VENTILATION OF LUNGS. TRANSPORT OF GASES. REGULATION OF RESPIRATION.
BIOMECHANICS OF RESPIRATORY ACT
I. Common characteristic of breathing. The respiratory system is divided into a respiratory zone, which is the site of gas exchange between air and blood, and a conducting zone, which conducts the air to the respiratory zone. The exchange of gases between air and blood occurs across the walls of tiny air sacs called alveoli, which are only a single cell layer thick to permit very rapid rates of gas diffusion.
The term respiration includes three separate but related functions: (1) ventilation (breathing); (2) gas exchange, which occurs between the air and blood in the lungs and between the blood and other tissues of the body; and (3) oxygen utilization by the tissues in the energy – liberating reactions of cell respiration.
Ventilation and the exchange of gases (oxygen and carbon dioxide) between the air and blood are collectively called external respiration. Gas exchange between the blood and other tissues and oxygen utilization by the tissues are collectively known as internal respiration.
Ventilation is the mechanical process that moves air into and out of the lungs. Since the oxygen concentration of air is higher in the lungs than in the blood, oxygen diffuses from air to blood. Carbon dioxide conversely moves from the blood to the air within the lungs by diffusing down its concentration gradient. As a result of this gas exchange, the inspired air contains more oxygen and less carbon dioxide than the expired air. More importantly blood leaving the lungs (in the pulmonary veins) has a higher oxygen and lower carbon dioxide concentration than the blood delivered to the lungs in the pulmonary arteries. This result bring the fact that lungs function is to give gaseous equilibrium between blood and the air.
Main process of the external respiration. The passage air respiratory systems are divided into two functional zones. The respiratory zone is the region where gas exchange occurs, it includes the respiratory bronchioles (which contain separate outpouchings of alveoli) and the terminal cluster of alveolar sacs.
Gas exchange between the air and blood occurs entirely by diffusion through lung tissue. This diffusion occurs very rapid because there is a large surface area within the lungs and a very short diffusion distance between blood and air.
Phases of respiratory act. Inspiration & Expiration
Pulmonary ventilation consists of two phases: inspiration and expiration. Inspiration (inhalation) and expiration (exhalation) are accomplished by alternately increasing and decreasing the volume of the thorax and lungs.
The thorax must be sufficiently rigid so that it can protect vital organs and provide attachments for many short and powerful muscles. Breathing, or pulmonary ventilation, requires the flexibility of the thorax to function as a bellow during the ventilation cycle. The rigidity and the surfaces for muscle attachment are provided by the bony composition of the rib cage. The rib cage is pliable, because the ribs are separate from one another and most of the ribs (upper ten of the twelve pairs) are attached to the sternum by resilient costal cartilages. The vertebral attachments also provide considerable mobility. The structure of the rib cage and associated cartilages provides continuous elastic tension, so that after stretched by muscle contraction during inspiration, the rib cage can return passively to its resting dimension when the muscles relax. This elastic recoil is greatly aided by the elasticity of the lungs.
Respiratory muscles cause passage of air into the Lung. Between the bony portions of the rib cage are two layers of intercostals muscles: the external intercostal muscles and internal intercostal muscles. Between the costal cartilages, there is only one muscle layer, which its fibers oriented in the same manner to those of the internal intercostal muscle. These muscles may called as the interchondral part of the internal intercostal muscle or parasternal intercostal muscle..
An unforced, or quiet, inspiration primarily results from contraction of the dome– shaped diaphragm, which become lowered and flattened. This increases thoracic volume in a vertical direction. Inspiration is also aided by the parasternal and external intercostal muscles, which raise the ribs when they contract and increase thoracic volume laterally. Other thoracic muscles involved in forced (deep) inspiration. The most important of these is the scalenus muscle, followed by the pectoralis minor muscle, and in extreme cases the sternocleidomastoid muscle. Contraction of these muscles elevates the ribs in an anteroposterior direction; simultaneously, the upper rib cage is stabilized so that the intercostal muscles become more effective.
Mechanism of normal quiet inspiration and expiration. Quiet inspiration is an active process. The contraction of the inspiratory muscles and diaphragm increases intrathoracic volume. This stretch the thorax and lungs. Quiet expiration is a passive process. The thorax and lungs recoil when the respiratory muscles relax. due to their elastic tension
During quiet breathing, the intrapleural pressure, which is about –
Mechanism forced ventilation. Strong inspiratory efforts reduce the intrapleural pressure value as low as —30 mm Hg, producing correspondingly greater degrees of lung inflation. When forced ventilation is increased, the extent of lung deflation is also increased by active contraction of expiratory muscles that decrease intrathoracic volume.
