Pressure-volume relationships in the right atrium were examined before and after the creation of acute exerimental tricuspid regurgitation in pigs. A 1.3 kHz multielectrode impedance catheter with a measuring current of 4 mA was used to determine instantaneous right atrial pressure and relative blood volume; right atrial dimension was assessed simultaneously with ultrasonic crystals attached to the atrial walls. Impedance volume waveforms and ultrasonic crystal dimensions closely paralleled each other at baseline and after the induction of tricuspid regurgitation. The normal right atrial pressure-volume plot exhibited a figure-of-eight configuration, with an "a-loop" and a "v-loop" corresponding to the a-wave and v-wave of the right atrial pressure tracing. With severe tricuspid regurgitation, atrial pump function was abolished, and the pressure-volume plot exhibited a single clockwise loop, consistent with complete ventricularization of the right atrium. Intermediate degrees of tricuspid regurgitation preserved the figure-of-eight loop, but the size of both the a-loop and the v-loop were increased, consistent with a Starling-type load imposed on the atrium by the regurgitant blood volume. Increased right ventricular afterload mediated by constriction of the pulmonary artery and infusion of methoxamine reversibly converted the right atrial pressure-volume loop from that of mild to that of severe tricuspid regurgitation. Alternatively, constriction of the inferior vena cava and infusion of nitroprusside changed the right atrial pressure-volume loop from that of a severe pattern of tricuspid regurgitation to a less severe type of pattern. Infusion of dobutamine increased the size of the a-loop relative to the v-loop both at baseline and after induction of tricuspid regurgitation. We conclude that tricuspid regurgitation induces changes in right atrial mechanics that can be detected and quantified with an impedance catheter. Circulation 73, No. 4, 799-808, 1986. TRICUSPID

SUMMARY. Myocardial ischemia due to increased oxygen demand (pacing tachycardia plus critical coronary stenoses) alters diastolic distensibility and relaxation more than ischemia of comparable duration due to coronary occlusion. To investigate the relationship between myocardial diastolic function and metabolism, we compared myocardial high energy phosphate content, tissue pH, and regional blood flow for these two types of ischemia in anesthetized open-chest dogs. Myocardial biopsies were done with a high-speed air-turbine biopsy drill, permitting rapid (<1-second) freezing of tissue samples from both nonischemic and ischemic areas, while myocardial pH was measured with a hydrogen ion-selective polymer membrane implanted in the subendocardium. After 3 minutes of pacing tachycardia in dogs with critical coronary stenoses (demand-type ischemia, n = 14), regional systolic function (% segment shortening by ultrasonic crystals) was mildly depressed (from 19 ± 2% control to 13 ± 2% post-pacing, P < 0.01), while left ventricular diastolic pressure-segment length relations shifted upward, indicating decreased distensibility of the ischemic myocardial segment. Associated with these changes in function, subendocardial adenosine triphosphate decreased (from 31.3 ± 1.5 to 27.9 ± 1.0 nmol/mg protein, P < 0.01), as did creatine phosphate (53.8 ± 2.1 to 39.6 ± 2.5 nmol/mg protein, P < 0.01), while myocardial pH declined slightly (ApH = -0.14 ± 0.02, P < 0.01). In contrast, at 3 minutes of coronary artery occlusion (primary ischemia, n = 14), regional segment shortening was replaced by systolic bulging (% shortening decreased from 17 ± 2% to -2 ± 1% during occlusion, P < 0.01), while left ventricular pressure-segment length relations were not shifted upward, and there was no decrease in diastolic distensibility of the ischemic segment. With coronary artery occlusion, subendocardial adenosine triphosphate declined slightly (33.2 ± 0.5 to 29.2 ± 2.0 nmol/mg, P < 0.05), while creatine phosphate decreased substantially (51.1 ± 2.3 to 7.8 ±1.4 nmol/mg protein, P < 0.01). Myocardial pH fell strikingly (ApH = -0.33 ± 0.03, P < 0.01), and the decline was 236% of that seen with demand-type ischemia. Regional myocardial blood flow (microsphere technique) showed a decreased endocardial:epicardial (endo:epi) ratio (1.04 ± 0.04 control vs. 0.40 ± 0.05 during pacing, P < 0.01) and absolute subendocardial flow (1.02 ± 0.47 to 0.47 ± 0.05 ml/min per g, P < 0.01) with demand-type ischemia. However, subendocardial blood flow in demand-type ischemia was still much greater than flow during coronary artery occlusion (0.10 ± 0.03 ml/min per g, P < 0.01). In summary, diastolic dysfunction was prominent during ischemia caused by increased oxygen demand, but was minimal during ischemia due to primary coronary flow reduction of equal duration. The diastolic dysfunction could not be explained simply by adenosine triphosphate depletion, which was modest and similar with both types of ischemia. Protection against diastolic dysfunction in primary ischemia m...

