detect volume responsive patients. In our
study, we found that in episodes with tachycardia, there was a higher number of
episodes with increased SVC -CI (55. 6% of episodes with increase SVC -CI vs
37% with decreased SVC-CI vs 7. 45 of episodes with no change in SVC-CI).
Global end diastolic volume (GEDV) is good indicator of cardiac preload. In
an animal model, nineteen anesthetised and mechanically ventilated piglets were
studied during volume loading. They found that after volume loading there was a
significant change in EDV (25+/-17%).67
GEDV was measured using trans
pulmonary thermodilution technique. In our study, more episodes of tachycardia
were associated with episodes of decrease in end -diastolic volume (59%). It could
55
Discussion
be that the tachycardia was due to hypovolemia. However, we did not ascertain fluid
responsiveness as it was not a part of our study.
Left ventricular filling pressure can be estimated by E/E’which is the ratio
between early mitral inflow velocity and mitral annular early diastolic velocity. The
gold standard in left ventricular pressure management is invasive cardiac
catheterization ,but echocardiography has been shown to provide a reliable estimate
for left ventricular filling pressures.68
The EAE/ASE guidelines also suggest
assessment of E/E’ as a measure of LV filling. In patients with cardiac disease’
velocity can be used as a corrective measure for the effect of LV relaxation on E
velocity. So E/E’ can be used as a measure of LV filling pressures.59
Estimation of
E/E’ by echocardiography will avoid the risks of invasive monitoring. Ventricular
diastolic function can be assessed by left ventricular filling pressure, as during
diastole the heart must normally fill without any elevation in filling pressures.69
In
the cardiac cycle, during isovolumetric relaxation, the LV pressure falls, producing a
gradient between the LA and LV, which causes blood to flow into the LV and fill it.
Hence, the myocardial relaxation (E’), precedes the onset of passive left ventricular
filling (E). In a failing left ventricle there is elevation of LA pressure and blood is
pushed into the LV. When this occurs, myocardial diastolic motion (E’) may be
secondary to filling. (E). So this difference in the mode of filling (E’) in a normal
and failing heart explains the different values of E/E’ in the two conditions.70
Using
the septal E/E’ ratio, a ratio of less than 8 is associated with normal filling pressures,
whereas a ratio of greater than 15 is associated with increased filling pressures.59
We found that there was a statistically significant change in blood pressure
with systemic vascular resistance. Episodes of fall in systolic blood pressure were
significantly associated with fall in SVR. (100% of episodes=0). There was an
increase in cardiac output despite a decrease in SBP. A possible explanation for this
could be the fall in SVR. Similarly increase in systemic blood pressure was
significantly associated with an increase in systemic vascular resistance (90% of
episodes=0. 008). Episodes with a decrease in MAP were significantly associated
with a decrease in SVR (81% of episodes=0. 009). Episodes of increase in MAP
56
Discussion
were also associated with increase in SVR (63%) of episodes, but this was not
statistically significant.
There can be many reasons for hypovolemia during the conduct of
anaesthesia. It could be specific to the surgery being undertaken- for instance, during
laproscopic cholecystectomy in fifteen nonobese patients monitored by invasive
hemodynamic monitoring, Joris et al found that after induction of anaesthesia and
positioning in the head up position, there was a fall in MAP, which increased after
peritoneal insufflation.71
Unclamping of the aorta during vascular surgery can lead
to hypotension.72
A common belief during the intraoperative period is that a fall in
blood pressure is due to hypovolemia caused by dehydration or blood loss. However
in our study, we found that a fall in SVR was a more common association with the
fall in blood pressure.
Fall in blood pressure should be treated according to its cause, as effect of
anaesthetic agents, hypovolemia, surgical position, effect of mechanical ventilation
and cardiac causes can lead to similar changes in blood pressure.73
Fall in pressure
due to decreased volume status requires fluids, whereas a fall in systemic vascular
resistance requires vasopressors.
Cardiovascular complications are known to occur with perioperative unstable
hemodynamics. Walsh et al studied data from 33, 330 noncardiac surgeries to study
the association between intraoperative hypotension and postoperative acute kidney
injury and myocardial ischemia. They determined that even short intraoperative
hypotensive events of MAP less than 55 mm of Hg were associated with acute
kidney injury and myocardial ischemia.74
Kheterpal et al studied the preoperative
and intraoperative hemodynamic data in more than 7000 patients undergoing non
cardiac surgery over a four-year period. They were studying the incidence and risk
factors for a cardiac adverse event (CAE) in patients undergoing non cardiac
surgery. The results of the study concluded that a high-risk patients experiencing a
CAE was more likely to have experienced an episode of mean arterial pressure < 50
mmHg (6% vs. 24%, P = 0. 02), experience an episode of 40% decrease in mean
57
Discussion
arterial pressure (26% vs. 53%, P = 0. 01), and an episode of heart rate > 100 (22%
vs. 34%, P = 0. 05).75
Hence it is vital that we accurately define the cause of hypotension. Using
TEE, we were able to more accurately estimate the reason for changes in blood
pressure and direct treatment towards the cause, rather than treatment in an
empirical manner.
TEE is being increasingly used in noncardiac surgery. Chew et al studied the
esophageal Doppler monitor to delineate its use in measuring cardiac index, preload
and systemic vascular resistance. They conducted a prospective pilot study in 12
mechanically ventilated patients with a diagnosis of septic shock. They found that
the esophageal Doppler had a good concordance with the pulmonary artery catheter
in measuring cardiac index, but was an unreliable measure of preload and SVR.76
In vascular surgery, transesophageal echocardiography was found to be 86 to
100% sensitive for the diagnosis of acute aortic syndrome which is potentially
fatal.77
TEE has a crucial role in surgical treatment of aortic diseases. It can be used
to delineate diseases in the thoracic aorta.78
TEE has been used to delineate areas of regional wall motion abnormality
indicate of myocardial ischemia in both cardiac and non-cardiac surgery.79,80,81
However, in our study we had no incidence of RWMA in any of our patients.
There is no single measured variable that can quantify preload, afterload or
contractility. It is a combination of the measured parameters and their interaction
that can clarify a particular clinical situation. The conventionally used clinical
parameters like heart rate and blood pressure in itself can be misleading in a
particular situation e.g. tachycardia in itself can be due to many reasons-pain,
anxiety, fever, decreased volume status. However, in combination with TEE
measures of preload such as stroke volume variation, afterload and contractility we
have greater clarity about the clinical situation we are facing. Hence, we are better
equipped to respond and can target our therapy appropriately in the perioperative
period.
