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Journal articles on the topic 'Pressure-volume curve'

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Published: 4 June 2025

Last updated: 15 July 2025

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Kunig, H. E. "Pressure-volume curve diagnosis." Journal of Cardiothoracic and Vascular Anesthesia 8, no. 5 (1994): 51. http://dx.doi.org/10.1016/1053-0770(94)90360-3.

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Wagers, Scott S., T. Glen Bouder, David A. Kaminsky, and Charles G. Irvin. "The Invaluable Pressure-Volume Curve." Chest 117, no. 2 (2000): 578–83. http://dx.doi.org/10.1378/chest.117.2.578.

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TAKEUCHI, MUNEYUKI, KHALED A SEDEEK, GUILHERME P P. SCHETTINO, KLAUDIUSZ SUCHODOLSKI, and ROBERT M KACMAREK. "Peak Pressure During Volume History and Pressure–Volume Curve Measurement Affects Analysis." American Journal of Respiratory and Critical Care Medicine 164, no. 7 (2001): 1225–30. http://dx.doi.org/10.1164/ajrccm.164.7.2101053.

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Dorn, Melissa, Anja Becher-Deichsel, Barbara Bockstahler, Christian Peham, and Gilles Dupré. "Pressure–Volume Curve during Capnoperitoneum in Cats." Animals 10, no. 8 (2020): 1408. http://dx.doi.org/10.3390/ani10081408.

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Laparoscopy is a growing field in veterinary medicine, although guidelines are lacking. The objective of this study was to evaluate the pressure–volume curve during capnoperitoneum in cats. A total of 59 female cats were scheduled for routine laparoscopy. Pressure and volume data were recorded and processed, and the yield point of the curve was calculated using a method based on a capacitor discharging function. For the remaining 40 cats, a linear-like pressure–volume curve was observed until a yield point with a mean cutoff pressure (COP) of 6.44 ± 1.7 mmHg (SD) (range, 2.72–13.00 mmHg) and a mean cutoff volume (COV) of 387 ± 144.35 mL (SD) (range, 178.84–968.43 mL) was reached. The mean mL/kg CO2 value in cats was 208 ± 34.69 mL/kg (range, 100.00–288.46 mL/kg). The COV correlated with COP and body weight but not with body condition score (BCS). COP correlated only with the COV. This study suggests that feline patients have a pressure–volume curve similar to that of canine patients, and the same pressure limit recommendations can be used for both species. After a yield point of 6.44 mmHg is reached, the increment in volume decreases exponentially as the intra-abdominal pressure (IAP) increases.

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Maggiore, Salvatore M., and Laurent Brochard. "Pressure-volume curve in the critically ill." Current Opinion in Critical Care 6, no. 1 (2000): 1–10. http://dx.doi.org/10.1097/00075198-200002000-00001.

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Pestaña, David. "Pressure-volume curve patterns in ARDS patients." Intensive Care Medicine 30, no. 5 (2004): 1002. http://dx.doi.org/10.1007/s00134-004-2219-3.

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Blanch, L. "Volume-pressure curve of the respiratory system." Intensive Care Medicine 24, no. 8 (1998): 886–87. http://dx.doi.org/10.1007/s001340050682.

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Shintani, H., and S. A. Glantz. "Influence of filling on left ventricular diastolic pressure-volume curve during pacing ischemia in dogs." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 4 (1994): H1373—H1385. http://dx.doi.org/10.1152/ajpheart.1994.266.4.h1373.

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The reversible upward shift of the diastolic pressure-volume curve that occurs during pacing-induced ischemia has not been fully explained by increases in passive chamber stiffness or reductions in relaxation rate. We measured the fully relaxed pressure-volume relation defined by both filling and nonfilling beats and the isovolumic relaxation time constant in nonfilling beats before and during demand ischemia using our in situ left ventricular volume clamping technique in 10 dogs. Pacing-induced ischemia shifted the diastolic pressure-volume curves in filling beats upward compared with the end-diastolic pressure-volume relation of the normally perfused heart. In contrast, the end-diastolic points for nonfilling beats during pacing-induced ischemia fell on the fully relaxed pressure-volume relation defined by the normally perfused heart. Left ventricular filling per se was necessary for the upward shift of the diastolic pressure-volume curve observed during pacing-induced ischemia. We speculate that active force developed during diastole induced by stretch activation or, perhaps, length-dependent changes in calcium sensitivity of the myofilaments in the ischemic myocardium due to stretch of the myocardium during rapid diastolic filling may contribute to the upward shift of the diastolic pressure-volume curve observed during pacing-induced ischemia.

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Nishida, Tomoyo, Klaudiusz Suchodolski, Guilherme P. P. Schettino, Khaled Sedeek, Muneyuki Takeuch, and Robert M. Kacmarek. "Peak volume history and peak pressure-volume curve pressures independently affect the shape of the pressure-volume curve of the respiratory system." Critical Care Medicine 32, no. 6 (2004): 1358–64. http://dx.doi.org/10.1097/01.ccm.0000128573.28173.2e.

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Venegas, José G., R. Scott Harris, and Brett A. Simon. "A comprehensive equation for the pulmonary pressure-volume curve." Journal of Applied Physiology 84, no. 1 (1998): 389–95. http://dx.doi.org/10.1152/jappl.1998.84.1.389.

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Venegas, José G., R. Scott Harris, and Brett A. Simon.A comprehensive equation for the pulmonary pressure-volume curve. J. Appl. Physiol. 84(1): 389–395, 1998.—Quantification of pulmonary pressure-volume (P-V) curves is often limited to calculation of specific compliance at a given pressure or the recoil pressure (P) at a given volume (V). These parameters can be substantially different depending on the arbitrary pressure or volume used in the comparison and may lead to erroneous conclusions. We evaluated a sigmoidal equation of the form, V = a + b[1 +[Formula: see text]]−1, for its ability to characterize lung and respiratory system P-V curves obtained under a variety of conditions including normal and hypocapnic pneumoconstricted dog lungs ( n = 9), oleic acid-induced acute respiratory distress syndrome ( n = 2), and mechanically ventilated patients with acute respiratory distress syndrome ( n = 10). In this equation, a corresponds to the V of a lower asymptote, b to the V difference between upper and lower asymptotes, cto the P at the true inflection point of the curve, and d to a width parameter proportional to the P range within which most of the V change occurs. The equation fitted equally well inflation and deflation limbs of P-V curves with a mean goodness-of-fit coefficient ( R 2) of 0.997 ± 0.02 (SD). When the data from all analyzed P-V curves were normalized by the best-fit parameters and plotted as (V − a)/ bvs. (P − c)/ d, they collapsed into a single and tight relationship ( R 2 = 0.997). These results demonstrate that this sigmoidal equation can fit with excellent precision inflation and deflation P-V curves of normal lungs and of lungs with alveolar derecruitment and/or a region of gas trapping while yielding robust and physiologically useful parameters.

