Anaesthesia 2014, 69, 436–444

doi:10.1111/anae.12623

Original Article Transthoracic echocardiography in women with treated severe pre-eclampsia* A. T. Dennis1,2 and J. M. Castro3 1 Specialist Anaesthetist, Director of Anaesthesia Research, Department of Anaesthesia, The Royal Women’s Hospital Parkville, Parkville, Victoria, Australia 2 Clinical Associate Professor, Department of Pharmacology and Department of Obstetrics and Gynaecology, The University of Melbourne, Melbourne, Victoria, Australia 3 Cardiologist, Department of Cardiology, St Vincent’s Hospital, Fitzroy, Victoria, Australia

Summary The aim of this study was to investigate cardiac function and haemodynamic indices using transthoracic echocardiography in women with severe pre-eclampsia who had already received treatment interventions. Fifteen women with treated severe pre-eclampsia were studied using transthoracic echocardiography. Mean (SD) cardiac output in women with treated disease was 5690 (1708) ml.min1. Systolic function was preserved in women with treated disease evidenced by mean (SD) fractional shortening 41 (9)%, fractional area change 62 (12)% and septal s0 velocities 9.0 (2.1) cm.s1. Left ventricle end-diastolic diameters were within healthy reference ranges at 4.7 (0.3) cm and the left ventricle was not dilated. Diastolic function was reduced, with a mean (SD) mitral valve E/septal e0 ratio of 12.6 (4.1). Left ventricular mass was increased at 182.0 (44.4) g. There was large variability in haemodynamics in women with treated severe pre-eclampsia. Transthoracic echocardiography is acceptable and applicable and enables quantification of cardiac function in women with severe pre-eclampsia. .................................................................................................................................................................

Correspondence to: A. Dennis Email: [email protected] *Presented in part at the Obstetric Anaesthetists’ Association Annual Meeting, Liverpool, UK, May 2012 and at the Australian Society of Anaesthetists National Scientific Congress, Hobart, Australia, September 2012. Accepted: 26 January 2014

Introduction Pre-eclampsia is a life-threatening hypertensive disease of pregnancy involving the heart and peripheral vasculature. It is a relatively common disease affecting 5–8% of pregnant women [1]. With an estimated 131 million women giving birth each year worldwide, it can be conservatively estimated that approximately 6.5 million women will develop pre-eclampsia in the next year [1–3]. Despite the large number of young women affected by this disease, morbidity and mortality from 436

pre-eclampsia has not decreased in the last decade [4]. The causes of maternal death and morbidity in women with pre-eclampsia are predominantly related to cerebral complications and cardiorespiratory failure [5, 6]. Due to expertise in resuscitation, airway management, pharmacology and physiology, women with these complications as well as women with severe preeclampsia in general are often managed within the multidisciplinary team by anaesthetists. © 2014 The Association of Anaesthetists of Great Britain and Ireland

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When considering appropriate interventions including antihypertensive medications, anaesthesia for caesarean birth, fluid resuscitation and postoperative high acuity care, it is important that anaesthetists understand cardiovascular function in women with pre-eclampsia. This includes an understanding of intravascular pressures, intravascular volume and blood flow, as well as the anatomical changes exhibited by the heart in women with severe pre-eclampsia. Currently, however, routine monitoring devices cannot give sufficient data regarding cardiac function and structure in the individual woman with pre-eclampsia. Therapeutic interventions are often instituted based on historical information about pre-eclampsia or summary data from groups of women with the disease. Anaesthetists frequently manage women after treatment has been commenced, and haemodynamics are further complicated by responses to interventions as well as possible progression of the underlying disease. The combination of pharmacological interventions, fluid resuscitation, underlying severe disease and anaesthesia, together with an inability to visualise or monitor cardiac function appropriately may lead to unpredictable responses to medical interventions. These may include hypotension, acute pulmonary oedema, refractory hypertension or fetal compromise. In this setting, transthoracic echocardiography may offer advantages in determining cardiac structure and function. Recent work has demonstrated the applicability and acceptability of transthoracic echocardiography in pregnant women including those with pre-eclampsia in whom treatment had not been commenced [7]. The aim of this study was to investigate cardiac function and haemodynamic indices using transthoracic echocardiography in women with severe pre-eclampsia who had already received treatment interventions.

