Biomedical subjects

J V Tyberg

Publications and source records attributed to J V Tyberg.

At least 19 recordsLinked to original sources

PubMed1992

Inosine--a natural modulator of contractility and myocardial blood flow in the ischemic heart?

The energetic role of inosine (INO) remains controversial. The aim of the present study was first to test whether endogenous INO consumption/production correlates with regional myocardial contractile performance and second to test whether locally increased levels of INO influence contractility and blood flow in severely ischemic myocardium. Fentanyl-anesthetized dogs with implanted sonomicrometry crystals and independently perfused left anterior descending coronary arteries were studied. Two relatively load-independent indexes of regional myocardial contractility derived from left ventricular pressure-segment length loops were used: the regional stroke work-end-diastolic segment length relationship (Wr/L(ed)) and the end-systolic pressure-segment length relationship (Plv/L(es)). Very good correlations between myocardial contractile performance (as measured by the slope of the regional Wr/L(ed) relationship) and endogenous INO consumption/production under both nonischemic and ischemic conditions were found. Ischemia severely depressed contractility, significantly shifting rightward the Wr/L(ed) and Plv/L(es) relationships. INO infused into the left anterior descending bypass, in a concentration of 600 to 800 mumol/L, partially restored contractile performance as evidenced by a significant leftward displacement of both relationships. Wr, measured at a common maximum L(ed), increased significantly by 61 +/- 5%. Border-zone collateral flow (microspheres) increased by 35 +/- 7% within the endocardial segments and by 34 +/- 9% in the epicardial segments, but no increase in flow in the ischemic region was measureable. With the current emphasis on recanalization with thrombolytic therapy and considering the apparent safety of INO, this naturally occurring nucleoside might prove to be a useful adjunctive agent in the treatment of acute myocardial ischemia.

Animals↗

PubMed1992

The importance of pericardial constraint in experimental pulmonary embolism and volume loading.

To clarify the magnitude of the contribution of pericardial constraint to the hemodynamic deterioration that is observed during acute pulmonary embolism, hemodynamics and chamber dimensions (sonomicrometry) were measured during pulmonary embolization and subsequent volume loading in six anesthetized and instrumented open-chest, open-pericardium dogs. Embolization markedly increased peak right ventricular systolic pressure (38 +/- 5 mm Hg before embolism to 64 +/- 12 mm Hg after repeated embolization, p less than 0.05). However, right ventricular stroke volume decreased by only an insignificant amount (17 +/- 7 ml to 15 +/- 6 ml, p = not significant). Indices of left ventricular end-diastolic volume (left ventricular area = anteroposterior x septum-to-left ventricle free wall diameters) and stroke work (stroke work = area of the left ventricular pressure-area loop) were also similar before and after repeated embolization. Volume loading after repeated embolization resulted in increased right ventricular stroke volume (15 +/- 6 ml to 20 +/- 4 ml, p = 0.06), left ventricular area (3320 +/- 600 mm2 to 3470 +/- 580 mm2, p less than 0.05) and stroke work (261 +/- 158 mm Hg to 425 +/- 170 mm Hg x mm2, p less than 0.05). These results are in marked contrast to those in a previously reported study in a closed-chest and closed-pericardium model in which there was a decrease in left ventricular preload and systolic function after similar embolization-induced right ventricular pressure loading. Moreover, there was a further decrease in these parameters as a result of volume loading after embolism in the closed pericardium experiments. In conclusion, pericardial constraint contributes to hemodynamic deterioration during both acute right ventricular pressure loading and subsequent volume loading. The hemodynamic response to both interventions in the intact animal is determined not only by the degree of right ventricular dysfunction but also by the degree of direct ventricular interaction.

Animals↗

PubMed1992

Venous modulation of ventricular preload.

