Left Ventricular Ejection Pressure Research Articles

Validation of the pulse decomposition analysis algorithm using central arterial blood pressure.

BackgroundThere is a significant need for continuous noninvasive blood pressure (cNIBP) monitoring, especially for anesthetized surgery and ICU recovery. cNIBP systems could lower costs and expand the use of continuous blood pressure monitoring, lowering risk and improving outcomes.The test system examined here is the CareTaker® and a pulse contour analysis algorithm, Pulse Decomposition Analysis (PDA). PDA’s premise is that the peripheral arterial pressure pulse is a superposition of five individual component pressure pulses that are due to the left ventricular ejection and reflections and re-reflections from only two reflection sites within the central arteries.The hypothesis examined here is that the model’s principal parameters P2P1 and T13 can be correlated with, respectively, systolic and pulse pressures.MethodsCentral arterial blood pressures of patients (38 m/25 f, mean age: 62.7 y, SD: 11.5 y, mean height: 172.3 cm, SD: 9.7 cm, mean weight: 86.8 kg, SD: 20.1 kg) undergoing cardiac catheterization were monitored using central line catheters while the PDA parameters were extracted from the arterial pulse signal obtained non-invasively using CareTaker system.ResultsQualitative validation of the model was achieved with the direct observation of the five component pressure pulses in the central arteries using central line catheters. Statistically significant correlations between P2P1 and systole and T13 and pulse pressure were established (systole: R square: 0.92 (p < 0.0001), diastole: R square: 0.78 (p < 0.0001). Bland-Altman comparisons between blood pressures obtained through the conversion of PDA parameters to blood pressures of non-invasively obtained pulse signatures with catheter-obtained blood pressures fell within the trend guidelines of the Association for the Advancement of Medical Instrumentation SP-10 standard (standard deviation: 8 mmHg(systole: 5.87 mmHg, diastole: 5.69 mmHg)).ConclusionsThe results indicate that arterial blood pressure can be accurately measured and tracked noninvasively and continuously using the CareTaker system and the PDA algorithm. The results further support the physical model that all of the features of the pressure pulse envelope, whether in the central arteries or in the arterial periphery, can be explained by the interaction of the left ventricular ejection pressure pulse with two centrally located reflection sites.

Ambulatory blood pressure monitoring in prepubertal idiopathic dilated cardiomyopathy children

BACKGROUND AND OBJECTIVES: Ambulatory blood pressure monitoring is recommended for several diseases in childhood; however, there are no reports about its use in the monitoring of children with dilated cardiomyopathy so far. We evaluated the pattern of ambulatory blood pressure monitoring in children with dilated cardiomyopathy and correlated it to height, weight, and body mass index. METHODS: Prepubertal children with dilated cardiomyopathy were assessed by ambulatory blood pressure monitoring. Data were collected for systolic and diastolic blood pressure. Means, for 24hours, daytime, and nighttime, dipping pattern and levels above the normal expected values were computed. RESULTS: Children with cardiomyopathy have the same blood pressure as normal kids. Weight was moderately but significantly correlated to nighttime systolic blood pressure. Children with left ventricular ejection fraction < 50% have 6% less diastolic blood pressure dipping. These same children were also receiving higher doses of carvedilol and captopril. CONCLUSIONS: Children with idiopathic dilated cardiomyopathy have the same blood pressure values and blood pressure dipping patterns on ambulatory blood pressure monitoring as normal healthy children are expected to have. Children with low left ventricular ejection pressure have lower dipping pattern.