Methods Institutional ethics approval was obtained and each woman provided informed written consent; women were recruited over an 18-month period at a single centre (Mercy Hospital for Women, Heidelberg, Vic, Australia). Inclusion criteria were women with severe pre-eclampsia in whom treatment had already been © 2014 The Association of Anaesthetists of Great Britain and Ireland

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started, who were not in labour and were non-smokers. These women were recruited as part of a large study investigating haemodynamics in women with pre-eclampsia. Data from women who had not been treated by the time of their echocardiographic examination have already been published [7]. Pre-eclampsia was defined as new onset, repeatedly high blood pressure (systolic blood pressure ≥ 140 mmHg and/or diastolic blood pressure ≥ 90 mmHg) occurring after 20 weeks’ gestation with an additional organ system involvement [8, 9]. Women were classified as having severe disease if they had symptomatic disease, severe hypertension (systolic blood pressure ≥ 160 mmHg, diastolic blood pressure ≥ 110 mmHg), neurological complications or other significant organ derangement, according to accepted classifications [7, 8]. All transthoracic echocardiography studies were performed by a single observer using a P17 5–1 MHz transducer (MicroMaxx, SonoSite Inc., Bothell, WA, USA) using 2-dimensional, M-mode, colour-flow, continuous, pulsed wave and tissue Doppler imaging according to American Society of Echocardiography guidelines and following the same methodology as previously published [7]. The echocardiographic examination was started after patients had rested in the left lateral position for a minimum of ten minutes. All echocardiography images were converted to digital images and communications in medicine (DICOM) format and all measurements were performed and analysed offline (ProSolvâ Fugifilm software Fugifilm Australia, Stafford, Qld, Australia). Each measurement was the average of three consecutive beats. While resting in the left lateral position, a calibrated sphygmomanometer was placed on the left arm and baseline systolic and diastolic blood pressures were obtained, recording the diastolic value as Korotkoff-5, according to the American Heart Association [10]. Measurements were made to the closest 2 mmHg and mean arterial pressure was then calculated. Haemodynamic measurements were performed according to the American Society of Echocardiography recommendations [11–13]. Cardiac output was calculated using measurements obtained from the left ventricular outflow tract diameter (cross-sectional area), the Doppler derived velocity time integral of the left ventricular outflow tract and the heart rate. The left ventricular 437

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outflow tract diameter measurement was made using the parasternal long axis view, and the left ventricular outflow tract velocity time integral was obtained from the apical four-chamber view. Fractional shortening was measured from the M-mode recording at the tip of the mitral valve leaflets in the parasternal long axis view. Fractional area change was measured during systole and diastole from the parasternal short axis image at the mid-papillary level. Systemic vascular resistance was calculated from mean arterial pressure and cardiac output. Measurements of diastolic function included left atrial diameter, mitral valve inflow velocities E and A, mitral valve deceleration time, mitral valve A wave duration and isovolumetric relaxation time. Tissue Doppler was used to record the interventricular septum diastolic velocities of e0 and a0 and the systolic velocity of s0 . Insonation angles were between 0 and 5 degrees. Measurements were made in accordance with the American Society of Echocardiography and European Association of Echocardiography expert consensus statement [14]. Left ventricular mass was calculated from measurements obtained from the parasternal long axis M-mode image of the left ventricle during diastole. The overall myocardial performance indicator, the Tei index, was measured according to accepted guidelines using tissue Doppler time intervals. Inter-observer and intra-observer reliability was determined using Bland–Altman methodology and expressed as bias (mean difference) and limits of agreement (2 9 SD mean difference). A second observer independently measured the left ventricular outflow tract diameter and left ventricular outflow tract velocity time integral on all women to enable interobserver reliability to be calculated and the single observer performed one repeated measurement of the left ventricular outflow tract diameter and left ventricular outflow tract velocity time integral to enable intra-observer reliability to be calculated.

