Appreciation of the large volume deficits which may occur in surgical or trauma patients due to blood loss has led to vigorous transfusion techniques designed to overt hypovolemic shock and ischemic damage to vital organs which may develop in minutes during the hypovolemic state. In a significant proportion of patients treated with massive rapid blood or fluid transfusion, hypervolemia occurs and life threatening pulmonary edema may develop. Especially, hypervolemia may occur during transfusion for preventing development of the so-called low output syndrome following cardiac surgery. However, the most effective indicator which reveals the adequate level of transfusion is not settled yet. The present study was aimed to compare the effectiveness of the indicators suggested thus far and to determine the most sensitive one. Eight dogs were experimentally studied in terms of left atrial pressure, pulmonary arterial systolic pressure, central venous pressure, mean systemic arterial pressure and heart rate before and after induced hypervolemia with infusion of 600ml heparinized homologous blood. Immediately after induced overtransfusion of the blood, pulmonary arterial systolic pressure increased 75.0%, in omparison with the control before transfusion, left atrial pressure 58.8%, central venous pressure 44.6%, and mean systemic arterial pressure 10.1%, one hour after transfusion, pulmonary arterial systolic pressure 40.0%, left atrial pressure 21.2%, central venous pressure 14.5%, and mean systemic arterial pressure 3.2%, central venous pressure 14.5%, and mean systemic arterial pressure 3.2%, respectively. Heart rate showed no significant change throughout the experiment. These result suggested that the changes of the pulmonary arterial systolic pressure is the most sensitive indicator for detection of hypervolemia during blood transfusion.
Proceedings of the Korean Institute of Information and Commucation Sciences Conference
/
2016.10a
/
pp.915-918
/
2016
Virtual testing devices are required due to rapid changes in the health care industry and the increase of the medical or nursing workforce. The importance of devices such as the simulator, blood vessels, and lab equipment for modeling blood flow to the heart is increasing too. In this study, we made heart pump by using a step motor and developed device which simulates arterial, venous blood pressure, and blood flow. We finally evaluated the function of proposed device. The proposed system is composed of the pump for simulating, the valve device to describe the resistance of the artery and vein, and a reducing device showing the characteristics of the venous system. We used BOXER pump for heart simulator and silicon tube for arterial and venous vessels, and designed a reducing device. We also used the pressure sensor to measure arterial blood pressure. For the evaluation of the proposed system, we selected a range of 50~100mmHg of the blood circuit 60 per minute and then compared the blood pressure of a person and the measured blood pressure.
Cardiac performances were analyzed in intact turtle heart(Amyda japonica), perfusing with turtle Ringer-Locke's solution containing various hydrogen ion concentration, at several levels of arterial and venous pressure. 1. Ventricular work increased when venous pressure, or venous filling pressure increased, and also increased when arterial pressure increased. 2. The higher the arterial pressure, the lower the cardiac to output, for arterial pressure is the resistance to the ventricular blood flow. On the other hand, in specific arterial pressure, cardiac output was proportional to the venous filling pressure. 3. Heart rates did not change significantly during the perfusion with Ringel· solution of various pH. 4. In the heart Perfused with Ringer solution of various pH, ventricular work was the highest at PH 7.6 (at 6 $cmH_2O$ arterial pressure and 8 $cmH_2O$ venous pressure, the ventricular work was 63.09m$\cdot$cm). However, within the range of pH $7.1{\sim}7.6$, there were no significant changes in cardiac output and ventricular work. Below the level of pH 7.0, ventricular work decreased to less than 56% of maximium value (at $6cmH_2O$ arterial pressure and $8cmH_2O$ venous Pressure, ventricular work was 36.0$gm{\cdot}$ at pH 7.0). At pH 7.7 ventricular work decreased to less than 48% of maximum value (ventricular work: 30.0 $gm{\cdot}$). The nature of the cardiac performance at the various arterial and venous pressures was similar to that of normal heart. 5. Turtle heart seemed to be relatively insensitive to acid-base disturbances. The mechanism of negative inotropic effect of hydrogen ion was discussed.
