What fills the space between the alveoli in the lungs?

What fills the space between the alveoli in the lungs?

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Do the lungs just consist of a large tree of alveoli, covered by the pleura, like this picture:

Or are they found "inside" the sac that is the lungs? If it's the later, what fills the space in-between the alveoli and forms the walls of the lung?

Alveolar tree is like a bunch of grapes. If you put a bunch of grapes into a plastic bag and put this bag into another bag, you can imagine how the lungs are covered.

Alveoli form the surface of the lungs. There is a membrane called visceral (or pulmonary) pleura that covers the alveoli and this membrane continues into another sheet called parietal (or thoracic) pleura that covers the inner side of the thoracic wall. The space between the membranes is called pleural space.

Here you can see how visceral pleura continues into parietal pleura:

Picture 1. Pleural space (source:

Picture 2. from page 1117 of "Cunningham's Text-book of anatomy" (1914) (source: Flickr)

I agree with Jan's answer generally, but thought I'd clarify a few points.

What fills the space between the alveoli in the lungs?

As Jan says, alveoli are packed together. In most cases, the thing next to any particular alveolus is another alveolus. In this case, the space between them is the alveolar wall, which (generally) consists of a pneumocyte and capillary (endothelial cell) with a shared basement membrane. You can see this in the following slide from Yale.

Alveolar sacs can abut other elements of lung parenchyma, including bronchioles, smooth muscle, nerves, and pleura. In this figure from Ross Histology, Ch. 19, you can see an alveolar sac adjacent to visceral pleura.

The relationship between lung parenchyma and pleural sac

I would encourage you to not think of the visceral and parietal pleura as two different bags, both of which contain the lung parenchyma (bag in a bag analogy). There is only one bag (per lung), and the only thing inside of it is the pleural fluid. The alveoli and associated parenchymal tissues are on the outside of the pleural sac just as much as the chest wall. They are just on opposite sides of the sac. This ubiquitous figure illustrates the relationship. The fist represents a lung, the ballon represents the pleura.

When a lung is removed what fills the space?

After a lobectomy, the remaining lobe(s) will fill the empty space. Pneumonectomy &ndash Removal of one entire lung (right or left). After a pneumonectomy, the remaining space (pleural cavity) fills with fluid.

Likewise, do lungs grow back after surgery? WEDNESDAY, July 18, 2012 (HealthDay News) -- Researchers have uncovered the first evidence that the adult human lung is capable of growing back -- at least in part -- after being surgically removed. The study showed a 64 percent increase in the number of alveoli in the woman's lung 15 years after surgery.

Regarding this, what happens to the space after a lung is removed?

The surgeon cuts some muscle and spreads the ribs apart. He or she surgically removes the affected lung. The sac that contained the lung (pleural space) fills up with air. Eventually, fluid takes the place of this air.

How long is recovery from lung lobectomy?

Generally speaking, people will spend at least five to seven days in hospital following an open lobectomy and three to four days following a video-assisted thoracoscopic surgery (VATS).

Gross Anatomy of the Lungs

The lungs are pyramid-shaped, paired organs that are connected to the trachea by the right and left bronchi on the inferior surface, the lungs are bordered by the diaphragm. The diaphragm is the flat, dome-shaped muscle located at the base of the lungs and thoracic cavity. The lungs are enclosed by the pleurae, which are attached to the mediastinum. The right lung is shorter and wider than the left lung, and the left lung occupies a smaller volume than the right. The cardiac notch is an indentation on the surface of the left lung, and it allows space for the heart (Figure 1). The apex of the lung is the superior region, whereas the base is the opposite region near the diaphragm. The costal surface of the lung borders the ribs. The mediastinal surface faces the midline.

Figure 1. Gross Anatomy of the Lungs

Each lung is composed of smaller units called lobes. Fissures separate these lobes from each other. The right lung consists of three lobes: the superior, middle, and inferior lobes. The left lung consists of two lobes: the superior and inferior lobes. A bronchopulmonary segment is a division of a lobe, and each lobe houses multiple bronchopulmonary segments. Each segment receives air from its own tertiary bronchus and is supplied with blood by its own artery. Some diseases of the lungs typically affect one or more bronchopulmonary segments, and in some cases, the diseased segments can be surgically removed with little influence on neighboring segments. A pulmonary lobule is a subdivision formed as the bronchi branch into bronchioles. Each lobule receives its own large bronchiole that has multiple branches. An interlobular septum is a wall, composed of connective tissue, which separates lobules from one another.

