an evaluation of hemodynamic instability during elective...

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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

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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

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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

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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

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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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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

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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

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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

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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.

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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

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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

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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,

12


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

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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


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


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


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


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


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


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


Figure 3: Assessment of E/A ratio

Figure 4: Assessment of E’/A’ and E/E’

22


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


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


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


Figure 8 Showing calculation of stroke volume

Figure 9 Showing stroke volume variation

26


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


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


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


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


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


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


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


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


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

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N

um

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(%)

SV

CC

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SV

CC

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dec

SV

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IVC

CI

-in

c

IVC

CI

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IVC

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no

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e

ED

V-

inc

ED

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dec

ED

V-n

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E/E’-

inc

E/E’-

dec

E/E’-

no

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SV

V-

INC

SV

V

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V N

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AN

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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

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ITY

AN

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HR

N

um

ber

(%)

TA

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dec

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R-

NC

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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.

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0

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5

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1

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2.

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0.

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8

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Y:

INC

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SE

, D

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RE

AS

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NC

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CH

AN

GE

38


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

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IVC

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1

05

(79

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42

(40

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47

(45

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15

(14

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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

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10

(38

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4

(15

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10

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1

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(95

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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


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


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


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


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


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


MEAN ARTERIAL PRESSURE DECREASE WITH PRELOAD


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


INCREASE IN MEAN ARTERIAL PRESSURE WITH PRELOAD


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


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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70. Park J-H, Marwick TH. Use and Limitations of E/e’ to Assess Left Ventricular

Filling Pressure by Echocardiography. J Cardiovasc Ultrasound. 2011 ;19 :169–

73.

71. Joris JL, Noirot DP, Legrand MJ, Jacquet NJ, Lamy ML. Hemodynamic

changes during laparoscopic cholecystectomy. Anesth Analg. 1993;76 :1067–

71.

72. Gelman S. The pathophysiology of aortic cross-clamping and unclamping.

Anesthesiology. 1995;82:1026–60.

73. Lonjaret L, Lairez O, Minville V, Geeraerts T. Optimal perioperative

management of arterial blood pressure. Integr Blood Press Control. 2014 ; 7:49–

59.

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

hypotension. Anesthesiology. 2013 ;119 :507–15.

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

general, vascular, and urological surgery. Anesthesiology. 2009 ;110 :58–66.

76. Chew HC, Devanand A, Phua GC, Loo CM. Oesophageal Doppler ultrasound in

the assessment of haemodynamic status of patients admitted to the medical

intensive care unit with septic shock. Ann Acad Med Singapore. 2009;38 :699–

703.

77. Mussa FF, Horton JD, Moridzadeh R, Nicholson J, Trimarchi S, Eagle KA.

Acute Aortic Dissection and Intramural Hematoma: A Systematic Review.

JAMA. 2016 ;316:754–63.

78. Erbel R, Aboyans V, Boileau C, Bossone E, Bartolomeo RD, Eggebrecht H, et

al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases:

Document covering acute and chronic aortic diseases of the thoracic and

abdominal aorta of the adult. The Task Force for the Diagnosis and Treatment of

Aortic Diseases of the European Society of Cardiology (ESC). Eur Heart J. 2014

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79. Yamaura K, Hoka S, Okamoto H, Takahashi S. Quantitative analysis of left

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cross-clamping. J Cardiothorac Vasc Anesth. 2003;17:703–8.

80. Couture P, Denault AY, Carignan S, Boudreault D, Babin D, Ruel M.

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transesophageal echocardiography. Can J Anaesth J Can Anesth. 1999 ;46 :827–

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81. Koolen JJ, Visser CA, Reichert SL, Jaarsma WJ, Kromhout JG, van Wezel HB,

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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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F65

165

1.72

recu

rren

t tu

bec

ulu

m s

ella

men

ingi

om

acr

anio

tom

y an

d d

eco

mp

ress

ion

Sup

ine

64n

on

o1.

