Showing papers on "Cardiac cycle published in 1983"

Atrial systole and left ventricular filling in hypertrophic cardiomyopathy: Effect of verapamil

Abstract: Many patients with hypertrophic cardiomyopathy (HC) have impaired left ventricular (LV) rapid diastolic filling. To quantitate the contribution of atrial systole to LV filling, we used radionuclide angiography to study 30 normal volunteers and 42 patients with HC before and after oral administration of verapamil (320 to 560 mg/day). LV time-activity curves were constructed by combined forward and reverse gating from the R wave, and the onset of atrial systole was determined by the P-R interval. The percent of LV stroke volume filled during rapid diastolic filling and atrial systole was then computed. Peak LV filling rate during rapid diastolic filling was expressed in end-diastolic volume (EDV)/second. Peak rate of rapid diastolic filling was not different in normal patients and those with HC (3.3 +/- 0.6 versus 3.3 +/- 1.1 EDV/s) and was within the normal range in 34 patients with HC (81%). However, the contribution to LV filling volume by rapid diastolic filling was diminished in patients with HC (83 +/- 7% normal, 67 +/- 17% HC, p less than 0.001) and the contribution of atrial systole was increased (16 +/- 8% normal, 31 +/- 18% HC, p less than 0.001). LV filling volume during atrial systole was above the upper normal limit of 31% in 17 patients (40%), including 13 patients with a normal peak filling rate. After verapamil, peak filling rate increased (to 4.2 +/- 1.2 EDV/s, p less than 0.001), percent LV filling during rapid diastolic filling increased (to 83 +/- 7%, p less than 0.001), and percent LV filling during atrial systole decreased (to 16 +/- 9%, p less than 0.001). Percent LV filling volume during atrial systole was abnormal after verapamil in only 3 patients (7%). Hence, although the peak rate of rapid diastolic filling may be normal in patients with HC, the contribution to LV filling by rapid diastolic filling is reduced and that of atrial systole is thereby increased. Increased rate and magnitude of rapid diastolic filling during verapamil is associated with decrease and normalization of the contribution of atrial systole to LV filling. These data suggest that many patients with HC are at risk of hemodynamic decompensation with the onset of atrial fibrillation or other tachyarrhythmias and loss of the atrial contribution to LV filling. This risk may be reduced during verapamil therapy.

The mitral valve orifice method for noninvasive two-dimensional echo Doppler determinations of cardiac output.

Abstract: We developed and validated a mitral valve orifice method for Doppler cardiac output determination. In 15 open-chest dogs, cardiac output was controlled and measured by a roller pump interposed between the right atrium and pulmonary artery as a right-heart bypass. Left heart flows were measured in the open-chest dog model by Doppler measurements at the mitral valve orifice and compared not only to volume flow measured by the roller pump, but to electromagnetic flow meters as well. The maximum mitral valve orifice area was measured off short-axis two-dimensional echocardiographic views by planimetry. The maximal orifice was then adjusted for its diastolic variation in size by calculating a ratio of mean-to-maximal mitral valve separation on a derived M-mode echocardiogram. Flow was sampled parallel to mitral valve inflow in a four-chamber plane. The multiplication of mean flow throughout the cardiac cycle by the mean mitral valve area after correction for diastolic size variation yielded a cardiac output determination that could be compared to the roller pump measurement. Fifty-two cardiac output determinations over roller pump values of 1-5 l/min yielded a high correlation between roller pump flows and Doppler (r = 0.97 +/- 0.23 l/min). Our study shows that the mitral valve orifice provides an accurate site for Doppler cardiac output measurements.

Dynamic ventricular interaction in the conscious dog.

