Hemodynamic responses of the acutely stressed neonatal right ventricle: a maturational study in lambs

Right ventricular Starling responses to acute volume infusion in newborn lambs were compared to those in older groups of lambs. When peak stroke volume/kg was reached during infusion, right ventricular end-diastolic pressures for the newborn group were significantly lower (p less than 0.001) than those obtained for older groups, in spite of significantly higher resting and peak stroke volumes in the two younger groups. Newborn lambs developed tricuspid regurgitation and right-to-left foraminal shunting, demonstrated by echocardiography, at a mean end-diastolic pressure of 7.5 mm Hg. No right-to-left shunting was noted in older lambs. This study demonstrated a blunted Starling response in the newborn lamb's right ventricle. The response to volume loading improved with maturation, but was still less than that reported for the left ventricle. Clinical implications regarding right ventricular immaturity and inadequate response to altered hemodynamic situations are raised.     

Optimal right ventricular filling pressures and the role of pericardial constraint in right ventricular infarction in dogs.

BACKGROUND. Previous studies have reported an important role for right ventricular function in the pathophysiology of the low cardiac output state that can accompany right ventricular infarction. Some studies have suggested that right ventricular distensibility impairs right ventricular filling and stroke output; others have demonstrated that the pericardium can mediate depressed left ventricular filling and stroke output. METHODS AND RESULTS. To determine the role of pericardial constraint and optimal volume loading in an experimental model of right ventricular wall infarction, six mongrel dogs were studied before and after right ventricular wall infarction and after volume loading. The pericardium was then opened in two phases. In the first phase, the pericardium was opened partially to allow the atria to distend freely, and in the second phase, the pericardium was opened completely. The animals were preinstrumented with two sets of piezoelectric crystals attached to the right ventricular free wall, one in the infarct and the other in the noninfarct territory. Left ventricular size was estimated by left ventricular crystals on the anterior wall of the left ventricle. Right ventricular and left ventricular Millar catheters were used to assess intracavitary pressure, and a flat balloon was used to assess intrapericardial pressure. Right ventricular infarction reduced cardiac output by 23% and stroke volume by 30%. End-diastolic segment length and transmural pressure of the left ventricle decreased. Volume loading restored cardiac output to baseline values and was mediated by a significant increase in end-diastolic length in the noninfarct territory. This was achieved by increasing right ventricular end-diastolic pressure from 9 +/- 2 to 16 +/- 3 mm Hg (p less than 0.01). Partial opening of the pericardium mediated significant increases in both end-diastolic segment lengths of the left ventricle and the noninfarct territory. Left ventricular end-diastolic pressure decreased slightly by 3 mm Hg (p = NS). Complete opening of the pericardium increased cardiac output and stroke volume and mediated a significant decrease in right and left ventricular end-diastolic pressures. Left ventricular transmural pressure and end-diastolic segment lengths of the left ventricle and the noninfarct territory increased. Left ventricular diastolic pressure-segment length relations were shifted upward by right ventricular infarction. A partial opening of the pericardium shifted this relation downward in all animals, and complete opening of the pericardium shifted the relation rightward and further downward. CONCLUSIONS. Cardiac output is restored to baseline values by volume loading sufficient to increase the right ventricular diastolic pressure to 16 +/- 3 mm Hg. Evidence of pericardial constraint was observed and appears to be mediated by an atrioventricular interaction in addition to the direct ventricular interaction.     

Left ventricular performance and contractility before and after volume infusion: a comparative study of preterm and full-term newborn lambs

