Lungs

Learning Objectives

• Describe the basic anatomy of the lung
• Discuss the basic principles of flow
• Describe the physiology of the lung including lung movement
• Locate and identify the main structures of the lung using cross-sectional medical imaging
• Discuss lung volumes, capacities, and gas exchange.
• Recognize how common pathological conditions affect the lung

Introduction

The lungs are two huffing and puffing sponge-like organs that dominate the chest cavity, essential in their function as the principle structures of respiration. An understanding of their unique anatomy and physiology brings understanding of how diseases will affect the lungs, and how these changes will manifest on X-ray and CT evaluation. In this first part of the series on the lung we emphasize principles, and outline how structure is integrated with function, disease, and imaging. The unique structural characteristics of the lungs include:

Dominance in the chest cavity
Ability to accommodate the entire cardiac output with every heartbeat
Asymmetric nature
Irregular and dichotomous branch pattern of the bronchovascular bundle
Tubular transport system, with a single system functioning for both delivery and removal
Spongy air-filled character
Pyramidal or cone shape
Dual blood supply

The unique functional aspects include:

The ability to move air efficiently
The ability to exchange gases efficiently

Anatomic Range of the Respiratory System

This collage reflects the anatomic range of the respiratory system from the macroscopic to the microscopic – a continuum of structure.

It seems a long way for the air to travel but the system can deliver the air to and from the outside in a single breath, and exchange the gases at the capillary level even more rapidly. It is a remarkable system.

Overview

As we progress through the module there is a recurring pattern of the dual function of the respiratory apparatus – an airway system that transports the air, and an exchange system that enables transfer of the gases across the alveolar membrane.

The lungs are part of a larger system called the respiratory system. The role of the lungs is to deliver ambient air (ventilation) to the alveoli and to act as the agent for gas exchange by contributing one layer of epithelium to the bilayered membrane, a double layer that serves as the ultimate interface for gas exchange. The primary role of the pulmonary arterial circulation is to transport blood to the alveolar interface (perfusion) and to also play a part in the exchange of carbon dioxide and oxygen by providing the second layer of the bilayered filter. It is the homeostatic aim of the body to match the ventilation with the perfusion, in order to maintain uniform ventilation (V) to perfusion (Q) ratio (V/Q).

The lungs are exposed directly to the air in the atmosphere and to the blood within the circulatory system. Through the lungs the blood is therefore exposed to the atmosphere, which on the one hand contains life-sustaining oxygen but on the other can present a hostile environment filled with microorganisms, industrial chemicals, and toxic fumes.

The lungs are made of expandable, sponge-like tissues. Their close proximity to the heart and circulatory system allows for rapid exchange of gases between the air and the circulatory system as noted above. This function is easily accomplished during rest, where resting respiratory rate in an adult is about 12 breaths per minute and heart rate 72 beats per minute. During exercise the respiratory rate can increase to 40-50 breaths per minute and the heart rate, increasing in concert, can reach 180-200 per minute. The interface of circulation with the respiratory system has to be sufficiently equipped to allow delivery, uptake, and exchange of gases at this accelerated pace. The key soldier in the exchange of oxygen is a complex protein called hemoglobin, which lies in the red cell.

I imagine the hemoglobin molecule scurried by the forces of the right ventricle into the pulmonary circulation. As it enters the chambers of exchange, the open windows of the lungs herald the fresh air. Under basal conditions, the hemoglobin gnome can work at a leisurely pace filling his baskets with oxygen. Under exercise conditions he has to start working like crazy, grabbing molecules of oxygen and stacking these into his storage baskets, surrounded by an accelerated pace with gale-like air forces and flood-like blood conditions. Hemoglobin is a remarkable molecule and can adapt its function to these extremes in physiology.

Carbon dioxide is a by product of body metabolism and is dissolved in the blood. Exchanges between the circulation and alveoli occur rapidly and efficiently across the alveolar membrane due to differences in the partial pressure of gas between the blood and the alveoli.

Examination of the lungs with a stethoscope

The presence of a structure in the body that is almost totally filled with air makes it a unique, challenging, and rewarding organ to examine clinically and radiologically. Examination of the lungs with a stethoscope enables the clinician to evaluate inspiratory and expiratory movement of air. Some pathologic conditions, including aspiration of a foreign body, collapsed lung, or inadvertent intubation of the bronchus, result in airway obstruction. In these conditions there is no air entry into the affected bronchus and subtended lung. The clinical finding of the lack of air entry, based simply on the lack of air sound, can be a life saving diagnostic maneuver.

Unusual but interesting words are used to describe the sounds of air character and movement on clinical examination. These include percussion, tactile fremitus, bronchophony, whispering pectoriloquy, and egophony and relate to the way air moves through the airways, and how the transmission may change when there is fluid in the pleural space or in the lungs. When the air mixes with the fluid, characteristic sounds such as rales and crepitus will result.

Imaging the Chest

From the radiological point of view, x-rays used in plain chest x-ray (CXR) or CT scan move almost unimpeded through the lungs, and present as a radiolucency or blackness on the image. On the other hand, the mediastinum serves as a moderate barrier to x-rays, and the ribs and spinal column present an even greater barrier. The tissues of the chest vary significantly in the degree to which they absorb or reflect x-rays. This difference presented a challenging problem to radiologists and physicists over the years, particularly related to technical factors that would optimize imaging of the mediastinum and heart on the one hand, and the lungs on the other. The advent of CT scanning with a superior gray scale, and with digital technology, has helped solve this problem, so that we are able to window in to the gray scale of the specific part being imaged. We can, for example, look specifically at the lungs using the gray scale and window level appropriate for the lung, (lung windows) for the mediastinum (mediastinal windows) or for the bones (bone windows).

What structures do we see on x-ray?

Why do we see structures on x-ray? We are able to define two side-by-side structures if they have contrasting x-ray absorption characteristics and hence densities. On a plain film of the chest for example, the trachea and main bronchi are usually visualized because the air filled trachea is surrounded by relatively thick soft tissue walls and other soft tissues of the mediastinum creating the necessary density differential to enable distinction. The air in the visible mainstem bronchi is surrounded and separated from the surrounding air filled parenchyma and by relatively thick walls of soft tissue density and this contrasting density allows the mainstem bronchi to be seen. As we progress to the smaller bronchi, usually after the fourth order of branching, the soft tissue walls become too thin to create an air-soft tissue interface and hence we cannot resolve nor see them.

Almost 90% of the lung is air and only about 10% is soft tissue, interstitium and blood. The dominant density of the lungs is therefore black or lucent. The soft tissues of the lung, including the blood vessels and the connective tissue (also called the interstitium), impede the x-ray, resulting in a gray or soft tissue density. The interface of lucent air (black) against a soft tissue background of the interstitium (gray) provides a sharp and contrasting interface of density, allowing an almost microscopic view of the lungs. If the pressure in the capillaries becomes abnormally high, for example more than 25 mmHg, fluid starts to leak into the interstitium. The clarity of the interstitial markings becomes reduced and blurry. The radiologist is able to imply pathophysiological changes based on the fuzziness of the blood vessels and can approximate the pressure in the capillaries. This change is best appreciated on a plain film of the chest. The plain chest film has stood the test of time, proving its value since Roentgen’s discovery in the late 19th century.

Most disease states replace the air of the lungs with fluid or soft tissue, and appear as increasing densities on the CXR. In pneumonia the alveoli become filled with pus or fluid. The air in the lung parenchyma is replaced by soft tissue elements. If there is persistence of air in the smaller airways, they will now be visualized, since the air in the airways is now in contrast to the surrounding density of the fluid filled parenchyma. This sign is called an “air bronchogram” and is characteristic of consolidated lung with a patent airway.

CT with a wider gray scale enables us to visualize subsegmental bronchi and bronchioles both in normal conditions and under various pathological situations.

Flow: Basic Principles

The function of air transport is the domain of the tracheobronchial tree, which as a tubular system has to obey the universal principles of flow within a tube. At the terminal end of these tubes are epithelial-layered grape-like clusters where gas exchange takes place. The principles of exchange of gases across a membrane are also universal in the body. If you understand flow in tubes, and exchange of gases, chemicals, and molecules across a membrane, you can apply the understanding to many aspects of body function.

Flow will only occur when a pressure difference exists between the two sides of the tubes. When we breathe in, the intercostal muscles contract and expand the chest laterally and the diaphragm moves down, increasing the volume of the chest cavity in a craniocaudal dimension. As a result, the alveoli expand, causing a negative pressure in the alveolar side of the tubes. The pressure in the atmosphere is higher and thus air will flow from a high-pressure system to a low-pressure system – i.e. from the atmosphere to the lungs. During expiration, the elastic nature of the chest, with the relaxation of intercostal muscles and diaphragm, result in a return of the chest to its pre inspiratory position. The chest therefore is in a contracted size, causing a relative increase of pressure in the alveoli when compared to the atmosphere, and air will flow from the alveoli to the atmosphere. Inspiration is therefore an active process requiring energy and muscle contraction, and expiration is a passive process of elastic recoil.

Flow: Basic Principles: Velocity of Flow

Velocity of flow relates to factors such as tubular diameter, resistance, friction, and pressure differences, as well as the nature of the medium being transported. Velocity of flow will also depend on whether the flow is laminar or turbulent. If it is laminar, it will be governed by Poiseuille’s law, which states that velocity of flow is directly proportional to the driving pressure.

As velocity increases, flow becomes turbulent and Poiseuille’s law does not apply.  Flow in the larger parts of the airways tends to be turbulent and in the smaller tubes it is laminar. Under resting conditions, laminar flow exists from the medium-sized bronchi onward down to the bronchioles. During exercise, the airflow is accelerated, and laminar flow may be confined only to the very small airways. Laminar flow is quiet while turbulent flow is noisy. Thus when your doctor or nurse places a stethoscope on your chest and asks you to breath in and out, they are listening to the turbulent flow in your larger airways. The audible “huffing and puffing” that occurs with exercise results from greater forcefulness of the muscles in an attempt to get more air in and out, and the turbulence becomes audible even without the stethoscope.

Quiz Me

If flow is turbulent, it will be governed by Poiseuille’s law.
True False

Resistance to flow depends on sympathetic tone of the smooth muscle, which governs the radius. Radius has a very powerful effect on the velocity of laminar flow. Very small changes in radius result in large changes in velocity. In health, the sympathetic tone is well balanced with the needs of a person’s physiology. However, if the tone is increased due to environmental allergens or exercise induced spasm, then tone may increase to the extent that it limits air movement and the patient becomes short of breath. Wheezing is the resulting sound of turbulent air through constricted bronchioles, which can be heard and felt by the clinician and the patient.

The tracheobronchial system is beautifully designed to enable rapid and efficient delivery of relatively clean air to the alveoli. Not only is the delivery rapid, but also it is uniform throughout the lung. The design is such that with a single inspiration, the fresh air reaches all alveoli (whether they are at the base or apex of the lungs), simultaneously. What a system! If we, in the world at large, could deliver an equal and adequate amount of supplies efficiently and simultaneously to all, at the precise time when needed, we would have a much happier world. Not only is it a system that delivers efficiently to the alveoli, but also its second function is to return with waste for delivery to the atmosphere. No other tube in the body performs this dual function of back and forth movement through the same piece of tubing. The gastrointestinal system will deliver via the esophagus, stomach and small bowel but excretion is via the large bowel. In the cardiovascular system the arteries deliver and the veins remove. They are one-way streets whereas the airways are a two-way system.

Flow: Airways and Blood Vessels

The lungs are divided into lobes, segments, subsegments, lobules, acini, and alveoli. An appropriate conduit group, meaning an artery, vein and lymphatic, accompanies each of these parts. The tracheobronchial tree is composed successively of the trachea, mainstem bronchi, lobar bronchi, segmental bronchi, terminal bronchioles, respiratory bronchioles, and alveolar ducts. The respiratory tree divides into paired branches of unequal length and diameter. This arborizing format is called an irregular dichotomy. Gas exchange starts at the respiratory bronchiole and becomes progressively more efficient and effective as the respiratory bronchiole progresses to the alveolar ducts, then alveolar sacs and finally the alveoli. The preliminary exchange of gases at the pre alveolar level enhances the delivery and exchange to the alveoli.

Flow: Airways and Blood Vessels: The Arteries

The accompanying arteries include the main pulmonary artery (MPA), the right pulmonary artery (RPA), and the left pulmonary artery (LPA). The lobar arteries, segmental and subsegmental arteries follow, which finally become the arterioles, which are the smallest arteries. When the arteriolar wall becomes one cell layer thick it is called a capillary.

Flow: Airways and Blood Vessels: The Bronchovascular Bundle

The bronchovascular bundle, as the name implies, consists of a combination of bronchi and vessels (in this case arteries), and it is positioned in the middle of the pulmonary lobule. The lobule (a.k.a. secondary lobule) is the unit of lung parenchyma consisting of three to five respiratory bronchioles and arteries with their progeny.  The progeny of the respiratory bronchioles are given specific names starting with the alveolar ducts, and progressing through the alveolar sacs and finally the alveoli.   The lobule is surrounded by a membrane of connective tissue that contains lymphatics and venules. We will describe this unit extensively in a coming section. The position of bronchovascular bundle is centrilobular, meaning that it is in the center of the lobule, while the venous and lymphatic conduits are distributed around the periphery of the lobules. Lymphatics sometimes accompany the bronchovascular bundle as well.

Flow: Airways and Blood Vessels: Venous Drainage

Venous drainage is usually via one major upper lobe and one major lower lobe pulmonary vein to each lung, but clinically significant variations do exist. Segmental and subsegmental veins and venules are the equivalent subdivisions of the veins. The capillaries surround the alveoli.

