Central Venous Waveform Analysis and Cardiac Output in a Porcine Model of Endotoxemic Hypotension and Resuscitation.

BACKGROUND Cardiac output (CO) is a valuable proxy for perfusion, and governs volume responsiveness during resuscitation from distributive shock. The underappreciated venous system has nuanced physiology that confers valuable hemodynamic information. In this investigation, deconvolution of the central venous waveform by the fast Fourier transformation (FFT) algorithm is performed to assess its ability to constitute a CO surrogate in a porcine model of endotoxemia-induced distributive hypotension and resuscitation. STUDY DESIGN Ten pigs were anesthetized, catheterized, and intubated. A lipopolysaccharides infusion protocol was used to precipitate low systemic vascular resistance hypotension. Four crystalloid boluses (10 cc/kg) were then given in succession, after which heart rate, mean arterial pressure, thermodilution-derived CO, central venous pressure (CVP), and the central venous waveform were collected, the last undergoing fast Fourier transformation analysis. The amplitude of the fundamental frequency of the central venous waveform's cardiac wave (f0-CVP) was obtained. Heart rate, mean arterial pressure, CVP, f0-CVP, and CO were plotted over the course of the boluses to determine whether f0-CVP tracked with CO better than the vital signs, or than CVP itself. RESULTS Distributive hypotension to a 25% mean arterial pressure decrement was achieved, with decreased systemic vascular resistance (mean 918 ± 227 [SD] dyne/s/cm-5 vs 685 ± 180 dyne/s/cm-5; p = 0.038). Full hemodynamic parameters characterizing this model were reported. Slopes of linear regression lines of heart rate, mean arterial pressure, CVP, f0-CVP, and CO were -2.8, 1.7, 1.8, 0.40, and 0.35, respectively, demonstrating that f0-CVP values closely track with CO over the 4-bolus range. CONCLUSIONS Fast Fourier transformation analysis of the central venous waveform may allow real-time assessment of CO during resuscitation from distributive hypotension, possibly offering a venous-based approach to clinical estimation of volume responsiveness.

[1]  O. Desebbe,et al.  Variations of pulse pressure and central venous pressure may predict fluid responsiveness in mechanically ventilated patients during lung recruitment manoeuvre: an ancillary study , 2022, BMC Anesthesiology.

[2]  M. Ismail,et al.  Comparison of inferior vena cava collapsibility and central venous pressure in assessing volume status in shocked patients , 2022, African journal of emergency medicine : Revue africaine de la medecine d'urgence.

[3]  Md. Abul Hayat,et al.  Critical Information from High Fidelity Arterial and Venous Pressure Waveforms During Anesthesia and Hemorrhage. , 2022, Cardiovascular engineering and technology.

[4]  P. Nowakowski,et al.  Methods of assessing fluid responsiveness in septic shock patients: a narrative review , 2022, Anaesthesiology intensive therapy.

[5]  S. Narayan,et al.  Uncommon Etiologies of Shock. , 2022, Critical care clinics.

[6]  J. Carcillo,et al.  Subtypes and Mimics of Sepsis. , 2022, Critical care clinics.

[7]  A. Chalmeh,et al.  Un‐fractionated heparin counteracts the systemic inflammatory responses and multiple organ damages caused by endotoxaemia in sheep , 2022, Veterinary medicine and science.

[8]  C. Sprung,et al.  Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. , 2021, Critical care medicine.

[9]  Jonathan S. Whitfield,et al.  Noninvasive Venous Waveform Analysis Correlates With Pulmonary Capillary Wedge Pressure and Predicts 30-Day Admission in Patients With Heart Failure Undergoing Right Heart Catheterization , 2021, Journal of Cardiac Failure.

[10]  A. Mahajan,et al.  Comparison of accuracy of two uncalibrated pulse contour cardiac output monitors in off-pump coronary artery bypass surgery patients using pulmonary artery catheter-thermodilution as a reference , 2021, BMC Anesthesiology.

[11]  D. Otsuki,et al.  Sildenafil in endotoxin-induced pulmonary hypertension: an experimental study. , 2021, Brazilian journal of anesthesiology.

[12]  T. Rasmussen,et al.  Measuring Cardiac Output in a Swine Model. , 2021, Journal of visualized experiments : JoVE.

[13]  G. Beilman,et al.  Hemodynamic Parameters in the Assessment of Fluid Status in a Porcine Hemorrhage and Resuscitation Model , 2021, Anesthesiology.

[14]  B. Rochwerg,et al.  How I Do It: Dosing Fluids in Early Septic Shock. , 2020, Chest.

[15]  T. Miyasho,et al.  Use of perfusion index to detect hemodynamic changes in endotoxemic pigs. , 2020, Journal of veterinary emergency and critical care.

[16]  C. Brophy,et al.  Non-Invasive Venous waveform Analysis (NIVA) for volume assessment during complex cranial vault reconstruction: A proof-of-concept study in children , 2020, PloS one.

[17]  C. Brophy,et al.  A brief report on the effects of vasoactive agents on peripheral venous waveforms in a porcine model , 2020, JRSM cardiovascular disease.

[18]  M. Cecconi,et al.  Hemodynamic resuscitation with fluids bolus and norepinephrine increases severity of lung damage in an experimental model of septic shock. , 2020, Medicina intensiva.

