Decrease In Pleural Pressure Research Articles

Mechanism of the increased rib cage expansion produced by the diaphragm with abdominal support.

When the abdomen in quadriplegic subjects is given a passive mechanical support, the expansion of the lower rib cage during inspiration is greater and the inward displacement of the upper rib cage is smaller. These changes have traditionally been attributed to an increase in the appositional force of the diaphragm, but the mechanisms have not been assessed. In this study, the inspiratory intercostal muscles in all interspaces were severed in anesthetized dogs, so that the diaphragm was the only muscle active during inspiration, and the displacements of the ribs 10 and 5 and the changes in pleural and abdominal pressure were measured during unimpeded breathing and during breathing with a plate applied on the ventral abdominal wall. In addition, external forces were applied to the 10th rib pair in the cranial and lateral directions, and the rib trajectories thus obtained were used as the basis for a vector analysis to estimate the relative contributions of the insertional and appositional forces to the rib 10 displacements during breathing. Application of the abdominal plate caused a marked increase in the inspiratory cranial and outward displacement of rib 10 and a decrease in the inspiratory caudal displacement of rib 5. Analysis of the results showed, however, that 1) the insertional and appositional forces contributed nearly equally to the increased inspiratory displacement of rib 10 and 2) the decrease in the expiratory displacement of rib 5 was the result of both the greater displacement of the lower ribs and the decrease in pleural pressure.

Fluid responsiveness in critically ill patients.

Fluid responsiveness in critically ill patients.

Determinants of the Y Descent and its Usefulness as a Predictor of Ventricular Filling

Our objective was to determine if the magnitude of the Y descent in the central venous pressure tracing could be used to determine which patients have restrictive hemodynamics. To better understand the determinants of the Y descent, we also examined the effects of changes in blood volume, changes in pleural pressure, and respiratory maneuvers on its magnitude. Studies were performed in both humans and dogs. In six anesthetized dogs, we examined the effect on the Y descent in central venous pressure (CVP) of an infusion of normal saline, a decrease in pleural pressure produced by having animals perform a Mueller maneuver, and the combination of a Mueller maneuver and volume loading. Observations were made with the chest closed, chest open, and chest and pericardium open. The state of the chest did not effect the Y descent. The Y descent was only significantly increased when a Mueller maneuver was combined with volume loading. There was a significant inverse relationship between the magnitude of the decrease in esophageal pressure and the Y descent. There was also a linear relationship between the CVP and Y descent. For the human studies, we examined patients undergoing routine cardiac surgery. They were examined during spontaneous breathing before intubation, with positive pressure breathing and closed chest, with positive pressure breathing and open chest, with an open pericardium, with a closed chest and positive pressure breathing postsurgery, and with spontaneous breathing after extubation following surgery. The Y descent was greater in spontaneous breaths postsurgery compared to before surgery, and this was associated with an increase in CVP. However, the magnitude of CVP did not correlate with the magnitude of the Y descent. A restrictive pattern in cardiac filling was identified by a lack of respiratory variation in right atrial pressure during spontaneous breaths. All patients with large Y descents had a restrictive pattern, but many patients with restrictive filling patterns did not have a large Y descent. The magnitude of the Y descent is affected by the volume status, the magnitude and direction of the changes in pleural pressure, and the compliance of the pericardial compartment. A large Y descent indicates a restrictive cardiac state, but a small Y descent does not rule out a restrictive condition because of the many interacting variables.

Determinants of the Y Descent and its Usefulness as a Predictor of Ventricular Filling

Our objective was to determine if the magnitude of the Y descent in the central venous pressure tracing could be used to determine which patients have restrictive hemodynamics. To better understand the determinants of the Y descent, we also examined the effects of changes in blood volume, changes in pleural pressure, and respiratory maneuvers on its magnitude. Studies were performed in both humans and dogs. In six anesthetized dogs, we examined the effect on the Y descent in central venous pressure (CVP) of an infusion of normal saline, a decrease in pleural pressure produced by having animals perform a Mueller maneuver, and the combination of a Mueller maneuver and volume loading. Observations were made with the chest closed, chest open, and chest and pericardium open. The state of the chest did not effect the Y descent. The Y descent was only significantly increased when a Mueller maneuver was combined with volume loading. There was a significant inverse relationship between the magnitude of the decrease in esophageal pressure and the Y descent. There was also a linear relationship between the CVP and Y descent. For the human studies, we examined patients undergoing routine cardiac surgery. They were examined during spontaneous breathing before intubation, with positive pressure breathing and closed chest, with positive pressure breathing and open chest, with an open pericardium, with a closed chest and positive pressure breathing postsurgery, and with spontaneous breathing after extubation following surgery. The Y descent was greater in spontaneous breaths postsurgery compared to before surgery, and this was associated with an increase in CVP. However, the magnitude of CVP did not correlate with the magnitude of the Y descent. A restrictive pattern in cardiac filling was identified by a lack of respiratory variation in right atrial pressure during spontaneous breaths. All patients with large Y descents had a restrictive pattern, but many patients with restrictive filling patterns did not have a large Y descent. The magnitude of the Y descent is affected by the volume status, the magnitude and direction of the changes in pleural pressure, and the compliance of the pericardial compartment. A large Y descent indicates a restrictive cardiac state, but a small Y descent does not rule out a restrictive condition because of the many interacting variables.