Flow: Applied
In the clinical world the sounds of air movement are caused by turbulent airflow and these sounds are evaluated by the stethoscope. The stethoscope is also a simple tubular structure with a membrane on its far end. There is normal airway turbulence in the larger airways and so it is normal to hear air movement in the lungs during inspiration and expiration. Inspiration is noisier and shorter in duration than expiration. The larger the diameter of the airway, the higher the pitch of the sound, while the smaller the diameter, the lower the pitch.

With anaphylaxis or foreign body inhalation, there are varying degrees of obstruction of the upper airways and an audible high-pitched sound on inspiration can be heard. This sound is called stridor. Anaphylaxis could affect the larger and / or the smaller airways. If the proximal larger airways are affected then stridor results, and if the smaller airways are affected then wheezing is heard.

If the stridor is caused by anaphylaxis then epinephrine may be required, whereas if it is caused by aspiration of a piece of poorly chewed steak then the Heimlich maneuver is required. If you are in a restaurant when a patron clutches his throat and stridorous noises are heard, the question to ask would be “meat or shrimp?” If the person were eating steak then the Heimlich maneuver would be indicated, and if it were shrimp and accompanying signs of hives and facial swelling were present and severe enough, epinephrine would be necessary. Either way, acute stridor is a serious and life threatening situation.

In an acute asthmatic attack the problem lies in the smaller airways. As stated above, in the normal patient, flow at this level is usually inaudible because of its laminar nature. The narrowing caused by muscle spasm and secretions occurs at the level of the smaller bronchi and the turbulence that results is heard as a wheezing sound on expiration. Why expiration and not inspiration? Good question. On inspiration the chest cavity expands and so do the alveoli and bronchioles. The change in size of the bronchioles with inspiration is often sufficient to allow laminar flow to persist, and hence no sound will result. On expiration the diminishing size of the chest cavity causes the bronchioles to recoil, resulting in a smaller diameter, and together with the spasm will result in air trapping, turbulence and wheezing. If the spasm is severe, there may be wheezing both on inspiration as well as expiration. Emphysema and chronic bronchitis are also causes of wheezing during exhalation. In all these conditions the overall intake of air exceeds the volume exhaled, and so the net result is air trapping and increase in the lung volume.

If there is a large amount of air trapping, the radiologist will see the larger air volumes as hyperexpanded or hyperinflated lungs. In such cases, if one counts the posterior ribs on the CXR, more than 10 posterior ribs will be visualized above the diaphragm. Flattening of the diaphragms also will occur and is best seen on the lateral CXR. Since a large portion of the air seen in the large lungs is static air, it will contain a higher level of carbon dioxide and relatively lower levels of oxygen. In severe asthma, poor oxygenation of the blood results and oxygen saturation falls. The air trapping seen in emphysema is caused by a loss of elasticity of the alveoli and abnormal overexpansion of the alveoli. With larger surface areas and hence volumes, there is an increase ventilation (V) without an overall appropriate increase in perfusion (Q), resulting in a V/Q mismatch, and thus inadequate gas exchange.

In an acute asthmatic attack, wheezing can be heard on inspiration.
True  False

Lung Movement: Basic Principles

The lung is often compared to a bellows system, meaning that with alternate expansion and contraction, air travels one way through a tube during expansion and is expelled the other way when the mechanism recoils.

Inspiration is an active process requiring muscle contraction and therefore energy, while expiration is a passive process of elastic recoil requiring no energy. As noted, one of the unique features of the lung is its ability to act as a two-way transport system. No other tube in the body is asked to perform this dual function. At first this seems like a simple demand on the system, but as you will see it is more complicated than a simple bellows system, and a fine balance exists between the complex forces of inspiration and the complex forces of expiration. Biology has had to make some considerable adaptations in order for the dual function of the airways to coexist.

Lung Movement: 5 Layers

There are five general functional layers to the bellows system. They include the bony cage, the muscle layer, the pleural layer, the lung and the layer of surfactant. The combination of bony, muscular, membranous, spongy, elastic, and chemical properties of the complex described, keeps the air moving in and out efficiently.

First Layer – Bone

The bony cage of ribs, sternum and spine create an outer protective layer with the sternum and spine being the relatively rigid components and the ribs acting as the pliable component. The ribs have been compared to bucket handles as they move up and out during inspiration pivoting on the sternum and spine  which act as two fixed points.

Second Layer – Muscle

The second layer includes the diaphragm inferiorly, the intercostal muscles circumferentially, the serratus anterior anterolaterally, scapular elevators posteriorly, and erector spinae muscles posteriorly. Superiorly the scalene and sternocleidomastoid muscles assist when necessary. The abdominal muscles also play a role as accessory muscles of respiration since movement of the chest cavity has effect on the abdomen, and vice versa. In fact, a principle to always keep in mind is that no cavity, system, organ, or cell is an isolated island – they all in the end work in concert for the greater health of the whole. John Donne, an English poet of the 17th century, proposed that “no man is an island,” promoting the same concept of the interconnectedness of all.

During inspiration the diaphragm moves down and intercostal muscle contraction causes outward chest vectors, resulting in chest cavity expansion. As a result there is a decrease in intrathoracic pressure and airflow into the lungs. When the muscles relax, the diaphragm flattens, the intercostals return to baseline position by passive and elastic recoil, and the chest moves inward, causing the chest volume to decrease. The intrathoracic pressure rises and becomes higher than the atmospheric pressure and therefore air will move outward from a position of high pressure to one of low pressure.

Third Layer – Pleura

The third layer is the double-layered pleura, with one component intimately attached to the chest wall, and the other layer intimately attached to the lung. Between them there is a thin layer of fluid that binds the two layers together by capillary action. The pleural surface constantly absorbs the fluid or gas that enters the space and a negative pressure of about 10mm Hg is maintained. We have all experienced the power of the thin fluid layer of water between two clean smooth surfaces of glass, which cannot be pulled apart because of the adhesive and cohesive capillary action. Capillary action is the interaction between contacting surfaces of a liquid and a solid. The cohesion and adhesion that result keep the outer chest cage of bone and muscle in intimate contact with the lungs, being pulled and pushed together in the harmonious dance of respiratory movement.

The adhesion and cohesion of the lung to the chest wall is a lifelong relationship of intimate contact, characterized by 10-15 in and out movements per minute at rest, and sometimes up to 20 – 40 breaths per minute during exercise. The harmony and intimacy continue despite the rigorous jolts of life including violent sneezes, cough whoops, jumps to the basketball hoops and the likes of usual rough and tumble. It is a simple but marvelous mechanism that keeps two structures bound together by such a simple but powerful physical principle. When there is a large effusion or pneumothorax then the cohesive and adhesive mechanisms fail, and collapse of the lung ensues.

Fourth Layer – Lung

The lung as a whole provides the next functional layer, but within the lung there is a combination of structures, each with different properties and needs. For the sake of understanding we will consider it a single layer. The relatively rigid upstream airways do not change much with the ins and outs of respiration, while the smaller airways and to greater extent the alveoli undergo significant change in size, expanding with inspiration and getting smaller with expiration.

The alveoli exhibit a surface tension which creates an environment for recoil during expiration and if held unchecked would undergo complete collapse. The tendency for recoil is necessary and healthy, while the collapse is of course harmful. The total collapse of the alveoli is prevented by the automatic rhythm of involuntary inspiration, which reverses the process, as well as the presence of surfactant (our fifth layer) that prevents the collapse. In the absence of surfactant the pressure required to keep the alveoli open is 20-30mmHg. Surfactant reduces this to about 3-5 mmHg.

Fifth Layer – Surfactant

Surfactant, the fifth and last layer, is a lipoprotein solution secreted by specialized cells of the alveolus. It serves to reduce the surface tension and ease the force necessary to open the alveoli during inspiration. In blowing up a balloon, we find that the most difficult part is when the radius of the balloon is small. Thus the surface tension on the balloon is high when the radius is small. As the radius increases the surface tension decreases and it becomes easier to blow up the balloon. Surfactant if it were present in the balloon would decrease the wall tension by an order of 15, to ease the energy and pressure necessary to inflate it.

Applied:  First Layer – Bone

We will now review the 5 layers and apply our knowledge of the physiology and anatomy to the diagnostic and therapeutic world.

First Layer – Bone: Fractured Ribs

The fracture of two to three ribs in one place does not result in respiratory difficulty. The pain that ensues can cause decreased respiratory excursion and consequent mild atelectasis. Pain limiting respiratory motion is a very common clinical and radiological scenario, often seen in patients who have had abdominal or chest surgery.

Flail chest, on the other hand, is fortunately not common, but is an urgent clinical problem following extensive blunt traumatic chest injury. Flail chest arises when three or more ribs are fractured both anteriorly and posteriorly, resulting in a loss of chest support. Paradoxical chest movement results so that during inspiration the fractured ribs follow the movement of the lung rather than the chest wall from which they have become detached. Thus during inspiration the isolated ribs and associated chest wall move inward instead of out, and during expiration they move out instead of inward. This injury is usually seen as a consequence of severe trauma, and associated lung parenchymal injury is common. Clinical consequences are a combination of the loss mechanical efficiency and loss of parenchymal function.

The following case represents a controlled situation of paradoxical motion of the chest. The patient was asked to take a deep breath in. Can you work out what the problem is?

First Layer – Bone: Scoliosis

The effects of scoliosis on respiratory function both before and after surgical correction have revealed that the degree of scoliosis did not correlate with the severity of respiratory difficulty, though there was improvement by about 10% of lung function following surgical correction.

 

Second Layer – Muscle

The ring of muscle is the next layer.

 

 

Second Layer – Muscle: Paralysis

It is not uncommon to see paralysis of one hemidiaphragm without untoward (has no functional consequence) effect. However, when both components of the diaphragm fail, therapeutic intervention is urgent. Diseases that affect the neural signal (polio, Guillain Barre, quadriplegic syndromes), transmission of the neural signal (myasthenia gravis), or disease of the muscle itself (tetanus, myopathy), can result in respiratory failure. In the acute situation when respiratory compromise is severe the patient will require a ventilator. The iron lung was developed to treat polio in 1927. It was the first respirator and was developed by a Harvard researcher Philip Drinker. He used an iron box and two vacuum cleaners to create a push and pull motion on the chest.

Third Layer – Pleura

The next layer is the pleura, which acts as the intermediary between the chest wall and the lungs.

The pleural adhesion/cohesion mechanism is quite a robust system, but like all mechanical systems under duress it can fail. Pneumothorax is a well-known failure of this system and is caused by air leaking from the lung, which intervenes in the bonding mechanism and separates the two pleural components.  Pleural effusions increase the distance between the lungs and the chest wall and when large can cause collapse or atelectasis of the lungs

Quiz Me

A pneumothorax is a collection of air in the pleural cavity.

True  False

Third Layer – Pleura: Pneumothorax

When a patient has a small pneumothorax we ask that the patient lie in bed with the affected lung on the down side (ipsilateral decubitus position) so that we limit the chest wall movement on that side and hence air movement into the lung. If the pneumothorax is large the patient can become symptomatic and a life-threatening event called tension pneumothorax can ensue. In tension pneumothorax, air leaks into the pleural space on inspiration and is trapped on expiration. The air subsequently accumulates until the pressure is sufficiently high in the pleural space to cause compression of the venous structures in the chest. The elevated venous pressure prevents venous return to the heart and cardiac output falls. Quick recognition of this entity and immediate decompression by a needle or a tube is life saving.

Third Layer – Pleura: Pleural Effusion

The following is also a problem with the pleural space – Can you solve the problem?

Fourth and Fifth Layer

Restrictive Lung Disease

The next layer is the lung. Restrictive lung disease occurs when the interstitial tissue of the lung lose elasticity and is replaced by fibrotic tissue. The patient has greater difficulty in expanding the lung and the recoil mechanism is also affected.

Hyaline Membrane Disease

The next layer is the surfactant.

Premature babies do not produce surfactant and therefore their tendency to collapse the alveoli during inspiration is increased. Also, greater forces are necessary to inflate the alveoli. Extensive atelectasis or lung collapse results in this condition and the baby may require a respirator to help keep the lungs open. This disease is called hyaline membrane disease, or respiratory distress syndrome.

ARDS

A parallel disease in older patients is called ARDS, or adult respiratory distress syndrome. It is characterized by diffuse alveolar damage (DAD), resulting in a relative lack of surfactant and consequent microatelectasis. There are many causes of DAD including sepsis, multisystem trauma, smoke inhalation, near drowning, and narcotic overdose. The absence of production of surfactant, in combination with the fluid accumulation in the alveoli, causes an increase in surface tension and more patient muscular effort is required to expand the alveoli. When this effort fails there is atelectasis and reduced oxygen delivery and carbon dioxide excretion.  The failing respiratory system requires a respirator to help keep the alveoli patent.

Breathing Instructions – The CXR

In general we intuitively know that when we take a deep breath we are using our muscles to actively inspire. When we breathe out it is a relaxation of that mechanism caused by actual muscle relaxation and the elastic recoil of the layers of the chest. We can of course breath out all the way until we have expired right to what we think is the last drop of air, and this takes effort and muscle contraction as well. When you as a technologist have a patient for a routine CXR you ask your patient to “take a deep breath in, blow it all the way out and hold it….” And you click your exposure. You can readily see that there is still quite a lot of air left in the lung. This is called the dead space of the lung, found in patients who are well and alive! Read on and learn all about what happens to the lung volumes and capacities during that process.

Lung Function Tests – Lung Volumes
In order to explain the process we will pretend that you are a lung function technologist for a moment. You are going to test your patient’s lung volumes, capacities, and velocities. We want you to think and apply what you see on these graphs to your own situation when you are doing a CXR, and to imagine the differences between an inspiration CXR and expiration CXR. We particularly want you to see the difference in volume of air between the inspiration film and the expiration film.

So we go back to our theoretical patient undergoing lung function tests and we place a mouthpiece over her mouth and attach the tubing on the other end to a recording device called a spirometer. As our patient lies on the table breathing quietly under resting conditions we notice a simple rhythmic pattern on the spirogram. This pattern is entirely involuntary caused by the production of a signal from the center of respiration located in the brain that causes the diaphragm and other muscles to contract and to expand the chest, and then as it switches off, the muscular relaxation and elastic recoil cause the chest to contract.