LIMITATIONS
58
Limitations of the Study
LIMITATIONS OF THE STUDY
1. The number of subjects studied was small. A larger study with a greater
number of subjects might have given more statistically significant
conclusions.
2. Unlike other equipment, use of the TEE requires adequate training and
knowledge for interpretation of the readings.
3. Our study was an observational study. It did not directly assess the outcome
of therapeutic intervention based on TEE readings.
4. Manipulation of the probe in patients in positions other than supine like
prone and lateral could be challenging at times. We were not able to get all
the views as per our protocol in some of these cases.
5. We studied only elective neurosurgical operations in the theatre. However
further studies could expand the site of use of TEE to include emergency
surgery, trauma and evaluation of patients in the critical care unit.
CONCLUSION
59
Conclusion
CONCLUSION
Our study shows insights into the common hemodynamic problems
encountered by the anesthesiologist in day to day non cardiac surgery practice and
the TEE guided approach in identifying the cause and management of the instability.
In our study of major neurosurgical procedures, we found that major hemodynamic
changes related to changes in heart rate, systolic and diastolic blood pressure were
frequent with at least 2-3 episodes occurring in each patient. These episodes have
been found to occur at any time during the intraoperative period and did not follow a
particular pattern of the anesthesia or surgical procedure.
In our study, we found that TEE was very useful in identifying the reason for
changes in hemodynamic parameters based upon preload, afterload and contractility.
We found that each episode had multiple factors causing changes. We could not find
a single TEE parameter which can identify all these changes.
Of all the TEE derived values, change in systemic vascular resistance was
the most consistent with hemodynamic changes, both for systolic blood pressure and
mean arterial pressure. In patients who developed tachycardia, preload indices were
altered whereas bradycardia alone did not cause significant change in the TEE
variables.
We conclude that a combination of TEE derived variables was very useful in
identifying the cause of hemodynamic instability that occurred in neurosurgical
patients. Our study was a pilot study and could not completely identify a particular
TEE variable that needs to be focused. We believe that future research with large
population would provide answers to the short coming in the present study.
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emergency department patients. Acad Emerg Med Off J Soc Acad Emerg Med.
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66. Sefidbakht S, Assadsangabi R, Abbasi HR, Nabavizadeh A. Sonographic
measurement of the inferior vena cava as a predictor of shock in trauma patients.
Emerg Radiol. 2007;14:181–5.
67. Renner J, Meybohm P, Gruenewald M, Steinfath M, Scholz J, Boening A, et al.
Global End-Diastolic Volume During Different Loading Conditions in a
Pediatric Animal Model: Anesth Analg. 2007;105:1243–9.
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70. Park J-H, Marwick TH. Use and Limitations of E/e’ to Assess Left Ventricular
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72. Gelman S. The pathophysiology of aortic cross-clamping and unclamping.
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73. Lonjaret L, Lairez O, Minville V, Geeraerts T. Optimal perioperative
management of arterial blood pressure. Integr Blood Press Control. 2014 ; 7:49–
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74. Walsh M, Devereaux PJ, Garg AX, Kurz A, Turan A, Rodseth RN, et al.
Relationship between intraoperative mean arterial pressure and clinical
outcomes after noncardiac surgery: toward an empirical definition of
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75. Kheterpal S, O’Reilly M, Englesbe MJ, Rosenberg AL, Shanks AM, Zhang L, et
al. Preoperative and intraoperative predictors of cardiac adverse events after
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33.
ANNEXURES
PATIENT CONSENT FORM
Title of the study: TRANSESOPHAGEAL ECHOCARDIOGRAPHIC (TEE) ASSESSMENT OF
CAUSES OF SIGNIFICANT HEMODYNAMIC CHANGES IN THE
INTRAOPERATIVE PERIOD DURING NEUROSURGERY
Name of the Investigators:
Dr Nilima Rahael Muthachen, Dr.Manikandan.S,
Hemodynamic changes (heart rate, rhythm, blood pressure) can occur during
neurosurgical procedures. You are being requested to participate in this study which
will detect changes in hemodynamics during your surgery. . This study will require
placement of invasive arterial cannula and use of transesophageal echocardiography.
Both these tools are used as part of Anaesthesia monitoring in this institute and
worldwide. We have planned to include about 200 people from this hospital in this
study.
.
What is TEE?
TEE is an ultrasound imaging of your heart. During TEE, a ultrasound probe is
inserted through your mouth into the esophagus (food pipe).The ultrasound shows the
structure and functions of the heart muscles and valves from different angles.This tool
has been used all over the world in neurosurgical patients undergoing major surgeries
and found to be safe.
What is invasive arterial BP?
Invasive arterial BP is the monitoring of blood pressure of the patient after
placing an arterial cannula in the peripheral artery of your hand/leg . This method of
BP monitoring is a part of standard anesthesia monitoring and has been used all over
the world in neurosurgical patients and found to be safe.
If you take part what will you have to do?
On the day of surgery you will be taken inside the Operation Theatre. Monitors
to check your heart beat, blood pressure and oxygen saturation level will be attached.
A small venous cannula will be inserted under local anesthesia in the hand for fluid
and drug administration. Arterial cannula also will be inserted under local anesthesia
for monitoring the blood pressure. General Anaesthesia will be induced as per the
routine anesthesia practice in the hospital. After the patient is fully sedated , and
paralyzed and connected to ventilator, a TEE probe will be inserted through the mouth
into the esophagus. Both the tools will be used to monitor the hemodynamic changes
throughout the surgery as per routine. At the end of surgery TEE probe will be
removed . Arterial line will be retained for post operative monitoring in ICU
Does TEE use have any side effects?
The majority of people have not had any side effects. The reported side effects
are sore throat and numbness of throat when used in awake patients but the incidence
of this complication in our study will be remote as the patient is in general anesthesia.
Other reported complications are very rare and include injuries to teeth and
esophagus. Esophageal intubation can induce vagal and sympathetic reflexes such as
hypertension or hypotension, tachy arrhythmias or bradycardia.These complications are
very rare in patients under general anesthesia as they are in deep sedation and paralysed
and anesthesia mostly blunts the hemodynamic effects of TEE.Futhermore the patients
with risk of getting injured are excluded by the exclusion criteria.
Does invasive arterial line use have any side effects?
The majority of people have not had side effects. The reported side
effects are hemorrhage, infection, vascular insufficiency, ischemia, thrombosis,
embolization, and neuronal or adjacent structure injury. These are very rare
complications and are prevented by preoperative testing for good collateral
circulation and avoiding long term cannulation.
