Victor V. Kislukhin

Theory and in vitro validation of a new extracorporeal arteriovenous loop approach for hemodynamic assessment in pediatric and neonatal intensive care unit patients.

Objectives: No simple method exists for repeatedly measuring cardiac output in intensive care pediatric and neonatal patients. The purpose of this study is to present the theory and examine the in vitro accuracy of a new ultrasound dilution cardiac output measurement technology in which an extracorporeal arteriovenous tubing loop is inserted between existing arterial and venous catheters. Design: Laboratory experiments. Setting: Research laboratory. Subjects: None. Interventions: None. Measurements and Main Results: In vitro validations of cardiac output, central blood volume, total end-diastolic volume, and active circulation volume were performed in a model mimicking pediatric (children 2–10 kg) and neonatal (0.5–3 kg) flows and volumes against flows and volumes measured volumetrically. Reusable sensors were clamped onto the arterial and venous limbs of the arteriovenous loop. A peristaltic pump was used to circulate liquid at 6–12 mL/min from the artery to the vein through the arteriovenous loop. Body temperature injections of isotonic saline (0.3–10 mL) were performed. In the pediatric setting, the absolute difference between cardiac output measured by dilution and cardiac output measured volumetrically was 3.97% ± 2.97% (range 212–1200 mL/min); for central blood volume the difference was 4.59% ± 3.14% (range 59–315 mL); for total end-diastolic volume the difference was 4.10% ± 3.08% (range 24–211 mL); and for active circulation volume the difference was 3.30% ± 3.07% (range 247–645 mL). In the neonatal setting the difference for cardiac output was 4.40% ± 4.09% (range 106–370 mL/min); for central blood volume the difference was 4.90% ± 3.69% (range 50–62 mL); and for active circulation volume the difference was 5.39% ± 4.42% (range 104–247 mL). Conclusions: In vitro validation confirmed the ability of the ultrasound dilution technology to accurately measure small flows and volumes required for hemodynamic assessments in small pediatric and neonatal patients. Clinical studies are in progress to assess the reliability of this technology under different clinical situations.

Determining lung water volume in stable hemodialysis patients

Lung water (LW) reflects the water content of the lung interstitium. Because hemodialysis patients have expanded total body water (TBW) they may also have increased LW. Hypertonic saline promotes a flux of water from lung to blood, which is measured by ultrasound flow probes on hemodialysis tubing. The volume of flux is an indirect measure of LW. Our purpose was to determine the feasibility and reproducibility of LW derived with ultrasound velocity dilution, to determine the effect of ultrafiltration on LW in stable hemodialysis patients, and to compare changes in LW with fluid compartment shifts using bioimpedance. Lung water, cardiac output, total body water, and extracellular and intracellular fluid volumes were measured in 24 stable hemodialysis patients at the beginning of hemodialysis and after ultrafiltration. The LW values at the beginning of hemodialysis (298.8 ± 90.2 ml or 3.67 ± 1.47 ml/kg) fell during hemodialysis (250.8 ± 55.8 ml or 3.12 ± 0.96 ml/kg; p < 0.05), as did TBW and extracellular fluid volumes (p < 0.001). Cardiac output, cardiac index, and central blood volume also decreased significantly with ultrafiltration (p < 0.005, p < 0.005, and p < 0.01, respectively). Results showed that stable hemodialysis patients have higher specific LW values (3.67 ml/kg) than the normal population (2 ml/kg) and ultrafiltration produces a significant decline in LW values.

Volume of extravascular lung fluid determined by blood ultrasound velocity and electrical impedance dilution.

