Showing papers on "Cardiac cycle published in 1986"

Left ventricular filling dynamics: influence of left ventricular relaxation and left atrial pressure.

Abstract: Peak rapid filling rate (PRFR) is often used clinically as an index of left ventricular relaxation, i.e., of early diastolic function. This study tests the hypothesis that early filling rate is a function of the atrioventricular pressure difference and hence is influenced by the left atrial pressure as well as by the rate of left ventricular relaxation. As indexes, we chose the left atrial pressure at the atrioventricular pressure crossover (PCO), and the time constant (T) of an assumed exponential decline in left ventricular pressure. We accurately determined the magnitude and timing of filling parameters in conscious dogs by direct measurement of phasic mitral flow (electromagnetically) and high-fidelity chamber pressures. To obtain a diverse hemodynamic data base, loading conditions were changed by infusions of volume and angiotensin II. The latter was administered to produce a change in left ventricular pressure of less than 35% (A-1) or a change in peak left ventricular pressure of greater than 35% (A-2). PRFR increased with volume loading, was unchanged with A-1, and was decreased with A-2; T and PCO increased in all three groups (p less than .005 for all changes). PRFR correlated strongly with the diastolic atrioventricular pressure difference at the time of PRFR (r = .899, p less than .001) and weakly with both T (r = .369, p less than .01) and PCO (r = .601, p less than .001). The correlation improved significantly when T and PCO were both included in the multivariate regression (r = .797, p less than .0001). PRFR is thus determined by both the left atrial pressure and the left ventricular relaxation rate and should be used with caution as an index of left ventricular diastolic function.

Left ventricular relaxation in the filling and nonfilling intact canine heart

Abstract: We studied left ventricular relaxation in the filling and transiently nonfilling working hearts of seven open-chest pentobarbital-anesthetized dogs by totally occluding the mitral annulus during one systole. In the completely isovolumic nonfilling cycle, the ventricle relaxes to a lower pressure minimum (usually negative) than in the normal filling cycle. By clamping the ventricle at end systole, we determined the pressure asymptote (Poo) under dynamic conditions. With this information, we evaluated the validity of a monoexponential characterization of relaxation. P = (P0 - Poo) exp(-t/T) + Poo (T, time constant, P0, pressure at t = 0). Plots of In(P-Poo) versus t are nonlinear and concave to the origin, thereby revealing that late relaxation is more rapid than predicted by a monoexponential relation. Nevertheless, the monoexponential T remains a useful index of relaxation and correlates well with other temporal indexes (isovolumic relaxation time and relaxation half-time). When T is calculated from a filling cycle by assuming a zero pressure asymptote, i.e., the conventional way, there is no significant difference with the true value based on the nonfilling cycle.

Hemodynamic effects of cardiac cycle-specific increases in intrathoracic pressure

Abstract: Changes in intrathoracic pressure (ITP) can influence cardiac performance by affecting ventricular loading conditions. Because both systemic venous return and factors determining left ventricular (LV) ejection may vary over the cardiac cycle, phasic increases in ITP may differentially affect preload or afterload if delivered at specific points within the cardiac cycle. We studied the hemodynamic effects of cardiac cycle-specific increases in ITP (pulses) delivered by a high-frequency jet ventilator in an acute closed-chested canine model (n = 11), using electromagnetic flow probes to measure biventricular stroke volume. Measurements were taken during a control condition after the induction of acute ventricular failure (AVF) by propranolol hydrochloride and volume infusion. ITP was independently varied without changing lung volume by the inflation of thoracoabdominal binders. Although synchronous pulses had minimal hemodynamic effects in unbound controls, binding pulses timed to occur in early diastole resulted in decreases in LV filling pressure and left ventricular stroke volume (SVlv) (P less than 0.05). In the AVF condition, pulses increased LV performance, evidenced by increases in SVlv (P less than 0.01), despite decreases in LV filling pressure (P less than 0.05). This effect is maximized by binding and by timing the pulses to occur in systole. We conclude that cardiac cycle-specific increases in ITP can significantly affect cardiac performance. These effects appear to be related to the ability of such timed pulses to selectively affect LV preload and afterload.

