The normal lung is capable of receiving and distributing a large flow of air and blood to its alveoli. In emphysema, the elastic recoil of the lung decreases with loss of alveolar septa, presumably because the reduced alveolar surface area exerts a lower surface tension. Inspiration lowers alveolar pressure, allowing air to flow into the lungs; the bronchiole dilates when the pressure in the surrounding alveoli is less than that within the lumen of the bronchiole. Conversely, in expiration, the airways are compressed because the alveolar pressure surrounding the bronchiole exceeds that within the bronchiolar lumen. There is a greater tendency for airflow obstruction during expiration. In emphysema, bronchiolar obstruction due to loss of alveolar structure is irreversible.

The bronchial glands and goblet cells may be hypertrophied, producing excessive amounts of mucus, which frequently obstructs bronchiolar lumina. One aspect of therapy focuses on increasing the fluidity and mobility of mucus. Submucosal edema and cellular infiltration cause a thickening of the bronchiolar wall and narrowing of the lumen. Because vasodilatation often leads to edema, another aspect of treatment is to cause vasoconstriction by means of alpha-adrenergics. The smooth muscle may be hypertrophied in bronchitis or asthma, narrowing the lumen. Adrenergic drugs are used to smooth the muscle. COPD is usually insidious, existing in an asymptomatic unrecognized form for years prior to the appearance of noticeable dyspnea on exertion. With mild to moderate COPD, bronchiolar obstruction is found in a patchy distribution throughout the lungs. This results in uneven ventilation/perfusion ratios, which will be discussed at the end of this section. The less involved, better-ventilated lung units become insufficient to compensate for the more involved, poorly ventilated units in cases of advanced COPD or superimposed viral or bacterial infections.

Severe arterial hypoxemia is likely to increase production of erythropoietin, which stimulates the bone marrow causing erythrocytosis. This erythrocytosis may be either useful or harmful. The higher hemoglobin associated with increased O₂ capacity is good; but the increased blood volume in the presence of a failing heart is not. Increased blood viscosity causes a harmful resistance to blood flow through the lungs and coronary vessels. Early medicine utilized phlebotomies to treat hypoxia instead of O₂. This resulted in a stimulus for increased erythropoiesis causing a snowball effect.

Patients with severe bronchitis have mismatched ventilation/­perfusion. This leads to arterial hypoxemia, secondary erythrocytosis, and cor pulmonale with congestive heart failure. They are called blue bloaters due to their cyanosis and edema, or anasarca. A patient with severe emphysema may have decreased cardiac output and a relatively small heart, but as long as he/she can effectively hyperventilate and match ventilation/perfusion, he/she will not develop hypoxemia. They are called pink puffers because they maintain a near normal PaO₂ and are hyperpneic.

Auscultation

Auscultation of the lungs provides information about the airflow through the tracheobronchial tree and the presence of fluid, mucus or obstruction of the airway. Vesicular breath sounds are normally heard over the chest. They are soft and low in pitch. Bronchovesicular breath sounds are medium in intensity and pitch and heard over the large, main stem bronchi. Bronchial breath sounds are loud and high in pitch and normally heard over the trachea. One type of bronchial breath sound rarely heard is the amphoric breath sound heard over a thick walled cavity that communicates freely with a large sized bronchus. The sound resembles blowing over the top of a wine bottle. Vesicular breath sounds last longest on inspiration and when airflow to an area is diminished, they may be decreased or absent. Bronchial breath sounds are longest on expiration. Consolidation of lung tissue, as occurs in pneumonia, blocks the passage of air through the affected area and prevents the exchange of sound quality.

Remember that a patient with particularly severe asthma may have a rather quiet chest on auscultation. This is probably because airflow is so slow that it can no longer generate much sound. Breath sounds will also be absent or decreased in COPD. This is caused by lung distention and poor transmission of sound to the chest wall.

Abnormal breath sounds (adventitious or “added”) include rales, rhonchi, wheezes and pleural friction rubs. Rales are noisy murmurs caused by passage of air through liquid. Moisture causes a sound like soda fizzing, cellophane crinkling, or the sound you hear when you roll your hair between your fingers near your ears. Rales are usually heard on inspiration. Coarse rales may clear after a cough but fine rales near the bases of long fields rarely do. Rales are sometimes called “crackles.” The crackles of interstitial lung disease, such as fibrosing alveolitis, are typically heard on late inspiration as opposed to crackles from secretions.

Rhonchi are rumbling, snoring or rattling sounds caused by obstruction of a large bronchus or the collection of secretions in a large bronchus. They are most prominent on expiration. Another name for rhonchus is a “wheeze.” Snoring sounds are called sonorous rhonchi, and high-pitched musical sounds are called sibilant rhonchi. Wheezes may be audible without a stethoscope.

Pleural friction rubs occur when the pleural fluid that normally lubricates the pleura is decreased or absent. The membranes rub together causing a loud creak or a soft click that resembles a grating sound. They are heard on inspiration and expiration and are associated with pain and splinting.

Ventilation/Perfusion (V/Q) Ratio

Effective gas exchange depends on uniform distribution of function throughout the lung. Ventilation must be distributed to 300 million alveoli through 23 generations of branching airways along with blood distribution through a myriad of capillaries. Even in normal lung function, distribution is not uniform. There is a gravity-dependent gradient of pleural pressure in the upright lung of about 0.3 cm H2O pressure/cm vertical distance. The pleural pressure over a normal adult lung 30 cm in height is about 9 cm H2O more negative at the apex than at the base. Lung units near the lung apex are distended by a greater trans­pulmonary pressure and are more fully inflated than those at the base.

Blood flow, like ventilation, is least at the apex and increases down the lung. However, alveolar ventilation and perfusion are not evenly matched, so the gradient of perfusion is steeper than that of ventilation. The average V/Q (Ventilation-Perfusion Ratio) is 0.8.

In regions of the lung where the V/Q ratio is increased above normal, wasted ventilation occurs. This has the effect of adding a space that is ventilated but does not participate adequately in gas exchange. An extreme example can occur when perfusion is virtually eliminated, by a blood clot or following ligation of a pulmonary artery.

Ventilation of regions of the lung with high V/Q ratios is partly wasted and contributes to alveolar dead space ventilation. In decreased states, this is not uncommon. It results in hyperventilation and increased work of breathing.