We studied left ventricular performance and contractility after volume loading in lambs at 122 days (group I, n = 9) and 139 days gestational age (group II, n = 9) and in 8-day-old full-term lambs (group III, n = 7). All were mechanically ventilated; each preterm lamb was treated with surfactant to stabilize pulmonary function and the ductus arteriosus was occluded with an inflated catheter balloon. Cineangiograms, left ventricular and vascular pressures, and the isovolumetric index of contractility, first derivative of left ventricular pressure (dP/dt), were recorded before and after three successive whole blood volume infusions of 10 ml/kg (total 30 ml/kg). The left ventricular end-diastolic volume per kilogram and stroke volume per kilogram increased significantly in all groups after volume infusion; these measurements and heart rate and systemic vascular resistance did not differ significantly between the groups either before or after the infusions. The left ventricular peak dP/dt did not change significantly within the groups during the volume infusions. The left ventricular stroke work was greatest in full-term animals and increased significantly in all groups after volume infusion. Thus, the left ventricles of the preterm and full-term lambs had quantitatively similar Frank-Starling responses and there was no increase in contractility during the infusions of whole blood. However, the left ventricle of the full-term lamb is capable of generating greater stroke work than that of the preterm lamb. These findings may contribute to the understanding of development aspects of postnatal circulatory adaptation.     

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.     

Radionuclide analysis of right and left ventricular response to exercise in patients with atrial and ventricular septal defects

In patients with ventricular or atrial septal defect, the ventricle which is chronically volume overloaded might not appropriately respond to increased demand for an augmentation in output and thereby might limit total cardiac function. In this study we simultaneously measured right and left ventricular response to exercise in 10 normal individuals, 10 patients with ventricular septal defect (VSD), and 10 patients with atrial septal defect (ASD). The normal subjects increased both right and left ventricular ejection fraction, end-diastolic volume, and stroke volume to achieve a higher cardiac output during exercise. Patients with VSD failed to increase right ventricular ejection fraction, but increased right ventricular end-diastolic volume and stroke volume. Left ventricular end-diastolic volume did not increase in these patients but ejection fraction, stroke volume, and forward left ventricular output achieved during exercise were comparable to the response observed in healthy subjects. In the patients with ASD, no rest-to-exercise change occurred in either right ventricular ejection fraction, end-diastolic volume, or stroke volume. In addition, left ventricular end-diastolic volume failed to increase, and despite an increase in ejection fraction, left ventricular stroke volume remained unchanged from rest to exercise. Therefore, cardiac output was augmented only by the heart rate increase in these patients. Right ventricular function appeared to be the major determinant of total cardiac output during exercise in patients with cardiac septal defects and left-to-right shunt.     

Effect of acutely increased right ventricular afterload on work output from the left ventricle in conscious dogs. Systolic ventricular interaction

In seven conscious, chronically instrumented dogs, left ventricular volume was calculated with an ellipsoidal model from the anteroposterior, septal-free wall, and base-to-apex left ventricular dimensions, measured by implanted ultrasonic transducers. Matched micromanometers measured left and right ventricular transmural and transseptal pressures. Ventricular pressures and volumes were varied by inflation of implanted vena caval and pulmonary arterial occluders. When compared with vena caval occlusion at matched left ventricular end-diastolic volumes, graded pulmonary arterial occlusions were associated with higher right ventricular systolic pressures, reduced left-to-right transseptal systolic pressure gradients, and leftward systolic septal displacement, with increased septal-free wall segment shortening (all p less than 0.05). Graded pulmonary arterial occlusions, like vena caval occlusions, reduced left ventricular end-diastolic volume, but left ventricular stroke work at a given end-diastolic volume was greater during pulmonary arterial occlusions (2,674 +/- 380 10(-3) erg) than during vena caval occlusion (1,886 +/- 450 10(-3) erg, p less than 0.05). These data indicate that, while transient pulmonary arterial occlusion reduces left ventricular preload, the concomitant increase in right ventricular systolic pressure, which is the pressure external to the interventricular septal segment of the left ventricle, augments septal shortening and assists left ventricular pump function at a given preload through direct systolic ventricular interaction.     

Dimensional changes of the left ventricle during acute pulmonary arterial hypertension in dogs

Left ventricular dimensions and volumes were measured by an endocardial marker technique in eight closed chest dogs during progressive increases of 10 mm Hg in mean pulmonary arterial pressure. Right ventricular volumes were measured by biplane cineanglography.