The objective of this discussion has been to describe a simple conceptual model of the circulation that emphasizes the role of the venous capacitance vasculature and is based on simplified vascular pressure-volume relationships. First, it is hoped that this approach will avoid some of the misunderstandings and contradictions that have resulted from an approach to the veins that is based on pressure-flow relationships. As mentioned at the outset, the confusion between venous volume and flow has led to the anomalous but logical conclusion that decreased venous pooling corresponds to increased venous return (which must equal cardiac output in the steady state). Second, it is also hoped that the model will prove to be a useful starting point from which to better understand how the veins modulate cardiac output in the normal individual and how alterations in venous capacitance affect the hemodynamic profile of congestive heart failure.

Arteries↗

PubMed1992

Effects of external constraint on the fetal left ventricular function curve.

To determine if external ventricular constraint significantly limits fetal left ventricular (LV) stroke volume and can thus account for the plateau of the fetal ventricular function curve, we studied nine fetal lambs (142 to 144 days' gestation) after partial delivery by cesarean section (halothane anesthetic). LV stroke volume (electromagnetic flow probe), LV end-diastolic pressure, and external ventricular constraint (intrapericardial pressure [liquid-filled balloon]) were measured over a range of end-diastolic pressures under two conditions: with a closed chest and closed pericardium and with an open chest and open pericardium. Stroke volume recorded during open chest and open pericardium exceeded those recorded during closed chest and closed pericardium at any given end-diastolic pressure (p less than 0.01). Decreases in external ventricular constraint significantly increased LV transmural pressure (preload) and substantially increased fetal LV stroke volume. Thus the plateau of the fetal ventricular function curve was largely a result of external ventricular constraint limiting LV preload, not necessarily a result of myocyte immaturity.

Animals↗

PubMed1992

The right and left ventricular intracavitary and transmural pressure-strain relationships.

The magnitude of pericardial pressure and therefore the shape of the right ventricular end-diastolic transmural pressure-volume relationship remains controversial. To investigate ventricular compliance, eight dogs anesthetized with fentanyl were instrumented as follows. Right and left ventricular intracavitary pressures were measured with micromanometer-tipped catheters. Right and left ventricular free wall segment lengths were measured by sonomicrometry. Pericardial pressure was measured over the right and left ventricles by means of flat liquid-containing balloon transducers, and transmural pressures were calculated as the difference between intracavitary and pericardial pressures. After defining the pressure-segment length relationship by vena caval constriction followed by release and blood transfusion, the pericardium and chest were opened widely and the cardiac volume manipulation was repeated; this allowed direct measurement of transmural right ventricular end-diastolic pressure for each level of strain recorded with the chest and pericardium closed. When intracavitary right or left ventricular end-diastolic pressure was raised from zero to 20 mm Hg, the respective transmural pressures increased from 0.2 +/- 0.6 (SD) mm Hg to 2.5 +/- 1.8 mm Hg and from 0.3 +/- 0.7 mm Hg to 6.0 +/- 2.5 mm Hg. Ventricular segmental strain increased by 7.0 +/- 0.8% and 6.0 +/- 0.2%, respectively. No statistically significant differences were found between right ventricular calculated (intracavitary minus pericardial pressure) and measured (open pericardium, open chest) transmural pressures at a given strain, thereby confirming the accuracy of our pericardial pressure measurements.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Changes in the radius of curvature of the ventricular septum at end diastole during pulmonary arterial and aortic constrictions in the dog.

