Diastolic Suction Research Articles

Effect of interconnecting collagen fibres on left ventricular function and intramyocardial compression.

The aim was to study the effects of the collagen mesh that interconnects the myocardial fibres on left ventricular mechanics and intramyocardial pressure. An earlier model which integrates a symmetrical left ventricular geometry and transmural muscle fibre structure with muscle fibre mechanics was expanded to include radial stiffness generated by dynamically stretched radial collagen fibres. The calculated end systolic pressure-volume relationship (ESPVR) was compared to left ventricular pressure and volume data from six open chest dogs, obtained over a wide load range. Midwall intramyocardial pressure measurements by flat intramyocardial transducer in six different dogs were also used. Consistent with the experiments, inclusion of radial stiffness yielded an ESPVR that was more curvilinear than the collagen-free model, and modified global left ventricular function in that the end systolic volume increased. A diastolic suction effect, manifested by a negative pressure with a steep diastolic pressure-volume relationship at low end systolic volumes, was predicted. The intramyocardial pressure was higher than the left ventricular pressure at the end of isovolumetric relaxation, when radial stretch is maximal and fibre stresses are relaxed. This is attributed to the radial fibre stress component. Intramyocardial pressure was only weakly dependent on left ventricular cavity pressure under wide load manipulations at constant contractility. The experiments also confirmed model predictions that (1) peak intramyocardial pressure is insensitive to load, (2) intramyocardial pressure is markedly higher than left ventricular pressure at the end of isovolumetric relaxation, and (3) intramyocardial pressure continues to rise during ejection towards a maximum value near end ejection. The transverse radial stiffness due to radial collagen interconnections between myocardial fibrils affects the global systolic left ventricular function, the diastolic suction effect, and the mechanism of systolic coronary compression.

Diastolic function of the nonfilling human left ventricle

Objectives. To investigate an early-diastolic left ventricular suction effect in humans, tip-micromanometer left ventricular pressure recordings were obtained in patients with mitral stenosis at the time of balloon inflations during percutaneous mitral valvuloplasty performed with a self-positioning Inoue balloon, which fits tightly in the mitral orifice.Background. When mitral inflow was impeded in anesthetized dogs. left ventricular pressure decayed to a negative asymptote value. This negative asymptote value was consistent with an early diastolic suction effect.Methods. Tip-micromanometer left ventricular pressure recordings were obtained in 23 patients with symptomatic mitral stenosis at the time of balloon inflations during percutaneous mitral valvuloplasty performed with a self-positioning Inoue balloon.Results. The left ventricular diastolic asymptote pressure (Pasy) was determined in 47 nonfilling beats with a sufficiently long (>200 ms) diastolic time interval (that is, the interval from minimal first derivative of left ventricular pressure to left ventricular end-diastolic pressure) and equaled 2 ± 3 mm Hg for beats with normal intraventricular conduction and 3 ± 2 mm Hg for beats with aberrant intraventricular conduction. Left ventricular angiography was performed in five patients during the first inflation of the Inoue balloon at the time of complete balloon expansion. Left ventricular end-diastolic volume of the nonfilling beats averaged 38 ± 14 ml and was comparable to the left ventricular end-systolic volume (39 ± 19 ml) measured during baseline angiography before mitral valvuloplasty. Time constants of left ventricular pressure decay were calculated on 21 nonfilling beats with a diastolic time interval >200 ms, normal intraventricular conduction and peak left ventricular pressure >50 mm Hg. Time constants (Toand Tbf) derived from an exponential curve fit with zero asymptote pressure and with a best-fit asymptote pressure were compared with a time constant (Tasy) derived from an exponential curve fit with the measured diastolic left ventricular asymptote pressure. The value for Tasy(37 ± 9 ms) was significantly smaller than that for Tbf(68 ± 28 ms, p < 0, 001) and the value for the measured diastolic left ventricular asymptote pressure (2 ± 4 mm Hg) was significantly larger than that for the best-fit asymptote pressure (-9 ± 11 mm Hg, p < 0.001). To(44 ± 20 ms) was significantly (p < 0.01) different from Tbfbut not from Tasy.Conclusions. During balloon inflation of a self-positioning Inoue balloon, left ventricular pressure decayed continuously toward a positive asymptote value and left ventricular cavity volume was comparable to the left ventricular end-systolic volume of filling beats. In these nonfilling beats, the best-fit asymptote pressure was unrelated to the measured asymptote pressure and towas a better measure of Tasythan was TbfReduced internal myocardial restoring forces, caused by different extracellular matrix of the human heart, reduced external myocardial restoring forces caused by low coronary perfusion pressure during the balloon inflation and inward motion of the balloon-occluded mitral valve into the left ventricular cavity could explain the failure to observe significant diastolic left ventricular suction in the human heart.