Increasing mean pulmonary arterial pressure caused a progressive increase in right ventricular volume; at a mean pulmonary arterial pressure of 60 mm Hg, right ventricular end-diastolic volume increased by 48 percent and end-systolic volume by 50 percent. Left ventricular volumes began to decrease significantly at a mean pulmonary arterial pressure of 30 mm Hg, and when a mean pulmonary arterial pressure of 60 mm Hg was reached, left ventricular end-diastolic volume had decreased by 30 percent and left ventricular end-systolic volume by 19 percent. Changes in ventricular filling pressure dlrectionally followed the volume changes of the respective ventricle. Left ventricular stroke volume decreased 45 percent at a mean pulmonary arterial pressure of 60 mm Hg but increasing heart rate prevented a decrease in cardiac output.

The decrease in left ventricular volume as pulmonary arterial pressure was Increased was associated with a disproportionate reduction in the left ventricular septal-lateral axis. At end-diastole, this dimension decreased by 22 percent at a mean pulmonary arterial pressure of 60 mm Hg, the anterior-posterior axis decreased by 8 percent and the base-apex axis by 4 percent. A similar disproportionate decrease of the septal-lateral axis occurred at end-systole. Even at the modest increase in mean pulmonary arterial pressure to 20 mm Hg, only the septal-lateral dimension was significantly shortened, and the right ventricular end-diastolic volume had increased by 17 percent but left ventricular end-diastolic volume was not significantly changed. Thus, during acute pulmonary hypertension, the right ventricle progressively dilates resulting in a distinctive change in the shape of the left ventricle that suggests septal buiging and that may impair left ventricular function.     

Influence of chronic captopril therapy on the infarcted left ventricle of the rat

To determine whether the relationship between infarct size and ventricular performance, volume, and compliance could be altered favorably, captopril was administered to rats for 3 months following coronary artery ligation. Baseline left and right ventricular and systemic arterial pressures and aortic blood flow, and maximal stroke volume and cardiac indices attained during a volume loading, were measured. Passive pressure-volume relations of the left ventricle were determined, and the slopes of segments of this relation were analyzed to characterize ventricular chamber stiffness. In untreated rats, left ventricular end-diastolic pressure progressively rose (from 5-28 mm Hg) as a function of infarct size, whereas, in captopril-treated rats, filling pressure remained within normal limits (5 +/- 1 mm Hg) in all but those with extensive infarcts. Chronic captopril therapy reduced baseline mean arterial pressure and total peripheral resistance, yet maintained cardiac and stroke outputs in rats both with and without infarcts. In untreated rats, maximal pumping ability progressively declined with increasing infarct size, whereas, in captopril-treated rats, peak stroke volume index remained within normal limits in all but those with extensive infarcts. The in vitro left ventricular volumes of captopril-treated rats were significantly less than those of untreated rats. The maintenance of forward output from a lesser dilated left ventricle yielded an index of ejection fraction for treated rats with moderate and large infarcts that was significantly elevated compared with that of untreated rats with infarcts of comparable size. Left ventricular chamber stiffness, which fell as infarct size increased in untreated rats, was normalized by chronic captopril therapy. Thus, captopril attenuated the left ventricular remodeling (dilation) and deterioration in performance that were observed in rats with chronic myocardial infarction.     

Atrial natriuretic peptide in a rat model of cardiac failure. Atrial and ventricular mRNA, atrial content, plasma levels, and effect of volume loading