Abstract: In nine conscious, chronically instrumented dogs, ultrasonic dimension transducers measured left ventricular anterior-posterior and septal-free wall minor axis and major axis diameters. Matched micromanometers measured right and left ventricular transmural and transeptal pressures. Ventricular pressures and volumes were varied by inflation of implanted vena caval and pulmonary artery occluders, and the functional significance of the two types of ventricular interaction, i.e., direct and series, was determined. The left ventricle was represented by a modified ellipsoidal geometry. Left ventricular stroke volume calculated from the dimension data correlated well with that measured directly from ascending aortic electromagnetic flow probes during all interventions (r greater than or equal to 0.96). Partial pulmonary artery occlusion significantly increased right ventricular diastolic and systolic pressures as compared to values obtained during control and venal caval occlusion. During pulmonary artery occlusion, latitudinal septal eccentricity was increased throughout the cardiac cycle compared to control and vena caval occlusion (P less than 0.05), indicating leftward interventricular septal shifting and significant alteration of left ventricular shape. The normalized diastolic pressure-volume curve was shifted to the left with pulmonary artery occlusion compared to control and indicated a decrease in left ventricular chamber compliance. However, when selected cardiac cycles with similar end-diastolic volumes from vena caval and pulmonary artery occlusions were compared, parameters of left ventricular systolic function (stroke volume, percent systolic shortening, peak aortic blood flow, peak left ventricular pressure, and its first derivative) remained relatively constant. These data suggest that mean myocardial fiber length is the major preload determinant of left ventricular systolic function independent of chamber pressure and shape, and that direct ventricular interaction mediated by interventricular septal shifting has minimal effects on systolic myocardial performance in this model. Thus, series ventricular interaction during acute imbalances in biventricular loading, where the output of the right ventricle determines the input of the left, seems to be far more important than direct interaction to the regulation of overall cardiac function.

The effect of variations of pulsed Doppler sampling site on calculation of cardiac output: an experimental study in open-chest dogs.

Abstract: We measured aortic flow by two-dimensional Doppler echocardiography in an open-chest dog model to examine how variations in Doppler sample volume length and position influence aortic hemodynamic flow calculations. Fourteen dogs underwent right-heart bypass, in which venous return from the venae cavae drained by gravity to a reservoir. A variable-speed roller pump returned the blood to the pulmonary artery, fixing left-sided cardiac input and output. Echo Doppler measurements were performed using a 3.5 MHz transducer placed directly on the aortic arch to determine internal aortic cross-sectional area. The transducer was then directed to image the aortic arch for Doppler velocity measurements and the various sampling sites were investigated. Doppler cardiac output could then be determined for each of the various sample volumes over a range of known roller pump settings. Doppler velocity was analyzed using fast Fourier transform spectral analysis. Mean velocity over the cardiac cycle was obtained by planimetry of the area under the Doppler velocity curve with a minicomputer. Doppler-derived determinations of cardiac output achieved a correlation of r = 0.98-0.99 to values obtained by the roller pump over a range of cardiac outputs from 0.75-5 l/min. The standard error of the estimate was 0.21/min. In this laminar flow model, there was no difference between the predictive accuracy of any of the sampling sites over the range of roller pump flows. Our study shows that Doppler velocity measurements can be used to quantify aortic flow over a clinically useful range and that variations of sample length and position did not produce significant differences in calculated flows.

Influence of atrial systole on the Frank-Starling relation and the end-diastolic pressure-diameter relation of the left ventricle.

Abstract: The influence of atrial systole on the left ventricular function curve (stroke volume vs end-diastolic pressure or end-diastolic diameter) and on the left ventricular end-diastolic pressure diameter relation was studied in nine anesthetized, open-chest dogs whose atrioventricular (AV) node had been completely blocked. Measurements were made during volume loading with the pericardium closed and opened and during alternate AV sequential pacing (to permit atrial contribution to ventricular filling) and AV simultaneous pacing (to prevent atrial contribution). When the pericardium was closed, withdrawal of the atrial contribution shifted the stroke-volume end-diastolic pressure relation downward, but did not shift the stroke volume-end-diastolic diameter relation, i.e., it reduced stroke volume for a given end-diastolic pressure according to a reduction in end-diastolic volume. The downward shift of the stroke volume-end-diastolic pressure relation was caused by an upward shift of the end-diastolic pressure-diameter relation, which, for a given end-diastolic pressure, resulted in a smaller end-diastolic diameter and, thus, in a smaller stroke volume. The reason for the upward shift in the end-diastolic pressure-diameter relation was that the atrium remained full and thus increased pericardial pressure by increasing pericardial volume. Opening the pericardium shifted the end-diastolic pressure-diameter relation downward and to the right, shifted the stroke volume-end-diastolic diameter relation upward and abolished the effect of withdrawal of the atrial contribution on these curves. We conclude that in the presence of an intact pericardium, atrial systole shifts the stroke volume-end-diastolic pressure relation because it shifts the end-diastolic pressure-diameter relation and it improves left ventricular performance by increasing preload.

Method and device for enhancement of cardiac contractility

Abstract: An apparatus for ultrasonic irradiation of the heart either when the chest is open after surgery or through the chest wall. It may also be used in conjunction with electrical defibrillation equipment or alone. The apparatus includes an EKG for detecting the heart beat, an ultrasonic generator and timing and pulsing circuits for providing timed pulses of ultrasound to coincide with selected events in the cardiac cycle.

