Comprehensive assessment of the aortic valve in critically ill patients for the non-cardiologist. Part I: Aortic stenosis of the native valve.

Aortic stenosis (AS) causes left ventricular outflow obstruction. Severe AS has major haemodynamic implications in critically ill patients, in whom increased cardiac output and oxygen delivery are often required. Transthoracic echocardiography (TTE) plays a key role in the AS severity grading. In this review, we will give an overview of how to use the simplified Bernoulli equation to convert the echo Doppler measured velocities (cm s-1) to AS peak and mean gra-dient (mm Hg) and how to calculate the aortic valve area (AVA), using the continuity equation, based on the principle of preservation of flow. TTE allows quantification of compensatory left ventricular (LV) hypertrophy, assessment of LV systolic function, and determination of LV diastolic function and LV loading. Subsequently, the obtained results from the TTE study need to be integrated to establish the AS severity grading. The pitfalls of echocardiographic AS severity assessment are explained, and how to deal with inconsistency between AVA and mean gradient. The contribution of transoesophageal echocardiography, low-dose dobutamine stress echo (in case of low-flow low-gradient AS), echocardiography strain imaging, cardiac magnetic resonance imaging, cardiac multidetector computed tomography and the relatively new concept of Flow Pressure Gradient Classification to the work-up for aortic stenosis is discussed. Finally, the treatment of AS is overviewed. Elective aortic valve replacement is indicated in patients with severe symptomatic AS. In the ICU, afterload reduction by vasodilator therapy and treatment of pulmonary and venous congestion by diuretics could be considered.

Comprehensive assessment of the aortic valve in critically ill patients for the non-cardiologist. Part II: Chronic aortic regurgitation of the native valve.

Inadequate diastolic closure of the aortic valve causes aortic regurgitation (AR). Diastolic regurgitation towards the left ventricle (LV) causes LV volume overload, resulting in eccentric LV remodelling. Transthoracic echocardiography (TTE) is the first line examination in the work-up of AR. TTE allows quantification of left ventricular end-diastolic diameter and volume and left ventricular ejection fraction, which are key elements in the clinical decision making regarding the timing of valve surgery. The qualitative echocardiographic features contributing to the AR severity grading are discussed: fluttering of the anterior mitral valve leaflet, density and shape of the continuous wave Doppler signal of the AR jet, colour flow imaging of the AR jet width, and holodiastolic flow reversal in the descending thoracic aorta and abdominal aorta. Volumetric assessment of the AR is performed by measuring the velocity time integral of the left ventricular outflow tract (LVOT) and transmitral valve (MV) plane, and diameters of LVOT and MV. We explain how the regurgitant fraction and effective regurgitant orifice area (EROA) can be calculated. Alternatively, the proximal isovelocity surface area can be used to determine the EROA. We overview the utility of pressure half time and vena contracta width to assess AR severity. Further, we discuss the role of transoesophageal echocardiography, echocardiography speckle tracking strain imaging, cardiac magnetic resonance imaging and computed tomography of the thoracic aorta in the work-up of AR. Finally, we overview the criteria for valve surgery in AR.

Prognostic value of bioelectrical impedance analysis for assessment of fluid overload in ICU patients: a pilot study.

INTRODUCTION: The non-invasive analysis of body fluid composition with bio-electrical impedance analysis (BIA) provides additional information allowing for more persona-lised therapy to improve outcomes. The aim of this study is to assess the prognostic value of fluid overload (FO) in the first week of intensive care unit (ICU) stay. MATERIAL AND METHODS: A retrospective, observational analysis of 101 ICU patients. Whole-body BIA measurements were performed, and FO was defined as a 5% increase in volume excess from baseline body weight. RESULTS: Baseline demographic data, including severity scores, were similar in both the fluid overload-positive (FO+, n = 49) patients and in patients without fluid overload (FO-, n = 52). Patients with FO+ had significantly higher cumulative fluid balance during their ICU stay compared to those without FO (8.8 ± 7.0 vs. 5.5 ± 5.4 litres; P = 0.009), VE (9.9 ± 6.5 vs. 1.5 ± 1.5 litres; P < 0.001), total body water (63.0 ± 9.5 vs. 52.8 ± 8.1%; P < 0.001), and extracellular water (27.0 ± 7.3 vs. 19.6 ± 3.7 litres; P < 0.001). The presence of 5%, 7.5%, and 10% fluid overload was directly associated with increased ICU mortality rates. The percentage fluid overload (P = 0.039) was an independent predictor for hospital mortality. CONCLUSIONS: A higher mortality rate in ICU-patients with FO was observed. FO is an independent prognostic factor because neither APACHE-II, SOFA, nor SAPS-II significantly differed on admission between survivors and non-survivors. Further research is needed to confirm these data prospectively and to evaluate whether BIA-guided deresuscitation in the subacute phase will improve mortality rates.

Energy expenditure of patients on ECMO: A prospective pilot study.

BACKGROUND: An optimal nutritional approach sustained by convenient monitoring of metabolic status and reliable assessment of energy expenditure (EE) may improve the outcome of critically ill patients on extracorporeal membrane oxygenation (ECMO). We previously demonstrated the feasibility of indirect calorimetry (IC)-the standard of care technique to determine caloric targets-in patients undergoing ECMO. This study aims to compare measured with calculated EE during ECMO treatment. We additionally provide median EE values for use in settings where IC is not available. METHODS: IC was performed in seven stable ECMO patients. Gas exchange was analyzed at the ventilator, and ECMO side and values were introduced in a modified Weir formula to calculate resting EE. Results were compared with EE calculated with the Harris-Benedict equation and with the 25 kcal/kg/day ESPEN recommendation. RESULTS: Total median oxygen consumption rate was 196 (Q1-Q3 158-331) mL/min, and total median carbon dioxide production was 150 (Q1-Q3 104-203) mL/min. Clinically relevant differences between calculated and measured EE were observed in all patients. The median EE was 1334 (Q1-Q3 1134-2119) kcal/24 hours or 18 (Q1-Q3 15-27) kcal/kg/day. CONCLUSION: Compared with measured EE, calculation of EE both over- and underestimated caloric needs during ECMO treatment. Despite a median EE of 21 kcal/kg/day, large variability in metabolic rate was found and demands further investigation.