Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Systole”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 685 records · Page 38Linked to original sources
PubMed2006

Myocardial systolic activation delay in patients with left bundle branch block and either normal or impaired left ventricular function.

AIM OF THE STUDY: to evaluate determinants of myocardial activation delay of both left (LV) and right (RV) ventricle in patients with left bundle branch block (LBBB) and either normal or impaired LV ejection fraction (EF). METHODS: From an initial cohort of patients with LBBB, 42 patients with dilated cardiomyopathy (group A) and 33 with normal global LV systolic function (group B), all comparable in age and sex, underwent standard Doppler echo, pulsed Doppler myocardial imaging (DMI), and coronary angiography. Using DMI, the following regional parameters were evaluated in five different basal myocardial segments (LV anterior, inferior, septal, lateral walls-RV lateral wall): systolic (Sm), early- and late-diastolic (Em and Am) peak velocities. As index of myocardial systolic activation was calculated: precontraction time (PCTm) (from the beginning of Q-wave of ECG to the onset of Sm). Intraventricular systolic dyssynchrony was analyzed by difference of PCTm in different LV myocardial segments. Interventricular activation delay was calculated by the difference of PCTm between the most delayed LV segment and RV lateral wall. RESULTS: Patients of group A showed increased heart rate (HR), QRS duration and LV end-diastolic diameter, and reduced LV EF. By DMI, patients of group A showed reduced myocardial peak velocities and a significant intraventricular delay in activation of LV lateral wall, with increased regional PCTm (P < 0.001). In addition, patients with dilated cardiomyopathy showed a more pronounced interventricular dyssynchrony, even after adjustment for HR and QRS duration. By receiver operating characteristic (ROC) curve analysis, a cut-off value of 55 msec of interventricular delay showed 86% sensitivity and 92% specificity in identifying patients with impaired EF. In the overall population, by use of stepwise forward multivariate linear regression analyses, LV end-diastolic diameter (beta coefficient = 0.52; P < 0.001) and LV EF (beta coefficient =-0.58; P < 0.0001) were the only independent determinants of interventricular activation delay. CONCLUSIONS: Pulsed DMI is an effective noninvasive technique for assessing the severity of regional delay in activation of LV walls in patients with LBBB. The impairment of interventricular systolic sychronicity is strongly related to LV dilatation and to the degree of global systolic dysfunction. Therefore, patients with dilated cardiomyopathy suitable for cardiac resynchronization therapy may be better selected.

Bundle-Branch Block↗
PubMedDate not supplied

Aortic valve replacement for aortic insufficiency: valve type as a determinant of systolic strain recovery.

BACKGROUND AND AIM: Left ventricular (LV) 3D systolic strain decreases in absolute value postoperatively and does not recover in patients who undergo aortic valve replacement (AVR) for chronic aortic insufficiency (AI). We investigated whether choice of valve prosthesis (mechanical [St. Jude], bioprosthetic [bovine pericardial], Ross procedure) had a significant impact on strain recovery in this surgical population. METHODS: MRI with tissue-tagging was performed on 14 patients with chronic AI both before and 28 +/- 13 months after AVR. Average values of LV systolic strain and end-systolic stress (ESS) were computed from MRI data for the LV. Three types of prosthetic valve were examined (Ross procedure n = 4, bovine pericardial n = 5, and St. Jude n = 5). RESULTS: Overall, systolic strain, ESS, LV volumes, ejection fraction, and LV mass all changed significantly following AVR. Comparisons between individual valve types revealed no differences in any of these measurements. Patients who received a mechanical valve had a greater decrease in the absolute value of systolic strain following surgery compared to patients from the nonmechanical group (Ross procedure and bioprosthetic valve). Comparisons between the Ross group and the prosthetic group (St. Jude and bioprosthetic) produced no significant differences in strain, ESS, LV volume, and mass. CONCLUSIONS: These early results suggest that valve prosthetic type may be a factor in efforts to improve strain recovery after AVR for AI, although further investigation is warranted. MRI with tissue-tagging may be a useful tool for comparing the impact of prosthetic valve choice on incompletely recovered systolic strain following AVR for chronic AI.

Adult↗
PubMed1999

A comparison of bioimpedance and echocardiography in measuring systolic heart function in cardiac patients.