This study examined the relation between synthesis, atrial storage, and plasma levels of atrial natriuretic peptide (ANP), and it examined plasma ANP levels and hemodynamic output in response to volume expansion in a rat model of myocardial infarction and failure. Arterial ANP concentrations did not correlate linearly with infarct size, but they did show an abrupt increase when infarct size exceeded 30% of the left ventricle, similar to the abrupt increase of left ventricular end-diastolic pressure with infarct size greater than 30%. Consequently, a close relation was found between plasma ANP levels and left ventricular end-diastolic pressure (n = 23, r = 0.89, p less than 0.001). Atrial ANP content per gram of tissue but not ANP content per pair of atria was reduced in rats with large infarcts (greater than 40%, p less than 0.05 vs. control animals). ANP mRNA level per pair of atria (related to total atrial RNA), determined by liquid hybridization (controlled by northern blot analysis), was increased by 38% in infarcted rats (p less than 0.05 vs. controls), but the ratio of atrial ANP mRNA relative to atrial beta-actin mRNA levels was not increased. Right and left ventricular ANP mRNA level increased by 90% and 380%, respectively, far exceeding the concomitant increase in beta-actin mRNA (+26% in the left ventricle). Plasma ANP increased with volume loading in controls and rats with moderate infarcts but not in rats with large infarcts despite a similar increase in right atrial pressure (compared with control animals); thus, the relation of delta ANP/delta right atrial pressure exerted by volume loading decreased in rats with large infarcts. Similarly, the response of cardiac output and renal blood flow (determined by radioactive microspheres) to volume loading was attenuated in rats with large infarcts. Thus, in this model of chronic cardiac failure, the activation of the ANP system is closely coupled with the increase in intracardiac pressures without correlating linearly to the extent of myocardial loss. Second, in severe cardiac failure, additional stimulation such as volume loading may elicit only an attenuated ANP secretion response, for example, due to saturation of the ANP receptor sensing system or to a limited transformation rate of pro-ANP. Third, the increase in atrial ANP synthesis and the increase in atrial ANP gene expression seems limited; however, substantial specific ANP gene expression occurs in the ventricles, which, in turn, may contribute to increased plasma ANP levels in chronic heart failure.     

Right and left ventricular pressure-volume response to elevated pericardial pressure

Because of the close anatomic connections, the volume in 1 ventricle can directly influence the volume in the other ventricle. We examined this ventricular mechanical coupling at elevated pericardial pressures in 6 mongrel dogs. The animals were anesthetized and were mechanically ventilated with intermittent positive-pressure ventilation. Right and left ventricular volumes and pressures and pericardial pressure were simultaneously measured during control and after infusing 25, 50, and 75 ml of saline with dextran into the pericardial cavity. The ventricular volumes were calculated from cine-radiographic positions of endocardial, radiopaque markers. In the control state, right ventricular end-diastolic volume (RVEDV) increased 9.2 +/- 0.9 ml (p less than 0.05) during expiration, whereas left ventricular end-diastolic pressure (LVEDP) increased 0.6 +/- 0.7 mmHg and left ventricular end-diastolic volume (LVEDV) decreased 0.6 +/- 0.4 ml. The increased transmural LVEDP with a decreased LVEDV indicates an apparent left ventricular distensibility decrease as right ventricular diastolic volume increased, possibly because of ventricular interdependence. At the highest pericardial pressure, RVEDV increased 6.7 +/- 1.4 ml (p less than 0.05) during expiration as LVEDP increased 1.2 +/- 0.6 mm Hg and LVEDV decreased 2.0 +/- 0.6 ml (p less than 0.05). Thus, at the higher pericardial pressures, smaller changes in RVEDV produced significantly greater changes in LVEDV. This coupling between the ventricles was further examined in 5 hearts studied postmortem. The hearts were placed in cold cardioplegic solution and balloons were inserted into both ventricles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Roles of the right ventricular free wall and ventricular septum in right ventricular performance and influence of the parietal pericardium during right ventricular failure in dogs

The roles of the right ventricular (RV) free wall and ventricular septum in RV performance were studied in the canine heart. The parietal pericardium was kept intact. Acute ischemia of the RV free wall from right coronary ligation decreased the RV stroke work index more than did that of the ventricular septum from the septal branch of the left coronary artery ligation (41 and 23%, respectively, p < 0.01). The response of the RV stroke work index to acute volume loading was also decreased. Left ventricular dysfunction was detected only with ventricular septal ischemia. Combined RV free wall and ventricular septal ischemia produced more severe and predominant RV dysfunction with disproportionate elevation of RV end-diastolic pressure. After combined ischemia, pericardiotomy improved the RV stroke work index as well as the left ventricular stroke work index (40 and 27%, respectively, p < 0.05), although the increase in RV stroke work index was greater than in left ventricular stroke work index (p < 0.05).The results of this study suggest that (1) the RV free wall has a more important role than the ventricular septum in RV performance, (2) predominant RV failure can be induced experimentally after combined RV free wall and ventricular septal ischemia, and (3) the pericardium has a restrictive effect on the damaged and dilated right ventricle.     

