Acta Clinica Belgica International Journal of Clinical and Laboratory Medicine

ISSN: 1784-3286 (Print) 2295-3337 (Online) Journal homepage: http://www.tandfonline.com/loi/yacb20

CARDIAC ULTRASOUND AND ABDOMINAL COMPARTMENT SYNDROME Y. Mahjoub & G. Plantefeve To cite this article: Y. Mahjoub & G. Plantefeve (2007) CARDIAC ULTRASOUND AND ABDOMINAL COMPARTMENT SYNDROME, Acta Clinica Belgica, 62:sup1, 183-189, DOI: 10.1179/ acb.2007.62.s1.024 To link to this article: http://dx.doi.org/10.1179/acb.2007.62.s1.024

Published online: 30 May 2014.

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Date: 06 April 2016, At: 11:26

CARDIAC ULTRASOUND AND ABDOMINAL COMPARTMENT SYNDROME

Original article – OA 23

CARDIAC ULTRASOUND AND ABDOMINAL COMPARTMENT SYNDROME Y. Mahjoub1, G. Plantefeve2

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Key words: Abdominal compartment syndrome. Hemodynamic. Doppler Echocardiography

INTRODUCTION ABSTRACT This review focuses on the available literature published about the evaluation of haemodynamic consequences of the abdominal compartment syndrome (ACS). Animal and clinical studies described decreased venous return, systemic vasoconstriction, systolic and diastolic dysfunction of left and right ventricles. Doppler echocardiography is a non-invasive bedside procedure which provides a complete haemodynamic evaluation of patients with ACS. Despite numerous evaluations in anesthesia during laparoscopic surgery, the use of echocardiography remains scarce in critically ill patients with ACS.

––––––––––––––– 1 Unité de réanimation polyvalente, Pôle d’anesthésie-réanimation, CHU Amiens, Amiens, France; 2 Réanimation Polyvalente, Hôpital Victor Dupouy, Argenteuil, France Address for correspondence: Dr. Gaëtan Plantefeve Service de Réanimation Polyvalente Centre Hospitalier Victor Dupouy 69, rue du Lieutenant Colonel Prudhon 95100 Argenteuil France Tel: +33 1 34 23 14 45 & +33 1 34 23 25 50 Fax: +33 1 34 23 27 91 E-mail: [email protected]

Cardiovascular dysfunction in abdominal compartment syndrome (ACS) is complex. It can be associated with decreased preload, excessive afterload, right and left ventricular dysfunction. The management of this complex haemodynamic status may be difficult especially when ACS is associated with septic shock and haemorrhage. Echocardiography, a non-invasive procedure, enables a full assessment of the haemodynamic status. Since the nineties, echocardiography has been routinely used in several intensive care units (ICU) to manage hemodynamically unstable patients. Several studies have demonstrated the main importance of echocardiography in ICU (1,2). The aim of this review is to describe the physiopathology of hemodynamic consequences of ACS and the use of echocardiography in this setting.

PHYSIOPATHOLOGY (FIGURE 1) Intra-abdominal hypertension (IAH) leads to reduction of cardiac output that may trigger subsequent organ failure. However, the effects of increased abdominal pressure (IAP) are different according to the level IAP. At lower IAP (near 5 to 10 mmHg), the venous return increases and cardiac output may increase in normovolemic patients as a sort of auto transfusion effect (3). When the IAP increases over 10 mmHg (as in IAH and ACS), the main consequence is the decrease of cardiac output. Several mechanisms have been proposed to explain this effect: decreased venous return, direct compression of heart by elevation of the diaphragm, and increased systemic vascular resistance (SVR).

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Increased intra-abominal pressure