Other Studies

  • Mechanism of surfactant secretion. Pulmonary surfactant maintains patency of alveoli, the sites of gas exchange in the lung. Vesicles containing surfactant in alveolar type 2 epithelial cells are held stationary by the actin cytoskeleton, while surfactant flows between the vesicles en route to the secretion locus in the plasma membrane (American Journal of Physiology: Lung, 2014).
  • Differential cadherin mobility determines endothelial barrier properties. Real-time confocal imaging of endothelial junctions shows mobile cadherins that assemble at focal points in a F-actin dependent manner to establish the protein selectivity filter that determines endothelial sieving properties (Nature Communications, 2012).
  • Red blood cells generate reactive species in lung hypoxia. Optically imaged lungs show that in hypoxia, erythrocytes flowing in lung microvessels generate peroxide that diffuses to the adjoining endothelium to induce proinflammatory activation (Blood, 2008 American Journal of Respiratory Cell & Molecular Biology, 2013)
  • Acid injury. Acid aspiration, modeled in mouse lung by micropuncturing alveoli and delivering concentrated acid directly in the alveolar space, caused pore formation in the alveolar epithelium, leading to generation of reactive oxygen species and inflammatory outcomes (American Journal of Physiology: Lung, 2012).Lung endothelial mitochondrial calcium determines shedding of the luminal TNF-&alpha receptor. Real-time confocal microscopy reveals that lung endothelial mitochondrial calcium increase induces TNF-&alpha receptor shedding. The findings indicate that endothelial mitochondria determine the severity of soluble TNF-&alpha-induced microvascular inflammation (J. Clin. Invest:2011).
  • Mechano-induction of mitochondrial calcium. Vascular stretch induced by an increase in the vascular pressure causes calcium release from endosomal stores and increase of mitochondrial calcium. Mitochondrial peroxide diffuses to the cytosol to activate expression of proinflammatory receptors (J. Clin. Invest: 2003.)
  • Protein therapy in ALI. We have developed a patented method for introducing purified, barrier-enhancing proteins in lung endothelium and alveolar epithelium. By this strategy, loading lung endothelium with focal adhesion kinase (FAK) protected against endotoxin-induced ALI.
  • Real-time studies of alveolar actin. Sub-cortical actin can act as a fence to negatively regulate surface expression of pro-inflammatory receptors in alveoli. We developed methods for real-time actin determination in live alveoli. In this project, we aim to determine the physiological regulation of the alveolar F-actin fence and the extent to which enhancement of alveolar F-actin fence is protective in ALI.
  • Liquid secretion in alveolar wall. Our goal in this project is to understand mechanisms underlying formation of the alveolar wall liquid (AWL), which constitutes the alveolar aqueous phase. The AWL enables surfactant phospholipids and proteins to distribute along the alveolar wall. As such it is critical for gas exchange and defense functions of the lung. However, factors underlying AWL formation are largely unknown.

What is ground glass opacity?

Ground glass opacity (GGO) refers to the hazy gray areas that can show up in CT scans or X-rays of the lungs. These gray areas indicate increased density inside the lungs.

The term comes from a technique in glassmaking during which the surface of the glass is blasted by sand. This technique gives the glass a hazy white or frosted appearance.

There are many potential causes of GGO, including infections, inflammation, and growths. One 2020 review also found that GGO was the most common anomaly among people with COVID-19-related pneumonia.

This article will look at what GGO is, some of its causes, and its treatment options.

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GGO refers to gray areas that can show up in lung X-rays or CT scans.

Normally, the lungs appear black in X-ray and CT scans. This indicates that they are free of any visible blockages.

However, gray areas indicate increased density, meaning that something is partially filling the air spaces inside the lungs. This could be due to:

  • the air spaces becoming partially filled with fluid, pus, or cells
  • the walls of the alveoli, which are the tiny air sacs in the lungs, thickening
  • the space between the lungs thickening

GGO can be due to many conditions. Sometimes, the cause is benign. Other times, it may be the temporary result of a short-term illness. However, it can also indicate a more serious or long-term condition.

