Claret Flowmeter

The Role of Nitric Oxide and the Regulation of Cardiac Metabolism

Elizabeth Kertowidjojo , ... Thomas H. Hintze , in Translational Research in Coronary Artery Disease, 2016

Function of Nitric Oxide and Reactive Dilatation in Coronary Artery Vasomotion

In the 1990s, emphasis was focused upon the command of the coronary circulation past means of endothelial shear stress. For many years it was known that the application of acetyl choline or carbachol to claret vessel strips resulted in relaxation of blood vessels that was variable and unpredictable. Through meticulous recording of data by Furchgott, Ignarro, and Murad, it was found that when the endothelium was damaged or missing, relaxation was either macerated or replaced by overt vasoconstriction in strips of blood vessels from multiple species.

Apoplexy of a large epicardial coronary artery in dogs results in characteristic reactive hyperemia like to that observed in the peripheral apportionment [12–20]. Transient occlusion of a large coronary artery for xxx   s results in a drop in period to zero, as calibrated with an electromagnetic claret catamenia transducer, following which release of the occluder results in marked increment in menses (Effigy 9.ii) associated with large avenue vasodilatation every bit measured past sonomicrometry.

Figure ix.2. Reactive hyperemia following release of transient apoplexy before and after administration of nitro-l-arginine. A small reduction in reactive hyperemia is observed to exist associated with the presence of this substituted arginine molecule.

Reactive dilatation is proportional to the duration of the occlusion, is independent of occlusion proximal or distal to the placement of the diameter sensing crystals, and is not altered by drugs to inhibit the production of adenosine, prostaglandins, or sympathetic receptor blocking agents. In contrast, it is entirely eliminated if blood flow is maintained at a constant velocity (Effigy 9.3), and is similarly eliminated by the inhibition of endothelial nitric oxide synthase (eNOS) with a substituted arginine molecule (Effigy 9.iv), hence confirming that this miracle is mediated past the endothelium [16,21].

Effigy 9.3. Big coronary artery dilation to adenosine is reduced past approximately 50% when the blood vessel blood flow is held constant, demonstrating that 50% of adenosine-mediated vasodilation is facilitated past adenosine receptor stimulation, while the remaining 50% results from a flow-dependent mechanism. In contrast, 100% of the big vessel dilation during reactive dilation is flow dependent.

Effigy ix.4. Change in diameter of the left circumflex coronary artery following twenty   s of apoplexy, administration of acetyl choline (ACH), cardiac pacing, adenosine infusion, and nitroglycerine (NTG) infusion. The open bars represent response to the stimulus alone, while the striped bars represent the arterial response post-obit blockade of nitric oxide synthase (NOS) with nitro-l-arginine (l-NNA). All or well-nigh all of the vasodilatory response to arterial occlusion or ACH is obliterated by l-NNA, as is the flow-mediated portion of the vasodilatory response to pacing and adenosine. The addition of exogenous nitrate eliminates the inhibitory effect of 50-NNA.

This demonstrates a precise, sensitive command machinery which employs shear stress as a stimulus for the endothelium to brand NO from arginine that tin be used to quantitatively estimate the damage to the endothelium in diverse vascular affliction states. Every bit at that place is a fixed relationship betwixt altered reactive dilation in the heart and forearm, studies of peripheral menses-mediated vasodilatation can predict disorders in coronary vasomotion [22]. Feldman et al. [23] take demonstrated that nitroglycerin causes transient dilatation of epicardial coronary arteries which is size related. Hence, dilatation in response to nitroglycerin becomes more and more than attenuated as one moves from epicardial to intermediate to small endocardial arteries [23]. The office of this segmental dilation in toto is 10% of the capacitance of coronary apportionment [1]. Effigy 9.v demonstrates the effect of prostaglandin-mediated dilation of a big coronary artery when exposed to arachidonic acid infusion, as compared to the more than robust response to NO in Effigy ix.vi.

Figure 9.five. Changes in large coronary avenue diameter when exposed to arachidonic acrid (lanes five and half dozen). Arachidonic acrid is the fatty acid precursor for eicosanoid vasodilators. Arachidonic acid-mediated vasodilation is blocked by nonsteroidal anti-inflammatory agents (NSAIDS) such equally indomethacin indicating that it is prostaglandin dependent.

Figure 9.6. In contradistinction to Figure ix.five, infusion of nitroglycerin causes profound dilatation (CD), when compared to arachidonic acid. Exogenous NTG donates NO which serves every bit a more than constructive vasodilator than prostacyclin.

