Cardiac Preload in Children With CV Dysfunction or Dilated CM
Cardiac Preload in Children With CV Dysfunction or Dilated CM
Objectives To characterize cardiac preload responsiveness in pediatric patients with cardiovascular dysfunction and dilated cardiomyopathy using global end-diastolic volume index, stroke volume index, cardiac index, and extravascular lung water index.
Design Prospective multicenter observational study.
Setting Medical/surgical PICUs of seven Spanish University Medical Centers.
Patients Seventy-five pediatric patients (42 male, 33 female), median age 36 months (range, 1–207 mo), were divided into three groups: normal cardiovascular status, cardiovascular dysfunction, and dilated cardiomyopathy.
Interventions All patients received hemodynamic monitoring with PiCCO2 (Pulsion Medical System SE, Munich, Germany). We evaluated 598 transpulmonary thermodilution sets of measurements. In 40 patients, stroke volume index, cardiac index, and global end-diastolic volume index were measured before and after 66 fluid challenges and loadings to test fluid responsiveness at different preload levels.
Measurements and Main Results Global end-diastolic volume versus predicted body surface area exhibits a power-law relationship: Global end-diastolic volume = 488.8·predicted body surface area (r = 0.93). Four levels of cardiac preload were established from the resulting "normal" global end-diastolic volume index (= 488.8·predicted body surface area). Stroke volume index and cardiac index versus global end-diastolic volume index/normal global end-diastolic volume index built using a linear mixed model analysis emulated Frank-Starling curves: in cardiovascular dysfunction group, stroke volume index (geometric mean [95% CI]) was 27 mL/m (24–31 mL/m) at "≤ 0.67 times normal global end-diastolic volume index," 37 mL/m (35–40 mL/m) at "> 0.67 ≤ 1.33 times normal global end-diastolic volume index" (Δ stroke volume index = 35%; p < 0.0001; area under the receiver-operating characteristic curve = 75%), 45 mL/m (41–49 mL/m) at "> 1.33 ≤ 1.51 times normal global end-diastolic volume index" (Δ stroke volume index = 21%; p < 0.0001; area under the receiver-operating characteristic curve = 73%), and 47 mL/m (43–51 mL/m) at "> 1.51 times normal global end-diastolic volume index" (Δ stroke volume index = 4%; p = 1; area under the receiver-operating characteristic curve = 54%). In dilated cardiomyopathy group, stroke volume index was 21 mL/m (17–26 mL/m) at "> 0.67 ≤ 1.33 times normal global end-diastolic volume index," 27 mL/m (21–34 mL/m) at "> 1.33 ≤ 1.51 times normal global end-diastolic volume index" (Δ stroke volume index = 29%; p = 0.005; area under the receiver-operating characteristic curve = 64%), and 25 mL/m (20–32 mL/m) at "> 1.51 times normal global end-diastolic volume index" (Δ stroke volume index = –8%; p = 1; area under the receiver-operating characteristic curve = 54%).
Conclusions This study provides "normal" values for global end-diastolic volume index and limits of cardiac preload responsiveness in pediatric patients with cardiovascular dysfunction and dilated cardiomyopathy: 1.33 times normal global end-diastolic volume index represents the upper limit of patent cardiac preload responsiveness, with the highest expected responsiveness being below 0.67 times normal global end-diastolic volume index. The maximum response of the Frank-Starling relationship and therefore the level of no additional preload reserve is 1.33 to 1.51 times normal global end-diastolic volume index. Above 1.51 times normal global end-diastolic volume index preload responsiveness is unlikely, and the risk of pulmonary edema is maximal.
Hypovolemia is the major cause of cardiovascular dysfunction in critically ill patients. Maintenance of adequate cardiac preload and cardiac output (CO) remains the primary targets to optimize hemodynamics for these patients. Nevertheless, increasing stroke volume (SV) does not necessarily follow after volume expansion as clinical examination is of minimal value for detecting inadequate cardiac preload, and the relationship between ventricular preload and SV is curvilinear, as described by Frank-Starling. Additionally, overly aggressive volume expansion may produce fluid overload leading to pulmonary edema and worsening gas exchange.
Fluid responsiveness is defined as a clinically meaningful increase in SV, generally greater than 15%, following a fluid challenge. According to the Frank-Starling curvilinear relationship, a patient is a "responder" to volume expansion only if both ventricles are preload responsive, which occurs when they are working in the steep part of the curve.
For predicting fluid responsiveness, it has been recommended that it should be determined on the part of the Frank-Starling relationship that the heart is actually working. Global end-diastolic volume (GEDV) is determined by transpulmonary thermodilution (TPTD) and measures the volume of blood in the four chambers of the heart, making it a good variable for evaluating cardiac preload in adults and children. Therefore, GEDV versus SV and/or CO may be used to establish the Frank-Starling relationship. Nevertheless, more information is currently needed to establish cutoff values of global end-diastolic volume index (GEDVI) for predicting cardiac preload responsiveness especially in children in whom the "normal" GEDVI values have not been established.
Pulmonary edema is a harmful consequence of fluid overload. Extravascular lung water (EVLW) determined at the bedside using TPTD has been shown to be a sensitive prognostic indicator of pulmonary edema, and its increase has recently been found to be associated with the Frank-Starling plateau.
We hypothesized that the limits for cardiac preload responsiveness could be ascertained using the combination of GEDV, SV (CO), and EVLW. The aim of the current study was to characterize the relationships of GEDV-based cardiac preload with SV (CO) and EVLW in pediatric patients with acute cardiovascular dysfunction and dilated cardiomyopathy.