.
Can you withdraw from this study after it starts?
Your participation in this study is entirely voluntary and you are also free to
decide to withdraw permission to participate in this study. If you do so, this will not
affect your usual treatment at this hospital in any way. In addition, if you experience
any side effects, the study will be stopped and you will be given additional treatment.
What will happen if you develop any study related injury?
We do not expect any injury to happen to you since the anaesthesia technique
and monitoring tools would be same even if you were not part of the study. But if you
do develop any side effects or problems due to the study, these will be treated at no
cost to you. We are unable to provide any monetary compensation, however.
Will you have to pay for the cost of using the devices?
Arterial BP monitoring and TEE are used as a part of routine anaesthesia
procedures for surgery. Any extra charge for monitoring purpose will be borne by the
Principal Investigator.
What happens after the study is over?
Arterial BP, Transesophageal Echocardiography is a routinely used tool for
monitoring heart and circulation during major neurosurgery.After the study is over the
same tools will be used to monitor hemodynamics throughout the length of the
surgery . After surgery is over the TEE probe will be removed before shifting the
patient to ICU.
Will your personal details be kept confidential?
The results of this study will be used for thesis submission as a part of
academic research and will be submitted to a medical journal for publication, but you
will not be identified by name in any publication or presentation of results. However,
your medical notes may be reviewed by people associated with the study, without
your additional permission, should you decide to participate in this study.
If you have any further questions, please ask Dr Nilima Rahael Muthachen (Principal
investigator) mobile number9496840423.. email: [email protected]
Participant’s name: Date of Birth / Age (in years):
I_________________________,son/daughter of ___________________________
Declare that (Please tick boxes)
• I have read the above information provided to me regarding
the study:
A study on the TRANSESOPHAGEAL ECHOCARDIOGRAPHIC (TEE)
ASSESSMENT OF CAUSES OF SIGNIFICANT HEMODYNAMIC
CHANGES IN THE INTRAOPERATIVE PERIOD DURING
NEUROSURGERY[ ]
• I have clarified any doubts that I had. [ ]
• I also understand that my participation in this study is entirely voluntary
and that I am free to withdraw permission to continue to participate at
any time without affecting my usual treatment or my legal rights [ ]
• I understand that the study staff and institutional ethics committee
members will not need my permission to look at my health records even if I
withdraw from the trial. I agree to this access [ ]
• I understand that my identity will not be revealed in any information
released to third parties or published [ ]
• I voluntarily agree to take part in this study [ ]
• I have been provided with the contact numbers of the principle investigator, in
case I want to know more about the study and participants rights [ ].
• I received a copy of this signed consent form [ ]
Name:
Signature:
Date:
Name of witness:
Relation to participant:
Signature :
Person Obtaining Consent
I attest that the requirements for informed consent for the medical research
project described in this form have been satisfied. I have discussed the research
project with the participant and explained to him or her in nontechnical terms all of
the information contained in this informed consent form,including any risks and
adverse reactions that may reasonably be expected to occur. I further certify that I
encouraged the participant to ask questions and that all questions asked were
answered.
Name : Signature : Date:
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tom
y an
d e
xcis
ion
late
ral
ND
ND
ND
ND
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8011
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77
3825
F48
154
1.43
Cer
ebel
lop
on
tin
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gle
ep
ider
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idcr
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tom
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mp
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ND
ND
ND
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102
134/
8493
3946
F65
155
1.64
L In
sula
r gl
iom
acr
anio
tom
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ine
59n
on
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130/
7387
4049
F65
165
1.72
recu
rren
t tu
bec
ulu
m s
ella
men
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om
acr
anio
tom
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Sup
ine
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129/
8899
4157
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155
1.59
R r
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ual
Ten
tori
al m
enin
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cran
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my
and
dec
om
pre
ssio
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Gra
de
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iast
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70
4255
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145
1.22
R F
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arie
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gio
ma
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my
and
dec
om
pre
ssio
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pin
e75
no
no
1sc
lero
tic
Ao
rtic
val
ve60
114/
5072
4328
M55
150
1.49
R p
arie
tal c
aver
no
ma
cran
ioto
my
and
exc
isio
nSu
pin
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DN
DN
DN
DN
D89
133/
8910
4
4462
M65
165
1.72
Left
fro
nta
l men
ingi
om
acr
anio
tom
y an
d e
xcis
ion
Sup
ine
68G
rad
e 1
dia
sto
lic d
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120/
4973
4536
M85
165
1.92
Bila
tera
l In
tern
al C
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tid
Art
ery
aneu
rysm
pte
rio
nal
cra
nio
tom
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Sup
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68n
on
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o66
120/
8685
sl n
oag
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nd
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eigh
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ght
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(m
2)Dia
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Cra
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170/
9511
0
4740
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165
1.72
Rig
ht
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lar
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gra
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pin
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no
no
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116/
4062
4855
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154
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on
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and
clip
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7612
6/85
102
4957
F65
155
1.64
L p
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tal m
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gio
ma
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no
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no
5611
9/68
89
5027
F65
155
1.64
L f
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Sup
ine
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7411
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5143
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152
1.56
L an
teri
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l cra
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ion
Sup
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71n
on
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M65
165
1.72
glio
ma
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and
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119/
6786
5352
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175
1.9
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212
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tran
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no
5810
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65
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155
1.65
Left
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lar
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ma
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om
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no
no
1.17
no
5511
5/53
75
5718
F46
151
1.39
Cra
nio
ph
aryn
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R p
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8411
4/68
83
5840
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L Fr
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8314
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110
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157
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L p
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6811
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6020
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147
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103/
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Rec
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l par
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83
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6712
0/77
92
sl n
o 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45
B-L
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VB
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B-L
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DB
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(cm
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%)B
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27
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9n
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276
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303.
57n
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no
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0.6
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no
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100
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7187
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59
9040
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5230
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90.
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60
7532
2.6
0.8
9759
5944
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29
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0.5
0.8
0.3
no
1.7
6610
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5056
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0.6
no
1.6
7212
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31
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0.9
60
8045
2.5
245
5050
251.
75n
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585
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no
no
no
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10.
80.
6n
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7570
122/
8497
1.9
1.7
1.4
0.9
40
7526
4.2
3.1
6536
3632
2.62
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0.5
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70.
51.
50.
738
5732
43.
444
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154
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no
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20.
50.
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675
126/
5879
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0.9
0.9
0.9
55
9532
4.4
3.9
6553
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3.49
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1.72
78.
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on
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70.
70.