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Rubber Pharmacology II-CV, GI, Respiratory and Renal Safety

Michael Williams , ... Pierre Lacroix , in xPharm: The Comprehensive Pharmacology Reference, 2007

1.3 Hemodynamic evaluation: Systemic, cardiac, renal and pulmonary hemodynamics in the anesthetized domestic dog

The purpose of a comprehensive hemodynamic evaluation is to examine the effects of NCEs on factors relevant to cardiac office, such as pump-muscle function and electric action. As many cardiovascular parameters are involved in this evaluation, big animals, such equally the dog or pig, are preferred. An analysis of the furnishings of NCEs on the 20–25 cardiovascular parameters usually recorded or calculated provides a detailed documentation of potential cardiac run a risk such as systemic, pulmonary, renal hypo/hypertension, undesirable cardio-stimulation/depressant effects, and electric disorders.

Exam agents are typically administered intravenously for hemodynamic evaluations, including cess of the electrocardiogram in anesthetized animals Lacroix et al (1991). In a standard assay, the following measurements are taken:

□

Hateful, systolic and diastolic aortic blood force per unit area (AoBP, mmHg), by fashion of a catheter filled with isotonic saline introduced into the left femoral artery or into the right carotid artery up to the aortic curvation

□

Left ventricular pressure (LVP, mmHg), by way of a Millar micro-tip catheter force per unit area transducer introduced into the right carotid avenue or into the left femoral artery and advanced into the left ventricle

□

Left ventricular end diastolic claret pressure level (LVEDP, mmHg) from LVP recording

□

Cardiac output (CO, l/min) past fashion of a Swann-Ganz thermodilution catheter introduced into the right jugular vein and advanced into the pulmonary artery

□

Renal blood flow velocity (RBF, cm/south) past way of a pulsed Doppler claret menstruum meter operating with a flow probe placed around the correct renal avenue

□

Center charge per unit (HR, bpm) by mode of an electrocardiogram recording (standard lead Ii)

□

Pulmonary artery blood pressure level (PAP, mmHg) by way of the Swann-Ganz thermodilution catheter

□

Pulmonary capillary wedge force per unit area (PCWP, mmHg), by style of the Swann-Ganz thermodilution catheter following transient balloon inflation

The following results are calculated from the above measurements:

□

dP/dt max, the first derivative of LVP (mmHg/s)

□

Total peripheral resistance (TP Res, dynes/s x cm-5) = [fourscore x AoBP (mmHg)]/CO (fifty/min)

□

An index of arteriolar renal resistance (R Res) = AoBP (mmHg)/RBF (cm/s)

□

Stroke volume (SV, ml) = CO (ml/min)/Hour (bpm)

□

Systolic ejection time (Gear up, ms) = time between the onset of the AoBP wave and the dichrotic notch (which corresponds to the closing of the aortic valvula)

□

Isometric contraction fourth dimension (ICT, ms) = time interval between the onset of the LVP moving ridge and the AoBP wave

□

Hemodynamic coefficient = SET (ms)/ICT (ms)

□

TTI, the tension time index = Hour (bpm) ten AoBP (mmHg) x SET (ms)/k

□

Left cardiac work (LCW, kgm/min) = AoBP (mHg) x CO (l/min) x 13.vi x ane.055

□

PR interval (ms)

□

QT interval (ms)

□

Corrected QT interval (QTc, ms), according to Fridericia's formula = QT(ms)/3√(60/HR(bpm)]

Normocapnia is verified by measuring arterial blood gases (pO2, pCO2, mmHg) and pH.

Supplementary studies non function of the standard battery are more than complex, investigating NCEs in animal models designed to provide explanations for the hemodynamic effects observed in the core tests. While not mandatory, such studies are frequently essential, depending on the cardiovascular profile of the test substance.

As an example, an NCE, compound X, was evaluated on systemic and cardiac hemodynamics in anesthetized dogs with or without to bistellectomy and bivagotomy Lacroix et al (1976) to cancel the influence of the autonomic sympathetic and parasympathetic systems (Fig. ii). In the cadre battery exam (normal middle), the NCE induced dose-dependent hemodynamic effects, in particular peripheral arteriolar vasodilatation, decreasing arterial blood force per unit area and increasing center rate. While it seems probable the increased heart charge per unit was partly due to a reflex response to the decrease in blood pressure, it is likewise possible the NCE exerted a direct positive chronotropic effect. This issue was addressed by studying the response to the compound in the denervated preparation. Measurements were taken before and and then during a 30-min period afterward the commencement of a ten-min intravenous (i.v.) infusion of 0 (vehicle only, such as xl% w/v hydroxypropyl-beta-cyclodextrin in water for injection) (Fig. 2). While in the normal preparation the vehicle caused hypertension and an associated bradycardia, in the denervated preparation it caused hypertension only no change in eye rate. In contrast, in the normal preparation the test substance caused a dramatic increase in heart rate together with a decrease in arterial blood pressure, whereas in the denervated preparation it failed to increment heart rate. These results indicated the increment in eye rate caused by the test substance is due to an autonomic reflex in response to hypotension, and non to a straight upshot on heart.