Dissociation between left ventricular untwisting and filling. Accentuation by catecholamines.

Efficient early diastolic filling is essential for normal cardiac function. Diastolic suction, as evidenced by a decreasing left ventricular pressure during early filling, could result from restoring forces (the release of potential energy stored during systolic deformation) dependent on myofilament relaxation. Although these restoring forces have been envisioned within individual myofibers, recent studies suggest that gross fiber rearrangement involving the connective tissue network occurs easy in diastole. This may lead to the release of potential energy stored during systole and suction-aided filling. To establish precisely the timing and extent of restoration of the systolic torsional deformation of the left ventricle with respect to early filling at baseline and with enhanced relaxation, we studied untwisting during control conditions and with catecholamine stimulation. Using noninvasive and nondestructive magnetic resonance tagging, torsional deformation of the left ventricle was measured at 20-msec intervals in 10 open-chest, atrially paced dogs, starting at aortic valve closure. Eight equiangular tags intersected the epicardium and endocardium in three short-axis imaging planes (base, mid, and apex). From the intersection points, epicardial and endocardial circumferential chord and arc lengths were measured and angular twist of mid and apical levels with respect to the base (maximal torsion and its reversal, untwisting) was calculated. Echo-Doppler provided timing of aortic valve closure and of mitral valve opening. Zero torsion was defined at end diastole. Torsion at the apical level reversed rapidly between its maximum and the time immediately after mitral valve opening: from 7.0 +/- 5.8 degrees to 3.2 +/- 5.4 degrees and 12.0 +/- 8.5 degrees to 6.9 +/- 7.8 degrees (mean +/- SD, both p less than 0.01) at the epicardium and endocardium, respectively. During the same period, no significant circumferential segment length changes occurred. As expected, after mitral valve opening, filling resulted in significant circumferential segment lengthening, whereas further reversal of torsion was small and nonsignificant. During dobutamine infusion, torsion at end systole was greater and reversal during isovolumic relaxation was much more rapid and greater in extent (p less than 0.01). Torsion reversed from 11.5 +/- 4.3 degrees to 5.7 +/- 4.8 degrees and 17.4 +/- 6.4 degrees to 6.9 +/- 7.7 degrees at epicardium and endocardium. Untwisting occurs principally during isovolumic relaxation before filling and is markedly enhanced in speed and magnitude by catecholamines. This partial return of the left ventricle to its preejection configuration before mitral valve opening could represent an important mechanism for the release of potential energy stored in elastic elements during the systolic deformation. These myocardial restoring forces would be markedly enhanced by physiological changes consequent to catecholamines such as during exercise, offsetting the concomitant shortening of the filling period.

Left ventricular function in rheumatic mitral stenosis

Haemodynamic factors contributing to clinical disability in patients with rheumatic mitral stenosis have been under discussion and investigation for decades. Prior to the development of left heart catheterization, a low cardiac output in the presence of little or no pulmonary hypertension was taken as evidence for a myocardial 'insufficiency'. With the use of left heart catheterization, it was possible to exclude the presence of coronary artery disease and to assess directly the size and function of the left ventricle. Such studies indicate a tendency toward low-normal left ventricular end-diastolic volumes and low-normal ejection fractions. Modest reductions in the ejection fraction may be due to: (1) a restriction or tethering of posterobasal myocardium by the scarred mitral apparatus, or (2) abnormal interventricular septal motion related to right ventricular overload and unequal filling of the two ventricles. These and other factors, such as limited LV distensibility and variable diastolic suction, may affect ventricular function in rheumatic mitral stenosis. Thus, left ventricular dysfunction can generally be explained without implicating a rheumatic myocardial factor.

Left ventricular diastolic suction as a mechanism of ventricular filling.

Physiological role of "suction" in diastolic ventricular filling is still controversial. In order to determine whether the beating intact heart induces negative left ventricular (LV) pressure, indicative of LV suction when the ventricular filling is prevented, we transiently prevented LV filling by occluding the mitral orifice in open chest dogs. In more than 80% of all runs with various hemodynamic conditions the minimal diastolic LV pressure (LVPmin) decreased below zero immediately after the mitral valve occlusion and remained negative throughout diastole. The negativity was augmented with a decrease in end-systolic volume and an increase in inotropic state. The diastolic pressure-volume relationships of the non-filling beating ventricle in control condition and high inotropic state (Ca++ infusion) demonstrated that LVPmin correlated with LV volume and intropic state. These results indicate that the negative diastolic LV pressure is augmented by a decrease in end-systolic volume and by an increase in contractility and thus, LV suction may play an important role in LV diastolic filling.

