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Research Article | Volume 15 Issue 1 (Jan - Feb, 2025) | Pages 354 - 362
Transthoracic Echocardiography: A real time hemodynamic monitoring tool during induction of anaesthesia in patients undergoing coronary artery bypass grafting surgery
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 ,
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1
Associate Professor, Department of Anaesthesiology, Karpagam faculty of medical sciences and research, Coimbatore. India
2
Assistant Professor, Department of Anaesthesiology, Karpagam faculty of medical sciences and research, Coimbatore. India
Under a Creative Commons license
Open Access
Received
Jan. 29, 2024
Revised
Dec. 8, 2024
Accepted
Dec. 30, 2024
Published
Jan. 28, 2025
Abstract

Objective: To evaluate the effectiveness of transthoracic echocardiography as a hemodynamic monitoring tool during induction of anesthesia and endotracheal intubation Design:  Prospective, single center, observational study Setting: Medical college teaching hospital Participants: Sixteen patients undergoing elective coronary artery bypass surgery Interventions: Patients were monitored with Transthoracic echocardiography and pulmonary artery catheter  Measurements and Main results: Baseline pre induction Transthoracic echocardiography was done to calculate fractional Shortening, fractional Area Change. Cardiac output and systemic vascular resistance were calculated by left ventricular outflow and mitral inflow Doppler. At the same time baseline pulmonary artery catheter measurements, cardiac output and calculated systemic vascular resistance were recorded. Measurements of Transthoracic echocardiography and pulmonary artery catheter were repeated during post induction and one minute after endotracheal intubation. Percent difference between baseline and post induction (Group A data) and percent difference between post induction and post intubation (Group B data) of all parameters were calculated. From group A and group B data estimated percent change in cardiac output and systemic vascular resistance correlated between two techniques. It also predicts the change in contractility during induction and endotracheal intubation. The change in cardiac output as estimated by the mitral inflow doppler and the left ventricular outflow doppler correlated well. Conclusion: Transthoracic echocardiography can be used as a replacement for pulmonary artery catheter to predict change in blood pressure, afterload and cardiac output during induction of anaesthesia in a non-invasive manner

Keywords
INTRODUCTION

Intense monitoring of hemodynamics. The invasive blood pressure (BP), central venous pressure (CVP), pulmonary artery catheter (PAC) is commonly used, in addition to electrocardiography (ECG) as hemodynamic monitoring tools in cardiac anesthesia practice. All of the above monitoring can be instituted before induction of anesthesia with minimal local analgesia.  

 

The PAC has been considered the gold standard for hemodynamic monitoring. However insertion of a PAC is not without its own risks. A good correlation has been shown between pulmonary capillary wedge pressure (PCWP) and left atrial pressure (LAP), LAP and left ventricular (LV) end diastolic pressure (LVEDP) under well defined physiologic circumstances. But under certain diseased states like coronary heart disease, valvular heart diseases there may be disparity between PCWP and LAP, LAP and LVEDP.1, 2 Although most of the monitoring techniques which are currently in clinical use, give numerical values for different parameters. The actual picture of cardiac structure and function is not presented by these monitoring techniques. Transoesophageal echocardiography (TOE) is nowadays well accepted as a real time monitoring tool during cardiac surgery. Because of interference with airway management and difficulty in toleration by awake patients, Transoesophageal echocardiography (TOE) cannot be used before induction of anesthesia.  Transthoracic echocardiography (TTE) has been used to monitor various hemodynamic parameters in patients where both PAC and TOE are contraindicated and it has been shown to predict hemodynamic changes quite accurately.3

 

There is a recent trend towards development of non invasive techniques for haemodynamic monitoring, which has inspired us to evaluate the effectiveness of TTE as a hemodynamic monitoring tool during induction of anesthesia and endotracheal intubation. We have compared the use of TTE with PAC monitoring in patients with coronary artery disease undergoing CABG

MATERIALS AND METHODS

The study protocol was approved by the institutional ethics committee. The study was conducted in a medical college teaching hospital. The study was done in a prospective randomized manner and it was an observational study.