Fig. two:. Hemodynamic evaluation: Effects of vehicle or substance X on mean aortic blood force per unit area and heart rate in heart innervated versus heart denervated anesthetized dog. n = half-dozen per group (cumulative doses). Means ± due south.e.m. (n = half-dozen).

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Drug Metabolism in Pregnancy

J.E. Moscovitz , ... L.M. Aleksunes , in Drug Metabolism in Diseases, 2017

Physiological Adaptations During Pregnancy

Throughout pregnancy, numerous maternal physiological and anatomical changes occur that alter the uterus and allow for the development of the placenta and fetus. These alterations include an increase in glomerular filtration rate, renal blood flow, and portal vein claret flow, which in plough impact pharmacokinetic determinants such equally plasma volume, oral absorption, and plasma protein binding among others. Additionally, changes in the expression and activity of maternal hepatic drug-metabolizing enzymes and transporters contribute to altered pharmacokinetics.

Hemodynamics, Hematology, and Hemodilution

A number of hemodynamic changes have been described in women during pregnancy. Using echocardiography, the cardiac output has been demonstrated to increase up to 60% in the second and third trimester when compared with nonpregnant women (Clark et al., 1989; Rubler et al., 1977). This enhanced cardiac output results from elevations in both stroke volume and heart rate. Subsequent analysis has revealed reductions in systemic and peripheral vascular resistance, pulmonary vascular resistance, and colloid oncotic pressure in women during pregnancy compared with the postpartum period (Clark et al., 1989).

Doppler ultrasonography has demonstrated that the portal venous blood period and total liver blood period are increased significantly in significant women after 28   weeks of gestation (Nakai et al., 2002). Past comparison, the hepatic arterial claret flow remains unchanged during pregnancy. Similar results have been determined past monitoring serial clearance of indocyanine dark-green at different time points in pregnancy (Robson et al., 1990). Although indocyanine green is a substrate of hepatic organic anion-type transporters (Chen et al., 2000), the extraction ratio of this dye (0.74) did not change across gestation, which supports its use as a liver blood catamenia probe. An alternative interpretation may involve potential adaptive regulation of transporters that balance physiological changes in claret catamenia.

The circulating blood supply increases steadily throughout pregnancy and approaches maximal increases (∼35–45%) by 30   weeks of gestation (Bader et al., 1955; Hytten and Paintin, 1963; Peck and Arias, 1979; Pritchard, 1965). Higher blood book results from both greater amounts of plasma and ruddy blood cells. The limerick of blood across pregnancy is too altered with a notable pass up in the concentration of plasma proteins such as albumin (Perucca and Crema, 1982). Equally a event of having less albumin in the circulation, the free fraction of drugs with narrow therapeutic indexes, such as valproic acid, phenytoin, and diazepam, can increment (Koerner et al., 1989; Riva et al., 1984).

Respiratory

At that place are a number of changes in respiratory anatomy and pulmonary office during pregnancy. Notably, meaning women oft complain of a stuffy nose that results from mucosal hypersecretion and edema due to elevated estradiol levels. Though the enlarged uterus pushes up on the diaphragm, breathing is not dumb. However, a number of changes in pulmonary function parameters have been noted during pregnancy. Throughout the 2d half of pregnancy, there is a progressive reject in expiratory reserve volume (up to 40%) and residual volume (up to 20%) without changes in total lung capacity, forced vital capacity, or tiptop menses rates (Baldwin et al., 1977; Elkus and Popovich, 1992). By contrast, tidal volume is enhanced from 450 to 700   mL equally a result of increased respiratory drive and rib muzzle volume deportation (Elkus and Popovich, 1992). In add-on, oxygen consumption at rest is enhanced by 30–40   mL/min in pregnant women (Pernoll et al., 1975).

Renal Blood Flow and Filtration

In response to pregnancy, renal blood flow and glomerular filtration charge per unit are increased by 30–50% (Davison and Dunlop, 1980; Dunlop, 1981). Both parameters begin to rising in the beginning trimester, superlative early in the 2nd trimester, and are sustained through the remainder of gestation. Studies have suggested that progesterone is natriuretic and thus, increases in this hormone throughout pregnancy may be responsible for the enhanced urine output (Barron and Lindheimer, 1984). Likewise, elevations in aldosterone during pregnancy take been proposed as a machinery for enhanced sodium reabsorption and prevention of excessive sodium filtration (Barron and Lindheimer, 1984).

Gastrointestinal Function

Pregnancy-related hormones, including progesterone, take been associated with a delay in gastric emptying and extended transit fourth dimension in the intestinal tract. As a result, the bioavailability of drugs tin exist contradistinct leading to shifts in the maximal concentrations and time to peak levels post-obit oral administration (Parry et al., 1970). For example, significant women at eight–12   weeks of gestation exhibit lower maximal concentrations of acetaminophen and greater times to maximum concentrations compared with nonpregnant controls (Levy et al., 1994). Too, nausea and vomiting during early and late pregnancy tin likewise alter drug assimilation in intestines.