6n
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103/
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0.7
0.6
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53
6837
4.4
3.4
4649
4935
2.52
no
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2.62
48.
51n
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0.6
0.4
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1.76
6912
7/77
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70.
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4326
3.8
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4051
5146
3.48
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1.03
2.06
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10.
70.
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963
100/
5671
0.7
0.6
1.9
1.6
50
6730
3.9
2.8
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4.39
no
3.11
2.97
78.
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on
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70.
60.
5n
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5576
134/
8299
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0.4
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40
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4.6
3.5
4362
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1.91
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90.
9n
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6
4015
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2.9
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2.15
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40.
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6
5616
3.8
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7055
5539
3.19
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474
11.5
no
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0.8
0.6
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6211
7/59
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61.
91.
139
8442
3.7
4.2
5062
6247
2.27
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5.18
2.99
810
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on
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80.
90.
7n
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694
131/
7694
0.5
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1.4
0.8
36
6521
3.9
2.5
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7230
4.16
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419
5.31
no
no
no
1.6
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0.8
0.8
no
1.6
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11.
61.
278
100
525.
34.
248
4444
392.
45n
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478.
98n
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on
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41
0.6
0.6
no
1.7
6611
6/84
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60.
51.
10.
741
8951
4.5
3.7
6637
3729
2.21
no
3.17
1.59
314
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on
on
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91.
40.
50.
4n
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590
136/
9080
0.6
0.5
1.4
0.9
44
8937
4.1
2.7
6670
7045
6.37
no
1.37
1.43
74.
21 2
+1+
no
1.5
1.2
1.6
1n
o1.
981
96/4
760
0.7
0.6
1.4
0.9
60
112
575
2.9
7445
4540
3.67
no
1.31
1.97
88.
97n
on
on
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50.
81.
70.
8n
o1.
694
95/5
772
0.7
0.4
1.1
0.6
55
9132
4.5
2.8
6572
7251
3.8
no
1.78
1.61
17.
85n
o1+
no
1.4
1.3
0.3
0.3
no
1.5
5393
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590.
30.
31.
31
62
8834
3.5
1.8
4859
5948
3.33
no
1.94
2.79
29.
71n
on
on
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51
11
no
1.6
8015
3/69
101
1.2
11.
41.
351
117
684.
43.
642
5555
443.
18n
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384.
536
6.03
no
no
no
1.4
0.9
0.7
0.6
no
1.7
6312
3/61
850.
70.
51.
41.
137
9841
4.2
363
6868
615.
08n
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691.
694
6.56
no
no
no
1.8
1.1
0.7
0.5
no
1.7
7313
4/62
831.
11.
11.
71.
165
9831
4.6
3.2
6851
5143
2.62
no
3.55
6.21
86.
79n
on
on
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21.
20.
80.
7n
o1.
660
130/
7093
0.7
0.7
1.1
164
6227
4.4
3.1
5655
5530
4.05
no
1.42
1.90
20.
98n
on
on
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40.
51.
50.
9n
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866
107/
6987
1.4
0.6
1.3
170
6127
3.5
2.5
5634
3416
2.15
no
2.05
1.96
89.
531+
1+n
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10.
50.
60.
6n
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762
112/
6077
1.5
1.2
1.1
0.9
32
127
424.
33
5840
4025
2.54
no
1.1
1.07
78.
6n
on
on
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91.
31.
30.
8n
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565
88/4
861
1.7
1.4
1.1
0.9
75
5944
4.3
3.6
6054
5430
3.5
no
1.58
0.84
7.5
no
no
no
21.
41.
10.
9n
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6
8833
3.1
2.1
6264
6434
2.95
AS
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2/1
71.
422.
094
21.5
no
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11.
40.
80.
7n
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843
109/
5372
1.5
1.4
1.4
0.7
37
7032
2.8
1.7
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1917
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24.8
no
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51.
10.
8n
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798
111/
8495
0.6
0.5
0.8
0.7
20
6546
4.7
3.2
3265
6530
4.25
no
2.56
0.40
112
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o2+
,ecc
entr
ic je
tn
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0.5
1.2
0.9
no
1.7
7514
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104
0.7
0.7
1.5
0.9
80
7135
5.1
3.3
5140
4029
2.67
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1.19
1.99
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51.
91.
2n
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5
4916
3.5
2.4
6857
5727
1.55
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2.12
1.60
214
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on
on
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10.
32.
91.
1n
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857
87/4
357
0.8
0.6
1.2
0.6
35
5430
4.3
445
6060
305.
71n
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462.
831
11.8
no
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30.
81
0.9
no
1.6
7810
3/50
662.
51.
81.
40.
846
9949
5.1
4.7
5180
8040
2.04
no
1.74
1.30
29.
37n
on
on
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40.
71.
51.
2n
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589
101/
5971
1.4
1.1
1.1
0.7
41
2214
3.9
3.3
3954
5435
3.28
no
1.48
3.48
89.
28n
on
on
o1.
10.
70.
80.
4n
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796
108/
6578
1.3
0.9
0.5
0.3
55
4827
2.9
1.9
4354
5449
3.62
no
1.59
2.29
116
.71+
no
no
1.4
11
0.9
no
2.2
6314
6/80
106
1.3
11.
40.
875
5024
3.4
2.3
6488
8845
7.43
no
1.23
1.58
39.
56n
o1+
no
1.4
0.9
0.7
0.5
no
1.6
7993
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560.
90.
71.
20.
873
5128
4.1
3.1
4643
4338
3.27
no
2.06
1.21
916
no
1+n
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40.
80.
50.
3n
o1.
511
411
0/70
811.
21
1.7
0.6
37
5421
4.1
3.5
6091
9170
4.98
no
1.54
1.33
315
.3n
o1+
no
1.2
0.6
0.8
0.3
no
11.6
7414
1/68
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30.
11.
30.
560
6323
4.2
3.4
6350
5044
4.82
no
1.37
1.77
312
.1n
on
on
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0.8
1.4
0.7
no
1.7
8413
0/79
961.
31.
10.
70.
647
6234
4.8
3.8
5352
5242
3.29
yes,
sep
tum
+ a
nte
rola
tera
l1.
652.
332
14.8
no
1+n
o1.
30.
71.
10.
5n
o1.
564
110/
4563
0.8
0.7
1.5
0.7
44
116
714.
63.
268
6868
544.
48n
o2.
332.
093
9.35
no
1+n
o1
0.5
1.6
0.9
no
1.7
7713
6/78
960.
40.
30.
90.