Intraventricular Pressure Differences

Like all fluids, blood tends to flow from areas of high pressure to low pressure. This seemingly trite observation hides a great deal of sophisticated pathophysiology that we are only beginning to exploit diagnostically and potentially therapeutically. In this issue of Circulation , Yotti and colleagues have exploited a new noninvasive technique to measure the small pressure differences generated within the normal left ventricular outflow tract in systole, demonstrating the utility of such measurements in quantifying ventricular systolic function.1 Because the fluid dynamics concepts behind these methods remain obscure to many cardiologists, it is worth reviewing the theoretical underpinnings in the hope that they will be more widely applied on the basis of articles like those of Yotti et al and others. See p 1771 Cardiologists have become comfortable with the use of the Gorlin equation in the cardiac catheterization laboratory and the simplified Bernoulli equation in the echocardiography laboratory to characterize the severity of valvular stenosis. Both equations are based on the principle of conservation of energy, relating the pressure drop (potential energy) across the valve to the rise in velocity (kinetic energy) as blood rushes through it. Several special circumstances combine to make these simple equations particularly applicable to flow through a restrictive orifice, including lack of a significant friction factor (viscosity) and a lack of pressure recovery as the blood rushes out of the abrupt obstruction. One of the most important simplifications is the absence of a significant “inertial” component to flow through a restrictive orifice. That is, the amount of blood actually moving at high velocity is tiny compared with the volume of the overall column of blood in the left ventricular outflow tract. Thus, very little pressure is expended in getting that small mass moving, and all of the potential energy lost across the …

Dynamic effects of positive-pressure ventilation on canine left ventricular pressure-volume relations.

Positive-pressure ventilation (PPV) may affect left ventricular (LV) performance by altering both LV diastolic compliance and pericardial pressure (Ppc). We measured the effect of PPV on LV intraluminal pressure, Ppc, LV volume, and LV cross-sectional area in 17 acute anesthetized dogs. To account for changes in lung volume independent of changes in Ppc and differences in contractility, measures were made during both open- and closed-chest conditions, during closed chest with and without chest wall binding, and after propranolol-induced acute ventricular failure (AVF). Apneic end-systolic pressure-volume relations (ESPVR) were generated by inferior vena caval occlusions. With the open chest, PPV had no effects. With the chest closed, PPV inspiration decreased LV end-diastolic volume (EDV) along its diastolic compliance curve and decreased end-systolic volume (ESV) such that the end-systolic pressure-volume domain was shifted to a point left of the LV ESPVR, even when referenced to Ppc. The decrease in EDV was greater in control than in AVF conditions, whereas the shift of the ESV to the left of the ESPVR was greater with AVF than in control conditions. We conclude that the hemodynamic effects of PPV inspiration are due primarily to changes in intrathoracic pressure and that the inspiration-induced decreases of LV EDV reflect direct effects of intrathoracic pressure on LV filling. The decreases in LV ESV exceed the amount explained solely by a reduction in LV ejection pressure.

Effects of Valve Replacement on Ventricular Mechanics in Mitral Regurgitation and Aortic Stenosis

This study in humans assessed changes in left ventricular function early and late after correction of mitral regurgitation (MR) (n = 9) or aortic stenosis (AS) (n = 10). Ventricular function was measured with radionuclide and micromanometer-derived pressure-volume loops during preload manipulation, thermodilution cardiac outputs, and echocardiograms. Late radionuclide and echocardiographic data were acquired at 24 hours and 20 months. Perioperative left ventricular performance (stroke work-end-diastolic volume relationship) did not change for patients with MR or AS. Significant changes in afterload occurred: ejection fraction (MR, 0.49 to 0.37; AS, 0.54 to 0.60; both, p = 0.013), mean left ventricular ejection pressure (MR, 73 to 91 mm Hg; AS, 138 to 93 mm Hg; both, p < 0.01), and end-systolic wall stress (MR, 26 to 42 x 10(3) dynes/cm2; AS, 37 to 22 x 10(3) dynes/cm2; both, p < 0.01). Ejection efficiency improved for MR patients (0.69 +/- 0.26 to 1.0 +/- 0.15; p < 0.05). The 20-month data showed improved New York Heart Association functional class, normal resting ejection fraction, and normal exercise response for both groups. Early after operation, a significant change in left ventricular load was seen with correction of MR and AS. Data obtained late after operation showed improvement consistent with ventricular remodeling.

Estimation of left ventricular function in patients with a left ventricular assist device.