 

After obtaining written informed patient consent, 16 patients scheduled for elective CABG were enrolled in the study. All the patients belonged to group II or group III, of the New York Heart Association classification. Patients with unstable hemodynamics, a rhythm other than sinus rhythm, poor echo windows (as in patients with COPD, obesity, crowded ribs), and those who were pre operative ventilatory support, were excluded from the study. Preoperative anti anginal medications & b blockers were continued preoperatively and the morning dose on the day of surgery was continued. All patients received 0.1 mg/kg of morphine and 0.5 mg/kg of promethazine, intramuscularly, 1 hour before the induction of anesthesia.  After arrival of the patient inside the operation theatre, 5 lead ECG, pulse oximetry, non-invasive blood pressure monitoring was started. Peripheral intra venous line (16 G), invasive radial arterial pressure (20 G) and a 7.5 F five lumen standard thermodilution PAC (Edwards life sciences LLC, Irvine, CA 92614) through right internal jugular vein was introduced under local analgesia.

 

After the above-mentioned procedures, the operation table was given a 30° left lateral tilt to improve echo windows. Baseline TTE (Philips sonos 5500, Dublin, Ireland) was done by an experienced echocardiographer, in short axis parasternal, apical four chamber and apical five chamber views. At the same time baseline PAC measurements, pulmonary artery systolic pressure (SYS-PAP), pulmonary artery diastolic pressure (DIA-PAP), mean pulmonary artery pressure, PCWP, CVP, cardiac output by thermo dilution (CO-TD) technique using 10 ml of ice-cold saline, calculated systemic vascular resistance (SVR-TD) and invasive arterial pressure were recorded. The baseline and subsequent CO were obtained from the average of three measurements during a brief period of apnea at end expiration; CO determinations were repeated until three consecutive measurements with less than 10% variability were obtained.  After baseline readings all patients received 1 mg midazolam and 2 mg/kg fentanyl intravenously. Anesthesia was induced with a sleep dose of 2.5% thiopentone sodium, and 0.9 mg/kg of rocuronium was administered for muscle relaxation and mask ventilation was started. Post induction measurements of TTE and PAC was repeated, endotracheal intubation was done with appropriate endotracheal tube and one minute after endotracheal intubation, post intubation measurements of TTE and PAC were repeated.

 

All pre intubation and post intubation measurements were performed in the expiratory phase of the respiratory cycle without applying positive end expiratory pressure (PEEP). The left ventricular end diastolic diameter (LV-EDD) and left ventricular end systolic diameter (LV-ESD) at the level of the chordae tendineae of the mitral valve were calculated from the short axis parasternal view. The left ventricular end diastolic area (LV-EDA- the largest LV cross sectional area immediately after the R wave peak on ECG) and left ventricular end systolic area (LV-ESA- defined as the frame corresponding to the smallest LV cross sectional area) were calculated from apical four chamber view. Time velocity integral (TVI) of left ventricular outflow tract (TVI-LVOT), TVI of mitral inflow (TVI-MV), LVOT diameter, mitral valve area (MVA) by pressure half time, fractional Shortening (FS = 100 ´ (LV-EDD - LV-ESD) / LV-EDD), fractional Area Change (FAC = 100 ´ (LV-EDA - LV-ESA) / LV-EDA) were calculated. CO was calculated by LVOT outflow doppler (area of LVOT C TVI-LVOT C HR) and mitral inflow doppler (MVA C TVI-MV C HR). Systemic vascular resistance (SVR) was calculated by mitral inflow Doppler (SVR-MV) and LVOT Doppler (SVR-LVOT). The end diastolic & end systolic views of each cardiac cycle were defined as the smallest and largest apical four chamber view. End diastolic & systolic assignment was verified by comparison with the peak of the R wave & end of T wave on a synchronous ECG signal respectively. Average of three consecutive cardiac cycles was used in all measurements. Apart from above mentioned quantitative measures, assessment was also done qualitatively by the echocardiographer.

 

From the above mentioned measured and derived parameters, percent difference between baseline and post induction (Group A data) and also percent difference between post induction and post intubation (Group B data) of mean blood pressure (M-BP), PCWP, LV-EDD, LV-EDA, FS, FAC, CO-TD, CO-MV, CO-LVOT, SVR-TD, SVR-MV and SVR-LVOT were calculated.