When ventilation is impaired without decreased blood flow or when perfusion continues to non-ventilated regions of the lung, as in atelectasis, there is a decreased V/Q. Gas exchange is extremely impaired or absent and perfusing blood is poorly oxygenated. Hyperventilation can help hypercapnia, but not hypoxemia. The addition of poorly oxygenated blood from areas of low V/Q to normally oxygenated blood acts like a shunt. This “physiologic shunting” must be differentiated from true venous admixture produced by an “anatomic” shunt.

A shunt study can be performed by having the patient breathe 100% O₂ for 20 minutes and then obtaining arterial blood gases. True venous admixture will not be changed by breathing 100% O₂. Use extreme caution in some patients, however, making sure hypoxic drive is what is keeping them ventilated.

Clinical Features of COPD:

History & Physical Findings

Patients with COPD have at least one symptom in common: undue breathlessness on exertion. Chronic bronchitis is unusual in nonsmokers and is more common in men than in women. Cough is often worse on arising due to accumulation of secretions while sleeping. Wheezing and exercise intolerance are often present and tend to worsen during acute infections of the lower respiratory tract. The sputum may become mucopurulent or purulent. Unless the patient has a hobby or job that requires strenuous exertion, the disease may go unnoticed until quite extensive.

In general, the COPDer appears anxious and malnourished, and complains of lost appetite, use of accessory muscles, muscle atrophy, jugular engorgement, cyanosis, and digital clubbing.

The COPDer’s chest will have increased AP diameter, barrel chest, or hyper-resonant chest, with decreased breath sounds and adventitious breath sounds. Their ventilatory pattern may include paradoxical movement of the abdomen, prolonged expiratory time, active exhalation and pursed lip breathing. In advanced disease, peripheral edema may be present.

Asthmatics who show some degree of persistent airway obstruction and exertional dyspnea are classified as COPD. The accompanying cough is often paroxysmal, and wheezing is severe. Asthma can be brought on by intrinsic or extrinsic factors. An example of an intrinsic factor would be an emotional upset that brings on an attack; extrinsic factors would include specific allergens, etc. Usually by the time an emphysema patient reaches the fifth decade, dyspnea is the primary complaint. Hyperventilation may be present if the patient becomes anxious, but true orthopnea is uncommon unless heart failure is present.

The history may be helpful to distinguish other conditions like chronic pulmonary fibrosis, recurrent pulmonary thromboembolism, polycythemia vera, the diseases of hypoventilation, and myxedema. Aerophagia with gastric distension causes early satiety. Patients often complain of upper abdominal soreness, distention, and fullness, or even epigastric pain. It is important to note that 20 to 25% of emphysema patients develop ulcers at some stage of their disease.

With deteriorating blood gases, there will be gradual impairment of mental acuity, memory, and judgment, along with headache and insomnia. Patients with cor pulmonale complain of easy fatigability, and may have anterior chest pain and palpitation on exertion. With right heart failure, ankle edema appears and liver enlargement with or without ascites develops.

Clinical features of bronchiectasis principally include a chronic, loose cough with mucopurulent, foul-smelling sputum. In advanced cases, the mucus settles out into three layers: cloudy on top, clear saliva in the middle, and cloudy, purulent material on the bottom. It is frequently associated with chronic paranasal sinusitis. Hemoptysis, occasionally severe, occurs in at least a half of all cases. Advanced cases result in chronic malnutrition, sinusitis, clubbing, cor pulmonale and right heart failure. Physical signs are variable; rales may be present at times. A plain chest film may not be helpful if dilatations of air fluid levels are not present.

Often the diagnosis of the disease can be made from history alone. It is confirmed by bronchography after vigorous treatment for at least one week. A lung resection may be indicated. Iodized oil and iodine in water have been the standard contrast media for many years. Powdered tantalum appears to offer a reliable substitute without the risk of iodine sensitivity. (We will be learning more about roentgenologic features in the next section.) Bronchoscopy in bronchiectasis often reveals a deep velvety red mucosa with pus swelling up from areas of involvement. Gram stains may show fusospirochetal organisms and cultures will reveal common mouth flora and anaerobic streptococci or others. Microscopic exam of sputum may show necrotic tissue, muscle fibers and epithelial debris.

Roentgenologic Features

Correlation among symptoms, physical findings, and the appearance of chest x-rays is often poor in COPD. Films of moderately advanced disease can be read “essentially normal,” but at least they can be used to rule out other complications. In acute asthma, hyperlucency may mask emphysema, but will clear after attack. Emphysema patients will show attenuation of the peripheral pulmonary vasculature. Those with alpha-1-antitrypsin will have scarcity of vascular markings in bases, and hilar shadows present.

“By far the best ways to treat COPD are to catch it early and to stop smoking.”

Increased prominence of the basal vascular markings is often seen in patients with severe chronic bronchitis or bronchiectasis, with or without emphysema. In patients with pulmonary hypertension and right ventricular enlargement, classically there is prominence of the main pulmonary artery segment, bulging of the anterior cardiac contour into the retrosternal space, and enlargement of the right and left pulmonary artery shadows. In combined right and left ventricular failure, the transverse diameter of the heart is widened, and the basal vascular markings show increased prominence. Comparison with x-rays previously taken may show progressive flattening of the diaphragm, increased radiolucency of the lung fields, increased size of bullous areas, and increased heart size.

The best radiologic criteria for the presence of emphysema is a flattened diaphragm, as seen in lateral view, and an increased depth of the retrosternal space of more than 3 cm between the anterior wall of the origin of the ascending aorta and the sternum. Fluoroscopy in COPD may be helpful because radiolucency of the lung bases tend to persist during forced expiration, in contrast to the increased density seen in normal subjects. Expiratory films should be obtained four or five seconds after the command to exhale is given, to allow time for the full effects of airway obstruction to be registered. CT Scans and modern MRI’s have replaced most need for older lung laminagrams to demonstrate size and location of bullae. Lung photoscans following intravenous injection of macroaggregated particles of serum albumin tagged with iodine are helpful in demonstrating areas of non-perfused or under-perfused areas. Occasionally, Xenon scans are used for this purpose. Pulmonary arteriograms may be indicated to rule out embolism.

EKG Aspects

The electrocardiogram is often normal in early or moderate emphysema. One of the most frequent changes in COPD is a shift of the P wave axis toward the right, often greater than +80 degrees in the frontal plane. Observing the P wave in a VL easily assesses this; it is isoelectric at the +60 degree axis and becomes increasingly negative as its axis moves further to the right, greater than +60 degrees. The P waves frequently are symmetrically peaked in leads II, III, and a VF; and when their height is 2.5 mm or more they are classified as “P pulmonale.”