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Youakim, Andro, and Ehab Daoud. "The Pressure-Volume curve, how to set PEEP." Journal of Mechanical Ventilation 2, no. 1 (2021): 45–47. https://doi.org/10.5281/zenodo.4542769.

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Risoe, C., C. Hall, and O. A. Smiseth. "Effect of enalaprilat on splanchnic vascular capacitance during acute ischemic heart failure in dogs." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 6 (1994): H2182—H2189. http://dx.doi.org/10.1152/ajpheart.1994.266.6.h2182.

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This study investigates the effect of angiotensin-converting-enzyme inhibition by intravenous enalaprilat (100 micrograms/kg) on splanchnic vascular capacitance during acute left ventricular failure induced by coronary microembolization in alpha-chloralose/urethan anesthetized dogs. Changes in hepatic and splenic vascular volumes were determined from organ diameters (sonomicrometry) at 15, 30, and 45 min after enalaprilat injection. Changes in vascular capacitance were assessed from organ pressure-diameter curves obtained during transient hepatic outflow occlusion. Thirty minutes after enalaprilat, hepatic volume was increased by 52 +/- 14 ml (P < 0.01), and portal and hepatic vein pressures were decreased from 10.2 +/- 0.9 to 8.7 +/- 0.8 mmHg (P < 0.01) and from 3.9 +/- 1.6 to 3.1 +/- 0.7 mmHg (P < 0.05), respectively. Splenic volume did not change. Enalaprilat shifted the hepatic pressure-diameter curve upward, resulting in a larger hepatic volume at any given pressure. Curve intercept was increased, suggesting an increase in unstressed vascular volume. Curve slope was unchanged. In conclusion, enalaprilat increased hepatic vascular volume during acute left ventricular failure in dogs. The pressure-diameter curve shift suggests a reduction in the smooth muscle tone of hepatic capacitance vessels.

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Shokry, Mia, and Kimiyo Yamasaki. "Ineffective trigger, the always missed sign." Journal of Mechanical Ventilation 1, no. 2 (2020): 57–58. http://dx.doi.org/10.53097/jmv.10014.

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Yellow curve: Pressure (cmH2O) on X-axis and Time (seconds) on Y-axis Pink curve: Flow (L/sec) on X-axis and Time (seconds) on Y-axis Green curve: Tidal volume (ml) on X-axis and Time (seconds) on Y-axis Orange curve: Esophageal pressure (cmH2O) on X-axis and Time (seconds) on Y-axis The blue arrows point to the inspiratory effort on flow and esophageal curves that is not followed by a breath

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Suga, H., O. Yamada, Y. Goto, and Y. Igarashi. "Peak isovolumic pressure-volume relation of puppy left ventricle." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 2 (1986): H167—H172. http://dx.doi.org/10.1152/ajpheart.1986.250.2.h167.

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We studied peak isovolumic pressure-volume (PV) relation of the left ventricle in 3-mo-old mongrel puppies. A puppy heart was excised and cross circulated with an adult dog. Left ventricular pressure and volume were measured with a water-filled balloon. Peak isovolumic PV curve in control contractile state was convex upward, reaching a maximum pressure of 130 mmHg. Epinephrine (0.6 microgram/min intracoronary) shifted the curve leftward and up to a maximum pressure of 160 mmHg. Propranolol (0.8 mg intracoronary) shifted it rightward and down to a maximum pressure of 110 mmHg. These PV curves were reasonably fitted by an asymptotic equation: P = A (1 - exp[-B (V - Vd)]), where V was normalized volume for 100 g left ventricle and Vd (6 ml/100 g) was V at which peak pressure was zero. A and B are regression coefficients. A was 149, 169, and 120 mmHg, and B was 0.16, 0.19, and 0.06 ml, respectively, in control, enhanced, and depressed contractile states. These changes in A and B were statistically significant. We conclude that the puppy left ventricular peak isovolumic PV curve is convex upward and shifts sensitively with inotropic changes.

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Peslin, R., M. Rotger, R. Farre, and D. Navajas. "Assessment of respiratory pressure-volume nonlinearity in rabbits during mechanical ventilation." Journal of Applied Physiology 80, no. 5 (1996): 1637–48. http://dx.doi.org/10.1152/jappl.1996.80.5.1637.

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The volume dependence of respiratory elastance makes it difficult to recognize actual changes in lung and chest wall elastic properties in artificially ventilated subjects. We have assessed in six anesthetized, tracheotomized, and paralyzed rabbits whether reliable information on the static pressure-volume (PV) curve could be obtained from recordings performed during step variations of the end-expiratory pressure without interrupting mechanical ventilation. Pressure and flow data recorded during 5- and 10-hPa positive-pressure steps were analyzed in the time domain with a nonlinear model featuring a sigmoid PV curve and with a model that, in addition, accounted for tissue viscoelastic properties. The latter fitted the data substantially better. Both models provided reasonably reproducible coefficients, but the PV curves obtained from the 5- and 10-hPa steps were systematically different. When the PV curves were used to predict respiratory effective elastance, the best predictor was the curve derived from the 10-hPa step with the viscoelastic model: unsigned differences averaged 8.6 +/- 11.1, 26.9 +/- 36.4, and 5.5 +/- 5.8% at end-expiratory pressures of 0, 5, and 10 hPa, respectively. This approach provides potentially useful, although not highly accurate, estimates of respiratory effective elastance-volume dependence.

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Thille, Arnaud W., Jean-Christophe M. Richard, Salvatore M. Maggiore, V. Marco Ranieri, and Laurent Brochard. "Alveolar Recruitment in Pulmonary and Extrapulmonary Acute Respiratory Distress Syndrome." Anesthesiology 106, no. 2 (2007): 212–17. http://dx.doi.org/10.1097/00000542-200702000-00007.

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Background Alveolar recruitment in response to positive end-expiratory pressure (PEEP) may differ between pulmonary and extrapulmonary acute respiratory distress syndrome (ARDS), and alveolar recruitment values may differ when measured by pressure-volume curve compared with static compliance. Methods The authors compared PEEP-induced alveolar recruitment in 71 consecutive patients identified in a database. Patients were classified as having pulmonary, extrapulmonary, or mixed/uncertain ARDS. Pressure-volume curves with and without PEEP were available for all patients, and pressure-volume curves with two PEEP levels were available for 44 patients. Static compliance was calculated as tidal volume divided by pressure change for tidal volumes of 400 and 700 ml. Recruited volume was measured at an elastic pressure of 15 cm H2O. Results Volume recruited by PEEP (10 +/- 3 cm H2O) was 223 +/- 111 ml in the pulmonary ARDS group (29 patients), 206 +/- 164 ml in the extrapulmonary group (16 patients), and 242 +/- 176 ml in the mixed/uncertain group (26 patients) (P = 0.75). At high PEEP (14 +/- 2 cmH2O, 44 patients), recruited volumes were also similar (P = 0.60). With static compliance, recruitment was markedly underestimated and was dependent on tidal volume (226 +/- 148 ml using pressure-volume curve, 95 +/- 185 ml for a tidal volume of 400 ml, and 23 +/- 169 ml for 700 ml; P &lt; 0.001). Conclusion In a large sample of patients, classification of ARDS was uncertain in more than one third of patients, and alveolar recruitment was similar in pulmonary and extrapulmonary ARDS. PEEP levels should not be determined based on cause of ARDS.