 

Statistics

Karl Pearson and Spearman correlation coefficient was used to determine the correlation between the various parameters. STATA.9 software (StataCorp LP, 4905 Lakeway Drive, College Station, Texas 77845, USA) was used to calculate the p value and the correlation coefficient

RESULTS

The demographic data of study patients is displayed in table -1. The haemodynamic and TTE data obtained at baseline, pre intubation and post intubation are summarized in table-2. Except FAC, all parameters show a decreasing trend from baseline to pre intubation values and increasing trend for pre intubation to post intubation values. The decreasing trend is statistically significant for SYS-BP, DIA-BP, M-BP, SYS-PAP, DIA-PAP, M-PAP, PCWP, CVP, LV-EDD, LV-ESD, LV-EDA, LV-ESA, CO-TD, CO-MV, CO-LVOT, SVR-TD.  The increasing trend is statistically significant for SYS-BP, DIA-BP, M-BP, SYS-PAP, DIA-PAP, M-PAP, PCWP, CVP, LV-EDD, LV-ESD, FS, LV-EDA, LV-ESA, CO-TD, CO-MV, CO-LVOT.

 

Table-1. Demographic data

 

 

 

1

Age

60.81

(±9.81)

 

 

2

Male :Female

13:3

3

Weight (kg)

67.06      (±7.16)

4

Height (cms)

169.25      (±5.7)

5

Left Ventricular function

 

Normal

 

Mild Left Ventricular dysfunction

 

2

14

6

Associated diseases

Diabetes

Hypertension

6

10

 

 Plus –minus are mean ± standard deviation

 

Table-2. Haemodynamic and echocardiographic data

 

Baseline

Post induction

Post intubation

Group A data

Group B data

HR

81.06 (±11.22)

77.5 (±12.68)

83.19 (±11.14)

 

 

SYS-BP

142.88 (±12.31)

112.38 (±11.46)

138.57 (±13.5)

 

 

DIA -BP

72.31 (±7.26)

58.81 (±5.90)

69.19 (±5)

 

 

Mean  BP

95.5 (±7.36)

76.75 (±6.39)

92.56 (±6.58)

-19.53 (±5.18)ƒ

+21.01 (±8.85) ƒ

PA-SYS

28.38 (±3.32)

23.75 (±2.93)

27.75 (±2.46)

 

 

PA-DIA

13.5 (±2.78)

11.44 (±2.31)

13.63 (±1.75)

 

 

PA-MEAN

18.3 (±2.77) 

15.81 (±2.69)

18.56 (±1.41)

-12.45ƒ (±17.4) ƒ

+20.47ƒ (±21.72) ƒ

PCWP

11.25 (±1.98)  

8.44 (±1.97)

10.13 (±1.54)

-24.92  (±12.65) ƒ

+24.24  (±25.29) ƒ

CVP

9.63 (±2.09)

7.19 (±1.52)

9.75 (±1.44)

 

 

LV-EDD

50.06 (±4.51)

42 (±4.55)

48.31 (±3.9)

-16.04 (±6.44) ƒ

+15.58 (±7.9) ƒ

LV-ESD

27.63 (±3.54)

23.63 (±3.03)

26.13 (±3.26)

 

 

FS

46.06 (±5.21)

43.69 (±5.72)        

45.94 (±5.52)

-6.4 (±12.23)

+5.68  (±8.73) ƒ

LV-EDA

51.75 (±4.45)

45.88 (±5.10)

50.25    (±3.94)

-11.4  (±5.43) ƒ

+10.1  (±7.59) ƒ

LV-ESA

27.69 (±3.84)

24.13 (±3.98)

26.63    (±3.4)

 

 

FAC

46.44 (±6.71)

47.31(±6.02)

46.63    (±5.88)

+2.61  (±10.24)

-1.06 (± 9)

CO- TD

4.31 (±0.41)

3.68 (±0.38)

4.2 (±0.42)

-14.37 (±6.14) ƒ

+14.35  (±7.67) ƒ

CO- MV

4.36 (±0.42)

3.66 (±0.34)

4.21    (±0.45)

-15.47 (± 6.24) ƒ

+15.12  (±7.91) ƒ

CO-LVOT

4.38 (±0.41)

3.67 (±0.36)

4.25    (±0.43)

-16.08  (±6.28) ƒ

+16.06  (±8.27) ƒ

SVR-TD

1604.19 (±139.73)

1524.63 (±93.49)

1584.44    (±124.24)

-4.47 (±7.98) ƒ

+4.1 (±8.01)