Endocardial pacing site affects left ventricular end-diastolic volume and performance in the intact anesthetized dog.

Abstract: We investigated how pacing from different endocardial sites affects the left ventricular three-dimensional contraction pattern and performance in intact anesthetized dogs. We used data from the motion of radiopaque markers implanted in the left ventricular endocardium in an analysis based on the polar decomposition theorem to determine the left ventricle's three-dimensional principal directions and magnitudes of deformation, and its axis and angle of rotation during the cardiac cycle. This paper also derives a new procedure that permits statistical comparison of different left ventricular cavity deformation patterns. During normal sinus rhythm and pacing from the right atrium, left ventricular septum, left ventricular apex, and right ventricular apex, the principal directions of left ventricular deformation remained relatively fixed with respect to the left ventricle's anatomy, independent of heart rate and pacing site. These directions were oriented in septum-free wall, anterior-posterior, and apex-base directions. End-systolic pressure and volume did not vary significantly among pacing sites. End-diastolic volume varied significantly among pacing sites, with right ventricular apical pacing producing the smallest end-diastolic and stroke volume. These results reveal that beats produced by right ventricular apical pacing eject less blood compared with beats produced by right atrial, left ventricular septal, or left ventricular apical pacing.

Quantitative relation between sites of atrial impulse origin and cycle length

Abstract: Having previously described the multicentric origin of the atrial impulse from sites widely distributed over the right atrium as well as an intrinsic link between these sites of origin and cycle length (CL), we undertook a quantitative study of this relationship. In 132 dogs anesthetized with pentobarbital sodium or fentanyl citrate, we recorded atrial activation sequence maps from 360 closely positioned electrodes and determined locations of impulse origin at heart rates between 80 and 240 (CL between 750 and 250). We used cardiac nerve stimulation and agonist-antagonist infusion to produce changes in CL and impulse origin. Results demonstrate a significant correlation between site of impulse origin and CL. These sites, associated with both the sinus node (SN) and extranodal sites, function predictably and consistently controlling impulse initiation at heart rates above and below rates at which the SN predominates. This relationship can be used to specify an anatomic-functional model of atrial pacemaker hierarchy and to quantitate the response of different atrial regions to specific pharmacological and physiological interventions.

Maximal Rate of Tachycardia Development: Sinus Tachycardia with Sudden Exercise vs. Spontaneous Ventricular Tachycardia

Abstract: In addition to providing basic physiologic information, knowledge of the maximal rate of sinus tachycardia development may be helpful in developing algorithms permitting new generations of antitachycardia pacemakers to distinguish accurately between sinus and ventricular tachycardia. To determine the maximal rate of sinus tachycardia development, 50 normal subjects rushed up 100 stairs as rapidly as possible, with continuous electrocardiographic monitoring. During the first second of exercise, the mean cardiac cycle length shortened from 709 to 570 ms, equivalent to an increase in heart rate from 85 to 105 beats per minute, or 20 beats per minute per second. Thereafter, a more gradual decrease in cycle length occurred. Differences between men and women, smokers and non-smokers, and sedentary compared to active subjects were all insignificant. Analysis of 50 spontaneous episodes of ventricular tachycardia also revealed a sequential but more abrupt decrease in the cycle length during the first second from 757 to 360 ms, equivalent to a rate increase from 79 to 167 beats per minute, or 88 beats per minute per second. After approximately 1 1/4 seconds, the ventricular tachycardia cycle length remained virtually constant. Baseline cycle lengths were similar in the sinus and ventricular tachycardia groups, but differed in all subsequent beats, although overlap for individual subjects did occur.

Assessment of left atrial dimensions by cross sectional echocardiography in patients with mitral valve disease.

