Abstract 12327: Intravenous Waveform Analysis Correlates With Volume Status in Resuscitation in In-Vivo Rat Model

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Matthew Barajas ◽  
Matthias L Riess ◽  
Franz J Baudenbacher ◽  
Matthew Hampton ◽  
zhu li ◽  
...  

Introduction: Current volume status markers under-perform. Dynamic markers demonstrate improved outcomes in goal directed fluid therapy but maintain validity in a narrow range of clinical parameters. In addition, they assess volume responsiveness over total volume status. Repeated echo assessments may be infeasible. Hypothesis: Intravenous waveform analysis-derived F1 more closely models volume status than current markers in a rat resuscitation model. Methods: Seven Sprague Dawley rats were anesthetized and mechanically ventilated. Pressure transductions occurred via cannulation of the right femoral vein, left femoral artery and right internal jugular vein. Hemorrhage and resuscitation occurred via the left femoral vein. Heparinized rats were bled to 80% of the estimated blood volume (EBV) then resuscitated with their own whole blood in increments of 2% of the EBV until euvolemia was reached. Cardiac output (CO) and left ventricular end diastolic area (LVEDA) were calculated with echocardiography. Fast Fourier transform was performed on venous waveforms to obtain the heart rate linked F1 amplitude. Pearson’s correlation coefficients were compared using Fisher’s Z transformation. Mixed effects modeling goodness-of-fit was assessed with Akaike information criterion (AIC). Significance was set at p=.05. Results: F1 had the strongest correlation with volume status, r= .70, followed by CO, r=.55, LVEDA, r=.55, mean arterial pressure (MAP), r=.50, central venous pressure r= -.02, and pulse pressure variation (PPV), r=.01. When compared, F1 rho was significantly greater than that of all variables except CO and LVEDA, p=.09 and p=.07, respectively. In mixed effects regression, F1 displayed the most significant AIC, -274, followed by CO at -239. Conclusions: The novel marker F1 is strongly correlated with volume status during whole blood resuscitation. F1 may be superior to current markers for directing volume resuscitation therapy.

Author(s):  
Ryan J. Lefevre ◽  
Claudius Balzer ◽  
Franz J. Baudenbacher ◽  
Matthias L. Riess ◽  
Antonio Hernandez ◽  
...  

Background Assessing intravascular hypovolemia due to hemorrhage remains a clinical challenge. Central venous pressure (CVP) remains a commonly used monitor in surgical and intensive care settings for evaluating blood loss, despite well-described pitfalls of static pressure measurements. The authors investigated an alternative to CVP, intravenous waveform analysis (IVA) as a method for detecting blood loss and examined its correlation with echocardiography. Methods Seven anesthetized, spontaneously breathing male Sprague Dawley rats with right internal jugular central venous and femoral arterial catheters underwent hemorrhage. Mean arterial pressure (MAP), heart rate, CVP, and IVA were assessed and recorded. Hemorrhage was performed until each rat had 25% estimated blood volume removed. IVA was obtained using fast Fourier transform and the amplitude of the fundamental frequency (f1) was measured. Transthoracic echocardiography was performed utilizing a parasternal short axis image of the left ventricle during hemorrhage. MAP, CVP, and IVA were compared with blood removed and correlated with left ventricular end diastolic area (LVEDA). Results All 7 rats underwent successful hemorrhage. MAP and f1 peak amplitude obtained by IVA showed significant changes with hemorrhage. MAP and f1 peak amplitude also significantly correlated with LVEDA during hemorrhage (R = 0.82 and 0.77, respectively). CVP did not significantly change with hemorrhage, and there was no significant correlation between CVP and LVEDA. Conclusions In this study, f1 peak amplitude obtained by IVA was superior to CVP for detecting acute, massive hemorrhage. In addition, f1 peak amplitude correlated well with LVEDA on echocardiography. Translated clinically, IVA might provide a viable alternative to CVP for detecting hemorrhage.