Lung Function Tests – Lung Volumes: Breath-hold  Deep Inspiration

We reset our spirometer to get our basal conditions set between the 3 and 4 liter mark so that we have room on the graph to see what happens with forced inspiratory effort and forced expiratory effort.

For those of you who require your patient to “breath hold” for MRI and CT, we are in fact asking them to stop this involuntary breathing pattern in order to prevent chest wall and lung movement that would otherwise cause motion artifact on our images.

For our CXR we now ask our patient to take as deep a breath in as possible and we see a dramatic change on the graph.

When you ask your patient to take a deep breath in for a CXR, the chest volume will increase by more than 3 liters. The patient will muster all their diaphragmatic forces to contract the intercostal muscles to enlarge the chest cavity and pull in air. The lung in the healthy patient will now contain about 6.7 liters of air. When our patients can take a deep breath and hold it in, the radiologists are better able to identify disease processes since the interface of air and the soft tissue of the disease are larger and therefore the disease is more easily seen.

For those of you who are ultrasound technologists you use the consequences “deep breath in” to bring the diaphragm and upper abdominal organs down, beyond the rib cage, in order to optimize your window to the upper abdomen.

Lung Function Tests – Lung Volumes: Expiration

Now as the patient reaches peak inspiration we tell her to breath out as completely and rapidly as possible, and our spirometer reading does the following:

The difference between the end of basal expiration and complete expiration is called the expiratory reserve volume (ERV).

For the lung function technologist the speed with which the expiration is performed is a key issue in lung function, but for you the degree to which the patient can empty their lungs is key for a good expiration film.

Lung Function Tests – Lung Volumes: Residual Volume

At the end of this complete expiration, there is still a volume of air left in the lungs and airways, and this is called the residual volume (RV), which is the air filled space that keeps everything open after a full expiration. When we perform a CXR in expiration, we ask our patients to breathe in and then all the way out, and to hold it out, and we then expose our film. The air you see in the lungs at the end of expiration is called the residual volume. The lungs are at their smallest volume in end expiration and at this point contain about 1.5-1.7 liters in our patient. In the normal adult the RV ranges between 1.0 and 2.4 liters.

 

Lung Capacities
We now move on to our patient’s lung capacities, which represent a combination of the volumes we have spoken about. What do you think inspiratory capacity is? It is of course the combination of the basal inspiration, which is our tidal volume of 500mls combined with the inspiratory reserve volume (3.2liters) giving us a total of a 3.7 liters capacity for inspiration.

The amount of air left in the lungs after a resting expiration includes the expiratory reserve volume and the residual volume is called the functional reserve capacity (FRC).

 

Lung Capacities: Vital Capacity

The vital capacity (VC) is defined, as is the maximum volume of air expelled after a maximum inspiration. For you, this is the difference in amount of air in the lungs between a CXR with maximum inspiration and a CXR with maximum expiration. In this patient it is about 5 liters – a large difference in volume and a large difference in the appearance of the chest, sometimes making the difference as to whether a pneumothorax is seen or not seen. Why is this so important? A small pneumothorax itself may not have any functional significance meaning the patient has no untoward effect. It does however reflect a leak, and a leak can get better or worse. In the situation in which it gets bigger it can cause a life-threatening situation and so it is essential to make the diagnosis of even a small pneumothorax. Using expiration technique for the clinical question of pneumothorax is essential.

 

Lung Capacities: Total Lung Capacity

The total lung capacity is a combination of the vital capacity and the residual volume. Thus it is a combination of the maximum volume of air that the patient can move in and out of his lungs and the air that remains in the lungs after a forced expiration.

 

The names and details of the volumes and capacities are not meant to confound you with impractical minutiae, which are not important to you in your day-to-day work. It is more meant to give you a sense of the volume changes that occur during quiet and forced breathing and the impact that these movements have on your work, whether it is taking a CXR where you want to optimize inspiration or expiration, during an MRI or CT examination where you want to minimize respiratory artifact, or during an ultrasound examination where you want to optimize your window to the upper abdomen.

Gas Exchange: Basic Principles

While the function of air transport is the domain of the tracheobronchial tree, it is the function of the alveoli to act as a membrane for gas exchange to and from the atmosphere and the blood. The principles of gas exchange across a membrane are also universal in the body. The movement of both oxygen and carbon dioxide is by diffusion. Diffusion is the movement of the gases, fluids, or chemicals from a higher level of concentration to a lower level. The partial pressure of the two gases is a measure of their concentrations. The greater the difference in partial pressure the greater the rate of diffusion. Oxygen is carried mostly by a macromolecule of protein called hemoglobin while carbon dioxide is mostly carried in the form of bicarbonate in the serum.

The membrane across which the gases have to move is between 0.3 – 1.0 micron thick and consists of two cell layers. One layer is the epithelium of the alveolus and the second layer is the epithelium (called endothelium) of the capillary.

Fick’s law governs the movement of air across a membrane. The net movement or diffusion rate of a gas across a fluid membrane is proportional to the difference in partial pressure, proportional to the area of the membrane, and inversely proportional to the thickness of the membrane. The total membrane surface area of the alveoli is about 80-100 square meters and the thickness is less than a millionth of a meter, so it is a very effective gas exchange interface.

At rest about 6-10 liters of air is moved through the tracheobronchial tree per minute. In this same minute about 600ccs of oxygen moves from the alveoli into the blood, while 600 ccs of carbon dioxide moves across the membrane into the alveoli. During exercise up to 100 liters of air can be moved through the airways per minute and about 3 liters of oxygen and 3 liters of carbon dioxide is moved across the membrane.

Gas Exchange: Applied Physiology

The alveolar membrane can get affected by disease processes that may accumulate fluid or pus within the alveoli causing a thickened membrane. Interstitial fibrosis is a second cause of thickening of the respiratory membrane that will affect the efficiency and speed of gas exchange.

Components of the Lung

The right and left lungs are asymmetric with the right having three lobes and the left two lobes. The lingula is part of the left upper lobe (LUL).

 

Right Lung Parts: Basic Anatomy
The right lung has three lobes: upper, middle, and lower. The lobes are subdivided into segments that are determined by the branching of the main bronchi. The right lung usually has the segments subtended by ten segmental bronchi. The right upper lobe (RUL) has three segments called the apical, posterior, and anterior segments. The right middle lobe (RML) has two segments named the lateral and the medial segments. The right lower lobe (RLL) has five segments also named according to position: superior, anterior basal, lateral basal, posterior basal, and medial basal segments. The superior segmental bronchus is the first branch of the RLL system and it is directed posteriorly. The superior segment is vulnerable in the supine patient who aspirates because of its posterior position.

 

Right Lung Anatomy Continued

The superior segment occupies the entire upper portion of the lower lobe. It sits atop the remaining four segments of the right lung: the anterior basal, lateral basal, posterior basal, and medial basal segments. These basal segments form the base of the almost pyramidal-shaped lower lobe, as well as the base of the lung.  The basal segments and base of the lung rest upon the diaphragm.

Right Lung Parts: Applied Anatomy

It is essential to know and understand the distribution of the lobes for accurate assessment of the CXR. For example, a disease process in the upper lung field on the right does not necessarily mean that the disease is in the RUL. Since the RLL is so large and extends almost the entire thoracic distance (see image 3a), it is difficult to localize on the P-A exam of the chest. However, if one reviews the lateral exam, the distinction between right upper and right lower lobe is much easier, since the lower lobe is mostly posterior and below the fissure, and the upper lobe mostly anterior and above the fissure.

The major fissure is the dividing line between the RLL on the one hand and the RUL and RML on the other. The minor fissure, also known as the transverse fissure, divides the RUL from the RML and is easily perceived on the lateral examination.

Right Lung Applied Continued
Sometimes there is an extra lobe in the right upper lung field called the azygous lobe and the azygous vein runs in the accessory fissure. The azygous lobe is an accessory lobe in the apex of the right lung that is found in approximately 0.5% of routine chest x-rays. It is recognized by a fissure in the apex that has an inverted comma shape.

The following diagram demonstrates the cross sectional appearance of the right lung at the level where both the major and minor fissures are seen. It correlates the CT scan with the anatomical specimen.

 

Left Lung Parts: Basic Anatomy

The left and right lungs are very different. We have already noted that the mainstem bronchi are different, with the left mainstem bronchus being long and thin, while the right mainstem bronchus is short and fat. The left lung has only two lobes. There is a left upper lobe (LUL) and a left lower lobe (LLL). The left lung does not have a middle lobe. Instead, the middle lobe equivalent is the lingula, which is in fact part of the LUL and not a separate lobe.

The two lobes of the left lung are separated by the major or oblique fissure, which is the only fissure on the left side. The left lung is smaller than the right and has eight segments compared to the ten segments on the right.

The upper lobe of the left lung has superior and lingula divisions. Both of these divisions have two segments each. The segments of the superior division are the apical-posterior and the anterior segments. The lingula is divided into superior and inferior segments. As noted there is no fissure between the upper segments of the LUL and the lingula – they are both part of the LUL.

The division of the lower lobe closely resembles that of the right except that there is consolidation of two of the left lower lobe segments. Thus, while the RLL has five segments, the LLL has only four. Again, as is characteristic, the left lung consolidates its component parts.

The superior segment of the LLL forms the top of the pyramid of the LLL. Inferiorly and at the base of this pyramid, the anterior and medial segments combine to form the anteromedial basal segment, followed by the lateral basal, and posterior basal segments.

 

Quiz Me

The left lower lung has _________ segments.
(Note: You will be given 2 tries to answer this question, then the answer will be provided.)
two
three
four
five

Left Lung Parts: Applied Anatomy

The overall volume of the left lung is smaller than the right, but the distribution of volume between LUL and LLL is more equalized and balanced. Again, in the P-A projection the two lobes overlap each other. A nodule in the upper lung field or lower lung field as seen on the P-A projection can be located either in the upper or lower lobe. The lateral examination is essential to accurately locate the disease. The LUL is anterior and above the fissure (see Fig 1b), while the LLL is posterior and below the fissure (see Fig 2b).

Quiz Me

A nodule in the lower lung field is always located in the lower lobe of the lung.

True  False

When we read plain films of the chest we use the position and relations of the lungs to the heart and the fissures to locate disease processes, including infiltrates, nodules, and regions of atelectasis. We use two principles to locate disease. The first is the described relations of structures to each other, and the second is the concept of “silhouetting.” The important facts that pertain are that the RML abuts the right heart border, the lingula the left heart border, and the lower lobes on both sides abut the diaphragm. The principle of “silhouetting” is commonly used to define the nature and location of a soft tissue process in the lung. We have described the fact that we are able to see and distinguish two different structures because their densities are different. Thus we are able to see the heart border or the diaphragm, for example, because they abut air- filled lung tissue that has a completely different density to their soft tissue nature. If, however, the air-filled lung is replaced by pus or exudates (pneumonia) or become airless (atelectasis), then the abutting structures both have soft tissue density and cannot be distinguished from one another. If there is a process that silhouettes the right heart border in the P-A projection then we know that this process is in the RML. Similarly, if the left heart border cannot be distinguished from the disease process, we know that it is in the lingula.

It is important to identify accurately the location of disease, particularly nodules and masses that may have to be surgically removed, since the surgeon has to know which part of the lung has to be removed.

Smaller Parts – The Acinus

The bronchi proceed from the mainstem bronchus via 16 to 23 divisions into the terminal bronchioles. Thereafter sac-like protrusions develop in the system, which allow gas exchange to start taking place. The first branch that is able to perform this gas exchange is called the respiratory bronchiole. After three divisions the respiratory bronchioles become alveolar ducts and after further division become alveolar sacs. Finally, at the terminal end of this pathway, are the alveoli. The system that starts at the respiratory bronchiole and terminates at the alveoli is called an acinus, and it is functionally characterized by having the ability to both conduct air as well as enable gas exchange. The acinus averages about 6-7mm in diameter. When it is filled with fluid, it can be visualized on a CXR as a 6-7mm density called an “acinar shadow.” As a structural entity it has little diagnostic utility. We will expand on the pulmonary lobule in the next section, which has greater implications for the imaging of the lung. Functionally however, the acinus can be considered as the unit of gas exchange in the lung.

 

The Secondary Lobule (a.k.a pulmonary lobule)

We will now move upstream toward the terminal bronchiole to gain an understanding of the secondary lobule. From a radiological point of view, it is structurally a more important unit than the acinus. It is a conglomerate of 3 to 5 acini enclosed in a membrane with a polyhedral (having many surfaces) shape. From a structural and radiological point of view it is important to understand this entity, since it has implications in the understanding of the CXR, conventional CT, high-resolution CT and in the structural changes that occur in some of the lung diseases.

We have already described the “buddy system” that exists in the lung, with the branches of arterioles and bronchi traveling together, and the venules and lymphatics going together. Lymphatics sometimes also accompany the bronchovascular bundle.

The Secondary Lobule (a.k.a. pulmonary lobule): Grapes of Exchange – A Romantic Story

From the minute I saw him I loved him and I knew that no matter what evolved, we would spend our lives together… little did I know what the working relationship would be.

Here follows a true story about me, the bronchiole, and my lifelong buddy the pulmonary arteriole.

He and I were on a mission. I had my origins in the atmosphere and he from the heart. We came from very different backgrounds and had come a long way on this trip on the highways and byways of the airways and circulation. My mission was to take products from the air in the atmosphere and deliver them to the grapes of exchange and his was to deliver blue blood to the same grapes. In this communication we will speak mostly of the journey to the grapes in the house of the pulmonary lobule. The grapes of exchange in my imagination had something to do with bonding and marriage – perhaps the exchange of vows. The story turns out quite differently. We had great travels together and took a lot of pictures!!