Patterns of global and regional systolic and diastolic function in the normal right ventricle assessed by ultrafast computed tomography

A detailed evaluation of global and regional systolic function and diastolic filling of the human right ventricle has not been previously reported. Ultrafast computed tomography enables simultaneous imaging of the right and left ventricles at an 8 mm slice thickness with a scanning rate of 17 frames/s (50 ms acquisition intervals). In 10 normal men (mean age 26 +/- 4 years) early diastolic filling data were fit to a third order polynomial curve and the peak rate of diastolic filling and time to peak filling were determined globally and regionally at three distinct ventricular levels (apex to base) within each ventricle. The right and left ventricular stroke volumes were not statistically different (89 +/- 8 ml and 90 +/- 8 ml, p = NS), neither were the peak filling rates as referenced to the stroke volume (4.9 +/- 0.9 and 5.3 +/- 0.8 stroke volumes/s, p = NS). Time to peak filling rate was not different between the two ventricles (154 +/- 33 and 161 +/- 18 ms, p = NS). However, reference of stroke volumes and absolute peak filling rates to end-diastolic volumes demonstrated lower dynamic values for the right ventricle (ejection fraction: right ventricle 57 +/- 4%; left ventricle 68 +/- 5%, p less than 0.05, and peak filling rate: right ventricle 2.7 +/- 0.4 end-diastolic volumes/s; left ventricle 3.6 +/- 0.5, p less than 0.05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of left and right ventricular function in acute myocardial infarction

Pulmonary arterial end-diastolic and mean right atrial pressures were compared in 25 patients with acute myocardial infarction and in one patient with unstable angina. No consistent relationship was observed between these pressures. Simultaneous ventricular function curves relating the stroke work of each ventricle to its respective filling pressure were constructed on 34 occasions, dextran infusion or diuresis being used to alter the filling pressure. The curves from each ventricle were described mathematically by a quadratic (parabolic) function as well as by a straight line function and then compared by canonical correlation analysis. Alterations in the left ventricular function curves occurred with and without depression of right ventricular function curves. These hemodynamic measurements demonstrate that acute myocardial infarction can alter the relationship between left and right ventricular function.     

Predominant right ventricular dysfunction after right ventricular destruction in the dog

Right and left ventricular function was assessed by observing the response to rapid blood volume expansion before and after extensive cauterization of the right ventricle in open chest dogs. In the control period, left ventricular end-diastolic pressure surpassed right ventricular end-diastolic pressure by an average of 11.5 mm Hg after volume expansion whereas, after destruction of the right ventricle, pressure in this chamber surpassed pressure in the left ventricle by an average of 4 mm Hg. In contrast, after left ventricular damage, left ventricular end-diastolic pressure averaged 25 mm Hg more than right ventricular end-diastolic pressure. Despite extensive damage to the right ventricular free wall, the right ventricle continued to generate a near normal pressure and aortic flow could be increased above control levels by volume expansion. We conclude that, in contrast to previous evidence, damage to the right ventricle produces a syndrome of predominant right ventricular dysfunction. However, cauterization of the entire free wall of the right ventricle does not reproduce the more profound right ventricular dysfunction noted in infarction of the right ventricle in man.     

