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Stroke Volume Measurements

ICG is impedance plethysmography based upon the measurement of thoracic electrical bioimpedance. It may also include a component from the resistivity dependence on blood flow (Sigman effect). If so this is not a plethysmographic but a blood velocity component. Usually a measuring frequency of 50—100 kHz has been used. A thoracic electrical bioimpedance measurement picks up both cardiac and respiration signals. The ambition is that the SV [L] and therefore CO [L/min] can be calculated with ICG, as well as the total thoracic fluid volume, for example, according to Eq. 10.1 v = GpL.  [Pg.440]

Nyboer (1950) used two band electrodes around the neck, one band electrode corresponding to the apex of the heart, and a fourth band further in caudal direction. Nyboer regarded the thorax as a cylinder volume of length L and used the expression  [Pg.441]

SV as developed by Kubicek et al. (1966) is still compatible with a basic physical model [Pg.441]

The first time derivative dZ/dt is called the ICG. T is the ventricular ejection time. [Pg.441]

Because the pick-up electrodes are positioned near the heart, they also pick up the ECG signal this is used for the time estimation. [Pg.441]


Calibrate the detector tube pump for proper volume measurement at least quarterly. Simply connect the pump directly to the bubble meter with a detector mbe in-line. Use a detector mbe and pump from the same manufacturer. Wet the inside of the 100 cc bubble meter with soap solution. For volume calibration, experiment to get the soap bubble even with the zero ml mark of the buret. For piston-type pumps, pull the pump handle all the way out (full pump stroke) and note where the soap bubble stops for bellows-type pumps, compress the bellows fully for automatic pumps, program the pump to take a full pump stroke. [Pg.249]

Sorensen AG, Copen WA, 0stergaard L, Buonanno FS, Gonzalez RG, Rordorf G, Rosen BR, Schwamm LH, Weisskoff RM, Koroshetz WJ. Hyperacute stroke simultaneous measurement of relative cerebral blood volume, relative cerebral blood flow, and mean tissue transit time. Radiology 1999 210 519-527. [Pg.34]

Pulmonary artery catheter An invasive device used to measure hemodynamic parameters directly, including cardiac output and pulmonary artery occlusion pressure calculated parameters include stroke volume and systemic vascular resistance. [Pg.1575]

An effect on blood pressure was shown in the study by Clark and Litchfield (1969) in which subcutaneous injections of PGDN to anesthetized rats at 5, 10, 20, 40, 80, or 160 mg/kg resulted in a dose-related fall in mean arterial blood pressure (measured in the cannulized femoral artery) within 30 min with recovery over the next 12 h. The maximum drop in blood pressure correlated with the maximum concentration of PGDN in the blood. However, a drop in blood pressure did not occur in human volunteers who inhaled 0.5 ppm PGDN for 7.3 h. Rather, a mean elevation of diastolic blood pressure of 12 mm Hg was associated with severe and throbbing headaches (Stewart et al. 1974). A drop in blood pressure and decreasing stroke volume can result in brain ischemia, causing the dizziness and weakness reported by one subject after exposure at 0.5 ppm for 6 h in the Stewart et al. (1974) study as well as in occupationally exposed workers (Horvath et al. 1981). [Pg.111]

Endpoint. An indicator measured in a patient or biological sample to assess safety, efficacy, or another trial objective. Some endpoints are derived from primary endpoints (e.g., cardiac output is derived from stroke volume and heart rate). Synonyms include outcome, variable, parameter, marker, and measure. See surrogate endpoint in the text. Also defined as the final trial objective by some authors. [Pg.992]

Cardiac output, pulmonary artery pressure (PAP) and stroke volume are measured by a thermodilution technique using a Cardiac Output Computer (Gould/Statham SP 1245) and a balloon-tip triple lumen catheter (Gould SP 5105, 5F) with the thermistor positioned in the pulmonary artery via the jugular vein. [Pg.89]

Dofetilide has a small positive inotropic effect in animal hearts (15,33). In a double-blind, placebo-controlled study of oral dofetilide 125, 250, or 500 mg bd for the maintenance of sinus rhythm after cardioversion of sustained atrial fibrillation or flutter in 201 patients, there were small changes in echocardiographic measures of atrial contractility, but no changes in stroke volume or cardiac output (34). [Pg.1173]