BACKGROUND: At end diastole, the position and shape of the ventricular septum depend on the transseptal pressure gradient. It is not clear, however, how the septal radius of curvature changes in response to the gradual change in transseptal pressure gradient during progressive pulmonary arterial constriction (PAC) and aortic constriction (AC). METHODS AND RESULTS: In 11 anesthetized open-chest dogs, the septal radius of curvature was measured from the short-axis two-dimensional echocardiogram, and the transseptal pressure gradient (left ventricular [LV] pressure minus right ventricular [RV] pressure) was calculated from ventricular pressures measured with micromanometers. Seven dogs were studied with both PAC and AC (group 1) and four dogs only with PAC, which was initiated before and after volume loading (group 2). The transseptal pressure gradient decreased during PAC. As the transseptal pressure gradient decreased, the septum shifted continuously leftward with decreases in the LV septum-free wall diameter and in LV cross-sectional area. The septal radius of curvature (Rs) increased until the septum became flat. The flat septum (i.e., Rs = infinity) occurred at a relatively constant value of transseptal pressure gradient (-4.6 +/- 1.4 mm Hg) independently of the absolute values of LV pressures when between 2 and 9 mm Hg, although necessarily a greater RV pressure was needed to make the septum flat when LV pressure was higher. After inversion, the septum again became curved, with a decrease in the absolute value of septal radius of curvature as the transseptal pressure gradient became increasingly negative. The septum was still concave to the LV cavity at zero transseptal pressure gradient, and its curvature decreased (i.e., its radius of curvature increased) with increases in ventricular pressures. During AC, the septal radius of curvature also increased, but with an increase in transseptal pressure gradient accompanied by increases in LV septum-free wall diameter and in LV area. In group 2 animals, at zero transseptal pressure gradient, the normalized septal radius of curvature was greater (p less than 0.005) at high LV pressure than at low LV pressure. The transseptal pressure gradient required to make the septum flat was not significantly different between low and high LV pressure, which confirmed the results of group 1. CONCLUSIONS: The results of the present study show that the shape and position of the ventricular septum are determined by the transseptal pressure gradient but that the shape of the septum is also affected by the ventricular pressures. The septum was not flat but rather still concave to the LV cavity at zero transseptal pressure gradient. Approximately 5 mm Hg of negative transseptal pressure gradient was required to displace the septum farther leftward and make it flat. The septal radius of curvature increased during both PAC (which decreased transseptal pressure gradient) and AC (which increased transseptal pressure gradient), indicating that the mechanisms involved in changing septal radius of curvature are different during PAC and AC.

Animals↗

PubMed1992

Changes in pericardial pressure during the perinatal period.

BACKGROUND: To determine how the tissues that surround the heart affect diastolic and systolic function during the perinatal period, we studied the pressure-diameter relation of the left ventricle in partially delivered fetal lambs. METHODS AND RESULTS: We anesthetized (1.5-2.0% halothane, balance O2) and ventilated six pregnant ewes (142-144 days of gestation) and then partially delivered each lamb by cesarean section. Each lamb was instrumented to record left ventricular anteroposterior diameters (endocardial ultrasonic transducers), pericardial pressure (liquid-containing balloon), and left ventricular pressure (transducer-tipped catheter). Left ventricular pressure-diameter relations were recorded under three conditions: initially, with a closed chest and closed pericardium (before ventilation); second, after interruption of the umbilical circulation and 1 hour of ventilation; and finally, when the lungs and the pericardium were retracted from the heart. Pericardial pressure (recorded at a common diameter, i.e., the maximal end-diastolic diameter recorded before ventilation) decreased by 48% after 1 hour of ventilation (p < 0.05). After ventilation, left ventricular anteroposterior diameters were 4-5% greater (p < 0.05) at each end-diastolic pressure compared (12.5, 15.0, 17.5, and 20 mm Hg). Thus, ventilation appeared to increase left ventricular diastolic compliance. Contractility also appeared to increase after ventilation when evaluated using ventricular stroke work as a function of end-diastolic pressure as preload. When we used a more appropriate measure of preload (i.e., transmural end-diastolic pressure), ventilation did not change left ventricular diastolic compliance or contractility. Thus, left ventricular systolic function increased because of an increase in preload. CONCLUSIONS: The tissues surrounding the fetal heart significantly augment pericardial pressure and limit left ventricular preload. The initiation of ventilation reduces pericardial pressure, increases left ventricular preload, and increases left ventricular systolic function. At birth, a decrease in pericardial pressure and the resulting increase in preload may help increase left ventricular output through the Frank-Starling mechanism.