To investigate the ability of bioimpedance cardiography to assess left ventricular systolic function in comparison with known echocardiographic parameters and to establish the most informative bioimpedance parameter, 28 cardiac patients were submitted to simultaneous echocardiography and bioimpedance cardiography. Bioimpedance systolic time ratio, Heather index, acceleration index, and index of contractility were compared with echocardiographically obtained left ventricular dimensions, 2D left ventricular ejection fraction, fractional shortening, and mean velocity of circumferential shortening. The systolic time ratio and Heather index correlated significantly well with, respectively, 2D ejection fraction (r = -0.73) and, respectively, fractional shortening (r = 0.69). The systolic time ratio was the best parameter in recognizing impaired left ventricular systolic function (F = 12.6) in comparison with the Heather index (F = 6.5). This study demonstrates the applicability of bioimpedance cardiography in assessing left ventricular systolic function similar to echocardiography in clinical cardiology.

Adult↗
PubMed2000

Risk assessment of left ventricular systolic dysfunction in primary care: cross sectional study evaluating a range of diagnostic tests.

OBJECTIVES: To assess the probability of left ventricular systolic dysfunction without echocardiography in patients from general practice. DESIGN: Cross sectional study using multivariate regression models to examine the relation between clinical variables and left ventricular systolic dysfunction as determined by echocardiography. SETTING: Three general practices in Copenhagen. SUBJECTS: 2158 patients aged >40 years were screened by questionnaires and case record reviews; 357 patients with past or present signs or symptoms of heart disease were identified, of whom 126 were eligible for and consented to examination. MAIN OUTCOME MEASURES: Clinical variables that were significantly (P<0.05) related to ejection fraction </=0.45 and their predictive value for left ventricular systolic dysfunction. RESULTS: 15 patients (12%) had left ventricular systolic dysfunction. The prevalence was significantly related to three questions: does the electrocardiogram have Q waves, left bundle branch block, or ST-T segment changes? (P=0.012); is resting supine heart rate greater than the simultaneous diastolic blood pressure? (P=0.002); and is plasma N-terminal atrial natriuretic peptide>0.8 nmol/l? (P=0.040)? Only one of 60 patients with a normal electrocardiogram had systolic dysfunction (2%, 95% confidence interval 0% to 9%) regardless of response to the other two questions. The risk of dysfunction was appreciable in patients with a yes answer to two or three questions (50%, 27% to 73%). CONCLUSIONS: A normal electrocardiogram implies a low risk of left ventricular systolic dysfunction. Patients can be identified for echocardiography on the basis of an abnormal electrocardiogram combined with increased natriuretic peptide concentration or a heart rate greater than diastolic blood pressure, or both.

Adult↗
PubMed1984

Regional left ventricular contraction abnormality during early systole in patients with angina pectoris. Assessment with radionuclide ventriculography.

To determine the presence and prevalence of regional contraction abnormalities in patients with angina pectoris, radionuclide ventriculography gated to an electrocardiogram was carried out in 22 control subjects (group 1) and in 22 patients with angina pectoris (group 2) with isolated stenosis of the left anterior descending coronary artery. No patients had had previous myocardial infarctions. A computer program subdivided the left ventricle into four regions at a geometric centre, and time-activity curves (30-40 ms/frame) of the global, septal, apical, and lateral regions were computed. There was no significant difference in the ejection fraction in the global or in any of the regions between the two groups. End systole in each region occurred close to global end systole in both groups. In the global region the percentage stroke volume ejected during the first third of systole was not significantly less in group 2 than in group 1. Regional analysis of the segments perfused by the stenosed vessel showed that the percentage stroke volume ejected during the first third of systole in group 2 was significantly less in the septal region and in the apical region compared with that in group 1. In contrast, in the normally perfused lateral region, there was no significant difference in the percentage stroke volume at the first third of systole between the two groups. This indicates that early contraction abnormalities are present in the region perfused by the stenosed vessel in patients with angina pectoris without previous myocardial infarction. Thus analysing the regional change in left ventricular volume during ejection in patients with coronary artery disease can show localised areas of contraction abnormalities during early systole that are not apparent when ventricular contraction is assessed as a whole.

Aged↗
PubMed2005

Systolic and diastolic function in middle aged patients with sickle beta thalassaemia. An echocardiographic study.