755
sl n
o
46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63
B-L
VED
VB
-LV
ESV
B-L
VID
DB
-LV
IDS
(cm
)B
-EF(
%)B
-SV
Svm
axSv
min
B-C
OB
-RW
MA
B-E
/AB
-E'/
A'
B-E
/E'
B-T
RB
-MR
B-A
RB
-SV
Cd
1B
-SV
Cd
2 B
-IV
Cd
1B-I
VC
d2
PFO
B-T
AP
SEH
R-1
BP
-1
MA
P-1
IVC
max
IVC
dm
inSV
Cd
max
SVC
dm
inSV
max
1
5440
3.5
2.5
4042
4238
2.22
no
1.71
0.64
712
.3n
on
on
o1.
61
0.4
0.3
no
1.5
5512
1/62
800.
60.
51.
71.
296
108
575
3.3
4745
4530
3.23
no
1.47
2.49
44.
931+
no
1+1.
70.
80.
70.
6n
o1.
774
91/5
165
1.2
0.9
1.6
0.9
71
4718
3.2
2.7
6244
4428
2.81
no
1.67
1.88
29.
03n
on
on
o1.
30.
90.
70.
5n
o1.
854
105/
6480
0.7
0.6
1.5
0.9
32
4927
3.3
2.5
5559
5942
3.28
no
24.
701
6.7
1+1+
no
1.2
0.7
0.9
0.7
no
1.5
5412
2/64
871
0.7
1.5
147
4218
3.4
3.1
5662
6262
3.91
no
2.23
2.71
411
1+1+
no
1.6
1.1
0.4
0.4
no
1.9
5912
3/71
880.
70.
61.
41.
179
8020
4.3
2.8
6571
7165
4.86
no
1.78
1.71
410
.9n
o1+
no
1.5
1.1
0.6
0.5
no
2.1
8014
2/81
105
0.9
0.9
1.7
152
8340
4.8
3.7
5265
6548
3.17
no
1.39
1.29
67.
18n
on
on
o2
10.
70.
6n
o2.
452
109/
6581
0.6
0.5
1.3
1.1
62
119
615
3.4
5981
8381
5.13
1n
o1.
721.
567
9.88
no
1+1+
21.
40.
80.
6n
o1.
554
110/
6582
0.9
0.7
1.6
1.1
68
8955
5.1
4.2
3831
3131
2.5
no
1.01
0.60
67.
9n
o2+
no
1.5
11.
11
no
1.5
6911
4/61
820.
90.
81.
50.
958
8948
3.8
2.8
5561
6154
3.46
hyp
ertr
op
hic
left
ven
tric
le1.
850.
762
17.1
no
no
no
1.3
1.2
0.6
0.5
no
2.5
5713
7/61
821.
20.
92
0.8
73
5835
42.
460
7373
734.
85n
o2.
821.
382
10.6
no
1+n
o1.
50.
90.
60.
4n
o2
6812
3/61
851.
51.
31.
70.
771
3010
3.6
2.4
5736
3629
2.95
no
1.42
3.24
612
.6n
on
on
o1.
10.
70.
70.
6n
o2
9513
5/82
102
0.6
0.4
10.
750
4915
3.4
2.2
7042
4235
2.85
no
1.31
1.34
211
.9n
on
on
o1.
10.
60.
80.
5n
o2.
472
117/
5477
0.8
0.7
10.
541
3216
3.7
2.7
5849
4948
3.13
no
1.56
1.79
95.
37n
on
on
o1.
10.
70.
90.
4n
o0.
981
125/
9610
80.
40.
31.
71
48
6330
3.8
3.1
4532
3220
3.13
no
3.22
4.87
25.
32n
o1+
no
1.2
0.6
0.7
0.4
no
1.6
7211
8/58
820.
70.
41.
60.
862
7442
4.5
3.5
4441
4138
2.73
no
4.12
1.83
313
2+1+
triv
ial
1.3
0.9
21.
1n
o1.
756
114/
7287
1.6
1.4
1.3
1.1
38
6157
3.8
2.8
5454
5437
3.45
no
1.5
1.64
28.
22n
on
on
o1.
70.
51.
10.
9n
o1.
569
121/
7093
1.7
1.4
1.8
0.9
61
5025
3.8
2.7
5680
8040
5n
o2
1.48
68.
35n
on
on
o1.
61.
31
0.8
no
1.7
sl n
o 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45
Svm
in 1
LVID
D-1
LVID
S-1
LVED
V-
1LV
ESV
-1T
AP
SE -
1EF
-1
SV -
1C
O -
1(L)E/
A -
1E'
/A' -
1E/
E' -
1M
R -
1TR
- 1
AR
VA
E 1
AP
1H
R-2
BP
-2
MA
P -
2IV
C d
maxI
VC
dm
inSV
Cd
2m
xSV
C d
mnS
vmax
2SV
min
2LV
IDD
2LV
IDS2
LVED
V -
2LVES
V-
2TAP
SE -
2
223
1.9
7035
1.5
6025
3.49
1.22
0.78
39.
73n
on
on
on
o18
104
77/5
059
0.8
0.7
0.9
0.5
3019
2.1
180
451.
7
303.
22
6530
1.6
6026
2.9
1.07
1.7
5.97
no
no
no
no
1510
113
9/83
102
10.
71.
10.
740
253.
52.
165
301.
7
404.
62.
270
351.
872
622.
113.
413.
082
0.47
no
no
no
no
15
304.
22.
470
301.
676
362.
361.
251.
055.
25n
on
on
on
o14
384.
32.
275
351.
868
604.
321.
31.
46.
25n
on
on
on
o15
283.
22.
780
361.
842
272
1.07
1.38
66.
65n
on
on
on
o16
6711
0/84
931.
20.
81.
81.
644
393.
72.
775
341.
6
273.
42.
668
331.
748
383.
232.
122.
023
7.62
no
no
no
no
1584
108/
7791
10.
81.
40.
830
284.
33
7731
1.4
403.
51.
953
241.
855
554.
132.
21.
2613
.54
no
no
no
no
2268
125/
6284
0.9
0.7
10.
614
110
14.
94.
510
362
1.7
413.
92.
150
361.
649
533
1.48
1.85
79.
16n
on
on
on
o17
5791
/75
710.
60.
30.
90.
756
553.
62.
162
251.
7
444
3.2
7535
1.8
6555
3.53
1.72
1.75
813
.04
no
no
no
no
1672
104/
6175
0.8
0.6
0.6
0.5
4943
4.5
3.2
4527
1.68
325.
44.
190
511.
744
503.
271.
862.
181
6.56
1+n
on
on
o14
5711
8/62
830.
