RESPIRATION III SEMESTER BOTANY MODULE II

Size: px

Start display at page:

Download "RESPIRATION III SEMESTER BOTANY MODULE II"

Liliana Boone
5 years ago
Views:

1 III SEMESTER BOTANY MODULE II RESPIRATION Lung Capacities and Volumes Tidal volume (TV) air that moves into and out of the lungs with each breath (approximately 500 ml) Inspiratory reserve volume (IRV) air that can be inspired forcibly beyond the tidal volume ( ml) Expiratory reserve volume (ERV) air that can be evacuated from the lungs after a tidal expiration ( ml) Residual volume (RV) air left in the lungs after strenuous expiration (1200 ml) Inspiratory capacity (IC) total amount of air that can be inspired after a tidal expiration (IRV + TV) Functional residual capacity (FRC) amount of air remaining in the lungs after a tidal expiration (RV + ERV) Vital capacity (VC) the total amount of exchangeable air (TV + IRV + ERV) Total lung capacity (TLC) sum of all lung volumes (approximately 6000 ml in males) Dead Space Anatomical dead space volume of the conducting respiratory passages (150 ml) Alveolar dead space alveoli that cease to act in gas exchange due to collapse or obstruction Total dead space sum of alveolar and anatomical dead spaces Oxygen Transport Transport of oxygen during external respiration: With its low solubility, only approximately 1.5% of the oxygen is transported dissolved in plasma. The remaining 98.5% diffuses into red blood cells and chemically combines with hemoglobin. 1

2 Hemoglobin Within each red blood cell, there are approximately 250 million hemoglobin molecules. Each hemoglobin molecule consists of: 1. A globin portion composed of 4 polypeptide chains. 2. Four iron-containing pigments called heme groups. Each hemoglobin molecule can transport up to 4 oxygen molecules because each iron atom can bind one oxygen molecule. When 4 oxygen molecules are bound to hemoglobin, it is 100% saturated; when there are fewer, it is partially saturated. Oxygen binding occurs in response to the high partial pressure of oxygen in the lungs. When hemoglobin binds with oxygen, it is called oxyhemoglobin. When one oxygen binds to hemoglobin, the other oxygen molecules bind more readily. This is called cooperative binding. Hemoglobin's affinity for oxygen increases as its saturation increases. Oxyhemoglobin and Deoxyhemoglobin The formation of oxyhemoglobin occurs as a reversible reaction, and is written as in this chemical equation: In reversible reactions, the direction depends on the quantity of products and reactants present. In the lungs, where the partial pressure of oxygen is high, the reaction proceeds to the right, forming oxyhemoglobin. In organs throughout the body where the partial pressure of oxygen is low, the reaction reverses, proceeding to the left. Oxyhemoglobin releases oxygen, forming deoxyhemoglobin, which is also called reduced hemoglobin. The affinity of hemoglobin for oxygen decreases as its saturation decreases. Oxygen-Hemoglobin Dissociation Curve The degree of hemoglobin saturation is determined by the partial pressure of oxygen, which varies in different organs throughout the body. 2

3 When these values are graphed, they produce the oxygen-hemoglobin dissociation curve. The axes on the graph are: partial pressure of oxygen and percent saturation of hemoglobin. In the lungs, the partial pressure of oxygen is approximately 100 millimeters of mercury. At this partial pressure, hemoglobin has a high affinity for oxygen, and is 98% saturated. In the tissues of other organs, a typical partial pressure of oxygen is 40 millimeters of mercury. Here, hemoglobin has a lower affinity for oxygen and releasess some but not all of its oxygen to the tissues. When hemoglobin leaves the tissuess it is still 75% saturated. The oxygen-hemoglobin dissociation curve is an S-shaped curve, with a nearly flat slope at high PO 2's and a steep slope at low PO 2's. A closer look at the flat region of the oxygen-hemoglobin dissociation curve between 80 and 100 millimeters of mercury: In the lungs at sea level, a typical PO 2 is 100 millimeters of mercury. At this PO 2, hemoglobin is 98% saturated. 3

In the lungs of a hiker at higher elevations or a person with particular cardiopulmonary diseases, the PO 2 may be 80 millimeters of mercury. At this PO 2, hemoglobin is 95% saturated.