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Below 10 mmHg

over 10 mmHg

Moderate splanchnic vascular compression

Splanchnic vascular compression

Increased venous return

decreased venous return

Increased cardiac preload

decreased cardiac preload

Increased cardiac output

Diaphragm elevation

Increased intrathoracic pressure

Cardiac compression Transient decreased cardiac contractility

Increased systemic afterload

Decreased cardiac output

Figure 1 Hemodynamic effects of increased intra-abdominal pressure

The increased IAP causes direct compression of the inferior vena cava (IVC) and portal vein. The increased IAP is transmitted to the thoracic cavity where it causes a reduction of inferior and superior vena cava flow. The effect of IAH on venous return depends on the difference between the right atrial pressure (RAP) and the IAP. When this gradient is positive (RAP>IAP), the venous return increases and the abdominal blood volume is redistributed towards the thoracic compartment (4). This phenomenon increases the left ventricular end diastolic pressure (LVEDP). The increase in LVEDP can lead to pulmonary oedema. When the gradient is negative (RAP 0.6 in the long axis in association with septal dyskinesia (20). In a dog experiment, IAH decreases cardiac output more markedly in hypovolemic compared to euvolemic animals (3). When the myocardial function was previously impaired, the deleterious effect of IAH on cardiac function were aggravated (21). Finally, the mean arterial pressure (MAP) is generally not modified during IAH. A transient enhanced MAP associated with increase in SVR is described in laparoscopy (22). When IAP increases towards IAH and ACS levels, the MAP can decrease but mostly remains stable for a long time.

TECHNIQUES AVAILABLE TO ASSESS HEMODYNAMIC STATUS IN ACS Recently, one study in septic critically ill patients demonstrated the lack of efficacy of central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP) to detect hypovolemia or more precisely preload dependence of the heart (23). When the combination of the both pressure values was considered instead of either pressure alone, the prediction of volume responsiveness was not improved. In IAH (with an IAP of only 10 mmHg) and in ACS, the CVP or PAOP values used are the sum of both the intravascular pressure and the surrounding intrathoracic pressure (24). Approximately 20-50% of the IAP is transmitted to the chest cavity by way of diaphragmatic bulging (25). The cardiac filling pressures tend to be erroneously increased similarly to the increase seen when positive end expiratory pressure (PEEP) is applied. As a result, CVP and PAOP values are often increased with IAH, despite the diminished venous return. The RV end diastolic volume indexed (RVEDVI) measured by volumetric thermodilution can be useful to evaluate preload in IAH (26). The intra-thoracic (ITBV) and the global end diastolic (GEDV) blood volume obtained by single thermal indicator dilution seem to be better markers of preload in IAH (27). A initial significant increase in ITBV (auto transfusion effect) can be observed during laparoscopy induced IAH (28). This increase persisted both in supine, head-up, and head-down positions. The fluid challenge performed

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before the induction of the pneumoperitoneum influences the variation of ITBV: an unchanged value may reflect a relative hypovolemia during IAH (29). Other studies showed a decrease in volumetric preload indices during sustained IAH.

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ECHOCARDIOGRAPHY FOR IAH ASSESSMENT Echocardiography exerts an increasing interest in the daily clinical practice of critical carephysicians. It’s a rapid and non-invasive technique which can be easily performed at the bedside in the ICU. A number of hemodynamic and cardiac function parameters can be measured and calculated. Different pathologies can be explored with echocardiography. Logically, since IAH and ACS influence left and right cardiac function, preload and afterload, there is a potential interest for the use of echocardiography. The difficulties of hemodynamic evaluation and the lack of reliable criteria argued for its use in ACS. Only few studies focused on echocardiography in ACS. Currently, data exist in animals and during pneumoperitoneum in humans.

and estimation of flow through the LVOT by pulsed wave Doppler. From these data, stroke volume and cardiac output are calculated as follows: - stroke volume = aortic valve area × the velocity time integral of aortic blood flow - cardiac output = stroke volume × heart rate This calculation of cardiac output is possible by either transthoracic or transoesophageal echocardiography. The echocardiographic method is at least as accurate as the thermodilution method (30). Assessment of hypovolemia (Figure 2 and 3) The Frank-Starling curve presents a steep portion followed by a plateau. When the plateau is reached, a volume expansion doesn’t increase cardiac output but is able to induce some adverse effects as pulmonary oedema and right ventricular dysfunction. Excessive

Figure 3. Ventilated patient with intra-abdominal hypertension (13 mmHg)

Measurement of cardiac output The measurement of cardiac output can be easily performed with bedside echocardiography. The most popular approach combines Doppler measurements with 2D diameter measurements allows volumetric flow to be calculated by LV outflow tract (LVOT) diameter

Figure 3A. No respiratory variation of aortic blood flow.

Figure 2. Respiratory variations of peak aortic velocities in a ventilated patient with intraabdominal hypertension (17 mmHg). This patient is preload-dependant with response to fluid challenge.