90.
62
1.8
5146
4.2
2.6
5221
1.8
313.
72.
855
261.
6546
403.
141.
92.
178
6.31
no
no
no
no
1310
012
3/84
950.
60.
32.
11.
135
333.
32.
233
231.
7
384.
32.
949
151.
7570
392.
411.
82.
028
9.78
no
no
no
no
1659
117/
6179
0.7
0.6
1.4
1.4
4743
4.5
2.3
5422
1.6
324.
93.
796
521.
846
363.
341.
91.
876
12.3
no
no
no
no
21
612.
92.
160
2952
785.
671.
321.
367
6.89
no
no
no
no
1784
133/
6588
0.6
0.6
1.4
1.4
110
984.
42.
453
341.
65
385
4.2
6741
1.6
3938
2.69
2.36
2.59
89.
8n
on
on
on
o17
7312
8/77
960.
60.
61.
50.
747
465.
64.
675
411.
7
224.
42.
672
531.
6573
443.
791.
381.
536
11.6
2n
on
on
on
o18
8713
2/77
970.
40.
31.
91.
138
294.
23
5184
1.8
603.
63.
277
481.
738
604.
772.
192.
646
6.65
1+2+
no
no
2010
013
3/71
970.
60.
51.
30.
766
533.
72.
552
171.
65
413.
12.
746
291.
736
555.
121.
311.
272
8.37
no
no
no
no
1693
84/5
465
1.6
10.
90.
642
393.
12.
142
231.
68
603.
92.
863
271.
857
623.
182.
531.
635
6.74
no
no
no
no
1960
116/
6279
0.3
0.3
1.7
177
624.
33.
479
371.
7
423.
32.
670
301.
7558
513.
941.
492.
975
6.87
no
no
no
no
2271
123/
6386
0.8
0.7
1.9
1.1
4534
3.3
257
311.
6
324.
33.
266
311.
653
372.
244.
12.
552
6.78
no
no
no
no
1361
98/4
766
0.6
0.4
1.5
1.1
5139
3.9
3.2
5828
1.6
624.
92.
515
641
1.6
7465
4.85
1.75
1.97
87.
61n
on
on
on
o22
6712
2/67
850.
90.
61.
40.
956
523.
92.
810
645
2.2
553.
62.
560
331.
467
643.
823.
373.
0611
.46
no
no
no
no
1668
116/
6584
0.9
0.8
1.3
167
524.
82.
971
261.
5
624.
33.
346
161.
565
704.
61.
61.
51.
17n
on
on
on
o14
6711
2/70
90
1.9
11.
21
5042
3.2
241
231.
62
263.
22.
352
321.
664
322.
531.
21.
86.
24n
on
on
on
o14
544
2.4
4825
1.7
4875
1.93
1.83
1.69
24.
19n
on
on
on
o14
6913
5/64
881.
41.
21.
90.
968
454.
23.
870
551.
7
364.
23
6832
1.6
6637
1.71
1.5
0.98
51+
no
no
no
1543
121/
5476
0.9
0.7
1.7
0.8
6850
4.4
3.4
8747
1.8
184.
52.
753
331.
752
201.
981.
220.
756
20.5
11+
no
no
no
1896
95/7
078
0.9
0.9
0.9
0.6
2018
5.1
2.2
5328
1.64
604.
22.
559
331.
875
806
1.71
1.59
29.
211+
no
no
no
14
343.
92.
539
201.
749
352.
232.
221.
285
0.13
no
no
no
no
1661
82/4
054
1.2
0.8
1.2
0.6
5044
4.3
3.1
5940
1.2
363.
82.
957
212
6346
4.03
1.53
0.83
310
.88
1+n
on
on
o20
8110
5/52
701.
10.
71.
21
6051
4.5
3.7
4828
1.4
204.
74.
349
201.
858
411.
32.
721.
921
7.16
no
no
no
no
1591
109/
6174
0.9
0.7
1.1
0.6
4113
4.7
4.4
6243
1.8
403.
52.
944
201.
755
302.
871.
811.
623
6.71
no
no
no
no
2097
103/
6776
0.6
0.4
10.
735
244.
63.
669
401.
7
684.
23
3412
1.6
6575
4.72
1.63
1.09
518
.33
no
no
no
no
2560
122/
7389
1.1
0.3
1.5
0.7
5046
3.1
2.9
4225
1.8
692.
61.
736
151.
757
735.
331.
611.
707
7.71
no
no
no
no
2179
104/
5473
0.6
0.3
1.8
0.8
8681
3.3
2.1
2927
1.6
254.
12.
659
351.
643
374.
381.
053.
801
9.92
1+n
on
on
o20
115
79/5
261
1.4
0.3
1.9
0.6
3635
3.8
2.4
3925
1.8
473.
22.
436
131.
765
603.
931.
191.
028
15.0
6n
on
on
on
o17
7411
8/60
791.
41.
31.
20.
773
513.
12.
635
171.
7
374.
63.
492
581.
733
473.
992
1.55
11.1
7n
on
on
on
o17
424.
84
6634
1.7
4844
2.74
1.69
1.84
118
.79
1+n
on
on
o20
6298
/42
591.
41.
31.
50.
928
263.
92.
952
351.
6
513.
23
6741
1.8
3955
4.35
1.21
1.78
311
.11
no
no
no
no
1475
105/
7483
10.
81.
10.
762
464
2.7
9744
1.7
sl n
o
46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63
Svm
in 1
LVID
D-1
LVID
S-1
LVED
V-
1LV
ESV
-1T
AP
SE -
1EF
-1
SV -
1C
O -
1(L)E/
A -
1E'
/A' -
1E/
E' -
1M
R -
1TR
- 1
AR
VA
E 1
AP
1H
R-2
BP
-2
MA
P -
2IV
C d
maxI
VC
dm
inSV
Cd
2m
xSV
C d
mnS
vmax
2SV
min
2LV
IDD
2LV
IDS2
LVED
V -
2LVES
V-
2TAP
SE -
2
793.
92.
672
461.
730
965.
111.
921.
111
18.6
7n
on
on
on
o19
4912
1/57
760.
50.
51.
61
5537
4.6
2.3
101
331.
6
564.
43.
285
471.
845
714.
721.
61.
601
9.23
no
no
1+n
o18
6410
5/51
741
0.7
1.6
0.8
6555
4.9
410
850
1.7
303.
42.
257
221.
761
321.
742.
624.
264
11.2
4n
on
on
on
o22
7414
4/86
110
0.7
0.7
1.4
0.5
3223
4.2
2.5
5339
1.8
353.