Abstract and Introduction
Abstract
Objectives To characterize cardiac preload responsiveness in pediatric patients with cardiovascular dysfunction and dilated cardiomyopathy using global end-diastolic volume index, stroke volume index, cardiac index, and extravascular lung water index.
Design Prospective multicenter observational study.
Setting Medical/surgical PICUs of seven Spanish University Medical Centers.
Patients Seventy-five pediatric patients (42 male, 33 female), median age 36 months (range, 1–207 mo), were divided into three groups: normal cardiovascular status, cardiovascular dysfunction, and dilated cardiomyopathy.
Interventions All patients received hemodynamic monitoring with PiCCO2 (Pulsion Medical System SE, Munich, Germany). We evaluated 598 transpulmonary thermodilution sets of measurements. In 40 patients, stroke volume index, cardiac index, and global end-diastolic volume index were measured before and after 66 fluid challenges and loadings to test fluid responsiveness at different preload levels.
Measurements and Main Results Global end-diastolic volume versus predicted body surface area exhibits a power-law relationship: Global end-diastolic volume = 488.8·predicted body surface area (r = 0.93). Four levels of cardiac preload were established from the resulting "normal" global end-diastolic volume index (= 488.8·predicted body surface area). Stroke volume index and cardiac index versus global end-diastolic volume index/normal global end-diastolic volume index built using a linear mixed model analysis emulated Frank-Starling curves: in cardiovascular dysfunction group, stroke volume index (geometric mean [95% CI]) was 27 mL/m (24–31 mL/m) at "≤ 0.67 times normal global end-diastolic volume index," 37 mL/m (35–40 mL/m) at "> 0.67 ≤ 1.33 times normal global end-diastolic volume index" (Δ stroke volume index = 35%; p < 0.0001; area under the receiver-operating characteristic curve = 75%), 45 mL/m (41–49 mL/m) at "> 1.33 ≤ 1.51 times normal global end-diastolic volume index" (Δ stroke volume index = 21%; p < 0.0001; area under the receiver-operating characteristic curve = 73%), and 47 mL/m (43–51 mL/m) at "> 1.51 times normal global end-diastolic volume index" (Δ stroke volume index = 4%; p = 1; area under the receiver-operating characteristic curve = 54%). In dilated cardiomyopathy group, stroke volume index was 21 mL/m (17–26 mL/m) at "> 0.67 ≤ 1.33 times normal global end-diastolic volume index," 27 mL/m (21–34 mL/m) at "> 1.33 ≤ 1.51 times normal global end-diastolic volume index" (Δ stroke volume index = 29%; p = 0.005; area under the receiver-operating characteristic curve = 64%), and 25 mL/m (20–32 mL/m) at "> 1.51 times normal global end-diastolic volume index" (Δ stroke volume index = –8%; p = 1; area under the receiver-operating characteristic curve = 54%).
Conclusions This study provides "normal" values for global end-diastolic volume index and limits of cardiac preload responsiveness in pediatric patients with cardiovascular dysfunction and dilated cardiomyopathy: 1.33 times normal global end-diastolic volume index represents the upper limit of patent cardiac preload responsiveness, with the highest expected responsiveness being below 0.67 times normal global end-diastolic volume index. The maximum response of the Frank-Starling relationship and therefore the level of no additional preload reserve is 1.33 to 1.51 times normal global end-diastolic volume index. Above 1.51 times normal global end-diastolic volume index preload responsiveness is unlikely, and the risk of pulmonary edema is maximal.
Introduction
Hypovolemia is the major cause of cardiovascular dysfunction in critically ill patients. Maintenance of adequate cardiac preload and cardiac output (CO) remains the primary targets to optimize hemodynamics for these patients. Nevertheless, increasing stroke volume (SV) does not necessarily follow after volume expansion as clinical examination is of minimal value for detecting inadequate cardiac preload, and the relationship between ventricular preload and SV is curvilinear, as described by Frank-Starling. Additionally, overly aggressive volume expansion may produce fluid overload leading to pulmonary edema and worsening gas exchange.
Fluid responsiveness is defined as a clinically meaningful increase in SV, generally greater than 15%, following a fluid challenge. According to the Frank-Starling curvilinear relationship, a patient is a "responder" to volume expansion only if both ventricles are preload responsive, which occurs when they are working in the steep part of the curve.
For predicting fluid responsiveness, it has been recommended that it should be determined on the part of the Frank-Starling relationship that the heart is actually working. Global end-diastolic volume (GEDV) is determined by transpulmonary thermodilution (TPTD) and measures the volume of blood in the four chambers of the heart, making it a good variable for evaluating cardiac preload in adults and children. Therefore, GEDV versus SV and/or CO may be used to establish the Frank-Starling relationship. Nevertheless, more information is currently needed to establish cutoff values of global end-diastolic volume index (GEDVI) for predicting cardiac preload responsiveness especially in children in whom the "normal" GEDVI values have not been established.
Pulmonary edema is a harmful consequence of fluid overload. Extravascular lung water (EVLW) determined at the bedside using TPTD has been shown to be a sensitive prognostic indicator of pulmonary edema, and its increase has recently been found to be associated with the Frank-Starling plateau.
We hypothesized that the limits for cardiac preload responsiveness could be ascertained using the combination of GEDV, SV (CO), and EVLW. The aim of the current study was to characterize the relationships of GEDV-based cardiac preload with SV (CO) and EVLW in pediatric patients with acute cardiovascular dysfunction and dilated cardiomyopathy.
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