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Lecture 11

Specific Pulmonary abnormalities

Chronic pulmonary emphysema: Emphysema means excess air in the lungs. This term describe complex obstructive and destructive process. It is caused by many years of smoking. It results from the following major pathophysiologic changes in the lungs:
1-chronic infection caused by inhaling smoke or other substances that irritate the bronchi and bronchioles. The chronic infection seriously deranges the normal protective mechanisms of the airways; including a-partial paralysis of the cilia of the respiratory epithelium (an effect caused by nicotine) leading to mucus cannot be moved easily out of the passageways. Also, b-stimulation of excess mucus secretion occurs, which further exacerbates the condition. Too, c- inhibition of the alveolar macrophages occurs, so that they become less effective in combating infection.
2. The infection excess mucus and inflammatory edema of the bronchiolar epithelium, both together cause chronic obstruction of many of the smaller airways.
3. The obstruction of the airways makes it especially difficult to expire, thus causing entrapment of air in the alveoli and overstretching them. This, combined with the lung infection, causes marked destruction of as much as 50 to 80 % of the alveolar walls.

The physiologic effects of chronic emphysema are depending on the severity of the disease:
Increases airway resistance during expiration (bronchiolar obstruction).
The marked loss of alveolar walls greatly decreases the diffusing capacity of the lung.
Extremely abnormal ventilation-perfusion ratios (The obstructive process is frequently much worse in some parts of the lungs than in other parts) with a very low VA/Q in some parts (physiologic shunt), and very high VA/Q in other parts (physiologic dead space).
Pulmonary vascular resistance often increases markedly, causing pulmonary hypertension (due to loss of large portions of the alveolar walls also decreases the number of pulmonary capillaries through which blood can pass).
Right-sided heart failure.
●The patient with emphysema progresses slowly over many years develops hypoxia and hypercapnia then air hunger and death.

Pneumonia

The term pneumonia includes any inflammatory condition of the lung in which some or all of the alveoli are filled with fluid and blood cells, This disease begins with infection in the alveoli; the pulmonary membrane becomes inflamed and highly permeable so that fluid, red and white blood cells leak out of the blood into the alveoli. Thus, the infected alveoli or aleveolis become progressively filled with fluid and cells, and the infection spreads by extension of bacteria or virus from alveolus to alveolus. And finally lead to consolidated alveoli or lob, this result in two major pulmonary abnormalities: (1) reduction in the total available surface area of the respiratory membrane and (2) decreased ventilation perfusion ratio (the blood passing through the aerated lung becomes 97 % saturated with oxygen, whereas that passing through the unaerated lung is about 60 % saturated. Therefore, the average saturation of the blood pumped by the left heart into the aorta is only about 78 %). Both these effects cause hypoxemia and hypercapnia.


Atelectasis
Atelectasis means collapse of the alveoli. It can occur in localized areas of a lung or in an entire lung. Its most common causes are:
Total obstruction of the airway: The airway obstruction type of atelectasis usually results from (1) blockage of many small bronchi with mucus or (2) obstruction of a major bronchus by either a large mucus plug or some solid object such as a tumor. The air entrapped beyond the block is absorbed within minutes to hours by the blood flowing in the pulmonary capillaries. If the lung flexible will lead simply to collapse of the alveoli. If the lung is rigid because of fibrotic tissue and cannot collapse absorption of air from the alveoli creates very negative pressures within the alveoli, which pull fluid out of the pulmonary capillaries into the alveoli, thus causing the alveoli to fill completely with edema fluid.
When an entire lung becomes atelectatic, a condition called massive collapse of the lung. Collapse of the lung tissue not only occludes the alveoli but also almost alway increases the resistance to blood flow through the pulmonary vessels of the collapsed lung. This resistance increase occurs a-partially because of the lung collapse itself, which compresses and folds the vessels as the volume of the lung decreases. In addition, b- hypoxia in the collapsed alveoli causes additional vasoconstriction. Fortunately blood flow shift to other ventilated areas and VA/Q is not much suffered and the aortic blood has only mild oxygen desaturation despite total loss of ventilation in an entire lung.
Or lack of surfactant in the fluids lining the alveoli. The surfactant decreases the surface tension in the alveoli 2- to 10-fold (Discussed earlier).

Asthma: spastic contraction of smooth muscles of bronchioles usually due to hypersensitivity of the bronchioles to foreign substances in the air (allergic as plant pollens or non allergic as smog). This allergic hypersensitivity leads to releasing factors which produce the following effect: (1) localized edema in the walls of the small bronchioles, as well as secretion of thick mucus into the bronchiolar lumens, and (2) spasm of the bronchiolar smooth muscle.
So the bronchiolar diameter reduced during expiration than during inspiration, caused by bronchiolar collapse during expiratory effort that compresses the outsides of the bronchioles. In addition to already partially occluded asthmatic bronchioles, creates severe obstruction during expiration. That is, the asthmatic person often can inspire quite adequately but has great difficulty expiring.
Clinical measurements show (1) greatly reduced maximum expiratory rate and (2) reduced timed expiratory volume. Also, all of this together result in dyspnea, or air hunger.
The functional residual capacity and residual volume of the lung become especially increased during the acute asthmatic attack because of the difficulty in expiring air from the lungs. Also, over a period of years, the chest cage becomes permanently enlarged, causing a barrel chest, and both the functional residual capacity and lung residual volume become permanently increased.