The QRS complexes often show low voltage in both the limb leads and the precordial leads, especially leads V5- 6. The mean QRS axis is displaced posteriorly and superiorly and shifted toward the left (clockwise rotation). The frontal electrical axis is often vertical, frequently more than +70 degrees. Superior rotation of the electrical vector manifested by a late R wave in a VR ABG gives rise to a SI, SII, SIII pattern with an indeterminate mean axis. With more severe rotation, axes greater than -30 degrees (left axis deviation) may be seen.

When right ventricular hypertrophy develops as a result of increased pulmonary vascular resistance and pulmonary hypertension, the QRS vector shift anteriorly and to the right. R waves then appear in the right precordial leads. Complete right bundle branch block is occasionally observed.

The QRS abnormalities may sometimes simulate those of myocardial infarction, particularly of the inferior portion of the heart. The presence of abnormal pulmonale-type P Ò26 waves suggests that emphysema is the sole cause of the EKG abnormality.

“Chronic obstructive pulmonary disease (COPD) is an ongoing lung condition caused by damage to the lungs. The damage results in swelling and irritation, also called inflammation, inside the airways that limit airflow into and out of the lungs. This limited airflow is known as obstruction. Symptoms include trouble breathing, a daily cough that brings up mucus and a tight, whistling sound in the lungs called wheezing.

COPD is most often caused by long-term exposure to irritating smoke, fumes, dust or chemicals. The most common cause is cigarette smoke.

Emphysema and chronic bronchitis are the two most common types of COPD. These two conditions usually occur together and can vary in severity among people with COPD}.”

MAYO CLINIC (https://www.mayoclinic.org/diseases-conditions/copd/symptoms-causes/syc-20353679)

Etiology

By far the most common etiological cause of COPD remains smoking. Even after the client quits smoking, the disease process continues to worsen. Air pollution and occupation also play an important role in COPD. Smog and second-hand smoke contribute to worsening of the disease.

Occupational exposure to irritating fumes and dusts may aggravate COPD. Silicosis and other pneumonoconioses may bring about lung fibrosis and focal emphysema. Exposure to certain vegetable dusts, such as cotton fiber, molds and fungi in grain dust, may increase airway resistance and sometimes produce permanent respiratory impairment. Exposures to irritating gases, such as chlorine and oxides of nitrogen and sulfur, produce pulmonary edema, bronchiolitis and at times permanent parenchymal damage.

Repeated bronchopulmonary infections can also intensify the existing pathological changes, playing a role in destruction of lung parenchyma and the progression of COPD.

Heredity or biological factors can determine the reactions of pulmonary tissue to noxious agents. For example, a genetic familial form of emphysema involves a deficiency of the major normal serum alpha-1 globulin (alpha-1 antitrypsin). A single autosomal recessive gene transmits this deficiency. The homozygotes may develop severe panlobular emphysema (PLE) early in adult life. The heterozygotes appear to be predisposed to the development of centrilobular emphysema related to cigarette smoking. The other better-known cause of chronic lung disease is mucoviscidosis or cystic fibrosis, which produces thickened secretions via the endocrine system and throughout the body.

Aging by itself is not a primary cause of COPD, but some degree of panlobular emphysema is commonly discovered on histopathologic examination. Age related dorsal kyphosis with the barrel-shaped thorax has often been called senile emphysema, even though there is little destruction of interalveolar septa. The morphologic changes consist of dilated air spaces and pores of Kohn.

Pathogenesis

The pathogenesis of COPD is not fully understood despite attempts to correlate the morphologic appearance of lungs at necropsy to the clinical measurements of functioning during life. Chronic bronchitis and centrilobular emphysema do seem to develop after prolonged exposure to cigarette smoke and/or other air pollutants. Whatever the causes, bronchiolar obstruction by itself does not result in focal atelectasis, provided there is collateral ventilation from adjacent pulmonary parenchyma via the pores of Kohn.

It has been proposed that airway obstruction at times may result in a check-valve mechanism leading to overdistension and rupture of alveolar septa, especially if the latter are inflamed and exposed to high positive pressure (i.e. barotrauma). This concept of pathogenesis of emphysema is entirely speculative. Airflow obstruction alone does not necessarily result in tissue destruction. Moreover, both centrilobular and panlobular emphysema may exist in lungs of asymptomatic individuals. It has been reported that up to 30% of lung tissue can be destroyed by emphysema without resulting in demonstrable airflow obstruction. Normally, radial traction forces of the attached alveolar septa support the bronchiolar walls. With loss of alveolar surface in emphysema, there is a decrease in surface tension, resulting in expiratory airway collapse. Additional investigative work continues in an effort to link disease states to pathogenesis.

Control of Ventilation

A brief description of respiratory control mechanisms will help the you with COPD or family members or the nurse better understand how the progression of COPD results in pathophysiologic changes. The respiratory centers impart rhythmicity to breathing. The sensory-motor mechanisms provide fine regulation of respiratory muscle tension and the chemical or humoral regulation that maintains normal arterial blood gases. This will help the nurse to understand why hypercapnia (increased PaCO₂) results in the COPDers’ extreme reliance on the hypoxic drive.

The reticular formation of the medulla oblongata constitutes the medullar control center responsible for respiratory rhythmicity. The mechanism whereby rhythmicity is established is not clear, but it may be the end result of the interaction of two oscillating circuits, one for inspiration and one for expiration, which inhibit each other. Although medullar centers are inherently rhythmic, medullar breathing without pontine influence is not well coordinated; therefore, pontine as well as medullar centers participate in producing normal respiratory rhythm.

In the pons, a neural mechanism has been identified as the pneumotaxic center. Stimulation of this center leads to an increase in respiratory frequency with an inspiratory shift, whereas ablation of the center leads to a slowing of respiration. The pneumotaxic center has no intrinsic rhythmicity but appears to serve by modulation of the tonic activity of the apneustic center. The latter is located in the middle and caudal pons. Stimulation of the apneustic center results in respiratory arrest in the maximal inspiratory position, or apneusis.