Animals↗

PubMed1991

The effect of nitroglycerin on pulmonary vascular capacitance in dogs.

In this study we investigated the hypothesis that the decrease in pulmonary vascular pressures observed after administration of nitroglycerin is in part due to a shift in the pulmonary vascular pressure-volume relationship. The experiments were done in six closed-chest dogs anesthetized with pentobarbital, in which pulmonary, cardiac, and intestinal relative blood volumes were determined by equilibrium blood pool scintigraphy. Nitroglycerin (30 micrograms/kg/min) caused 7% (p less than 0.02) and 12% (p less than 0.02) reductions in pulmonary and total cardiac blood volume, respectively, and a 7% (p less than 0.01) increase in intestinal blood volume. This shift of blood from the heart and the pulmonary circulation to the systemic (intestinal) circulation was accompanied by reductions in mean pulmonary artery pressure from 16 +/- 2 mm Hg to 12 +/- 1 mm Hg (p less than 0.01), in mean pulmonary capillary wedge pressure from 11 +/- 2 mm Hg to 6 +/- 1 mm Hg (p less than 0.01), and in mean portal pressure from 9 +/- 1 mm Hg to 8 +/- 1 mm Hg (p less than 0.01). The position of the pulmonary vascular pressure-blood volume relationship was unaffected by nitroglycerin, whereas the portal pressure-intestinal blood volume relationship was shifted to the left and upward. These changes suggest that pulmonary vascular tone remained unchanged, whereas intestinal vascular tone decreased during administration of nitroglycerin. In conclusion, nitroglycerin decreased pulmonary vascular pressures through a passive emptying of the pulmonary circulation as a result of increased systemic (intestinal) vascular capacitance.

Animals↗

PubMed1991

Left and right ventricular diastolic function during acute pericardial tamponade.

The aim of the study was to determine the effect of acute pericardial tamponade on left (LV) and right ventricular (RV) intracavitary and transmural pressure-volume (P-V) relations and to assess the effect of changing blood volume during tamponade on LV and RV volumes. The experiments were done in 11 acutely instrumented anaesthetized dogs in which LV and RV volumes were determined by computed tomography (CT) (n = 5) and LV and RV diameters by sonomicrometry (n = 6). Pressures were measured in the pericardium (balloon transducer), in the aorta and in the ventricles. Incremental pericardial infusion (up to 180 ml) caused a progressive left and upward shift of the LV and the RV intracavitary P-V relationship. This shift was entirely due to increased pericardial pressure (PP). The induction of tamponade caused no change in the LV and RV transmural P-V relationship. During tamponade with ventricular filling pressures above 10-15 mmHg, blood volume expansion caused only minimal increase in LV and RV volumes. In conclusion, pericardial tamponade shifted the LV and the RV intracavitary diastolic P-V relation by increasing PP. However, there was no change in the transmural P-V relationship, indicating unchanged myocardial compliance. Volume loading caused only minimal increase in LV and RV volumes during tamponade.

Animals↗

PubMed1991

Differences in distensibility between the anterior and posterior walls of the left ventricle in dogs.

Nonuniformity of myocardial systolic and diastolic performance in the normal left ventricle has been recognized by a number of investigators. Lack of homogeneity in diastolic properties might be caused by or related to differences in the distensibility of different regions of the left ventricular (LV) wall. Thus, we compared the end-diastolic transmural pressure-strain relations in both the anterior and posterior LV walls in seven anesthetized dogs during two interventions (pulmonary artery constriction and aortic constriction). Transmural pressure was defined as the difference between LV intracavitary pressure and local pericardial pressure. LV pressure was measured using a micromanometer; pericardial pressures over the LV anterior and posterior walls were measured with balloon transducers. Circumferentially oriented pairs of sonomicrometer crystals were implanted in the midwall of the anterior and posterior walls of the LV to measure segment lengths. Strains were calculated as (L-L0)/L0, where L was the instantaneous segment length and L0 was the segment length when transmural pressure was zero. The pattern of end-diastolic transmural pressure--strain relations was similar in all dogs. The change in strain in the posterior wall was always greater than that in the anterior wall. Opening the pericardium did not affect the difference in distensibility of the anterior and posterior walls. The results suggest that the posterior wall is more compliant than the anterior wall (that is, for a given difference in transmural pressure, the local segment length change of the posterior wall was greater). This seems consistent with other observations, which suggest that the posterior wall might make a greater contribution to diastolic filling.

