Effects of decreasing lung compliance with oleic acid on the cardiovascular response to PEEP

1977 ◽  
Vol 233 (6) ◽  
pp. H635-H641 ◽  
Author(s):  
S. M. Scharf ◽  
R. H. Ingram

In 12 anesthetized mongrel dogs on a constant volume ventilator, the response of the cardiovascular system to increasing positive end-expiratory pressure (PEEP) was examined before and after inducing acute lung injury with oleic acid. As PEEP was raised to approximately 16 mmHg, lung volume increased by approximately 900 ml before oleic acid and only 350 ml after. Pleural pressure increased by the same amount, indicating that both lung and chest wall compliance decreased with oleic acid. Right atrial pressure, the back pressure to venous return, also increased by the same amount. Although cardiac output at PEEP = 0 was lower after oleic acid, the relative decrements produced by increasing PEEP were the same as before oleic acid.

1987 ◽  
Vol 63 (1) ◽  
pp. 36-43 ◽  
Author(s):  
Z. Hantos ◽  
B. Daroczy ◽  
B. Suki ◽  
S. Nagy

modified forced oscillatory technique was used to determine the respiratory mechanical impedances in anesthetized, paralyzed rats between 0.25 and 10 Hz. From the total respiratory (Zrs) and pulmonary impedance (ZL), measured with pseudorandom oscillations applied at the airway opening before and after thoracotomy, respectively, the chest wall impedance (ZW) was calculated as ZW = Zrs - ZL. The pulmonary (RL) and chest wall resistances were both markedly frequency dependent: between 0.25 and 2 Hz they contributed equally to the total resistance falling from 81.4 +/- 18.3 (SD) at 0.25 Hz to 27.1 +/- 1.7 kPa.l–1 X s at 2 Hz. The pulmonary compliance (CL) decreased mildly, from 2.78 +/- 0.44 at 0.25 Hz to 2.36 +/- 0.39 ml/kPa at 2 Hz, and then increased at higher frequencies, whereas the chest wall compliance declined monotonously from 4.19 +/- 0.88 at 0.25 Hz to 1.93 +/- 0.14 ml/kPa at 10 Hz. Although the frequency dependence of ZW can be interpreted on the basis of parallel inhomogeneities alone, the sharp fall in RL together with the relatively constant CL suggests that at low frequencies significant losses are imposed by the non-Newtonian resistive properties of the lung tissue.


1995 ◽  
Vol 78 (1) ◽  
pp. 179-184 ◽  
Author(s):  
C. Papastamelos ◽  
H. B. Panitch ◽  
S. E. England ◽  
J. L. Allen

Development of chest wall stiffness between infancy and adulthood has important consequences for respiratory system function. To test the hypothesis that there is substantial stiffening of the chest wall in the first few years of life, we measured passive chest wall compliance (Cw) in 40 sedated humans 2 wk-3.5 yr old. Respiratory muscles were relaxed with manual ventilation applied during the Mead-Whittenberger technique. Respiratory system compliance (Crs) and lung compliance (Cl) were calculated from airway opening pressure, transpulmonary pressure, and tidal volume. Cw was calculated as 1/Cw = 1/Crs - 1/Cl during manual ventilation. Mean Cw per kilogram in infants < 1 yr old was significantly higher than that in children > 1 yr old (2.80 +/- 0.87 vs. 2.04 +/- 0.51 ml.cmH2O–1.kg-1; P = 0.002). There was an inverse linear relationship between age and mean Cw per kilogram (r = -0.495, slope -0.037; P < 0.001). In subjects with normal Cl during spontaneous breathing, Cw/spontaneous Cl was 2.86 +/- 1.06 in infants < 1 yr old and 1.33 +/- 0.36 in older children (P = 0.005). We conclude that in infancy the chest wall is nearly three times as compliant as the lung and that by the 2nd year of life chest wall stiffness increases to the point that the chest wall and lung are nearly equally compliant, as in adulthood. Stiffening of the chest wall may play a major role in developmental changes in respiratory system function such as the ability to passively maintain resting lung volume and improved ventilatory efficiency afforded by reduced rib cage distortion.


1983 ◽  
Vol 54 (4) ◽  
pp. 1039-1047 ◽  
Author(s):  
T. W. Wallis ◽  
J. L. Robotham ◽  
R. Compean ◽  
M. K. Kindred

Recent reports have suggested that positive end-expiratory pressure (PEEP) depresses left ventricular (LV) function or shifts LV pressure-volume (PV) relationships due to neural, humoral, or mechanical events. These studies have usually utilized pressures measured during expiration. To study the mechanical effects of PEEP in expiration and inspiration, the circulation was arrested in 12 open-chest dogs, and the coronaries were perfused with a cold cardioplegic agent. Balloons were placed in the ventricles to measure ventricular pressures. Shifts in cardiopulmonary blood volume were prevented by venting the atria to atmosphere. Having ablated neural reflexes and humoral changes, we varied ventricular volumes, chest wall compliance, tidal volume, and PEEP. We found that isovolumic ventricular pressures (relative to atmosphere) increase with PEEP (P less than 0.001), and heart-lung interaction with PEEP is significantly greater in inspiration (P less than 0.001). The effect of PEEP is modified by heart volume (P less than 0.01) and respiratory system compliance (P less than 0.01). We conclude that a mechanical compressive force can be applied to the heart by the lungs as they expand, and this may explain the previous reports of diminished LV function or LV diastolic compliance with PEEP and, in part, explain the decreased cardiac output associated with PEEP. The marked increase in mechanical compressive forces applied to the heart during inspiration with PEEP may have far greater hemodynamic consequences than events during expiration.