SVR-MV

1585.13    (±160.44)

1535.25 (±122.68)

1582.81    (±121.72)

-2.4  (±11)

+3.55  (±9.63)

SVR-LVOT

1579.19    (±171.14)

1530.69 (±121.21)

1564.13    (±98.05)     

-2.42  (±8.96)

+2.68  (±9.04)

 

ƒ =p < 0.05 statistically significant, HR- Heart rate, SYS- Systolic, BP- Blood Pressure, DIA- Diastolic, PA – Pulmonary artery, PCWP – Pulmonary Capillary Wedge Pressure, CVP- Central Venous Pressure, LV – Left Ventricle, EDD – End Diastolic Diameter, ESD- End Systolic Diameter, FS- Fractional shortening, EDA – End Diastolic Area, ESA – End Systolic Area, FAC – Fractional Area of Change, CO – Cardiac Output, TD- Thermo dilution, MV – Mitral Valve, LVOT - Left Ventricular Outflow Tract, SVR – Systemic Vascular Resistance, TD – Thermo dilution, ± plus minus values are mean ± standard deviation.

 

The baseline to pre intubation PAC measured preload parameters (CVP- 2.44 mmHg and PCWP-24.92 (12.65) %) show a decreasing trend, the same trend as was observed in TTE estimated preload parameters (LV-EDD-16.04 (6.44)%  and LV-EDA-11.4  (5.43)%). The pre intubation to post intubation PAC measured preload parameters (CVP + 2.56 mmHg and PCWP +24.24 (25.29) %) show an increasing trend, the same trend as was observed in TTE estimated preload parameters (LV-EDD +15.58 (7.9) % and LV-EDA +10.1 (7.59) %).

 

Both TEE and PAC estimated baseline to pre intubation CO measurements (CO- TD-14.37 (6.14) %, CO-MV-15.47 (6.24) %, CO- LVOT-16.08 (6.28) %) show a decreasing trend and the change is statistically significant. Pre intubation to post intubation CO measurements (CO- TD+14.35 (7.67) %, CO-MV+15.12 (7.91) %, CO- LVOT+16.06 (8.27) %) show an increasing trend and the change is statistically significant.

 

Both TEE and PAC estimated baseline to pre intubation SVR measurements (SVR- TD-4.47 (7.98) %, SVR-MV-2.4  (11) %, SVR- LVOT-2.42  (8.96) %) show a decreasing trend and the change is not statistically significant, pre intubation to post intubation SVR measurements (SVR- TD+4.1 (8.01) %, SVR-MV+3.55  (9.63) %, SVR- LVOT+2.68  (9.04) %) show an increasing trend and the change is not statistically significant.

 

Correlation analyses of preload, afterload and cardiac output parameters displayed in Table-3. From the Group A data, percent change in CO-TD positively correlates with percent change in CO -MV (p 0.00, r 0.836) and CO -LVOT (p 0.00, r 0.798).  From the Group B data, percent change in CO-TD positively correlates with percent change in CO -MV (p 0.004, r 0.679) and CO -LVOT (p 0.006, r 0.657).  From the Group A data, percent change in SVR-TD positively correlates with percent change in SVR-MV (p 0.000, r 0.847) and SVR -LVOT (p 0.000, r 0.874). From the Group B data, percent change in SVR-TD positively correlates with percent change in SVR-MV (p 0.000, r 0.835) and SVR -LVOT (p 0.000, r 0.797).  (Table -3)

 

Table-3. Correlation analysis of change in preload, after load and cardiac output measured by transthoracic echocardiography and pulmonary artery catheter

Group

 

Correlation between

p value

r value

A

Preload correlation

PCWP´LV-EDD

PCWP´LV-EDA

0.496

0.456

-

-

B

Preload correlation

PCWP´LV-EDD

PCWP´LV-EDA

0.979

0.866

-

-

A

CO correlation

 

CO-TD´CO-MV

CO-TD´CO-LVOT

<0.001 ƒ

<0.001 ƒ

0.836

0.798

B

CO correlation

CO-TD´CO-MV

CO-TD´CO-LVOT

0.004 ƒ

0.006 ƒ

 

0.679

0.657

A

Afterload correlation

SVR-TD´SVR-MV

SVR-TD´SVR-LVOT

<0.001 ƒ

<0.001 ƒ

 

