Transmural Left Ventricular End-diastolic Pressure Research Articles

Ventricular interaction and external constraint account for decreased stroke work during volume loading in CHF.

The slope of the stroke work (SW)-pulmonary capillary wedge pressure (PCWP) relation may be negative in congestive heart failure (CHF), implying decreased contractility based on the premise that PCWP is simply related to left ventricular (LV) end-diastolic volume. We hypothesized that the negative slope is explained by decreased transmural LV end-diastolic pressure (LVEDP), despite the increased LVEDP, and that contractility remains unchanged. Rapid pacing produced CHF in six dogs. Hemodynamic and dimension changes were then measured under anesthesia during volume manipulation. Volume loading increased pericardial pressure and LVEDP but decreased transmural LVEDP and SW. Right ventricular diameter increased and septum-to-LV free wall diameter decreased. Although the slopes of the SW-LVEDP relations were negative, the SW-transmural LVEDP relations remained positive, indicating unchanged contractility. Similarly, the SW-segment length relations suggested unchanged contractility. Pressure surrounding the LV must be subtracted from LVEDP to calculate transmural LVEDP accurately. When this was done in this model, the apparent decrease in contractility was no longer evident. Despite the increased LVEDP during volume loading, transmural LVEDP and therefore SW decreased and contractility remained unchanged.

Estimating cardiac filling pressure in mechanically ventilated patients with hyperinflation.

When positive end-expiratory pressure (PEEP) is applied, the intracavitary left ventricular end-diastolic pressure (LVEDP) exceeds the LV filling pressure because pericardial pressure exceeds 0 at end-expiration. Under those conditions, the LV filling pressure is itself better reflected by the transmural LVEDP (tLVEDP) (LVEDP minus pericardial pressure). By extension, end-expiratory pulmonary artery occlusion pressure (eePAOP), as an estimate of end-expiratory LVEDP, overestimates LV filling pressure when pericardial pressure is >0, because it occurs when PEEP is present. We hypothesized that LV filling pressure could be measured from eePAOP by also knowing the proportional transmission of alveolar pressure to pulmonary vessels calculated as index of transmission = (end-inspiratory PAOP--eePAOP)/(plateau pressure--total PEEP). We calculated transmural pulmonary artery occlusion pressure (tPAOP) with this equation: tPAOP = eePAOP--(index of transmission x total PEEP). We compared tPAOP with airway disconnection nadir PAOP measured during rapid airway disconnection in subjects undergoing PEEP with and without evidence of dynamic pulmonary hyperinflation. Prospective study. Medical intensive care unit of a university hospital. We studied 107 patients mechanically ventilated with PEEP for acute respiratory failure. Patients without dynamic pulmonary hyperinflation (group A; n = 58) were analyzed separately from patients with dynamic pulmonary hyperinflation (group B; n = 49). Transient airway disconnection. In group A, tPAOP (8.5+/-6.0 mm Hg) and nadir PAOP (8.6+/-6.0 mm Hg) did not differ from each other but were lower than eePAOP (12.4+/-5.6 mm Hg; p < .05). The agreement between tPAOP and nadir PAOP was good (bias, 0.15 mm Hg; limits of agreement, -1.5-1.8 mm Hg). In group B, tPAOP (9.7+/-5.4 mm Hg) was lower than both nadir PAOP and eePAOP (12.1+/-5.4 and 13.9+/-5.2 mm Hg, respectively; p < .05 for both comparisons). The agreement between tPAOP and nadir PAOP was poor (bias, 2.3 mm Hg; limits of agreement, -0.2-4.8 mm Hg). Indexing the transmission of proportional alveolar pressure to PAOP in the estimation of LV filling pressure is equivalent to the nadir method in patients without dynamic pulmonary hyperinflation and may be more reliable than the nadir PAOP method in patients with dynamic pulmonary hyperinflation.

Effects of Pericardial Constraint on Left Ventricular Mechanoreceptor Activity in Cats

The purpose of this study was to assess the effect of pericardial constraint on the activity of left ventricular (LV) mechanoreceptors with nonmyelinated vagal afferents. Single-unit activity of cervical vagal afferents (conduction velocity, 1.6 +/- 0.5 m/s) was recorded in six cats anesthetized with alpha-chloralose. Discharge frequency during diastole (DFdiastole) and systole (DFsystole) was determined after correction for conduction delay of the nerve action potential. When the pericardium was closed and LV end-diastolic pressure (LVEDP) was approximately 5 mm Hg, DFdiastole and DFsystole were 1.3 +/- 1.0 and 0.3 +/- 0.1 impulses per second, respectively. Volume expansion increased LVEDP, LV transmural LVEDP, and segment length and was associated with a significant increase in DFdiastole. At a given LVEDP, DFdiastole was significantly greater in the absence of the pericardium than with the pericardium closed. Removal of the pericardium increased the slope of the relation between DFdiastole and intracavitary LVEDP but did not alter the slope of the relations between DFdiastole and transmural LVEDP and LV segment length. These results suggest that, rather than the absolute value of intracavitary LVEDP, transmural LVEDP and distension appear to be more important determinants of diastolic LV mechanoreceptor activity and that pericardial constraint may attenuate mechanoreceptor activity by limiting cardiac distension.