Negative diastolic pressure in the intact canine right ventricle. Evidence of diastolic suction.

To determine whether the canine right ventricle (RV) can develop a negative diastolic pressure indicative of suction, RV pressure was measured in 15 dogs, with catheter-tip micromanometers. Six dogs were studied only with the chest closed. In these dogs, intrapleural pressure was measured medially (near the heart) in four and laterally in two. In nine dogs, RV pressure was evaluated with the chest closed and after the chest had been opened. In all dogs, with the chest closed, minimal RV diastolic pressure during expiration was negative, -4.8 +/- 0.3 mm Hg. The lowest diastolic pressures occurred during early diastole. Intrapleural pressure during expiration was never this low. Intrapleural pressure measured medially in four dogs was positive during expiration (1.0 +/- 0.6 mm Hg). In the two dogs which it was measured in the lateral pleural space, it was somewhat negative during expiration (-2.5 and -1.3 mm Hg, respectively). After the chest had been opened (nine dogs) minimal RV pressure during early diastole was negative in six dogs and positive in three (range: -1.8 to 0.8 mm Hg). These results indicate that the negative RV diastolic pressure during expiration did not result from a negative intrathoracic pressure. It appears that the RV during early diastole can create a sucking effect which may contribute to the filling process.

Negative intraventricular diastolic pressure in patients with mitral stenosis: Evidence of left ventricular diastolic suction

Left ventricular diastolic pressure was evaluated in 15 patients with mitral stenosis and 16 patients with no significant heart disease to determine if a stenotic mitral valve can cause the left ventricle to produce a negative diastolic pressure, indicative of ventricular diastolic suction. The minimal level of diastolic pressure in patients with mitral stenosis ranged between 6 and -7 mm Hg; in normal subjects it did not fall below 0. The average value of minimal diastolic pressure in patients with mitral stenosis (-2 +/- 1 mm Hg [mean +/- standard error of the mean]) was significantly lower than in patients without significant heart disease (5 +/- 1 mm Hg) (p less than 0.001). These observations indicate that the human left ventricle, in the presence of mitral stenosis, can generate a negative diastolic pressure. The presence of a negative diastolic pressure in patients with mitral stenosis suggests that the dynamics of the ventricle during diastole may contribute to the filling process.

Negative diastolic pressure in the isolated hypothermic dog heart.

Pressure relationships in the left ventricle of the dog were studied under conditions in which left ventricular inflow was controlled by means of an artificial circuit. Hypothermia was used to slow the dynamics of the heart beat. When all inflow to the left ventricle was suddenly stopped, the succeeding beats showed negative diastolic pressures. The greatest drop in pressure occurred early in diastole; in most instances, end-diastolic pressures remained negative. Early diastolic pressures before occlusion average +2.6 mm. Hg; early diastolic pressures after occlusion of inflow averaged -4.7 mm. Hg. A physical model was proposed which could explain the occurrence and decay of the observed subatmospheric pressure. These experiments indicate that diastolic suction can be a factor that accomplishes ventricular filling during diastole in a heart following systolic discharge against a wide range of aortic pressures.

Ventricular filling by diastolic suction

Ventricular filling by diastolic suction

Evidence for left ventricular diastolic suction in closed-chest dogs.

The question of ventricular filling by "suction" was investigated by recording the transmural ventricular pressure in normally breathing animals who had recovered from surgery. This transmural pressure was recorded as the difference between the thoracic pressure and the intraventricular pressure. It was considered positive whenever the ventricular pressure exceeded the thoracic pressure as is the case during systole, and negative when it was less than the thoracic pressure. During diastole the difference between these pressures are always small (±10 mm Hg or less). In the normal untraumatized animal it is zero or positive (filling by venous pressure). After the animal deteriorates from repeated experiments it may become negative, (filling by an action of the ventricular wall or suction). This suction is greater as a result of conditions which interfere with venous return and diminish the size of the ventricles by x-ray (mitral stenosis or bleeding). The force of suction is lessened after transfusions which increase the size of the ventricles. Considerations are advanced for believing that the suction force originates in elastic recoil of the ventricular wall and that it is not clearly an important factor in the mechanism of cardiac pumping.

Effects of increased residual volume, increased output resistance and autonomic drugs on ventricular suction in the turtle.