0.847

0.874

B

Afterload correlation

 

SVR-TD´SVR-MV

SVR-TD´SVR-LVOT

<0.001 ƒ

<0.001 ƒ

 

0.835

0.797

 

PCWP – Pulmonary Capillary Wedge Pressure,

LV – Left Ventricle, EDD – End Diastolic Diameter, EDA – End Diastolic Area,

CO – Cardiac Output, TD – Thermodilution, MV – Mitral Valve, LVOT – Left ventricular outflow tract, SVR – Systemic Vascular Resistance, ƒ =P < 0.05 is statistically significant

 

Correlation analysis of change in preload and afterload parameters and change in mean blood pressure are displayed in table-4. From the Group A data, percent change in mean blood pressure does not significantly correlate with percent change in PCWP (p 0.823), LV-EDD (p 0.231) and LV-EDA (p 0.771). ). From the Group B data, percent change in mean blood pressure does not significantly correlate with percent change in PCWP (p 0.601), LV-EDD (p 0.308) and LV-EDA (p 0.519). From the Group A data percent change in mean blood pressure positively correlates with percent change in SVR-MV (p 0.037, r 0.526) and SVR-LVOT (p 0.05, r 0.496). Group A data percent change in mean blood pressure does not correlate with percent change in SVR-TD (p 0.07). From Group B percent change in mean blood pressure positively correlates with percent change in SVR-MV (p 0.048, r 0.5), SVR-LVOT (p 0.022, r 0.568) and SVR-TD (p 0.01, r 0.625).

 

Table - 4. Correlation analysis of change in preload and afterload parameters and change in mean blood pressure

Group

 

Correlation between

p value

r value

A

Preload correlation

PCWP´M-BP

LV-EDD´M-BP

LV-EDA´M-BP

 

0.823

0.231

0.771

 

-

-

-

B

Preload correlation

PCWP´M-BP

LV-EDD´M-BP

LV-EDA´M-BP

 

p 0.601

p 0.308

0.519

-

-

-

A

Afterload correlation

SVR-MV´M-BP

SVR-LVOT´M-BP

SVR-TD´M-BP

0.037 ƒ

 0.05 ƒ

 0.07

0.526

0.496

-

B

Afterload correlation

SVR-MV´M-BP

SVR-LVOT´M-BP

SVR-TD´M-BP

0.048 ƒ

0.022 ƒ

0.01 ƒ

0.500

0.568

0.625

 

ƒ =p < 0.05 statistically significant, M-BP- Mean Blood Pressure, PCWP – Pulmonary Capillary Wedge Pressure, LV – Left Ventricle, EDD – End Diastolic Diameter, EDA- End Diastolic Area,  TD- Thermo dilution, MV – Mitral Valve, LVOT - Left Ventricular Outflow Tract, SVR – Systemic Vascular Resistance,  ± plus minus values are mean ± standard deviation.

 

Correlation analysis of change in preload, afterload and cardiac output parameters as measured by two different methods of transthoracic echocardiography are displayed in table-5. The correlation between LV-EDD, LV-EDA is significant (p 0.002) and positive (r 0.702 The correlation between LV-EDD, LV-EDA is significant (p 0.005) and positive (r 0.661). Percent change in CO -MV positively correlates with percent change in CO -LVOT (p 0.00, r 0.874). Percent change in CO -MV positively correlates with percent change in CO -LVOT (p 0.002, r 0.716). Percent change in SVR -MV is positively correlates with percent change in SVR -LVOT (p 0.000, r 0.89). Percent change in SVR-MV positively correlates with percent change in SVR-LVOT (p 0.000, r 0.85). 

 

Table - 5. Correlation analysis of change in preload, afterload and cariac output parameters measured by two different methods of transthoracic echocardiography

Group

 

Correlation between

p value

r value

A

Preload correlation

LV-EDD´LV-EDA

0.002 ƒ

0.702

B

Preload correlation

LV-EDD´LV-EDA

0.005 ƒ

0.661

A

CO correlation

 

 

 

CO-MV´CO-LVOT

<0.001 ƒ

0.874

B

CO correlation

CO-MV´CO-LVOT

0.002 ƒ

0.716

A

Afterload correlation

SVR-MV´SVR-LVOT

 

<0.001 ƒ

 

0.890

 

B

Afterload correlation

SVR-MV´SVR-LVOT

 

<0.001 ƒ

 

0.850

 

ƒ =p < 0.05 statistically significant, LV – Left Ventricle, EDD – End Diastolic Diameter, EDA – End Diastolic Area, CO – Cardiac Output, TD- Thermo dilution, MV – Mitral Valve, LVOT - Left Ventricular Outflow Tract, SVR – Systemic Vascular Resistance, ± plus minus values are mean ± standard deviation.