Physiologic effects of positive end-expiratory pressure and mask pressure support during exacerbations of chronic obstructive pulmonary disease.

To assess physiologic effects of continuous positive airway pressure (CPAP) and positive end-expiratory pressure (PEEP) during noninvasive pressure support ventilation (PSV) in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD), we measured in seven patients the breathing pattern, lung mechanics, diaphragmatic effort (PTPdi), and arterial blood gases under four conditions: (1) spontaneous breathing (SB); (2) CPAP; (3) PSV of 10 cm H2O; and (4) PSV plus PEEP (PEEP + PSV). CPAP and PEEP were set between 80 and 90% of dynamic intrinsic PEEP (PEEPidyn) measured during SB and PSV, respectively. PEEPidyn was obtained (1) from the decrease in pleural pressure (delta Ppl) preceding inspiration, and (2) subtracting the fall in gastric pressure (delta Pga) caused by relaxation of the abdominal muscles from the delta Ppl decrease. Abdominal muscle activity made PEEPidyn overestimated in almost all instances (p < 0.0001). PSV increased minute ventilation, improved gas exchange, and decreased PTPdi. PEEP added to PSV, likewise CPAP compared with SB, further significantly decreased the diaphragmatic effort (PTPdi went from 322 +/- 111 to 203 +/- 63 cm H2O.s) by counterbalancing PEEPidyn, which went from 5.4 +/- 4.0 to 3.1 +/- 2.3 cm H2O. These data support the use of low levels of PEEP (80 to 90% of PEEPidyn) to treat acute exacerbation of COPD by means of mask PSV.

Influence of pleural pressure variations on cardiovascular system dynamics: a model study.

A mathematical model of the human cardiovascular system (CVS) is used to study the effect of different respiratory manoeuvres on the circulation. The model simulates the normal CVS and the interaction between the heart and the intrathoracic pressure. The vascular system is represented by resistive, capacitive and inertial elements whereas the ventricles are assumed to function according to the time-varying elastance concept based on their transmural pressures. The model predicts that normal inspiratory effeort effects an increase in the venous return, an increase in the pulmonary flow and a slight decrease in the left ventricular stroke volume (LVSV), which represents a decrease in ejection due to the increased LV transmural pressure. A step decrease in pleural pressure to −40 mm Hg, representing the Muller manoeuvre (MM), accentuates these findings, showing a decrease in LVSV in spite of an increase in the LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV) and the LV filling pressure, expressed as the mean left atrial transmural pressure. Simulating intermittent positive pressure ventilation (IPPV) with added positive end expiratory pressure (PEEP) shows an 18·6 per cent decrease in the cardiac output compared with quiet respiration. The calculated results of the model are in good agreement with available experimental data, suggesting that most of these findings may be explained by basic haemodynamic principles in the uncontrolled CVS.

Cardiovascular performance during bronchospasm in dogs.

In 8 anesthetized mongrel dogs, we studied the effects of carbachol-induced bronchoconstriction (BC) on the cardiovascular system. Inhalation of carbachol in an amount sufficient to produce at least a 50% decrease in lung conductance (GL) did not lead to significant changes in cardiac output, mean transmural left atrial (Pla) or right atrial pressure, end-diastolic left ventricular septal-lateral dimension, left ventricular apex to base dimension, or in end-diastolic right ventricular septal to lateral dimension during expiration. Mean transmural pulmonary arterial pressure rose and mean transmural aortic pressure (Pao) fell during BC. During inspiration, there were significant increases in transmural left atrial pressure, Pla, associated with decreases in end-diastolic left ventricular septal-lateral and apex-base dimensions. End-diastolic right ventricular septal-lateral dimension increased during inspiration. Beat-to-beat aortic flow (Qao) decreased during inspiration, while pulmonary arterial flow increased. There were no changes in transmural Pao during inspiration measured at the nadir of aortic flow. During BC, these changes were exaggerated, but remained qualitatively the same. The magnitude of the inspiratory decrease in pleural pressure (Ppl) was shown to be linearly related to the magnitude of the change in GL, and the magnitude of the inspiratory decrease in Pao and Qao (pulsus paradoxus) was shown to be linearly related to the magnitude of the inspiratory swing in Ppl. Although vagotomy significantly altered the pattern of respiration such that tidal volume increased and respiratory rate decreased, it did not substantially alter the responses of the cardiovascular system to breathing during BC. We conclude: the inspiratory decrease in Pao and Qao (pulsus paradoxus) is associated with a decrease in left ventricular end-diastolic filling, and a stiffening of the left ventricle; these changes are exaggerated during BC as a result of the exaggerated inspiratory swings in Ppl; the effects on left ventricular dynamics are mediated only in part through increases in right ventricular end-diastolic filling operating through the mechanism of ventricular interdependence; changes in left ventricular afterload appear to play little role in determining the responses seen.