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Brute Models for Cardiovascular Enquiry

Yous-Tang Shen , ... Richard P. Shannon , in Creature Models for the Study of Human Illness (Second Edition), 2017

2.1 Brief Coronary Avenue Occlusion-Induced Myocardial Stunning

Coronary artery spasm, myocardial revascularization, and coronary artery bypass grafting often produce a issue of a brief myocardial ischemia with a reversible, but prolonged, regional myocardial dysfunction for hours to days in patients. This clinical miracle has been termed as "myocardial stunning." The beginning postischemia induced myocardial dysfunction in conscious dog model was described by Heyndrickx et al. (1975). During the past three decades, myocardial stunning was extensively studied in different creature species, primarily dogs, pigs, rabbits, and nonhuman primates (Bolli and Marban, 1999; Shen and Vatner, 1996). Brief coronary artery occlusion and reperfusion can be achieved by transiently inflating and deflating a surgically-implanted hydraulic occluder around either the left circumflex or left anterior descending coronary avenue. The duration of coronary avenue occlusion should not be more than 15 min to avert irreversible myocardial injury. The regional myocardial dysfunction is closely correlated with the duration of coronary artery occlusion. Thus, the confirmation of consummate coronary artery occlusion and reperfusion is disquisitional for a reproducible consistent pattern of myocardial dysfunction within and among experiments when same ischemic protocol is utilized. Ideally, a coronary blood flow probe proximal to the occluder needs to be implanted for continuously monitoring of coronary blood menstruation during the entire experiment. The regional myocardial function in both potential ischemic zone and contralateral nonischemic zone, which is the cease point for myocardial stunning, can exist measured directly using a transit time dimension gauge technique (Shen and Vatner, 1996; Shen et al., 2008a). Concomitant continuous measurements of both coronary blood menstruation and regional myocardial office are essential for the study of myocardial stunning. Other physiological measurements should be as well considered which include arterial pressure, centre charge per unit, as well equally left ventricular (LV) pressure, and its first derivative (dP/dt). These parameters along with regional myocardial part and coronary blood flow provide a comprehensive contour for assessment of myocardial stunning. Fig. vi.1 illustrates the changes in continuous waveforms of LV pressure, LV dP/dt, wall thickness of posterior and anterior left ventricular walls, coronary blood flow, and heart charge per unit in a chronically instrumented conscious dog during brief coronary artery apoplexy.

Figure 6.1. Effects of cursory left circumflex coronary artery occlusion on systolic wall thickening in posterior ischemic and inductive nonischemic walls.

Note that wall thickening in the posterior wall was diminished during the coronary avenue occlusion which was confirmed by consummate loss of coronary blood flow (Shen et al., 1988).

The degree of myocardial stunning is characterized by both the level of regional myocardial dysfunction and the duration of myocardial function recovery. There are several factors to impact the degree of myocardial stunning, which can pb to increase variability or lack of reproducibility. First, incomplete coronary artery occlusion, even residual leak of coronary blood flow, can consequence in significantly less myocardial stunning every bit compared to a complete coronary artery occlusion. Usually, this can be easily detected from coronary claret flow and regional myocardial part in the ischemic zone. However, the change in regional part tin can also be induced by opening collateral channels, rather than incomplete coronary artery occlusion, particularly in dog species, where coronary precollateral channels are present.

Second, where regional myocardial office is measured within the ischemic area tin can produce marked variability of myocardial stunning in different animals. The closer the center of ischemic area the more severity of myocardial dysfunction is. When the location of myocardial function measured is shut to boarder zone, the myocardial stunning oftentimes cannot exist conspicuously detected. Thus, it is important to know the exact potential ischemic zone then find the center of ischemic zone for measurement of regional myocardial role before study is performed. This can be easily accomplished past a cursory coronary artery occlusion, that is, less than x s during the surgery, to induce a temporal color change of epimyocardium to outline of the ischemic zone. The dimension estimate should be placed every bit shut to cardinal ischemic zone as possible. A representative regional myocardial role recording in a chronically instrumented conscious domestic dog during control, left circumflex coronary artery occlusion, and later coronary artery reperfusion is shown in Fig. 6.two.

Figure 6.2. Phasic waveforms of left ventricular (LV) pressure, rate of change of LV pressure (dP/dt), and posterior and inductive wall thickness in a conscious dog subjected to 10 min of coronary artery occlusion (CAO) followed by iii h of coronary artery reperfusion.

Note at that place was no major effect on systolic wall thickening in nonischemic (anterior) zone, whereas systolic wall thickening in ischemic (posterior) wall zone reversed to wall thinning during CAO and was depressed at 3 h of CAR (Shen and Vatner, 1996).

