Inferior vena cava collapsibility index as a predictor of fluid responsiveness in sepsis-related acute circulatory failure

Background Assessing fluid responsiveness is the key to successful resuscitation of critically-ill sepsis patients. The use of IVC variation is favored among the dynamic methods of fluid responsiveness assessment in the ICU because it is non-invasive and inexpensive; moreover, it does not demand a high level of training. The aim of this study is to determine the value of the IVC respiratory variability for predicting fluid responsiveness in spontaneously breathing sepsis patients with acute circulatory failure. Results In this prospective observational study, fifty-eight spontaneously breathing sepsis patients admitted in the ICU were enrolled after the approval of the departmental Research Ethical Committee, and the informed written consent had been taken from the patients. Ultrasonographic and echocardiographic parameters were measured “IVC parameters and stroke volume (SV)” with calculation of the inferior vena cava collapsibility index (IVCCI) and cardiac output. These values were obtained before (baseline) and after volume expansion with a fluid bolus. The study showed that twenty-nine patients (50%) were considered to be responders, with an increase in CO by 10% or more after fluid challenge. There was a significant difference between responders and non-responders in baseline IVCCI (p value < 0.001). There were no significant differences between responders and non-responders in terms of demographic and baseline clinical characteristics. Also, there was statistically significantly larger maximum (IVC max) and minimum (IVC min) inferior vena cava diameters before volume expansion in non-responders than in responders with p value 0.037 and 0.001 respectively. The suggested cut off value regarding baseline IVCCI to predict response to fluid infusion is 0.32 with a high chance of response above this figure (a sensitivity of 72.41% and a specificity of 82.76%). Conclusions Inferior vena cava collapsibility index assessment can be a sensitive and a good predictor of fluid responsiveness, being based on a safe and a non-invasive technique compared to other methods such as central venous pressure (CVP) measurement and pulmonary artery catheter insertion.

Hyperoxia during extracorporeal cardiopulmonary resuscitation for refractory cardiac arrest is associated with severe circulatory failure and increased mortality

Background High levels of arterial oxygen pressures (PaO2) have been associated with increased mortality in extracorporeal cardiopulmonary resuscitation (ECPR), but there is limited information regarding possible mechanisms linking hyperoxia and death in this setting, notably with respect to its hemodynamic consequences. We aimed therefore at evaluating a possible association between PaO2, circulatory failure and death during ECPR. Methods We retrospectively analyzed 44 consecutive cardiac arrest (CA) patients treated with ECPR to determine the association between the mean PaO2 over the first 24 h, arterial blood pressure, vasopressor and intravenous fluid therapies, mortality, and cause of deaths. Results Eleven patients (25%) survived to hospital discharge. The main causes of death were refractory circulatory shock (46%) and neurological damage (24%). Compared to survivors, non survivors had significantly higher mean 24 h PaO2 (306 ± 121 mmHg vs 164 ± 53 mmHg, p < 0.001), lower mean blood pressure and higher requirements in vasopressors and fluids, but displayed similar pulse pressure during the first 24 h (an index of native cardiac recovery). The mean 24 h PaO2 was significantly and positively correlated with the severity of hypotension and the intensity of vasoactive therapies. Patients dying from circulatory failure died after a median of 17 h, compared to a median of 58 h for patients dying from a neurological cause. Patients dying from neurological cause had better preserved blood pressure and lower vasopressor requirements. Conclusion In conclusion, hyperoxia is associated with increased mortality during ECPR, possibly by promoting circulatory collapse or delayed neurological damage.

Oximetric studies in chronic nonspecific lung diseases

Oximetric studies were carried out in 48 patients, of whom 18 were with chronic emphysema of the lungs, pneumosclerosis with circulatory failure of 2 and 3 degrees (cor pulmonale II).

Extrapericardial cardiac tamponade secondary to traumatic hemorrhage of the thymus

This report describes a 90-year-old man who sustained blunt chest trauma that progressed to circulatory failure from an enlarging anterior mediastinal hematoma. Emergent sternotomy was performed, revealing a hematoma primarily involving the thymus that was promptly evacuated. Extrapericardial cardiac tamponade is an uncommon event that occurs when fluid collects within the mediastinum but outside the pericardium. Hemodynamically significant hemorrhage of the thymus is rare because the gland begins to involute early in development. To our knowledge, cardiac tamponade secondary to traumatic hemorrhage of the thymus has not been previously described. Early recognition and hematoma evacuation can be lifesaving.