26n

il74

129/

8899

4157

F60

155

1.59

R r

esid

ual

Ten

tori

al m

enin

gio

ma

cran

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my

and

dec

om

pre

ssio

nla

tera

l70

Gra

de

1 d

iast

olic

dys

fun

ctio

nno

0.93

MR

1+

7611

0/53

70

4255

F36

145

1.22

R F

ron

top

arie

tal m

enin

gio

ma

cran

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my

and

dec

om

pre

ssio

nSu

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

eN

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

ysfu

nct

ionn

o0.

82n

o66

120/

4973

4536

M85

165

1.92

Bila

tera

l In

tern

al C

aro

tid

Art

ery

aneu

rysm

pte

rio

nal

cra

nio

tom

y an

d c

lipp

ing

Sup

ine

68n

on

o1.

33n

o66

120/

8685

sl n

oag

ege

nd

erw

eigh

thei

ght

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(m

2)Dia

gno

sis

surg

ery

po

siti

on

P-L

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(%)P-d

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P-R

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alve

P-H

R P

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4652

M65

165

1.72

AC

OM

art

ery

aneu

rysm

Cra

nio

tom

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d C

lipp

ing

Sup

ine

66n

on

o1.

28n

o54

170/

9511

0

4740

M65

165

1.72

Rig

ht

insu

lar

low

gra

de

glio

ma

cran

ioto

my

and

dec

om

pre

ssio

nSu

pin

e66

no

no

1.33

TR1

+,A

R 1

+74

116/

4062

4855

M65

154

1.63

R IC

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om

mu

nic

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g se

gmen

t an

eury

smp

teri

on

al c

ran

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my

and

clip

pin

gSu

pin

e70

no

no

1.52

no

7612

6/85

102

4957

F65

155

1.64

L p

aras

aggi

tal m

enin

gio

ma

cran

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my

and

dec

om

pre

ssio

nsi

ttin

g62

no

no

1.27

no

5611

9/68

89

5027

F65

155

1.64

L f

ron

to-p

arie

tal h

igh

gra

de

lesi

on

cr

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tom

y an

d d

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mp

ress

ion

Sup

ine

ND

ND

ND

ND

ND

7411

0/70

84

5143

F60

152

1.56

L an

teri

or

on

e th

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par

asag

gita

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ingi

om

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fro

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l cra

nio

tom

y an

d e

xcis

ion

Sup

ine

71n

on

o1.

1n

o84

98/5

470

5245

M65

165

1.72

glio

ma

cran

ioto

my

and

dec

om

pre

ssio

nsu

pin

eN

DN

DN

DN

DN

D51

119/

6786

5352

M75

175

1.9

R M

CA

bif

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atio

n a

neu

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and

clip

pin

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no

1.43

AR

1+,

scle

roti

c A

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212

2/74

92

5459

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1.75

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tran

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an

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nio

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up

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dia

sto

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73M

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134/

8910

0

5554

M75

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1.9

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cran

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and

dec

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pre

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pin

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Gra

de

1 d

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dys

fun

ctio

nno

<1

no

5810

2/56

65

5647

F66

155

1.65

Left

rec

urr

ent

fro

nto

insu

lar

glio

ma

cran

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my

and

dec

om

pre

ssio

nSu

pin

e75

no

no

1.17

no

5511

5/53

75

5718

F46

151

1.39

Cra

nio

ph

aryn

gio

ma

R p

eric

oro

nal

par

asag

gita

l cra

nio

tom

ySup

ine

ND

ND

ND

ND

ND

8411

4/68

83

5840

F61

162

1.65

L Fr

on

tal C

on

vexi

ty m

enin

gio

ma

L Fr

on

tal c

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my

and

dec

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pre

ssio

nSu

pin

e60

no

E>A

no

8314

1/94

110

5937

F58

157

1.58

L p

aras

aggi

tal m

enin

gio

ma

cran

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my

and

exc

isio

nSu

pin

e62

nil

1.5

no

6811

5/77

92

6020

F47

147

1.38

R p

arie

tal l

esio

n (

glio

ma)

cran

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my

and

dec

om

pre

ssio

nSu

pin

eN

DN

DN

DN

DN

D88

103/

5166

6134

M80

165

1.96

Rec

urr

ent

R F

ron

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per

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r le

sio

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exp

lora

tory

Cra

nio

tom

y an

d d

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mp

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ion

Sup

ine

64n

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5256

112/

7083

6256

M51

136.