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Figure 3B. Mitral blood flow : E/A=1.2 and EDT=12 ms

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fluid resuscitation may also lead to further increase in IAP (31). Within this regard, dynamic variables have been demonstrated to be accurate predictors of fluid responsiveness (32). Doppler echocardiography provides interesting indices. Vena cava diameter The respiratory variations of vena cava can be used to assess the response to fluid challenge in critically ill patients. The superior vena cava (SVC) can be easily accessed with transoesophageal echocardiography (33). A variation threshold of 36% allowed discrimination between responders and non responders to volume expansion. The respiratory variation of inferior vena cava (IVC) diameter can be evaluated by transthoracic echocardiography via the subcostal view (34). When the IAP exceeds the right atrial pressure, the abdominal IVC collapses, the venous return reduces, and the measurement may be difficult (5). Aortic Blood velocity The respiratory changes of aortic blood velocity are predictors of fluid responsiveness in mechanically ventilated patients (35). Measurement of aortic blood flow can be easily performed by transophageal echocardiography via the transgastric short axis view. This measure may also be done with transthoracic echocardiography using the apical five-chamber view. The peak velocity of the aortic blood (Vpeak) flow is measured by continuous–wave Doppler beam. As demonstrated by Feissel et al., the threshold value of 12% in the variation of the peak velocity of aortic blood allowed discrimination between responders and non-responders to a fluid challenge with a sensitivity of 100% and a specificity of 89% (35). In the ACS conditions, this parameter has not been validated. Evaluation of right ventricular function In the clinical situation, right ventricular function is classically assessed by transoesophageal or transthoracic echocardiography. The assessment of right ventricular systolic function may be difficult due to the shape of the right ventricle. Furthermore, ejection fraction alone is not relevant to describe the right ventricular function. The best indices to evaluate right ventricle function are the association of right ventricular dilatation associated with septal dyskinesia (20). Echocardiography may provide a reliable and non invasive assessment of the right ventricular function. In ARDS, cor

pulmonale or pulmonary embolism, these parameters are well validated (20). In IAH, only one preliminary study performed in septic patients was published only as abstract form. Patients with IAH had more frequently right ventricular dysfunction than patients without IAH (19). This study did not validate the method because no comparison with other techniques was made. Evaluation of left ventricular function The vasoconstriction occurring in IAH induces an increase of left ventricle (LV) afterload. This increase could be assessed by echocardiographic measurement of left ventricle systolic wall stress (LVSWS) (36). Despite the fact that this index is a rather complex way of expressing afterload, it could be useful in IAH where increased afterload could induce left ventricular diastolic dysfunction. Actually, no study assessed this index in IAH or ACS. Even with a slight increase of 14 mmHg, the IAP transmitted to the thoracic compartment could lead to cardiac compression which could impair the diastolic function (11). The diastolic dysfunction is assessed by the study of mitral flow, pulmonary venous blood flow, and Doppler tissue imaging of the mitral annulus velocity (37,38,39). The ratio of transmitral (E) velocity to the early diastolic velocity at the mitral annulus (Ea) ratio is also a fast and easy parameter to estimate the PAOP (Figure 4) (40). As in other disease, the impairment of diastolic function in ACS can lead to pulmonary oedema especially with massive fluidresuscitation. In many situations, the

Figure 4. Doppler tissue imaging of mitral annulus velocity of the same patient. E/Ea=10.5. With E wave deceleration time (EDT) fewer than 15 and E/Ea ration over 7. The PAOP is estimated over 15mmHg

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LV filling pressure elevation alerts the physician whereas these values are inappropriate in ACS (24). Assessment of LV systolic function is easily done by echocardiography. LV Ejection fraction, LV fractional area change or myocardial performance index are validated as accurate index of LV systolic function (41,42,43). No study demonstrated their (lack of) efficacy to assess the LV systolic function in ACS.

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CONCLUSION IAH and ACS impair cardiovascular function. The hemodynamic status of patients suffering from ACS may be associated with hypovolemia, false increased filling pressures, right and left ventricular dysfunctions. These impairments must be assessed to improve our management of these patients. Echocardiography offers rapid and non-invasive important diagnostic information about the hemodynamic disturbances. It also can be reapplied as the clinical situation changes. Despite the lack of specific validation in ACS, echocardiography could be helpful to assess the hemodynamic status in the future.

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