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Biomedical subjects

F R Badke

Publications and source records attributed to F R Badke.

17 recordsLinked to original sources
PubMed1985

Left ventricular geometry during positive end-expiratory pressure in dogs.

We evaluated changes in left ventricular (LV) geometry in ten dogs during intermittent positive-pressure ventilation (IPPV) with and without 10 cm H2O of positive end-expiratory pressure (PEEP). The dimensions during expiration and inspiration decreased in all three orthogonal axes during PEEP, consistent with decreased LV end-diastolic (ED) and end-systolic (ES) volumes. Within a respiratory cycle, the anterior-posterior (AP) ED dimension during inspiration increased with IPPV alone but decreased when PEEP was added, consistent with presumed differences in pulmonary venous return. This caused opposite changes in AP percent regional shortening. Septal-lateral free wall (SL) percent regional shortening decreased during inspiration with both IPPV and PEEP, but the respiratory variation was significantly less during PEEP. Thus, PEEP did not simply produce a smaller version of the same events seen during IPPV alone. The larger decreases with PEEP observed in ED compared to ES dimensions in the AP and SL axes suggest a dominant regional preload effect, whereas the larger fall in the long axis ES compared to ED dimension suggests a primary regional decrease in afterload. Measurements of the right ventricular SL axis in three dogs showed an overall reduction with PEEP, with the inspiratory dimensions being minimal during both IPPV alone and with PEEP. Thus, ventricular interdependence cannot account for the diminished LV SL dimension with PEEP during any part of the respiratory cycle. These findings suggest that the motion of the LV free wall influenced by changes in lung volume may be at least as important as septal motion in determining LV geometry with PEEP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Validation of attenuation-corrected equilibrium radionuclide angiographic determinations of right ventricular volume: comparison with cast-validated biplane cineventriculography.

To determine the accuracy of attenuation-corrected equilibrium radionuclide angiographic determinations of right ventricular volumes, we initially studied 14 postmortem human right ventricular casts by water displacement and biplane cineventriculography. Biplane cineventriculographic right ventricular cast volumes, calculated by a modification of Simpson's rule algorithm, correlated well with right ventricular cast volumes measured by water displacement (r = .97, y = 8 + 0.88x, SEE = 6 ml). Moreover, the mean volumes obtained by both methods were no different (73 +/- 28 vs 73 +/- 25 ml). Subsequently, we studied 16 patients by both biplane cineventriculography and equilibrium radionuclide angiography. The uncorrected radionuclide right ventricular volumes were calculated by normalizing background corrected end-diastolic and end-systolic counts from hand-drawn regions of interest obtained by phase analysis for cardiac cycles processed, frame rate, and blood sample counts. Attenuation correction was performed by a simple geometric method. The attenuation-corrected radionuclide right ventricular end-diastolic volumes correlated with the cineventriculographic end-diastolic volumes (r = .91, y = 3 + 0.92x, SEE = 27 ml). Similarly, the attenuation-corrected radionuclide right ventricular end-systolic volumes correlated with the cineventriculographic end-systolic volumes (r = .93, y = - 1 + 0.91x, SEE = 16 ml). Also, the mean attenuation-corrected radionuclide end-diastolic and end-systolic volumes were no different than the average cineventriculographic end-diastolic and end-systolic volumes (160 +/- 61 and 83 +/- 44 vs 170 +/- 61 and 86 +/- 43 ml, respectively). Comparison of the uncorrected and attenuation-corrected radionuclide right ventricular volumes demonstrated narrower 95% confidence intervals for the attentuation-corrected right ventricular volume determinations over a wide range of cineventriculographic volumes. Thus we conclude that: (1) attenuation-corrected radionuclide right ventricular end-diastolic and end-systolic volumes compare closely with those obtained by a cast-validated biplane cineventriculographic method and (2) attenuation-corrected radionuclide right ventricular volumes correspond more closely to determinations of biplane cineventriculographic right ventricular volumes and are thus likely to be more accurate than uncorrected radionuclide right ventricular volumes.