Results Fifteen women underwent transthoracic echocardiography examination after treatment for pre-eclampsia had started (Table 1). Nine women were scanned in the birthing suite, one in the emergency department and five in the antenatal ward. Pre-eclampsia treatment fol438

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Table 1 Characteristics and haematological, urinary, obstetric and outcome data of women with treated severe pre-eclampsia (n = 15). Values are mean (SD) or number (proportion).

Age; years Gestation; weeks Body mass index; kg.m2 Number with body mass index > 40 kg.m2 Height; m Weight; kg Nulliparous Haematocrit Haemoglobin; g.l1 Protein/creatinine ratio; g.mmol1 Interventions Magnesium sulphate Labetalol a-methyldopa Hydralazine Anaesthetic interventions Delivered by caesarean section Neuraxial analgesia for vaginal birth Admitted to higher acuity area for management Severe maternal morbidity in addition to severe pre-eclampsia* Morbidities Major obstetric haemorrhage Renal dysfunction Septic shock Liver dysfunction (HELLP) Cerebrovascular event (eclampsia) Intensive care unit admission

31 32 32 1

(4.2) (5.1) (7.2) (7%)

1.64 86 8 0.33 116 0.29

(0.68) (18.9) (53%) (0.04) (13.1) (0.36)

7 7 4 2 14 13 1 8

(47%) (47%) (27%) (13%) (93%) (87%) (7%) (53%)

7 (47%)

2 2 1 2 0 1

(13%) (13%) (7%) (13%) (7%)

*Categories of maternal morbidity from the Scottish Confidential Audit of Severe Maternal Morbidity report 2008 [4]. HELLP, haemolysis, elevated liver enzymes, low platelets.

lowed clinician preference and no set protocol was used. No woman was given intravenous fluid. Eight women were treated in the 30 min before echocardiography examination and seven women were treated in the previous 24 h. Systolic, diastolic and structural variables were obtained in all women and there were no complications due to the study. All women stated they would participate in the study again. No woman was breathless, in acute pulmonary oedema, or in labour at the time of transthoracic echocardiography examination. Obesity was a common co-morbidity in women with severe pre-eclampsia. Seven (47%) women with treated severe pre-eclampsia were having their second or subsequent baby, the remainder were nulliparous. The most common pharmacological interventions were © 2014 The Association of Anaesthetists of Great Britain and Ireland

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magnesium sulphate and labetalol. Involvement of an anaesthetist occurred in 93% of women with treated severe pre-eclampsia with the majority of women undergoing caesarean section. Seven (47%) women with treated severe pre-eclampsia, in addition to the disease itself, experienced severe maternal morbidity, defined according to the World Health Organization as ‘very ill pregnant or recently pregnant woman who would have died had it not been that luck and good care was on her side’ [15]. Eight (53%) women were admitted to a higher acuity area for monitoring and one woman was admitted to the intensive care unit for management. The haemodynamic, systolic, diastolic and structural data are shown in Table 2. Systolic function, evidenced by fractional shortening, fractional area change and septal s0 velocities, was relatively preserved in women with treated pre-eclampsia (Table 2). Left Table 2 Haemodynamic and echocardiographic data in women with treated severe pre-eclampsia (n = 15). Values are mean (SD) or number (proportion).

Systolic blood pressure; mmHg Diastolic blood pressure; mmHg Mean arterial pressure; mmHg Cardiac output; ml.min1 Heart rate; beats.min1 Stroke volume; ml Systemic vascular resistance; dyne.s1.cm5 Fractional area change; % Fractional shortening; % Septal s0 velocity; cm.s1 Left ventricular end-diastolic diameter; cm Left atrial diameter; cm Septal e0 velocity; cm.s1 Septal a0 velocity; cm.s1 Septal e0 /a0 Isovolumetric relaxation time; ms Mitral valve E/A Mitral valve deceleration time; ms A wave duration; ms Mitral valve E/septal e0 Mitral valve E/septal e0 > 15 Mitral valve E/e0 > 8 and ≤ 15 Mitral valve E/e0 ≤ 8 Tei index Left ventricular mass; g Pericardial effusion Pericardial effusion > 1 cm

150 91 111 5690 82 69 1716

(15) (16) (15) (1708) (15) (14) (631)