A hypertonic sodium chloride bolus passing through the lung has a sound velocity transient that is biphasic when it reaches the carotid artery. This transient is compatible with water moving into the hypertonic bolus from the lung parenchyma, thereby leaving the lung parenchyma hypertonic. Subsequently, as the bolus leaves the lung vasculature, water passes from the blood into the tissue to return the lung tonicity to baseline, giving a moment when net movement is zero, an instant of osmotic equilibrium. Concurrent measurements of impedance track the sodium chloride transient. A theoretic basis for the calculation of extravascular lung water is derived from the water transferred to the blood, the amount of sodium chloride moved from blood to the lung, and the increase in blood osmolarity measured at the moment of equilibrium. Examples from measurements on sheep suggest that two intravenous injections of hypertonic and isotonic sodium chloride, with observations of sound velocity and electrical impedance in the systemic arterial circulation (which could also provide the cardiac output), provide a basis for calculation of lung permeability, water and salt movements, and extravascular lung water estimation.

Vasomotion model explanation for urea rebound.

Urea rebound after hemodialysis is generally attributed to urea entering the circulation from poorly perfused tissue and/or entering from regions with low membrane permeability for urea. Another explanation for rebound is based on disorders in the microcirculation, connected with the phenomenon of vasomotion, i.e., cyclic opening and closing of microvessels. The purpose of the following mathematical model is to explain observed urea rebound by the vasomotion phenomenon. The significance of vasomotion is related to the fact that a significant fraction, up to 80–95%, of all microvessels are closed while others are being perfused. The rate with which open microvessels “migrate” through the tissue determines quality of perfusion. A stochastic scheme for describing vasomotion is developed. Probabilities to change the state of microvessels are defined as follows: &agr; = probability to be open and remain open; &bgr; = to be open and become closed; &ngr; = to be closed and remain closed; &mgr; = to be closed and become open. The activity of vasomotion is defined by the rate of vasomotion, R, R = &bgr; + &mgr;, and can be measured using a curve of urea concentration.

Hemodynamic recovery after hypovolemic shock with lactated Ringer's and keratin resuscitation fluid (KRF), a novel colloid.

Abstract Death after severe hemorrhage remains an important cause of mortality in people under 50 years of age. Keratin resuscitation fluid (KRF) is a novel resuscitation solution made from keratin protein that may restore cardiovascular stability. This postulate was tested in rats that were exsanguinated to 40% of their blood volume. Test groups received either low or high volume resuscitation with either KRF or lactated Ringers solution. KRF low volume was more effective than LR in recovering cardiac function, blood pressure and blood chemistry. Furthermore, in contrast to LR-treated rats, KRF-treated rats exhibited vital signs that resembled normal controls at 1-week.

782 New Dilution Method For QP/QS Measurement in Patients with Single Ventricle (SV) Anatomy

Background and Aims Major challenge for treatment of Hypoplastic left heart syndrome by Norwood procedure is in achieving the adequate Qp/Qs value. The absence of routine method of assessing the Qp/Qs value can lead to hypoxia, brain injury, for Qp/Qs< < 1 or to insufficient tissue perfusion and lung edema for Qp/Qs>>1. The aim of the study was to develop routine method for Qp/Qs assessment for PICU and NICU patients. Method development: A mathematical model of indicator movement for SV anatomy was developed. After intravenous injection and mixing in SV the first portion of the indicator enters systemic circulation via aorta. Second portion of the indicator enters lungs via PA, then again enters SV via left atria etc. The model suggests that Qp/Qs may be calculated from dilution curve (Pic.1) Qp/Qs=S2/S1. Results COstatus monitor, (Transonic Systems Inc., NY, USA) was used in NICU and PICU patients to measures cardiac output, blood volumes and to identify shunts and PDA. According to Transonic curve data archive recoded by COstatus for single ventricle patients the actual shape of dilution curves (example, Pic.2) well agrees with model data. Abstract 782 Figure 1 Dilution Curve Model Abstract 782 Figure 2 SV Patient Dilution Curve Conclusions Mathematical model for indicator movement in SV anatomy proved that Qp/Qs value can be calculated from indicator dilution curve. Next step is to validate the Qp/Qs values measured by COstatus in animal model and in patients. Grant NIH SBIR # R43 HL111852–01.