31.
547
141.
371
472.
452.
343.
298
11.1
61+
1+n
on
o18
5911
0/48
710.
90.
61.
40.
763
583.
42.
337
141.
3
604
2.9
4022
1.4
4579
4.74
1.78
2.78
14.4
41+
1+n
on
o17
6611
7/70
850.
60.
61.
30.
957
444.
13.
142
191.
1
443.
82.
852
192.
163
523.
94.
971.
583
9.27
1+n
on
on
o19
8013
0/72
950.
60.
52.
11.
363
593.
72.
852
221.
9
566.
34.
412
956
2.6
5762
3.32
1.44
1.13
515
.37
no
no
no
no
1455
116/
6786
0.7
0.6
1.6
0.8
5050
5.8
413
367
2.1
555.
13.
210
839
2.5
6768
3.81
2.32
1.58
66.
04`1
+n
o1+
no
1758
153/
8311
20.
80.
52.
21.
278
614.
93.
210
246
2.2
493.
93.
761
362
4258
3.85
0.97
0.64
46.
11+
no
no
no
2068
116/
6586
0.6
0.5
1.5
0.7
5855
4.7
3.7
9356
3.6
364.
93.
710
949
255
733.
861.
511.
189
9.62
no
no
no
no
2156
127/
5979
0.7
0.6
1.4
0.9
6867
4.7
2.5
107
662.
4
683.
41.
736
141.
771
714.
641.
752.
428.
941+
no
no
no
2471
122/
5982
1.8
1.6
1.4
0.9
6349
3.7
2.3
5719
2.5
462.
92.
123
121.
654
505.
012.
081.
014
10.7
5n
on
on
on
o13
108
125/
6786
0.5
0.5
1.4
0.9
5443
3.3
2.6
2513
1.9
372.
92.
134
92.
164
412.
871.
271.
682
6.86
no
no
no
no
2180
100/
5067
0.9
0.7
10.
747
333.
52.
538
142.
6
333.
22.
241
161.
361
483.
91.
061.
954
8.45
no
no
no
no
1979
109/
7388
0.6
0.4
1.3
0.5
4637
3.3
2.3
4419
1
454.
12.
873
302.
266
624.
772.
672.
0112
.81
1+n
on
on
o15
8610
7/51
680.
90.
41.
20.
945
345
3.4
7926
1.4
374.
12.
956
221.
460
382.
20.
842.
314
18.0
81+
2+tr
ivia
lno
2559
125/
7389
1.5
1.4
1.4
0.9
5439
42.
869
221.
5
563.
92.
868
311.
855
614.
221.
241.
349
9.53
no
no
1+n
o19
6311
0/67
870.
90.
81.
80.
963
544
2.2
6125
1.8
sl n
o 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45
EF 2
SV2
CO
- 2
E/A
-2
E'/A
' -2E/E'
2 M
R -
2Tr 2
AR
V
AE
2AP
2H
R 3
BP
3M
AP
3IV
C d
3IV
Cd
3SV
C d
3SV
Cd
3SV
V 3
Svm
ax 3S
V m
in 3L
VID
d 3
LVID
s 3L
VED
V 3
LVES
V 3
TAP
SE 3
EF 3
SV 3
CO
3E/
A 3
E'/A
' 3E/
E' 3
MR
TRA
RV
AE
AP
3
6533
3.46
1.07
18.
4n
on
on
on
o18
5220
2.27
1.19
1.3
10.5
no
no
no
no
16
4944
2.99
1.5
1.2
6.25
no
no
no
no
1683
190/
9012
31
.51.
11.
31
68/4
568
453.
42.
185
501.
669
604.
90.
881.
380.
4n
on
on
on
o17
6030
2.67
3.2
2.3
7.86
no
no
no
no
1690
120/
6786
1.2
1.1
1.6
1.2
27/2
627
264.
22.
483
221.
373
272.
23.
612.
276.
6n
on
on
on
o15
4014
19.
530.
842
8.34
no
no
no
no
2173
118/
5574
0.9
0.7
0.7
0.3
88/7
588
754.
32.
585
451.
6570
888.
50.
830.
857.
2n
on
on
on
o21
5556
2.95
1.62
1.8
7.87
no
no
no
no
17
4049
3.83
3.91
2.5
14.9
no
no
no
no
16
8151
3.07
1.93
2.7
8.94
1+n
on
on
o14
7035
3.13
2.03
29.
03n
on
on
on
o13
5547
2.84
2.09
2.5
8.81
no
no
no
no
1669
114/
5575
0.5
0.4
1.5
1.3
63/5
763
573.
92.
847
241.
770
634.
41.
852
10n
on
on
on
o16
4211
08.
781.
281.
76.
84n
on
on
on
o18
4647
3.61
1.46
2.2
9.54
no
no
no
no
1772
128/
7393
0.5
0.5
1.3
0.9
50/4
950
494.
94.
250
351.
739
505.
61.
31.
658.
8n
on
on
on
o16
5438
3.31
1.4
1.4
8.11
no
no
no
no
1885
130/
7092
0.4
0.4
1.3
0.9
33/2
333
234
3.1
8751
1.7
3933
2.9
2.16
2.33
7.8
no
no
no
no
17
6866
6.71
1.7
3.4
5.42
1+2+
no
no
2190
116/
6584
0.9
0.7
1.4
0.6
53/4
853
484
2.9
109
411.
6863
535.
22
2.5
6.1
2+TR
max
17
no
no
21
3542
4.02
3.25
1.2
9.33
no
no
no
no
1593
121/
7796
1.7
1.1
10.
644
/34
4434
3.8
2.3
115
121.
771
444.
10.
482.
849.
3n
on
on
on
o15
5377
4.45
1.6
2.7
8.19
no
no
no
no
19
5545
3.37
1.39
2.3
8.03
no
no
no
no
2366
101/
5170
0.6
0.6
1.8
143
/31
4331
3.3
2.2
4527
1.5
5243
2.6
2.22
4.09
8.1
no
no
no
no
22
5251
2.87
2.56
4.5
7.56
no
no
no
no
13
7056
3.68
1.41
1.6
11.4
no
no
no
no
2066
113/
6178
0.8
0.6
1.7
154
/49
5449
3.7
2.7
7137
2.5
6554
3.5
1.94
26.
1n
on
on
on
o20
6167
4.44
5.68
3.5
10.5
no
no
no
no
1661
120/
8497
0.9
0.7
1.3
0.9
69/5
069
504.
53.
268
151.
671
694.
33.
763.
