Relationship of Structural to Functional Impairment during Alveolar-Capillary Membrane Development

The pathway of oxygen through the body consists of the diffusion of oxygen across the alveolar-capillary membrane and then the peripheral tissue membranes, followed by the convective transport of oxygen in the blood. Any transport process will have its choke points and limitations. In the case of oxygen, the constraints can take 1 of 2 forms, perfusion limitation or diffusion limitation.

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The Two Doctors Fick

Just Enough Physiology ◽

10.1093/med/9780199797790.003.0012 ◽

2011 ◽

pp. 94-100

Author(s):

James R. Munis

Keyword(s):

Cardiac Output ◽

Steady State ◽

Transfer Rate ◽

Dialysis Membrane ◽

Solute Transfer ◽

Fick Principle ◽

Capillary Membrane ◽

The Difference ◽

Physical Laws ◽

Alveolar Capillary

We often confuse the ‘Fick principle’ with ‘Fick's law of diffusion.’ They are not the same. Ironically, Fick borrowed heavily from already known physical laws when he first described both his law of diffusion and his principle. Borrowing from Ohm's law of electricity, Fick applied concepts of diffusion and transfer across a resistance to formulate a law of diffusion that could be applied to gas or solute transfer across a membrane. Whether we are talking about transfer across the alveolar-capillary membrane or across a dialysis membrane, the concept is the same. The concept is similar to electricity—you have a transfer rate, resistance, and a gradient. Now let's consider the Fick principle. On the basis of another physical law he understood that, in the steady state, the difference between the amount of oxygen going into a tissue bed minus that leaving the tissue bed must be equal to the oxygen consumed. With a little reworking, this became the Fick principle: Cardiac output = O2 consumption / (arterial O2 - venous O2).

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Effect of temperature on arterial blood gas tensions and pH during exercise

Journal of Applied Physiology ◽

10.1152/jappl.1964.19.2.243 ◽

1964 ◽

Vol 19 (2) ◽

pp. 243-245 ◽

Cited By ~ 23

Author(s):

Alf Holmgren ◽

Malcolm B. McIlroy

Keyword(s):

Metabolic Acidosis ◽

Normal Subjects ◽

Bicycle Ergometer ◽

Effect Of Temperature ◽

Membrane Diffusion ◽

Arterial Blood Gas ◽

Arterial Blood ◽

Capillary Membrane ◽

Severe Exercise ◽

Alveolar Capillary

We measured arterial blood Po2, Pco2 and pH at rest and during a standard exercise test on a bicycle ergometer in ten normal subjects. In five we measured esophageal and five arterial blood temperature during the exercise and corrected the arterial blood values to the temperature at the time the samples were collected. We found an average rise in temperature of 1 C (range 0.2–1.6 C) during exercise lasting about 30 min at loads up to an average of 1,200 kg-m/min. At the highest load the average correction for PaOO2 was 5.6 mm Hg, for PaCOCO2 1.6 mm Hg and for pH 0.014 units. Our corrected values showed a fall in PaCOCO2 and pH and a rise in PaOO2 during severe exercise. These findings are compatible with the development of a metabolic acidosis during severe exercise and indicate that our subjects were not limited by diffusion across the alveolar-capillary membrane. metabolic acidosis; alveolar capillary membrane diffusion; hyperventilation; PaOO2 and PaCOCO2 in severe exercise Submitted on June 17, 1963

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Effect of negative intra-alveolar pressure on pulmonary diffusing capacity

Journal of Applied Physiology ◽

10.1152/jappl.1960.15.3.372 ◽

1960 ◽

Vol 15 (3) ◽

pp. 372-376 ◽

Cited By ~ 15

Author(s):

J. E. Cotes ◽

D. P. Snidal ◽

R. H. Shepard

Keyword(s):

Carbon Monoxide ◽

Venous Pressure ◽

Capillary Blood ◽

Breath Holding ◽

Diffusing Capacity ◽

Alveolar Pressure ◽

Holding Period ◽

Capillary Membrane ◽

Capillary Blood Volume ◽

Alveolar Capillary

In one of two subjects studied in detail, using 0.1% carbon monoxide in the test gas and a 10-second breath-holding period, the alveolar capillary blood volume (Vc) was found to increase by nearly 100% when the intra-alveolar pressure was made negative during breath holding. This was accompanied by a reduction in venous pressure in the forearm. In both subjects Vc was increased on exercise. The diffusing capacity of the alveolar capillary membrane (Dm) remained relatively constant in spite of large changes in Vc. The findings suggest that stationary blood is present in some alveolar capillaries at rest. The implications of this finding and a likely mechanism for the increase in Vc with negative pressure are discussed. xsSubmitted on September 14, 1959

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Effects of Ischemic Acute Kidney Injury on Lung Water Balance: Nephrogenic Pulmonary Edema?