Adolescent↗
PubMed1984

Left ventricular dimensions and function during exercise in dogs with chronic right ventricular pressure overload.

Left ventricular (LV) dimensions and shortening at rest and during treadmill exercise were examined before and after 4 weeks of pulmonary artery (PA) constriction in 6 conscious dogs. The dogs were preinstrumented with LV and right ventricular (RV) catheters, an LV micromanometer, a PA inflatable cuff occluder and ultrasonic crystals to measure an LV anteroposterior, a septal-lateral, an apex-base and a free wall segment chord. With PA constriction, RV pressures increased from 49 +/- 4/2 +/- 1 mm Hg (systolic/end-diastolic) to 104 +/- 5/2 +/- 1 at rest and from 71 +/- 9/2 +/- 1 to 133 +/- 8/14 +/- 2 at peak exercise (mean +/- standard error of the mean). Heart rate, LV pressure and LV dP/dt were similar before and after RV pressure overload at rest and with exercise. During exercise at control, systolic shortening increased significantly in all chords. With chronic PA constriction at rest, shortening of all chords also remained normal despite decreases in end-diastolic dimensions, which were most marked in the septal-lateral chord (23% decrease, p less than 0.01). However, during exercise in the presence of RV pressure overload, septal-lateral shortening decreased 46% (p less than 0.01) despite increases in systolic shortening in the other chords similar to the control response. Therefore, although LV function at rest in chronic RV pressure overload is normal, exercise may induce regional abnormalities of LV contraction that appear to be mediated by a reduced contribution of the ventricular septum to LV ejection.

Animals↗
PubMed1984

Effect of right ventricular pressure on the end-diastolic left ventricular pressure-volume relationship before and after chronic right ventricular pressure overload in dogs without pericardia.

We studied the effect of chronic right ventricular pressure overload on diastolic ventricular interdependence in dogs without pericardia, instrumented to measure left ventricular pressure, right ventricular pressure, and 3 left ventricular dimensions. We studied 12 dogs before (control) and nine dogs after 6 weeks of pulmonary artery constriction producing systolic right ventricular pressure greater than or equal to 70 mm Hg. Compared to control, following pulmonary artery band there was greater (P less than 0.01) interventricular septal mass (53 +/- 15 vs. 35 +/- 7 mg, mean +/- SD), thickness (15 +/- 2 vs. 10 +/- 1 mm), and ratio of the surface area of the interventricular septal to total left ventricular surface area (0.38 +/- 0.03 vs. 0.33 +/- 0.02), but unchanged left ventricular free wall mass (81 +/- 12 vs. 84 +/- 14 mg) and thickness (11 +/- 2 vs. 11 +/- 2 mm). End-diastolic right and left ventricular pressures and left ventricular volume were varied by vena cava and pulmonary artery occlusions and releases. Volume was calculated as an ellipsoid and the data in each dog fit to: left ventricular pressure = a0 + a1V + a2V2 + a3V3 + a4V4 + bPRV, r greater than or equal to 0.91 in each dog. During control, b was similar, whether calculated from both pulmonary artery and vena cava occlusions (0.47 +/- 0.09) or from vena cava occlusions alone (0.43 +/- 0.11), and was greater than the ratio of the interventricular septal surface area to left ventricular surface area (0.33 +/- 0.02, P less than 0.05). Following the pulmonary artery band, b decreased to 0.21 +/- 0.10 (P less than 0.05) and was less than the ratio of interventricular septal surface area to the left ventricular surface area which increased to 0.38 +/- 0.03 (P less than 0.05). We conclude that the effect of alterations in right ventricular pressure on the end-diastolic left ventricular pressure volume relationship, independent of the pericardium, is reduced following the pulmonary artery band that produces interventricular septal hypertrophy. These results are consistent with the hypothesis that the effect of alterations of right ventricular pressure on the diastolic left ventricular pressure-volume relationship depends on the relative elastance of the interventricular septum and left ventricular free wall, and not simply on the ratio of the interventricular septal surface area to the left ventricular surface area.