Regional changes in hemodynamics and cardiac myocyte size in rats with aortocaval fistulas. 2. Long-term effects

Regional changes in hemodynamics and cardiac myocyte size were examined in adult rats 5 months after creating a large aortocaval fistula. At that time, cardiac output, left and right ventricular pressures, and left and right ventricular dP/dtmax were measured. Subsequently, isolated cardiac myocytes were collected from the left ventricle, right ventricle, and septum for cell size measurements. Compared with sham-operated controls, percent dry weight was reduced in the liver and kidney but was unchanged in the lung. Heart rate, left ventricular systolic pressure, left ventricular dP/dtmax, and systolic aortic pressure were not changed in rats with fistulas. However, cardiac output, stroke volume, left ventricular end-diastolic pressure, and all measured parameters in the right ventricle were significantly increased. Mean cell volume and the ratio of heart weight to body weight were both elevated 92%. Cell volume, cell length, and cross-sectional area increased significantly in each heart region examined. Hypertrophy was more pronounced in cells from the right ventricle and the endomyocardium of the left ventricle. The percentage of cells with mononucleation or binucleation was not changed in any heart region of rats with fistulas. In summary, despite evidence of renal and hepatic congestion, most indexes of cardiac function were normal or elevated 5 months after creation of a large volume-overload-induced hypertrophy. Data from isolated cardiac myocytes suggested that cellular hypertrophy, rather than hyperplasia, was responsible for the increased cardiac mass.     

Alterations of cardiac performance in rats with established spontaneous hypertension.

To characterize intact cardiac performance during the progression from moderate to severe left ventricular hypertrophy, peak pumping ability, maximal pressure-generating capacity and passive pressure-volume relations were determined in ether-anesthetized 6 and 18 month old female spontaneously hypertensive rats, in 18 month old male spontaneously hypertensive rats and in sex- and age-matched normotensive rats. Ejection phase indexes of young female hypertensive rats were comparable with those of age-matched normotensive rats. Both groups ejected the same peak stroke volumes from similar end-diastolic volumes so that their indexes of ejection fraction were identical. However, in old female and male hypertensive rats, these characteristics of ventricular performance were greatly diminished. A reduced peak stroke volume was ejected from a normal end-diastolic volume in old female hypertensive rats and from a significantly larger end-diastolic volume in old male hypertensive rats, so that ejection fraction indexes were moderately and substantially reduced, respectively. Maximal pressure developed during an aortic occlusion was always significantly greater in hypertensive rats. Despite elevated systemic arterial blood pressures, young female hypertensive rats ejected a normal stroke volume from a normal end-diastolic volume. Even though the severity of hypertension did not further progress with age, cardiac mass increased, yet systolic function decreased in old hypertensive rats. Therefore, hypertrophic growth of the left ventricle in the hypertensive rat is associated with both a compensated and a depressed phase of cardiac performance.     

Quantitative dynamics of left ventricular emptying and filling as a function of heart size and stroke volume in pure aortic regurgitation and in normal subjects.

Quantitative understanding of the dynamics of left ventricular (LV) emptying and filling as the left ventricle dilates but maintains ejection fraction is limited. Cine computed tomography was used to quantify peak LV emptying and filling characteristics in 30 patients with normal ejection fraction but variable end-diastolic and stroke volumes. Group I consisted of 15 normal male patients and group II of 15 male patients with chronic, well-compensated, isolated aortic regurgitation. For each patient global LV volumes, absolute peak emptying and peak early diastolic filling rates and the timing of these maximal slopes were quantified. Mean arterial pressure and heart rate were within the normal range and ejection fraction and ages similar between groups I and II. Between-group analyses showed significantly increased end-diastolic and stroke volumes in group II compared with group I but nearly identical end-systolic volumes. Likewise, absolute peak emptying and filling rates were significantly greater in group II than in group I patients. The ratio of peak emptying rate to peak filling rate remained constant between groups. Timing of peak emptying and filling were similar in both groups. Absolute LV peak emptying and filling rates were found to vary linearly with end-diastolic and stroke volumes in all subjects examined. However, referencing peak emptying or peak filling rates to end-diastolic or total stroke volumes eliminated intergroup differences. Thus, in the presence of preserved ejection fraction and normal arterial pressure, the dynamic rates of LV emptying and early diastolic filling increase in direct proportion to absolute end-diastolic and stroke volumes, but the ratio of peak emptying to peak filling rate remains constant.     