I think by this time you know what we had already been through. He had started out as a large elastic vessel off the right heart called the main pulmonary artery (nickname “MPA”) and I had started out as the trachea. (nickname “trach”). We met at the doorway of the lung called the hilum, and took a fancy to each other right away and so we decided to travel together. We had traveled a long way by the time our story begins both experiencing many divisions and were right in the middle of an inspiration. We both looked quite different at this point having given birth to many offspring. In the new language – we had both “morphed” quite a bit but this was a necessary part of the mission. Of course we were much smaller than we had been. He had lost some of his elasticity and developed a bit of muscle. I had lost my entire cartilaginous skeleton and had developed some muscle as well. We were told that from now on we were both going to lose muscle and I in particular was going to change drastically. I could not wait! I secretly hoped that this change would make me more attractive and bring me closer to a happy union since I was promised a happy union in the end. My name at this stage was “terminal bronchiole”. A foreboding and deathly chill rattled down my muscularis as I said the word “terminal” knowing that I was going to lose the small amount of muscle that I had.

We reached the doorway surrounding the secondary lobule and faced the polyhedral entrance. It was quite beautiful I thought in my teal blue outfit.

We took a quick walk around the polyhedral structure.

We returned to the entrance and took a closer look at the goings on inside through the large front entrance windows of the pulmonary lobule. Below is a picture of what we saw.

As we were ushered into the lobule, we were faced by a refreshing atmosphere of comforting air and a hub of activity. In addition to the swishing sounds of air movement we heard a hubbub of clinking and clanking. We were told that the sounds were coming from the grapes of exchange (wedding bells?). We also noticed that there were at least three other couples that looked like the people of our tribe – three other bronchovascular bundles. We called our tribe the “bronchovascular bundle” with the one part of the bundle being the progeny of the bronchus and the other, the progeny of the pulmonary artery.A group picture inside the lobule is shown below. Fortunately the flash was working because it was a little dark inside.

We noted there were other pairs of people they called the pulmonary venules (red) and lymphatics (yellow). A joyous union with these pairs was also promised. I could not imagine how. They looked so different to each other – the lymphatic, tiny and dressed in a bright yellow suit and the vein in passionate red. They seemed so foreign, almost from another space, time zone and culture. At this vantage point we got a vague sense of what was to come, but in our wildest dreams we could not have imagined how our bodies were going to change and what was to happen as we moved inward into the chambers of gas exchange.

 

I did not realize that my body had already started to morph at the time of the picture – little sac-like love handles spreading all along my formerly sleek and beautiful body. Yech! I did not look good at all. My buddy the arteriole on the other hand as well as members of the other tribe maintained their sleek tubular looks. “Why me?” I shouted. “All for the good of the nation and good gas exchange!!” they shouted above the swishing of air and clanging of the factories. “Easy for you to say,” I replied. “Some of us have to suffer some bad morphs for the good of the whole” they said, “but those love handles kind of suit you,” they exclaimed with a wry smile. I was so sad.

Well the divisions started coming rapidly and so we all became smaller very quickly. I was getting rounder and rounder while they were getting thinner and sleeker. Things seemed to be rushing at an accelerated pace and I must say that there was some excitement in the air as we all got closer and closer to each other. In the big picture we seemed to be coming together as a team, and the whole landscape seemed more colorful and more promising. We reached out to the other tribe and they too us.

 

I remained on the plump side as my love handles grew more pronounced and rounder while the clanging noises grew louder and louder. I was dividing into alveolar ducts and alveolar sacs and finally into alveolus which of course is a complete transformation from my former tube like shape to the spherical shape of the grape. In the mean time my buddy the artery grew as small as an 8-micron red cell and remained true to his tubular form. He started to surround me completely but was more in concert with that beastly red vein as he ran headstrong in blind passion to join her in capillary union. For a moment they each lost their identity becoming the tiniest of tubes neither arteriole nor venule. I on the other hand became at one with the fruit of the vine and in stuporous state I think I became the grape itself. Through my waist I felt the pleasant freshness of gusts of air going back and forth through my skin. My delivery of fresh air moved very quickly into the capillary. Little did I know that it was the oxygen that I carried which gave my competition the beautiful red glow of health. The odious carbon dioxide moved the other way. This toxic waste came directly from the man I had known and trusted for so long. Thanks for nothing.

I do not like to show the next picture much since for me it is a sad one. There I am a ditched lover, fat as a grape, in the middle of the capillary union between my blue “ex” and his new partner in crime, the red beast. Yes of course it was for the better – they all say that – but what about me?

As you have learned already, the blood circulation needs two types of vessels: one to carry the blood to the lungs and a second to carry it from the lungs. I on the other hand do it all by myself. On inspiration I take air to the lungs and on expiration I take it away through the same vessel to the atmosphere. This is the lot of all women. We do double the amount of work schlepping here and there and everywhere and get no respect for it.

So at this junction we are in the middle of an inspiration (for me – what kind of inspiration could I feel in my morphed format) and we were just about to start the expiration. While I was traveling to the exit of the lobule during this phase of my life, my “ex” was going in the same direction – now transformed into a beautiful vessel with that healthy glow. Despite my odious load and my downtrodden feeling I moved with a sense of optimism.

What do you know? As I left the chamber of the lobule I shed my love handles one by one and my saccular form started to take on the sleek and tubular look again. I looked and felt brand new. “Hmm… I thought – perhaps he will fall in love with me again. I was hoping for another inspiration, just to show him once again how beautiful I was both on the outside and the inside. And that my friends was my nightmare in the Grapes of Exchange.

The Secondary Lobule: Applied Anatomy

The secondary lobule contains all the structural elements of the lung compacted into a small space and it is a recognizable structural entity that measures about 1 – 2.5cms. There are 3-5 bronchovascular bundles per secondary lobule. Prior to entering the secondary lobule the bronchovascular bundles branch at approximately 1cm intervals. However, once they enter the confines of the lobule the branching becomes fast furious and a new branch originates every 1 – 3mms. A lot of structure subsequently is packed into a small space. The lobules are well formed in the apices and the peripheral aspects of the lungs and poorly formed posteriorly.

The Secondary Lobule: Applied: Disease of the Secondary Lobule

The interlobular septa and the secondary lobules are not normally visualized. However, any disease of the lung, particularly if the lymphatics are involved, will expose the lobules mostly by providing better visualization of the interlobular septa. If more than three contiguous secondary lobules are visualized then the lung is abnormal.

Quiz Me

If more than _____ contiguous secondary lobules are visualized then the lung is abnormal.

One
Two
Three

The Secondary Lobule: Applied: CT Example
At the level of the terminal bronchiole the arteriole and bronchiole measure about 0.2 mms each and it is the challenge of our CT technology to resolve these structures. At this level we are starting to push the limits of resolution. Thin collimation allows us to optimally visualize the lobule. We are thus better able to visualize the septa and the lobules with 1.5mm collimation than with 3mm collimation and our chances diminish, as collimation gets thicker. The evolution of high resolution CT scan has allowed us insight into the lobule and provides a better understanding of the diseases that affect the lobule.

The Secondary Lobule: Applied: Congestive Heart Failure

We are never able to visualize the normal lobule on a plain film, but in diseases such as congestive cardiac failure when the lymphatics become overwhelmed they distend and become visible. In congestive cardiac failure the heart fails as a pump. In left ventricular failure the resulting congestion is reflected in the left ventricle (LV), left atrium (LA), pulmonary veins, and capillaries as increased pressure. It is reflected structurally as dilatation of the chambers and vessels. The increased fluid and pressure not only cause dilatation but also cause the fluid to leak out into the interstitium. The lymphatics are able to remove and mop up some of the excess fluid, but there is a point when the volume overwhelms the lymphatics and the excess fluid remains in the interstitium. On a CXR the findings include dilatation and cephalization of the arterioles, peribronchial cuffing, Kerley B lines (thickening of the interlobular septa), pleural effusion, and subpleural edema.

Kerley B lines are interesting manifestations of the thickened interlobular septa. After the discussion on the polygonal shape of the secondary lobule one might think that on the CXR we would identify a polygonal shape. However, the interlobular septa take on a linear shape, at the periphery and base of the lungs. It just so happens that the septa between the lobules run at right angles to the pleural surface at the costophrenic angles and so Kerley B lines are defined as linear, non-tapering, horizontal lines measuring 1-2cms., positioned at right angles to, and in contact with the pleural surface. Kerley B lines are best seen on a CXR.

The Secondary Lobule: Applied: Carcinoma Sarcoidosis

Conclusion

In this first part of the series on the lung we have emphasized the structure of the lung, and outlined how structure is integrated with function, disease, and imaging. We have focused on the principles describing a tubular system involved with transport, and a membranous system involved with gas exchange. The manner in which the lungs in concert with the muscles, bones, and membranes of the chest accomplish movement of air is remarkable. The principles of physics is an important aspect of understanding flow and exchange, but as you will see again and again, biological systems have changing needs under changing physiological conditions, and therefore we cannot treat the system as a simple tube or a simple filtering mechanism. The physics can only guide our understanding of a biological system. Diseases of the lungs are common and varied, and the chest x-ray is still the most common radiological examination that is performed. Imaging of the chest and lungs has been significantly advanced by the advent of multidetector CT and tailored examinations are required depending on the part of the lung that is deemed suspect. Thus a CT for pulmonary embolism will have little need for high-resolution technique for interstitial lung structure, and similarly a study for the evaluation for interstitial disease in sarcoidosis has little need for conventional CT technique. The technique applied is going to be guided by the clinical question.

 

Introduction

The devil is in the detail. The following module presents the anatomic detail in greater depth so that the finer points of diagnosis, particularly related to imaging and imaging techniques can be elaborated. What is the indication for high resolution CT for example? How do we time the bolus to optimize pulmonary arterial imaging? What anatomical and physiological facts do we use? Why do we change the position of the patient in the evaluation of interstitial lung disease? What is an air bronchogram, and what is ground glass opacity? What is the future for the plain film of the chest?

Components of the Lung

The detailed anatomy of the right and left lung can be found in

Part 1-Applied Anatomy of the Lung: Basic Principles. 

For continuity of thought we will pictorially illustrate the parts of the lung.The lung is divided into a right and left side with the right lung being composed of an upper, middle, and lower lobe, and the left lung being composed of an upper lobe (with the lingula as part of the upper lobe) and the lower lobe.

The same specimen as seen above is viewed from its posterior aspect showing the upper lobes in red and the lower lobes in green. Note that the lower lobes have a majority of their parenchyma posteriorly while the upper lobes are dominantly positioned anteriorly.
Courtesy of: Ashley Davidoff, M.D.
32557b01The lobes are subdivided into segments that are determined by the branching of the main bronchi. The right lung usually has the segments subtended by ten segmental bronchi. The right upper lobe (RUL) has three segments called the apical, posterior, and anterior segments. The right middle lobe (RML) has two segments named the lateral and the medial segments. The right lower lobe (RLL) has five segments also named according to position: superior, anterior basal, lateral basal, posterior basal, and medial basal segments. The superior segmental bronchus is the first branch of the RLL system and it is directed posteriorly. The superior segment is vulnerable in the supine patient who aspirates because of its posterior position.

The left lung is smaller than the right and has eight segments compared to the ten segments on the right. The upper lobe of the left lung has superior and lingula divisions. Both of these divisions have two segments each. The segments of the superior division are the apical-posterior and the anterior segments. The lingula is divided into superior and inferior segments. The division of the lower lobe closely resembles that of the right except that there is consolidation of two of the left lower lobe segments. Thus, while the RLL has five segments, the LLL has only four.

The segments are divided into the secondary lobules.  The lobules are made up of the small airways including the terminal bronchioles, respiratory bronchioles, alveolar ducts, alveolar sacs and the alveoli themselves.

 

 

 

Size and Surface Anatomy

The lungs are one of the more voluminous organs in the body but in terms of weight are relatively light for their size, since they are filled mostly with air. Additionally, their size can change dramatically since the difference in volume between a deep inspiration and deep expiration can be as much as 3.5 liters.

Within the thorax the lungs extend superiorly passed the clavicle into the base of the neck, with a craniocaudal length in inspiration of approximately 24 cm. Posteriorly, on a chest X-ray they reach to the 10th  rib. Cranially they extend to the first thoracic vertebrae and inferiorly to the dome of the diaphragm and costophrenic sulci more inferiorly.

In patients with COPD (chronic obstructive pulmonary disease) or an acute asthmatic attack, the lung volumes are expanded and the lungs will be seen beyond the 6th rib anteriorly and the 10th rib posteriorly.

Weight and Volumes

In the living and breathing adult, the lungs weigh approximately 900 to 1200 grams, of which nearly 40% to 50% is blood. The weight will depend on how much blood is running through the lungs. At rest it is 5L/min, but during exercise, the blood flowing through the lungs can be up to 25L/min and at any one time during exercise, the lungs will be that much heavier. At rest the lungs together weigh about the same as the liver, which is 1/3 the volume of the lungs.

The left lung is smaller since the heart, which is dominantly a left sided structure, occupies part of the left chest.

The total volume of the lungs is about 6300ml in adult men and 4200ml in adult women. At end-expiration, the volume of air within the lungs is about 2.5 L, whereas at maximal inspiration it may be 6 L. Taking a rate of 10-15 breaths per minute (about 17,000 breaths per 24 hours) results in approximately 10,000 liters of air inspired per day. Of course an equal amount has to be expired per day as well, and so there is the back and forth movement of about 20,000 liters per day.

Alveoli make up approximately 50% of entire lung volume. The outer 1/3 of the lung contains 50% of the alveoli. Thus alveoli are the major component of the lung and they are situated dominantly in the periphery while the tubular transport systems are located centrally by the hilum. The lung and the kidney have structural similarities in that the outer third of the kidney called the cortex contains most of the key functioning and filtering aspects of the kidney, whereas the inner and more central medulla houses the tubular system. The similarity is such that some refer to the lung as having an outer cortex and an inner medulla.