Patients with profound left ventricular (LV) dysfunction supported by a left ventricular assist device (LVAD) may have recovery of LV function, but current methods for assessing this are difficult or not readily available. A new method to estimate LV performance was tested in 6 patients on LVAD (age, 47 +/- 12 years). Simultaneous measures of LV cross-sectional area (substitute for volume) using transesophageal echocardiographic automated border detection and femoral arterial pressure (substitute for LV ejection pressure) were recorded during brief periods on and off LVAD. During the LVAD off period, femoral arterial pressure and LV area signals were combined on-line to generate arterial pressure-LV area loops. The slope of the linear regression line connecting the end systolic points generated during LV filling after LVAD off was used as an estimate of end systolic elastance denoted by Ees. The average Ees was 3.8 +/- 3.1 mmHg/cm2. These values are significantly lower than those of 13 control patients (22.3 +/- 15.4 mmHg/cm2). This method of estimating Ees may be clinically useful in assessing LV recovery in patients on LVAD after extended support.

Left ventricular function depends on previous beat ejection but not previous beat pressure load.

Previous beat contraction history, in which the performance of the left ventricle on any one beat is influenced by the mechanical events of the previous beat, may be important in the beat-to-beat regulation of left ventricular performance in the intact cardiovascular system. Prior studies of this phenomenon have established that mechanical events of the previous beat influence the function of the current beat, but it is not known whether the important mechanical influence is exerted by previous beat ejection or previous beat pressure. In addition, the magnitude of the effect of previous beat contraction history on left ventricular performance is unknown. To make these determinations, we performed experiments in six isolated rabbit left ventricle preparations buffer perfused at 30 degrees C. Left ventricular pressure and volume were controlled precisely with a servo-controlled linear motor system. After steady-state ejecting conditions were established by clamping left ventricular ejection pressure at 60% of peak isovolumic pressure, single test beats, which were pressure clamped at 40%, 60%, 80%, and 100% of peak isovolumic pressure, were introduced and followed by an isovolumic reference beat. As the level of pressure clamp decreased from 100% to 40%, developed pressure on the isovolumic beat following the single test beats increased from 139 +/- 15 (mean +/- SD) to 151 +/- 13 mm Hg. Similarly, peak positive left ventricular dP/dt increased from 1,718 +/- 209 to 1,864 +/- 181 mm Hg.sec-1 (both p less than 0.01). Multiple regression analysis showed that this increase in left ventricular function was related to previous beat ejection but not to previous beat pressure load or relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Diminished stroke volume during inspiration: a reverse thoracic pump.

In 12 conscious dogs, a three-dimensional array of pulse-transit ultrasonic transducers was used to measure left ventricular anterior-posterior minor, septal-free wall minor, and basal-apical major diameters. Matched micromanometers measured left ventricular, right ventricular, and intrapleural pressures. Electromagnetic ascending aortic blood flow and right ventricular transverse diameter were measured in five of the dogs. A major cause of the inspiratory decline in stroke volume in this preparation appeared to be reflex tachycardia and autonomic changes associated with inspiration. However, when heart rate was controlled by atrial pacing or pharmacologic autonomic attenuation (propranolol and atropine), stroke volume still decreased around 10%, with an inspiratory decrease in pleural pressure of 10 mm Hg. Based on the measurements of ventricular dimension, venous return to the right ventricle appeared to be augmented significantly during inspiration and the transient increase in right ventricular volume was associated with leftward interventricular septal shifting and altered diastolic left ventricular geometry. However, left ventricular end-diastolic volume was changed minimally, implying that alterations in preload were not important. Moreover, transmural left ventricular ejection pressure, calculated as intracavitary minus pleural pressure, was not significantly changed, and it seemed that neither pressure nor geometric components of afterload were altered significantly by inspiration. The inspiratory fall in left ventricular stroke volume correlated best with the decline in intracavitary left ventricular ejection pressure referenced to atmospheric pressure. It is hypothesized that during ejection, left ventricular pressure referenced to atmospheric pressure is the hydraulic force effecting stroke volume and that the decline in this effective left ventricular ejection pressure is responsible for the inspiratory fall in stroke volume through a reverse thoracic pump mechanism.