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Bartlett, M. K., G. Sinclair, G. Fontanesi, T. Knipfer, M. A. Walker, and A. J. McElrone. "Root pressure–volume curve traits capture rootstock drought tolerance." Annals of Botany 129, no. 4 (2021): 389–402. http://dx.doi.org/10.1093/aob/mcab132.

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Abstract Background and Aims Living root tissues significantly constrain plant water uptake under drought, but we lack functional traits to feasibly screen diverse plants for variation in the drought responses of these tissues. Water stress causes roots to lose volume and turgor, which are crucial to root structure, hydraulics and growth. Thus, we hypothesized that root pressure–volume (p–v) curve traits, which quantify the effects of water potential on bulk root turgor and volume, would capture differences in rootstock drought tolerance. Methods We used a greenhouse experiment to evaluate relationships between root p–v curve traits and gas exchange, whole-plant hydraulic conductance and biomass under drought for eight grapevine rootstocks that varied widely in drought performance in field trials (101-14, 110R, 420A, 5C, 140-Ru, 1103P, Ramsey and Riparia Gloire), grafted to the same scion variety (Vitis vinifera ‘Chardonnay’). Key Results The traits varied significantly across rootstocks, and droughted vines significantly reduced root turgor loss point (πtlp), osmotic potential at full hydration (πo) and capacitance (C), indicating that roots became less susceptible to turgor loss and volumetric shrinkage. Rootstocks that retained a greater root volume (i.e. a lower C) also maintained more gas exchange under drought. The rootstocks that previous field trials have classified as drought tolerant exhibited significantly lower πtlp, πo and C values in well-watered conditions, but significantly higher πo and πtlp values under water stress, than the varieties classified as drought sensitive. Conclusions These findings suggest that acclimation in root p–v curve traits improves gas exchange in persistently dry conditions, potentially through impacts on root hydraulics or root to shoot chemical signalling. However, retaining turgor and volume in previously unstressed roots, as these roots deplete wet soil to moderately negative water potentials, could be more important to drought performance in the deep, highly heterogenous rooting zones which grapevines develop under field conditions.

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SCHULTE, P. J., and T. M. HINCKLEY. "A Comparison of Pressure-Volume Curve Data Analysis Techniques." Journal of Experimental Botany 36, no. 10 (1985): 1590–602. http://dx.doi.org/10.1093/jxb/36.10.1590.

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HICKLING, KEITH G. "The Pressure–Volume Curve Is Greatly Modified by Recruitment." American Journal of Respiratory and Critical Care Medicine 158, no. 1 (1998): 194–202. http://dx.doi.org/10.1164/ajrccm.158.1.9708049.

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Servillo, Giuseppe, Edoardo De Robertis, Salvatore Maggiore, François Lemaire, Laurent Brochard, and Rosalba Tufano. "The upper inflection point of the pressure-volume curve." Intensive Care Medicine 28, no. 7 (2002): 842–49. http://dx.doi.org/10.1007/s00134-002-1293-7.

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Vieillard-Baron, Antoine, and Fran�ois Jardin. "Pressure-volume curve patterns in ARDS patients?authors? reply." Intensive Care Medicine 30, no. 5 (2004): 1003. http://dx.doi.org/10.1007/s00134-004-2218-4.

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He, Xingdong, Peifang Cong, Yubao Gao, et al. "Drought resistance of four grasses using pressure-volume curve." Frontiers of Biology in China 2, no. 4 (2007): 425–30. http://dx.doi.org/10.1007/s11515-007-0065-8.

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Osanai, K., K. Takahashi, S. Sato, et al. "Changes of lung surfactant and pressure-volume curve in bleomycin-induced pulmonary fibrosis." Journal of Applied Physiology 70, no. 3 (1991): 1300–1308. http://dx.doi.org/10.1152/jappl.1991.70.3.1300.

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We investigated whether alveolar surface force increased and participated in the lung pressure-volume relationship in bleomycin-induced pulmonary fibrosis in hamsters and, if so, whether lung surfactant was hampered in the lungs. On the air-filled pressure-volume curve, decreases of lung volume from control level were significantly higher at 3-8 cmH2O pressure on day 10 than on day 30. Because the change of lung tissue elasticity evaluated from the saline-filled pressure-volume curve was equal for the 2 days, the higher decrease of air volume on day 10 was due primarily to contribution of alveolar surface force. Pressure differences between deflation limbs of air-filled and saline-filled pressure-volume curves, which represented net alveolar surface force, were significantly higher at any lung volume between 50 and 90% total lung capacity on day 10, but almost no significance was observed on day 30. Phospholipid concentration in bronchoalveolar lavage fluid significantly decreased on day 10 but had improved by day 30. Analysis of phospholipid species in purified lung surfactant showed decreased fractions of disaturated phosphatidylcholine and phosphatidylglycerol on day 10. Surface-active properties of the surfactant, measured by a modified Wilhelmy balance, were remarkably hampered on day 10, but most of them had improved by day 30. We consider that the quantitative and functional abnormalities of lung surfactant have a part in the aggravation of lung mechanics in the acute phase of pulmonary fibrosis.

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Gugger, M., P. K. Wraith, and M. F. Sudlow. "A new method of analysing pulmonary quasi-static pressure-volume curves in normal subjects and in patients with chronic airflow obstruction." Clinical Science 78, no. 4 (1990): 365–69. http://dx.doi.org/10.1042/cs0780365.

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1. Exponential analysis of lung pressure-volume curves is used to deal with the non-linearity of the pressure-volume relationship. A major problem of this procedure is to define the lower volume limit for exponential curve fitting. 2. In 12 healthy subjects and 24 patients with chronic airflow obstruction, a cubic function was fitted to the quasi-static pressure-volume curves to define an inflection point. 3. The exponential function of Colebatch et al. (Colebatch, H.J.H., Ng, C.K.Y. & Nikov, N. J. Applied Physiol. 1979; 46, 387–93) was then fitted to the data for volumes above the inflection point. 4. Exponential analysis with a cubic determination of an inflection point provides an objective way to describe the elastic properties of the human lungs in vivo.

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Luecke, Thomas, Juergen P. Meinhardt, Peter Herrmann, Gerald Weisser, Paolo Pelosi, and Michael Quintel. "Setting Mean Airway Pressure during High-frequency Oscillatory Ventilation According to the Static Pressure–Volume Curve in Surfactant-deficient Lung Injury." Anesthesiology 99, no. 6 (2003): 1313–22. http://dx.doi.org/10.1097/00000542-200312000-00012.