OBJECTIVE: To evaluate the right and left ventricular systolic and diastolic function in middle aged patients with sickle beta thalassaemia. METHODS: Forty three patients with sickle beta thalassaemia were recruited for echocardiographic study while 55 controls, matched for age and sex, served as the control group. Parameters measured included: dimensions and wall thickness of left (LV) and right (RV) ventricle and left atrium, LV mass, and cardiac index. LV and RV contractility variables--ejection fraction, circumferential fibre shortening velocity, end systolic stress, end systolic stress/volume index ratio, mitral and tricuspid annulus systolic excursion, and Tei index--were also calculated. The study also evaluated parameters of RV and LV diastolic function including early and late atrioventricular flow velocities (E and A wave respectively), E/A ratio, deceleration time (DT), isovolumic relaxation time (IVRT) as well as pulmonary and hepatic veins systolic to diastolic (S/D) ratio. RESULTS: Chamber enlargement, greater LV mass index, cardiac index, and RV wall thickness were found in the anaemic group compared with controls. The LV and RV contractility variables of the patients were similar to controls. Conversely the LV and RV Tei index was significantly greater in the patient group. Diastolic dysfunction was present in the anaemic patients resulting from the increased LV and RV A-wave, the longer LVIVRT, RVIVRT, and RVDT, as well as the higher hepatic and pulmonary veins S/D ratio. CONCLUSIONS: The results show that in middle aged patients with sickle beta thalassaemia the diastolic function is abnormal in both ventricles but still more in RV, whereas the systolic function remains unchanged.

Blood Flow Velocity↗
PubMed2006

Cardiac dilatation and pump dysfunction without intrinsic myocardial systolic failure following chronic beta-adrenoreceptor activation.

There is no direct evidence to indicate that pump dysfunction in a dilated chamber reflects the impact of chamber dilatation rather than the degree of intrinsic systolic failure resulting from myocardial damage. In the present study, we explored the relative roles of intrinsic myocardial systolic dysfunction and chamber dilatation as mediators of left ventricular (LV) pump dysfunction. Administration of isoproterenol, a beta-adrenoreceptor agonist, for 3 mo to rats (0.1 mg.kg(-1).day(-1)) resulted in LV pump dysfunction as evidenced by a reduced LV endocardial fractional shortening (echocardiography) and a decrease in the slope of the LV systolic pressure-volume relation (isolated heart preparations). Although chronic beta-adrenoreceptor activation induced cardiomyocyte damage (deoxynucleotidyl transferase-mediated dUTP nick-end labeling) as well as beta(1)- and beta(2)-adrenoreceptor inotropic downregulation (attenuated contractile responses to dobutamine and salbutamol), these changes failed to translate into alterations in intrinsic myocardial contractility. Indeed, LV midwall fractional shortening (echocardiography) and the slope of the LV systolic stress-strain relation (isolated heart preparations) were unchanged. A normal intrinsic myocardial systolic function, despite the presence of cardiomyocyte damage and beta-adrenoreceptor inotropic downregulation, was ascribed to marked increases in myocardial norepinephrine release, to upregulation of alpha-adrenoreceptor-mediated contractile effects as determined by phenylephrine responsiveness, and to compensatory LV hypertrophy. LV pump failure was attributed to LV dilatation, as evidenced by increased LV internal dimensions (echocardiography), and a right shift and increased volume intercept of the LV diastolic pressure-volume relation. In conclusion, chronic sympathetic stimulation, despite reducing beta-adrenoreceptor-mediated inotropic responses and promoting myocyte apoptosis, may nevertheless induce pump dysfunction primarily through LV dilatation, rather than intrinsic myocardial systolic failure.

Adrenergic beta-1 Receptor Agonists↗
PubMed1980

Effect of systole on coronary pressure-flow relations in the right ventricle of the dog.

Downey and Kirk's hypothesis that ventricular systole inhibits coronary blood flow by forming vascular waterfalls was examined in conscious chronically instrumented dogs by studying the effect of right ventricular systole on right coronary blood flow. Diastolic and systolic pressure-flow relations were constructed at resting-level flow and peak flow reactive hyperemia from phasic pressure and flow tracings recorded in nine dogs with right ventricular pressures ranging between 14 and 154 mmHg. Linear relations were found between aortic pressure and right coronary flow during diastolic and during systole when peak ventricular pressure was less than systemic. At resting-level flow and when peak ventricular pressure was less than one-half systemic, systole translated the diastolic relation to a higher zero-flow-intercept pressure and did not alter the slope of the relation. We interpret the data as showing that ventricular systole inhibits coronary blood flow by augmenting a vascular waterfall mechanism that exists during diastole.

Animals↗
PubMed1987

Ventricular systolic interdependence: volume elastance model in isolated canine hearts.

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

Algorithms↗
PubMed1988

Isochronal behavior in left ventricular systolic pressure-wall thickness relations.