Surface Area

There are about 20,000 acini and 300 million alveoli in the normal lung. During inspiration the radius of the alveolus doubles from about 0.05 mm to 0.1 mm. The total surface area of the lung is about 80 square meters, about the size of a tennis court. The extent and volume of air that is moved across the alveoli is simply stunning.As we have already seen about 5-10 liters of air is moved through the tracheobronchial tree per minute at rest. During exercise up to 100 liters of air can be moved through the airways per minute and about 3 liters of oxygen and 3 liters of carbon dioxide moved across the membrane. There are many factors that allow for the exchange to take place but the lung does its part by providing a large patent surface area by virtue of its alveolar structure.

The lungs create an increased space by bubbling, or ballooning out in the form of the alveoli. The gastrointestinal tract and kidney have more time to do their work. The lungs need all the time they can get since most of the exchange is done during inspiration and even more effectively between inspiration and expiration. The air that is inspired must present itself to the functional surface at large almost immediately, and the exchange has to take place before expiration starts when the air is whisked away to prepare for the next load.

Surface Area: Applied Anatomy

In the clinical realm, there are certain diseases that make the lungs abnormally large and those that reduce the size of the lungs or segments of the lungs.

The lungs will usually take up the available space in the chest so that if one part of the lung is collapsed or surgically removed then the remaining lung will take up the space. Similarly, if one lung is blocked or becomes smaller, then the other becomes hyperinflated resulting in shape and size changes to accommodate the deficiency.

In the COPD group, including emphysema, there is air trapping so that what goes in does not come out because of the structural changes in the lung, resulting in hyperinflation and large lungs. In an acute asthmatic attack there is air trapping making the lungs larger in volume than normal. The diaphragm gets pushed down and becomes flattened. Atelectasis is also part of the disease because thickened mucus plugs the smaller airways, and therefore air cannot get in and subsegmental collapse occurs. Less commonly the mucus may block the airways at segmental and lobar level with significant consequences to an already compromised system. The diaphragm on the same side of the collapse becomes elevated to the degree that depends on the size of the collapse. The larger the collapse the greater the volume loss in the lungs, the greater the space that needs to be filled in, and hence the greater the elevation of the diaphragm. The concept of filling in space is also witnessed when a patient has had resection of part of the lung. The space usually is filled in by the remaining segments of the ipsilateral lung, but if there is insufficient ipsilateral lung to do the job, (fill in the space) it may be filled in by contralateral lung.

 

Shape

The lungs are funnel, conical, or even pyramidal in shape, with a narrow apex and a broad, concave base.

The apex, also called the cupola is dome shaped, fitting snuggly into the space created by the soft tissue confluence of the mediastinal parietal pleura with the costal parietal pleura and the bony frame formed by the clavicle and first rib. It is positioned 2-3cm superior to the medial third of the clavicle where it projects through the superior thoracic inlet.

 

 

Lung parenchyma is relatively exposed at the apex making it vulnerable to penetrating injuries of the neck.The base of the lung is concave so that there is a snug fit with the hemidiaphragms bilaterally. An intimate and parallel contact is maintained during all phases of respiration. This contact is necessary since the function of these two structures is intimately linked. The shape of the base will of course change with respiration and, like two dancers doing the tango, the diaphragm and lung move gracefully, intimately, and sometimes dramatically together with each phase of respiration – even with the sharp turn of events of a hiccup or a cough (or the tango equivalents – the gancho or the giro!).

Each lobe of the lungs has a characteristic shape, and may look very different in the A-P projection and lateral projection. The right upper lobe (RUL) is roughly triangular in shape but with blunted or rounded angles. Its A-P shape is very similar to its lateral shape. The right middle lobe (RML) and the right lower lobe (RLL) are both rectangular in the A-P projection but triangular in the lateral view, (apex at hilum and base anteriorly), though the RML is comparatively smaller.

The left upper lobe (LUL) from the A-P projection resembles a rectangle with the upper edge being rounded, while from the lateral view it is shaped like half an oval, the bottom part being pointed. The left lower lobe (LLL), from the A-P projection, is almost a perfect rectangle, and from the lateral view is almost a perfect triangle.

Shape: Applied Anatomy

In a hyperinflated state such as exists in emphysema, the lungs are full, bulging with air, and less pliant, causing the diaphragm to flatten. Clinically, the patient is described as having a barrel shaped chest, a pigeon shaped chest, or in Latin, pectus carinatum. The chest X-ray (CXR) in this circumstance will show flattened hemidiaphragms, reflecting the almost fixed shape of the lungs, and an increase in the air space behind the sternum, (the retrosternal air space) which causes the barrel shape.

 

 

Position

The lungs are located within the thorax, within the thoracic cavity and within the pleura. They occupy about 3/4 of the thoracic cavity, with the rest occupied by the heart and the mediastinum. The right lung occupies almost the entire right hemi thorax and the left is displaced by the heart and occupies a lesser amount of space.

The lungs are divided into upper and lower lobes being somewhat of a conceptual misnomer, since the lower lobes creep up posteriorly to almost the apex of the lungs and the upper lobes (together with the lingula and middle lobe) reach more inferiorly in the anterior location. The lobes may have just as well been called the posterior lobes and the anterior lobes but because the upper lobes reach the most superior position in the chest and the lower lobes the most inferior and diaphragmatic parts, they were reasonably labeled upper and lower.

The segments are named according to their position, and include the apical anterior and posterior segments in the upper lobes, the lateral and medial components of the RML, the superior and inferior of the lingula, and the superior (apical) lateral medial anterior and posterior basal segments. Note that all the names relate to the position of the segments. There is a move to give these segment numbers – but it seems far easier to understand the spatial positioning by naming the segments according to their position.

The middle lobe has a very intimate relation to the right heart border (RA), while the lingula has a similar relationship with the left ventricle. This has relevance in the evaluation of infiltrates on the CXR since disease in the RML will cause silhouetting of the right heart border (RA), while an infiltrate in the lingula will silhouette the left heart border. On the lateral examination since both of these are anterior segments they will be seen as anterior infiltrates. Hence the position of infiltrates as seen on the CXR can be accurately localized to segments by looking at the relationship to the heart in the P-A and whether the infiltrate is anterior or posterior on the lateral.

Position: Applied Anatomy

Situs inversus (reversal of position or location) has a wide variation of clinical presentations. Some patients with situs inversus may live a completely normal life without ever being aware of the condition. At the other extreme, the aberrant morphology, particularly related to the heart is life threatening.

Anatomy of the Structures Surrounding the Lungs

The lungs are completely surrounded by the pleura, a variety of muscles and the bony thoracic cage. The heart and other structures of the mediastinum form the medial relations of the lungs.

Within the mediastinum lies the heart and pericardium, the trachea and main stem bronchi, esophagus, thoracic duct, lymph nodes, and both phrenic and vagus nerves. The mediastinum is situated anterior to the sternum and ventral to the spinal column, nestled between the pleural sacs of the right and left lungs. Superiorly it reaches the level of the fourth thoracic vertebrae and rests upon the diaphragm inferiorly. Below the diaphragm lie the liver, gall bladder, and spleen.

Surrounding the lungs are the thoracic muscles and the diaphragm itself. These are the muscles related to respiration. Their operation alters the pressure within the thorax. When the thorax expands, the pressure decreases allowing air from the trachea into the lungs. When it contracts, the lungs compress and air leaves the lungs. When the diaphragm contracts, it flattens and sinks as much as 7-10 cm below its normal level at rest. As the muscles relax the thorax returns to normal pressure and air from the lungs is released. This is known as abdominal respiration and accounts for approximately 70% of respiration in a resting body.

Character of the Lungs

Leonardo da Vinci in the late 15th century accurately depicted the spongy and elastic nature of the lungs by the following observation.”The substance of the lung is dilatable and extensible like the tinder made from a fungus. But it is spongy and if you press it, it yields to the force which compresses it, and if the force is removed, it increases again to its original size.”

The lungs are filled with air, and they look and feel like a soft sponge. Their infrastructure of thin septa and air filled cavities is very reminiscent of the architecture of a sponge. The lung “crepitates”, or has a characteristic “crackling” feeling when handled. If it is inflated with air ex vivo, the healthy lung will float. The value of the relative amounts of air, and hence floatability, is well known to swimmers and snorkelers who can control their buoyancy by titrating the amount of air in their lungs against where they want to passively float in the water.

The chest wall and lungs are also characterized by an elastic nature allowing the apparatus to recoil after inspiration. The act of expiration is thus a passive process requiring no energy as the elastic recoil brings the lung back to unexpanded state.

Color

The color of the healthy lungs is affected by age and geographic location. In the young, they are pink and healthy appearing. In an industrial society the lungs are directly exposed to a smoky environment, and carbon particles are retained in the lungs and lymph nodes giving the lungs a dark slate gray color with a mottled appearance. With advancing age, the slate gray mottling changes to a black. The carbon-type granules are mostly deposited in the tissue near the surface of the lung.

The Mediastinum

The mediastinum is densely populated with important structures including the aorta, esophagus, trachea and heart. Often the first signs of disease are recognized on the chest X-ray as a result of subtle changes in the shape of the mediastinum. It is therefore imperative that radiologists are extremely familiar with the normal shape of the mediastinum. Review of the shape may start with the left side at the apex – Think of yourself skiing down a mogul trail and consider the bumpy ride that may challenge you. There is a left sided slope and the right sided slope – both are black diamonds. Get your skis and helmets on– these are tough slopes.

The Mediastinum: Applied Anatomy

The following image represents one of the many shape changes that occurs in the mediastinum that will tip the radiologist off to a disease process in the chest.

 

 

The Trachea

The trachea is a tubular portion of the respiratory system that connects the larynx to the bronchi. It is relatively thin walled, about 6 inches long in the adult, consists of a series of c-shaped cartilaginous rings anteriorly and a membrane posteriorly. At the level of the carina it divides into left and right bronchi.

The trachea, although it is a tube, is made up of 15 – 20 C-shaped cartilaginous rings with a posterior membranous surface, giving it a horseshoe shape in cross section. Its A-P dimension is thus longer than its transverse dimensions.

The shape of the tracheobronchial tree at large is very similar to a branching tree. If you took an image of the tracheobronchial tree and turned it upside down you would see the following. It has an irregular dichotomous branching pattern meaning it divides into paired branches of unequal length and diameter.

The Trachea: Applied Anatomy

Tracheomalacia is softening of the tracheal cartilages which results in relative collapse of the trachea during inspiration and thus affecting airflow. The cause can be due to congenital weakening of the cartilage, due to extrinsic disease such as vascular rings and slings, or acquired from prolonged intubation or chronic infection. (eMedicine).

The Trachea: Position of the Trachea

The trachea is central in its position, and lies anterior to the esophagus. It originates below the pharynx and ends at the carina where it bifurcates into left and right main stem bronchi.

Bronchi and Bronchioles

The mainstem bronchi taken together have 40% more cross sectional area than the trachea. This progressive increase in cross sectional area continues as we progress downstream resulting in an overall reduction in resistance, evolution of laminar flow, and facilitation of airflow. This structural feature allows air from a single breath to reach all the alveoli almost simultaneously.There is considerable discrepancy in diameter and length between the right and left mainstem bronchi. The right mainstem bronchus is short and plump while the left mainstem bronchus is the long and thin.

The right mainstem bronchus measures about 1.4 cms in diameter while the left mainstem bronchus is about 1.3cm both being slightly smaller in the female (Hampton , et al).
The RUL bronchus is about 1cm in diameter, with the apical segment being 4-7mm, and the RML bronchus is about 8mms.

The LUL bronchus resembles its uncle, the right main stem bronchus, since it is also relatively short and fat possibly because it is responsible to give rise to the lingula as well as the left apical segments. It measures 11mm in diameter (but only 9mm in length). The ascending upper division bronchus is approximately 7mm in diameter.

Bronchi and Bronchioles: Applied Anatomy

The failure of air delivery is one of the major causes of fatality during an anaphylactic reaction or a severe asthma attack. Return of airway patency is the first consideration in resuscitation. In fact, in any resuscitation, the “A” of the “ABC” of resuscitation is to ensure patency of the airway first.  Maintenance of airway diameter is provided by cartilage in the upper components of the airways. In the trachea a C-shaped cartilaginous ring surrounds the anterior and lateral walls while the posterior wall consists of a membrane allowing for some pliability during the phases of respiration. The trachea lengthens and dilates during inspiration while it shortens and narrows during expiration.Some disease states compromise the patency of the airways. Tracheomalacia is a softening of the cartilage of the trachea and during inspiration the trachea will be unable to maintain its diameter. This will result in a relative collapse during inspiration and hence diminished air flow.

More downstream, support of airway patency transforms from cartilagenous support to muscular support. Asthma, inflammation, or infection can affect the diameter by inducing muscle spasm while the presence of edema of the wall would also result in narrowing of the lumen. In most of these diseases the airways of both lungs are diffusely involved and respiratory decompensation can easily result due to the extent of involvement. Collapse of a lobe, segment, or sub segment of a lung on the other hand may not affect respiratory function at all when the remaining lung is normal or near normal. Localized collapse may occur with inhalation of a foreign body, mucus or purulent impaction, and tumor growth into the lumen. Patients who have undergone a pneumonectomy usually have normal or near normal pulmonary function, unless there is disease in the other lung.

The Tracheobronchial Tree

The tracheobronchial tree changes its morphology (and so its nature) as it progresses from a relatively rigid cartilaginous structure strengthened by C-shaped cartilages. The cartilage accompanies and supports the bronchi but disappears at the level of the bronchioles. The structure of the walls progresses to muscular, elastic, and mucus secreting bronchioles and then to delicate one cell layered airways at the alveolar level. The bronchi contain cartilage but the bronchioles do not.