Selective positive end-expiratory pressure and cardiac function in dogs

Effects of general (G) versus selective (S) right (R) and left (L) positive end-expiratory pressure (PEEP) were compared during differential lung ventilation in 11 anaesthetized dogs in the supine position. GPEEP 20 cmH2O decreased cardiac output (1 min-1) from 2.9 +/- 0.2 (mean +/- SE) to 1.7 +/- 0.5 (p less than 0.05), RPEEP from 2.8 +/- 0.2 to 2.2 +/- 0.2 (p less than 0.05) while LPEEP caused no significant change in cardiac output. GPEEP increased pleural pressure more than SPEEP. Pleural pressure was asymmetric during SPEEP. Both SPEEP and GPEEP increased pericardial pressure uniformly, but the increase was less marked with SPEEP. During GPEEP 20 cmH2O transmural left ventricular end-diastolic pressure (LVEDP) decreased markedly. SPEEP caused less marked reductions in transmural LVEDP. Qualitatively similar, but less marked changes were observed with PEEP 10 cmH2O. In conclusion, cardiac output decreased less with selective PEEP than with general PEEP. This was explained by less increase in pleural and pericardial pressure, and accordingly less decrease in LV transmural filling pressure.

Plasma concentrations of atrial natriuretic factor during positive end‐expiratory pressure ventilation in dogs with normal or impaired left ventricular function

The influence of positive end-expiratory pressure (PEEP) ventilation on plasma concentrations of atrial natriuretic factor (ANF) was studied in dogs anesthetized with sodium pentobarbital during normal cardiac function and during acutely impaired left ventricular function. Left ventricular impairment was induced by injecting repeated doses of polystyrene microspheres with a diameter of 50 microns into the main left coronary artery, causing a severe depression of left ventricular performance. This was accompanied by doubling of ANF concentrations measured in blood sampled from aorta. Application of PEEP (10 cmH2O (0.98 kPa] reduced plasma ANF in dogs both with normal and impaired left ventricular function. The decrease was significantly greater during left ventricular impairment compared to control, 31 and 19%, respectively. A positive correlation was observed between plasma ANF and transmural left ventricular end-diastolic pressure when all data were pooled, but not between ANF and transmural right atrial pressure. This implies that transmural left ventricular end-diastolic and hence transmural left atrial pressure probably is the principal determinant of acute ANF release in this model. Reduced plasma ANF in response to PEEP even during acute left ventricular impairment when ANF release was augmented, was probably due to diminished atrial distension during PEEP ventilation.

Ventricular interaction during experimental acute pulmonary embolism.

Although stroke volume may decrease markedly after acute pulmonary embolism, left ventricular end-diastolic pressure (LVEDP) usually changes very little, which suggests that compliance or contractility or both are reduced. To test the hypothesis that the altered LV function during pulmonary embolism is primarily due to reduced preload mediated by increased pericardial constraint, hemodynamics and chamber dimensions (measured by sonomicrometry) were assessed in seven anesthetized dogs during control volume loading, after pulmonary embolism (with autologous blood clot), and after repeated pulmonary embolism in the volume-loaded state. The correlation between LVEDP and an index of LVED volume (LVED area index) throughout a wide range of LVEDP before and after embolism was poor (mean r = 0.42; range, 0-0.82). However, the correlation between transmural LVEDP (LVEDP-directly measured pericardial pressure) and LVED area index (mean r = 0.78; range, 0.61-0.94) was significantly higher (p = 0.03). Similarly, an index of stroke work (LV area stroke work) correlated less well (p less than 0.01) with LVEDP (mean r = 0.43; range, 0.07-0.77) than with transmural LVEDP (mean r = 0.82; range, 0.68-0.92). LV area stroke work also correlated well with the LV area index (mean r = 0.84; range, 0.70-0.95). These data indicate that neither compliance nor contractility is substantially altered during acute pulmonary embolism. The altered LV performance is due to reduced LV preload as reflected by a decrease in transmural LVEDP. This study also demonstrates that LVEDP is a poor index of LV preload during pulmonary embolism, whereas transmural LVEDP accurately reflects LVED dimensions.

Right and left ventricular pressure-volume response to elevated pericardial pressure.