Respiratory muscles, like other skeletal muscles, possess muscle spindles, which, by sensing length, form a part of a reflex loop that assures that the muscle contraction is appropriate to the anticipated respiratory load and required effort. This servo-­mechanism facilitates fine regulation of respiratory movements and may stabilize the normal respiration in spite of changes in mechanical loading. Breathing is automatic when the respiratory load is constant or when changes in load are subconsciously anticipated. Thus, because it is anticipated, we are not consciously aware of the increase in expiratory resistance during phonation. Under such circumstances the increase in effort is not sensed because it is appropriate to the expected load.

It has been suggested that signals from respiratory muscle and joint mechano-receptors are integrated to produce a sensation that may reach consciousness when there is this “length tension appropriateness.”

Humoral regulation of the medullar centers is mediated by chemosensitive areas in the medulla and through peripheral chemoreceptors. Peripheral chemoreceptors are primarily responsible for the hypoxic drive. These receptors are highly vascular structures located at the carotid bifurcation and arch of the aorta. A diminution of oxygen supply results in anaerobic metabolism in cells of these carotid and aortic bodies. The resulting locally produced metabolites stimulate receptor nerve endings and, through signals conveyed to medullar control centers, lead to increased ventilation. The extremely high blood flow of the chemoreceptors and their almost immeasurable arterial-venous difference make them sensitive to reduced arterial oxygen tension (PaO₂) but not to a reduction in oxygen content alone. However, a decrease in blood flow to these chemoreceptor organs, by permitting accumulation of metabolites, results in their stimulation and an increase in ventilation. Very high PaCO₂ minimizes receptor stimulation regardless of blood flow.

A decrease in arterial pH also stimulates these peripheral chemoreceptors. The stimulation resulting from an increase in arterial carbon dioxide tension (PaCO₂) is probably secondary to the increase in pH. The effect of pH has been attributed to dilatation of arteriovenous anastomoses in the periphery of the chemoreceptor bodies, with resulting reduction in blood flow to the chemosensitive cells. However, the effect of carbon dioxide and pH on respiration is mediated only to a limited extent by peripheral chemoreceptors. Denervation of these receptor organs abolishes the hypoxic drive to respiration but has little effect on the influence on ventilation of carbon dioxide or pH.

Changes in PaCO₂ have a profound effect on central chemoreceptors located in the medulla. These are primarily responsible for mediating the hypercapnic respiratory drive. The precise location and characteristics of these central chemoreceptor sites nor their neural connections with the medullar respiratory control centers have been established. The chemosensitive areas appear to be directly responsive to hydrogen ions rather than to carbon dioxide.

Central chemoreceptors are sensitive to changes in pH, and through this mechanism they appear to be specifically responsive to PaCO₂. Hydrogen ions themselves do not readily traverse the blood-brain barrier. Under normal circumstances, CO₂ plays the primary role in chemical control of ventilation while PaO₂ and extracellular pH have lesser roles. Normal subjects increase their ventilation more than two-fold while breathing 5% CO₂ gas mixture.

Chronic elevation of PaCO₂ (hypercapnia) is found in patients having COPD. The respiratory response to CO₂ is markedly diminished in these clients and they become markedly sensitive to their diminished PaO₂ (hypoxemia). An exuberant use of oxygen for hours may have dire consequences by removing the dominant respiratory stimulus in these clients.  If a patient has Emphysema whose brain is use to high carbon diozide levels in their blood secondary to bad breathing and getting low 02 blood levels in their body so their brain gets use to being messaged to tell the patient to breath on low levels of carbon dioxide blood levels when reaching the brain.  If this emphysema pt is given high doses of O2 for hours it turns the brain off making it think it doesn’t need to send messages to the person to breath.  A normal person with no emphysema COPD is use to breathing due to hypoxia but a emphysema is use to breathing when they have hypocapnia.  That is why when a emphysema pt who is no respiratory arrest is given 2L or less daily.  When is distress high 02 levels temporarily unlikely to hurt the pt, since the high 02 is given for a short period.

”WHO statistics on COPD:

• Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide, causing 3.5 million deaths in 2021, approximately 5% of all global deaths.
• Nearly 90% of COPD deaths in those under 70 years of age occur in low- and middle-income countries (LMIC).
• COPD is the eighth leading cause of poor health worldwide (measured by disability-adjusted life years)
• Tobacco smoking accounts for over 70% of COPD cases in high-income countries. In LMIC tobacco smoking accounts for 30–40% of COPD cases, and household air pollution is a major risk factor.”

World Health Organization – WHO (https://www.who.int/news-room/fact-sheets/detail/chronic-obstructive-pulmonary-disease-(copd))

   Usually due to smoking

This is Healthy Lung Month covering COPD.

What is Chronic Obstructive Pulmonary Disease (COPD)?

Chronic obstructive pulmonary disease (COPD) is a term that applies to patients with chronic bronchitis, bronchiectasis, emphysema and, to a certain extent, asthma. A brief review of normal functional anatomy will provide a background for the discussion of pathology.

The airway down to the bronchioles normally is lined with ciliated pseudo-stratified columnar cells and goblet cells. Mucus derives from mucus glands that are freely distributed in the walls of the trachea and bronchi. The cilia sweep mucus and minor debris toward the upper airway. Low humidity, anesthesia gases, cigarette smoking and other chemical irritants paralyze the action of these cilia. The mucociliary action starts again after a matter of time. This is why people awaken to “smokers cough.”

“Chronic obstructive pulmonary disease (COPD) is a term that applies to patients with chronic bronchitis, bronchiectasis, emphysema and, to a certain extent, asthma.”

Bronchi run in septal connective tissue, but bronchioles are suspended in lung parenchyma by alveolar elastic tissue. The elastic tissue extends throughout alveolar walls, air passages, and vessels, connecting them in a delicate web. Bronchiolar epithelium is ciliated, single-layered and columnar or cuboidal. Beyond the bronchioles the epithelium is flat and lined with a film of phospholipid (surfactant), which lowers surface tension and thereby helps to keep these air spaces from collapsing. Remember that the phospholipid develops during later gestation in utero. This is the reason why premature infant’s lungs cannot stay inflated without the addition of surfactant therapy. Macrophages are found in alveolar lining. Smooth muscles surround the walls of all bronchi, bronchioles, and alveolar ducts and when stimulated they shorten and narrow the passages. Cartilage lends rigidity and lies in regular horse-shaped rings in the tracheal wall. Cartilage is absent in bronchi less than 1 mm in diameter.