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Background Numerous studies suggest setting positive end-expiratory pressure during conventional ventilation according to the static pressure-volume (P-V) curve, whereas data on how to adjust mean airway pressure (P(aw)) during high-frequency oscillatory ventilation (HFOV) are still scarce. The aims of the current study were to (1) examine the respiratory and hemodynamic effects of setting P(aw) during HFOV according to the static P-V curve, (2) assess the effect of increasing and decreasing P(aw) on slice volumes and aeration patterns at the lung apex and base using computed tomography, and (3) study the suitability of the P-V curve to set P(aw) by comparing computed tomography findings during HFOV with those obtained during recording of the static P-V curve at comparable pressures. Methods Saline lung lavage was performed in seven adult pigs. P-V curves were obtained with computed tomography scanning at each volume step at the lung apex and base. The lower inflection point (Pflex) was determined, and HFOV was started with P(aw) set at Pflex. The pigs were provided five 1-h cycles of HFOV. P(aw), first set at Pflex, was increased to 1.5 times Pflex (termed 1.5 Pflex(inc)) and 2 Pflex and decreased thereafter to 1.5 times Pflex and Pflex (termed 1.5 Pflex(dec) and Pflex(dec)). Hourly measurements of respiratory and hemodynamic variables as well as computed tomography scans at the apex and base were made. Results High-frequency oscillatory ventilation at a P(aw) of 1.5 Pflex(inc) reestablished preinjury arterial oxygen tension values. Further increase in P(aw) did not change oxygenation, but it decreased oxygen delivery as a result of decreased cardiac output. No differences in respiratory or hemodynamic variables were observed when comparing HFOV at corresponding P(aw) during increasing and decreasing P(aw). Variation in total slice lung volume (TLVs) was far less than expected from the static P-V curve. Overdistended lung volume was constant and less than 3% of TLVs. TLVs values during HFOV at Pflex, 1.5 Pflex(inc), and 2 Pflex were significantly greater than TLVs values at corresponding tracheal pressures on the inflation limb of the static P-V curve and located near the deflation limb. In contrast, TLVs values during HFOV at decreasing P(aw) (i.e., 1.5 Pflex(dec) and Pflex(dec)) were not significantly greater than corresponding TLV on the deflation limb of the static P-V curves. The marked hysteresis observed during static P-V curve recordings was absent during HFOV. Conclusions High-frequency oscillatory ventilation using P(aw) set according to a static P-V curve results in effective lung recruitment, and slice lung volumes during HFOV are equal to those from the deflation limb of the static P-V curve at equivalent pressures.

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Wang, Yang, Jun Teng, Qi Huang, Wei Wang, and Yong Zhong. "Insight on the Swelling Pressure–Suction Relationship of Compacted Bentonite during Hydration." Materials 16, no. 15 (2023): 5403. http://dx.doi.org/10.3390/ma16155403.

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Investigation of the swelling pressure of buffer/backfill materials is a critical aspect in the design of high-level radioactive waste (HLW) disposal repositories. In this study, to clarify the swelling pressure–suction relation for compacted bentonite upon the hydration path, constant-volume swelling pressure tests with suction control were conducted. The swelling pressure–suction curves indicated that the swelling pressure of the specimens increased significantly with increasing dry density, while the shape of the curves during hydration depended on the dry density. Moreover, the swelling pressure–suction curves exhibited a distinction between unsaturated and saturated segments divided by the critical saturated state (CSS) curve, which proves the unique existence of a CSS curve in the stress space independent of the stress path. With the introduction of the CSS curve into the s–p space, the conventional stress space of unsaturated soil could expand to that of unsaturated expansive soil. The results obtained in this study could provide the mechanical parameters for the construction of disposal repositories. In addition, the stress space with CSS curve proposed in this study provides a new approach to building constitutive models of bentonite materials.

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Freeman, G. L., and W. C. Little. "Comparison of in situ and in vitro studies of pericardial pressure-volume relation in dogs." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 2 (1986): H421—H427. http://dx.doi.org/10.1152/ajpheart.1986.251.2.h421.

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Whether the material properties of the pericardial membrane are the key determinants of the in situ pericardial pressure-volume relation is not known. Although both the pressure-volume relation of the intact pericardium and the stress-strain relation of isolated pericardial samples are nonlinear, it is not clear how closely these phenomena are related. To directly examine this question we compared the pressure-volume, pressure-normalized volume, and stress-strain relations of pericardia from six dogs tested both in situ and in vitro. The curves generated under the two sets of conditions were different. The transition from the compliant to the noncompliant portion of the curve was more acute under in vitro conditions. Nonlinear regression analysis using a monoexponential function of the form Y = alpha (e beta chi-1) showed beta, the proportionality constant for the slope of the curve, to be larger for each form of analysis under in vitro testing conditions as follows: 0.002 +/- 0.009 vs. 0.078 +/- 0.029, P less than 0.002 for pressure-volume; 3.52 +/- 1.75 vs. 11.03 +/- 5.31, P less than 0.005 for pressure-normalized volume; and 19.6 +/- 6.6 vs. 62.3 +/- 18.8, P less than 0.001 for stress-strain. These differences in the pressure-volume relation of the intrapericardial space in situ and the isolated pericardium in vitro suggest that pericardial attachments present in situ may buffer the loading of the membrane itself. We conclude that the pressure-volume relation of the intrapericardial space is only partly determined by the properties of the isolated pericardium alone and is also influenced by other components of the intact pericardium.

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Meilani, Inge, Harianto Rahardjo, and Eng-Choon Leong. "Pore-water pressure and water volume change of an unsaturated soil under infiltration conditions." Canadian Geotechnical Journal 42, no. 6 (2005): 1509–31. http://dx.doi.org/10.1139/t05-066.

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Triaxial shearinginfiltration tests were conducted to study the pore-water pressure and volume change of unsaturated soils subjected to infiltration conditions. A modified triaxial apparatus with three Nanyang Technological University (NTU) mini suction probes along the specimen height was used for the experimental program. Elastic moduli were obtained for the soil structure with respect to changes in net confining pressure (E) and matric suction (H). Water volumetric moduli associated with changes in net confining pressure (Ew) and matric suction (Hw) were also obtained from the shearinginfiltration tests. Water volumetric strain and pore-water pressure during the shearinginfiltration tests were computed based on volume change theory. This paper presents the significance of obtaining the parameter Hw from an appropriate scanning curve of a soil-water characteristic curve (SWCC) for the computation of water volumetric strain and pore-water pressure changes during a shearinginfiltration test. The appropriate scanning curve should be obtained from the wetting curve of the SWCC at the matric suction where the infiltration test commences.Key words: infiltration, matric suction, triaxial, unsaturated soils, pore-water pressure, water volume change.

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Linehan, J. H., C. A. Dawson, D. A. Rickaby, and T. A. Bronikowski. "Pulmonary vascular compliance and viscoelasticity." Journal of Applied Physiology 61, no. 5 (1986): 1802–14. http://dx.doi.org/10.1152/jappl.1986.61.5.1802.