The effect of acute hypoxia on right ventricular function in healthy adults

Right ventricular ejection fraction and right ventricular volumes were derived in 12 healthy male subjects using krypton-81m equilibrium radionuclide ventriculography whilst subjects breathed 30% (high inspired oxygen) and then 8-12% oxygen in nitrogen mixture (hypoxia). 'Physiological' tricuspid valve regurgitation was identified in 7 of the subjects by Doppler echocardiography, and right ventricular peak systolic pressure was estimated during high inspired oxygen and during hypoxia. Mean right ventricular peak systolic pressure was 24.1 +/- 3.3 mmHg during high inspired oxygen and increased to 41.3 +/- 8.4 mmHg during hypoxia (P less than 0.01). Mean right ventricular ejection fraction was 0.612 +/- 0.075 during high inspired oxygen and was unchanged at 0.590 +/- 0.073 during hypoxia. There was no significant change in right ventricular end-diastolic volume or stroke volume in response to hypoxia. The systolic performance of the normal right ventricle is well-maintained during an acute rise in afterload induced by hypoxia.     

Relation of size of secondary ventricles to exercise performance in children after fontan operation

The effects of the nondominant or secondary ventricle on the Fontan circulation are not known. The present study used cardiac magnetic resonance imaging to investigate the relations between secondary ventricular size and global cardiac performance. The Fontan cross-sectional study collected data from 7 centers participating in the Pediatric Heart Network. Subjects with complete cardiac magnetic resonance imaging data and an identifiable secondary ventricle were included in the analysis. Relationships between body surface area-adjusted parameters of the secondary ventricle (mass, end-diastolic volume, mass/volume ratio, and stroke volume) and the following measures were assessed. These measures included the percentage of predicted peak oxygen consumption and oxygen consumption at the ventilatory anaerobic threshold, ejection fraction of the main ventricular chamber, echocardiographic diastolic function grade, serum B-type natriuretic peptide, primary ventricular end-diastolic pressure, and parent-reported physical functioning summary score on the Child Health Questionnaire. Of the 546 enrolled subjects, 123 (age 12.1 ± 3.3 years, 56% male) had undergone cardiac magnetic resonance imaging, and 38 had achieved maximal aerobic capacity. A larger secondary ventricular end-diastolic volume, lower mass/volume ratio, and greater secondary/total ventricular stroke volume ratio were associated with a greater exercise capacity. No significant relationships were found between the measures of the secondary ventricle and the other outcomes. In conclusion, in children after the Fontan operation, a larger and less hypertrophied secondary ventricle with a greater contribution to stroke volume was associated with a better exercise capacity.     

Ventricular interaction during mechanical ventilation in closed-chest anesthetized dogs

The cardiac effects of positive pressure ventilation and positive end-expiratory pressure are incompletely understood. External constraint due to increased intrathoracic pressure decreases left ventricular end-diastolic volume; the effects on venous return and ventricular interaction are less clear. Phasic changes in inferior vena caval flow, end-diastolic ventricular dimensions and output were measured in seven anesthetized, ventilated normal dogs. During inspiration, caval flow, right ventricular diameter and output decreased; end-diastolic transseptal pressure gradient, septum-to-left ventricular free wall diameter, left ventricular area (ie, left ventricular volume index) and output increased despite the decreased sum of the septum-to-free wall diameters. The reverse occurred during expiration. Increased positive end-expiratory pressure decreased the left ventricular area, but the end-expiratory right ventricular diameter was unchanged. At given airway pressures, right ventricular diameter was greater at higher positive end-expiratory pressures, suggesting that a leftward septal shift (direct ventricular interaction) added to the effect of external constraint on left ventricular end-diastolic volume. In conclusion, positive pressure ventilation reduced right ventricular end-diastolic volume during inspiration and increased the transseptal pressure gradient, which shifted the septum rightward, increasing left ventricular end-diastolic volume and output. The reverse occurred during expiration. Positive end-expiratory pressure constrained left ventricular filling and decreased left ventricular end-diastolic volume further by a leftward septal shift.