Because of the close anatomic connections, the volume in 1 ventricle can directly influence the volume in the other ventricle. We examined this ventricular mechanical coupling at elevated pericardial pressures in 6 mongrel dogs. The animals were anesthetized and were mechanically ventilated with intermittent positive-pressure ventilation. Right and left ventricular volumes and pressures and pericardial pressure were simultaneously measured during control and after infusing 25, 50, and 75 ml of saline with dextran into the pericardial cavity. The ventricular volumes were calculated from cine-radiographic positions of endocardial, radiopaque markers. In the control state, right ventricular end-diastolic volume (RVEDV) increased 9.2 +/- 0.9 ml (p less than 0.05) during expiration, whereas left ventricular end-diastolic pressure (LVEDP) increased 0.6 +/- 0.7 mmHg and left ventricular end-diastolic volume (LVEDV) decreased 0.6 +/- 0.4 ml. The increased transmural LVEDP with a decreased LVEDV indicates an apparent left ventricular distensibility decrease as right ventricular diastolic volume increased, possibly because of ventricular interdependence. At the highest pericardial pressure, RVEDV increased 6.7 +/- 1.4 ml (p less than 0.05) during expiration as LVEDP increased 1.2 +/- 0.6 mm Hg and LVEDV decreased 2.0 +/- 0.6 ml (p less than 0.05). Thus, at the higher pericardial pressures, smaller changes in RVEDV produced significantly greater changes in LVEDV. This coupling between the ventricles was further examined in 5 hearts studied postmortem. The hearts were placed in cold cardioplegic solution and balloons were inserted into both ventricles.(ABSTRACT TRUNCATED AT 250 WORDS)

Volume-dependent effects of positive airway pressure on intracavitary left ventricular end-diastolic pressure.

To test the hypothesis that the effects of positive end-expiratory airway pressure (PEEP) on intracavitary left ventricular end-diastolic pressure (LVEDP) depend on the ventricular filling conditions under which PEEP is applied, the effects of PEEP on pressure in and around the left ventricle were determined before and after stepwise expansion of intravascular blood volume in 10 closed-chest dogs. Over a range of 0 to 20 cm of water, PEEP progressively increased both intrapericardial and intracavitary right ventricular end-diastolic pressures. These increases in pressure around the left ventricle were approximately linear and were relatively unaffected by volume loading. At the same time, PEEP always decreased transmural LVEDP by decreasing ventricular filling. However, transmural LVEDP fell more when ventricular volume was initially large, due to the nonlinear relationship between left ventricular transmural pressure and volume. As a result, intracavitary LVEDP (which reflected the sum of decreased transmural LVEDP and increased external pressure) increased when baseline ventricular volume was small and decreased when baseline ventricular volume was large. At intermediate volumes the fall in transmural pressure equaled the rise in external pressure, and intracavitary LVEDP did not change. These findings demonstrate that changes due to PEEP in intracavitary LVEDP are a complex function of increased intrathoracic pressure, decreased ventricular filling, and the operative level of left ventricular compliance.

Left ventricular contractility using isovolumic phase indices during PEEP in ARDS patients.

The effects of incremental increases in PEEP during mechanical ventilation on left ventricular (LV) contractility before and after intravascular volume expansion (IVE) were studied in 10 patients treated for ARDS. A pulmonary artery (PA) catheter, a LV catheter-tip micromanometer, and an esophageal balloon catheter were inserted in these patients. We measured transmural right atrial and PA pressures, transmural LV end-diastolic and systemic arterial pressures, the first derivative of LV pressure (LV dP/dt), the ratio of LV dP/dt at transmural developed LV pressure (dP/dt/DPt) with DPt = 5, 10, 40 mm Hg, cardiac index (CI) at every level of PEEP and after IVE at the highest PEEP. Stepwise increases in PEEP (from 0-20 cm H2O) were associated with progressive fall in CI whereas heart rate remained unchanged. Transmural right atrial and PA pressures did not change; transmural LV end-diastolic and systemic arterial pressures and peak dP/dt decreased significantly with PEEP, except for dT/dt/dPt. IVE reversed this fall in CI and peak dP/dt. Whereas transmural LV end-diastolic pressure rose markedly. We conclude that the observed fall in LV performance during PEEP is not the result of a depressed LV contractility because PEEP does not induce a decrease in dP/dt/DPt, the least sensitive to change in preload isovolumic phase indices of contractility.

Effect of positive end-expiratory pressure on left ventricular mechanics in patients with hypoxemic respiratory failure.