Pulmonary Medicine ◽

10.1155/2011/414253 ◽

2011 ◽

Vol 2011 ◽

pp. 1-6 ◽

Cited By ~ 5

Author(s):

Rajit K. Basu ◽

Derek Wheeler

Keyword(s):

Acute Kidney Injury ◽

Pulmonary Edema ◽

Disease Process ◽

Kidney Injury ◽

Fluid Accumulation ◽

Lung Water ◽

Edema Formation ◽

Bulk Fluid ◽

Capillary Membrane ◽

Alveolar Capillary

Pulmonary edema worsens the morbidity and increases the mortality of critically ill patients. Mechanistically, edema formation in the lung is a result of net flow across the alveolar capillary membrane, dependent on the relationship of hydrostatic and oncotic pressures. Traditionally, the contribution of acute kidney injury (AKI) to the formation of pulmonary edema has been attributed to bulk fluid accumulation, increasing capillary hydrostatic pressure and the gradient favoring net flow into the alveolar spaces. Recent research has revealed more subtle, and distant, effects of AKI. In this review we discuss the concept of nephrogenic pulmonary edema. Pro-inflammatory gene upregulation, chemokine over-expression, altered biochemical channel function, and apoptotic dysregulation manifest in the lung are now understood as “extra-renal” and pulmonary effects of AKI. AKI should be counted as a disease process that alters the endothelial integrity of the alveolar capillary barrier and has the potential to overpower the ability of the lung to regulate fluid balance. Nephrogenic pulmonary edema, therefore, is the net effect of fluid accumulation in the lung as a result of both the macroscopic and microscopic effects of AKI.

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Aerosolized Antibiotics for Ventilator-associated Pneumonia

Anesthesiology ◽

10.1097/aln.0b013e3182755d7a ◽

2012 ◽

Vol 117 (6) ◽

pp. 1364-1380 ◽

Cited By ~ 53

Author(s):

Jean-Jacques Rouby ◽

Belaïd Bouhemad ◽

Antoine Monsel ◽

Hélène Brisson ◽

Charlotte Arbelot ◽

...

Keyword(s):

Experimental Studies ◽

Systemic Exposure ◽

Ventilator Associated Pneumonia ◽

Bacterial Killing ◽

Capillary Membrane ◽

Flow Turbulence ◽

Jet Nebulizers ◽

High Doses ◽

Reduced Toxicity ◽

Alveolar Capillary

The aim of this review is to perform a critical analysis of experimental studies on aerosolized antibiotics and draw lessons for clinical use in patients with ventilator-associated pneumonia. Ultrasonic or vibrating plate nebulizers should be preferred to jet nebulizers. During the nebulization period, specific ventilator settings aimed at decreasing flow turbulence should be used, and discoordination with the ventilator should be avoided. The appropriate dose of aerosolized antibiotic can be determined as the intravenous dose plus extrapulmonary deposition. If these conditions are strictly respected, then high lung tissue deposition associated with rapid and efficient bacterial killing can be expected. For aerosolized aminoglycosides and cephalosporins, a decrease in systemic exposure leading to reduced toxicity is not proven by experimental studies. Aerosolized colistin, however, does not easily cross the alveolar-capillary membrane even in the presence of severe lung infection, and high doses can be delivered by nebulization without significant systemic exposure.

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Influence of pulmonary blood flow on management and outcome

10.1093/med/9780199228188.003.0005 ◽

2011 ◽

Keyword(s):

Blood Flow ◽

Heart Disease ◽

Pulmonary Circulation ◽

Early Life ◽

Pulmonary Blood Flow ◽

Venous Blood ◽

Cyanotic Heart Disease ◽

Capillary Membrane ◽

Pulmonary Vascular Development ◽

Alveolar Capillary

Introduction 50Pulmonary vascular development in early life 50Cyanotic heart disease and pulmonary blood flow 52Delivery of systemic venous blood to the alveolar capillary membrane to allow release of waste CO2 and uptake of O2 depends on the integrity of the pulmonary circulation. Too little blood flow to the lungs and the patient is hypoxic; too much and the lungs become oedematous....

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Acute Lung Injury Induced by Staphylococcal enterotoxin B: Disruption of Terminal Vessels as a Mechanism of Induction of Vascular Leak

Microscopy and Microanalysis ◽

10.1017/s1431927612000190 ◽

2012 ◽

Vol 18 (3) ◽

pp. 445-452 ◽

Cited By ~ 16

Author(s):

Ali Imran Saeed ◽

Sadiye Amcaoglu Rieder ◽

Robert L. Price ◽

James Barker ◽

Prakash Nagarkatti ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Staphylococcal Enterotoxin ◽

Pulmonary Vasculature ◽

Tunel Staining ◽

Staphylococcal Enterotoxin B ◽

Vascular Leak ◽

Capillary Membrane ◽

Enterotoxin B ◽

Alveolar Capillary

AbstractThe current hypothesis of alveolar capillary membrane dysfunction fails to completely explain the severe and persistent leak of protein-rich fluid into the pulmonary interstitium, seen in the exudative phase of acute lung injury (ALI). The presence of intact red blood cells in the pulmonary interstitium may suggest mechanical failure of pulmonary arterioles and venules. These studies involved the pathological and ultrastructural evaluation of the pulmonary vasculature in Staphylococcal enterotoxin B (SEB)-induced ALI. Administration of SEB resulted in a significant increase in the protein concentration of bronchoalveolar lavage fluid and vascular leak in SEB-exposed mice compared to vehicle-treated mice. In vivo imaging of mice demonstrated the pulmonary edema and leakage in the lungs of SEB-administered mice. The histopathological studies showed intense clustering of inflammatory cells around the alveolar capillaries with subtle changes in architecture. Electron microscopy studies further confirmed the diffuse damage and disruption in the muscularis layer of the terminal vessels. Cell death in the endothelial cells of the terminal vessels was confirmed with TUNEL staining. In this study, we demonstrated that in addition to failure of the alveolar capillary membrane, disruption of the pulmonary arterioles and venules may explain the persistent and severe interstitial and alveolar edema.

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