DISCUSSION

In 1970 Swan et al introduced pulmonary artery catheterization, 38 years of invasive monitoring have made the balloon tipped flow directed PAC a gold standard for hemodynamic monitoring includes filling pattern of left ventricle, systolic& diastolic functions of heart, valvular function, assessment of CO, SVR, etc.4 It provides information unavailable by clinical examination, and has been shown to alter the diagnostic and therapeutic decisions.5

 

The use of PAC in peri operative medicine is one of the most controversial subjects in anesthesia and in critical care medicine. The changes in intrathoracic pressure resulting from mechanical ventilation and / or application of PEEP and the position of the PAC in different areas of the lung (west zones) may lead to misinterpretation of the data from PAC. The impact of variations in the distribution volume, i.e., the volume between the injection port of the bolus and the thermistor, on the thermodilution measurement of cardiac output by was never discussed.6 The calculation of resistance in low-pressure pulmonary circulation is atleast under intensive care settings, controversial.

 

Insertion of a PAC is not without its own risks. These include the well-known complications of central venous catheterization and additional complications specific to introduction of a PAC such as arrhythmias, catheter coiling, knotting, damage to endocardium, tricuspid, pulmonic valve, pulmonary infarction, pulmonary artery rupture, etc.

 

Almost 50% of respondents to a questionnaire in a multicenter study of physician’s knowledge about PAC were unable to adequately deal with a PAC and with the data obtained.7, 8 So the PAC may give inaccurate data and its use may be associated with unwanted side effects. A monitoring technique is needed to replace the PAC with accuracy equal to or greater than the PAC.

 

In our study we found that the TTE estimated fall in afterload correlate well with the PAC derived fall in afterload during the induction of anesthesia. The TTE estimated fall in afterload not only correlates with the PAC measured fall in afterload, but it also correlates with the fall in blood pressure during induction. Along with the above-mentioned predictors, a change in LV-EDD and a change in LV-EDA also predict the decrease in contractility during induction of anesthesia. The fall in blood pressure during induction of anesthesia is because of a fall in SVR and myo-depression induced by the balanced anesthesia technique used.

 

We also found that TTE estimated increase in afterload correlates well with the PAC estimated raise in afterload during intubation. TTE estimated raise in afterload not only correlated well with the PAC measured raise in afterload, but it also correlated well with raise in blood pressure during intubation. Along with the above-mentioned predictors, a change in LV-EDD, LV-EDA and FS also predicted the increase in contractility during intubation. So, an increase in blood pressure during intubation is because of an increase in SVR and contractility, secondary to sympathetic stimulation.

 

In our study change in FAC does not predicts the change in contractility, both during induction and intubation. The presence of LV dysfunction may be the reason for the FAC s failure to predict the change in contractility. With TTE monitoring we can find the reason for change in hemodynamics during induction of anesthesia in a particular patient and we can initiate the appropriate treatment if needed. However, based on echo data we did not use any intervention in our study, as it is an observational study. We also found that TEE estimated changes in CO correlate well with PAC derived changes in CO, both during induction and intubation.

 

Controversy exists not only regarding the use of a PAC, but also with the timing of insertion of PAC. More pharmacological interventions were performed before tracheal intubation based on hemodynamic data obtained in patients in whom the PAC was placed before induction of GA.9,10  The time taken for PAC insertion in awake patients was longer, it was a stressful painful and unnecessary intervention before induction of anesthesia and leads to hemodynamic changes or ischemia.11-13 Access to hemodynamic data before and during induction may however be crucial in patients with poor LV function. The TTE is a good replacement for a PAC, to monitor hemodynamic parameters during induction of anesthesia.