4 In the lungs of a hiker at higher elevations or a person with particular cardiopulmonary diseases, the PO 2 may be 80 millimeters of mercury. At this PO 2, hemoglobin is 95% saturated. Even though the PO 2 differs by 20 millimeters of mercury there is almost no difference in hemoglobin saturation. This means that although the PO 2 in the lungs may decline below typical sea level values, hemoglobin still has a high affinity for oxygen and remains almost fully saturated. Factors that affect the affinity of hemoglobin for oxygen include: Temperature: A higher temperature cause a decrease in affinity. In more active tissue with a higher temperature O 2 unloads more easily. ph: Hydrogen ion increases (ph decreases) in more active tissue. This decreases the affinity of hemoglobin by the Bohr effect which can be expressed in this equation Hb + O 2 --> Hb-O 2 + H + In more active tissue ph decreases and O 2 is more easily unloaded P CO2 : CO 2 binds reversibly with Hb to form carbaminohemoglobin a molecule which has a lesser affinity for O 2. This decrease in the affinity of Hb for oxygen in the presence of CO 2 is called the carbamino effect These first three factors work together to promote O 2 unloading in respiring tissues and O 2 loading in the lungs. 4

5 The hemoglobin oxygen disassociation curve can shift either to the left or to the right. When the curve shifts to the right, the affinity of oxygen for hemoglobin decreases and oxygen can be more easily unloaded. When the curve shifts to the left, the affinity of oxygen for hemoglobin increases and oxygen can be more easily loaded. CO 2 Transport 1. Carbon dioxide is produced by cells throughout the body. 2. It diffuses out of the cells and into the systemic capillaries, where approximately 7% is transported dissolved in plasma. 3. The remaining carbon dioxide diffuses into the red blood cells. Within the red blood cells, approximately 23% chemically combines with hemoglobin, and 70% is converted to bicarbonate ions, which are then transported in the plasma. CO 2Transport: Carbaminohemoglobin (Tissues) Of the total carbon dioxide in the blood, 23% binds to the globin portion of the hemoglobin molecule to form carbaminohemoglobin, as written in this equation: Carbaminohemoglobin forms in regions of high PCO 2, as blood flows through the systemic capillaries in the tissues. CO 2Transport: Carbaminohemoglobin (Lungs) The formation of carbaminohemoglobin is reversible. In the lungs, which have a lower PCO 2, carbon dioxide dissociates from carbaminohemoglobin, diffuses into the alveoli, and is exhaled. 5

6 CO 2 Transport: Bicarbonate Ions (Tissues) 1. Of the total carbon dioxide in the blood, 70% is converted into bicarbonate ions within the red blood cells, in a sequence of reversible reactions. The bicarbonate ions then enter the plasma. 2. In regions with high PCO 2, carbon dioxide enters the red blood cell and combines with water to form carbonic acid. This reaction is catalyzed by the enzyme carbonic anhydrase. The same reaction occurs in the plasma, but without the enzyme it is very slow. 3. Carbonic acid dissociates into hydrogen ions and bicarbonate ions. The hydrogen ions produced in this reaction are buffered by binding to hemoglobin. This is written as HHb. 4. In order to maintain electrical neutrality, bicarbonate ions diffuse out of the red blood cell and chloride ions diffuse in. This is called the chloride shift. 5. Within the plasma, bicarbonate ions act as a buffer and play an important role in blood ph control. CO 2 Transport: Bicarbonate Ions (Lungs) 1. In the lungs, carbon dioxide diffuses out of the plasma and into the alveoli. This lowers the PCO 2in the blood, causing the chemical reactions to reverse and proceed to the left. 2. In the lungs, the bicarbonate ions diffuse back into the red blood cell, and the chloride ions diffuse out of the red blood cell. Recall that this is called the chloride shift. 3. The hydrogen ions are released from hemoglobin, and combine with the bicarbonate ion to form carbonic acid. 4. Carbonic acid breaks down into carbon dioxide and water. This reverse reaction is also catalyzed by the enzyme carbonic anhydrase. Tobacco Smoking Considering the globe, the adverse effects of tobacco smoking out number all the effects of other pollutants. It is considered as one of the most important preventable causes of death. Tobacco smoking affects not only those who are actively 6