Animals↗

PubMed1991

Experimental instrumentation and left ventricular pressure-strain relationship.

Pericardial pressure measurement with a balloon transducer requires opening and reapproximating the pericardium. If this instrumentation significantly compromises pericardial volume, the heart may be constrained, exaggerating the magnitude of pericardial pressure and thus altering the left ventricular end-diastolic pressure-volume relationship. In open-chest dogs, we studied the effects of opening the pericardium, inserting a pericardial balloon transducer and myocardial sonomicrometer crystals, and reapproximating the pericardium on the left ventricular end-diastolic pressure-strain relationship (LVEDPSR). After a thoracotomy, sonomicrometer crystals were inserted through small holes (less than 3 mm) in the pericardium to measure LV segment length. A micromanometer with a reference lumen was used to measure LV pressure. LVEDPSRs were recorded in the following situations: 1) before the pericardium was opened (but after the crystals were inserted); 2) after the pericardium was opened, the heart was instrumented (4 pairs of crystals and 1 balloon), and the pericardium was reapproximated with interrupted sutures; and 3) after the pericardium was removed. For each dog, a cubic regression equation was fitted to the data obtained before opening the pericardium, and the 95% confidence intervals for the individual data points were determined. In each case, the LVEDPSR obtained after instrumentation was similar to the LVEDPSR described before opening the pericardium. Furthermore, data obtained after instrumentation were uniformly located within the confidence intervals of the LVEDPSR obtained before opening the pericardium and instrumenting the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

The dependence of the time constant of left ventricular isovolumic relaxation (tau) on pericardial pressure.

The purpose of this study was to investigate the dependence of tau, the time constant of left ventricular (LV) isovolumic relaxation, on pericardial pressure and to compare values of tau as determined by the methods of previous investigators and by a standard exponential curve fit. All of the more recent methods involve an additional parameter--the pressure to which the exponential relaxation finally declines (PB, the pressure intercept in the method of Craig and Murgo and the asymptote in the exponential fits). An additional purpose of the study was to determine the relation of these parameters to pericardial pressure. In eight closed-chest anesthetized dogs, tau was calculated from intracavitary (Plv) and transmural LV pressure (Plv = Plv-Pper) by each method as pericardial (Pper) and LV end-diastolic pressure were changed by pericardial infusion and intravenous volume loading. The time constant determined by the method of Weiss et al was dependent on pericardial pressure; the time constants determined by the other methods were not. PB and the asymptotes were found to be similar and to increase almost equally with pericardial pressure. When pericardial pressure was zero, these values were approximately -20 mm Hg. Thus, both these parameters seem to indicate the same baseline pressure, a pressure that increases pari passu with pericardial pressure. Reported changes in the value of tau calculated from intracavitary LV pressure by the method of Weiss et al may reflect factors other than changes in LV diastolic function.

Animals↗

PubMed1990

Assessment of the splanchnic vascular capacity and capacitance using quantitative equilibrium blood-pool scintigraphy.