The terminal bronchiole is lined with columnar epithelium and is the last purely conducting airway. An acinus includes a terminal bronchiole and its distal structures. Five to ten acini together constitute a secondary lobule, which is generally 1 to 2 cm in diameter and is partly surrounded by grossly visible fibrous septa. Passages distal to the terminal bronchiole include an average of three but as many as nine generations of respiratory bronchioles lined with both columnar and alveolar epithelium. Each of the last respiratory bronchioles gives rise to about six alveolar ducts, each of these to one or two alveolar sacs, and finally each of the sacs to perhaps seventy-five alveoli. Alveolar pores (pores of Kohn) may connect alveoli in adjacent lobules.

Two different circulations supply the lungs. The pulmonary arteries and veins are involved in gas exchange. The pulmonary arteries branch with the bronchi, dividing into capillaries at the level of the respiratory bronchiole, and supplying these as well as the alveolar ducts and alveoli. In the periphery of the lung, the pulmonary veins lie in the interlobular septa rather than accompanying the arteries and airways. The bronchial arteries are small and arise mostly from the aorta. They accompany the bronchi to supply their walls. In some cases of COPD, like bronchiectasis, extensive anastomoses develop between the pulmonary and bronchial circulations. This can allow major shunting and recirculation of blood, therefore contributing to cardiac overload and failure. Lymphatics run chiefly in bronchial walls and as a fine network in the pleural membrane. The lumina of the capillaries in the alveolar walls are separated from the alveolar lining surfaces by the alveolar-capillary membrane, consisting of thin endothelial and epithelial cells and a minute but expansile interstitial space. This interface between air and blood, only 2 microns in thickness, is the only place where gases may be exchanged effectively.

Disease Specific Review

Chronic Bronchitis

Chronic bronchitis is a clinical disorder characterized by excessive mucus secretion in the bronchi. It was traditionally defined by chronic or recurrent productive cough lasting for a minimum of three months per year and for at least two consecutive years, in which all other causes for the cough have been eliminated. Today’s definition remains more simplistic to include a productive cough progressing over a period of time and lasting longer and longer. Sometimes, chronic bronchitis is broken down into three types: simple, mucopurulent or obstructive. The pathologic changes consist of inflammation, primarily mononuclear, infiltrate in the bronchial wall, hypertrophy and hyperplasia of the mucus-secreting bronchial glands and mucosal goblet cells, metaplasia of bronchial and bronchiolar epithelium, and loss of cilia. Eventually, there may be distortion and scarring of the bronchial wall.

Asthma

Asthma is a disease characterized by increased responsiveness of the trachea and bronchi to various stimuli (intrinsic or extrinsic), causing difficulty in breathing due to narrowing airways. The narrowing is dynamic and changes in degree. It occurs either spontaneously or because of therapy. The basic defect appears to be an altered state of the host, which periodically produces a hyperirritable contraction of smooth muscle and hypersecretion of bronchial mucus. This mucus is abnormally sticky and therefore obstructive. In some instances, the illness seems related to an altered immunologic state.

Histological changes of asthma include an increase in the size and number of the mucosal goblet cells and submucosal mucus glands. There is marked thickening of the bronchial basement membrane and hypertrophy of bronchial and bronchiolar smooth muscle tissue. A submucosal infiltration of mononuclear inflammatory cells, eosinophils and plugs of mucus blocks small airways. Patients who have had asthma for many years may develop cor pulmonale and emphysema.

Emphysema

Pulmonary emphysema is described in clinical, radiological and physiologic terms, but the condition is best defined morphologically. It is an enlargement of the air spaces distal to the terminal non-respiratory bronchiole, with destruction of alveolar walls.

Although the normal lung has about 35,000 terminal bronchioles and their total internal cross-sectional area is at least 40 times as great as that of the lobar bronchi, the bronchioles are more delicate and vulnerable. Bronchioles may be obstructed partially or completely, temporarily or permanently, by thickening of their walls, by collapse due to loss of elasticity of the surrounding parenchyma, or by influx of exudate. In advanced emphysema, the lungs are large, pale, and relatively bloodless. They do not readily collapse. They many contain many superficial blebs or bullae, which occasionally are huge. The right ventricle of the heart is often enlarged (cor pulmonale), reflecting pulmonary arterial hypertension. Right ventricular enlargement is found in about 40% of autopsies of patients with severe emphysema. The distal air spaces are distended and disrupted, thus excessively confluent and reduced in number. There may be marked decrease in the number and size of the smaller vascular channels. The decrease in alveolar-capillary membrane surface area may be critical. Death may result from infection that obliterates the small bronchi and bronchioles. There is often organized pneumonia or scarring of the lung parenchyma due to previous infections.

Classification of emphysema relies on descriptive morphology, requiring the study of inflated lungs. The two principal types are centrilobular and panlobular emphysema. The two types may coexist in the same lung or lobe.

Centrilobular emphysema (CLE) or centriacinar emphysema affects respiratory bronchioles selectively. Fenestrations develop in the walls, enlarge, become confluent, and tend to form a single space as the walls disintegrate. There is often bronchiolitis with narrowing of lumina. The more distal parenchyma (alveolar ducts and sacs and alveoli) is initially preserved, then similarly destroyed as fenestrations develop and progress.

The disease commonly affects the upper portions of the lung more severely, but it tends to be unevenly distributed. The walls of the emphysematous spaces may be deeply pigmented. This discoloration may represent failure of clearance mechanisms to remove dust particles, or perhaps the pigment plays an active role in lung destruction. CLE is much more prevalent in males than in females. It is usually associated with chronic bronchitis and is seldom found in nonsmokers.

Panlobular emphysema (PLE) or panacinar emphysema is a nearly uniform enlargement and destruction of the alveoli in the pulmonary acinus. As the disease progresses, there is gradual loss of all components of the acinus until only a few strands of tissue, which are usually blood vessels, remain. PLE is usually diffuse, but is more severe in the lower lung areas. It is often found to some degree in older people, who do not have chronic bronchitis or clinical impairment of lung function. The term senile emphysema was formerly applied to this condition. PLE occurs as commonly in women and men, but is less frequent than CLE. It is a characteristic finding in those with homozygous deficiency of serum alpha-1 antitrypsin. It has also been found that certain populations of IV Ritalin abusers show PLE.