End-systolic and end-diastolic ventricular interaction.

Abstract: Right ventricular volume affects left ventricular volume via direct interaction across the interventricular septum and series interaction because the right and left hearts are connected in series through the lungs. Because it is difficult to sort out complex physiological mechanisms in the intact circulation, the relative importance of these two effects is unknown. We used statistical analyses of transient changes in left and right ventricular pressures and dimensions following pulmonary artery and venae caval constrictions to separate and quantitate the direct (immediate) from the series (delayed) interaction effects on left ventricular size at end systole and end diastole. With the pericardium closed, direct interaction was one-half as important as series interaction at end diastole and was one-third as important at end systole. With the pericardium removed, direct interaction was one-fifth as important as series interaction at end diastole and one-sixth as important at end systole. These results suggest that differences between transient and steady-state end-systolic pressure-volume relationships are largely explained by direct interaction and that direct end-systolic interaction is important for maintaining balanced right and left heart outputs.

MRI of the normal pericardium

Abstract: The visibility and thickness of the pericardium, as depicted by MRI, and the changes of these parameters over the cardiac cycle were determined in 18 normal subjects. Gated, cycled, multisection images were obtained in the transaxial orientation. Using a score-point system for quantification, there was better visualization of the low-intensity pericardial line during systole as compared with diastole (p less than 0.005). Pericardial thickness was 1.2 +/- 0.5 mm in diastole and 1.7 +/- 0.5 mm in systole (p less than 0.001) as measured in a midventricular section in front of the right ventricle; both values exceeded the thickness of 0.4 to 1.0 mm reported for anatomic measurements of pericardial thickness. The layer of normal pericardial fluid present in the pericardial space should also have low intensity, and it likely contributes to the overall pericardial thickness as visualized by MRI. Since MRI is sensitive to the small amount of normal pericardial fluid and depicts its anatomic distribution, it should be valuable in detection and quantification of even small pericardial effusions.

Phasic blood flow velocity pattern in epimyocardial microvessels in the beating canine left ventricle.

Abstract: We quantitated phasic epimyocardial microcirculatory coronary blood flow velocity patterns in the beating left ventricle. Using a newly developed floating objective and high-speed cinematography, red cell velocities in small arterioles, capillaries, and small venules and microvascular diameters in the superficial layer of the epimyocardium of beating left ventricle were determined throughout the entire cardiac cycle in open-chest anesthetized dogs. Heart rate was maintained at 140 beats/min by means of left atrial pacing. Peak red cell velocity was observed in midsystole in small arterioles and capillaries, and in late systole in small venules. Abrupt decline in red cell velocity and, in many cases, a momentary cessation or reverse of flow, was observed in these microvessels during the pre-ejection period. The internal diameter of small venule was increased in late systole, while that of small arteriole remained almost constant during the cardiac cycle. Furthermore, in these epimyocardial microvessels, a higher percentage of the total area under the velocity curve occurred during the ejection phase; 51% in small arterioles, 43% in capillaries, and 40% in small venules. These findings indicate that the phasic blood flow pattern is markedly different in the subepimyocardial microvessels from that in the large epicardial artery and the septal artery. During vasodilation following dilazep (50 micrograms/kg, i.v.), an adenosine potentiator, red cell velocity increased throughout the entire cardiac cycle in epimyocardial microvessels with significant increases in the total area under the velocity curves accompanied by significant dilation of the arterioles. The present data will provide information useful in predicting or simulating transmural differences in the phasic blood flow pattern.