[19]  C. Brophy,et al.  Non-invasive venous waveform analysis (NIVA) for volume assessment in patients undergoing hemodialysis: an observational study , 2020, BMC Nephrology.

[20]  D. Foster,et al.  Importance of Endotoxin Clearance in Endotoxemic Septic Shock: An Analysis From the Evaluating Use of PolymyxinB Hemoperfusion in a Randomized Controlled Trial of Adults Treated for Endotoxemic Septic Shock (EUPHRATES) Trial , 2020, Critical care explorations.

[21]  G. Ospina-Tascón,et al.  Use of Pulse Pressure Variation as Predictor of Fluid Responsiveness in Patients Ventilated With Low Tidal Volume: A Systematic Review and Meta-Analysis , 2020, Clinical medicine insights. Circulatory, respiratory and pulmonary medicine.

[22]  Daniel R. Brophy,et al.  Non-Invasive Venous waveform Analysis (NIVA) for monitoring blood loss in human blood donors and validation in a porcine hemorrhage model. , 2019, Journal of clinical anesthesia.

[23]  L. Lindberg,et al.  Indirect Calorimetry Overestimates Oxygen Consumption in Young Children: Caution is Advised Using Direct Fick Method as a Reference Method in Cardiac Output Comparison Studies , 2019, Pediatric Cardiology.

[24]  D. Paniagua,et al.  Thermodilution Cardiac Output: A Concept Over 250 Years in the Making , 2019, Cardiology in review.

[25]  P. Pickkers,et al.  Experimental human endotoxemia as a model of systemic inflammation. , 2019, Biochimie.

[26]  K. Sexton,et al.  Fast Fourier Transformation of Peripheral Venous Pressure Changes More Than Vital Signs with Hemorrhage , 2019, Military medicine.

[27]  F. Baudenbacher,et al.  Peripheral Intravenous Volume Analysis (PIVA) for Quantitating Volume Overload in Patients Hospitalized With Acute Decompensated Heart Failure-A Pilot Study. , 2018, Journal of cardiac failure.

[28]  Robert G. W. Kirk,et al.  Recovering The Principles of Humane Experimental Technique , 2017, Science, technology & human values.

[29]  J. Fraser,et al.  An Ovine Model of Hyperdynamic Endotoxemia and Vital Organ Metabolism , 2018, Shock.

[30]  F Baudenbacher,et al.  Peripheral i.v. analysis (PIVA) of venous waveforms for volume assessment in patients undergoing haemodialysis , 2017, British journal of anaesthesia.

[31]  P. Marik,et al.  Prediction of fluid responsiveness: an update , 2016, Annals of Intensive Care.

[32]  T. Fanshawe,et al.  Fluid responsiveness prediction using Vigileo FloTrac measured cardiac output changes during passive leg raise test , 2016, Journal of Intensive Care.

[33]  F. Baudenbacher,et al.  Peripheral Venous Waveform Analysis for Detecting Hemorrhage and Iatrogenic Volume Overload in a Porcine Model , 2016, Shock.

[34]  Yoshitsugu Yamada,et al.  Reliability of cardiac output measurements using LiDCOrapid™ and FloTrac/Vigileo™ across broad ranges of cardiac output values , 2016, Journal of Clinical Monitoring and Computing.

[35]  S. Sondergaard,et al.  Central venous pressure: we need to bring clinical use into physiological context , 2015, Acta anaesthesiologica Scandinavica.

[36]  J. Bakker,et al.  Starling curves and central venous pressure , 2015, Critical Care.

[37]  Y. Mehta,et al.  Newer methods of cardiac output monitoring. , 2014, World journal of cardiology.

[38]  O. Viklicky,et al.  The effect of immunosuppression on manifestations of sepsis in an animal model of cecal ligation and puncture. , 2013, Transplantation proceedings.

[39]  D. Ganea,et al.  Cecal ligation puncture procedure. , 2011, Journal of visualized experiments : JoVE.

[40]  G. Nieman,et al.  A clinically applicable porcine model of septic and ischemia/reperfusion-induced shock and multiple organ injury. , 2011, The Journal of surgical research.

[41]  S. Opal.  Endotoxins and other sepsis triggers. , 2010, Contributions to Nephrology.

[42]  N. Nakagawa,et al.  EXPERIMENTAL MODELS OF SEPSIS AND THEIR CLINICAL RELEVANCE , 2008, Shock.

[43]  T. Martin,et al.  Animal models of acute lung injury , 2008, American journal of physiology. Lung cellular and molecular physiology.

[44]  C. Hartley,et al.  DISTRIBUTION OF NOS ISOFORMS IN A PORCINE ENDOTOXIN SHOCK MODEL , 2007, Shock.

[45]  A. Arner,et al.  Endotoxemic pulmonary hypertension is largely mediated by endothelin-induced venous constriction , 2008, Intensive Care Medicine.

[46]  P. Germann,et al.  INFUSION OF INCREASING DOSES OF ENDOTOXIN INDUCES PROGRESSIVE ACUTE LUNG INJURY BUT PREVENTS EARLY PULMONARY HYPERTENSION IN PIGS , 2006, Shock.

[47]  F. Bach,et al.  Carbon monoxide pretreatment prevents respiratory derangement and ameliorates hyperacute endotoxic shock in pigs , 2005, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.