Noninvasive techniques, such as echocardiograph, are more limited in sensitivity. It is too relatively difficult to repeatedly measure the regional myocardial function in the exact same location over the time, a limitation not present with the direct measurement via fixed, chronically implanted ultrasonic dimension gauge. Further, when longitudinal or repeated myocardial stunning information are compared in the same animal, the slight change in location of measurement via noninvasive techniques should be carefully considered.

Although myocardial stunning in the dog model has been studied extensively, one of the major concerns for this particular species is that myocardial stunning cannot be reproduced when the same experiment is performed several days later. Our previous report demonstrated that reductions in regional myocardial office, assessed by systolic wall thickening via surgically implanted dimension gauge, were significantly less in the 2nd and tertiary myocardial stunning experiments as compared to the 1st experiment (Shen and Vatner, 1996). Interestingly, the same repeated ischemic protocol studied in pigs does not evidence the "preconditioning-similar effects" as seen in the domestic dog model (Shen and Vatner, 1996). The effects of three separate x-min coronary artery occlusions, each 2 days apart, on systolic wall thickening in both ischemic and nonischemic zone in conscious dogs and pigs are shown in Figs. six.three and 6.4, respectively. Conspicuously, repeated myocardial stunning performed in dog model results in a nifty variability compared to that observed in pigs. Understanding the different characteristics of myocardial stunning in different species is of import for choosing a correct model to meet goals of different studies.

Figure vi.iii. Three divide x min of coronary artery occlusion (CAO) and reperfusion, performed ii days apart, in conscious dogs.

Annotation that following coronary artery reperfusion, depression of systolic wall thickening in the ischemic zone was more severe and prolonged afterwards 1st coronary occlusion than later on 2nd and third occlusions. *P < 0.05, 1st versus 2d and 3rd coronary occlusions (Shen and Vatner, 1996).

Figure 6.4. Three split up 10 min of coronary artery occlusion (CAO) and reperfusion, performed 2 days apart, in conscious pigs.

Note that following coronary artery reperfusion, low of systolic wall thickening in the ischemic zone was similar among iii separate performed coronary artery occlusion and reperfusion. (Shen and Vatner, 1996).

Myocardial stunning can too be performed in conscious or tranquilized nonhuman primate models, that is, monkey or baboon. The bones implanted transducers and experimental protocols are similar to those used in domestic dog or sus scrofa models. Since left ventricular wall thickness in nonhuman primates are often smaller than those seen in dogs and pigs, regional myocardial function normally is assessed using left ventricular segmental length, rather than wall thickness, via implanted ultrasonic dimension gauges in the remote, adjacent, and fundamental risk areas. Fig. vi.5 shows a schematic illustration for instrumentation and direct measurements for cardiac global and regional myocardial segmental length in a conscious monkey subjected to a brief coronary artery occlusion. A typical experimental ready up in conscious nonhuman primates is shown in Fig. six.vi.

Figure 6.5. During cursory coronary artery apoplexy (CAO), there was a consummate loss of regional segmental length in the central ischemic zone (C) during systolic phase, while remote nonischemic zone was reduced normally (A). The office in the next to ischemic zone (B) became nonsynchronous, every bit compared to the remote nonischemic zone (unpublished written report).

Effigy half-dozen.6. Illustration of experiment conducted in conscious monkey via a tether organization (unpublished written report).

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Technical Aspects of Hemodialysis

Bryan N. Becker , Gerald Schulman , in Therapy in Nephrology & Hypertension (Third Edition), 2008

THE HEMODIALYSIS Process

Blood Circuit

Blood in the extracorporeal circuit is contained within tubing that is connected to the venous and arterial sides of a patient's access (Fig. 77-i). Needles are inserted into the patient's claret access, and blood tubing is connected to the needle hubs. Claret is withdrawn from the arterial segment by the blood pump and pumped through the dialyzer dorsum to the patient via the venous segment of tubing. Inadvertent entry of air into the dialysis circuit, air embolism, is a potentially lethal complication and is virtually likely to occur between the vascular access site and the blood pump. Air tin enter the dialysis excursion from areas effectually the arterial needle, through leaky or broken tubing or tubing connections, and through the saline infusion fix. Air traps are located in the claret tubing to trap air and forestall it from entering the patient'south circulation. Air detectors are linked to a relay switch that automatically clamps the venous blood line and shuts off the blood pump if air is detected.