Animals↗
PubMed1984

Evaluation of left ventricular contractile performance utilizing end-systolic pressure-volume relationships in conscious dogs.

The relationship between left ventricular end-systolic pressure and volume has been proposed as a model of left ventricular contraction which may be useful for quantifying inotropic state independent of preload and afterload. Although the model has been well-validated in isolated hearts, systematic evaluation in conscious animals with an intact peripheral circulation has been limited. Accordingly, we derived end-systolic pressure-volume relationships in twelve conscious dogs, chronically instrumented to measure left ventricular pressure and dimensions from endocardial ultrasonic crystals in three orthogonal axes. We examined the linearity of the end-systolic pressure-volume relationship, its response to alterations of inotropic state and the peripheral circulation, and the influence of beta-adrenergic reflexes. End-systolic pressure-volume relationships were constructed by linear regression of end-systolic pressure-volume coordinates produced by transient inferior vena caval occlusions during atrial pacing. The relations were highly linear; of 127 inferior vena caval occlusions, the correlation coefficient was 0.96 +/- 0.05 (mean +/- SD). The slope of the end-systolic pressure-volume relationship was not significantly altered either by a moderate resistive afterload induced by angiotensin II infusion, or by a moderate increase in preload produced by dextran, but was increased from 4.7 +/- 2.3 to 6.5 +/- 2.2 mm Hg/ml (P less than 0.05) in response to the positive inotropic stimulus of dobutamine. The volume intercept at zero end-systolic pressure was unaffected by dextran or dobutamine, but was decreased from 12 +/- 8 to 5 +/- 11 ml (P less than 0.01) by angiotensin II infusion, indicating a leftward shift of the end-systolic pressure-volume relationship.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1983

Effect of the undisturbed pericardium on left ventricular size and performance during acute volume loading.

Studies in instrumental dogs have suggested that the pericardium alters left ventricular diastolic pressure-volume relations and thus may influence systolic performance. However, the instrumentation used in these studies disrupts the pericardium and may have influenced the results. We therefore studied five conscious dogs by methods not traumatic to the pericardium, before and after pericardiectomy. Although heart rate and left ventricular systolic and end-diastolic pressures were not different before or after pericardiectomy, either at rest or during volume loading, end-diastolic volume measured by biplane two-dimensional echocardiography increased post pericardiectomy at rest from 38 +/- 4 (SE) to 61 +/- 4 ml (p less than 0.05) and during volume loading from 68 +/- 5 to 79 +/- 5 ml (p less than 0.005). After pericardiectomy, ejection fraction was unchanged, but the peak value of the first derivative of left ventricular systolic pressure (dP/dt) increased significantly at rest from 17 +/- 2 to 26 +/- 4.0 x 10(2) mm Hg/sec. We conclude that pericardiectomy shifts the left ventricular end-diastolic pressure-volume curve to the right and increases the systolic isovolumic index of dP/dt in the basal state.

Animals↗
PubMed1983

Regional left ventricular performance during normal and obstructed spontaneous respiration.

