Walter H. Pritchard

The Determination of Cardiac Output by the Dilution Method without Arterial Sampling I. Analytical Concepts

The selection of an external site for a radioisotope determination of cardiac output is discussed with respect to satisfying the analytical conditions of the Stewart-Hamilton dilution equation. Examples of both single-chamber and multichamber recording are illustrated, along with a discussion of the difficulties of curve calibration and extrapolation from multiple sites. The development of a method independent of critical placement or patient variability is described.

The Determination of Cardiac Output by the Dilution Method without Arterial Sampling II. Validation of Precordial Recording

Technics for determining the cardiac output by recording the dilution curve of injected iodinated I131 human serum albumin from precordial sites have been described. By viewing predominantly either the right or left side of the heart and by rapid delivery of the isotope, quantitation of the dilution curves for cardiac output has been possible without critical requirements for placement of the counter. In a series of 26 determinations in normal patients cardiac output values calculated from simultaneously recorded precordial curves and withdrawn arterial blood showed an average agreement within ± 8 per cent. In a smaller series of 8 determinations on patients in heart failure, an average deviation of ± 9 per cent was found.

Recording of Intracavity Potentials Through a Single Lumen, Saline Filled Cardiac Catheter

Summary A new technic is described to obtain intracavitary cardiac potentials through the single lumen saline filled cardiac catheter without use of the usual copper wire electrode. If the exploring terminal of an electrocardiograph is connected to the open arm end of a column of blood or saline in a catheter which has been introduced into the cavity of the heart, and if the indifferent electrode is connected to a central terminal, the completed curve will represent chiefly the fluctuations of intra-cardiac potential at the tip of the catheter.

The Determination of Cardiac Output by a Continuous Recording System Utilizing Iodinated (I131) Human Serum Albumin I. Animal Studies

A method is outlined for the determination of cardiac output by the injection of iodinated (I131) human serum albumin and continuous recording of the dilution curve. The calibration of the flow system by means of the final dilution and blood volume is discussed along with the possible application to an external measuring method. The results of eight dilution curves obtained from dogs are presented and the calculated cardiac outputs compared with the values measured by the rotameter method.

Correlation of renal blood flow determined by the single injection of Hippuran-I131 with direct measurements of flow☆

Abstract 1. 1. In 21 determinations in 11 dogs, the clearance values of I131-labeled Hippuran calculated from the time-concentration curve of arterial blood after a single injection were compared with flows measured simultaneously by collecting the total renal venous drainage from one kidney. 2. 2. The average agreement was 7.6 per cent in a range of flows from 94 to 340 ml. per minute and under conditions of altered blood and urine flow rates. 3. 3. The accuracy and simplicity of the method indicates its clinical usefulness in the area of renal blood flow studies. 4. 4. Classic clearance techniques utilizing Hippuran-I131 also gave excellent agreement with simultaneously measured flow, although renal A-V differences were large.

Vasopressor Material in Experimental Renal Hypertension

Transfer of blood from rats with acute renal hypertension to normal recipient rats demonstrated that a vasopressor substance was present in the circulation of the hypertensive animals. This is consistent with the view that a humoral mechanism plays a role in the origin of the hypertension. In contrast to the acute stage, no vasoactive material could be demonstrated in the blood after the second week of hypertension. Either the amount of pressor substance was too small to detect or none was being produced. In the latter case, chronic renal hypertension cannot be attributed to a humoral mechanism.

Measurement of Total Myocardial Blood Flow in Dogs with 43K and the Scintillation Camera

To establish an innocuous method for evaluating myocardial ischemia, a technique was devised utilizing a scintillation camera to record the distribution of 43K in the myocardium following an intravenous injection of the tracer. The objective was achieved by determining with the camera the fraction of the total amount of injected material deposited in the myocardium and calculating the total myocardial blood flow as a fraction of cardiac output according to the indicator fractionation principle. Following in vivo measurements in dogs, the entire heart was excised, compared with an aliquot of the injected dose as a standard, and assayed by a well scintillation counter. Reasonable agreement was achieved between estimations determined in vivo and those determined in vitro. Because of difficulties in ascertaining the heart border on the scans, a deconvolution program which used a digital computer was applied to the 40 × 40 matrix of digitized scan data to sharpen the transition between counting levels and improve the distributional image of 43K deposition in the myocardium.

Relation of Renal Arterial Pressure to Activity of Renin-Angiotensin System in Renal Hypertension.

Summary Unilateral renal hypertension was produced in rats by constricting the aorta just above the ostium of the left renal artery. This caused a sharp reduction in renal arterial pressure which usually remained below 80 mm Hg for 1 to 2 weeks. During this interval the renal vein blood contained a potent vasopres-sor agent and an elevated content of renin. By 2 weeks the left renal arterial pressure had returned to normal levels in most animals and this was associated with disappearance of the vasopressor agent from renal vein blood as well as a marked reduction in the output of renin. Not a single rat was encountered in which a low renal arterial pressure persisted indefinitely or in which the kidney continued to produce excess vasopressor material or to discharge an increased amount of renin. These findings indicate that(1) in unilateral renal hypertension the renal arterial pressure probably governs the release of renin by the kidney and that(2) low renal arterial pressure and hence increased activity of the renin-angiotensin system are limited to the early or acute stage of renal hypertension.

I131-labeled serum albumin: its use in the study of cardiac output and peripheral vascular flow.

During the past several years a method for measuring plasma volumes has been under investigation in our laboratory (1, 2). This method involved the use of a tagged serum protein (I131-tagged albumin) and gave promising results which appeared useful. It became obvious that the slow rate of disappearance of tagged albumin from the blood would make this a satisfactory substance for the study of vascular flow measurements. Before this could be achieved, however, it was necessary to develop a number of instruments which would make it possible to detect small amounts of radioactivity by their gamma emission and to record the events rapidly enough so that critical alterations in dilution and mixing of the radioactive albumin could be recorded. The essence of the method which will be described concerns itself with measuring and recording the manner and rate in which iodinated plasma is mixed and diffused through the blood. The character of the curve which is obtained on isolated arteries has proved suitable for q...

Role of a Pressor Substance in Unilateral Renal Hypertension.

Summary Unilateral renal hypertension was produced by constricting the aorta of the rat between the ostia of the main renal arteries. The acute stage of hypertension probably depended on a renal humoral mechanism since during the first 2 or 3 weeks of the hypertensive state, blood from the renal vein of the ischemic left kidney contained a potent vasoconstrictor substance, probably angiotensin, which was also present in arterial blood but not in renal vein blood from the untouched right kidney. After 3 weeks the left kidney ceased to release a pressor agent and in addition no such agent was demonstrable in the general circulation by bioassay. Hence the chronic stage of unilateral renal hypertension could not be attributed to the direct vasoconstructive effect of a humoral pressor agent.