62 41 9.0 4.7

(12.0) (9) (2.1) (0.3)

3.7 7.8 8.9 0.92 70 1.2 166.2 98.9 12.6 7 9 2 0.47 182 11 2

(0.3) (1.8) (2.3) (0.28) (14.5) (0.3) (30) (26) (4.1)* (47%)* (60%) (13%) (0.08) (44)* (73%) (18%)

*Abnormal values compared with healthy pregnant and non-pregnant adults. © 2014 The Association of Anaesthetists of Great Britain and Ireland

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ventricular end-diastolic diameters were not increased; i.e. the left ventricle was not dilated, compared with normal pregnant values. With regards to diastolic function, septal a0 velocity was greater than e0 velocity in some women with treated disease. Women with treated disease had diastolic impairment evidenced by mitral value E/e0 values of 15 or greater. Left ventricular mass was increased; however, the Tei index was within the healthy reference range. Figures 1 and 2 incorporate data from our previously published work in women with untreated preeclampsia, gestationally-matched healthy pregnant women and non-pregnant controls [7], and are included in order to aid an understanding of the ranges of haemodynamic variables and comparisons in these different groups of women. Figures 1 and 2 show there are a wide range of values for cardiac output, fractional shortening, septal s0 velocity, left ventricular end-diastolic diameters and diastolic function in women with treated severe pre-eclampsia as well as the other three groups of women. Abnormal values are shown in the shaded grey areas of the graphs. The graph of cardiac output (a) demonstrates wide ranges of cardiac output in the women with treated severe pre-eclampsia, similar to the variability seen in women with untreated disease. The fractional shortening graph (b) illustrates the wide range of fractional shortening values in the group of women with treated severe pre-eclampsia as well as the groups of healthy pregnant and untreated pre-eclampsia woman. Some healthy pregnant and non-pregnant women had fractional shortening values less than the lower reference range limit for non-pregnant adults. Despite some women with severe pre-eclampsia, both treated and untreated, having fractional shortening values less than the lower limit reference range value, none had clinical signs of reduced cardiac output. The highest mean velocities for septal systolic myocardial velocities (s0 ) were found in women with treated severe pre-eclampsia; however, some women in each of the four groups had reductions in septal s0 velocities. The graph of left ventricular end-diastolic diameter (d) shows that women with treated severe pre-eclampsia all had left ventricular end-diastolic diameters within the healthy reference range (i.e. none had a dilated ventricle). Some women in the healthy pregnancy group and 439

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(a)

Cardiac output 80

Fractional shortening (%)

Cardiac output (ml.min–1)

10000

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8000

6000

4000

2000

0

60

40 28 20

0

(c)

Pregnant Healthy n = 40

Pre-eclampsia Pre-eclampsia Severe untreated Severe treated n = 19 n = 15

Septal s' velocity

15

10 7.5 5

0 Non-pregnant Healthy n = 20

Pregnant Healthy n = 40

Pre-eclampsia Pre-eclampsia Severe untreated Severe treated n = 19 n = 15

Non-pregnant Healthy n = 20

Left ventricular end-diastolic diameter (cm)

Non-pregnant Healthy n = 20

Septal s' velocity (cm.s–1)

Fractional shortening

(b)

(d)