1965 ◽  
Vol 20 (6) ◽  
pp. 1211-1216 ◽  
Author(s):  
Charles Mittman ◽  
Norman H. Edelman ◽  
Arthur H. Norris ◽  
Nathan W. Shock

Chest wall and pulmonary compliance were measured in 42 normal males aged 24—78 years. Measurements were made using the static method and the positive-pressure breathing method of Heaf and Prime. Chest wall compliance decreased significantly with age. Pulmonary compliance measured at functional residual capacity was similar in old and young subjects. As lung volume increased pulmonary compliance decreased more in the young than in the old. The latter age difference may result from a loss of lung elastic recoil in the elderly or may be due totally to the age difference in chest wall compliance. The observed age differences in lung compartment volumes can largely be accounted for by the decrease in chest wall compliance. aging; chest wall compliance; lung compliance; static measurement of compliance; positive-pressure measurement of compliance; lung volumes; residual volume Submitted on July 17, 1964


2003 ◽  
Vol 94 (3) ◽  
pp. 849-859 ◽  
Author(s):  
George L. Brengelmann

A. C. Guyton pioneered major advances in understanding cardiovascular equilibrium. He superimposed venous return curves on cardiac output curves to reveal their intersection at the one level of right atrial pressure (Pra) and flow simultaneously consistent with independent properties of the heart and vasculature. He showed how this point would change with altered properties of the heart (e.g., contractility, sensitivity to preload) and/or of the vasculature (e.g., resistance, total volume). In such graphical representations of negative feedback between two subdivisions of a system, one input/output relationship is necessarily plotted backward, i.e., with the input variable on the y-axis (here, the venous return curve). Unfortunately, this format encourages mistaken ideas about the role of Pra as a “back pressure,” such as the assertion that elevating Pra to the level of mean systemic pressure would stop venous return. These concepts are reexamined through review of the original experiments on venous return, presentation of a hypothetical alternative way for obtaining the same data, and analysis of a simple model.


1988 ◽  
Vol 65 (3) ◽  
pp. 1093-1098 ◽  
Author(s):  
G. M. Davis ◽  
A. L. Coates ◽  
A. Papageorgiou ◽  
M. A. Bureau

The measurement of pulmonary mechanics has been developed extensively for adults, and these techniques have been applied directly to neonates and infants. However, the compliant chest wall of the infant frequently predisposes to chest wall distortion, especially when there is a low dynamic lung compliance (CL,dyn). We describe a technique of directly measuring the static chest wall compliance (Cw,st), developed initially in the newborn lamb and subsequently applied to the premature neonate with chest wall distortion. The mean CL,dyn in seven intubated newborn lambs in normoxia was 2.45 +/- 0.41 ml.cmH2O-1.kg-1, whereas Cw,st was 11.81 +/- 0.25 ml.cmH2O-1.kg-1. These values did not change significantly in seven animals breathing through a tight-fitting face mask or with hypercapnia-induced tachypnea. For the eight premature infants the mean CL,dyn was 1.35 +/- 0.36 ml.cmH2O-1.kg-1, whereas the mean Cw,st was 3.16 +/- 1.01 ml.cmH2O-1.kg-1. This study shows that, under relaxed conditions when measurements of static compliance are performed, the chest wall is more compliant than the lung. The measurement of Cw,st may thus be used to determine the contribution of the respiratory musculature in stabilizing the chest wall.


2011 ◽  
Vol 301 (3) ◽  
pp. H629-H633 ◽  
Author(s):  
Daniel A. Beard ◽  
Eric O. Feigl

Based on observations that as cardiac output (as determined by an artificial pump) was experimentally increased the right atrial pressure decreased, Arthur Guyton and coworkers proposed an interpretation that right atrial pressure represents a back pressure restricting venous return (equal to cardiac output in steady state). The idea that right atrial pressure is a back pressure limiting cardiac output and the associated idea that “venous recoil” does work to produce flow have confused physiologists and clinicians for decades because Guyton's interpretation interchanges independent and dependent variables. Here Guyton's model and data are reanalyzed to clarify the role of arterial and right atrial pressures and cardiac output and to clearly delineate that cardiac output is the independent (causal) variable in the experiments. Guyton's original mathematical model is used with his data to show that a simultaneous increase in arterial pressure and decrease in right atrial pressure with increasing cardiac output is due to a blood volume shift into the systemic arterial circulation from the systemic venous circulation. This is because Guyton's model assumes a constant blood volume in the systemic circulation. The increase in right atrial pressure observed when cardiac output decreases in a closed circulation with constant resistance and capacitance is due to the redistribution of blood volume and not because right atrial pressure limits venous return. Because Guyton's venous return curves have generated much confusion and little clarity, we suggest that the concept and previous interpretations of venous return be removed from educational materials.


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