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When dog lung lobes were perfused at constant arterial inflow rate, occlusion of the venous outflow (VO) produced a rapid jump in venous pressure (Pv) followed by a slower rise in both arterial pressure (Pa) and Pv. During the slow rise Pa(t) and Pv(t) tended to converge and become concave upward as the volume of blood in the lungs increased. We compared the dynamic vascular volume vs. pressure curves obtained after VO with the static volume vs. pressure curves obtained by dye dilution. The slope of the static curve (the static compliance, Cst) was always larger than the slope of the dynamic curve (the dynamic compliance, Cdyn). In addition, the Cdyn decreased with increasing blood flow rate. When venous occlusion (VO) was followed after a short time interval by arterial occlusion (AO) such that the lobe was isovolumic, both Pa and Pv fell with time to a level that was below either pressure at the instant of AO. In an attempt to explain these observations a compartmental model was constructed in which the hemodynamic resistance and vascular compliance were volume dependent and the vessel walls were viscoelastic. These features of the model could account for the convergence and upward concavity of the Pa and Pv curves after VO and the pressure relaxation in the isovolumic state after AO, respectively. According to the model analysis, the difference between Cst and Cdyn and the flow dependence of Cdyn are due to wall viscosity and volume dependence of compliance, respectively. Model analysis also suggested ways of evaluating changes in the viscoelasticity of the lobar vascular bed. Hypoxic vasoconstriction that increased total vascular resistance also decreased Cst and Cdyn and appeared to increase the vessel wall viscosity.

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Risoe, C., C. Hall, and O. A. Smiseth. "Blood volume changes in liver and spleen during cardiogenic shock in dogs." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 6 (1991): H1763—H1768. http://dx.doi.org/10.1152/ajpheart.1991.261.6.h1763.

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Changes in vascular capacitance of the liver and spleen were studied in seven anesthetized dogs during cardiogenic shock induced by coronary microembolization. Left ventricular end-diastolic pressure increased from 2 +/- 2 to 28 +/- 4 mmHg (P less than 0.001), and mean aortic pressure decreased from 111 +/- 7 to 56 +/- 9 mmHg (P less than 0.001). Hepatic venous pressure increased from 1.8 +/- 0.6 to 5.0 +/- 1.0 mmHg (P less than 0.05). Portal venous pressure did not change. Blood volume changes were assessed from sonomicrometric measurements of organ diameters. Hepatic diameter increased after embolization, corresponding to an estimated 54 +/- 14 ml increase of hepatic blood volume (P less than 0.01). Splenic diameter gradually decreased during shock until an estimated 33 +/- 12 ml of blood had been released (P less than 0.05). Occlusion of hepatic venous outflow by a balloon catheter was used to cause ramp changes in hepatic volume and hepatic venous pressure so that a pressure-volume curve could be estimated. Analysis of the hepatic curves showed an increase in unstressed volume with no change in vascular compliance during shock. The blood volume increase could in part be attributed to increased outflow pressure, but active dilation of hepatic capacitance vessels probably contributed. Splenic curves were shifted downward, suggesting expulsion of blood by active contraction.

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Berard, David, Saul J. Vega, Sofia I. Hernandez Torres, et al. "Development of the PhysioVessel: a customizable platform for simulating physiological fluid resuscitation." Biomedical Physics & Engineering Express 8, no. 3 (2022): 035017. http://dx.doi.org/10.1088/2057-1976/ac6196.

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Abstract Uncontrolled hemorrhage is a leading cause of death in trauma situations. Developing solutions to automate hemorrhagic shock resuscitation may improve the outcomes for trauma patients. However, testing and development of automated solutions to address critical care interventions, oftentimes require extensive large animal studies for even initial troubleshooting. The use of accurate laboratory or in-silico models may provide a way to reduce the need for large animal datasets. Here, a tabletop model, for use in the development of fluid resuscitation with physiologically relevant pressure-volume responsiveness for high throughput testing, is presented. The design approach shown can be applied to any pressure-volume dataset through a process of curve-fitting, 3D modeling, and fabrication of a fluid reservoir shaped to the precise curve fit. Two case studies are presented here based on different resuscitation fluids: whole blood and crystalloid resuscitation. Both scenarios were derived from data acquired during porcine hemorrhage studies, used a pressure-volume curve to design and fabricate a 3D model, and evaluated to show that the test platform mimics the physiological data. The vessels produced based on data collected from pigs infused with whole blood and crystalloid were able to reproduce normalized pressure-volume curves within one standard deviation of the porcine data with mean residual differences of 0.018 and 0.016, respectively. This design process is useful for developing closed-loop algorithms for resuscitation and can simplify initial testing of technologies for this life-saving medical intervention.

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Fraites, Thomas J., Akio Saeki, and David A. Kass. "Effect of Altering Filling Pattern on Diastolic Pressure-Volume Curve." Circulation 96, no. 12 (1997): 4408–14. http://dx.doi.org/10.1161/01.cir.96.12.4408.

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Hatakeyama, S., K. Harada, N. Saoyama, and Y. Monden. "Pressure-Volume Curve of the Remaining Lung after Lung Resection." European Surgical Research 21, no. 3-4 (1989): 168–74. http://dx.doi.org/10.1159/000129020.

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De Pascalis, Riccardo, I. David Abrahams, and William J. Parnell. "Predicting the pressure–volume curve of an elastic microsphere composite." Journal of the Mechanics and Physics of Solids 61, no. 4 (2013): 1106–23. http://dx.doi.org/10.1016/j.jmps.2012.11.005.

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Weissenberg, Sarah, and Revital Lavy. "Pressure-Volume Curve and Compliance of a Balloon: a Simulation." Advances in Physiology Education 27, no. 4 (2003): 244–45. http://dx.doi.org/10.1152/advan.00021.2003.

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As educators, we are continually designing new methods and procedures to enhance learning. During this process, good ideas are frequently generated and tested, but the extent of such activities may not be adequate for a full manuscript. Nonetheless, the ideas may be quite beneficial in improving the teaching and learning of physiology. Illuminations is a column designed to facilitate the sharing of these ideas (illuminations). The format of submissions is quite simple: a succinct description of about one or two double-spaced pages (less title and authorship) of something you have used for the classroom, teaching, lab, conference room, etc. You may include one or two simple figures or references. Submit ideas for inclusion in Illuminations directly to the Associate Editor in charge, Stephen DiCarlo (sdicarlo@med.wayne.edu).

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van den Berg, B., H. Stam, and JM Bogaard. "Effects of PEEP on respiratory mechanics in patients with COPD on mechanical ventilation." European Respiratory Journal 4, no. 5 (1991): 561–67. http://dx.doi.org/10.1183/09031936.93.04050561.