The main pulmonary artery (MPA) is usually about 3-4 cm in diameter being very similar to the ascending aorta and twice the size of the trachea. The branch pulmonary arteries are each about the same size as the trachea. Although the right and left mainstem bronchi are in combination and thus the right pulmonary artery (RPA) and left pulmonary artery (LPA) are quite a bit larger than their counterparts, the right and left mainstem bronchi. However, at the segmental level there is a catch up, so that the bronchi and arteries are equal in size.

These comparative sizes are very important in the imaging world and size evaluation is very useful in the diagnosis of tracheomalacia, COPD (big trachea), tracheal narrowing, bronchiectasis, aortic aneurysm, pulmonary congestion, and pulmonary hypertension – all common medical conditions that have characteristic changes in size that are evaluated by comparing the sizes of the airways to the vessels. It should be noted that in dependant positions the artery might normally appear slightly larger than its airway counterpart. This means that if the patient is supine, blood will be more dependent posteriorly and so the posterior vessels may be slightly larger than their bronchial brother or sister.

In the normal patient the pulmonary arterial branches and the bronchi are about the same size until they reach the hallowed halls of the pulmonary lobule.

 

The Tracheobronchial Tree: The Tracheobronchial Tree Continued

The reason we are able to see the air filled bronchi within the air filled lung is because they have wall that is made up of the soft tissue allowing for an interface. As the bronchi get smaller their walls will get proportionately thinner until they are too thin to resolve at which time they will blend into the parenchyma. They become invisible as discrete structures on high resolution CT when they reach 2mm in size, which corresponds to the bronchioles that are about 2 cm from the lung periphery. The arterioles on the other hand maintain their soft tissue character and their interface with air of the lung is maintained allowing detection even in subpleural regions of the lung periphery.Bronchiectasis is a condition where disease within the walls of the airways results in weakening resulting in enlargement and hence ectasia. In this condition, therefore, the bronchioles will be larger than their arteriole counterpart and they will be seen within 1 cm distance of the pleura.

The Tracheobronchial Tree: Length

The length of the airways does have practical significance as well, contributing to velocity of flow. Knowledge of the length of structures is also important for safe execution of procedures such as endoscopy, intubation, and stent placement.In adults, the trachea ranges from 9 to 15cm in length, terminating distally at the carina which represents the origins of the left and right mainstem bronchi. The distance from mouth to carina is about 25cm.

As previously stated, the right and left bronchus show considerable difference in their morphology. The right is short and plump while the left is long and thin.

The Tracheobronchial Tree: Important Dimensions

The right lung has 10 bronchopulmonary segments while the left has 8. There are approximately 23 airway divisions from the mainstem bronchi to the level of the alveoli.

The number of branches from hilum to periphery is variable with the shortest path to a terminal bronchiole being about 7 divisions and total length of 7 to 8 cm, and the longest pathway having about 25 branch divisions with total length of more than 22 cm. In the upstream portions of the airways the tree does not divide as frequently as they do downstream. The lungs are large organs and the aim of the airways is to deliver the air to the alveoli. Distance needs to be covered from the hilum where alveoli are relatively sparse, to the periphery where the alveoli are abundant. Prior to entering the secondary lobule, the bronchovascular bundle branches at approximately 1 cm intervals. Once they enter the confines of the lobule, branching becomes fast, furious and a new branch originates every 1 – 3mm. This frequency of division in the hallowed halls of gas exchange makes intuitive sense as surface area becomes the dominant focus.

The left main stem bronchus leaves the trachea at a 135-degree angle. The right mainstem bronchus is more vertically oriented, with a 155-degree angle of origin. The carinal angle should be about 55 degrees and should not be more than 90 degrees. In patients with subcarinal disease including pathological lymph nodes (lymphoma and metastatic lung carcinoma), left atrial enlargement (mitral stenosis, regurgitation and left heart failure), and large hiatus hernia, the carinal angle may be widened. The carinal angle is therefore a very important landmark in the evaluation of the chest X-Ray.

The Tracheobronchial Tree: Position

The trachea is central in its position, and lies anterior to the esophagus. It originates below the pharynx and ends at the carina where it bifurcates into left and right main stem bronchi. The right bronchus lies more vertical in its axis than the left. When we look at a normal CXR we find that the right hilum is slightly lower than the left. Since the hilum is made up of vessels and airways and since the RPA runs below the right mainstem bronchus, the superior most structure in the right hilum is the bronchus. The left bronchus is hyparterial, meaning that it runs below the LPA. (i.e. the LPA does the high jump over it) Thus, the left hilum is higher than the right. The RPA cannot make the jump over the right mainstem bronchus, (called the eparterial bronchus) resulting in a right hilum that is slightly lower than the left.

The Tracheobronchial Tree: Applied Anatomy

Knowledge of the relationship of the trachea and esophagus is extremely important for those who are intubating patients or placing nasogastric tubes. The trachea and esophagus lie very close to each other, and so it is not uncommon for the intubations to be misplaced.

Upper lobe disease such as tuberculosis (TB) will cause fibrosis and shrinkage of the lung structures with consequent traction effect and elevation of the hilum so that it is pulled upward.

The Pleura

The pleura consist of a double layer of glistening, semitransparent serous membranes, which surround the pleural space. The secreting surfaces face each other across the pleural space. One of these layers, the visceral pleura, is intimately attached to the lung and follows the fissures, while the second component, the parietal layer, is intimately related to the thoracic cage, mediastinum, and diaphragm. There is no communication between the right and left pleural spaces. The pleura have elastic qualities in order to accommodate the changes in size with the expansion and contraction of the chest cavity. During the respiratory cycle the two layers of pleura move in tandem gliding smoothly over each other, lubricated by a small amount of serous fluid. As the chest wall expands during inspiration, the parietal pleura moves with it, while the visceral pleura moves with the expansion of the lung, the two being held together by the negative pressure caused by capillary forces of the fluid that lies between the two smooth surfaces. Try the experiment of putting a small film of water between two clean, smooth, and flat glass surfaces. The two cannot be easily separated, unless a small amount of air can be introduced between the opposing surfaces.

The cells lining the pleura are called mesothelial cells. They are responsible for the production of pleural fluid. Although we describe two components to the pleura, it is really one structure into which the developing lung bud grows, similar to a fist pushing its way into a balloon. At the hilum of the lung, the bronchovascular and lymphatic bundles acting as the fist, push their way into the pleura and become enveloped by the pleura, with the most distal progeny of the lung bud coming into intimate contact with the visceral pleura.

Despite the apparent single embryologic origin of the visceral and parietal pleura, they are in fact functionally and structurally different. The visceral pleura, for example, have no pain fibers; whereas the parietal pleura are extremely sensitive to pain. The visceral pleura receive its nerve supply through the autonomic nervous system, whereas the parietal pleural innervation is via the somatic intercostal nerves and the phrenic nerve.

The blood supply of the visceral and parietal pleura is also different. The parietal pleura are supplied only by the systemic circulation from the intercostal arteries while the visceral pleura are supplied by the bronchial arteries and the pulmonary arteries.

The visceral pleura follow the lung surface and therefore will follow the fissures. The parietal pleura follow the chest wall and therefore will not follow the fissures of the lung. The pleural cavity is larger than the total lung volume, allowing the lung to expand during respiration. It is particularly obvious in the pleural recesses at the inferior aspect of the thoracic cavity.

The visceral pleura are subdivided into three distinct parts, including the mediastinal, the diaphragmatic, and the costal pleura.

There is continued production of pleural fluid by the mesothelial cells into the pleural space. There is also a continued drainage of the fluid by the subpleural lymphatic system which lies between the visceral pleura and lung coursing into the interlobular septa.

The Pleura: Applied Anatomy

On a plain film of the chest the easiest method of identifying fluid is the lateral upright examination where fluid accumulates in the posterior pleural recesses and causes “blunting” of the posterior costophrenic angles. CT is far more sensitive in the detection of the fluid and to some extent in the characterization of the fluid. When the fluid layers with a meniscus that is parallel to the floor and falls into expected dependant positions (just as water would in a glass on a flat table top) then the effusion can be expected to be free flowing. If the fluid falls in a non-dependant fashion it is considered “loculated” and it is more likely to be complex. Under these circumstances the level is tilted. Ultrasound however is better able to identify septations and other soft tissue components of the fluid collection. Thoracentesis however is still necessary to enable the chemical evaluation of the fluid.

When there is an accumulation of fluid in the pleural space (pleural effusion) or air (pneumothorax) the underlying lung gets pushed away from the chest wall and the harmonious interaction of chest wall pleura and lung is lost. As the accumulation gets larger, the underlying lung collapses without the support mechanisms, and functional lung tissue is lost, with ensuing respiratory difficulty. The lungs are relatively forgiving in that they have enough reserve to accommodate effusions (even large) and moderate degrees of atelectasis, particularly when this occurs gradually, enabling compensatory mechanisms to evolve.

Tension pneumothorax is an acute life threatening event, where there is not only collapse of the lung from the pneumothorax but also a pressure build up in the pleural space that causes the heart and great vessels to be compressed. This acute loss of support of the system is life threatening and if not treated by emergency decompression will lead to death. It would only take a small open-ended needle placed into the pleural space to decompress the tension and save a life. Sometimes when a patient suddenly collapses, and the condition of tension pneumothorax is a clinical consideration, physicians emergently put a small needle into the chest wall even before the chest X-ray confirms their clinical suspicions.

Clinical Aspects

Acute inflammatory conditions of the pleura results in pleuritic chest pain. When the patient inspires the inflamed pleural surfaces rub against each other causing exquisite localized pain. The motion of the pleura becomes restricted by fibrinous exudates, and may cause a pleural “rub” – a squeaking sound caused by the restricted motion. As the pleural effusion enlarges the chances of contact of the two surfaces becomes less likely, and hence the pleural rub cannot be heard. Instead the large effusion compresses the adjacent lung causing a condition called “compressive atelectasis”.  Percussion of the fluid results in dullness and auscultation results in amplification of sound called egophony.In the laboratory it is important to distinguish between a transudative effusion and an exudative effusion. This is done by evaluating the concentration of protein in the fluid. A transudate usually results from pulmonary congestion and contains limited protein and no fibrin, whereas an exudate is more complex and contains fibrin. Empyema is an infected pleural effusion and one of its hallmarks is the relatively low PH of the fluid.

Connective Tissues and Supporting Structures

There is a continuous network of connective tissue through the lung, starting from the hilum and ending at the pleura and sub pleural tissues. There are two basic systems, one known as the axial fiber system and the second the peripheral fiber system (Weibel). They are connected at the level of the alveolus by an intra lobular system of fine reticular fibers. Conceptually, it is easiest to consider the axial system starting at the hilum, and going in the direction of flow of the pulmonary arteries, and the peripheral system starting at the periphery and going in the direction of the pulmonary veins and lymphatics.

Connective Tissues and Supporting Structures: Axial Fiber System

The axial fiber system surrounds the bronchovascular bundle, which contains the bronchi, arteries, and their respective segmental and subsegmental progeny, up to the alveolar sacs. Thus the bronchovascular bundle starts at, and is anchored at the hilum, and ends within the acinus at the alveolar ducts and alveolar sacs. Presumably it is called the axial system because it courses along this major axis of the airways and pulmonary artery.

Connective Tissues and Supporting Structures: Peripheral Fiber System

The second system, the peripheral fiber system, consists of the sub-pleural, pleural, and interlobular network and is closely linked to the veins and lymphatics (Weibel). One may think of it as starting in the subpleural space, extending into the pleura and then the interlobular septa, running along and supporting the veins and lymphatics and ending at, and anchored by, the hilum. Flow of both the veins and lymphatics is from the periphery toward the hilum. Presumably the origin of the term “peripheral system” relates to the concept that it functionally starts in the periphery.

Connective Tissues and Supporting Structures: Intralobular System

A less distinct system called the intralobular system consists of a fine reticulin meshwork surrounding the capillaries. It acts as the skeleton for the support of the alveoli. This network in effect connects the axial system and the peripheral system. In the end, all connective tissue systems are connected from head to toe.  This is the fate and function of the connective system – they connect and support structures. Thus in the lung, identifying distinct axial, peripheral, and intralobular system is artificial, but is extremely helpful in the understanding of the structure and the changes that occur in disease.

Connective Tissues and Supporting Structures: Applied Anatomy

Congestive cardiac failure with interstitial fluid accumulation results in a thickened interstitium. The chest X-ray will show effects of fluid accumulation in the interstitium. Within the peripheral system, this congestion will be reflected in subpleural edema, while at the alveolar level and axial level it will be reflected by Kerley B lines, and peribronchial cuffing.

Additionally, at the alveolar level the thickened interstitium inhibits gas exchange. Antifailure therapy which includes diuretics results in a decrease in the fluid and clearing of the interstitium. Other acute interstitial diseases include acute viral syndromes which are usually self limiting but their effect on the interstium with fluid and exudation can also affect gas exchange. Most acute interstitial diseases respond to medical therapy, or resolve, while the chronic interstitial fibrotic diseases are less likely to respond to therapy.Plain film examination of the lungs is remarkably sensitive to disease in the interstitium and pleural space. High resolution CT is able to show more exquisite detail of this part of the lung. We almost have a microscopic view of the lungs with both the plain film and CT. The plain film is also extremely helpful in the detection of pleural space disease, whether there is a pleural effusion or a small pneumothorax. Peribronchial cuffing is caused as a result of edema.

The clinical question surrounding a patient with shortness of breath or respiratory difficulty is such a common hospital and ICU scenario, and the diagnosis of alveolar disease (pneumonias) vs. acute interstitial disease (congestive cardiac failure) is very important. The distinction is made with the CXR and treatment with antibiotics vs. diuretics often rests on the findings of the CXR.

Blood Supply

In this section we discuss the blood supply to the lungs. There are two sets of arteries. The transport system needs a relatively small amount of oxygenated blood and the bronchial system is supplied by the bronchial arteries, while the exchange system has needs to supply a tennis court sized surface are and is supplied by the larger pulmonary arterial system.