Regional left ventricular systolic pressure-thickness relations have been used to assess regional load-insensitive contractility with the assumption that they possess linear isochrones that are fundamental to the time-varying elastance model of global pressure-volume relations. We examined the shape and time-varying behavior of pressure-thickness isochrones in six open-chest canine preparations. Transmural wall thickening (sonomicrometry) and ventricular pressure were altered by abrupt preload alterations during control, dobutamine, and propranolol. In all dogs and interventions, linear isochrones (r2 mean +/- SE = 0.91 +/- 0.11) were found at 5-ms intervals. During control, linear isochrone slope rose monotonically from onset to end of systole. Thickness-axis intercepts also varied continuously in time, but peak intercept and maximal slope were asynchronous. Dobutamine caused a steeper earlier maximum slope and increased slope-intercept asynchrony. Propranolol reduced maximum slope and slope-intercept asynchrony. Isochronal data during early systole were better fitted to a parabolic than to the linear model; however, fits to linear and parabolic models were equally good near end of systole. Linear isochronal behavior exists in systolic pressure-thickness relations especially near end systole and is maintained during modest inotropic alterations.

Animals↗
PubMed1994

Effects of free wall ischemia and bundle branch block on systolic ventricular interaction in dog hearts.

Systolic direct ventricular interaction is thought to occur via the ventricular septum and the coordinated contraction of common fibers shared by both ventricles. The purpose of the present study was to evaluate the effects of transient free wall ischemia and bundle branch block, which disrupt the coordinated contraction of shared common fibers, on left-to-right systolic ventricular interaction. We produced transient right and left ventricular free wall ischemia by 2-min coronary artery occlusions and bundle branch block by ventricular pacing in nine in situ dog hearts. To eliminate any confounding effect of series interaction, we used an abrupt hemodynamic perturbation (aortic constriction), and we measured systolic interaction gain (IG) as delta right ventricular peak systolic pressure/delta left ventricular peak systolic pressure (IG(peak)) and instantaneous delta right ventricular pressure/delta left ventricular pressure at matched data sampling times (IG(inst)), along with changes in right ventricular stroke volume and stroke work before and on the beat immediately after the aortic constriction. To achieve equivalence of the interventricular septal pressure transmission contribution to ventricular interaction, the delta left ventricular peak systolic pressure produced by the aortic constriction was matched under all experimental conditions [average increase: 64 +/- 19 (SD) mmHg]. Control IG(peak) was 0.12 +/- 0.05, and control IG(inst) was 0.11 +/- 0.05. These values did not change with either free wall ischemia or ventricular pacing, with or without an intact pericardium. The changes in right ventricular stroke volume and stroke work produced by the aortic constriction were not different from zero, during either ischemia or ventricular pacing, with or without an intact pericardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Left ventricular systolic dysfunction precedes diastolic dysfunction during myocardial ischemia in conscious dogs.

We studied the initial effects of regional and global left ventricular (LV) ischemia induced by left circumflex and left main coronary artery occlusion (CAO), respectively, on indexes of systolic and diastolic LV function in conscious dogs to determine whether diastolic abnormalities precede systolic dysfunction or vice versa during the onset of either regional or global myocardial ischemia. With regional myocardial ischemia, within four beats after left circumflex CAO, there was a significant decrease in end-systolic wall thickness in the ischemic zone followed by significantly enhanced postsystolic wall thickening in the nonischemic zone at beat 6. Both peak negative first derivative of left ventricular pressure (LV dP/dt) and the isovolumic relaxation half-time (T 1/2) were prolonged, but later (i.e., by the 9th beat). During sustained CAO T1/2 was normalized shortly after postsystolic thickening in the nonischemic zone had disappeared despite persistent regional systolic asynchrony and shortened ejection time. Thus postsystolic thickening in the nonischemic zone played a major role in the early, transient changes in isovolumic relaxation after acute induction of regional ischemia. With global myocardial ischemia, induced by left main coronary occlusion, indexes of systolic function (e.g., LV dP/dt, ejection fraction, and velocity of circumferential endocardial fiber shortening) were also depressed significantly before (by 5-15 beats) indexes of LV diastolic function [e.g., time constant of isovolumic relaxation and LV myocardial and chamber stiffness (by 35-45 beats)]. Similar results were observed in the presence of autonomic blockade, when heart rate did not change with CAO. Thus, during the induction of either acute regional or acute global LV ischemia in conscious dogs, LV systolic dysfunction occurs before diastolic dysfunction.