When positive end-expiratory pressure (PEEP) is added to intermittent positive pressure ventilation, cardiac output and stroke volume frequently fall despite unchanged or increased transmural left ventricular end-diastolic pressure. To determine whether a part of the fall in stroke volume with PEEP is explained by depressed left ventricular systolic function (increased end-systolic volume at a given end-systolic pressure on PEEP) the authors measured left ventricular end-diastolic volume (EDV), end-systolic volume (ESV), and the corresponding pressures in nine patients with acute hypoxemic respiratory failure. Measurements were made before and after 10 cm H2O PEEP was added to the ventilator. PEEP reduced mean stroke volume from 71 to 62 ml and this was explained entirely by a reduction in end-diastolic volume from 135 to 112 ml (P less than 0.005). Despite reduced EDV, pulmonary wedge pressure increased from 12 to 14 torr on PEEP, indicating reduced diastolic compliance or unstressed volume of the left ventricle in these patients similar to that reported in dogs. The authors conclude that PEEP reduces venous return and cardiac output without depressing left ventricular pumping function because end-systolic volume decreased from 64 to 49 ml on PEEP despite identical blood pressures (78 torr). They speculate that PEEP might improve ventricular performance by increasing intrathoracic pressure and left ventricular pressure relative to systemic blood pressure in extrathoracic vessels.

Canine left ventricular volume response to mechanical ventilation with PEEP.

To determine the cause of decreased cardiac output (CO) resulting from the use of PEEP, hemodynamic and pulmonary parameters and radiographic estimates of left ventricular volumes were observed in nine dogs under three conditions: control, PEEP (15 cm H2O), and PEEP with intravascular (IV) volume expansion. Volume expansion was sufficient to return the CO to control values. Cardiac index (CI), stroke volume index (SI), left ventricular stroke work index (LVSWI) all decreased approximately 30 per cent with the application of PEEP. Ejection fraction remained unchanged. With IV volume expansion, the CI, SI, left ventricular end-diastolic volume index, and LVSWI returned to approximate control values. The transmural left ventricular end-diastolic pressure (TMLVEDP) did not change significantly. The authors therefore conclude that reduced left ventricular preload is the cause of decreased cardiac output by PEEP and that indirect evidence of preload (transmural left ventricular end-diastolic pressure) is not an adequate assessment of the force-length relationship under the conditions stated.

Effect of positive end-expiratory pressure on ventricular function in dogs

Artificial ventilation with positive end-expiratory pressure (PEEP) reduces venous return by raising intrathoracic pressure. To determine whether PEEP decreases cardiac output further by depressing myocardial function, we constructed Starling curves, using rapid dextran infusion in 7 anesthetized dogs ventilated with zero (ZEEP) and 20 cm PEEP. The changes in stroke volume and in left ventricular stroke work (LVSW) when PEEP was added or removed were significantly greater than could be attributed to the corresponding change in transmural left ventricular end-diastolic pressure (LVEDPTM) on these Starling curves. To the extent that PEEP did not alter left ventricular diastolic volume-pressure characteristics, these data indicated PEEP depressed ventricular function. Identical changes with PEEP in cardiac output (-30%), esophageal pressure (+10 cmH2O), and left ventricular function were observed after pulmonary edema was induced with oleic acid. These results confirm and extend recent suggestions that high levels of PEEP depress left ventricular function in dogs, accounting for about half of the reduction in cardiac output before and during acute pulmonary edema.

The effect of haemodynamic changes induced by angiographic contrast media on aortic regurgitation in the sedated dog.

Summary: Angiographic contrast media induce changes in cardiac and circulatory function. Their effect on the extent of aortic regurgitation in closed-chest sedated dogs was studied. Ascending aortic flow was measured by an electromagnetic transducer, implanted five to ten days earlier when aortic regurgitation had been produced. Sodium iothalamate 80% or 76% sodium methylglucamine diatrizoate (0.5 ml/kg body weight) were injected into the left ventricle. Seconds later there was a decrease in peak rate of left ventricular pressure rise and inconsistent elevation of trans-mural left ventricular end-diastolic pressure but no change in aortic regurgitation. Twelve to sixteen seconds after injection significant hypotension, due to decreased systemic vascular resistance, appeared and was usually accompanied by tachycardia. Diastolic regurgitant volume fell 48‡ 13 (SD)% (p < 0.001) but total stroke volume fell only 10%, regurgitant fraction decreasing 43‡ 11% (p < 0.001). Duration of regurgitation per minute fell, but not consistently (8‡ 11%; p < 0.1), and most of the decrease in regurgitation was due to a fall in regurgitant flow rate early in diastole (36‡ 16%p < 0.001) associated with decrease in aortoventricular pressure difference. Effective cardiac output increased 84‡ 50%. Hypotension and tachycardia disappeared by one minute; then persistent increase in forward flow parameters became associated with variable increase in regurgitation. Left ventricular end-diastolic pressure became elevated. The early changes are consistent with mild depression of left ventricular contractility, but there was no change in aortic regurgitation. Thereafter, hypotension, with or without prominent tachycardia, led to decrease in aortic regurgitation. Subsequently, regurgitation tended to increase above the control value, other concomitant changes being consistent with expansion of intravascular volume. Changes induced in aortic regurgitation by angiographic contrast media are importantly time dependent and secondary to other haemodynamic effects.