Arterial pressure ramps provoke linear increases of heart period in humans

Abstract: A variety of methods has been used experimentally to increase baroreceptor activity and provoke transient, vagally mediated cardiac slowing in humans. We studied baroreceptor-cardiac reflex physiology in eight resting volunteers by measuring R-R interval changes during and after spontaneous brief elevations of arterial pressure, preceded by bursts of muscle sympathetic nerve activity. Arterial pressure was measured with a catheter in a brachial artery, and muscle sympathetic activity was measured with a microelectrode positioned transcutaneously in a peroneal nerve. R-R intervals were related to preceding systolic pressures with linear regression analysis. When systolic pressures were correlated with R-R intervals of the next cardiac cycle, slopes (+/- SE) averaged 12.4 +/- 2.2 ms/mmHg and correlation coefficients averaged 0.81 +/- 0.09. Baroreflex slopes were inversely related to base-line systolic pressures. These results are similar to those obtained when baroreceptors are stimulated experimentally; they suggest that elevations of arterial pressure, which are preceded by bursts of muscle sympathetic activity, trigger with one heart-beat latency highly linear increases of efferent vagal-cardiac nerve activity.

Interatrial conduction during cardiac pacing.

Abstract: DDD pacemakers sense and pace right-sided cardiac chambers. The relationship of atrial to ventricular systole on the left side of the heart is of importance for systemic hemodynamics. Effective atrioventricular synchrony is partially determined by interatrial conduction time (IACT). At the time of DDD pacemaker implantation, interatrial conduction was measured using an intraesophageal pill electrode in 25 patients who were on no cardiac medications. Mean interatrial conduction time for all patients prolonged from 95 +/- 18 ms during sinus rhythm to 122 +/- 30 ms during right atrial pacing (p less than 0.001). In 16 patients with P wave duration less than 110 ms interatrial conduction prolonged from 85 +/- 10 ms during sinus rhythm to 111 +/- 9 ms during right atrial pacing (p less than 0.01) compared to 114 +/- 20 ms prolonging to 111 +/- 19 ms (p less than 0.01) in 9 patients with P wave duration greater than 110 ms. In each patient, while atrioventricular conduction prolonged with incremental right atrial pacing, interatrial conduction times did not vary. Interatrial conduction prolongs from baseline during atrial pacing and remains constant at all paced rates from 60-160 beats per minute. In addition to longer interatrial conduction times during sinus rhythm, patients with electrocardiographic P wave prolongation have longer interatrial conduction times during right atrial pacing than do normals (p less than 0.001). Based on interatrial conduction times alone, the AV interval during DDD cardiac pacing should be approximately 25 ms longer during AV pacing as compared to atrial tracking.

Regional variation in the timing and extent of left ventricular wall motion in normal subjects.

Abstract: Right anterior oblique cineangiograms from 19 subjects without evidence of heart disease were analysed to assess regional non-uniformity in the time of onset of systolic inward motion, amplitude of systolic motion, time of peak inward motion, and wall motion during the isovolumic relaxation period. The left ventricular silhouette was digitised frame by frame for a full cardiac cycle. These four wall motion variables were quantitatively measured along 40 chords drawn from equally spaced points on the end diastolic silhouette to the nearest point on the end systolic silhouette. Onset of systolic inward motion was significantly non-uniform, being delayed by up to 120 ms in the anterior apical chords compared with the areas of earliest inward motion near the base of the heart. More uniformity was noted in time of peak inward motion; the differences between regions were not statistically significant. Amplitude of systolic motion was significantly less at the apical and mid-anterior segments than elsewhere in the heart. Wall motion during the isovolumic relaxation period is outward and greatest in the mid-anterior segments, but inward in the proximal inferior segments and mitral valve region. These data suggest that contraction of muscle fibres in the anterior apical segments is initially isometric due to the considerable afterload at the onset of contraction, this afterload being the result of earlier contraction elsewhere in the ventricle. This may partly explain the propensity for aneurysms to be located in the anterior apical region. When the timing and extent of wall motion in disease states are analysed, account must be taken of the non-uniformity in the normal heart.

Superior vena caval blood flow velocities in adults: a Doppler echocardiographic study.

Abstract: Superior vena caval blood flow velocity was measured in 30 normal adults (age 20–65, mean 36 yr). The flow velocities were measured by pulsed Doppler echocardiography, using a Duplex system with the transducer at the right supraclavicular fossa, approximating a 0 degrees Doppler angle. Four distinct flow waveforms were found during each cardiac cycle: A, a small retrograde flow during right atrial contraction (peak flow velocity 12.4 +/- 2.2 cm/s); B, a small antegrade flow during right atrial relaxation (15.7 +/- 5.0 cm/s); S, a large antegrade flow during ventricular systole (35.2 +/- 7.3 cm/s); and D, a large antegrade flow during ventricular diastole (23.2 +/- 3.1 cm/s). The wave duration was inversely related to heart rate. The peak flow velocities of the S and D waves were inversely related to the patients' ages. This study provides recognition of the pattern and range of normality essential to extension of this noninvasive technique to the diagnosis of pathological conditions.