Abstract: Left atrial dimensions were measured using cross sectional echocardiography in 37 patients with mitral valve disease and 30 normal subjects of similar ages. The anteroposterior (AP), superior-inferior (SI), and medial-lateral (ML) left atrial dimensions were determined at the end of ventricular systole using parasternal long and short axis and apical four chamber views (for SIa and MLa). To assess the reliability of these measurements cross sectional echocardiographic and angiographic left atrial volumes were compared in 19 patients with mitral valve disease, giving an excellent correlation. A moderate correlation was found between the anteroposterior dimension of the left atrium obtained using M mode echocardiography and that obtained using the parasternal short axis and long axis projections. In normal subjects a good correlation was found between SI and ML dimensions, while a lower correlation was found between SI and AP, and ML and AP dimensions. The SI dimension was the major axis of the left atrium and AP dimension the minor axis. In patients with mitral valve disease a good correlation was found between SI and ML dimensions, while SI and ML dimensions had a low correlation with AP dimensions. The AP dimension was the minor axis of the left atrium, while the SI and ML dimensions were not significantly different. All left atrial dimensions were significantly greater in patients with mitral valve disease than in normal subjects. Of 30 patients with at least one dimension increased, all three dimensions were abnormal in 16, two dimensions were increased in 10, and only one dimension was increased in four. AP, SI, and ML dimensions were abnormal in 25, 20, and 27 patients, respectively. Cross sectional echocardiography may provide a reliable estimate of left atrial dimensions. In patients with mitral valve disease a thorough examination of the left atrium using multiple cross sectional views is necessary to detect asymmetric left atrial enlargement and to measure the degree of left atrial dilatation.

Diastolic "locking" of the mitral valve: the importance of atrial systole and intraventricular volume.

Abstract: Diastolic mitral valve "locking," defined as sustained diastolic closure of the mitral valve after atrial systole, was investigated by simultaneous hemodynamic and echocardiographic recordings during a protocol of programmed pacing in six dogs with surgically induced atrioventricular block. Atrial extrasystoles were introduced at progressively increasing coupling intervals during programmed prolonged pauses in ventricular pacing. As the coupling interval of the atrial extrasystole was increased, both the mitral reopening time (MRT) and the calculated left ventricular volume (LVV) at the end of the MRT increased proportionally. These interrelations could be best expressed by a general logarithmic function of the form y = a + b ln (x), where x = the coupling interval of the atrial extrasystole and y = the MRT or the LVV. Correlations between the measured data and the predicted data were excellent (r greater than or equal to 0.95). In each dog, a specific LVV had to be attained to allow a diastolic "locking" of the mitral valve. Atrial standstill and atrial fibrillation were also induced in each dog to study the relative role of atrial systole in locking of the mitral valve. During either atrial standstill or atrial fibrillation, the mitral valve closed transiently, but did not lock, despite the accumulation of a LVV larger than the LVV necessary to lock the valve during sinus rhythm. Thus, diastolic locking of the mitral valve has several determinants, including the presence of active atrial systole and the accumulation of a sufficient intraventricular volume.

Left bundle branch block and mechanical events of the cardiac cycle

Abstract: Left bundle branch block (LBBB) is associated with a prolongation of the interval from the QRS onset to the onset of left ventricular (LV) ejection. The locus and prevalence of specific sites of delay were examined in 56 patients with complete LBBB using echocardiography, phonocardiography and external pulse recordings. The results were compared with those in 52 control subjects without LBBB. The onset of the QRS complex was used as the initial reference point of measurement of time intervals. The following abnormalities were found in patients with LBBB: (1) delayed mitral valve closure (Q-MC greater than 0.08 second) was the major site of delay in 23% of patients; (2) prolongation of the LV isovolumetric contraction time (greater than 0.06 second) was the major site of delay in 41%; (3) both Q-MC and LV isovolumetric contraction time were prolonged in 18%; and (4) in 26% of patients the onset of ventricular contraction determined by the onset of the increase of the apex impulse was delayed (Q-VC greater than 0.07 second). The most common cause of delayed ejection was a prolonged LV isovolumetric contraction time, which occurred in 59% of patients. A control group of 20 patients with abnormal LV function but without LBBB had a low incidence of the 3 types of delay in LV ejection (0 to 15%). Thus, the major abnormalities in the cardiac cycle in LBBB are due to the conduction defect and not to LV dysfunction. The results of this study suggest the presence of variable abnormalities of conduction in complete LBBB.

Phasic effects of repetitive vagal stimulation on atrial contraction.

Abstract: The vagus nerves of anesthetized dogs were stimulated once each cardiac cycle with a brief burst of pulses, and the timing of the stimulus bursts was changed by a fixed increment on successive cardiac cycles. The effects of such vagal stimulation on atrial contraction depended on the number of pulses per stimulus burst, on the interval between pulses within the burst, and on the timing of the stimulus bursts within the cardiac cycle. The vagal stimulus bursts had the least negative inotropic effect when they were given less than 100 msec before the next atrial depolarization, and they were most effective when given about 330 msec before the next atrial depolarization. This dependence of the inotropic response on the timing of the vagal activity within the cardiac cycle indicates that the following conditions must prevail with respect to the vagal innervation of the atrium: (1) the acetylcholine released from the vagal nerve endings is hydrolyzed at a critically rapid rate in the atrial tissues, (2) the neurally released acetylcholine must exert its major influence on atrial contraction during some preferential fraction of the cardiac cycle (presumably, during depolarization), and (3) after a vagal stimulus of a given strength, the concentration of acetylcholine in the region of the myocardial cells will attain its maximum value during this critical phase of the cardiac cycle when the vagal stimuli are given at the optimal time in the cardiac cycle.