Blood pumps used for hemodialysis (HD) are roller pumps that utilize the principles of peristaltic pumping to move blood through tubing. A compressible function of the tubing (the pump segment) is occluded between rollers and a curved rigid runway. Elastic recoil refills the pump tubing afterward the roller has passed over it. The menstruum rate of the blood pump is dependent on the stroke volume, the speed of rotation of the rollers, and the volume of the pump segment. The blood period rate displayed on the dialysis automobile is based on these three parameters, rather than an bodily value from a blood period probe. This can lead to significantly higher values for the displayed blood flow compared to the truthful claret flow rate. Incomplete occlusion of the pump segment due to a pump maladjustment leads to a reduced book of claret with each pump rotation. This is a common crusade of overestimation of blood flow and hence clearance. Conscientious maintenance of the pump is essential to ensure that the prescribed dialysis dose is actually delivered to the patient.

Pressure monitors are usually located proximal to the blood pump and immediately distal to the dialyzer. The proximal monitor, the arterial monitor, guards against excessive suction on the vascular access site by the blood pump; the distal monitor, the venous monitor, gauges the resistance to blood return to the venous side of the vascular access. Some machines place the arterial monitor distal to the blood pump and proximal to the dialyzer to detect clotting in the dialyzer and more precisely guess pressure in the dialyzer blood compartment. To forestall blood clotting in the dialyzer, an anticoagulant such every bit heparin is oft infused into the circuit. A peristaltic pump or syringe pump delivers the anticoagulant into blood in the circuit via a T-tube or T-plumbing equipment ordinarily located betwixt the blood pump and the dialyzer.

A blood leak detector is unremarkably placed in the dialysis circuit in the dialysate outflow line. If a claret leak develops through the dialysis membrane, the blood leaking into the dialysate is sensed by the blood leak detector and the advisable alarm is activated.

Dialysis Solution Circuit

Ii backdrop of the dialysis solution that require constant monitoring are conductivity and temperature. A proportioning system dilutes a concentrated dialysis solution with water. If this system malfunctions, patient claret tin exist exposed to a hyperosmolar dialysis solution, resulting in hypernatremia, or a hypo-osmolar dialysis solution, leading to hyponatremia and hemolysis. The chief solutes in the dialysis solution are electrolytes. Therefore, the concentration of the dialysis solution is reflected by the concentration of electrolytes and their electrical electrical conductivity. Advisable proportioning of h2o and the dialysis solution is monitored past a meter measuring electrical conductivity of the dialysis solution fed into the dialyzer.

A temperature monitor prevents complications related to warm dialysis solution. In about situations, the dialysate temperature is higher than that of the patient, resulting in the transfer of thermal energy into the patient. The energy transfer may prevent a ascension in full peripheral resistance as fluid is removed by ultrafiltration (UF), resulting in hypotension during hemodialysis. A cool dialysis solution (i.e., 35°C) tin exist uncomfortable for the patient and may be unsafe when the patient is unconscious. Nevertheless, the use of cool dialysate otherwise may take therapeutic value in preventing hypotension. Overheated dialysis solution (>42°C), however, tin can lead to hemolysis. If the conductivity or the temperature is outside the normal range, a bypass valve diverts the dialysis solution around the dialyzer and straight to a drain.

On-line Monitoring

Dialysis machines part every bit more than just dialysis commitment systems. Built-in monitors appraise the physical characteristics of the dialysis solution, as noted to a higher place, and accrue data ranging from patient blood pressure and heart rate to treatment parameters, medication data, measures of delivered dialysis dose, plasma volume, thermal energy loss, and even dialysis access recirculation. Computerized medical information systems take been linked with dialysis delivery systems to provide data networks that can control treatments at individual patient stations while maintaining data and treatment records for future utilize. Some of these systems include the Smart Connection from Baxter Healthcare, RenalSoft, and a like system designed by Fresenius Medical Intendance. Real-time information regarding treatment parameters and patient data also tin can be visualized during dialysis treatments with the Cobe Centry Arrangement 3, the Althin Drake Willock System k, and the Fresenius 2008H organisation. It is now possible to integrate data, such as comparing present and past dialysis treatments, into a real-fourth dimension display to assistance approximate therapy, change prescription and ultrafiltration goals, and generate better firsthand assessment of a patient'southward and unit's overall status. one,ii Such on-line monitoring that allows sensors from the auto to change treatment parameters has been termed a biofeedback arrangement (Fig. 77-2). Automated biofeedback systems have the potential to reduce adverse events such equally hypotension, to monitor the land of the hemodialysis access, and to increment the efficiency of the hemodialysis treatment (Table 77-1).