Assessment of slope of end-systolic pressure-volume line of in situ dog heart.

Abstract: The purpose of this study was to establish a new method of assessment of the slope (Emax) of the end-systolic pressure-volume line (ESPVL) of the in situ heart. In anesthetized open-chest dogs, an isovolumic contraction was produced by an aortic occlusion after steady-state ejecting contractions in the left ventricle. We plotted ventricular pressure measured with a catheter-tip manometer against time integral of aortic flow measured with an electromagnetic flowmeter of the last ejecting and the first isovolumic contraction, assuming the same end-diastolic volume. ESPVL was drawn from the peak isovolumic pressure-volume point tangential to the left upper corner of the +/- 3.0 (SE) mmHg/ml (n = 9 dogs) in control run and was increased by 59 +/- 19% under isoproterenol and decreased by 47 +/- 9% after propranolol. Emax was little changed by atrial pacing. We conclude that Emax by this aortic occlusion method is useful for assessment of left ventricular contractility of the in situ dog heart.

Echocardiographic assessment of tricuspid regurgitation during ventricular demand pacing

Abstract: Twenty patients from our pacemaker clinic population were assessed clinically and by saline contrast echocardiography (subxiphoid view) to determine the prevalence of tricuspid regurgitation (TR) and, if TR was present, its mechanism. The patients had no known TR before lead placement, a single transvenous right ventricular pacing lead present more than 6 months (mean 52, range 7 to 138), ventricular demand pacing alternating with sinus rhythm and rate programmability. Each patient was studied in sinus rhythm and during ventricular pacing. Using the criterion of inferior vena cava (IVC) contrast reflux during ventricular systole to diagnose TR, no patient had evidence of TR in sinus rhythm, consistent with clinical examination. During ventricular demand pacing, jugular venous pulse cannon A waves developed in 10 patients, and 18 patients (including these 10) had IVC contrast reflux during ventricular systole. Analysis of the timing of IVC reflux revealed its close temporal relation to the timing of atrial systole rather than a fixed timing during ventricular systole. This reflux occurred with loss of normal atrioventricular (AV) synchrony and the underlying mechanism in all cases was shown to be right atrial contraction against a closed tricuspid valve. Two patients who did not have such a pattern with pacing maintained normal AV synchrony. These observations indicate that: (1) TR is an uncommon accompaniment of ventricular demand pacing; (2) the jugular venous pulse and IVC echocardiographic contrast patterns during ventricular demand pacing simulate TR when AV synchrony occurs; and (3) the IVC contrast pattern of pacing-induced AV synchrony is best termed the cannon A wave synchronous pattern.

Mitral valve closure and left ventricular filling time in patients with VDD pacemakers: assessment of the onset of left ventricular systole and the end of diastole

Abstract: The effect of mitral valve closure on left ventricular filling time and its relation to the onset of systole were assessed from mitral valve echocardiograms and simultaneous apex cardiograms in 21 normal subjects, 11 patients with left bundle branch block, and 19 patients with VDD pacemakers programmed for atrioventricular intervals of 50, 150, and 250 ms. The interval between the electrocardiograph Q wave and the apex cardiogram upstroke was similar in normal subjects and patients with left bundle branch block, but was significantly longer in patients with VDD pacemakers at all atrioventricular intervals. Similarly there was little difference in the time interval between the Q wave and mitral valve closure in normal individuals and patients with left bundle branch block but this was considerably delayed in VDD pacemaker patients with the atrioventricular interval set at 50 ms. With increasing atrioventricular intervals the mitral valve closed significantly earlier, whereas the onset of left ventricular systole and the timing of mitral valve opening remained unchanged. Thus as a result of earlier mitral valve closure left ventricular filling time decreased progressively as the atrioventricular interval was increased. Since the onset of left ventricular systole, with respect to left ventricular stimulation, is considerably delayed in VDD pacemaker patients a short atrioventricular interval is required in these patients to maintain the normal time relations between atrial and ventricular contraction and hence maximise left ventricular filling.