Anesthetized dogs were tilted from horizontal to the upright and head down position. Tilting to the upright position was followed by an increase in heart rate. In the head down position a decreased heart rate was obtained. The arterial blood pressure was decreased in the upright position and was decreased markedly in the head down position. The central venous pressure was decreased in the upright position and was markedly decreased down to the negative pressure in the head down position. The respiratory rate was slightly increased in the upright position comparing to that in the horizontal position. No remarkable changes were noted in the head down position. From the above results the following factors were discussed The decreased arterial blood pressure during the upright position was supposed to be the secondary effect from the diminished venous return that was suggested by the decreased central venous pressure. The decreased arterial blood pressure in the head down position was also supposed as the above reason as the diminished central venous pressure during the tilt. In addition the cardioinhibitory effects originated from the baroreceptors might have been operated during head down tilting. In the heart rate there was slight tachycardia in the upright position this was assumed as the abolished cardioinhibitory impulses from the baroreceptor in the upright position. On the contrary, despite of the decrease of arterial blood pressure in the head down position as well as in the upright, the bradycardia have been appeared. This was suggestive of cardioinhibitory impulses from the baroreceptors which was stretched during head down tilting. From the above findings there is a possibility of continous cardioinhibitory responses during head down tilting for this kind of the short period of 10 minutes which was chosed in this study.
Kim, Kyu-Soo;Oh, Sang-Yu;Choi, Byung-Ok;Lee, Joong-Kil
The Korean Journal of Physiology
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v.3
no.2
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pp.25-31
/
1969
Effects of graded increase of positive lung inflation upon heart rates and arterial blood pressure were observed in the anesthetized dogs to analyze the mechanical and neural regulatory factor in response to the positive inflation of the lung. The results obtained were summarized as followings: 1) When the low grade of positive lung inflation was employed under the mild to moderate anesthesia, central venous pressure was linearly increased while heart rate was decreased. After bilateral vagotomy, central venous pressure was obviously increased while heart rate was constant. 2) When the high degree of positive lung inflation was employed, changes of central venous pressure and heart rate were not significant. 3) The low grade of intrapulmonary pressure increase caused reflex tachycardia in phase 2 and overshooting in phase 4 in response to the systemic arterial blood pressure change. 4) On the other hand, the high degree of intrapulmonary pressure increase caused paradoxical bradycardia in phase 2 and lack of overshooting in phase 4 in response to the systemic arterial blood pressure change. 5) It may be noted that the experimental model employed in the present study is a useful tool to evaluate and analyze the neural and mechanical regulatory factor in response to the graded increase of the positive lung inflation.
Pulmonary function is the determinant of blood gas tension. However, Acid-Base disturbances can also alter partial pressures of oxygen and carbon dioxide in arterial blood. During respiratory acidosis $PO_2$ will be lowered and reverse changes will be produced during respiratory alkalosis. On the other hand, in metabolic acidosis $PO_2$ will be elevated and $PCO_2$ will be lowered by the respiratory compensation, and reverse response will be induced in metabolic alkalosis. Urinary gas tension has many influencing factors than arterial blood and difficult to estimate the tendency of its alterations. Urinary $PO_2$ and $PCO_2$ are not always identical level as venous blood. It is to be altered by blood gas tension, flow rate of urine, metabolic rate of kidney, and Acid-Base status of blood. Particularly countercurrent exchange of oxygen and carbon dioxide in the renal medulla will make larger alteration of gas tension than venous blood. After induction of Acid-Base disturbances [disturbances] arterial and urinary $PCO_2$, $PO_2$, urinary volume, and osmolarity were determined in dogs, and the relationships between arterial and urinary $PCO_2$ , $PO_2$ Acid-Base disturbances, urinary volume, and osmolarity were investigated. 1. During the acute Metabolic and Respiratory disturbances urinary pH did not respond on respiratory origin. However, there were immediate urinary response in pH on metabolic origin. 2. Urinary $PO_2$, $PCO_2$, did not always follow arterial or venous gas tension and Acid-Base disturbance. Urinary $PCO_2$, correlate well with the urinary volume. The larger the urinary volume, $PCO_2$ lowered to the venous level. The smaller the urinary volume, urinary $PCO_2$ tends to be higher. However urinary $PO_2$ did not have any particular correlation with urinary volume. 3. Correlation between urinary $PCO_2$ and $PO_2$ were inversely proportional to arterial blood. Differences of $PCO_2$ between arterial blood and urine also did not have any particular correlation with urinary volume. This may suggest that changes on blood gas tensions can influence on urinary $PCO_2$. 4. There were eminent clear inverse correlation between urinary $PCO_2$ and osmolar concentrations of urine. Above results strongly suggest that partial pressure of gas in urine primarily depend upon counter-current exchanges in renal medullary tissues.