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We studied the effects of positive end-expiratory pressure (PEEP) applied by the ventilator on respiratory mechanics in ventilated patients with chronic obstructive pulmonary disease (COPD). Airway pressures, relaxed expiratory flow-volume curves and end-expiratory volumes (EEV) were measured. In all patients investigated without PEEP applied by the ventilator, an intrinsic PEEP level (PEEPi) and a concavity in the flow-volume curve was present. Ventilator-PEEP caused a significant decrease in PEEPi in all patients (p less than 0.01). In patients in whom ventilator-PEEP exceeded PEEPi, significant increases occurred in airway pressures and EEV (p less than 0.05) and moreover the shape of the flow-volume curve was changing. In patients in whom the level of ventilator-PEEP was below the PEEPi level, no significant changes in airway pressures, EEV or flow-volume curves were found. We conclude: 1) PEEP applied by the ventilator can reduce PEEPi in ventilated patients with COPD without significant changes in airway pressures, EEV or flow-volume curves. 2) Expiratory flow-volume curves can be used to estimate the effects of ventilator-PEEP on EEV.

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Moreno, R. H., G. S. McCormack, J. Brendan, et al. "Effect of intravenous papain on tracheal pressure-volume curves in rabbits." Journal of Applied Physiology 60, no. 1 (1986): 247–52. http://dx.doi.org/10.1152/jappl.1986.60.1.247.

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To investigate the effects of airway cartilage softening on tracheal mechanics, pressure-volume (PV) curves of excised tracheas were studied in 12 rabbits treated with 100 mg/kg iv papain, whereas 14 control animals received no pretreatment. The animals were killed 24 h after the injection and the excised specimens studied 24 h later. Treated tracheas exhibited decreased ability to withstand negative transmural pressures, reflected in increased collapse compliance: 6.2 +/- 2.1 vs. 2.0 +/- 0.5% peak volume (Vmax)/cmH2O means +/- SD, P less than 0.001, (Vmax = extrapolated maximal tracheal volume), increased kc (exponential constant that reflects the shape of collapse limb of the PV curve): 0.244 +/- 0.077 vs. 0.065 +/- 0.015 (P less than 0.001). The distension limb of the PV curve greater than 2.5 cmH2O transmural pressure (Ptm) was no different. Compliance between 0 and 2.5 cmH2O Ptm was increased in papain-treated rabbits: 4.97 +/- 1.73 vs. 2.30 +/- 0.31% Vmax/cmH2O (P less than 0.001). Tracheal volume, and therefore mean diameter, was decreased at 0 Ptm: 2.7 +/- 0.26 vs. 3.2 +/- 0.27 mm (P less than 0.001). We conclude that airway cartilage softening increases the compliance of the trachea at pressures less than 2.5 cmH2O Ptm.

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Cornish, K. G., M. W. Barazanji, T. Yong, and J. P. Gilmore. "Volume expansion attenuates baroreflex sensitivity in the conscious nonhuman primate." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 3 (1989): R595—R598. http://dx.doi.org/10.1152/ajpregu.1989.257.3.r595.

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We examined the effect of intravascular volume expansion (VE) on the arterial baroreflex control of pulse rate (PR) in conscious, chronically instrumented monkeys tethered in their cages. A total of five monkeys was studied after surgical implantation of catheters in the descending aorta, the left atrium, and the internal jugular vein. Mean arterial blood pressure (MABP)-PR stimulus response curves were constructed by decreasing and increasing blood pressure with nitroprusside and phenylephrine, respectively. The data were analyzed with a regression analysis that generated a sigmoid curve and the maximum sensitivity (slope) of the curve. The data were obtained before and after VE with an isotonic isoncotic dextran solution equal to 20% of the estimated blood volume. After VE, the MABP-PR curve shifted to the right at the high blood pressures, and there was a significant decrease in the maximum sensitivity from 5.65 +/- 1.44 for control to 2.14 +/- 0.63 after VE (P less than 0.05). We concluded that VE attenuates the baroreflex control of heart rate in the conscious nonhuman primate.

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Wagner, E. M., W. A. Mitzner, and E. R. Bleecker. "Peripheral circulatory alterations in canine anaphylactic shock." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 5 (1986): H934—H940. http://dx.doi.org/10.1152/ajpheart.1986.251.5.h934.

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We have examined peripheral circulatory variables that might contribute to the decrease in cardiac output and arterial pressure characteristic of anaphylactic shock. In six dogs instrumented with a right heart bypass, the intravenous administration of Ascaris suum antigen caused a 53% decrease in cardiac output and a 58% decrease in arterial pressure. Resistance to venous return increased from 0.0038 +/- 0.0004 to 0.0056 +/- 0.0006 mmHg X ml-1 X min (P less than 0.05), mean systemic pressure decreased from 7.0 +/- 0.6 to 4.4 +/- mmHg (P less than 0.005), and vascular compliance did not change. Assuming a constant vascular volume, the decrease in mean systemic pressure could be explained by a rightward shift of the systemic pressure volume curve. This constant-volume assumption was tested in intact (n = 6) and splenectomized dogs (n = 7). Serial measurements of protein oncotic pressure and hematocrit were used to estimate plasma volume changes during anaphylaxis. Both methods for estimating volume showed small increases in plasma volume at the time of the largest decrease in arterial pressure in both groups of animals. These results suggest that the primary circulatory mechanisms responsible for anaphylactic shock are an increase in resistance to venous return and a shift of the systemic pressure volume curve and not an acute loss of plasma volume.

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Davidson, Shaun, Chris Pretty, Antoine Pironet, et al. "Minimally invasive, patient specific, beat-by-beat estimation of left ventricular time varying elastance." BioMedical Engineering OnLine 16, no. 1 (2017): 42. https://doi.org/10.1186/s12938-017-0338-7.

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Background: The aim of this paper was to establish a minimally invasive method for deriving the left ventricular time varying elastance (TVE) curve beat-by-beat, the monitoring of which's inter-beat evolution could add significant new data and insight to improve diagnosis and treatment. The method developed uses the clinically available inputs of aortic pressure, heart rate and baseline end-systolic volume (via echocardiography) to determine the outputs of left ventricular pressure, volume and dead space volume, and thus the TVE curve. This approach avoids directly assuming the shape of the TVE curve, allowing more effective capture of intra- and inter-patient variability.Results: The resulting TVE curve was experimentally validated against the TVE curve as derived from experimentally measured left ventricular pressure and volume in animal models, a data set encompassing 46,318 heartbeats across 5 Piétrain pigs. This simulated TVE curve was able to effectively approximate the measured TVE curve, with an overall median absolute error of 11.4% and overall median signed error of −2.5%.Conclusions: The use of clinically available inputs means there is potential for real-time implementation of the method at the patient bedside. Thus the method could be used to provide additional, patient specific information on intra- and inter-beat variation in heart function.

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Mahmud, Walid Mohamed. "Rate-Controlled Mercury Injection Experiments to Characterize Pore Space Geometry of Berea Sandstone." E3S Web of Conferences 366 (2023): 01016. http://dx.doi.org/10.1051/e3sconf/202336601016.