Central thrombi in pulmonary arterial hypertension detected by MR imaging.

Abstract: Differentiation of thrombi from slow flow in the pulmonary arteries, sometimes observed in the presence of pulmonary arterial hypertension, can be equivocal. Magnetic resonance (MR) imaging was performed in a patient with chronic pulmonary thromboembolism and pulmonary arterial hypertension using an electrocardiographically gated technique that allowed visualization of the pulmonary arteries at the end of diastole and multiple times during systole. These images were compared with those of a patient with primary pulmonary hypertension and those of healthy subjects. Thrombi were discrete structures, seen throughout the cardiac cycle on both the first and second spin-echo images, and decreased in signal intensity on the second image. Slow flow increased in signal intensity and changed in structure during the cardiac cycle and was seen best on the second image. MR may play an important role in excluding large central thrombi as the cause of pulmonary arterial hypertension. It is a noninvasive method for defining pulmonary arterial wall thickness and for direct visualization of chronic pulmonary thrombus.

Development of aortic and mitral valve continuity in the human embryonic heart.

Abstract: The anatomic relationship of the aortic and mitral valves is a useful landmark in assessing congenital heart malformations. The atrioventricular and semilunar valve regions originate in widely separated parts of the early embryonic heart tube, and the process by which the normal fibrous continuity between the aortic and mitral valves is acquired has not been clearly defined. The development of the aortic and mitral valve relationship was studied in normal human embryos in the Carnegie Embryological Collection, and specimens of Carnegie stages 13, 15, 17, 19, and 23, prepared as serial histologic sections cut in the sagittal plane, were selected for reconstruction. In stage 13, the atrioventricular valve area is separated from the semilunar valve area by the large bend between the atrioventricular and outflow-tract components of the single lumen heart tube created by the left interventricular sulcus. In stages 15 and 17, the aortic valve rotates into a position near the atrioventricular valves with development of four chambers and a double circulation. In stage 19, there is fusion of aortic and mitral endocardial cushion material along the endocardial surface of the interventricular flange, and this relationship is maintained in subsequent stages. Determination of three-dimensional Cartesian coordinates of the midpoints of valve positions shows that, while there is growth of intervalvular distances up to stage 17, the aortic to mitral distance is essentially unchanged thereafter. During the period studied, the left ventricle increases in length over threefold. The relative lack of growth in the saddle-shaped fold between the atrioventricular and outflow tract components of the heart, contrasting with the rapid growth of the outwardly convex components of most of the atrial and ventricular walls, may be attributed to the different mechanical properties of the two configurations. It is postulated that the pathogenesis of congenital heart malformations, which characteristically have failure of development of aortic and mitral valve continuity, may involve abnormalities of rotation of the aortic region or malpositioning of the fold in the heart tube.

Spatial Velocity Distributions in the Ascending Aorta of Healthy Humans and Cardiac Patients

Abstract: Blood velocity profiles in the human ascending aorta were assessed with the aid of ultrasonic Doppler echocardiography. To this end, the transducer was placed in the suprasternal notch, and the spatial velocity profiles along an axis passing through the center of the aortic cross section were recorded by a multigate Doppler instrument. The profiles are analyzed with respect to characteristics independent of the angle of incidence and the cross sectional area. Data from 10 healthy individuals, 10 patients with hypertrophic obstructive cardiomyopathy (HOCM), and 10 patients with severe aortic insufficiency (AI) are compared. Five instantaneous profiles recorded at different times during systole and the temporal average of all profiles recorded during the entire cardiac cycle at 16 ms intervals are examined. Considerable differences between the three groups of subjects are observed visually as well as quantitatively in terms of specific parameters. The representation of the velocity maps in the form of contour graphs is particularly incisive. The results demonstrate that the temporal velocity patterns measured depend, in general, on both the disease and the location of the sampling volume within the aortic lumen. Reliable aortic volume flow rate measurements may have to be based on a method which takes into account the velocity at every point of the entire vascular cross section of patients with HOCM or AI.