There are several types of GGO. These include:

  • Diffuse: Diffuse opacities show up in multiple lobes of one or both lungs. This pattern occurs when the air in the lungs is replaced with fluid, inflammation, or damaged tissue.
  • Nodular: This type can indicate both benign and malignant conditions. GGO that persists over several scans may indicate either premalignant or malignant growths.
  • Centrilobular: This type appears within one or several lobules of the lung. Lobules are the hexagonal divisions of the lung. The connective tissue between the lobules is unaffected.
  • Mosaic: This pattern develops when small arteries or airways within the lung are blocked. The opaque areas vary in intensity.
  • Crazy paving: Crazy paving shows up as a linear pattern. It can occur when the spaces between the lobules widen.
  • Halo sign: This type of opacity fills the area around the nodules.
  • Reversed halo sign: A reversed halo sign is an area that is almost totally surrounded by liquid-filled tissue.

The shape, size, quantity, and location of opacities will vary depending on the cause. Some conditions cause only one type, but others may cause a mixture.

The sections below will look at some potential causes in more detail.

Infections are common causes of GGO. Such infections include:


Pneumonia is a serious infection in the lungs. It can result from viruses, bacteria, or fungi. Most often, it occurs as a result of a viral illness, such as influenza (flu), measles, or respiratory syncytial virus.

The symptoms can vary depending on the cause, but they typically include:

  • a cough that produces yellow, green, or bloody mucus and fingernails and sweating
  • extreme fatigue or delirium
  • a sharp pain in the chest that gets worse when coughing or breathing deeply
  • loss of appetite

Most cases of viral pneumonia improve on their own. Fluids, rest, and oxygen therapy may help.

Doctors treat bacterial and fungal pneumonia with medications.


A 2020 review and meta-analysis found that just over 83% of people with COVID-19-related pneumonia had GGO.

Another 2020 study in 54 participants found that GGO most commonly showed up in the lower lobes of the lungs as round opacities, but that as the disease progressed, it became more patchy and affected all lobes.

The symptoms of COVID-19 can include any of the following :

If a person has symptoms that could indicate COVID-19, they should remain at home, self-isolate from others, and seek information from their local authority about getting tested.

Pneumonitis, or inflammation in the lungs, can occur if a person inhales:

  • allergens or irritants, which can contribute to hypersensitivity pneumonitis smoke, which can cause e-cigarette or vaping product use-associated lung injury (EVALI)
  • toxins, such as asbestos

Certain drugs can also cause pneumonitis and accompanying GGO. Typically, this type of pneumonitis occurs shortly after a person begins taking a new drug.

Hypersensitivity pneumonitis

The symptoms of hypersensitivity pneumonitis can include:

Other names for this condition include farmer’s lung and hot tub lung.

In the short term, doctors treat this condition by trying to identify and remove the trigger of a person’s symptoms. The person may also require medications and oxygen therapy.

In the long term, the condition may cause chronic fatigue, weight loss, and irreversible scarring.


E-cigarettes and vaping devices contain nicotine concentrates, solvents, and other chemicals. These products can cause EVALI.

EVALI may cause numerous types of GGO, including crazy paving and reversed halo sign, to show up on a scan.

Vaping can also cause alveolar hemorrhage. There is more detail on this condition below.


It is evident that both the connective tissue fiber system and the surfactant system are essential and interdependent components of alveolar micromechanics (Weibel and Bachofen 1997). For alveolar physiology and pathophysiology, it is not only relevant what is going on in the alveolar wall𠅋ut also what is going on on its surface. In that sense, surfactant is certainly more than “mere paint on the alveolar wall” (Nicholas 1996). Nevertheless, despite considerable efforts over the last decades, we are still far from a comprehensive understanding of alveolar micromechanics.

The development of real-time in vivo microscopy techniques have undoubtedly advanced the understanding of alveolar micromechanics during mechanical ventilation under physiological and pathophysiological conditions as outlined above. Due to technical constraints, the access to the alveoli is, however, limited so that most studies using in vivo microscopy analyzed subpleurally located alveoli which might not be representative of the whole population of alveoli within the lung. In addition, while in vivo microscopy allows the analyses of alveolar volume changes, the mechanisms of deformation occurring within the inter-alveolar septa cannot be evaluated since the resolution is not sufficient for this purpose. Hence, if the volume change within an alveolus results in a real stretching of cells in the inter-alveolar septa or is linked with an unfolding of pleats and shape changes remains unanswered by these investigations. In-depth analyses to answer these questions would require electron microscopic resolution (for review, see Ochs et al. 2016) to visualize the basal lamina (and the epithelial cells) which might be stretched so that its surface area increases or simply unfold as ultrastructural investigations from fixed lungs suggest. Until now, however, there is no direct visual evidence whether these mechanisms are really involved during spontaneous or mechanical ventilation in a living subject.