Other monitoring systems have been developed and are used to monitor admission flow and office during dialysis and to make accurate determinations of circulating blood volume during the dialytic process. Single- and dual-sensor systems using saline injections and sound velocity dilution calibration accept been investigated as a method for accurately determining admission flow during hemodialysis. 3 Similar efforts take led to noninvasive optical hematocrit monitoring that continually measure hematocrit during dialysis to improve determine circulating claret volume. four As blood volume deceases, hematocrit increases. It is often possible to define a hematocrit to a higher place which hypotension is likely to occur in a patient. A critical hematocrit can be adamant with these devices in a higher place which hypotension can be reliably predicted in upwardly to 75% of patients. 5

The measurement of on-line claret book with these devices can place patients who are not almost their estimated dry weight. In eighteen% of hemodialysis patients, a less than v% decrease in claret volume was noted during routine hemodialysis sessions. In subsequent treatments, increased volume was successfully removed without hypotensive episodes. 6 The patients were able to have intradialytic fluid removal intentionally increased by 47% (boilerplate, 0.eight L). The alter in blood book can be determined noninvasively during hemodialysis with these devices. seven Thus, these devices provide an added on-line safe measure out to the handling.

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Biomedical Sensors

Yitzhak Mendelson PhD , in Introduction to Biomedical Technology (Third Edition), 2012

10.vi.eight Surface Plasmon Resonance Sensors

When monochromatic polarized low-cal (e.thou., from a light amplification by stimulated emission of radiation source) impinges on a transparent medium having a conducting metallized surface (e.g., Ag or Au), in that location is a accuse density oscillation at the interface. When light at an appropriate wavelength interacts with the dielectric-metallic interface at a divers bending, called the resonance bending, there is a match of resonance betwixt the energy of the photons and the electrons at the metal interface. Equally a result, the photon energy is transferred to the surface of the metallic equally packets of electrons, called plasmons, and the light reflection from the metallic layer volition be adulterate. This results in a miracle known as surface plasmon resonance (SPR) and is shown schematically in Figure ten.43. The resonance is observed equally a abrupt dip in the reflected light intensity when the incident bending is varied. The resonance angle depends on the incident wavelength, the type of metal, the polarization state of the incident lite, and the nature of the medium in contact with the surface. Any modify in the refractive alphabetize of the medium will produce a shift in the resonance angle and thus provide a highly sensitive ways of monitoring surface interactions.

Figure ten.43. Principle of a surface plasmon resonance (SPR) detection arrangement.

 Courtesy of Biacore AB, Uppsala, Sweden.

SPR is more often than not used for sensitive measurement of variations in the refractive index of the medium immediately surrounding the metallic picture show. For example, if an antibody is jump to or absorbed into the metal surface, a noticeable change in the resonance bending can exist readily observed because of the change of the refraction index at the surface if all other parameters are kept constant. The advantage of this concept is the improved ability to detect the direct interaction between antibody and antigen as an interfacial measurement.

10.7

Exercises

1.

Requite an example of a biomedical transducer that is used to monitor patients in the intensive care unit.

2.

Discuss the important considerations in the option of materials for packaging of an implantable biosensor.

3.

Judge the response time of an airflow transducer to monitor changes in breathing rate.

four.

Explain why low migrate is an important specification for implantable sensors.

5.

The scale tests of a new pressure transducer produced the readings in Table 10.4.

(a)

Plot the input-output calibration for this transducer.

(b)

Discover the offset for readings between 0 to 200   mmHg.

(c)

Detect the sensitivity for readings betwixt 0 to 200   mmHg.

(d)

Gauge the average sensitivity for readings ranging between 200 to 300   mmHg.

(e)

Country whether the response of this transducer over the unabridged measurement range is linear or nonlinear.

Table 10.4. Sample Calibration Data for a Pressure Sensor

Pressure (mmHg) Reading (μV)
xx   0
40   20
60   40
fourscore   threescore
100   eighty
120 100
140 120
160 135
180 150
200 165
220 180
240 190
260 200
280 210
300 220
320 225
340 230
360 235
380 237
400 239
420 240
440 240
6.

Suggest a method to measure hysteresis in a claret period transducer.

7.

Discuss the problem of using a pressure level transducer with hysteresis to monitor blood pressure level.

8.

Explain how the accurateness of a new temperature sensor can be determined.

9.

Two identical silver electrodes are placed in an electrolyte solution. Calculate the potential drib between the 2 electrodes.

ten.

Cadmium and zinc electrodes are placed in an electrolyte solution. Calculate the current that volition catamenia through the electrodes if the equivalent resistance of the solution is equal to 14   kΩ.

11.

Explain what will happen when the Ag/AgCl gel of an ECG electrode used to monitor a patient in the ICU dries out over time.

12.

By how much would the inductance of an inductive displacement transducer curlicue alter if the number of curl turns is decreased by a factor of vi?

13.

Determine the ratio betwixt the cross-sectional areas of two blood vessels assuming that the voltage ratio induced in identical magnetic menstruum probes is equal to 2:three and the ratio of blood flows through these vessels is 1:v.

14.

A 4.5   kΩ linear rotary transducer is used to measure out the angular displacement of the knee joint. Calculate the change in output voltage for a 165° modify in the bending of the human knee. Assume that a constant electric current of 14   mA is supplied to the transducer.

fifteen.