Tuberculosis

In tuberculosis, the tubercle bacilli cause a tissue reaction in the lungs, including (1) invasion of the infected tissue by macrophages and (2) walling off of the lesion by fibrous tissue to form the so-called tubercle (which is the protective process against extension of the infection).
In untreated case the bacilli spread lead to extreme destruction of lung tissue with formation of large abscess cavities and then in late stage fibrosis throughout the lung as well as reduced total amount of functional lung tissue. This lead to:
(1) Increased work on the part of the respiratory muscles to cause pulmonary ventilation and reduced vital capacity and breathing capacity;
(2) Reduced total respiratory membrane surface area and increased thickness of the respiratory membrane, causing progressively diminished pulmonary diffusing capacity; and (3) abnormal ventilation-perfusion ratio in the lung.

Hypoxia: decrease O2 to the cells.

Causes of hypoxia:
1-Inadequate oxygenation of the blood in the lungs because of extrinsic reasons (Deficiency of oxygen in the atmosphere & hypoventilation as neuromuscular disorders).
2- Pulmonary disease.
3-Venous-to-arterial shunts (right-to-left cardiac shunts).
4- Inadequate oxygen transport to the tissues by the blood.
a. Anemia or abnormal hemoglobin.
b. General circulatory deficiency.
c. Localized circulatory deficiency (peripheral, cerebral, coronary vessels)
d. Tissue edema
5-Inadequate tissue capability of using oxygen:
Poisoning of cellular oxidation enzymes.
Diminished cellular metabolic capacity for using oxygen, because of toxicity, vitamin deficiency, or other factors.
The classic cause of inability of the tissues to use oxygen is cyanide poisoning, in which the action of the enzyme cytochrome oxidase is completely blocked by the cyanideto such an extent that the tissues simply cannot use oxygen even when plenty is available. Also, deficiencies of some of the tissue cellular oxidative enzymes or of other elements in the tissue oxidative system can lead to this type of hypoxia e.g in beriberi in which several important steps in tissue utilization of oxygen and formation of carbon dioxide are compromised because of vitamin B deficiency. Oxygen therapy is of hardly any measurable benefit.


Effects of Hypoxia on the Body: Hypoxia, if severe enough, can cause death of cells throughout the body, but in less severe degrees it causes principally (1) depressed mental activity, sometimes culminating in coma, and (2) reduced work capacity of the muscles.

Oxygen therapy in different types of hypoxia

Oxygen can be administered by (1) placing the patients head in a tent that contains air fortified with oxygen, (2) allowing the patient to breathe either pure oxygen or high concentrations of oxygen from a mask, or (3) administering oxygen through an intranasal tube.
Oxygen therapy in different types of hypoxia as follow:
In atmospheric hypoxia, provide 100 % effective therapy.
In hypoventilation hypoxia, a person breathing 100 % oxygen can extremely beneficial.
In impaired alveolar membrane diffusion, O2 therapy is beneficial because oxygen therapy can increase the PO2 in the lung alveoli from the normal value of about 100 mm Hg to as high as 600 mm Hg so increase O2 diffusion across respiratory membrane to pulmonary capillaries.
In hypoxia caused by anemia, abnormal hemoglobin transport of oxygen, circulatory deficiency, or physiologic shunt, O2 therapy lead to a small amount of extra oxygen, between 7 and 30 %, can be transported in the dissolved state.
In inadequate tissue use of oxygen, oxygen therapy is of hardly any measurable benefit.

Cyanosis

Cyanosis is the blueness of the skin, and its cause is excessive amounts of deoxygenated hemoglobin in the skin blood vessels, especially in the capillaries. This deoxygenated hemoglobin has an intense dark blue purple color that is transmitted through the skin. In general, definite cyanosis appears whenever the arterial blood contains more than 5 grams of deoxygenated hemoglobin in each 100ml of blood. A person with anemia almost never becomes cyanotic because there is not enough hemoglobin for 5 grams to be deoxygenated in 100 ml of arterial blood. Conversely, in a person with excess red blood cells, as occurs in polycythemia vera, the great excess of available hemoglobin that can become deoxygenated leads frequently to cyanosis, even under otherwise normal condition.

Hypercapnia

Hypercapnia means excess carbon dioxide in the body fluids. It is not always associated with hypoxia, hypercapnia usually occurs in association with hypoxia only when the hypoxia is caused by hypoventilation or circulatory deficiency, other type of hypoxia is not associated with hypercapnia.
When the alveolar PCO2 rises above about 60 to 75 mm Hg, an otherwise normal person by then is breathing about as rapidly and deeply as he or she can, and air hunger, also called dyspnea, becomes severe.
If the PCO2 rises to 80 to 100 mm Hg, the person becomes lethargic and sometimes even semicomatose. Anesthesia and death can result when the PCO2 rises to 120 to 150 mm Hg. At these higher levels of PCO2, the excess carbon dioxide now begins to depress respiration rather than stimulate it, thus causing a vicious circle: (1) more carbon dioxide, (2) further decrease in respiration, (3) then more carbon dioxide, and so forthculminating rapidly in a respiratory death.

Dyspnea

Dyspnea (air hunger) means mental distress associated with inability to ventilate enough to satisfy the demand for air. At least three factors often enter into the developmentof the sensation of dyspnea:
Abnormality of respiratory gases in the body fluids, especially hypercapnia and, to a much less extent, hypoxia.
The amount of work that must be performed by the respiratory muscles to provide adequate ventilation.
State of mind. This is called neurogenic dyspnea or emotional dyspnea. (For instance, almost anyone momentarily thinking about the act of breathing may suddenly start taking breaths a little more deeply than ordinarily because of a feeling of mild dyspnea. This feeling is greatly enhanced in people who have a psychological fear of not being able to receive a sufficient quantity of air, such as on entering small or crowded rooms).





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