Animals↗
PubMed1997

Left atrial systolic and diastolic function after cessation of pacing in tachycardia-induced heart failure.

Studies in the rapid-pacing model of heart failure have shown that left ventricular (LV) systolic function normalizes on cessation of pacing and LV diastolic dysfunction persists, but there is no information regarding atrial function under these conditions. To determine the effects of cessation of pacing on left atrial (LA) systolic and diastolic function, ten dogs with rapid pacing-induced heart failure (250 beats/min for 3-4 wk), six dogs with regression of heart failure (4 wk after cessation of rapid pacing), and seven control dogs were instrumented with LA sonomicrometers and micromanometers. At matched LA pressure, LA ejection (10.2 +/- 3.0 vs. 17.4 +/- 5.5%), reservoir volume fractions (19 +/- 8 vs. 35 +/- 11%), and heart rate-corrected mean normalized systolic ejection rate (1.25 +/- 0.33 vs. 1.60 +/- 0.44 EF/s) were significantly less, and the volume-normalized diastolic stiffness constant (4.9 +/- 0.8 vs. 3.2 +/- 1.1) was significantly greater, in regression versus control dogs; these changes were associated with incomplete regression of LA hypertrophy and a persistent 77.4% increase in beta-myosin heavy chain (beta-MHC) in the LA body. LV systolic function and weight were not significantly different, whereas the time constant of LV relaxation was longer (52.5 +/- 4.4 vs. 40.8 +/- 7.6 ms; P < 0.05) and LV end-diastolic pressure was greater (12.2 +/- 1.8 vs. 7.1 +/- 2.0 mmHg; P < 0.05) in regression compared with control dogs. Thus, unlike the normalization of LV systolic function observed with cessation of rapid pacing, LA systolic function is persistently abnormal, owing in part to persistent LV diastolic dysfunction, residual LA hypertrophy, and MHC isoform switches.

Animals↗
PubMed1997

Alpha-adrenergic vasoconstriction reduces systolic retrograde coronary blood flow.

There is a paradoxical alpha-adrenoceptor-mediated coronary vasoconstriction whenever there is adrenergic activation of the heart, as during cardiovascular reflexes or exercise. A previous study demonstrated that this paradoxical vasoconstriction helps maintain blood flow to the vulnerable inner layer of the left ventricular wall during exercise, but the mechanism for this effect was not elucidated. The purpose of the present investigation was to test the hypothesis that alpha-adrenoceptor-mediated vasoconstriction lessens the to-and-fro oscillation of blood flow that occurs in the coronary arterial tree during systole and diastole. Septal coronary artery blood velocity was measured in anesthetized open-chest dogs with a 20-MHz pulsed Doppler velocimeter. Systolic retrograde velocity and diastolic forward velocity were compared during norepinephrine infusion before and after alpha-adrenoceptor blockade with phenoxybenzamine. Systolic aortic pressure was held constant by aortic banding; heart rate was controlled by pacing at 80, 140, and 200 beats/min; and maximum left ventricular dP/dt was unchanged by alpha-blockade. At each pacing rate, systolic retrograde velocity was significantly greater after alpha-blockade, indicating that alpha-vasoconstriction reduced systolic retrograde flow by changing coronary vascular impedance. Transmural blood flow was measured with microspheres in a second group of dogs during the same experimental conditions, and flow to the inner layer of the left ventricle was diminished by alpha-adrenoceptor blockade at a heart rate of 250 beats/min, demonstrating a beneficial effect of alpha-vasoconstriction. In conclusion, adrenergic alpha-adrenoceptor-mediated coronary vasoconstriction reduces systolic retrograde coronary flow during norepinephrine infusion. This lessens to-and-fro flow oscillation in the coronary circulation and probably is the mechanism whereby alpha-vasoconstriction helps maintain blood flow to the inner layer of the left ventricle during exercise.

Adipose Tissue↗
PubMed2000

Maturation of end-systolic stress-strain relations in chick embryonic myocardium.