Development of the atrioventricular valve region in the human embryo

Abstract: Severe cardiac malformations may involve the atrioventricular valve region, but the sequence of embryonic development of this important area has been little studied. In particular, the basis of atrioventricular muscular discontinuity, except at the conduction system, has remained unexplained. To examine this question, serial histologic sections of human embryos from the Carnegie Embryo-logical Collection and from the Hopkins Pathology Collection were studied and six embryos were reconstructed. The atrioventricular sulcus can be identified in Carnegie stage 10 as an indentation or crease on the right side separating the heart tube from the umbilical vein. By stage 12 the sulcus has deepened and rotated anteriorly as the atria appear and the heart tube elongates rapidly within the confining pericardial space. Selective accumulation of cardiac jelly on the endocardial aspect of the constriction of the heart tube produced by the atrioventricular sulcus is pronounced by stage 14. By stage 16 the separation of the atrioventricular orifice into right and left components is well advanced, and by stage 18 the septation of the atria and ventricles is largely complete. The muscular connection between the atria and the ventricles becomes interrupted around most of the artioventricular sulcus, except for the His bundle, during the latter part of the embryonic period. The topography of the original sulcus assumes a catenoidal or saddle-shaped configuration, i.e., convex in one plane and concave in the perpendicular plane. The tension and pressure relationships in such a structure would favor cardiac jelly accumulation and the eventual disintegration of lines of myocyte connections passing across the groove. The preservation of the His bundle connection is explained by the failure of the sulcus to completely encircle the heart.

Rate responsive pacing using the magnitude of the repolarization gradient of the ventricular gradient

Abstract: A rate responsive cardiac pacing system is provided. In the illustrative embodiment, electrical stimulus pulses are applied to the heart ventricle and the evoked potential of the applied electrical stimulus pulses is detected. The detected potential is integrated over time to obtain a repolarization gradient magnitude. The repolarization gradient magnitude is compared with a corresponding repolarization gradient magnitude of at least one previous cardiac cycle. The rate of the electrical stimulus pulses is controlled in response to this comparison.

Comparative aspects of the dual role of the human atrioventricular node.

Abstract: As well as transmitting the impulse from the atria to the ventricles the atrioventricular node has two other important functions namely: synchronisation of atrial and ventricular contractions by a varying delay; and protection of the ventricles from rapid atrial arrhythmias. The relative importance of these two functions appears to differ in large and small mammalian hearts. In small mammals synchronisation of atrial and ventricular contractions is the major function of the atrioventricular node, whereas protection from rapid atrial arrhythmias may be its most important function in large mammals. Atrioventricular conduction time in sinus rhythm is ten times longer in the whale (500 ms) than in the rat (50 ms). A whale heart, however, is about 100 000 times heavier than a rat heart. During atrial fibrillation the ventricular rate in a dog heart is only three times faster than in a horse, whereas a horse heart may be 40 times as heavy as that of a dog. Hence there is a considerable discrepancy between the size of the mammalian heart and the functions of its atrioventricular node. Analysis of several anatomical and functional aspects of atrioventricular conduction systems in mammals of all sizes showed that the importance of the delaying role of the atrioventricular conduction system diminishes as the size of the mammal increases, whereas the protective role of the atrioventricular node probably increases. The function of the human atrioventricular node seems to be intermediate between that of of the small and large mammals.

Rate responsive pacing system using the integrated cardiac event potential

Abstract: A rate responsive cardiac pacing system is provided. In the illustrative embodiment, electrical stimulus pulses are applied to the heart ventricle and the evoked potential of the applied electrical stimulus pulses is detected. The detected potential is integrated over time to obtain a depolarization gradient magnitude. The depolarization gradient magnitude is compared with a corresponding depolarization gradient magnitude of at least one previous cardiac cycle. The rate of the electrical stimulus pulses is controlled in response to this comparison.