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.

Effects of negative pleural pressure on left ventricular hemodynamics

Negative pleural pressure alters left ventricular (LV) function. LV volume changes have been studied in human subjects, but little is known of the hemodynamic effects. The effect of changes of pleural pressure on LV hemodynamics during a Mueller maneuver (inspiration against an obstruction) was studied in 11 subjects and during quiet, unobstructed inspiration in 3. During the Mueller maneuver, there was an initial decrease in pulmonary wedge pressure and aortic systolic pressure, almost as great as the decrease in pleural pressure. Thereafter, these pressures increased despite a sustained reduction in pleural pressure. Toward the end of the Mueller maneuver, pulmonary wedge transmural pressure averaged 31 ± 12 mm Hg and in 6 patients large v waves developed. The increase in aortic transmural pressure averaged 30 ± 16 mm Hg. Aortic pulse pressure decreased on the first beat from control levels of 59 ± 21 to 47 ± 21 (p < 0.001) and then returned to control levels. During normal breathing in 3 subjects, studied with intraesophageal balloons, there was a similar increase in both transmural aortic and transmural pulmonary wedge pressures with a decrease in pleural pressure 6 mm Hg during inspiration. Thus, increased negative pleural pressure was associated with a marked increase in pulmonary wedge transmural pressure; the increase was approximately proportionate to the decrease in pleural pressure. It is suggested that this increase was due to increased impedance to LV ejection and to right ventricular expansion interfering with LV diastolic filling.

Cardiovascular disturbances in chronic respiratory insufficiency

The mechanical factors by which chronic respiratory insufficiency may influence right and left ventricular performance during both spontaneous and mechanical ventilation are reviewed. During a spontaneous inspiration the right heart distends because of increased inflow and increased pulmonary vascular resistance. This decreases the effective left ventricular compliance, through ventricular interdependence, reducing the gradient for pulmonary venous return. The inspiratory decrease in pleural pressure also effectively increases the impedance to left ventricular ejection. An inspiratory increase in abdominal pressure further increases the left ventricular afterload. These factors combine to impair left ventricular performance. During intermittent positive pressure ventilation, left ventricular stroke volume increases early in inspiration. This increased inspiratory flow cannot be attributed to a phase lag in the right heart output reaching the left heart chambers because, even with a constant pulmonary arterial inflow, aortic flow increases during inspiration. Several factors may act in concert to improve left ventricular performance, despite the adverse effects of intermittent positive pressure ventilation on the right ventricle. These include (1) a decrease in right heart volume, increasing left ventricular compliance and hence the gradient for pulmonary venous return; (2) anterograde emptying of the alveolar capillary bed with lung inflation; (3) the increase in pleural pressure decreasing impedance to left ventricular emptying; and (4) physical compression of the heart by the lungs.

A model of the effects of respiration on left ventricular performance

We have investigated the interaction of left ventricular afterload and right-heart volume on left ventricular performance. By utilizing a right-heart bypassed heart-lung preparation, we have been able to control independently each factor. We have previously suggested that the major influences of the inspiratory decrease in pleural pressure in decreasing left ventricular stroke volume (LVSV) may be via the inspiratory increases in left-heart afterload and right-heart volume (RHV). Thus, our preparation serves as a model to study in detail the specific effects on the left ventricle of changes that are induced by respiration. Our results show that increases in transmural (relative to pleural pressure) aortic pressure (Pao) caused an increased left ventricular end-diastolic pressure (LVEDP), and that the effect of equivalent increases in Pao was greater when RHV was greater. Increase in RHV had minimal effects at low volume, but resulted in large increases in LVEDP at large RHV. These effects were markedly attenuated after pericardiectomy. Rapid increases in either RHV or Pao produced transient falls in LVSV. Our results are consistent with the hypothesis that increases in both right-heart volume and LV afterload contribute to the inspiratory decrease in LVSV and increase in LVEDP.

Cardiovascular changes in conscious dogs during spontaneous deep breaths.

Cardiovascular functions were evaluated beat by beat during 29 spontaneous deep breaths in three conscious dogs. When pleural pressure was significantly lower than during quiet breathing, stroke volume was reduced, heart rate elevated, as well as transmural pressure in the pulmonary artery (PPA-Ppl) and in the thoracic aorta (PAO-Ppl); the left ventricular filling pressure (LVEDP-Ppl) did not decrease. The authors suggest that these findings are not consistent with the classical hypothesis which explains the decrease in left ventricular output primarily by a reduction in the venous return to the left heart. The results indicate that the decrease in pleural pressure is responsible for an increase in the afterload on the left heart and suggest that this is the predominate factor in the reduction of the stroke volume without decrease in left ventricular filling pressure.