Bullae are common in both CLE and PLE, but may exist in the absence of either. Air-filled spaces in the visceral pleura are commonly termed blebs, and those in the parenchyma greater than 1 cm in diameter are called bullae. A valve mechanism in the bronchial communication of a bulla permits air trapping and enlargement of the air space. This scenario may compress the surrounding normal lung. Blebs may rupture into the pleural cavity causing a pneumothorax, and through a valve mechanism in the bronchopleural fistula a tension pneumothorax may develop.

Paracicatricial emphysema occurring adjacent to pulmonary scars represents another type of localized emphysema. When the air spaces distal to terminal bronchioles are increased beyond the normal size but do not show destructive changes of the alveolar walls, the condition is called pulmonary overinflation. This condition may be obstructive, because of air trapping beyond an incomplete bronchial obstruction due to a foreign body or a neoplasm. Many lung lobules may be simultaneously affected as a result of many check-valve obstructions, as in bronchial asthma. Pulmonary overinflation may also be nonobstructive, less properly called “compensatory emphysema”, when associated with atelectasis or resection of other areas of the lung.

Bronchiectasis

Bronchiectasis means irreversible dilation and distortion of the bronchi and bronchioles. Saccular bronchiectasis is the classic advanced form characterized by irregular dilatations and narrowing. The term cystic is used when the dilatations are especially large and numerous. Cystic bronchiectasis can be further classified as fusiform or varicose.

Tubular bronchiectasis is simply the absence of normal bronchial tapering and is usually a manifestation of severe chronic bronchitis rather than of true bronchial wall destruction.

Repeated or prolonged episodes of pneumonitis, inhaled foreign objects or neoplasms have been known to cause bronchiectasis. When the bronchiectatic process involves most or all of the bronchial tree, whether in one or both lungs, it is believed to be genetic or developmental in origin.

Mucoviscidosis, Kartagener’s syndrome (bronchiectasis with dextrocardia and paranasal sinusitis), and agammaglobulinemia are all examples of inherited or developmental diseases associated with bronchiectasis. The term pseudobronchiectasis is applied to cylindrical bronchial widening, which may complicate a pneumonitis but which disappears after a few months. Bronchiectasis is true saccular bronchiectasis but without cough or expectoration. It is located especially in the upper lobes where good dependent drainage is available. A proximal form of bronchiectasis (with normal distal airways) complicates aspergillus mucus plugging.

Advanced bronchiectasis is often accompanied by anastomoses between the bronchial and pulmonary vessels. These cause right-to-left shunts, with resulting hypoxemia, pulmonary hypertension and cor pulmonale.

Keeping a healthy lung prevents emphysema.  So for starters don’t smoke and exercise; which includes don’t be exposed to smoke frequently!

Overall numbers the CDC reports in statistics up to 2021:

“OVERALL NUMBERS:

• Prevalence: In 2021, 38.4 million Americans, or 11.6% of the population, had diabetes.
  • 2 million Americans have type 1 diabetes, including about 304,000 children and adolescents
• Diagnosed and undiagnosed: Of the 38.4 million adults with diabetes, 29.7 million were diagnosed, and 8.7 million were undiagnosed.
• Prevalence in seniors: The percentage of Americans age 65 and older remains high, at 29.2%, or 16.5 million seniors (diagnosed and undiagnosed).
• New cases: 1.2 million Americans are diagnosed with diabetes every year.
• Prediabetes: In 2021, 97.6 million Americans age 18 and older had prediabetes.”

“Diabetes was the eighth leading cause of death in the United States in 2021 based on the 103,294 death certificates in which diabetes was listed as the underlying cause of death. In 2021, diabetes was mentioned as a cause of death in a total of 399,401 certificates.

Cost of diabetes

Updated November 2, 2023

$412.9 billion: Total cost of diagnosed diabetes in the United States in 2022

$306.6 billion was for direct medical costs

$106.3 billion was in indirect costs

After adjusting for population age and sex differences, average medical expenditures among people with diagnosed diabetes were 2.6 times higher than what expenditures would be in the absence of diabetes.”

American Diabetes Association (https://diabetes.org/about-diabetes/statistics/about-diabetes)

Diabetes is still common in the United States. From 1980 through 2011, the number of Americans with diagnosed diabetes has more than tripled as of 2011 (from 5.6 million to 20.9 million).

30.3 million – The number of people in the U.S. who had diabetes in 2022.  According to a the CDC’s most recent “National Diabetes Statistics Report” in 2023, an estimated 136 million adults in the United States are living with either diabetes or prediabetes.

Do you know how much it is costing in our country?  Its a combination of factors that has caused such and increase in the disease of Diabetes in the U.S.

Factors:

-Look how much our population has increased with fast food companies pushing the  unhealthy foods the sell in restaurants or food stores.

-Also people from other countries who permanently came into America becoming a citizen from 1980 to now and came in to the U.S. already eating poor OR picked up the bad habits of eating poor foods that the U.S. media pushes that is acceptable to enough by U.S. society (that just continues).  This factor is adding to the diabetic population whether they came in the U.S. with it or got it when coming to live in America.

-Than people born in the U.S. with family having a history of diabetes or worse parents who did not watch good eating habits when raising their children who got obese putting them at high risk for diabetes.

–Ending line, these factors massively increased making the number of Diabetic Americans 3x higher since 1980.

-Than another factor is the illegals with diabetes also adds to the number of diabetic people in America; for they are not left out and are treated in hospitals with citizens of the U.S.  If they come to an ER in the U.S. we treat them.  Think of what the count is now with all these illegal people coming in the U.S. since the past 4 years with Former President Bidon and Harris in the office.

These factors all IMPACT an increase in the number of Diabetics in America!

Wake up America!  We need to get this disease under better control!  Diabetes increasing in the U.S. will not help disease overall in America!

Statistics:

That’s right. The metabolic condition is about as American as you can get, according to a the CDC’s most recent “National Diabetes Statistics Report” in 2023, an estimated 136 million adults in the United States are living with either diabetes or prediabetes, with the highest prevalence of diagnosed diabetes among American Indian/Alaskan Native adults, followed by non-Hispanic Black adults, Hispanic adults, non-Hispanic Asian adults, and then non-Hispanic White adults; the report also highlights disparities in diabetes prevalence based on socioeconomic factors like income and education level.

The report shows that nearly half of Americans have diabetes or prediabetes, which puts them at high risk for the condition. A good number of these folks haven’t been diagnosed and don’t even realize their predicament.