Hemodynamic measurements in human subjects and in experimental animals are generally made in the supine position; not much attention is paid to potential beneficial or harmful effects of right or left lateral positions on cardiac output or other hemodynamic variables. To evaluate the potential influence of such positional changes on cardiac performance, we measured cardiac output and left and right ventricular pressures (with micromanometer catheters) in anesthetized experimental animals (eight dogs and nine pigs) in the supine, right lateral, and left lateral positions. Cardiac output increased from supine to left lateral (mean SD, 2.6 +-0.9 to 3.1 ± 1.0 liters/min; p < .001) and from supine to right lateral positions (2.6 ± 0.9 to 3.1 ± 1.1 liters/min; p < .001). There was an associated decrease in arteriovenous oxygen saturation difference from supine to left lateral position (31 + 8% to 24 ± 4%; p < .001) and from supine to right lateral position (32 ± 9% to 25 ± 6%; p < .001). Left ventricular systolic and end-diastolic pressures increased from supine to left lateral (128 17/9 ± 2 to 147 19/16 ± 4 mm Hg; both p < .001) and from supine to right lateral positions (128 + 19/9 ± 2 to 141 16/16 ± 7 mm Hg; p < .01 and p < .001, respectively). Similarly, right ventricular systolic and end-diastolic pressures also increased from supine to left lateral (30 ± 7/3 + 2 to 38 + 7/8 ± 2 mm Hg; both p < .001) and from supine to right lateral positions (31 ± 8/3 + 2 to 43 + 8/11 + 4 mm Hg; both p < .001). Systolic and end-diastolic right ventricular pressures were significantly higher in the right lateral position than in the left (both p < .001). Heart rate did not change with positional maneuvers. Neither the sequence of positional changes nor the species of animal (dog vs pig) had any apparent influence on the results. Roentgenographic analysis of the differences in height of the right ventricle relative to the inferior vena cava suggests that changes in hydrostatic pressure may be entirely responsible for the increases in right ventricular end-diastolic pressure when animals are changed from the supine to the left or right lateral positions. We conclude that a change from supine to lateral position significantly increases intracardiac pressures and cardiac output in experimental animals. If confirmed in humans, these findings may have significant implications for the assessment of hemodynamic status of patients in intensive care unit and catheterization laboratory settings and for the treatment of patients in low-cardiac output states. Circulation 73, No. 3, 579-585, 1986. IN INTENSIVE CARE UNITS, catheterization laboratories, and animal research facilities, cardiac output is usually measured with the patient or animal in the supine position; not much attention is paid to potential From the Charles A.

Assessment of the complex relations between pressure and volume in the right atrium has been hampered in the past by difficulties in the measurement of atrial volume. Accordingly, in the present study the dynamics of right atrial pressure-volume relations were examined (with the use of an impedance catheter to measure right atrial volume) in patients with and without an atrial septal defect. Right atrial pressure and impedance volume were measured in 16 patients at the time of cardiac catheterization with the use of a multi-electrode impedance catheter to provide continuous, on-line, pressure-volume data. Eleven patients without evidence of an interatrial shunt were examined during normal respiration and during the Valsalva maneuver and contrasted with five patients with an atrial septal defect documented by oxygen saturation step-up and echocardiographic studies. Right atrial pressure-volume diagrams in patients without an atrial septal defect exhibited the normal figure eight pattern, with an A loop (atrial contraction) and a V loop (passive filling), corresponding to the A wave and V wave of right atrial pressure, respectively. During inspiration, mean right atrial pressure decreased and mean right atrial volume increased, consistent with augmented venous return. With the Valsalva maneuver, right atrial pressure increased and both right atrial stroke volume and mean right atrial volume decreased compared with baseline. Patients with an atrial septal defect demonstrated baseline pressure-volume diagrams similar to those of patients without an interatrial shunt. However, no change in mean right atrial volume occurred with either respiration or the Valsalva maneuver despite changes in right atrial pressure similar to those seen inpatients without an atrial septal defect.(ABSTRACT TRUNCATED AT 250 WORDS)