7 smoking but it also has an adverse consequence on the health of those who are by the vicinity of the smoker. These individuals are termed as passive Smokers. Active Smoking and disease The cigarette smoke that is taken through the mouth into the lung has several types of chemicals that have diverse & serious effects on our health. The composition depends on the type of tobacco, length of the cigarette, and presence and effectiveness of filter tips. Usually present are (1) Carcinogens whose effects have been verified in lower animals (e.g.polycyclic hydrocarbons, betanaphthylamine, nitrosamines). (2) Cell irritants and toxins (e.g. Ammonia, formaldehyde, and oxides of nitrogen). (3) Carbon monoxide, and (4) nicotine, which has various effects on the sympathetic nervous system, blood pressure, heart rate etc. The more common adverse health effects of tobacco are lung cancer, coronary heart disease, COPD (Chronic bronchitis, emphysema), and systemic atherosclerosis. And the less common effects are peptic ulcer, Cancer that can originate from larynx, esophagus, pancreas, bladder & kidneys. Fetuses are also adversely affected by maternal smoking. Several studies have shown that maternal smoking could cause low birth weight, prematurity, still birth and infant mortality. Moreover other complications of pregnancy like abruptio placentae, placenta previa, and premature rupture of membranes have been found to be caused by maternal smoking. The risk of mortality is dose dependent. The number of pack years i.e. number of packs per day times number of years is directly related to mortality rate. The more pack years of smoking the higher the risk of mortality. Coronary heart disease causes most of the deaths when it comes to effects of cigarette smoking. Lung cancer closely follows causing a huge number of deaths. Involuntary smoke exposure (Passive Smoking) The effect of passive smoking has been identified during the last few decades. Its effect comes when non-smoking people inspire the ambient air, which is polluted by cigarette smoke. The health impact depends on the volume of the air in the room, number of active smokers, rate of air exchange and duration of exposure. Data from different countries show that the risks of lung cancer increase by 1.5 due to passive smoking. There is also increased risk of cardiovascular diseases specially MI, and high incidence of lower respiratory tract diseases in infants & children of smoking parents. 7

8 Children & infants of smoking mothers will have an obvious intense exposure and hence retardation of physical and intellectual growth is likely to occur. Benefits of cessation or reducing exposure to cigarette smoke When a person stops smoking the risks of diseases and subsequent death start to decline. The risk to reach to that of non-smoking people may take 20 years of smoke-free period. The amount of cigarettes smoked daily, and duration of smoking determines the rate of decrease of risks. The relative risk of lung cancer and laryngeal cancer start to decline after 1 to 2 smoke free years. However considering lung cancer former smokers will have slightly higher risk than non-smokers even after 30 years of smoke-free years. When it comes to coronary diseases the decline of risk is rapid and it can level with those of non-smokers after 5 to 20 years. Once COPD has been developed quitting does not have any significant effect in reversing the situation. Hypercapnia and hypocapnia An increase in partial pressure of CO 2 (pco 2) above 43 mm Hg is called hypercapnia. Hypercapnia produces acidosis. This stimulates the chemosensitive area in the medulla and chemoreceptors in the carotid and aortic sinuses. This activates the inspiratory area and thereby causes hyperventilation (increase in the rate of respiration). Hyperventilation removes more CO 2 until pco 2 is lowered to normal. When the pco 2 is less than 37 mm Hg the condition is called hypocapnia. It is the common cause of alkalosis. Alkalosis inhibits respiration (hyperventilation), therby allows metabolic C 2 to accumulate in blood. Emphysema This disease is characterized by the irreversible distension of respiratory bronchioles, alveolar ducts and alveoli. Distension of these structures reduces the surface area available for exchange of gases. Hypoxia, pulmonary hypertension, heart failure etc. are the consequences of the disease. Persistent coughing, cigarette smoking and infections are the predisposing factors. Apnoea It refers to the temporary cessation of breathing. A sudden severe pain or cold can bring about apnoea. 8

9 Asphyxia Asphyxia refers to oxygen starvation as result of low-atmospheric oxygen or other such situations as drawning. Acute asphyxia involves a combination of respiratory, circulatory and nervous system failure. Hypoxia Hypoxia is a condition in which the body or a region of the body is deprived of adequate oxygen supply. Hypoxia may be classified as either generalized, affecting the whole body, or local, affecting a region of the body. Generalized hypoxia occurs in healthy people when they ascend to high altitude. Hypoxia also occurs in healthy individuals when breathing mixtures of gasses with low oxygen content. 9

Physiology Unit 4 RESPIRATORY PHYSIOLOGY

Physiology Unit 4 RESPIRATORY PHYSIOLOGY In Physiology Today Respiration External respiration ventilation gas exchange Internal respiration cellular respiration gas exchange Respiratory Cycle Inspiration