To clarify the effects of respiration on left ventricular (LV) dimensions and shortening, we studied chronically instrumented dogs with endocardial sonomicrometer crystals in the anterior-posterior (AP), septal to lateral (SL), and long axes (LA) following pericardiectomy. Ten anesthetized dogs were examined during spontaneous unobstructed respiration, partial inspiratory obstruction (PIO), and Mueller maneuvers (MM). During unobstructed inspiration, end-diastolic dimensions (EDD) demonstrated a significant increase in the AP and a similar decrease in the SL axis (i.e., noncongruent shape changes). During PIO only the SL EDD diminished significantly, while no significant changes occurred in any EDD during MM. Individual dogs also demonstrated noncongruent shape changes at end systole during inspiration. However, the end-systolic dimensions for the entire group demonstrated a significant increase in one dimension during each inspiratory mode with no significant changes in the other two axes suggesting an increased ventricular volume. Regional shortening declined only in the SL axis during both unobstructed respiration and PIO. Spontaneous sighs with large tidal volumes, yet smaller changes in pleural pressure than during the MM, were associated with marked noncongruent shape changes in both diastole and systole. We conclude that 1) estimates of LV volumes during respiration based on only one or two axes and assuming regional congruent shape changes may be misleading; and 2) lung volume changes can affect LV geometry independently of changes in pleural pressure.

Airway Obstruction↗
PubMed1983

Differential effects of diltiazem and nitroprusside on left ventricular function in experimental chronic volume overload.

To compare the hemodynamic effects of a calcium-channel blocker with those of a conventional vasodilator in the awake preinstrumented dog, diltiazem and nitroprusside were administered in equihypotensive infusions before (decrease in mean aortic pressure by 10%; p less than .001, n = 6) and after (decrease in mean aortic pressure by 12%; p less than .001) chronic volume overload (CVO) produced by an infrarenal aortocaval fistula. Diltiazem had no effect on preload either before or after CVO. The maximal rate of change in left ventricular pressure (dP/dtmax) was unaffected by diltiazem before the aortocaval fistula (decrease in dP/dtmax by 6%; p = NS) but was significantly reduced by calcium-channel blockade after CVO (decrease in dP/dtmax by 22%; p less than .001). By contrast, at matched aortic pressures nitroprusside significantly reduced left ventricular end-diastolic dimension (LVEDD) and pressure (LVEDP) in the same animals before (decrease in LVEDD by 10%, p less than .05; decrease in LVEDP by 7 +/- 2 mm Hg, p less than .001) and after CVO (decrease in LVEDD by 7%, p less than .05; decrease in LVEDP by 5 +/- 2 mm Hg, p less than .001) without altering dP/dtmax. We conclude that the calcium entry blocker diltiazem, unlike conventional vasodilators, may depress left ventricular function in CVO by direct negative inotropic properties in amounts that are without myocardial depressant effects in the presence of normal left ventricular performance.

Animals↗
PubMed1982

Comparative hemodynamic effects of digoxin vs nitroprusside in conscious dogs with aortocaval fistula-induced chronic left ventricular volume overload and normal systolic performance.

We compared the effects of IV digoxin (0.04 mg/kg) and nitroprusside (NP) (1.2 and 1.8 microgram/kg/min) on left ventricular (LV) performance in six preinstrumented conscious dogs with 3 and 6 hours after digoxin administration (serum level, 3.5 +/- 0.6 ng/ml), there were no changes in heart rate, LV systolic (LVSP) and end-diastolic (LVEDP) pressures, LV dimensions, LV dP/dtmax, or percent minor diameter shortening as compared to control values in the resting state, after beta blockade, or during phenylephrine infusion. By contrast, NP produced a significant reduction (p less than 0.05) in LVEDP (16 +/- 3 to 10 +/- 3 mm Hg) at the smaller dose which caused no change in mean aortic pressure. The larger dose of NP further reduced LVEDP and evoked significant (p less than 0.05) decreases in LVSP (124 +/- 5 to 117 +/- 7 mm Hg), mean aortic pressure (85 +/- 3 to 78 +/- 5 mm Hg), and LV end-diastolic dimension (LVEDD) (53.0 +/- 5.5 to 52.0 +/- 5.7 mm), while augmenting LV dp/dtmax (3288 +/- 266 to 3647 +/- 130 mm Hg/sec). Beta blockade with IV propranolol (2.0 mg/kg) prevented the rise in LV dP/dtmax after high-dose NP administration but did not alter the reductions in mean aortic pressure, LVEDP, and LVEDD. This study indicates that NP, but not digitalis, has a favorable effect on LV hemodynamics in the volume-overloaded heart with normal LV systolic contraction and high-output CHF resulting from increased blood volume and reduced LV diastolic compliance. At least part of the apparent improvement in LV performance observed with high-dose NP is sympathetically mediated since it can be attenuated by beta blockade.