RV function. Another technique to assess RV function is the measurements of isovolumic relaxation time (IVRT). Prolonged right ventricular IVRT in IPAH patients was found to be the strongest predictor of clinical status and survival (35). Another novel method of predicting outcomes in patients with IPAH is Doppler measurement of pulmonary vascular capacitance, which is calculated by utilization of the relationship between stroke volume and pulmonary pulse pressure. In multivariate analysis, echo-calculated pulmonary vascular capacitance correlated more strongly with outcomes than invasively measured mPAP, RA pressure, and pulmonary vascular resistance (PVR) (36). [Pg.148]

Figure 13-2. Ventricular function (Frank-Starling) curves. The abscissa can be any measure of preload—fiber length, filling pressure, pulmonary capillary wedge pressure, etc. The ordinate is a measure of useful external cardiac work—stroke volume, cardiac output, etc. In congestive heart failure, output is reduced at all fiber lengths and the heart expands because ejection fraction is decreased. As a result, the heart moves from point A to point B. Compensatory sympathetic discharge or effective treatment allows the heart to eject more blood, and the heart moves to point C on the middle curve. Figure 13-2. Ventricular function (Frank-Starling) curves. The abscissa can be any measure of preload—fiber length, filling pressure, pulmonary capillary wedge pressure, etc. The ordinate is a measure of useful external cardiac work—stroke volume, cardiac output, etc. In congestive heart failure, output is reduced at all fiber lengths and the heart expands because ejection fraction is decreased. As a result, the heart moves from point A to point B. Compensatory sympathetic discharge or effective treatment allows the heart to eject more blood, and the heart moves to point C on the middle curve.
Murphy, B.D., et al.. Identification of penumbra and infarct in acute ischemic stroke using computed tomography perfusion-derived blood flow and blood volume measurements. Stroke, 2006. 37(7) p. 1771-7. [Pg.119]

Thijs VN, Somford DM, Bammer R, Robberecht W, Moseley ME, Albers GW. Influence of arterial input function on hypoperfusion volumes measured with perfusion-weighted imaging. Stroke. 2004 35 94-98... [Pg.196]

Much of the criticism of the interpretation of Starling s original measured input-output relations was resolved by the introduction of a family of cardiac function curves [74], which accommodated neural and metabolic stimulation of the heart. Such influences manifest themselves in graphs of input (preload)-output (stroke volume, stroke work, etc.) as counter clockwise rotation (steeper) and stretch along the output (vertical) axis. Alteration in parameter c in Equation 18.1 and Equation 18.2 carries major responsibility for these modifications. In addition, it has recently been found that the cardiac function curve can be shifted along the horizontal (preload) axis [75]. This shift is effected by changes in air pressure, pe, external to the cardiac chambers, such as caused by the respiratory system, or by CPR, and modifies Equation 18.2 by approximation to... [Pg.298]

There are many direct and indirect (noninvasive) methods of measuring cardiac output. Of equal importance to the number that represents cardiac output is the left-ventricular ejection fraction (stroke volume divided by diastolic volume), which indicates the abUity of the left ventricle to pump blood. [Pg.209]

Holt [1] described the method of injecting an indicator into the left ventricular during diastole and measuring the stepwise decrease in aortic concentration with successive beats (Figure 13.5). From this concentration-time record, end-diastolic volume, stroke volume, and ejection fraction can be calculated. No assumption need be made about the geometric shape of the ventricle. The following describes the theory of this fundamental method. [Pg.217]

Martin RW, Bashein G (1989) Measurement of stroke volume with three-dimensional transesophageal ultrasonic scanning comparison with thermodilution measurement. Anesthesiology 70 470-476... [Pg.210]


See other pages where Stroke Volume Measurements is mentioned: [Pg.82]    [Pg.389]    [Pg.440]    [Pg.82]    [Pg.389]    [Pg.440]    [Pg.33]    [Pg.35]    [Pg.462]    [Pg.305]    [Pg.292]    [Pg.37]    [Pg.129]    [Pg.145]    [Pg.388]    [Pg.390]    [Pg.53]    [Pg.579]    [Pg.184]    [Pg.1621]    [Pg.221]    [Pg.148]    [Pg.58]    [Pg.194]    [Pg.195]    [Pg.44]    [Pg.343]    [Pg.433]    [Pg.146]    [Pg.207]   


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