scholarly journals Transpulmonary thermodilution-derived cardiac function index identifies cardiac dysfunction in acute heart failure and septic patients: an observational study

Critical Care ◽  
2009 ◽  
Vol 13 (4) ◽  
pp. R133 ◽  
Author(s):  
Simon Ritter ◽  
Alain Rudiger ◽  
Marco Maggiorini



2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Jessica Perny ◽  
Antoine Kimmoun ◽  
Pierre Perez ◽  
Bruno Levy

Introduction. The PiCCO transpulmonary thermodilution technique provides two indices of cardiac systolic function, the cardiac function index (CFI) and the global ejection fraction (GEF). Both appear to be correlated with left ventricular ejection fraction (LVEF) measured by echocardiography in patients with circulatory failure, especially in septic shock. The aim of the present study was to test the reliability of CFI as an indicator of LVEF in patients with cardiogenic shock.Methods. In thirty-five patients with cardiogenic shock, we performed (i) simultaneous measurements of echocardiography LVEF and cardiac function index assessed by transpulmonary thermodilution (n=72) and (ii) transpulmonary thermodilution before/after increasing inotropic agents (n=18).Results. Mean LVEF was 31% (+/−11.7), CFI 3/min (+/−1), and GEF 14.2% (+/−6). CFI and GEF were both positively correlated with LVEF (P<0.0001,r2=0.27). CFI and GEF were significantly increased with inotropic infusion (resp.,P=0.005,P=0.007). A cardiac function index <3.47/min predicted a left ventricular ejection fraction ≤35% (sensitivity 81.1% and specificity 63%). In patients with right ventricular dysfunction, CFI was not correlated with LVEF.Conclusion. CFI is correlated with LVEF provided that patient does not present severe right ventricular dysfunction. Thus, the PiCCO transpulmonary thermodilution technique is useful for the monitoring of inotropic therapy during cardiogenic shock.





2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Foulkes ◽  
B Costello ◽  
E.J Howden ◽  
K Janssens ◽  
H Dillon ◽  
...  

Abstract Background Young cancer survivors are at increased risk of impaired cardiopulmonary fitness (VO2peak) and heart failure. Assessment of exercise cardiac reserve may reveal sub-clinical abnormalities that better explain impairments in fitness and long term heart failure risk. Purpose To investigate the presence of impaired VO2peak in pediatric cancer survivors with increased risk of heart failure, and to assess its relationship with resting cardiac function and cardiac reserve Methods Twenty pediatric cancer survivors (aged 8–24 years) treated with anthracycline chemotherapy underwent cardiopulmonary exercise testing to quantify VO2peak, with a value &lt;85% of predicted defined as impaired VO2peak. Resting cardiac function was assessed using 3-dimensional echocardiography, with cardiac reserve quantified from resting and peak exercise heart rate (HR), stroke volume index (SVi) and cardiac index (CI) using exercise cardiac magnetic resonance imaging. Results 12 of 20 survivors (60%) had impaired VO2peak (97±14% vs. 70±16% of age and gender predicted). There were no differences in echocardiographic or CMR measurements of resting cardiac function between survivors with normal or impaired VO2peak. However, those with reduced VO2peak had diminished cardiac reserve, with a lesser increase in CI (Fig. 1A) and SVi (Fig. 1B) during exercise (Interaction P=0.001 for both), whilst the HR response was similar (Fig. 1C; P=0.71). Conclusions Resting measures of cardiac function are insensitive to significant cardiac dysfunction amongst pediatric cancer survivors with reduced VO2peak. Measures of cardiopulmonary fitness and cardiac reserve may aid in early identification of survivors with heightened risk of long-term heart failure. Figure 1 Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): National Heart Foundation



Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Satoshi Okumura ◽  
Yunzhe Bai ◽  
Meihua Jin ◽  
Sayaka Suzuki ◽  
Akiko Kuwae ◽  
...  

The sympathetic nervous system and proinflammatory cytokines are believed to play independent roles in the pathophysiology of heart failure. However, the recent identification of Epac (exchange protein activated by cyclic AMP), a new cyclic AMP-binding protein that directly activates Rap1, have implicated that there may be a potential cross talk between the sympathetic and cytokine signals. In order to examine the role of Epac in cytokine signal to regulate cardiac function, we have generated transgenic mice expressing the human Epac1 gene under the control of alpha-cardiac myosin heavy chain promoter (Epac1-TG), and examined their response in lipopolysaccharide (LPS)-induced cardiac dysfunction, a well established model for sepsis-induced cardiac dysfunction. Sepsis-induced cardiac dysfunction results from the production of proinflammatory cytokines. At baseline, left ventricular ejection fraction (LVEF) was similar (TG vs. NTG, 67±1.7 vs. 69±2.1%, n =7–9). The degree of cardiac hypertrophy (LV(mg)/tibia(mm)) was also similar at 3 months old (TG vs. NTG 4.0±0.1 vs. 4.2±0.1, n =5–6), but it became slightly but significantly greater in Epac1-TG at 5 month old (TG vs. NTG 4.9±0.1 vs. 4.4±0.1, p< 0.05, n =5–7). LPS (5mg/kg) elicited a significant and robust reduction of LVEF in both Epac1-TG and NTG, but the magnitude of this decrease was much less in Epac1-TG at 6 hr after injection (TG vs. NTG 48±2.4 vs. 57±1.8%, p< 0.01, n =6–9). At 24 hr after injection, cardiac function was restored to the baseline in both Epac1-TG and NTG. We also examined the activation of JAK-STAT pathway at 24 hr after injection. The tyrosine phosphorylation of STAT1 (Tyr701) and STAT3 (Tyr705) in LV, which is an indicator of STAT activation, was reduced to a greater degree in Epac1-TG by 31±8.8% ( p< 0.05, n =4) and 29±5.9% ( p< 0.05, n =7), respectively, relative to that in NTG. Taken together, Epac1 protects the heart from the cytokine-induced cardiac dysfunction, at least in part, through the inhibition of the JAK-STAT pathway, suggesting the beneficial role played by sympathetic signal to antagonize proinflammatory cytokine signal in heart failure.



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