Adrenergic beta-Antagonists↗
PubMed1982

Left ventricular dimensions and function during right ventricular pressure overload.

The effects of right ventricular (RV) pressure overload on left ventricular (LV) function is controversial. Therefore, we examined LV dimensions and shortening after acute and chronic pulmonary artery (PA) constriction in six conscious dogs, preinstrumented with LV and RV catheters, an LV micromanometer, a PA inflatable cuff occluder, and ultrasonic crystals to measure an LV anteroposterior, a septal-lateral, and a free wall segment chord. Studies were performed before, immediately after, and 2, 4, and 6 wk after PA constriction. With acute cuff inflation, RV systolic- and end-diastolic pressures rose, but LV end-diastolic pressure fell. Both septal-lateral end-diastolic length and systolic shortening declined 4.1 +/- 0.7 mm and 5.9 +/- 2.3% respectively (P less than 0.01), whereas the anteroposterior and segment chords were unaffected. With chronic RV pressure overload septal-lateral shortening but not end-diastolic length returned to control levels. Also the first derivative of LV pressure (LV dP/dt) fell 540 +/- 164 mmHg/s by 6 wk compared with control, but this decline was reversed by volume expansion with dextran. We conclude that RV pressure overload displaces the septum toward the LV free wall; acutely this displacement is primarily at end diastole, but chronically it occurs at end systole as well, maintaining the septal contribution to LV ejection. Thus chronic RV pressure overload is associated with significant changes in LV diastolic shape but maintenance of normal LV function.

Animals↗
PubMed1981

Differential effects of systemic and intracoronary calcium channel blocking agents on global and regional left ventricular function in conscious dogs.

We examined the differential effects of intravenous (IV) equimolar doses of diltiazem (D), verapamil (V), and nifedipine (N) upon left ventricular (LV) function in 12 healthy unsedated dogs. We also attempted to isolate direct myocardial effects of these agents from reflex and peripheral effects by using intracoronary (IC) equimolar drug administration in an additional six animals. Despite equivalent dose-related increases in heart rate and declines in arterial pressure intravenous V (0.04, 0.1, 0.17 mg/kg) and N (0.3 mg/kg) but not D (0.04, 0.1, 0.17 mg/kg) depressed LV function. Peak effects after high dose V included increased heart rate (HR) (68%) and reduced mean aortic pressure (MAP) (17%), dP/dt max (22%), and percent shortening of the LV minor diameter (% delta D) (33%) (all p less than or equal to 0.001). By contrast, equimolar D increased HR (68%) and decreased MAP (20%) but produced no change in dP/dt or % delta D while low dose N (0.03 mg/kg) depressed dP/dt and % delta D by 37% and 45%, respectively (both p less than or equal to 0.001) despite similar changes in HR and MAP. Pretreatment with propranolol (2 mg/kg) and matching HR and loading conditions to control failed to uncover myocardial depression after D. Equimolar IC D, V (4, 8, 16 micrograms/kg), or N (3 micrograms/kg) each produced dose-related reductions in percent regional shortening which were greatest with N (58% at 3 micrograms/kg) and least with D (9% at 16 micrograms/kg). These data suggest that calcium channel blockers vary in their propensity to reduce LV function and that the myocardial depressant effects of these agents are partially offset by reflex and peripheral vascular actions.

Animals↗
PubMed1981

Effects of experimental volume-overload hypertrophy on myocardial blood flow and cardiac function.