Left ventricular longitudinal strain variations assessed by speckle-tracking echocardiography after a passive leg raising maneuver in patients with acute circulatory failure to predict fluid responsiveness: A prospective, observational study

Background An association was reported between the left ventricular longitudinal strain (LV-LS) and preload. LV-LS reflects the left cardiac function curve as it is the ratio of shortening over diastolic dimension. The aim of this study was to determine the sensitivity and specificity of LV-LS variations after a passive leg raising (PLR) maneuver to predict fluid responsiveness in intensive care unit (ICU) patients with acute circulatory failure (ACF). Methods Patients with ACF were prospectively included. Preload-dependency was defined as a velocity time integral (VTI) variation greater than 10% between baseline (T0) and PLR (T1), distinguishing the preload-dependent (PLD+) group and the preload-independent (PLD-) group. A 7-cycles, 4-chamber echocardiography loop was registered at T0 and T1, and strain analysis was performed off-line by a blind clinician. A general linear model for repeated measures was used to compare the LV-LS variation (T0 to T1) between the two groups. Results From June 2018 to August 2019, 60 patients (PLD+ = 33, PLD- = 27) were consecutively enrolled. The VTI variations after PLR were +21% (±8) in the PLD+ group and -1% (±7) in the PLD- group (p<0.01). Mean baseline LV-LS was -11.3% (±4.2) in the PLD+ group and -13.0% (±4.2) in the PLD- group (p = 0.12). LV-LS increased in the whole population after PLR +16.0% (±4.0) (p = 0.04). The LV-LS variations after PLR were +19.0% (±31) (p = 0.05) in the PLD+ group and +11.0% (±38) (p = 0.25) in the PLD- group, with no significant difference between the two groups (p = 0.08). The area under the curve for the LV-LS variations between T0 and T1 was 0.63 [0.48–0.77]. Conclusion Our study confirms that LV-LS is load-dependent; however, the variations in LV-LS after PLR is not a discriminating criterion to predict fluid responsiveness of ICU patients with ACF in this cohort.

Comparison of mean systemic pressure in patients with acute circulatory failure receiving passive leg raising vs. pneumatic leg compression

Background: Driving pressure of venous return (VR) is determined by a pressure gradient between mean systemic pressure (Pms) and central venous pressure (CVP). While passive leg raising (PLR) and pneumatic leg compression PC (PC) can increase VR, no study has explored the effects of these two procedures on Pms and VR-related hemodynamic variables. Methods: Forty patients with acute circulatory failure were enrolled in this analysis. All patients obtained both PLR and PC, and were measured for Pms, CVP, mean arterial pressure (MAP), cardiac output (CO), VR resistance (RVR), and systemic vascular resistance (SVR) at baseline and immediately after procedures. To minimize carry over effect, the patients were divided in 2 groups based on procedure sequence which were 1) patients receiving PLR first then PC (PLR-first), and 2) patients receiving PC first then PLR (PC-first). Both groups waited for a washout period before performing the 2 second procedure. Primary outcome was difference in Pms between PLR and PC procedures. Secondary outcome were differences in CVP, MAP, CO, RVR, and SVR between PLR and PC procedures. Results: No difference was found in baseline characteristics and no carry over effect was observed between the 2 groups of patients. Compared with baseline, both PLR and PC significantly increased Pms, CVP, MAP, and CO. PLR increased Pms (9.0±2.3 vs 4.8±1.7 mmHg, p<0.001), CVP (4.5±1.2 vs. 1.6±0.7 mmHg, p<0.001), MAP (22.5±5.6 vs. 14.4±5.0 mmHg, p<0.001), and CO (1.5±0.5 vs. 0.5±0.2 L/min, p<0.001) more than PC. However, PC, also significantly increased RVR (16 ± 27.2 dyn.s/cm5, p=0.001) and SVR (78.4 ± 7.2 dyn.s/cm5, p<0.001) but no difference in PLR group. Conclusion: Among patients with acute circulatory failure, PLR increased Pms, CVP, MAP, and CO more than PC.

Comparison of mean systemic pressure in patients with acute circulatory failure receiving passive leg raising vs. pneumatic leg compression

Background: Driving pressure of venous return (VR) is determined by a pressure gradient between mean systemic pressure (Pms) and central venous pressure (CVP). While passive leg raising (PLR) and pneumatic leg compression PC (PC) can increase VR, no study has explored the effects of these two procedures on Pms and VR-related hemodynamic variables. Methods: Forty patients with acute circulatory failure were enrolled in this analysis. All patients obtained both PLR and PC, and were measured for Pms, CVP, mean arterial pressure (MAP), cardiac output (CO), VR resistance (RVR), and systemic vascular resistance (SVR) at baseline and immediately after procedures. To minimize carry over effect, the patients were divided in 2 groups based on procedure sequence which were 1) patients receiving PLR first then PC (PLR-first), and 2) patients receiving PC first then PLR (PC-first). Both groups waited for a washout period before performing the 2 second procedure. Primary outcome was difference in Pms between PLR and PC procedures. Secondary outcome were differences in CVP, MAP, CO, RVR, and SVR between PLR and PC procedures. Results: No difference was found in baseline characteristics and no carry over effect was observed between the 2 groups of patients. Compared with baseline, both PLR and PC significantly increased Pms, CVP, MAP, and CO. PLR increased Pms (9.0±2.3 vs 4.8±1.7 mmHg, p<0.001), CVP (4.5±1.2 vs. 1.6±0.7 mmHg, p<0.001), MAP (22.5±5.6 vs. 14.4±5.0 mmHg, p<0.001), and CO (1.5±0.5 vs. 0.5±0.2 L/min, p<0.001) more than PC. However, PC, also significantly increased RVR (16 ± 27.2 dyn.s/cm5, p=0.001) and SVR (78.4 ± 7.2 dyn.s/cm5, p<0.001) but no difference in PLR group. Conclusion: Among patients with acute circulatory failure, PLR increased Pms, CVP, MAP, and CO more than PC.