We utilized pulmonary artery pressure monitoring system in risky patients for preventing the postoperative pulmonary hypertensive crisis and for sampling the mixed venous blood. And this mixed venous blood oxygen saturation [MVSO2] or partial pressure [MVPO2]tells us many meaningful patients state. We selected 59 cyanotic congenital heart diseased patients, who were operated in our hospital from Nov. 1987 to Oct. 1988, in the Department of Thoracic and Cardiovascular Surgery, Seoul National University Children\ulcorner Hospital, who had pulmonary artery pressure monitoring catheter and who made us know their mixed venous oxygen condition. We found that there was no close relationship between MVPO2 and Cardiac Index [C.I.] during early postoperative period, but on the first and second day after operation the correlation coefficient was increased as r=0.35[p=0.008], r=0.78[p=0.0001]. So we concluded that the correlation between MVPO2 and C.I. was more reliable with time going as hemodynamic stabilization. And we experienced no survivors whose MVPO2 was under 20 torr, but that was not the only factor for death. From these results, we conclude that we can consider the MVPO2 [or MVSO2] representing C.I. after stabilized postoperative condition of the open heart surgery patients, but during early postoperative period, in addition to this MVPO2, we should do also apply other parameter such as urine output, arterial blood pressure, left atrial pressure and pulmonary arterial pressure for exact estimation of the patients status.
Various factors influencing the lymph flow from thoracic duct were investigated in an attempt to evaluate their contributing degree and the mechanisms. Sixteen mongrel dogs weighing between 10 and 16 kg were anesthetized and polyethylene catheters were inserted into the thoracic duct and femoral veins. Arterial blood pressure, heart rate, central venous pressure, lymph pressure and lymph flow were measured under various conditions. Electrical stimulation of left sciatic nerve, stepwise increase of central venous pressure, manual application of rhythmical depressions onto abdomen, injection of hypertonic saline solution and histamine infusion were employed. Measurement of cental venous pressure was performed through the recording catheter inserted into abdominal inferior vena cava. Changes in central venous pressure were made by an air-ballooning catheter located higher than the tip of the recording catheter in the inferior vena cava. Lymph flow from thoracic duct was measured directly with a graduated centrifuge tube allowing the lymph to flow freely outward through the inserted cannula. The average side pressure of thoracic lymph was $1.1\;cmH_2O$ and lymph flow was 0.40 ml/min or 1.9 ml/kg-hr. Hemodynamic parameters including lymph flow were measure immediately before and after (or during) applying a condition. Stimulation of left sciatic nerve with a square wave (5/sec, 2 msec, 10V) caused the lymph flow to increase 1.4 times. The pattern of lymph flow from thoracic duct was not continuous throughout the respiratory cycle, but was continuous only during Inspiration. Slow and deep respiration appeared to increase the lymph flow than a rapid and shallow respiration. Relationship between central venous pressure and the lymph flow revealed a relatively direct proportionality; Regression equation was Lymph Flow (ml/kg-hr)=0.09 CVP$(cmH_2O)$+0.55, r=0.67. Manual depressions onto the abdomen in accordance with the respiratory cycle caused the lymph flow to increase most remarkably, e.g,. 5.5 times. The application of manual depressions showed a fluctuation of central venous pressure superimposed on the respiratory fluctuation. Hypertonic saline solution (2% NaCl) administered Intravenously by the amount of 10 m1/kg increased the lymph flow 4.6 times. The injection also increased arterial blood pressure, especially systolic Pressure, and the central venous pressure. Slow intravenous infusion of histamine with a rate of 14-32 ${\mu}g/min$ resulted in a remarkable increase in the lymph flow (4.7 times), in spite of much decrease in the blood pressure and a slight decrease in the central venous pressure.