51.

35L

Fro

nta

l par

afal

cin

e m

enig

iom

acr

anio

tom

y an

d e

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ion

Sup

ine

62n

on

o1.

28A

R 2

+,sc

lero

tic

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5810

8/64

83

6320

F45

154

1.4

L re

curr

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ma

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late

ral

ND

ND

ND

ND

ND

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

VED

VB

-LV

ESV

B-L

VID

DB

-LV

IDS

(cm

)B

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%)B

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Svm

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min

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OB

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Cd

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Cd

2 B

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VC

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PFO

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IVC

max

IVC

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inSV

Cd

max

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dm

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max

1

5815

4.2

373

6060

401.

5n

o1.

711.

27

no

no

no

1.4

0.9

10.

9n

o1.

610

910

2/54

700.

60.

30.

90.

730

8034

3.3

276

4141

303.

57n

o1.

321.

515

5.51

no

no

no

0.8

0.6

0.6

0.5

no

1.5

100

120/

7187

1.3

0.8

0.8

0.4

59

9040

4.7

4.1

4952

5230

2.37

no

2.21

2.81

60.

16n

on

on

o1.

20.

90.

90.

7n

o1.

757

80/4

053

0.6

0.5

1.2

0.9

60

7532

2.6

0.8

9759

5944

2.38

no

1.11

0.61

29

no

no

no

1.2

0.5

0.8

0.3

no

1.7

6610

0/56

711.

51.

31.

10.

559

7234

2.8

1.4

5056

5640

3.35

no

1.88

2.36

0.3

1+2+

no

1.4

0.9

1.1

0.6

no

1.6

7212

4/80

951.

31

1.4

0.9

60

8045

2.5

245

5050

251.

75n

o1.

161.

585

5.71

no

no

no

1.4

10.

80.

6n

o1.

7570

122/

8497

1.9

1.7

1.4

0.9

40

7526

4.2

3.1

6536

3632

2.62

no

1.17

2.51

58.

49n

on

on

o1.

21

0.7

0.5

yes

1.5

9093

/53

660.

70.

51.

50.

738

5732

43.

444

154

154

134

11.6

no

1.12

1.68

514

.7n

on

on

o1.

31.

20.

50.

5n

o1.

675

126/

5879

1.2

0.9

0.9

0.9

55

9532

4.4

3.9

6553

5344

3.49

no

1.74

1.72

78.

96n

on

on

o1.

40.

70.

70.

6n

o1.

665

103/

5876

0.7

0.6

0.7

0.5

53

6837

4.4

3.4

4649

4935

2.52

no

3.72

2.62

48.

51n

on

on

o1

0.4

0.6

0.4

no

1.76

6912

7/77

940.

90.

90.

70.

654

4326

3.8

3.1

4051

5146

3.48

no

1.03

2.06

64.

96n

on

on

o1.

91.

10.

70.

6ye

s1.

963

100/

5671

0.7

0.6

1.9

1.6

50

6730

3.9

2.8

5654

5446

4.39

no

3.11

2.97

78.

22n

on

on

o1.

70.

70.

60.

5n

o1.

5576

134/

8299

0.5

0.4

1.4

1.1

40

8753

4.6

3.5

4362

6257

4.9

no

1.31

1.91

99.

09n

on

on

o1.

50.

90.

90.

9n

o1.

6

4015

3.3

2.9

6136

3631

2.48

no

2.34

2.15

714

.7n

on

on

o1.

40.

70.

40.

3ye

s1.

6

5616

3.8

2.3

7055

5539

3.19

no

21.