1994 ◽  
Vol 267 (1) ◽  
pp. R97-R106 ◽  
Author(s):  
H. S. Huang ◽  
J. C. Longhurst

The cardiovascular effects of regional abdominal ischemia and reperfusion were studied in cats anesthetized with alpha-chloralose. In group 1 (n = 9), central venous pressure was kept constant by a servo-controller while the celiac and superior mesenteric arteries were occluded by loop snares for 10 min. In group 2 (n = 9), a constant-perfusion circuit to the celiac and superior mesenteric arteries that could divert flow to the femoral vein was used to induce abdominal ischemia. In group 3 (n = 7), venous return from the inferior vena cava was controlled, and a constant-perfusion circuit was used to induce abdominal ischemia. Abdominal ischemia significantly (P < 0.05) increased portal venous blood lactate from 4.3 +/- 0.6 to 6.0 +/- 0.6 mM in group 3. The early increases in blood pressure caused by passive volume shifts in groups 1 and 2 were abolished in group 3. The late, i.e., 10 min, response to abdominal ischemia consisted of significant (P < 0.05) increases in mean arterial pressure (29 +/- 7, 24 +/- 7, and 33 +/- 8 mmHg in groups 1, 2, and 3, respectively). Abdominal ischemia also significantly (P < 0.05) increased the first derivative of left ventricular pressure at 40 mmHg developed pressure from 4,355 +/- 377 to 4,839 +/- 407 mmHg/s in group 3. Celiac and superior mesenteric ganglionectomy abolished the late but not the early hemodynamic changes. Ganglionectomy also significantly (P < 0.05) enhanced the decrease in mean arterial pressure during reperfusion in all groups. We conclude that the pressor and contractile responses during 10 min of abdominal ischemia and the relative maintenance of blood pressure during reperfusion after ischemia are reflex in nature.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zhihang Ma ◽  
Jiaxin Gai ◽  
Yinghan Sun ◽  
Yunpeng Bai ◽  
Hongyi Cai ◽  
...  

Abstract Background Currently, the accepted effective method for assessing blood volume status, such as measuring central venous pressure (CVP) and mean pulmonary artery pressure (mPAP), is invasive. The purpose of this study was to explore the feasibility and validity of the ratio of the femoral vein diameter (FVD) to the femoral artery diameter (FAD) for predicting CVP and mPAP and to calculate the cut-off value for the FVD/FAD ratio to help judge a patient’s fluid volume status. Methods In this study, 130 patients were divided into two groups: in group A, the FVD, FAD, and CVP were measured, and in group B, the FVD, FAD, and mPAP were measured. We measured the FVD and FAD by ultrasound. We monitored CVP by a central venous catheter and mPAP by a Swan-Ganz floating catheter. Pearson correlation coefficients were calculated. The best cut-off value for the FVD/FAD ratio for predicting CVP and mPAP was obtained according to the receiver operating characteristic (ROC) curve. Results The FVD/FAD ratio was strongly correlated with CVP (R = 0.87, P < 0.0000) and mPAP (R = 0.73, P < 0.0000). According to the ROC curve, an FVD/FAD ratio ≥ 1.495 had the best test characteristics to predict a CVP ≥ 12 cmH2O, and an FVD/FAD ratio ≤ 1.467 had the best test characteristics to predict a CVP ≤ 10 cmH2O. An FVD/FAD ratio ≥ 2.03 had the best test characteristics to predict an mPAP ≥ 25 mmHg. According to the simple linear regression curve of the FVD/FAD ratio and CVP, when the predicted CVP ≤ 5 cmH2O, the FVD/FAD ratio was ≤ 0.854. Conclusion In this study, the measurement of the FVD/FAD ratio obtained via ultrasound was strongly correlated with CVP and mPAP, providing a non-invasive method for quickly and reliably assessing blood volume status and providing good clinical support.


Perfusion ◽  
1995 ◽  
Vol 10 (5) ◽  
pp. 323-326 ◽  
Author(s):  
James R Beck ◽  
Linda B Mongero ◽  
Daniel J Goldstein ◽  
Mehmet C Oz

A simple heparin-bonded circuit to facilitate a femoral vein to femoral artery shunt for the treatment of right-sided circulatory failure is proposed. Desaturated venous blood is shunted to the left-sided circulation to increase systemic blood pressure at the expense of saturation. The circuit comprised ¼ inch x 3/32 inch tubing with a paediatric Bio-Medicus centrifugal pump head allowing adequate regulation of flow. Paediatric Bio- Medicus cannulae provide flows between 500 and 2000 ml/min. Measurements of pulmonary artery pressure, central venous pressure, arterial pressure, arterial saturation and cardiac output were recorded. In the four case studies presented, the treatment included unloading of the right ventricle with venous to arterial shunting. Likewise, eight Holstein calves underwent shunt utilization after placement of a left ventricular assist device and induction of right ventricular failure. The future use of this device may be instrumental in aiding the cardiothoracic surgical team in the treatment of right-sided circulatory failure.