Blood Supply: Blood Supply to the Airways

There are usually two bronchial arteries. The left artery arises from the aorta, and the right arises either from the 3rd intercostal artery (30%), with the 3rd intercostal as a common origin (intercostobronchial artery), from the thoracic aorta, or from one of the other proximal intercostal arteries. It is not uncommon to have 3 or 4 intercostal arteries.

The bronchial arteries supply the bronchi and the tissue of the lungs with oxygenated blood. As systemic vessels their pressure is at systemic levels, with a mean pressure that is 5-6 times higher than the mean pulmonary pressure (15 mmHg.).

The bronchial venous system drains into the right atrium and the azygos system.

This CT in the early arterial phase shows four small arteries surrounding the carina, and represent branches of the normal bronchial arteries. The arteries are overlaid in red in the second image.
Courtesy of: Ashley Davidoff, M.D.

Blood Supply: Blood Supply to the Lungs

When we speak of an artery, we tend to think of a high pressured system with oxygenated blood. The common characteristic that defines them however is the fact that they carry blood away from the heart and toward an end organ. Hence the pulmonary artery, true to definition, carries blood away from the heart, but it is deoxygenated and is under relatively low pressure.

The pulmonary circulation receives more blood per minute than any other organ in the body since it receives the entire cardiac output from the right ventricle, together with a small component (1-2% of total pulmonary blood flow) from the bronchial arterial flow.

Blood Supply: Blood Supply to the Lungs Continued

The right ventricular outflow tract (RVOT) gives rise to the MPA which in turn divides into left and right pulmonary arteries. We have noted the difference in the anatomy of the right and left mainstem bronchi (right short and fat, left long and thin), and the similarity in the branching patterns of the distal bronchi and distal arterial system. While the RPA and LPA are similar in size they bear no resemblance to each other or to the mainstem bronchi.The direction that the two vessels are oriented is also completely different. The LPA courses directly posteriorly while the RPA courses directly laterally.

The right pulmonary artery (RPA) takes almost a 140-degree turn from the main pulmonary artery. It rests on the top of the left atrium (LA) and has a straight shot in the direction of the midaxillary line. Thus on a lateral examination of the chest the LPA has the shape of an umbrella handle and the RPA is seen as an ovoid or rounded structure as we look down its barrel. The pulmonary veins are all inferior to the pulmonary arteries at the hilum.

Distal to the main pulmonary arteries, the branches follow the branching of the irregular dichotomous branching of the airways, and their morphology is similar till they enter the pulmonary lobule at the level of the respiratory bronchiole. At the capillary level, all the blood supplied by the pulmonary artery drains into the alveolar capillaries where they become oxygenated and then drain into the pulmonary venules within the interlobular septa, and finally back to the left atrium.

Blood Supply: Applied Anatomy

The distinction between the arteries and veins on plain film examination is often difficult. At the level of the hilum, it is a little easier since the LPA is superior to the more easily identified left bronchus and the RPA lies under the similarly easily identified right bronchus. The confluence of the veins into the LA is always inferior to the pulmonary artery.

As we proceed beyond the hilum the artery can be identified, as long as its low-density air filled bronchus buddy is with it. As the structures move more peripherally the bronchioles get more difficult to see and the distinction between artery and vein becomes difficult.

In the lower lung fields the veins are horizontal as they course toward the left atrium while the arties have a more vertical course.

On CT, the same principles hold, but an added feature of the difference in branching angles of the vessels sometimes is helpful. Arteries usually branch at acute angles, and veins branch at 90° angle.

Pulmonary hypertension is characterized by enlarging arteries. The margins of the main arteries are usually quite distinct on the plain film. The lower lobe arteries should not measure more than 16mm in the male and more than 14mm in the female. They become blurred when there is interstitial edema, most commonly caused by heart failure.

Two of the common diseases of the pulmonary arteries include pulmonary embolism and pulmonary arterial hypertension. Pulmonary embolism has been an elusive diagnosis in the past and had been a commonly life threatening condition that was frequently missed. The advent of CT angiography with multidetector scanners has made the diagnosis much easier.

Pulmonary hypertension may be idiopathic, due to underlying chronic lung disease, or due to the less common congenital heart disease. In congenital heart disease pulmonary arterial abnormalities are common. In left to right shunts, including ASD, VSD, and PDA, there is an increase in flow in the pulmonary arteries due to the left to right shunt, with resulting increase in pulmonary pressure.

Another serious anomaly is a variety of hypoplastic growth abnormalities of the pulmonary outflow tract ranging from stenosis to total atresia.

The other arterial circulation to the lungs – the bronchial circulation, can also be the source of disease. In chronic disease states such as cystic fibrosis, and bronchiectasis for example, chronic increase flow due to the inflammation and infection occurs, and the combination of an infected and friable mucosa with enlarged arteries, is a cause for hemoptysis. The treatment of choice for recurrent hemoptysis is embolization of the bronchial arteries.

Venous Drainage

Venous drainage is usually via one major upper lobe and one major lower lobe pulmonary vein to each lung, but clinically significant variations do exist. Segmental and subsegmental veins and venules are the equivalent subdivisions of the veins. The capillaries surround the alveoli.

The pulmonary veins drain the lungs of the blood supplied by the pulmonary artery, and the bronchial veins drain the blood from the areas supplied by the bronchial artery. Whereas the pulmonary veins contain oxygenated blood, the bronchial veins contain deoxygenated blood. 98-99% of the blood in the lungs is in the pulmonary arterial – venous circulation while the remaining blood is in the bronchial circulation.

The bronchial veins have a deep and a superficial system. The deep bronchial veins drain either into the pulmonary veins or into the left atrium. The superficial bronchial veins drain the extra pulmonary bronchi, visceral pleura, and hilar lymph nodes and drain into the azygous system on the right side and the superior intercostal vein or the hemiazygous system on the left.

Pulmonary Veins

There are usually 4 pulmonary veins. They are the superior and inferior right pulmonary veins and the superior and inferior left pulmonary veins.

The right superior pulmonary vein drains the right upper and middle lobe. The two veins join to form the most anterior structure in the hilum. The left superior pulmonary vein drains the left upper and lingular segments.  The inferior veins drain the lower lobes.

The veins are the shortest of the three major vessels originating in the hilum. The longest structures are the bronchi and second to them are the pulmonary arteries. This has implication in cross sectional imaging where all these structures converge. Therefore when the central areas are viewed, there will be a single bronchus and artery, but usually two veins on either side. The upper veins will be anterior to the bronchus and artery and the lower veins will be posterior and inferior.

Venous Drainage – Applied Anatomy

Diseases of the pulmonary veins are most commonly secondary to left sided heart disease where an elevated left ventricular or left atrial pressure is reflected in the pulmonary veins. There are a series of congenital anomalies of the pulmonary veins including partial and total anomalous venous return.
Total anomalous pulmonary venous return (TAPVR) can occur with the final destination either above the diaphragm or below. Sometimes, the TAPVR below the diaphragm connects to primitive venous origins of the hepatic circulation so that pulmonary venous return is to the sinusoids of the liver. This condition as an untreated anomaly, cannot sustain life since the pressure of the oxygenated blood in the sinusoids is close to zero, and there is therefore no driving force to allow it to traverse the sinusoids. Hence there is a functional obstruction.

Nerve Supply

There are three types of nerve fibers that connect the lungs to the autonomic nervous system. Autonomic afferent fibers travel to the vagus nerve via the pulmonary plexuses, originating in the airways and the lungs. They transmit information from stretch receptors. Parasympathetic efferent fibers are all contained in the vagus nerve. They carry motor impulses to the airways and lungs which cause bronchiolar muscle contraction, gland secretion, and vasodilatation. The third group is the sympathetic efferent fibers which relax bronchial muscles, inhibit glandular secretion, and cause vasoconstriction.

The walls of the bronchi and bronchioles are innervated by the autonomic nervous system. There are b2 adrenergic receptors in the bronchial epithelium and smooth muscle. The b2 receptors are responsible for bronchodilation and secretion. The a1 adrenergic receptors, on the other hand, inhibit secretion.

Lymphatic Drainage

Two sets of lymphatic vessels drain the lung of lymph. A subpleural lymphatic network collects the lymph from the peripheral lung tissue and drains it along the veins leading toward the hilum. There is a deeper lymphatic system that originates around the bronchi and the bronchioles. The deep system joins the lymphatics around the larger bronchi and pulmonary arteries and they finally enter the mediastinum where they join the bronchomediastinal trunks. The final common pathway for all the lymphatic is via the thoracic duct which enters the left subclavian vein.

Most of the visible lymph nodes are within the hila and mediastinum. However, there are lymph nodes that lie close to the periphery of the lung. These are relatively small measuring approximately 2mm in diameter. They become larger towards the hila, reaching diameters of between 5 to 10mm.

The mediastinal nodes have been divided into 4 main groups:

Superior mediastinal
Aortic
Inferior mediastinal
N node
Within these groups there are 14 nodal stations. These 14 stations have been given both names and numbers to aid in the classification and staging of disease.

Lymphatic Drainage: Subpleural System

Certain diseases have a predilection for the lymphatic system at the subpleural level including sarcoidosis. On the other hand, diseases such as lung carcinoma have a predilection for the deep and central nodal system. Since the systems do connect and are both usually involved, it is imperative to evaluate both systems.

Sarcoidosis and sarcoid nodules in particular, specifically seek out the lymphatics of both the subpleural and the deep systems. Thus when nodules or focal changes are identified on the pleural surfaces, including the fissures, interlobular septa, and bronchovascular bundles then sarcoidosis is a prime suspect. Pleural effusions on the other hand are distinctly uncommon in sarcoidosis.(1-4%). In lymphangitic spread of disease, malignant cells get bundled into the lymphatics causing obstruction and reducing pulmonary capacity. Thickening of the interlobular septa is a characteristic finding in these cases. In anthracosis, lymph nodes and lymphatics become filled with carbon colored soot.

Lymphatic Drainage: Mediastinal Nodes

In general, although we often measure the size, and specifically the short axis size of the nodes to determine the presence of disease, we understand that this is a fairly inaccurate method with low specificity . A short axis of more than 10mm implies a pathologically involved node. Often the large node may be reactive and may not contain malignant disease. PET scanning has been an important advance to aid in the distinction between reactive and malignant lymphadenopathy.

Aging of the Lungs

While the number of bronchi one has at birth is the same as the number in old age, the number of alveoli increases until the age of about 8 years. Thereafter the alveoli increase in size until about 18 years. As the lungs progress through age there is a mild, functionally insignificant increase in size due to loss of elasticity. The respiratory bronchioles and alveolar ducts increase in size in middle age, but there is no destruction of the walls of the alveolar septa. Thus in old age there is a mild increase in the size of the lungs but without concomitant destruction of lung tissue that is seen in emphysema. There is glandular hypertrophy and progressive calcification of the cartilage of the medium sized bronchi.

The Lung and Disease

The lungs are closely connected to the immediate environment and hence they are directly exposed to any and all pathogenic entities in the environment, including biological and non biological elements.

Bacteria and viruses are universal and therefore are common pathogens and affect everybody. Immune status is key to survival from these infections, and so the young and the old, and those with immune deficiencies are particularly vulnerable to these unseen enemies. Other diseases such as the dust diseases and pneumoconiosis, occur in isolated work related environments, but there are some diseases, like bird fancier’s disease that have both acute and chronic manifestations due to exposure to the antigen which is found in the droppings of birds – most commonly pigeon’s but also from domestic birds like budgerigars (small parakeets).

The Lung and Disease: Infection – Pneumonia

Infections to the lungs are caused by a host of organisms and most commonly are viral or bacterial in origin. Anatomically they can affect the airways causing epiglottitis, pharyngitis, tracheitis, bronchitis or bronchiolitis. The infection, on the other hand may affect the alveolar components of the lungs causing lobar or segmental pneumonia, or the interstium of the lungs causing an interstitial pneumonitis. Since the airways and alveoli by definition are connected the involvement of one part does not preclude the involvement of the other, though certain organisms have a predilection for certain parts of the respiratory epithelium. Additionally an infection may start out as viral and progress and become complicated by secondary bacterial infection. Within the lung, interstitial infections (usually viral), will appear on a chest X-ray with a linear pattern while the classical bacterial pneumonia will present as a consolidation.

The most common form of pneumonia in the population is viral in origin while the most common bacterial pneumonia is streptococcal in origin.

There are some characteristic features about the bacterial pneumonias that are sometimes helpful in the differential diagnosis, though it is often difficult to make an organism specific diagnosis based on imaging. In general the bronchopneumonias affect infants’, young children and the elderly and are caused by streptococcus pneumonia and affect airways and alveoli contiguous to the larger bronchioles. Bronchopneumonia is characterized by peribronchial thickening, lobular nodules of patchy airspace disease, which may progress to lobar disease. Lobar pneumonia affects young adults and presents as a consolidated mass affecting segments, lobes, singly or at multiple locations. Lobar pneumonia is also usually caused by Streptococcus pneumoniae (aka pneumococcal pneumonia) (Todar’s On Line Text of Bacteriology), and Klebsiella. It is primarily a disorder of the alveoli resulting in segmental or lobar consolidation with the air bronchogram being characteristic.

Klebsiella infection tends to occur in the upper lobes and causes significant swelling of the lung so that bulging fissures may be seen. It also can cause cavitation.
Legionella has a tendency to affect the lower lobes.
Mycoplasma has a tendency to affect the lower lobes.

The Lung and Disease: Viral Pneumonia

The most common agents causing viral pneumonia are influenza A, respiratory syncitialk virus (RSV) and paraifluenza 1,2,3.

 

Radiological findings are classically of a linear interstitial nature but they may also show alveolar changes such as consolidation. Pleural effusion and peribronchial thickening are associated findings.