474

11.5

no

no

no

1.5

1.2

0.8

0.6

no

1.5

6211

7/59

780.

70.

61.

91.

139

8442

3.7

4.2

5062

6247

2.27

no

5.18

2.99

810

.7n

on

on

o1.

60.

80.

90.

7n

o1.

694

131/

7694

0.5

0.4

1.4

0.8

36

6521

3.9

2.5

7472

7230

4.16

1n

o1.

727.

419

5.31

no

no

no

1.6

1.1

0.8

0.8

no

1.6

6312

0/70

871

11.

61.

278

100

525.

34.

248

4444

392.

45n

o1.

971.

478.

98n

on

on

o1.

41

0.6

0.6

no

1.7

6611

6/84

910.

60.

51.

10.

741

8951

4.5

3.7

6637

3729

2.21

no

3.17

1.59

314

.5n

on

on

o1.

91.

40.

50.

4n

o1.

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

o1.

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

/46

590.

30.

31.

31

62

8834

3.5

1.8

4859

5948

3.33

no

1.94

2.79

29.

71n

on

on

o1.

51

11

no

1.6

8015

3/69

101

1.2

11.

41.

351

117

684.

43.

642

5555

443.

18n

o4.

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

o1.

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

o1.

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

o1.

40.

51.

50.

9n

o1.

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

o1.

10.

50.

60.

6n

o1.

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

o1.

91.

31.

30.

8n

o1.

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

o1.

6

8833

3.1

2.1

6264

6434

2.95

AS

+IS

,sco

re 1

2/1

71.

422.

094

21.5

no

1+n

o2.

11.

40.

80.

7n

o1.

843

109/

5372

1.5

1.4

1.4

0.7

37

7032

2.8

1.7

4919

1917

1.9

apic

al,m

idp

ort

ion

hyp

oki

nes

ia2.

380.

515

24.8

no

1+n

o0.

80.

51.

10.

8n

o1.

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

.3n

o2+

,ecc

entr

ic je

tn

o1

0.5

1.2

0.9

no

1.7

7514

0/86

104

0.7

0.7

1.5

0.9

80

7135

5.1

3.3

5140

4029

2.67

no

1.19

1.99

96.

071+

1+n

o0.

90.

51.

91.

2n

o1.

5

4916

3.5

2.4

6857

5727

1.55

no

2.12

1.60

214

.7n

on

on

o1.

10.

32.

91.

1n

o1.

857

87/4

357

0.8

0.6

1.2

0.6

35

5430

4.3

445

6060

305.

71n

o4.

462.

831

11.8

no

1+n

o1.

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

o1.

40.

71.

51.

2n

o1.

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

o1.

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

/43

560.

90.

71.

20.

873

5128

4.1

3.1

4643

4338

3.27

no

2.06

1.21

916

no

1+n

o1.

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

930.

30.

11.

30.

560

6323

4.2

3.4

6350

5044

4.82

no

1.37

1.77

312

.1n

on

on

o1

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

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INA

LIT

Y R

EPO

RT

PRIM

AR

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UR

CES

jour

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.lww

.com

Inte

rnet

ww

w.w

ildca

tane

sthe

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com

Inte

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guid

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ejec

hoca

rd.p

rod-

oup.

high

wire

.org

Inte

rnet

lib.b

ioin

fo.p

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ww

w.n

cbi.n

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tern

et

ajrc

cm.a

tsjo

urna

ls.o

rgIn

tern

et

Bala

chun

dhar

Sub

ram

ania

m. "

Impa

ct o

f TE

E in

Non

card

iac

Surg

ery"

, Int

erna

tiona

l Ane

sthe

siol

ogy

Clin

ics,

200

8C

ross

ref

ww

w.c

ja-jc

a.or

gIn

tern

et

Zora

b, J

.S.M

.. "M

akin

g se

nse

of m

onito

ring"

, Cur

rent

Ana

esth

esia

& C

ritic

al C

are,

199

005

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

%

an evaluation of hemodynamic instability during elective...

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