Some of these limitations might be addressed by computational simulations (Burrowes et al. 2018). Computational modelling has the potential to advance our understanding of the acinar micromechanics and alveolar interdependence including the effects down to the cellular level. Measurements of lung mechanical properties such as elastance and compliance at the organ level, so-called macromechanics, reflect mechanisms which occur at the alveolar level such as alveolar R/D or overdistension (Knudsen et al. 2018). With this regard, computational modelling of alveolar micromechanics has been employed to investigate pathologic alterations in R/D in mice with VILI during injury progression (Smith and Bates 2013) to understand the injurious mechanical forces (Hamlington et al. 2016), and to predict the open fraction of respiratory units and alveolar distension as a function of airway pressure and disease severity (Smith et al. 2013, 2015 Knudsen et al. 2018). These empirical models of alveolar R/D are based on the assumption that at a microscopic level the lung is composed of respiratory units (e.g. alveoli) ventilated in parallel. Each alveolus has a certain elastance and viscoelasticity and the collectivity of all alveoli defines the mechanical properties at the organ scale. During the respiratory cycle, the transpulmonary pressure increases during inspiration and decreases during expiration. Depending on the surface tension and “stickiness” of the fluid alveolar lining, alveoli can derecruit (i.e. collapse) if the pressure falls below a certain limit, the alveolar closing pressure. During inspiration, however, alveoli can again be recruited in case the transpulmonary pressure exceeds a certain alveolar opening pressure (Bates and Irvin 2002). These model-assumptions were advanced in recent years and have been demonstrated to be able to reproduce empirically measured lung mechanical properties as well as structural data in several studies (Smith et al. 2013 Knudsen et al. 2018).

Spring network models were developed for simulations of the mechanics of lung parenchyma. In its original description, the spring model was composed of a two-dimensional network of springs (i.e. inter-alveolar septa) forming hexagonal (i.e. alveolar) spaces (Mead et al. 1970). This model was further developed and applied to simulate the time course and lung mechanical impairment of pulmonary fibrosis as well as pulmonary emphysema including response to lung volume reduction surgery (Bates et al. 2007 Mishima et al. 1999 Mondoo and Suki 2017). In addition, spring models were used to understand aspects of alveolar and alveolar-airway interdependence (Ma and Bates 2012, 2014 Ma et al. 2013a, b, 2015 Mead et al. 1970 Makiyama et al. 2014 Bates et al. 2007). It has long been understood that alveolar interdependence plays an important role in the determining strain at the level of individual septa (Mead et al. 1970 Perlman et al. 2011). However, the influence of surfactant dysfunction and derecruitment on the septal strain distribution is not well described, in particular during disease progression. In this regard, it has been proposed that surfactant dysfunction, R/D dynamics, and alveolar interdependence with increased strain play critical roles in the pathogenesis of fibrotic lung disease (Todd et al. 2015 Lopez-Rodriguez et al. 2017 Knudsen et al. 2017 Cong et al. 2017). Recent imaging studies in lungs suffering from idiopathic pulmonary fibrosis (IPF) provided evidence for instability of distal airspaces in regions of the lung which were not yet subject to fibrotic remodeling (Mai et al. 2017 Petroulia et al. 2018). Mai and co-workers used micro-computed tomography of IPF lung explants and found microatelectases in areas close to fibrotic tissue but not yet affected by fibrosis. Based on these observations microatelectases might be attributed the roles of stress concentrators which trigger disease progression including lung injury, alveolar collapse, fibrotic remodeling and collapse induration (Burkhardt 1989 Knudsen et al. 2017).

The nervous system

Your breathing usually does not require any thought, because it is controlled by the autonomic nervous system, also called the involuntary nervous system.

  • The parasympathetic system slows your breathing rate. It causes your bronchial tubes to narrow and the pulmonary blood vessels to widen.
  • The sympathetic system increases your breathing rate. It makes your bronchial tubes widen and the pulmonary blood vessels narrow.

Your breathing changes depending on how active you are and the condition of the air around you. For example, you need to breathe more often when you do physical activity. At times, you can control your breathing pattern, such as when you hold your breath or sing.

To help adjust your breathing to changing needs, your body has sensors that send signals to the breathing centers in the brain.