The embryonic myocardium increases functional performance geometrically during cardiac morphogenesis. We investigated developmental changes in the in vivo end-systolic stress-strain relations of embryonic chick myocardium in stage 17, 21, and 24 white Leghorn chick embryos (n = 10 for each stage). End-systolic stress-strain relations were linear in all developmental stages. End-systolic strain decreased from 0.50 +/- 0.02 to 0.31 +/- 0.01 (mean +/- SE, P < 0.05), while average end-systolic wall stress was similar at 3.29 +/- 0.34 to 4.19 +/- 0.43 mmHg (P = 0.14) from stage 17 to 24. Normalized end-systolic myocardial stiffness, a load-independent index of ventricular contractility, increased from 2.98 +/- 0.19 to 6.03 +/- 0.39 mmHg from stage 17 to 24 (P < 0.05). Zero-stress midwall volume increased from 0.024 +/- 0.002 to 0.124 +/- 0.004 microl from stage 17 to 24 (P < 0.05). These results suggest that the embryonic ventricle increases normalized ventricular "contractility" while maintaining average end-systolic wall stress over a relatively narrow range during cardiovascular morphogenesis.

Animals↗
PubMed2001

Enhanced systolic function of the right ventricle during respiratory distress syndrome in newborn lambs.

Respiratory distress syndrome (RDS) causes pulmonary hypertension. It is often suggested that this increased afterload for the right ventricle (RV) might lead to cardiac dysfunction. To examine this, we studied biventricular function in an experimental model. RDS was induced by lung lavages in seven newborn lambs. Five additional lambs served as controls. Cardiac function was quantified by indexes derived from end-systolic pressure-volume relations obtained by pressure-conductance catheters. After lung lavages, a twofold increase of mean pulmonary arterial pressure (from 15 to 34 mmHg) was obtained and lasted for the full 4-h study period. Stroke volume was maintained (5.2 +/- 0.6 ml at baseline and 6.1 +/- 1.4 ml at 4 h of RDS), while RV end-diastolic volume showed only a slight increase (from 6.5 +/- 2.3 ml at baseline to 7.7 +/- 1.3 ml at 4 h RDS). RV systolic function improved significantly, as indicated by a leftward shift and increased slope of the end-systolic pressure-volume relation. Left ventricular systolic function showed no changes. In control animals, pulmonary arterial pressure did not increase and right and left ventricular systolic function remained unaffected. In the face of increased RV afterload, the newborn heart is able to maintain cardiac output, primarily by improving systolic RV function through homeometric autoregulation.

Algorithms↗
PubMed1988

Transient analysis of cardiopulmonary interactions. II. Systolic events.

The etiology of the fall in left ventricular stroke volume (LVSV) and arterial pressure with a negative intrathoracic pressure (NITP) during inspiration is controversial. An increase in LV afterload produced by NITP has been proposed as one explanation but is difficult to evaluate if preload is also altered. To test the hypothesis that a systolic event alone, i.e., a change in LV afterload or contractility, can reduce LVSV during inspiration independent of changes in LV preload, a rapid transient NITP confined to systole was produced by electrocardiogram-triggered phrenic nerve stimulation in eight anesthetized dogs. Intrathoracic descending aortic diameters were measured by sonomicrometry to transduce qualitative changes in aortic transmural pressure. With the airway completely obstructed systolic NITP resulted in a decrease in LVSV (-8.1%, P less than 0.001) but an increase in the systolic anteroposterior (0.54 mm, P less than 0.01) and right-to-left (0.45 mm, P less than 0.01) aortic diameters compared with preceding beat. Similar significant changes were observed with the airway unobstructed. These observations are consistent with an increased afterload imposed on the LV reducing LVSV and egress of blood out of the thorax. Prolonging NITP to include both systole and diastole, a profound fall in LVSV is observed, consistent with the independent influences of systolic and diastolic events combining to diminish LVSV.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Obstruction↗
PubMed1992

Effect of the pericardium on atrial systolic function.

The effect of pericardial constraint on atrial systolic function was investigated in nine acutely instrumented anesthetized dogs. Left and right atrial pressures were recorded by high-fidelity catheters; auricular diameters and free wall segment lengths were measured by sonomicrometry. Atrial function curves were constructed by relating atrial systolic dimensional shortening to atrial end-diastolic pressure during progressive volume loading. With the pericardium closed, the function curves were shifted markedly downward and rightward, such that atrial systolic shortening was reduced at any given pressure. There was a concomitant leftward and upward shift of the atrial end-diastolic pressure-dimension relationship. The relationship between atrial systolic shortening and atrial end-diastolic dimension was not shifted. These results suggest that the apparent depression of atrial systolic function with the pericardium closed is due to a restrictive effect of the pericardium on atrial filling. In conclusion, in the acutely dilated heart, the pericardium restricts atrial filling and thus causes a reduction in atrial systolic contribution to ventricular filling.

Animals↗