Pregnant Healthy n = 40

Pre-eclampsia Pre-eclampsia Severe untreated Severe treated n = 19 n = 15

Left ventricular end-diastolic diameter

6.5 6.0 5.5 5.3 5.0 4.5 4.0 3.5 Non-pregnant Healthy n = 20

Pregnant Healthy n = 40

Pre-eclampsia Pre-eclampsia Severe untreated Severe treated n = 19 n = 15

Figure 1 Box and whisker graphs showing minimum and maximum values, the median value (line inside the box) and the IQR for (a) cardiac output, (b) fractional shortening, (c) septal s0 velocity and (d) left ventricular end-diastolic diameter in four groups of women: non-pregnant; healthy pregnant; women with untreated pre-eclampsia and women with treated pre-eclampsia. The grey shaded areas represent abnormal values for cardiac function for the particular variable. The threshold value above or below which the abnormal values occur is shown on the y-axis. Data presented in non-pregnant women, healthy pregnant women and women with untreated pre-eclampsia are from [7]. severe pre-eclampsia group had left ventricular enddiastolic diameters greater than the upper healthy reference range value of 5.3 cm for non-pregnant women. There was no correlation found between reduced fractional shortening and cardiac output (Pearson r = 0.36). Figure 2 shows the mitral valve E/septal e0 ratio; some women with treated pre-eclampsia had values > 15, indicating significant diastolic impairment. Inter-observer reliability determined the mean (SD) differences in left ventricular outflow tract diameter and left ventricular outflow tract velocity time integral between two observers to be 0.1 (1.0) mm and 1.1 440

(1.5) cm.s1, respectively. For the left ventricular outflow tract diameter, this equates to 95% of the interobserver measurements being within 2.1 mm (10.7%) of the mean left ventricular outflow tract measurement of 19.7 mm. For the left ventricular outflow tract velocity time integral this equates to 95% of the interobserver measurements’ being within 4.1 cm.s1 (18.3%) of the mean value of 22.4 cm.s1. Intra-observer reliability, using Bland–Altman methodology, for the left ventricular outflow tract diameter and left ventricular outflow tract velocity time integral for the group of 15 women determined the mean (SD) differences in the left ventricular © 2014 The Association of Anaesthetists of Great Britain and Ireland

Mitral valve E velocity/septal e' velocity ratio

Dennis and Castro | Echocardiography in treated pre-eclampsia Mitral valve E/e' ratio 25

20

15

10 8 5

0 Non-pregnant Healthy n = 20

Pregnant Healthy n = 40

Pre-eclampsia Pre-eclampsia Severe untreated Severe treated n = 19 n = 15

Figure 2 Box and whisker graphs showing minimum and maximum values, the median value (line inside the box) and the IQR for the mitral E/septal e0 velocity ratio in four groups of women: non-pregnant; healthy pregnant; women with untreated pre-eclampsia and women with treated pre-eclampsia. The grey shaded areas represent abnormal values for cardiac function for the particular variable. The threshold value above or below which the abnormal values occur is shown on the y-axis. The lower dashed line represents the threshold value of 8. Values below 8 are associated with normal diastolic function whereas values between 8 and 15 may be associated with diastolic impairment. Values of 15 or above represent abnormal diastolic function [13]. Data presented in non-pregnant women, healthy pregnant women and women with untreated pre-eclampsia are from [7]. outflow tract diameter and left ventricular outflow tract velocity time integral between two observations for the single observer to be 0.0 (0.5) mm and 0.0 (0.2) cm.s1, respectively. For the left ventricular outflow tract diameter, this equates to 95% of the intraobserver measurements’ being within 1.0 mm (5%) of the mean left ventricular outflow tract measurement for the two observations of 20.0 mm. For the left ventricular outflow tract velocity time integral, this equates to 95% of the intra-observer measurements’ being within 0.33 cm.s1 (1.5%) of the mean value for the two observations of 22.1 cm.s1.

Discussion This study examined women with treated severe preeclampsia and quantified haemodynamics using transthoracic echocardiography. Women were rested in the © 2014 The Association of Anaesthetists of Great Britain and Ireland