The Lung and Disease: Pneumonia in the Immunocompromised Host

There is a high incidence of pneumocystis pneumonia (PCP) in patients with AIDS. Other organisms such as gram negative bacilli, staphylococcus, aspergillus and cytomegalovirus are also well known pathogenic organisms in this population of patients. (eMedicine – Fernandes). Up to 45% of all HIV respiratory infections are bacterial in origin occurring at any CD4 count. As the CD4 count decreases the incidence increases, particularly when the CD4 count is less than 200 cells/mm 3.

The Lung and Disease: Mycoplasma Pneumonia

Mycoplasma is a genus of bacteria that lacks cell walls. When it affects the respiratory system it presents with fever, headache, malaise, and anorexia. The white cell count is usually normal but may show a left shift. Cold agglutinins are detected in 50-70% of patients and the diagnosis is made with a PCR assay of a nasopharyngeal swab or serologic testing.. The CXR has a variable appearance and can present both with airspace disease in segmental or lobar fashion (45-60%) or with an interstitial pattern of nodular or reticular type (15-50%). Pleural effusions are relatively uncommon (<20%). On CT they may present with a bronchioloitis with centrilobular nodules, alveolar consolidation, interstitial thickening of the axial interstitium or of the interlobular septa.

Most infections resolve and the morphology of the lung returns to normal. With repeated infection and or untreated disease, there may be permanent and ongoing structural damage to the lung or the airways and entities such as bronchiectasis may result.

The Lung and Disease: Inflammatory Diseases

Inflammatory diseases such as the collagen vascular diseases, interstitial pulmonary fibrosis, and sarcoidosis are idiopathic and slowly advancing. Understanding of the causes of these diseases and the underlying pathology is one of an inflammatory process affecting the airways, vessels, connective tissues or the parenchyma.

The Lung and Disease: Malignant Disease and Other Growth Abnormalities

The malignant diseases of the lungs commonly have a cigarette smoking habit to blame, and the aggressive, space occupying, spreading nature of the disease usually has a negative outcome as we struggle with different and new therapeutic regimens to prolong life. The small cell carcinomas of the lung are usually bulky and aggressive, respond dramatically to therapy but then tend to recur. The non small cell cancers have surgical options and a potential cure. The potential for cure rests on the staging of the disease.

The Lung and Disease: Congenital Disease

Congenital and genetic disease of the lungs is not common in the adult population but sporadic cases do occur. Progress in the management of patients with cystic fibrosis has resulted in an enlarging adult population with this disease which was previously fatal in childhood.

The Lung and Disease: Mechanical Diseases

Emphysema can be considered a mechanical disease of the lungs since the loss of elasticity of the lung tissue that occurs together with the destruction of tissue results in mechanical disadvantage. As a result air cannot be moved efficiently and there is an increase in air that is trapped in “dead” space and which cannot be efficiently moved to the capillaries for exchange nor efficiently removed. Emphysema is a major cause of morbidity and mortality in the smoking population.

Asthma, another common disorder is an obstructive disease that inhibits the transport of air to and from the lungs as well.

The Lung and Disease: Pulmonary Embolism

The advent of multidetector CT has brought about a revolution in our ability to diagnose this relatively common and often fatal disorder. Our ability to diagnose pulmonary embolism (PE) with CT requires meticulous care to the technique and bolus timing since contrast volume limitations precludes a second injection because of the nephrotoxicity of the contrast.

The Lung and Disease: Pulmonary Embolism with Infarction

Although pulmonary embolism is a common pulmonary infarction it is distinctly uncommon because the lung receives blood supply from the bronchial as well as the pulmonary artery and can also be oxygenated directly from the alveoli.

The Lung and Disease: Heart Failure

Heart failure is a very common entity and despite the progress with MDCT, the CXR is still the most sensitive imaging technique for this entity.

Imaging of the Lungs – Technical Aspects

The plain film chest X-ray (CXR) is still the most commonly used radiological examination and the PA and lateral view when possible provide the most information.The PA is taken with the anterior portion of the chest on the cassette, with tube being 72 inches away minimizing divergence and so the heart is relatively small. When the projection is AP,  the source is only 40 inches away (i.e. X-rays enter from anterior). Under these circumstances, divergence is a factor and the heart and mediastinum become relatively magnified.

Deep inspiration on a routine CXR gives us the best opportunity to study all the structures we have discussed above. The mediastinum contains soft tissue structures while the lungs are lucent. The lungs therefore require less penetration of X-rays and the mediastinum and the heart require more. The left lower lung can be invisible on the CXR if the film is underpenetrated and so it is better to be over than underpenetrated.

Important anatomic structures relevant to evaluation of the P-A view, are the interfaces of the lungs with the mediastinum, the ability to evaluate the left lower lung field, the ability to clearly see the bronchovascular bundles.

The advent of CT scanning with a superior gray scale, and with digital technology, has helped solve this problem, so that we are able to window in to the gray scale of the specific part being imaged. We can, for example, look specifically at the lungs using the gray scale and window level appropriate for the lung, (lung windows) for the mediastinum (mediastinal windows) or for the bones (bone windows).  CT enables us to visualize subsegmental bronchi and bronchioles in normal conditions.

Computed Tomography (CT)

CT technique employed in the examination of the lungs is based on the clinical indication. There are a few techniques that are utilized:

Conventional Routine Examination without Contrast:        3-5mm thickness slices
Conventional Routine Examination with Contrast:            3-5mm thickness slices
High Resolution CT:                                                      0.75-1mm thickness slices
Rule Out Pulmonary Embolism:                                    0.75-1mm thickness slices

Conventional technique with 64 slice multiple-row detector (MDCT) scanner uses 3mm thickness slices with detector collimation of 0.6mm. If contrast is needed then 120cc’s of Omnipaque 350 is used at an injection rate of 1cc/second with a scan delay of 60 seconds.

For high resolution imaging using the 64-slice MDCT scanner, a slice thickness of 3mm and 0.75mm are acquired with collimation width of 0.6mm. Contrast is not generally used.

If there are pulmonary changes at the posterior dependant portions this may be due to passive atelectasis due to poor movement of air and prone imaging may help inflate these regions and provide a more accurate evaluation of the disease process.

For a pulmonary embolism (PE) study on the 64 slice MDCT scanner, the slice thickness used is 0.75mm, collimation is .6mm, and 100-120ccs of Visipaque 320 is used with a scan delay of 25-30 seconds or patient specific bolus timing or tracking can be employed.

Conventional 3 – 5mm slice thickness imaging is used for the evaluation of pneumonia, pleural effusion, lung nodule follow up for example. The addition of contrast in these studies is based on the need to identify lymphadenopathy and other structures in the mediastinum. This is particularly necessary in the evaluation of lung carcinoma and in most cases of inflammatory diseases of the lungs including sarcoidosis, which has a predilection for lymph nodes but is also required in imaging the patient with lymphoma. If empyema is a clinical concern then contrast is helpful to determine if there is rim enhancement of the pleura a sign indicating inflammation in the pleura. Contrast is also essential if there is clinical concern for an arteriovenous malformation.

High resolution imaging (0.75 -1mm slice thickness) is utilized when interstitial lung disease is a clinical or radiological consideration. As conventional MDCT gets down to the 3mm thickness slice range we are close to high resolution of yester year, but the 1mm collimation still offers significant advantage in spatial resolution. It is imperative that the patient is able to lay still and breathhold for this technique.

Timing the bolus presents a technical challenge since the cardiovascular status in the ill is so variable. One may suspect that bolus tracking would have been the answer to our problems but in fact it does not give us the consistently well timed bolus. We aim for a density of contrast in the pulmonary artery of about 90 HU.

Several methods of bolus administration have been employed. A uniphase injection with a rate of 4mls/sec has been suggested as the preferred technique. (Bae et al Radiology, 2000, 216:872-880) If the injection duration is prolonged then recirculation of contrast causes an additive effect of existing contrast and increases the density in the artery. Bolus tracking would start the injection relatively early and cumulative effect would not be accomplished. One could argue that the threshold level could be set higher but in the face of poor cardiac output the higher threshold may not be reached and the scan would never be triggered. A scan delay of 25 – 30 seconds usually allows for optimal technique in most patients and individual tailoring based on age and hemodynamic status must always be considered.

Technical Aspects: PET Scanning

The advent of PET scanning has revolutionized the diagnosis and staging of lung cancer. The technology is based on the avidity of tissue for fluorodeoxyglucose (FDG) which is tagged with fluorine 18. Metabolically active tissues, exemplified by malignant tissue as well as some inflammatory diseases have avidity for the fluorodeoxyglucose. Lesions usually have to be more than 7mms in order for them to be seen by PET imaging. Some carcinomas such as the bronchiolar alveolar carcinomas do not take up the FDG and are notoriously negative. Thus a negative PET scan does not exclude the diagnosis of malignancy, and a positive PET study does not definitely imply malignancy.

Imaging the Chest

From the radiological point of view, X-rays used in plain chest X-ray or CT scan, move almost unimpeded through the lungs, and present as a radiolucency or blackness on the image. On the other hand, the mediastinum serves as a moderate barrier to X-rays, and the ribs and spinal column present an even greater barrier. The tissues of the chest vary significantly in the degree to which they absorb or reflect X-rays. This difference presented a challenging problem to radiologists and physicists over the years, particularly related to technical factors that would optimize imaging of the mediastinum and heart on the one hand, and the lungs on the other. The advent of CT scanning with a superior gray scale, and with digital technology, has helped solve this problem, so that we are able to window in to the gray scale of the specific part being imaged. We can, for example, look specifically at the lungs using the gray scale and window level appropriate for the lung, “lung windows” for the mediastinum “mediastinal windows” or for the bones “bone windows”.

Imaging of the Chest: Imaging – Chest X-ray

Why do we see structures on X-ray? We are able to define two side by side structures if they have contrasting X-ray absorption characteristics and hence densities. On a plain film of the chest for example, the trachea and main bronchi are usually visualized because the air filled trachea is surrounded by relatively thick soft tissue walls and other soft tissues of the mediastinum creating the necessary density differential to enable distinction. The air in the visible mainstem bronchi is surrounded and separated from the surrounding air filled parenchyma and by relatively thick walls of soft tissue density and this contrasting density allows the mainstem bronchi to be seen. As we progress to the smaller bronchi, usually after the fourth order of branching, the soft tissue walls become too thin to create an air-soft tissue interface and hence we cannot resolve nor see them.

Almost 90% of the lung is air and only about 10% is soft tissue, interstitium and blood. The dominant density of the lungs is therefore black or lucent. The soft tissues of the lung, including the blood vessels and the connective tissue (also called the interstitium), impede the X-ray, resulting in a gray or soft tissue density. The interface of lucent air (black) against a soft tissue background of the interstitium (gray) provides a sharp and contrasting interface of density, allowing an almost microscopic view of the lungs. If the pressure in the capillaries becomes abnormally high, for example more than 25 mmHg, fluid starts to leak into the interstitium. The clarity of the interstitial markings becomes reduced and blurry. The radiologist is able to imply pathophysiological changes based on the fuzziness of the blood vessels and can approximate the pressure in the capillaries. This change is best appreciated on a plain film of the chest. The plain chest film has stood the test of time, proving its value since Roentgen’s discovery in the late 19th century.

Most disease states replace the air of the lungs with fluid or soft tissue, and appear as increasing densities on the CXR. In pneumonia the alveoli become filled with pus or fluid. The air in the lung parenchyma is replaced by soft tissue elements. If there is persistence of air in the smaller airways, they will now be visualized, since the air in the airways is now in contrast to the surrounding density of the fluid filled parenchyma.

Imaging of the Chest: The Secondary Lobule Revisited

CT with a wider gray scale enables us to visualize subsegmental bronchi and bronchioles both in normal conditions and under various pathological situations. The secondary lobule is a unit of the lung that is enclosed by an incomplete capsule called the interlobular septum, best developed in the periphery of the lung and specifically at the lung bases and the apex, and incompletely formed in the rest of the lung. In the evaluation of lung diseases the diagnostic dilemma starts with the anatomic question as to which part of the lung is involved with disease – the so called anatomical differential diagnosis. Is it the tubular airways, the alveoli, the interstitium, the arteries, the lymphatics or the veins?  Since we know that the center of the secondary lobule contains the airway and the arteriole, the matrix contains the alveoli, and the periphery contains the interlobular septum, the lymphatic and the vein, we always search for the polygonal structure or vestiges of it to help us hone down on the structure that is involved.

Imaging of the Chest: Small Airway Disease

 

Imaging of the Chest: The Alveoli

When the alveoli become diseased they fill to variable extent with fluid, whether it be pus, transudate, exudate, or cellular material, and radiologically present on CT with a pattern called ground glass when they are only half filled, or an alveolar pattern when they are fully filled. In the ground glass pattern there is a haze over the parenchyma, and we are still able to see vessels running through the density. In the alveolar consolidation the vessels cannot be seen since they have the same density as the alveoli, and we start to see air bronchograms.

Conclusion

The following module presents the anatomic detail of the lung in great depth so that the finer points of diagnosis, particularly related to imaging and imaging techniques, can be elaborated. We have taken you through the anatomy of the bronchi on their journey to the histological level of the lung. Understanding the anatomy and histology is an essential step needed to understand lung imaging particularly in the world of high resolution CT. Imaging the chest is central to the management of the ICU patient where day-to-day life sustaining decisions are based on the CXR. Accurate placement of tubes and hardware is essential to survival. It is therefore important that meticulous care is taken to perform these studies in optimal fashion with optimal technique.

The innate contrast between the blackness of air and the whiteness of the soft tissues of the lungs gives us an unique opportunity to evaluate microscopic structures of the lungs, down to the thickening of sub-millimeter interstitial tissues. Prudent use of contrast and high resolution imaging has brought important understanding of lung disease. The consistent diagnosis of pulmonary embolism eluded us for years, and we now have a tool that has high sensitivity and specificty for this life threatening disease. PET scanning has added a functional tool that is essential in the management of the oncological patient, and has given us a non invasive method that has improved the diagnosis and hence the management of our patients.