1996 ◽  
Vol 80 (1) ◽  
pp. 69-76 ◽  
Author(s):  
M. R. Eichinger ◽  
B. R. Walker

We sought to examine the influence of nitric oxide (NO) and the second messengers guanosine 3′,5′-cyclic monophosphate (cGMP) and intracellular Ca2+ on fluid flux in lungs isolated from male Sprague-Dawley rats and perfused with saline (containing 4% albumin) or with whole blood. Lungs were allowed to equilibrate for a period of 30 min without treatment (control group) or with one of the following agents: the exogenous NO donor spermine NONOate, the nitric oxide synthase inhibitor N omega-nitro-L-arginine (L-NNA), 8-BrcGMP, the Ca2- ionophore ionomycin, or the endothelial injurious agent protamine. After equilibration, perfusate reservoir height was increased to five incremental settings to increase pulmonary venous pressure and enhance fluid flux. Perfusate reservoir weight was monitored continuously as an index of fluid flux. The lung wet-to-dry weight ratio was determined on completion of the experiments. Increasing reservoir height was associated with an increase in pulmonary arterial, pulmonary capillary, and pulmonary venous pressures and an increase in fluid flux. However, treatment with exogenous NO or inhibition of endogenous NO was without effect on fluid flux in saline lungs at two different flow rates or in whole blood-perfused lungs. Similarly, treatment with cGMP and ionomycin did not alter fluid flux. Protamine pretreatment resulted in a significant increase in fluid flux at the highest reservoir setting, although exogenous NO and L-NNA pretreatments were without further effect on the protamine-treated lungs. Thus a role for NO and the second messengers cGMP and Ca2+ in modulating fluid flux could not be demonstrated in the isolated rat lung.


Author(s):  
CL Hastings ◽  
RD Carlton ◽  
FG Lightfoot ◽  
AF Tryka

The earliest ultrastructural manifestation of hypoxic cell injury is the presence of intracellular edema. Does this intracellular edema affect the ability to cryopreserve intact myocardium? To answer this guestion, a model for anoxia induced intracellular edema (IE) was designed based on clinical intraoperative myocardial preservation protocol. The aortas of 250 gm male Sprague-Dawley rats were cannulated and a retrograde flush of Plegisol at 8°C was infused over 90 sec. The hearts were excised and placed in a 28°C bath of Lactated Ringers for 1 h. The left ventricular free wall was then sliced and the myocardium was slam frozen. Control rats (C) were anesthetized, the hearts approached by median sternotomy, and the left ventricular free wall frozen in situ immediately after slicing. The slam frozen samples were obtained utilizing the DDK PS1000, which was precooled to -185°C in liguid nitrogen. The tissue was in contact with the metal mirror for a dwell time of 20 sec, and stored in liguid nitrogen until freeze dry processing (Lightfoot, 1990).


2021 ◽  
pp. 039139882110168
Author(s):  
Dilushi Wijayaratne ◽  
Vasantha Muthu Muthuppalaniappan ◽  
Andrew Davenport