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left lateral position before echocardiography in order to achieve baseline haemodynamic observations and minimise aortocaval compression [7, 16–18]. There were four major haemodynamic findings in this study related to women with treated severe pre-eclampsia: there was preserved systolic function; the left ventricle was not dilated; there was impairment of diastolic function; and transthoracic echocardiography was applicable and acceptable. These data suggest that cardiac output is not reduced in women with treated severe pre-eclampsia compared with women with untreated pre-eclampsia. This is consistent with previous work using the pulmonary artery catheter in preterm pregnant women [19]. None of the women had clinical signs of reduced cardiac output, indicating that at rest in the left lateral position, compensation mechanisms maintain an adequate cardiac output despite seemingly lower than expected cardiac output in some women. Transthoracic echocardiography is useful in identifying women with lower than expected cardiac output. Further serial studies are needed to examine the effects of further interventions such as fluid, physiological stress or worsening disease on cardiac output. Fractional shortening and fractional area change correlate with ejection fraction and are indicators of contractility. Fractional shortening was calculated to quantify myocardial wall movement during systole and diastole as a clear view and measurement of the left ventricular end-diastolic and end-systolic diameters were possible from the parasternal long axis view. This measurement was performed, rather than Simpson’s biplane measurement, as it was achievable in all women and there was assumed to be no regional wall motion abnormalities. Furthermore, the apical long and short axis views were not as clearly seen in all the third trimester women and therefore measurement errors generated from calculating volumes from images in two planes during diastole and systole would be significant. Fractional shortening was preserved in women with treated severe pre-eclampsia, indicating that systolic function and contractility is not reduced in the group of women with treated disease. The finding that some women with severe pre-eclampsia, both treated and untreated, had fractional shortening values less than the lower limit reference range value may 441

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indicate a reduction in contractile function and a reduced cardiac reserve in some women across all groups. Further research is needed to investigate the clinical implications of these findings. Myocardial wall movement during systole, measured at the interventricular septum (s0 velocity) using tissue Doppler imaging, was preserved in women with severe pre-eclampsia. Due to the orientation of the pregnant woman’s heart and the left lateral position, the septal tissue Doppler velocities were measured preferentially to lateral wall velocities as the angle of insonation was between 0 and 5 degrees, enabling accurate measurements of these values. The highest mean velocities for septal systolic myocardial velocities (s0 ) were found in women with treated severe preeclampsia, indicating preserved systolic function. Left ventricular end-diastolic diameter was not increased in women with treated severe pre-eclampsia. This suggests that women with severe pre-eclampsia do not have a dilated ventricle and that dilated cardiomyopathy is not a feature of either treated or untreated [7] severe pre-eclampsia. Some women in the healthy pregnancy group and severe pre-eclampsia group had left ventricular end-diastolic diameters greater than the upper healthy reference range value of 5.3 cm for non-pregnant women, indicating that some individual women may have a dilated ventricle both in healthy seemingly uncomplicated pregnancy and in severe pre-eclampsia. Further research and serial studies are needed to examine the effects of interventions on cardiac function in healthy and unwell pregnant women, in order to understand the effect of a dilated ventricle on outcomes. The mitral valve E velocity/septal e0 velocity dimensionless ratio is widely used as a measure of diastolic function as it is positively correlated with left ventricular filling pressures recorded during cardiac catheterisation. The relationship is such that mitral valve E/septal e0 > 15 correlates with increased left ventricular filling pressures and < 8 correlates with a normal left ventricular diastolic pressure [13]. It is one of the most reproducible echocardiographic measurements to estimate the pulmonary capillary wedge pressure and is predictive of adverse events in hypertensive heart disease in the non-pregnant population [13, 20]. The hypertensive women in this study with treated 442

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severe pre-eclampsia had evidence of abnormal diastolic function, with nearly 30% of women having echocardiographic findings of increased left ventricular diastolic pressure quantified by mitral valve E/e0 > 15. This occurred in the presence of preserved ejection fraction and systolic function. The significance of this finding is that elevated left ventricular end-diastolic pressure increases the risk of acute pulmonary oedema, and therefore these women may be at increased risk of developing acute pulmonary oedema if they experience additional cardiovascular stressors such as increased preload (fluids), increased afterload (further elevated blood pressure or untreated blood pressure), or increased heart rate (pain, exercise). Preserved ejection fraction, diastolic impairment and hypertension in non-pregnant adults is associated with poor ability to tolerate increased metabolic demands such as exercise, and also poor ability to tolerate rapid increases in preload such as when intravenous fluids are administered rapidly. It is commonly associated with the development of preserved ejection fraction heart failure. Common treatment modalities in non-pregnant adults, some of which are uncommonly used in pregnant women, include diuretics, angiotensin converting enzyme inhibitors, angiotensin-2 receptor antagonists and beta-adrenoceptor blockers [21]. This study suggests that women with severe pre-eclampsia have preserved ejection fraction and diastolic impairment in the presence of hypertension. Under these conditions, preserved ejection fraction heart failure or acute hypertensive pulmonary oedema may occur when there is disproportionate intravenous fluid administration or increasing metabolic demands such as labour and birth, concurrent infection or postoperative recovery from major surgery (i.e. caesarean section) [22]. Abnormalities of cardiac function have been found in asymptomatic non-pregnant and healthy pregnant women and there are a wide range of all haemodynamic variables in these groups, with some values being beyond accepted reference ranges [7]. This means that relying on symptoms and signs to assess cardiac function and cardiac reserve may be misleading in pregnant women. It is because of this unreliability in clinical settings that in non-pregnant adults there is widespread application and accepted appropriateness of the use of © 2014 The Association of Anaesthetists of Great Britain and Ireland