0411
no
no
no
no
16
4350
1.43
3.4
7n
on
on
on
o
6539
2.88
1.5
1.7
6.5
no
no
no
no
15
5481
3.73
2.65
1.8
191+
no
no
no
6120
2.03
1.7
0.3
111+
no
no
no
18
3250
5.05
2.38
2.9
6.31
no
no
no
no
1659
129/
6083
1.4
0.6
1.1
0.6
41/3
541
354.
12.
571
301.
557
412.
71.
581.
618
no
no
no
no
16
4060
5.32
1.64
1.9
17.8
no
no
no
no
2091
105/
5270
1.2
11
0.7
45/3
845
384.
53.
537
221.
841
454.
21.
781.
1813
no
no
no
no
20
3241
1.31
1.95
4.5
7.86
no
no
no
no
15
4235
3.4
3.23
1.6
10.4
no
no
no
no
2199
100/
5970
0.5
0.5
1.1
0.8
28/2
328
234.
33.
653
311.
741
283
1.71
2.35
10n
on
on
on
o22
4150
3.11
1.42
1.5
11.5
no
no
no
no
2162
119/
6886
1.2
0.9
1.5
0.6
47/4
547
453.
52.
641
221.
646
472.
81.
881.
6614
no
no
no
no
22
3286
6.23
1.7
2.3
9.3
no
no
no
no
2184
103/
5470
0.9
0.8
1.4
0.9
67/5
267
523
2.4
6043
1.65
5267
5.5
1.87
1.91
7.7
no
no
no
no
21
3636
4.18
1.03
1.7
5.54
1+n
on
oye
s23
5173
5.45
1.25
1.2
17.1
no
no
no
no
16
5128
1.7
1.57
12.
331+
no
no
no
20
4662
4.68
1.25
1.7
9.79
no
no
no
no
1479
109/
7285
10.
80.
90.
653
/47
5347
4.6
2.9
107
361.
767
534.
11.
342.
110
no
no
no
no
sl n
o
46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63
EF 2
SV2
CO
- 2
E/A
-2
E'/A
' -2E/E'
2 M
R -
2Tr 2
AR
V
AE
2AP
2H
R 3
BP
3M
AP
3IV
C d
3IV
Cd
3SV
C d
3SV
Cd
3SV
V 3
Svm
ax 3S
V m
in 3L
VID
d 3
LVID
s 3L
VED
V 3
LVES
V 3
TAP
SE 3
EF 3
SV 3
CO
3E/
A 3
E'/A
' 3E/
E' 3
MR
TRA
RV
AE
AP
3
3855
2.71
2.85
1.7
9.34
no
no
no
no
19
5465
4.8
1.97
3.4
7.8
no
no
1+n
o18
4032
2.34
1.64
2.1
11n
on
on
on
o22
6912
5/68
900
.60.
41.
20.
533
/25
3325
3.1
2.4
5725
1.8
5233
2.5
1.98
3.04
8.6
no
no
no
no
23
6163
3.66
1.43
1.9
131+
1+n
on
o19
5557
3.7
2.12
213
.81+
1+n
on
o18
6411
8/71
870
.70.
41.
40.
662
/60
6260
3.3
2.3
5013
1.2
5762
3.7
1.66
2.07
101+
1+n
on
o18
5863
4.85
3.3
1.8
6.95
1+n
on
on
o19
8610
9/77
920
.60.
41.
51
45/3
945
393.
52.
655
232.
553
453.
92.
961.
339.
11+
no
no
no
19
5050
2.6
1.16
1.3
12.7
no
no
no
no
1455
100/
6176
0.5
0.5
1.3
0.8
63/6
163
615.
43.
910
641
2.2
5563
3.2
1.38
1.05
13n
on
on
on
o14
5478
4.69
1.4
1.7
10.2
no
no
1+n
o17
5411
0/64
800
.90.
81.
71.
181
/71
8171
5.1
412
068
2.1
4381
41.
461.
985.
7n
on
o1+
no
17
4058
4.06
1.24
0.8
10.8
1+n
on
on
o20
6511
0/70
870
.80.
71.
60.
855
/45
5545
4.9
3.7
120
542.
855
553.
61.
270.
5214
1+n
on
on
o20
5368
3.74
1.52
0.9
15n
on
on
on
o21
5610
6/52
680
.60.
51.
71
61/5
661
564.
32.
982
452.
446
613.
41.
571.
0413
no
no
no
no
21
6763
4.26
1.77
2.3
6.48
1+n
on
on
o23
7210
8/55
740
.70.
61.
40.
863
/50
6350
3.5
1.9
4115
2.2
6763
42.
072.
598.
71+
no
no
no
24
4254
5.65
3.65
2.2
10.2
no
no
no
no
1410
710
8/64
780
.60.
50.
90.
639
/36
3936
3.4
2.8
2915
1.5
4039
3.5
3.27
1.08
14n
on
on
on
o14
6447
3.99
1.23
1.1
11.4
no
no
no
no
2185
103/
5267
0.7
0.6
1.1
0.5
35/2
935
293.
41.
737
81.
772
352.
80.
981.
4812
no
no
no
no
21
5646
3.56
1.57
2.3
6.07
no
no
no
no
1977
105/
7486
0.8
0.6
1.7
0.9
43/3
243
323.
62.
553
231.
250
433
11.
4114
no
no
no
no
19
6045
4.02
4.01
1.4
11.2
no
no
no
no
14
6854
2.8
5.38
3.8
10.1
1+2+
triv
ialno
2564
162/
104
122
1.9
1.6
1.4
0.9
56/2
956
294.
32.
987
331.
962
563.
63.
543.
418.
81+
2+tr
ivia
lno
25
5963
3.85
11.
211
.8n
on
o1+
no
1965
99/6
479
1.9
1.6
1.7
155
/51
5551
3.8
2.5
5420
1.3
4855
3.4
1.21
1.15
11n
on
o1+
no
19
18%
SIM
ILA
RIT
Y IN
DEX
1 2 3 4 5 6 7 8 9 10Nilim
a_TH
ESI
S PL
AGIR
ISM
.doc
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Bala
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Sub
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m. "
Impa
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Non
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sthe
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Clin
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200
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.. "M
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Ana
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& C
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199
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Cro
ssre
f
259
wor
ds —
4%
142
wor
ds —
2%
135
wor
ds —
2%
107
wor
ds —
2%
94 w
ords
— 2
%
52 w
ords
— 1
%
47 w
ords
— 1
%
44 w
ords
— 1
%
38 w
ords
— 1
%
35 w
ords
— 1
%