Introduction: Serum cancer antigen 125(SeCA125) has been reported to be increased in patients with heart failure and correlate with both extracellular water (ECW) overload and poor prognosis. Ultrafiltration failure and ECW overload are a major cause of peritoneal dialysis (PD) technique failure. We wished to determine whether SeCA125 could also be a marker of volume status in PD patients. Methods: We contemporaneously measured SeCA125, serum N terminal brain natriuretic peptide (NTproBNP) and ECW by bioimpedance in adult PD patients attending for outpatient assessment of peritoneal membrane function. Results: The median SeCA125 was 19 (12–33) U/mL in 489 PD patients, 61.3% male, median age 61.5 (interquartile range 50–75) years. SeCA125 was positively associated with the ratio of ECW/total body water (TBW) ( r = 0.29, p < 0.001), 4-h peritoneal dialysate to serum creatinine ratio ( r = 0.23, p < 0.001), NTproBNP) ( r = 0.18, p < 0.001), and age ( r = 00.17, p = 0.001) and negatively with 24-h PD ultrafiltration volume ( r = −0.28, p < 0.001) serum albumin ( r = −0.22, p < 0.001), and echocardiographic left ventricular ejection fraction ( r = −0.20, p < 0.001), but not with residual renal function or C-reactive protein. Patients with above the median SeCA125, had greater median ECW/TBW 0.403(IQR 0.394–0.410) vs 0.395(0.387–0.404), p < 0.001 and NTproBNP (6870 (IQR 1936–20096) vs 4069 (1345–12291) vs) pg/mL, p = 0.03. Conclusion: Heart failure studies have reported SeCA125 is a marker of ECW overload. Our retrospective analysis suggests that SeCA125 is also associated with ECW volume in PD patients. Further studies are required to determine whether serial measurements of SeCA125 trend with changes in ECW status in PD patients and can be used to aid volume assessments.


1995 ◽  
Vol 73 (3) ◽  
pp. 378-382 ◽  
Author(s):  
Yi-Tsau Huang ◽  
Chuang-Ye Hong ◽  
Pi-Chin Yu ◽  
Ming-Fang Lee ◽  
May C. M. Yang ◽  
...  

The purpose of this study was to investigate the vascular contractile and inositol phosphate responses in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL) in Sprague–Dawley rats. Sham-operated rats served as controls. Pressures, vasoconstrictor responses, and inositol phosphate responses were determined at 14 days after surgery. The portal venous pressure was significantly higher, while systemic arterial pressure and heart rate were lower, in PVL rats. Dose-dependent contractile responses were observed for both norepinephrine (1 × 10−8 – 3 × 10−6 M) and vasopressin (3 × 10−10 – 3 × 10−8 M) in the tail artery of both groups. The contractile response to norepinephrine was significantly decreased in PVL rats compared with controls at all doses. The contractile response to vasopressin was significantly decreased in PVL rats at higher doses. After myo-[3H]inositol incorporation in tail artery, the levels of 3H-labelled phosphatidylinositols (cpm/mg) were similar between the two groups. Norepinephrine (10−7 – 10−5 M) and vasopressin (10−10 – 10−8 M) dose dependently stimulated the 3H-labelled inositol phosphate production in the tail artery of both PVL and sham-operated rats. However, the response was significantly lower in PVL rats. The results suggested that the attenuation of vascular contractile responses in portal hypertension was reflected in the phosphoinositide messenger system.Key words: portal hypertension, inositol phosphates, phosphoinositide, tail artery, contractile response.


Author(s):  
Christos Iliadis ◽  
Maximilian Spieker ◽  
Refik Kavsur ◽  
Clemens Metze ◽  
Martin Hellmich ◽  
...  

Abstract Background Reliable risk scores in patients undergoing transcatheter edge-to-edge mitral valve repair (TMVR) are lacking. Heart failure is common in these patients, and risk scores derived from heart failure populations might help stratify TMVR patients. Methods Consecutive patients from three Heart Centers undergoing TMVR were enrolled to investigate the association of the “Get with the Guidelines Heart Failure Risk Score” (comprising the variables systolic blood pressure, urea nitrogen, blood sodium, age, heart rate, race, history of chronic obstructive lung disease) with all-cause mortality. Results Among 815 patients with available data 177 patients died during a median follow-up time of 365 days. Estimated 1-year mortality by quartiles of the score (0–37; 38–42, 43–46 and more than 46 points) was 6%, 10%, 23% and 30%, respectively (p < 0.001), with good concordance between observed and predicted mortality rates (goodness of fit test p = 0.46). Every increase of one score point was associated with a 9% increase in the hazard of mortality (95% CI 1.06–1.11%, p < 0.001). The score was associated with long-term mortality independently of left ventricular ejection fraction, NYHA class and NTproBNP, and was equally predictive in primary and secondary mitral regurgitation. Conclusion The “Get with the Guidelines Heart Failure Risk Score” showed a strong association with mortality in patients undergoing TMVR with additive information beyond traditional risk factors. Given the routinely available variables included in this score, application is easy and broadly possible. Graphic abstract


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