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Interpretation of the relationship between heterogeneity and the flow in porous media is very important in increasing the recovery factor for an oil or gas reservoir. Capillarity for instance, controls fluids static distribution in a reservoir prior to production and remaining hydrocarbons after production commences. Therefore, capillary pressure data are used by petroleum engineers, geologists, and petrophysicists to evaluate production characteristics of petroleum accumulations. Conventional pressure-controlled mercury porosimetry produces an overall capillary pressure curve and pore throat size distribution data that provide little information about the porous medium structure and pore geometry. The present study provides information on three capillary pressure curves obtained from rate-controlled mercury injection porosimetry; one describes the larger pore spaces or pore bodies of a rock, another describes the smaller pores or pore throats that connect the larger pores, and a final curve which corresponds to the overall capillary pressure curve obtained from the conventional pressure-controlled mercury injection. An experimental constant-rate mercury injection apparatus was constructed that consists of a piston displacement pump, a computer controlled stepper motor drive and a core sample cell designed to minimize dead volume. The apparatus was placed in a glass chamber and subjected to an air bath to maintain a constant temperature of 27o C throughout the experiments. Then constant rate mercury injection experiments were performed on three Berea Sandstone core plugs. Results show that volume-controlled or rate-controlled porosimetry provides considerably more detailed data and information on heterogeneity and the statistical nature of pore space structure than the conventional pressure-controlled porosimetry as pressure fluctuations with time reveal menisci locations in pore bodies and pore throats. Moreover, pore size distributions based on volume-accessed pores and pore radii were obtained from the pressure versus saturation relationship.

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Ohya, N., J. Huang, T. Fukunaga, and H. Toga. "Airway pressure-volume curve estimated by flow interruption during forced expiration." Journal of Applied Physiology 67, no. 6 (1989): 2631–38. http://dx.doi.org/10.1152/jappl.1989.67.6.2631.

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We attempted to estimate the pressure-volume characteristics of airways downstream from the choke point when the airflow was abruptly interrupted during forced expiration. The change of gas volume of the downstream segment after interruption could be estimated by multiplying the maximum flow (Vmax) immediately before interruption by the interruption time because the Vmax is maintained for a short period after airflow interruption at the mouth, as described in our previous report (J. Appl. Physiol. 66: 509-517, 1989). For the pressure of the downstream segment, we used the mouth pressure itself. Airway compliance, a slope of the pressure-volume curve, was measured in an airway model in eight normal subjects, in six patients with chronic obstructive pulmonary disease (COPD), and in one patient with tracheobronchopathia osteochondroplastica. Airway compliance was 0.96 ml/cmH2O in normal subjects and 2.49 ml/cmH2O in COPD patients. This difference of airway compliance was believed to be caused by the longitudinal expansion of the downstream segment and changes in the properties of the airway wall.

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Takeuchi, M., T. Shimatani, M. Kyogoku, and T. S. Nishida. "Lung Recruitability Assessment Using Pressure-volume Curve May Be Affected by Its Peak Pressure." American Journal of Respiratory and Critical Care Medicine 211, Abstracts (2025): A1518. https://doi.org/10.1164/ajrccm.2025.211.abstracts.a1518.

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Wang, Pan-Pan, Ju-Xiang Shao, and Qi-Long Cao. "Melting properties of Pt and its transport coefficients in liquid states under high pressures." International Journal of Modern Physics B 30, no. 01 (2016): 1550250. http://dx.doi.org/10.1142/s0217979215502501.

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Molecular dynamics (MD) simulations of the melting and transport properties in liquid states of platinum for the pressure range (50–200 GPa) are reported. The melting curve of platinum is consistent with previous ab initio MD simulation results and the first-principles melting curve. Calculated results for the pressure dependence of fusion entropy and fusion volume show that the fusion entropy and the fusion volume decrease with increasing pressure, and the ratio of the fusion volume to fusion entropy roughly reproduces the melting slope, which has a moderate decrease along the melting line. The Arrhenius law well describes the temperature dependence of self-diffusion coefficients and viscosity under high pressure, and the diffusion activation energy decreases with increasing pressure, while the viscosity activation energy increases with increasing pressure. In addition, the entropy-scaling law, proposed by Rosenfeld under ambient pressure, still holds well for liquid Pt under high pressure conditions.

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Zhixia, Guofang Fei, Qi Zhang, and Yi Ru. "Clinical application of a ventilation strategy based on the P-V curve in obese patients undergoing gynaecological laparoscopic surgery." Journal of the Pakistan Medical Association 75, no. 05 (2025): 743–47. https://doi.org/10.47391/jpma.20946.

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Objective: To explore the clinical value of pressure-controlled ventilation-volume guaranteed (PCV-VG) strategy based on the pressure-volume curve method in obese patients undergoing gynaecological laparoscopic surgery. Method: The retrospective study was conducted in December 2021 after approval from the ethics review committee of Huzhou Maternal and Child Health Hospital, China, and comprised clinical records of obese patients who underwent elective gynaecological laparoscopic surgery between January 2020 and October 2021. The patients were divided into study group A, who underwent surgery with PCV-VG, and control group B, who underwent surgery without the PCV-VG. Ventilation parameters in group A were individually set according to the pre-pneumoperitoneum pressure-volume curves. Respiratory parameters, peak airway pressure, end-tidal carbon dioxide partial pressure, mean arterial pressure and patients' postoperative comfort scores were compared between the groups after tracheal intubation, pneumoperitoneum, and postural positioning. Data was analysed using SPSS 22. Results: Of the 200 patients, 40(20%) were cases of laparoscopy myomectomy, 152(76%) cases of ovarian cystectomy, and 8(4%) cases of hysterectomy. There were 100(50%) females in group A with a mean age of 43.15±4.24 years, and 100(50%) were in group B with a mean age of 42.69±4.01 years (p=0.12). The peak airway pressure, mean arterial pressure, pneumoperitoneum pressure, and head-down tilt of the patients in group A were significantly lower post-pneumoperitoneum and post-positioning (p<0.05). At the same time, the respiratory rate was considerably higher (p<0.05) than that in group B. The end-tidal carbon dioxide partial pressure value at all time points was not significantly different between the groups (p>0.05). Postoperative comfort scores of patients in group A were significantly higher than those of group B (p<0.05). Conclusion: PCV-VG, based on the pressure-volume curve, significantly reduced intraoperative peak airway pressure, was associated with smoother hemodynamic, and regulated intraoperative pneumoperitoneal pressure and position in obese patients undergoing gynaecological laparoscopic surgery. The ventilation method also significantly improved the patients' postoperative comfort. Key Words: P-V curve, PCV-VG, Obese, Posture, Pneumoperitoneum pressure, Laparoscopy.

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Augé, Robert. "PVCURVE: A COMPUTER SPREADSHEET TEMPLATE FOR EVALUATING PRESSURE-VOLUME CURVES." HortScience 25, no. 9 (1990): 1096e—1096. http://dx.doi.org/10.21273/hortsci.25.9.1096e.