People with diabetes have too much sugar in their blood. If the disease isn’t controlled, they can wind up with heart disease, nerve damage, kidney problems, eye damage and other serious health problems.

Type 1 diabetes was previously called insulin-dependent mellitus (IDDM) or juvenile-onset diabetes. This type of diabetes happens when the immune system ends up destroying beta cells in the body that come from our pancreas and they are the only cells in the human body that make the hormone INSULIN the regulates your glucose. Insulin allows glucose to transfer into the cells and tissues of our body to give them their energy to do their job in the body and nutrition to work properly=sugar-glucose. To live with this diabetes the person must have their insulin delivered by injection or a pump. This form of diabetes usually occurs in children or young adults but can occur at any age.

Type 2 diabetes was called non-insulin dependent diabetes mellitus (NIDDM) or adult-onset diabetes. In adults, type 2 diabetes accounts for about 90-95% of all diagnosed cases of diabetes. It usually begins as insulin resistance, a disease in which the cells do not use insulin properly due to the pancreas not making enough or the pancreas not secreting the correct form o of insulin to do its function. Ending line the insulin isn’t working properly. As the need for insulin rises, the pancreas gradually loses its ability to produce it.

Type 2 diabetes is associated with older age, OBESITY, family history of diabetes, history of gestational diabetes, impaired glucose metabolism, physical inactivity and race/ethnicity.

Gestational diabetes is a form of glucose intolerance diagnosed during pregnancy. Gestational diabetes occurs more frequently among African Americans, Hispanic/Latino Americans, and American Indians. It is also more common among obese women and women with a family history of diabetes. During pregnancy, gestational diabetes requires treatment to optimize maternal blood glucose levels to lessen the risk of complications in the infant.

Other types of diabetes result from; specific genetic conditions (such as maturity-onset diabetes of youth), surgery, medications, infections, pancreatic disease, and other illnesses. Such types of diabetes account for 1% to 5% of all diagnosed cases.

Treatment for Diabetes:

Diet, insulin, and oral medication to lower blood glucose levels are the foundation of diabetes treatment and management. Patient education and self-care practices are also important aspects of disease management that help people with diabetes lead normal lives or as normal as possible.

To survive, people with type 1 diabetes must have insulin delivered by injection or a pump.

Many people with type 2 diabetes can control their blood glucose by following a healthy meal plan and exercise program, losing excess weight, and taking oral medication.

Medications for each individual with diabetes will often change during the course of the disease. Some people with type 2 diabetes may also need insulin to control their blood glucose.

Self-management education or training is a key step in improving health outcomes and quality of life. It focuses on self-care behaviors, such as healthy eating, being active, and monitoring blood sugar.

The medications used for diabetes would be that your endocrinologist doctor would decide:

-Insulins-commonly in Type I DM but can be used if needed in Type II DM which the MD decides:

If you have type 1 diabetes, your body can’t make its own insulin. The goal of treatment is to replace the insulin that your pancreas can’t make.

Insulin is the most common type of medication used in type 1 diabetes treatment. There are more than 20 types sold in the United States.

It’s given as an infusion under the skin (with the help of an insulin pump) or as an injection.

There are multiple types of insulin. They vary based on how quickly they start working, how long they work, and whether they have a peak level of action.

The type of insulin you need depends on your body’s sensitivity to insulin and the severity of your insulin deficiency.

There are short acting, rapid acting, intermediate acting  long acting, and combination insulins.

Also there is amylinomimetic. It’s an injectable medication that’s used before meals.  It works by delaying the time your stomach takes to empty itself. It also reduces the secretion of the hormone glucagon after meals. These actions lower your blood sugar.  Specifics are another topic in itself.

-Oral medications commonly used in type II diabetics; again specifics are another topic in itself.

If not doing treatment the diabetic will end up with severe complications to possibly death sooner in life than a compliant diabetic.

Pretty simple isn’t it but you have to  the make a move quick if you haven’t yet!  Take action and make changes if you need to!

How the cost of diabetes impacts America:

Diabetes is not only common and serious; it is also VERY COSTLY!  This impacts medical insurance being so high since our population is so high in America. Let us take a look how:

The cost of treating diabetes is staggering. According to the American Diabetes Association, the annual cost of diabetes in medical expenses and lost productivity rose for $98 billion in 1997 to $132 billion in $2002 to $174 billion in 2007.

Two years ago in this post it stated one out of every 5 U.S. federal health care dollars is spent treating people with diabetes. The average yearly health care costs for a person without diabetes is 2,560 dollars; for a person with diabetes that figure soars to $11,744. Much of the human and financial costs can be avoided with proven diabetes prevention and management steps.

Now in 2022 the American Diabetes Association states “People with diagnosed diabetes incur average medical expenditures of $16,752 per year, of which about $9,601 is attributed to diabetes. On average, people with diagnosed diabetes have medical expenditures approximately 2.3 times higher than what expenditures would be in the absence of diabetes.”   https://diabetes.org/about-us/statistics/cost-diabetes

Diabetes.org states now that “The estimated total economic cost of diagnosed diabetes in 2017 is $327 billion, a 26% increase from our previous estimate of $245 billion (in 2012 dollars).

The CDC states the following:

“Natural insulin (i.e. insulin released from your pancreas) keeps your blood sugar in a very narrow range. Overnight and between meals, the normal, non-diabetic blood sugar ranges between 60-100mg/dl and 140 mg/dl or less after meals and snacks.  To keep the blood sugar controlled overnight, fasting and between meals, your body releases a low, background level of insulin. When you eat, there is a large burst of insulin. This surge of insulin is needed to dispose of all the carbohydrate or sugar that is getting absorbed from your meal. All of this happens automatically!  Insulin is continuously released from the pancreas into the blood stream. Although the insulin is quickly destroyed (5-6 minutes) the effect on cells may last 1-1/2 hours. When your body needs more insulin, the blood levels quickly rise, and, the converse – when you need less, the blood levels rapidly fall —The situation is different when you have diabetes and are getting insulin replacement therapy. Once you have injected a dose of insulin, it is going to get absorbed into your bloodstream whether you need it or not.

Insulin pump therapy is increasingly popular. Because insulin pumps more closely mimic what your body does naturally, you can improve your blood sugar control. With that control comes a more flexible lifestyle. Remember, though, that the pumps still require a lot of input from users.