Mina Stephanos;Christopher M. B. Stewart;Ameen Mahmood;Christopher Brown;Shahin Hajibandeh;Shahab Hajibandeh;Thomas Satyadas
Annals of Hepato-Biliary-Pancreatic Surgery
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v.28
no.2
/
pp.115-124
/
2024
To compare the outcomes of low central venous pressure (CVP) to standard CVP during laparoscopic liver resection. The study design was a systematic review following the PRISMA statement standards. The available literature was searched to identify all studies comparing low CVP with standard CVP in patients undergoing laparoscopic liver resection. The outcomes included intraoperative blood loss (primary outcome), need for blood transfusion, mean arterial pressure, operative time, Pringle time, and total complications. Random-effects modelling was applied for analyses. Type I and type II errors were assessed by trial sequential analysis (TSA). A total of 8 studies including 682 patients were included (low CVP group, 342; standard CVP group, 340). Low CVP reduced intraoperative blood loss during laparoscopic liver resection (mean difference [MD], -193.49 mL; 95% confidence interval [CI], -339.86 to -47.12; p = 0.01). However, low CVP did not have any effect on blood transfusion requirement (odds ratio [OR], 0.54; 95% CI, 0.28-1.03; p = 0.06), mean arterial pressure (MD, -1.55 mm Hg; 95% CI, -3.85-0.75; p = 0.19), Pringle time (MD, -0.99 minutes; 95% CI, -5.82-3.84; p = 0.69), operative time (MD, -16.38 minutes; 95% CI, -36.68-3.39; p = 0.11), or total complications (OR, 1.92; 95% CI, 0.97-3.80; p = 0.06). TSA suggested that the meta-analysis for the primary outcome was not subject to type I or II errors. Low CVP may reduce intraoperative blood loss during laparoscopic liver resection (moderate certainty); however, this may not translate into shorter operative time, shorter Pringle time, or less need for blood transfusion. Randomized controlled trials with larger sample sizes will provide more robust evidence.
Human circulatory system between heart and tissue is not directly connected in normal condition but mandatory to go through the capillary system in order to fulfill its physiologic aim to deliver oxygen and nutrients, etc. to the tissue and retrieve used blood together with waste products from the tissue properly. When abnormal connection between arterial and venous system (AV fistula), these two circulatory systems respond differently to the hemodynamic impact of this abnormal connection between high pressure (artery) and low pressure (vein) system. Depending upon the location and/or degree (e.g. size and flow) of fistulous condition, each circulatory system exerts different compensatory hemodynamic response to this newly developed abnormal inter-relationship between two systems in order to minimize its hemodynamic impact to own system of different hemodynamic characteristics. Pump action of the heart can assist the failing arterial system directly to maintain arterial circulation against newly established low peripheral resistance by the AV fistula during the compensation period, while it affects venous system in negative way with increased venous loading. However, the negative impact of increased heart action to the venous system is partly compensated by the lymphatic system which is the third circulatory system to assist venous system independently with different hemodynamics. The lymphatic system with own unique Iymphodynamics based on peristaltic circulation from low resistance to high resistance condition, also increases its circulation to assist the compensation of overloaded venous system. Once these compensation mechanisms should fail to fight to newly established hemodynamic condition due to this abnormal AV connection, each system start to show different physiologic ${\underline{de}compensation}$ including heart and lymphatic system. The vicious cycle of decompensation between arterial and vein, two circulatory system affecting each other by mutually negative way steadily progresses to show series of hemodynamic change throughout entire circulation system altogether including heart. Clinical outcome of AV fistula from the compensated status to decompensated status is closely affected by various biological and mechanical factors to make the hemodynmic status more complicated. Proper understanding of these crucial biomechanical factors iii particular on hemodyanmic point of view is mandatory for the advanced assessment of biomechanical impact of AV fistula, since this new advanced concept of AY fistula based on blomechanical information will be able to improve clinical control of the complicated AV fistula, either congenital or acquired.
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