Provide a step-by-step derivation of Eq. (x.xi).

16.

An elastic resistive transducer with an initial resistance, R o, and length, l o, is stretched to a new length. Assuming that the cross-sectional area of the transducer changes during stretching, derive a mathematical relationship for the change in resistance ΔR as a part of the initial length, l o; the change in length, Δl; the book of the transducer, V; and the resistivity, ρ.

17.

The area of each plate in a differential capacitor sensor is equal to 5.6   cm2. Calculate the equilibrium capacitance in air for each capacitor assuming that the equilibrium displacement for each capacitor is equal to three   mm.

18.

Plot the capacitance (y-axis) versus displacement (ten-axis) characteristics of a capacitance transducer.

19.

Calculate the sensitivity of a capacitive transducer (i.due east., ΔC/Δd) for small changes in displacements.

20.

A capacitive transducer is used in a mattress to measure changes in breathing patterns of an babe. During inspiration and expiration, the rate of change (i.e., dV/dt) in voltage across the capacitor is equal to ±1V/s, and this modify tin be modeled past a triangular waveform. Plot the corresponding changes in electric current flow through this transducer.

21.

Derive the relationship for the current through the capacitor-equivalent piezoelectric crystal every bit a role of V and C.

22.

2 identical ultrasonic transducers are positioned across a blood vessel, as shown in Effigy 10.44. Calculate the bore of the blood vessel if it takes 380   ns for the ultrasonic sound moving ridge to propagate from one transducer to the other.

Figure ten.44. 2 identical ultrasonic transducers positioned across a blood vessel.
23.

Discuss the advantages of MEMS-blazon sensors.

24.

Calculate the resistance of a thermistor at 98°F assuming that the resistance of this thermistor at 12°C is equal to 7.0   kΩ and β = iv,600.

25.

The resistance of a thermistor with a β = 5,500 measured at 18°C is equal to 250 Ω. Find the temperature of the thermistor when the resistance is doubled.

26.

Calculate the β of a thermistor assuming that information technology has a resistance of four.4   kΩ at 21°C (room temperature) and a resistance of 2.85   kΩ when the room temperature increases by xx percent.

27.

A Chromel/Constantan thermocouple has the post-obit empirical coefficients:

C 0 = −ii.340 × x−two

C 1 = 4.221 × 10−two

C 2 = 3.284 × 10−5

Find the EMF generated by this thermocouple at a temperature of 250°C.

28.

Find the Seebeck coefficient for the Chromel/Alumel thermocouple at a temperature of 200°C.

29.

Explain why the temporal artery thermometer is not used to measure out core body temperature over the radial avenue.

30.

Compare and contrast the temporal artery and tympanic thermometers.

31.

Compare and contrast a temperature pill with a temporal artery thermometer.

32.

Sketch the electric current (y-axis) versus pOii (10-centrality) characteristics of a typical polarographic Clark electrode.

33.

Explain why the value of the normalized ratio (R) in a pulse oximeter is contained of the volume of arterial blood entering the tissue during systole.

34.

Explicate why the value of the normalized ratio (R) in a pulse oximeter is independent of skin pigmentation.

35.

Explain the departure between a potentiometric and amperometric sensor.

36.

Explain the deviation between intravascular fiber optic pO2 and SvO2 sensors.

37.

A pH electrode is attached to a sensitive voltmeter that reads 0.652 V when the electrode is immersed in a buffer solution with a pH of six.7. Afterward the pH electrode is moved to an unknown buffer solution, the reading of the voltmeter is decreased by xx percent. Summate the pH of the unknown buffer solution.

38.

Plot the optical density, OD, of an absorbing solution (y-axis) as a function of the concentration of this solution (10-axis). What is the gradient of this bend?

39.

An unknown sample solution whose concentration is 1.55 × ten−3 g/50 is placed in a i   cm clear holder and plant to have a transmittance of 44 percentage. The concentration of this sample is changed such that its transmittance has increased to 57 percent. Calculate the new concentration of the sample.

twoscore.

Calculate the angle of the refracted light ray if an incident light ray passing from air into water has a 75-degree angle with respect to the normal.

41.

Explain why cobweb optic sensors typically require simultaneous measurements using 2 wavelengths of calorie-free.

42.

Plot the fluorescence intensity of a fiber optic pOtwo sensor (y-centrality) as a function of oxygen concentration (x-axis).

43.

A chemical sensor is used to measure the pH of a dye with an absorbance spectrum shown in Effigy 10.45. Assume that the absorbance of each form of the dye is linearly related to its pH. Devise a method to mensurate the pH of the dye.

Figure ten.45. Optical absorbance spectra of a dye in its acrid (pH = 5.0) and base (pH = 8.0) forms.
44.

Explain the difference between absorption-based and fluorescence-based measurements.

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