A series of human and animal experiments were carried out to assess the usefulness of equilibrium blood pool scintigraphy (EBPS) to study acute changes of the splanchnic vascular capacity and the splanchnic vascular pressure-volume (P-V) relationship. Corrected regional abdominal count rate changes, before and after various pharmacologic interventions, were used to assess regional splanchnic vascular volume changes. Animals were instrumented to manipulate and record splanchnic venous pressures. In patients, splanchnic vascular capacity increased by 5.2 +/- 6.9% (p less than 0.001) after 0.6 mg sublingual nitroglycerin while no significant change was noted after sugar pills (0.9 +/- 5.2%, p greater than 0.3). In dogs, splanchnic vascular capacity decreased by a mean of 16% during infusion of angiotensin (p less than 0.001) and increased by a mean of 32% during infusion of nitroprusside (p less than 0.001). The splanchnic vascular P-V curve was shifted rightwards during nitroglycerin administration. Thus, using the radionuclide technique we detected the expected qualitative and quantitative shifts in splanchnic capacity and capacitance. We conclude that EBPS is a useful method to assess acute changes of 1) the splanchnic vascular P-V relationship, in invasive animal studies, and 2) the splanchnic vascular capacity in noninvasive human and animal studies.

Adult↗

PubMed1990

Ventricular diastole and the role of the pericardium.

In order to understand the mechanics of left ventricular (LV) diastolic filling it has become important to understand the role of the pericardium. This is because it has been demonstrated that the LV pressure-volume relationship can be shifted by previously unrecognized changes in pericardial "pressure" and, therefore, LV end-diastolic pressure (LVEDP) may be ambiguous as a measure of preload. The key to this understanding is to appreciate that (except in the case of pericardial effusion or tamponade) the pericardium impedes cardiac filling by exerting a stress, not by raising the pressure in the pericardial fluid, and that the magnitude of this stress is variable and relatively great. When animals or humans are volume loaded acutely, this stress is approximately equal to right ventricular (RV) filling pressure. Thus, while it may not be possible to estimate true preload from simple measurements of LVEDP, subtracting RV filling pressure from LVEDP may provide a useful estimate of transmural LVEDP. As an example of the effect of the pericardium, recent laboratory results indicated that the decrease in stroke volume which resulted from acute pulmonary embolization could be explained by reductions in LV preload. Transmural LVEDP and end-diastolic volume decreased in spite of the fact that LVEDP rose markedly. Since LVEDP increased while stroke volume decreased, it might have been concluded that contractility had decreased. However, this was shown not to be the case, since the reduction in stroke volume only corresponded to the reductions in transmural LVEDP and end-diastolic volume. Thus, appropriately accounting for pericardial constraint may allow many changes in LV systolic performance, hitherto thought to represent changes in contractility, to be explained on the basis of preload changes and the Frank-Starling mechanism.

Diastole↗

PubMed1989

Pericardial pressure attenuates release of atriopeptin in volume-expanded dogs.

The role of the pericardium in the release of atriopeptin (AP) was examined, utilizing two separate protocols, in alpha-chloralose-anesthetized dogs. Protocol I consisted of an experimental group (9 dogs), in which the pericardium was incised to allow instrumentation and reapproximated, and a control group (6 dogs), in which the pericardium was left undisturbed. In the experimental group, mean right atrial pressure (Pra) was elevated from a control value of 1.8 +/- 0.9 mmHg (mean +/- SD) to 8.3 +/- 0.8 mmHg for 40 min by volume expansion with isoncotic, lactated Ringer solution. After this period of volume expansion, the pericardium was removed while holding Pra at 8 mmHg. During volume expansion, arterial blood samples for AP analysis were taken at 5, 10, 15, 20, 30, and 40 min, pre- and postpericardiectomy. A similar protocol was followed in the control group. At a Pra of 8 mmHg prepericardiectomy, the plasma AP concentration was 76 +/- 17 pM/l and 74 +/- 38 pM/l in the experimental and control groups, respectively. However, after pericardiectomy, AP levels increased significantly in both the experimental group (136 +/- 41 pM/l; P less than 0.001) and the control group (107 +/- 53 pM/l; P less than 0.025). In protocol II (6 dogs), the pericardium was removed before volume expansion, and Pra was elevated by 2- to 3-mmHg increments and maintained for periods of 13 min at each pressure. AP concentration did not increase until Pra reached 3-4 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Quantification of effect of pericardium on LV diastolic PV relation in dogs.