To examine the effects of volume-overload hypertrophy on regional myocardial perfusion, we determined myocardial blood flows with microspheres at rest, during exercise, and during exercise with adenosine infusion in dogs with aortocaval fistulas for 12 wk (group 2) and sham-operated controls (group 1). A subgroup of six animals (group 3) was studied both before and after shunt closure in order to separate the influences of hypertrophy from the hemodynamic effects of the fistula. Epicardial blood flows in animals with patent fistulas were significantly greater than in controls under all conditions (P less than 0.05). However, endocardial blood flows were lower at maximal exercise and with adenosine, so that the endocardial-to-epicardial blood flow ratios were reduced 36 and 28%, respectively(P less than 0.05). These flow abnormalities were reversed by closing the fistula prior to regression of hypertrophy. Moreover, coronary resistance per unit of myocardium was not different for the three groups. These results suggest that the blood-flow abnormalities seen in the exercising dog with an aortocaval fistula are secondary to hemodynamic considerations and not to hypertrophy itself. Low aortic diastolic pressures and high myocardial oxygen demands during exercise may combine to produce subendocardial hypoperfusion in this model.

Animals↗
PubMed1981

Hemodynamic effects of n-acetylprocainamide compared with procainamide in conscious dogs.

We examined the hemodynamic actions of clinically relevant i.v. doses (20 mg/kg and 10 mg/kg) of n-acetyl procainamide (NAPA) in conscious dogs preinstrumented with a left ventricular (LV) micromanometer, LV and aortic catheters, and ultrasonic crystals for measurement of LV internal diameter shortening (% delta D). Within 30 seconds after the 20-mg/kg dose, there were significant increases in heart rate (27 +/- 7 beats/min, mean +/- SEM; n = 6), maximum dP/dt (655 +/- 206 mm Hg/sec), and % delta D (2.2 +/- 0.9%; all p less than or equal to 0.05). However, by 6 hours after the dose there were reductions compared with control in peak LV pressure (19 +/- 9 mm Hg), dP/dt (610 +/- 210 mm Hg/sec), and % delta D (2.3 +/- 0.6%; all p less than or equal to 0.05). In contrast, equimolar doses of procainamide or drug vehicle alone evoked no response, as did NAPA after pretreatment with reserpine (0.25 mg/kg/day for 2 days) or hexamethonium (10-15 mg/kg). These data suggest NAPA produces a biphasic hemodynamic response with enhancement of LV performance early and a decrease later; this response is different from that of the parent compound, procainamide. These effects are likely mediated by the adrenergic nervous system at either a ganglionic or a central level.

Acecainide↗
PubMed1980

Effects of ventricular pacing on regional left ventricular performance in the dog.

Changes in regional left ventricular (LV) performance induced by ventricular pacing were studied in two groups of open-chest anesthetized dogs. In the first group of five dogs, local function at the LV anterior base, anterior apex, and posterior apex was assessed by ultrasonic crystal pairs with atrial, right ventricular, LV apical, and LV base pacing. Ventricular pacing produced asynchrony of contraction and marked changes in the shortening pattern at each site, as well as an average 27% reduction in peak systolic pressure and peak dP/dt compared to atrial pacing. Moreover, the extent of shortening during LV ejection was reduced or unchanged at all sites measured during ventricular pacing. In the second group of five dogs, function of the septum and opposing LV lateral wall was studied with atrial and LV lateral wall pacing. Lateral function was assessed with a crystal pair and septal function by cineradiography of a lead bead implanted in the septum. Ventricular pacing produced reciprocal interaction between the two walls, with early lateral shortening inducing septal bulging and late septal shortening inducing lateral wall systolic lengthening. We conclude that ventricular pacing produces significant changes in regional myocardial function, likely induced by reciprocal interaction of opposing myocardial regions. Furthermore, such interaction appears deleterious to global ventricular function, presumably because volume is sequestered and pressure is dissipated into relatively inactive segments that are out of phase with the bulk of contracting myocardium.

Animals↗