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The determination of tissue water potential components is important for understanding plant growth and response to the environment. Pressure-volume (PV) analysis is often considered to give the most accurate estimate of symplastic osmotic potential. Additional information about tissue water relations can also be computed from PV curves estimates of bulk cell wall elasticity, symplastic water volume, and turgor potential at various states of tissue water content. The generation of PV curves is a time-consuming procedure, however, and involves considerable computation. This presentation describes a computer spreadsheet template for traditional evaluation of a PV curve through linear regression of the zero turgor segment. The template allows real-time plotting of the inverse ψ/ water loss relating, provides estimates of most commonly calculated PV characteristics and permits instant graphic visualizations of changes in water potential components and elasticity with changes in water potential, total tissue water and symplastic water content. The advantages of spreadsheet analysis of PV curves are simplicity, consistency, thoroughness and speed. A fleeting acquaintance with spreadsheet software and a thorough understanding of pressure-volume theory on the part of the user is assumed.

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Henzler, Dietrich, Nadine Hochhausen, Rolf Dembinski, Sandra Orfao, Rolf Rossaint, and Ralf Kuhlen. "Parameters Derived from the Pulmonary Pressure–Volume Curve, but Not the Pressure–Time Curve, Indicate Recruitment in Experimental Lung Injury." Anesthesia & Analgesia 105, no. 4 (2007): 1072–78. http://dx.doi.org/10.1213/01.ane.0000278733.94863.09.

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Shapiro, Kenneth, and Arno Fried. "Pressure-volume relationships in shunt-dependent childhood hydrocephalus." Journal of Neurosurgery 64, no. 3 (1986): 390–96. http://dx.doi.org/10.3171/jns.1986.64.3.0390.

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✓ The pressure-volume index (PVI) technique of bolus manipulation of cerebrospinal fluid (CSF) was used to measure neural axis volume buffering capacity and resistance to absorption of CSF (Ro) in 20 shunt-dependent hydrocephalic children acutely ill from shunt malfunction. All children had had ventricles that were near normal or subnormal in size when the shunts were functioning. The mean intracranial pressure (ICP, ± standard deviation (SD)) at the time of revision was 10.6 ± 6.4 mm Hg. The mean measured PVI (± standard error of the mean) was 18.4 ± 1.1 ml compared to the normal PVI of 17.5 ± 4.4 ml (± SD) predicted for these children. According to paired t-tests, these measured values were similar to those predicted on the basis of neural axis volume for each child, indicating that these children had normal neural axis volume buffering capacity. While the study was in progress, abrupt increases of ICP were documented in all children. These waves were observed spontaneously as well as in response to the addition of volume to the neural axis. In each child a specific threshold pressure along the pressure-volume curve corresponded to the appearance of unstable ICP. The threshold pressures at which this occurred corresponded to a mean neural axis compliance of 0.32 ± 0.07 ml/mm Hg (± SD). The Ro varied as a function of ICP. The Ro measured at ICP's below 15 mm Hg ranged from 2 to 7.5 mm Hg/ml/min and rose to 12 to 30 mm Hg/ml/min at pressures in the 20 to 25 mm Hg range. The results of this study indicate that neural axis volume buffering capacity is normal in shunt-dependent children who respond to shunting by reconstitution of the cortical mantle. This study indicates that the proximate cause of their abrupt clinical deterioration is unstable ICP, which occurred at a similar point on the pressure-volume curve of all children studied. The correlation of Ro to ICP suggests that CSF absorption does not increase in these children as ICP rises, resulting in movement along relatively normal pressure-volume curves. The functional implications of these parameters are discussed.

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Duggan, C. J., W. D. Castle, and N. Berend. "Effects of continuous positive airway pressure breathing on lung volume and distensibility." Journal of Applied Physiology 68, no. 3 (1990): 1121–26. http://dx.doi.org/10.1152/jappl.1990.68.3.1121.

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In this study the effects on lung elastic behavior of 10 min of breathing at a continuous positive airway pressure (CPAP) of 10 cmH2O were examined in 10 normal subjects. To investigate whether any changes were induced by release of prostaglandins, the subjects were also pretreated with the cyclooxygenase inhibitor indomethacin. CPAP produced a significant (P less than 0.001) upward shift of the pressure-volume (PV) curve [change in total lung capacity (delta TLC) 374 +/- 67 (SE) ml, mean delta volume at a transpulmonary pressure of 15 cmH2O (delta VL15) 279 +/- 31 ml] with no change in K, an index of lung distensibility. After CPAP the PV curves returned to normal base line within 20 min. The same pattern was observed after indomethacin, but the increase in TLC was significantly less (P less than 0.01) (mean delta TLC 206 +/- 42 ml) mainly because of a slight and not statistically significant increase in base-line TLC. In five subjects further PV curves with and without CPAP were obtained greater than or equal to 7 days after indomethacin. The responses were not significantly different from those obtained before indomethacin (mean delta TLC 366 +/- 89, mean delta VL15 296 +/- 42 ml). We conclude that CPAP produces an upward shift of the PV curve without a change in lung distensibility. In addition, there may be a small degree of resting alveolar duct tone that is influenced by indomethacin.

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Mercer, R. R., J. M. Laco, and J. D. Crapo. "Three-dimensional reconstruction of alveoli in the rat lung for pressure-volume relationships." Journal of Applied Physiology 62, no. 4 (1987): 1480–87. http://dx.doi.org/10.1152/jappl.1987.62.4.1480.

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To determine alveolar pressure-volume relationships, alveolar three-dimensional reconstructions were prepared from lungs fixed by vascular perfusion at various points on the pressure-volume curve. Lungs from male Sprague-Dawley rats were fixed by perfusion through the pulmonary artery following a pressure-volume maneuver to the desired pressure point on either the inflation or deflation curve. Tissue samples from lungs were serially sectioned for determination of the volume fraction of alveoli and alveolar ducts and reconstruction of alveoli. Alveoli from lungs fixed at 5 cmH2O on the deflation curve (approximating functional residual volume) had a volume of 173 X 10(3) microns3, a surface area of 11,529 microns2, a mouth opening diameter of 72.7 microns, and a mean caliper diameter of 91.8 micron (SE). Alveolar shape changes during deflation from total lung capacity to residual volume was first (30 to 10 cmH2O) associated with little change in the diameter of the alveoli (102.7 +/- 2.4 to 100.3 +/- 3.3 microns). In the range overlapping normal breathing (10 to 0 cmH2O) there was a substantial decrease in diameter (100.3 +/- 3.3 to 43.3 +/- 2.3 microns). These measurements and others made on the relative changes in the dimensions of the alveolus suggest that the elastic network, particularly around the alveolar ducts, are predominant in determining lung behavior near the volume expansion limits of the lung while the elastic and surface tension properties of the alveoli are predominant in the volume range around functional residual capacity.

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