  • Sensors in the airways detect lung irritants. The sensors can trigger sneezing or coughing. In people who have asthma, the sensors may cause the muscles around the airways in the lungs to contract. This makes the airways smaller.
  • Sensors in the brain and near blood vessels detect carbon dioxide and oxygen levels in your blood.
  • Sensors in your joints and muscles detect the movement of your arms or legs. These sensors may play a role in increasing your breathing rate when you are physically active.

In central sleep apnea, the brain temporarily stops sending signals to the muscles needed to breathe. Learn more at our Sleep Apnea Health Topic.

A small pneumothorax may go away on its own over time. You may only need oxygen treatment and rest.

The provider may use a needle to allow the air to escape from around the lung so it can expand more fully. You may be allowed to go home if you live near the hospital.

If you have a large pneumothorax, a chest tube will be placed between the ribs into the space around the lungs to help drain the air and allow the lung to re-expand. The chest tube may be left in place for several days and you may need to stay in the hospital. If a small chest tube or flutter valve is used, you may be able to go home. You will need to return to the hospital to have the tube or valve removed.

Some people with a collapsed lung need extra oxygen.

Lung surgery may be needed to treat collapsed lung or to prevent future episodes. The area where the leak occurred may be repaired. Sometimes, a special chemical is placed into the area of the collapsed lung. This chemical causes a scar to form. This procedure is called pleurodesis.

The structure of the lungs and thoracic cavity control the mechanics of breathing. Upon inspiration, the diaphragm contracts and lowers. The intercostal muscles contract and expand the chest wall outward. The intrapleural pressure drops, the lungs expand, and air is drawn into the airways. When exhaling, the intercostal muscles and diaphragm relax, returning the intrapleural pressure back to the resting state. The lungs recoil and airways close. The air passively exits the lung. There is high surface tension at the air-airway interface in the lung. Surfactant, a mixture of phospholipids and lipoproteins, acts like a detergent in the airways to reduce surface tension and allow for opening of the alveoli.

Breathing and gas exchange are both altered by changes in the compliance and resistance of the lung. If the compliance of the lung decreases, as occurs in restrictive diseases like fibrosis, the airways stiffen and collapse upon exhalation. Air becomes trapped in the lungs, making breathing more difficult. If resistance increases, as happens with asthma or emphysema, the airways become obstructed, trapping air in the lungs and causing breathing to become difficult. Alterations in the ventilation of the airways or perfusion of the arteries can affect gas exchange. These changes in ventilation and perfusion, called V/Q mismatch, can arise from anatomical or physiological changes.

[Biology] What is going on when a lung "collapses"?

I have a hard time creating a clear picture of how the lungs mechanically work and what happens when the thorax is punctured.

A collapse of the lung is not necessarily a puncture in the thorax. YOu can have a collapsed lung without even getting a cut, or even breaching the lung itself.

This is because a a collapsed lung is a breach of the pleura, not really a breach of the lung itself. It usually (not always) does involve a breach of the lung, though.

Surrounding each lung is a double-walled membrane called the pleura. One of the membranes (the visceral pleura) is attached to the lung and the other (the parietal pleura) is attached to the chest wall. The pleura are not attached to each other *.

In between is a "negative space" with a small amount of lubricant. This functions to prevent the lung from rubbing against the chest wall. Like I said, they are not actually attached, but are held together by negative pressure, kind of like how a suction cup grips against a smooth surface.

When you inhale, your chest cavity expands. Because the parietal pleura is attached to the chest wall, it expands **. Because of the suction cup thing, the only way to compensate for the pressure change is for the visceral pleura to be pulled along for the ride. Because the visceral pleura is attached to the lung, the lung expands as well. This causes a negative pressure inside the lung relative to the outside air, and you draw in air.

However, if that negative space is breached and something else can come in and compensate for the pressure change, the lung won't expand the suction cup has a hole in it.

This "something else" is generally air bubbling out from the lung. It fills the negative space, and now when the chest cavity expands, the gas in there simply expands along with it, and that pressure gradient sucks air right out of the lung. And then you have a collapsed lung.

* They are actually attached, kind of. The pleura is really one thing, like a collapsed balloon. Imagine a jar and a tied off, partially inflated and really flexible balloon. Take the jar and set it on top of the balloon. The push it down "into" the balloon, so it gets swallowed up. Once it's all the way in, pull the air out of the balloon. You now have a double walled sac around the jar. that's kind of like the pleura.

** Actually, the chest wall itself doesn't usually move much. The diaphragm pulls down, and the pleura keeps the lung in place, anchored to the more stationary chest wall.

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