Sheep cardiac Purkinje fibers: configurational changes during the cardiac cycle.

Abstract: Previous attempts to study the cytoarchitecture of cardiac Purkinje fibers with the scanning electron microscope (SEM) have been limited by the surrounding dense connective tissue. In this study the connective tissue was removed by treatment with 8N HCl, after adult sheep hearts were fixed in diastole or systole and tissue taken for SEM and transmission electron microscopy (TEM). In SEM, Purkinje fibers freely anastomosed in false tendons and formed a subendocardial plexus. In systole, medium and small-sized Purkinje fibers formed deep clefts not observed in diastole. The clefts are thought to be due to sarcolemmal folding and fiber buckling and may therefore affect conduction. The myofibrils beneath the laterally apposed sarcolemmas of adjacent Purkinje cells when fixed in systole were often observed as tightly curved arches in series. Similar configurations with expanded arches were observed in diastole. The formation of arches by myofibrils is unique to Purkinje fibers and is interpreted as the mechanism responsible for their compliance to stretch. The significance of contraction in producing the observed geometric changes in Purkinje fibers and the implications of their cytoarchitecture with respect to conduction are discussed.

Muscle pathway geometry in the heart wall

Abstract: Muscle fiber pathways in the heart wall are described. Procedures are introduced which permit data to be standardized from cadaver and animal hearts fixed at different points of the cardiac cycle or obtained in vivo from patients with different ejection fractions and heart masses. Design criteria are also developed here to construct a hypothetical standard left ventricle to compare the data from different hearts. The equations allow the nested set of toroidal fiber-shells to be depicted with typical muscle fiberpaths. With this formulation the heart wall and typical elements in it can be shown computergraphically as they move from the contracted state to the distended. Man-made fiber structures that simulate the fail-safe shockload absorbing features of the heart can now be designed and tested computergraphically by use of the mathematical procedures described here.

The valve of the foramen ovale in interatrial right-to-left shunt: echocardiographic cineangiocardiographic and hemodynamic observations.

Abstract: In postpartum persistent right-to-left shunt at the atrial level, the valve of the foramen ovale fails to close. As a thin valve-flap the septum primum is pushed to the left during the phases of right atrial pressure predominance and closes to the septum secundum, when left atrial pressure exceeds right atrial pressure. Thus, it performs a marked movement during the cardiac cycle, reflecting the interatrial pressure-flow dynamics. With use of M-mode echocardiography, this movement pattern was studied in 24 patients: 13 with cyanotic heart disease (age 2 days to 21 years) and 11 newborns with persistent transatrial right-to-left shunt due to noncardiac disease. Cardiac defects were confirmed by cardiac catheterization and cineangiocardiography. Interatrial right-to-left shunts were proved by M-mode and 2-dimensional contrast echocardiography. The comparison of the M-mode echocardiographic findings in our patient groups with normal atrial septal movement studied in 20 healthy infants and children revealed considerable differences. The characteristic movement of the valve of the foramen ovale also was compared with results obtained by cineangiography and 2-dimensional echocardiography. Analysis of interatrial blood pressure difference provided a pathophysiologic explanation of the septum primum movement in transatrial right-to-left shunt.

Prosthetic mitral valve motion during cardiac dysrhythmias as determined by echocardiography.

Abstract: To assess the changes and physiologic mechanisms of prosthetic valve motion during cardiac dysrhythmias as well as the role of atrial systole in the closure of the mitral valve, M-mode echocardiography was performed in 36 patients with normally functioning prosthetic mitral valves (Bjork-Shiley, Starr-Edwards, and Beall valve). Premature closure of the prosthetic mitral valve in diastole with a "sharp" closing motion was seen during first-degree atrioventricular block, atrial fibrillation with ventricular rates less than 60 beats/min, and atrial flutter. A "rounded" premature valve closure due to atrial systole was seen during atrial tachycardia and complete heart block. Atrial systole initiates a closing motion of the prosthetic mitral valve at end-diastole, and ventricular systole completes this closure during normal sinus rhythm. When first-degree atrioventricular block is present, atrial systole alone completes this closure before ventricular contraction. Atrial contraction alone also can effectively close the prosthetic mitral valve during atrial flutter and atrial tachycardia. Other factors (such as left ventricular diastolic volume) may play a role in the effective closure of the prosthetic mitral valve during atrial fibrillation with slow ventricular rates and complete heart block. These findings must be considered in the echocardiographic evaluation of suspected malfunctioning prosthetic mitral valves. A baseline postoperative echocardiogram after prosthesis insertion is important for future evaluation when clinically indicated.