The aim of the present study was to quantify the effect of the pericardium on the left ventricular (LV) diastolic pressure-volume relation. The experiments were done in 10 anesthetized closed-chest dogs. Pericardial and cardiac volumes were determined by computed tomography. Pericardial effusion (n = 5) and volume loading (6% dextran iv; n = 5) were used to increase pericardial volume. Volumes were normalized as multiples of the LV volume measured when LV transmural pressure was 6 mmHg (VLV6). Using the data from the pericardial effusion experiments, we calculated the best-fit exponential equations for the pericardial pressure-volume relations. From these equations we calculated that the changes in pericardial volume necessary to shift the LV diastolic pressure-volume curve upward by 2, 5, 10, and 20 mmHg were 0.6 +/- 0.1, 1.1 +/- 0.2, 1.6 +/- 0.2, and 2.2 +/- 0.3 times VLV6, respectively. Using the data from the volume loading experiments, we also calculated the degree of upward shift of the LV pressure-volume relation caused by volume loading, which increased LV mean diastolic pressure by 12 mmHg. (The upward shift is that increment in pericardial pressure caused by the total increase in volume of the extra-LV contents of the pericardium, i.e., the atria, the right ventricle, and any pericardial effusion.) This volume loading increased the total volume of the right ventricle and the atria by 1.0 +/- 0.1 VLV6, which, in itself, increased pericardial pressure by 3.6 +/- 0.8 mmHg. We conclude that in situations in which heart or pericardial volume increases acutely, the pericardium shifts the diastolic pressure-volume relation of the LV upward by a significant amount.

Animals↗

PubMed1979

Reduction in ventricular endocardial and epicardial potentials during acute increments in left ventricular dimensions.

Unipolar potentials were recorded from the endocardium (Endo-Pot) and the epicardium (Epi-Pot) of the left and right ventricles of anesthetized open-chested dogs during acute changes in left ventricular dimension by blood transfusion. A pair of implanted ultrasonic crystals were used to detail changes in left ventricular (LV) anteroposterior diameter. When the diameter increased by an average of 11 per cent, LV Endo-Pot decreased by 28 per cent and LV Epi-Pot decreased by 15 per cent. Right ventricular Endo-Pot and Epi-Pot concurrently decreased by similar magnitude (-36 per cent). The relationship between potentials and LV diameter showed negative linearity over the ranges examined, and was not influenced by changes in hematocrit. No inverse relation between changes in Endo-Pot and Epi-Pot was observed. It is suggested that potentials when recorded directly from the endocardium or epicardium mainly reflect the electrical activity of the tissues in the immediate vicinity of the electrode. It is postulated that an increase in ventricular volume by producing stretching and thinning of ventricular walls, reduces the effective tissue mass represented in the electrode signal, thereby accounting for a reduction in both endo and epicardial potentials. Although the precise mechanisms of changes in ventricular potentials remains unclear, such changes, nevertheless, may indicate, in clinical circumstances, an acute shift in left ventricular volume.

Action Potentials↗

PubMed1979

Determination of frequency response from step response: application to fluid-filled catheters.

The performance of a fluid-filled catheter can be described by reporting its undamped natural frequency and damping ratio. These parameters can be measured by subjecting the catheter to sinusoidally varying pressures at a wide variety of frequencies to obtain the frequency response. They can also be computed from the response to a step change in pressure, which is often easier to produce. This paper derives the required equations and includes a graph which permits one to look up the undamped natural frequency after measuring the period and decay rate of the oscillation following a step change in pressure.

Cardiac Catheterization↗