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transthoracic echocardiography in the assessment of cardiovascular disease [11, 13]. In contrast, there are very few studies examining the use of transthoracic echocardiography as a diagnostic tool in pregnant women and it is not routinely used, even in critically unwell women with severe pre-eclampsia [23, 24]. Abnormalities found on echocardiography in non-pregnant adults may trigger further diagnostic tests, additional interventions or changes in interventions. This same level of diagnostic rigour and tailored interventional approach does not occur in the management of pregnant women with severe pre-eclampsia, where the choice of antihypertensive agent and fluid management is often left to a clinician’s experience rather than objective haemodynamic measurements. Similar to its use in non-pregnant adults, echocardiographic quantification of variables such as fractional shortening, left ventricular end-diastolic diameter, fractional area change and mitral valve E/e0 in women with severe pre-eclampsia may allow rational haemodynamic-based decisions regarding the quantity and rate of administration of fluids, the need for diuresis, the choice of antihypertensive agents, the intra- and postoperative monitoring, and the longerterm surveillance and cardiovascular risk reduction strategies. This study has several limitations. This is a small study of 15 women, limited by the number of women who required immediate treatment before transthoracic echocardiography examination or who were already receiving treatment but still meeting the diagnostic criteria for severe pre-eclampsia, rather than because of a pre-determined sample size calculation. This study was a single-point study and not a serial study before and after interventions, and there was heterogeneity in the pharmacological interventions. It is therefore not possible to make any inferences about the effect of treatment interventions on cardiac function in these women. It is likely that the 15 women presented here represent a more severely affected group of women as treatment interventions were deemed to be more urgent than for women who had been examined in the untreated state. Another possibility regarding the treatment of pre-eclampsia may be that treatment interventions do not improve, or may in fact worsen, other haemodynamic variables such as diastolic function. Our current practice of treating to the cardiovascular © 2014 The Association of Anaesthetists of Great Britain and Ireland

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endpoint of a particular blood pressure target may be wrong, and a more haemodynamic approach targeting changes in the absolute value and distribution of cardiac output, as well as improvements in diastolic function, may be more beneficial. Further research is needed in this area to test these hypotheses. In conclusion, as a group, women with treated severe pre-eclampsia have preserved systolic function and cardiac output, do not have a dilated left ventricle, have increased left ventricular mass and have significant diastolic abnormalities with evidence of increased left ventricular end-diastolic pressure. We urge clinicians looking after women with pre-eclampsia to consider echocardiography in this particularly challenging group of patients to aid diagnostic evaluation and help guide treatment.

Acknowledgements The investigators would like to acknowledge the support provided by Professor Colin Royse, Professor Michael Permezel, Associate Professor Scott Simmons and Mrs Caroline Carr. Financial support for this work was provided from the Australian Society of Anaesthetists PhD Research Support Grant and the Laryngeal Mask Airway/Pacific Medical/Australian Society of Anaesthetists Fellowship. SonoSite Australasia Pty. Ltd provided the transthoracic echocardiography machine used in this study and Fugifilm Australia provided the ProSolv software for data measurement. These companies had no influence or involvement in any part of the study, data analysis or manuscript preparation.

Competing interests No conflicts of interest declared.

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Transthoracic echocardiography in women with treated severe pre-eclampsia.

The aim of this study was to investigate cardiac function and haemodynamic indices using transthoracic echocardiography in women with severe pre-eclam...
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