The end-systolic pressure-volume relation has been postulated as a load-independent measure of cardiac contractility, but has been difficult to measure because of technical problems associated with the serial measurement of intracardiac volume over a physiologic range of ventricular loading conditions. Utilizing a multielectrode impedance catheter to assess continuous, on-line left ventricular relative volume during transient inferior vena cava occlusion, a method is described for determining the end-systolic pressure-volume relation and for assessing changes in this relation secondary to inotropic modulation. In particular, using this method, the relative inotropic properties were determined of four drugs: dobutamine, milrinone, epinephrine and an experimental cardiotonic agent (Ro 13-6438, Posicor). Left ventricular micromanometer pressure and impedance catheter volume were measured continuously in 10 open chest, anesthetized dogs and 14 pigs. Arterial pressure was altered over a range of 20 to 60 mm Hg by brief inferior vena cava constriction. A linear end-systolic pressure-volume relation was observed in pressure-volume diagrams constructed from on-line pressure and impedance catheter recordings. Administration of dobutamine, milrinone and epinephrine resulted in a leftward shift and an increase in the slope of the end-systolic pressure-volume relation as compared with baseline; Posicor did not alter the slope over a range of doses, despite an increase in the cardiac output secondary to arterial vasodilation. Volume changes as measured by the impedance method closely paralleled simultaneous changes in the ultrasonic crystal-determined segment length, and the impedance end-systolic pressure-volume relation slope was reproducible with repeated load-altering maneuvers.(ABSTRACT TRUNCATED AT 250 WORDS)

Volume measurements obtained with an impedance catheter (impedance volume measurements) have been used previously in determining pressure-volume relationships in the right and left ventricles and in the right atrium. The purpose of the present study was to determine the utility of impedance volume techniques in the assessment of aortic pressure-volume relationships in animals and humans. Experiments to develop this methodology were first performed in ten anesthetized dogs, with simultaneous measurements of aortic pressure (micromanometer), diameter (ultrasonic crystals), and impedance volume. Transient (20 sec) inferior vena cava (IVC) occlusion and nitroprusside infusion resulted in a reproducible series of aortic pressure-volume and pressure-diameter points. In each case changes in impedance volume closely paralleled changes in diameter. From the wide range of pressure-volume points, it was possible to construct pressure-volume plots for a single cardiac cycle, as well as longer loops over a 20-40 mm Hg pressure range. End-systolic and end-diastolic pressure-volume points could subsequently be identified, which outlined a more precise pressure-volume relationship that was linear in six cases and curvilinear in four cases, depending on the level of aortic pressure. We extended these techniques to human subjects undergoing diagnostic cardiac catheterization. Studies using the impedance catheter in the aorta were performed in 11 patients. Aortic pressure-volume curves were elicited during Valsalva maneuver to obtain data over a range wider than that of a single cardiac cycle. Measurements of relative volume were calibrated with simultaneous M-mode echocardiography in three patients. We conclude that pressure-volume relationships in the aorta can be assessed with impedance volume techniques, making possible in vivo measurements of arterial compliance. Potential nonlinearities in aortic P-V relationships require that the assessment of aortic compliance encompass as much as possible of the physiologic range of pressure and volume.

Venous return determines cardiac preload and is in turn affected by respiration and vasodilation. The purpose of the present study was to examine the dynamics of venous return and venous volume, using impedance volume measurements in the venous system. In order to develop a methodology for the assessment of venous volume and venous return in man, we first studied 17 endotracheally intubated and ventilated anesthetized closed-chest dogs. We measured central venous and inferior vena cava (IVC) pressure (micromanometer) and volume (impedance catheter). Studies were done above and below the diaphragm with normal ventilation, with positive end-expiratory pressure (PEEP), and with beta-adrenergic blockade and i.v. nitroglycerin. Intrathoracic IVC volume fell and extrathoracic IVC volume rose with lung inflation, while PEEP raised extrathoracic IVC volume and lowered intrathoracic IVC volume. Nitroglycerin lowered intrathoracic IVC volume. Beta blockade did not affect IVC volume, ventilatory variation, or response to PEEP and nitroglycerin. We performed similar studies in 14 human subjects during normal quiet respiration, with measurements above and below the diaphragm, and with interventions including Valsalva maneuver and i.v. nitroglycerin. Intrathoracic IVC volume fell and extrathoracic IVC volume rose with expiration and Valsalva maneuver. Nitroglycerin again lowered intrathoracic IVC volume. We conclude that venous volume and the dynamics of venous return can be assessed in animals and man with an impedance catheter. Specifically, we show the divergent effects of respiration, ventilation, PEEP, and nitroglycerin on IVC volumes above and below the diaphragm. Beta-adrenergic blockage does not appear to play a role in altering any of these effects.(ABSTRACT TRUNCATED AT 250 WORDS)