Type 1 diabetes is caused by a loss or malfunction of the insulin producing cells, called pancreatic beta cells. Damage to beta cells results in an absence or insufficient production of insulin produced by the body.

You have Type 2 diabetes if your tissues are resistant to insulin, and if you lack enough insulin to overcome this resistance. Type 2 diabetes is the most common form of diabetes of diabetes worldwide and accounts for 90-95% of cases.”

University of California (https://dtc.ucsf.edu)

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Insulin is a hormone made by the pancreas that allows your body to use sugar (glucose) from carbohydrates in the food that you eat for energy or to store glucose for future use. Insulin helps keeps your blood sugar level from getting too high (hyperglycemia) or too low (hypoglycemia).  How it works; when the glucose gets in your body after digestion starting from eating or even if your not eating by mouth but through IV with Dextrose in it (a form of sugar) or just on a feeding tube via a nasogastric tube or gastric tube (PEG) with Dextrose or some form of sugar in it will put glucose in your blood.  When you eat or drink, much of your food is broken down into a simple sugar called “glucose.”   All 3 routes of getting nutrition can cause your glucose count in the bloodstream to go up, if some form of sugar is in the nutrition supply you get in your body for the cells in our bloodstream.  Now glucose is food to our cells but the food has to get into the cells.  For glucose to pass into our cells it needs a hormone to allow the glucose to pass in the cell to be the food for the cell.  This is where Insulin comes into play!  Insulin is released by the pancrease and put in our bloodstream to do one of its MAIN functions to allow glucose in the cell.  For without insulin what happens is the glucose just will pile up outside of the blood cells and in time cause what we call Diabetes.  Without glucose going into our cells through insulin allowing it to pass in the cells we would not have energy that helps us in doing our activities of daily living.

So in review, the amount of glucose in your bloodstream is tightly regulated by the hormone insulin. Insulin is always being released in small amounts by the pancreas but especially after eating and when digestion takes place releasing the broken down sugar to “glucose” being released into our blood. When the amount of glucose in your blood rises to a certain level, the pancreas will release more insulin to push more glucose into the cells.

Diabetes mellitus (sometimes called “sugar diabetes“) is a condition that occurs when the body can’t use glucose (a type of sugar) normally. Glucose is the main source of energy for the body’s cells. The levels of glucose in the blood are controlled by a hormone called insulin, which is made by the pancreas that it releases into the blood- stream when glucose level goes up allowing for it to be utilized by our body in allowing the glucose to transfer over the cell membranes into the cells as the main source of energy-a major form of nutrition for out cells to do its functions especially transfer oxygen throughout the body to keep our tissues healthy and alive.  Without oxygen we would have tissue and cell starvation.  Think in a diabetic when blood flow gets thick due to high glucose levels in the bloodstream making it difficult for the blood to move throughout our body to oxygenate our tissues the first place the body compensates to allow oxygenated blood by our cells to get to our vital organs like heart, lungs, brain and not areas far away from the body like feet.  That is why you commonly hear of amputations of lower legs with uncontrolled or badly controlled diabetics (arms amputated is very, very rare due to diabetes, more its due to trauma.

People with diabetes either don’t make insulin or their body’s cells are resistant to insulin, leading to high levels of sugar circulating in the blood, called simply high blood sugar. By definition, diabetes is having a blood glucose level of 126 milligrams per deciliter (mg/dL) or more after an overnight fast (not eating anything).

So ending line without Insulin no glucose, a energy nutrition for our cells. we would not get glucose inside the cells. This as a ending result would cause cellular starvation of energy resulting into death in time (much sooner than other people without this problem) unless they take their insulin!

Another function of insulin is after our body uses all the glucose it needs at that time it needs to be stored somewhere.  Insulin helps control blood glucose levels by signaling the liver and muscle and fat cells to take in glucose from the blood.  To get the glucose level in therapeutic range for the body in time.

The 2 major groups of Diabetes occurs if someone has a problem with this role function of insulin resulting in one of the following:

Type 1 Diabetes occurs because the insulin-producing cells of the pancreas (called beta cells) are destroyed by the immune system. People with type 1 diabetes produce no insulin and must use insulin injections to control their blood sugar.  This is most commonly seen in people under age 20 but may occur at any age.

Type 2 Diabetes is the most common form of diabetes, affecting almost 18 million Americans. While most of these cases can be prevented, it remains for adults the leading cause of diabetes-related complications such as blindness, non-traumatic amputations, and chronic kidney failure requiring dialysis. Type 2 diabetes usually occurs in people over age 40 who are overweight, but can occur in people who are not overweight as well.Sometimes referred to as “adult-onset diabetes,” type 2 diabetes has started to appear more often in children because of the rise in obesity in young people.

Sometimes referred to as “adult-onset diabetes,” type 2 diabetes has started to appear more often in children because of the rise in obesity in young people.

Some people can manage their type 2 diabetes by controlling their weight, watching their diet, and exercising regularly. Others may also need to take a pill that helps their body use insulin better, or take insulin injections.

Often, doctors are able to detect the likelihood of type 2 diabetes before the condition actually occurs. Commonly referred to as pre-diabetes, this condition occurs when a person’s blood sugar levels are higher than normal, but not high enough for a diagnosis of type 2 diabetes.

Know this diabetes can be hereditary as well.

Maybe you might want to get your glucose checked by your M.D. and make sure your insulin is functioning well for the side effects of uncontrolled diabetes are detrimental and could shorten your life!

“Research shows that type 2 diabetes increases a person’s risk of developing dementia. Dementia risk also increases with the length of time someone has diabetes and how severe it is. However, it is important to note that diabetes is only a risk factor and does not mean that a person with diabetes will go on to develop dementia.

In people with type 1 diabetes. severe blood sugar highs and lows are also associated with increased risk of developing dementia.As you get older, you are more likely to develop certain health conditions, including diabetes.

To manage this, speak to your GP about going for a health check.

Eating a healthy, balanced diet may reduce your risk of type 2 diabetes. No single ingredient, nutrient or food can improve health by itself. Instead, eating a range of different foods in the right proportions is what makes a difference. This is known as a ‘balanced’ diet.

By eating a balanced diet you are more likely to get all the nutrients you need to stay healthy.”

Alzheimer’s Society (https://www.alzheimers.org.uk/about-dementia/managing-the-risk-of-dementia/reduce-your-risk-of-dementia/diabetes)