Estimation of instantaneous blood flow through a rigid, coronary artery stenosis in anaesthetised domestic swine

Abstract: This study tested the hypothesis that instantaneous coronary flow rate (Q) through a severe rigid coronary artery stenosis of known dimensions can be reliably estimated by measuring the instantaneous pressure gradient (ΔP) across the stenosis. A non-linear model for stenosis ΔP was employed (Δ P=RQ+SQ2, where R and S are constants describing stenosis geometry). Flow rate was determined by solving for the positive root of the quadratic equation, Q=(−R+√R2+4S (ΔP))/2S. Four open chest, anaesthetised, domestic swine were studied. A 7.0 mm long rigid stenosis (82% reduction in vessel diameter) was placed in the left anterior descending (LAD) coronary artery. Pressure distal to the stenosis was obtained with a fluid filled catheter (ID=1.4 mm) the distal end of which was secured within and open to the distal end of the stenosis. Aortic pressure corrected for phase delay in the time domain was taken as pressure proximal to the stenosis. An electromagnetic (EMF) flow probe positioned just proximal to the stenosis measured instantaneous flow. All pressure wave forms and the EMF flow signal were digitised on line and transmitted to a computer for analysis. Simultaneous computed and EMF flows for an average cardiac cycle were obtained in each animal: 1) at control; 2) after 10 min of adenosine infusion into the distal LAD; and 3) at a second control period. Computed and measured flow signals were compared on a point by point basis (5 ms resolution). The correlation coefficient (r) was 0.94±0.04 (mean±1SD) for the entire cycle (P<0.0001), 0.86±0.09 for systole (P<0.001) and 0.97±0.04 for diastole (P<0.0001). The absolute value of mean flow rate computed (0.50±0.15, cm3·s−1) correlated well (r=0.95, P<0.001), with mean flow rate measured (0.53±0.22). Computed mean diastolic flow rate (0.64±0.15) also correlated well (r=0.79, P<0.002) with measured mean diastolic flow rate (0.69±0.21). Thus, instantaneous coronary blood flow through a severe, rigid stenosis of known dimensions can be reliably estimated from instantaneous measurement of stenosis pressure gradient and a non-linear, quadratic model of stenosis pressure-flow relations.

Effects of cardiac contraction on segmental coronary resistances and collateral perfusion.

Abstract: This study examined the reactions of coronary arteries and microvessels to changes in left ventricular pressure, as well as their significance for collateral circulation. Collateral perfusion pressure was measured as peripheral coronary pressure of an occluded coronary artery after embolisation of its terminal vascular bed with 20 micron microspheres in 9 anesthetized dogs. With measurement of collateral perfusion pressure it was then possible to determine the segmental coronary resistances of the coronary arteries and the microvasculature. Left ventricular pressure was increased by aortic clamping during autoregulation and after maximal pharmacological dilation of the coronary circulation. During autoregulation, the increase in left ventricular pressure induced a resistance decrease mainly in the postcollateral microvessels. With maximal vasodilation, the increase in left ventricular pressure induced a resistance increase mainly in the postcollateral microvessels. Finally with ventricular fibrillation, the resistance of the postcollateral microvasculature was markedly decreased. We conclude that both metabolic regulation of coronary blood flow and extravascular compression of coronary circulation by cardiac contraction act predominantly on postcollateral microvessels. Coronary collateral circulation may be impaired at increased left ventricular pressure.

Doppler Ultrasound Measurement of Cardiac Output in Patients with Physiologic Dual Chamber Pacemakers

Abstract: Dual chamber pacemakers have recently come into widespread use. They offer practical advantages in restoring atrio-ventricular synchrony and in allowing rate variability in response to physiologic stresses. Doppler ultrasound allows non-invasive assessment of cardiac output in man. We used this technique to determine the changes in resting cardiac output itt patients with DDD pacemakers when the mode of pacing was varied from VVI to DDD at fixed heart rates.