 

P.G. Barash and Wendy J. Wolt used TTE to evaluate the anesthetic effects on ventricular function in children and they found that echo provides a more sensitive and discriminating way to monitor changes in the cardiovascular system than routine hemodynamic monitoring and is the potential tool for clinical anesthesiology that may supplant the invasive monitoring currently available.14, 15

 

Filipovic used TTE as a monitoring tool in two patients, one with dilated cardio myopathy and the second with a severe mitral secondary to bacterial endocarditis who underwent caesarean delivery under regional anesthesia. The management strategy was to give intra venous fluid when BP and LVDD decreased simultaneously and to give vasoactive drugs when BP decreased without changes in LV dimension.3

 

D.R. Redwood found that acute changes in LVEDV and LVESV were easily detected by TTE.16 In our study also we found that changes in preload parameters LV-EDD, LV-EDA and PCWP were easily detectable and significant during induction and intubation. However, both TTE and PAC derived preload parameters; do not predict a fall or an increase in blood pressure. This may indicate that changes in preload during induction were very minimal in our study.

 

CO as determined by TEE using continuous wave Doppler (CWD) across the aortic valve is in very good agreement with CO-TD in anesthetized patients with regular heart rhythm, stable hemodynamics and if there is no evidence of aortic valve disease.17 The use of TEE in place of PAC/ TTE can be continued after intubation to monitor CO and the various derived parameters. The use of a PAC for CO measurement alone seems no longer justified, given the more varied and complete data that can be obtained from TTE.

 

In our study we also found that the change in preload as estimated by LV-EDD and LV-EDA, the change in afterload as estimated by mitral inflow doppler and left ventricular outflow doppler, the change in CO as estimated by the mitral inflow Doppler and the left ventricular outflow doppler correlated well. We can interchangeably use the two different methods of estimation of CO by TTE especially in patients with free of aortic and mitral valve disease.

 

The use of positive end expiratory pressure (PEEP) has been shown to cause a decrease in right ventricular preload, left ventricular preload and CO.18 So in order to avoid inaccuracy, we performed all measurements in our patients in the expiratory phase of the respiratory cycle without applying PEEP.

 

PAC pressure measurement fail to reflect changes in either LV pressure or LV size during or after cardiac procedures.1,2 A substantial increase in EDV may occur with minimal corresponding changes in PCWP, whereas direct echocardiographic measurement of chamber volumes provides more accurate information.19

Fig 1. The trend of mean blood pressure from baseline to pre intubation was decreasing and the trend of mean blood pressure for pre intubation to post intubation values was increasing. p < 0.05, statistically significant. Data are mean values

Fig 2.  Decreasing trend of CO-TD, CO- MV, CO- LVOT from baseline to pre intubation values and increasing trend of CO-TD, CO- MV, CO- LVOT from pre intubation to post intubation values. p < 0.05, statistically significant . Data are mean values. CO  = Cardiac output, TD = Thermodilution, MV = Mitral valve, LVOT = Left Ventricular Outflow Tract.

Fig 3.  Decreasing trend of SVR-TD, SVR- MV, SVR- LVOT from baseline to pre intubation values and increasing trend of SVR-TD, SVR- MV, SVR- LVOT from pre intubation to post intubation values. Data are mean values. SVR = systemic Vascular Resistance, TD = Thermodilution, MV = Mitral Valve, LVOT = Left Ventricular Outflow Tract.

 

Limitations

The feasibility of using standard precardial echocardiography is often technically difficult during mechanical ventilation with PEEP, because the transducer moves with the respiratory movements & the expanded lung interferes with ultrasound beam. Hence all pre intubation and post intubation measurements were done in expiratory phase of respiratory cycle without applying PEEP. For clinical application we need real time display of hemodynamic data. Future improvement in software technology may help us with the automatic calculation of hemodynamic data. USCOM device gives real time CO values, but this device utilizes nomogram derived LVOT diameter rather than calculated true LVOT diameter and a non-imaging probe is used to get a Doppler sample, so alignment with blood flow may not be accurate and reproducible.20  The small number of cases evaluated is a drawback of our study.

CONCLUSION

From our study we found TTE can be used as a replacement for PAC to estimate the change in hemodynamics, to predict change in blood pressure, to estimate preload, afterload and CO during induction of anaesthesia in a non-invasive manner. However, expertise in the use and interpretation of images in the TTE is required. Further studies in a larger population will be helpful to define the role of TTE as a hemodynamic monitor in cardiac surgical patients.

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