Immersed, isolated turtle ventricles were allowed to beat when filling only by suction. Obstruction of ejection at various volumes showed an inverse relationship between residual volume and volume aspirated. Diastolic aspiration occurred even with residual volumes of at least 0.55 ml. Ventricles, filling by suction only, maintained continuous output of up to 3 ml./min. working against pressures of 16 to 22 cm. H 2 O. In these circumstances ejection was diminished or abolished by acetylcholine and usually increased by epinephrine. This work amplifies and further quantitates recent work showing ventricular diastolic suction in a variety of species.

Critical review of recent work on ventricular diastolic suction.

Unequivocal evidence in favor of the concept that a ventricular diastolic vis a fronte contributes to ventricular filling has been established only in the following conditions: a. When the ventricle contains an abnormally small residual volume (rat, dog, turtle) b. When the ventricle contains a more nearly normal, residual volume due to ejection against the resistance of a fluid column (dog, turtle). The quantitative contribution of the ventricular vis a fronte to ventricular filling at various residual volumes and various levels of cardiac activity is still unknown. The physiological significance of diastolic suction for the return flow of blood can therefore not yet he evaluated.

Ventricular diastolic suction at normal arterial pressures.

It has been shown previously that an empty ventricle can suck in a small amount of fluid during diastole, but the question of whether a normal ventricle does so was not answered. In the present experiments it was demonstrated that even a ventricle with a more nearly normal endsystolic residual volume draws blood into its cavity and that this ventricular vis a fronte is augmented by the action of epinephrine.

STUDIES ON THE CONSECUTIVE PHASES OF THE CARDIAC CYCLE

ArticleSTUDIES ON THE CONSECUTIVE PHASES OF THE CARDIAC CYCLEI. The Duration of the Consecutive Phases of the Cardiac Cycle and the Criteria for their Precise DeterminationCarl J. WiggersCarl J. WiggersFrom the Department of Physiology, Western Reserve University School of Medicine, Cleveland, OhioPublished Online:01 Jul 1921https://doi.org/10.1152/ajplegacy.1921.56.3.415MoreSectionsPDF (3 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByConstructing the Wiggers diagram using core concepts: a classroom activityDee U. Silverthorn10 November 2022 | Advances in Physiology Education, Vol. 46, No. 4The Wright table of the cardiac cycle: a stand-alone supplement to the Wiggers diagramBruce E. Wright, Gretchen LeFever Watson, and Nancy J. Selfridge3 September 2020 | Advances in Physiology Education, Vol. 44, No. 4Contractile work directly modulates mitochondrial protein levels in human engineered heart tissuesRonald Ng, Lorenzo R. Sewanan, Allison L. Brill, Paul Stankey, Xia Li, Yibing Qyang, Barbara E. Ehrlich, and Stuart G. Campbell5 June 2020 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 318, No. 6What global diastolic function is, what it is not, and how to measure itCharles S. Chung, Leonid Shmuylovich, and Sándor J. Kovács1 November 2015 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 309, No. 9Cardiac phase-dependent time normalization reduces load dependence of time-varying elastanceTaco Kind, Nico Westerhof, Theo J. C. Faes, Jan-Willem Lankhaar, Paul Steendijk, and Anton Vonk-Noordegraaf1 February 2009 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 296, No. 2Left ventricular endocardial longitudinal and transverse changes during isovolumic contraction and relaxation: a challengeWolfgang A. Goetz, Emmanuel Lansac, Hou-Sen Lim, Patricia A. Weber, and Carlos M. G. Duran1 July 2005 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 289, No. 1Reservoir and conduit function of right atrium: impact on right ventricular filling and cardiac outputSydney L. Gaynor, Hersh S. Maniar, Sunil M. Prasad, Paul Steendijk, and Marc R. Moon1 May 2005 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 288, No. 5Assessment of left ventricular diastolic suction in dogs using wave-intensity analysisZhibin Wang, Fereshteh Jalali, Yi-Hui Sun, Jiun-Jr Wang, Kim H. Parker, and John V. Tyberg1 April 2005 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 288, No. 4Cardiovascular physiology in the twentieth century: great strides and missed opportunitiesHarris J. Granger1 December 1998 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 275, No. 6Carl J. Wiggers and the pulmonary circulation: a young man in search of excellenceJohn T. Reeves1 April 1998 | American Journal of Physiology-Lung Cellular and Molecular Physiology, Vol. 274, No. 4 More from this issue > Volume 56Issue 3July 1921Pages 415-438 Copyright & PermissionsCopyright © 1921 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1921.56.3.415History Received 26 March 1921 Published online 1 July 1921 Published in print 1 July 1921 Metrics