Movement of the diaphragm accounts for 75% of the change in intrathoracic volume during quiet inspiration. This muscle attached around the bottom of the thoracic cage, and it arches over the liver and moves downward like a piston when it contracts.
The other important inspiratory muscles are the external intercostals muscles, which run obliquely downward and forward from rib to rib. The ribs pivot as if hinged at the back, so that when the external intercostals contract they elevate the lower ribs. This pushes the sternum outward and increases the anteroposterior diameter of the chest. The transverse diameter is actually changed little if at all. Either the diaphragm or the external intercostals muscles alone can maintain adequate ventilation at rest. Transaction of the spinal cord above the third cervical segment cause fatal without artificial respiration, but transaction below the origin of the phrenic nerves that innervate the diaphragm (third to fifth cervical segments) is not fatal; conversely, in patients with bilateral phrenic nerve palsy, respiration is somewhat labored, but adequate to maintain life. The scalene and sternocleidomastoid muscles in the neck are accessory inspiratory muscles that they help to elevate the thoracic cage during deep labored respiration.
A decrease in intrathoracic volume and forced expiration result when the expiratory muscles contract. The internal intercostals have this action because they pass obliquely downward and posterior from rib to rib and therefore pull the rib cage downward when they contract. Contractions of the muscles of the anterior abdominal wall also aid expiration by pulling the rib cage downward and inward and by increasing the intraabdominal pressure, which pushes the diaphragm upward.
Change of pressure in pleural cavity in correlation from phases of respiratory act. The lungs and the chest wall are elastic structures. Normally, there is no more than a thin layer of fluid between the lungs and the chest wall. The lungs slide easily on the chest wall but resist being pulled away from it in the same way as 2 moist pieces of glass slide on each other but resist separation. The pressure in the “space” between the lungs and chest wall (intrapleural pressure) is sub atmospheric. The lungs are stretched when they are expanded at birth, and at the end of quiet expiration their tendency to recoil from the chest wall is just balanced by the tendency of the chest wall to recoil in the opposite direction. If the chest wall is opened, the lungs will collapse; and if the lungs lose their elasticity, the chest expands and becomes barrel-shaped.
Movement of blood on venous in correlation from phases of respiratory act.
Contraction of the diaphragm during inhalation also improves venous return. As the diaphragm contracts, it lowers to increase the thoracic volume and decrease the abdominal volume. This creates a partial vacuum in the thoracic cavity (negative intrathoracic pressure) and a higher pressure in the abdominal cavity. The pressure difference thus produced favors blood flow from abdominal to thoracic veins.
Change of pressure in alveoli. The respiratory muscles cause pulmonary ventilation by alternatively compressing and distending the lungs, which in turn causes the pressure in the alveoli to rise and fall. During inspiration the intra-alveolar pressure becomes slightly negative with respect to atmospheric pressure, normally slightly less than
During maximum expiratory effort (with the glottis closed )the intra-alveolar pressure can be increased to as much as
Recoil Tendency of the Lungs, and the Intrapleural Pressure. The lungs have a continual elastic tendency to collapse and therefore to pull away from the chest wall. This is called the recoil tendency of the lungs, and it is caused by two different factors. First, throughout the lungs are many elastic fibers that are stretched by lung inflation and therefore attempt to shorten. Second, and even more important, the surface tension of the fluid lining the alveoli also causes a continual elastic tendency for the alveoli to collapse. This effect is caused by intermolecular attraction between the surface molecules of the alveolar fluid. That is, each molecule pulls on the next one so that the whole lining sheet of fluid on the alveolar surfaces acts like many small elastic balloons continuously trying to collapse the lung.
Ordinarily, the elastic fibers in the lungs account for about one third of the recoil tendency, and the surface tension phenomenon accounts for about two thirds.
The total recoil tendency of the lungs can be measured by the amount of negative pressure in the pleural space required to prevent collapse of the lungs; this pressure is called the pleural pressure or, occasionally, the lung recoil pressure. It is normally about –
“Surfactant” in the alveoli, and its effect on the collapse tendency.
A lipoprotein mixture called “surfactant” is secreted by special surfactant-secreting cells (the “type II granular pneumocytes”) which are the component parts of the alveolar epithelium. This mixture, containing especially the phospholipids dipalmitoyl lecithin, decreases the surface tension of the alveolar fluid lining. In the absence of surfactant, lung expansion is extremely difficult, which often requires negative pleural pressures as low as – 20 to –
Control of Bronchial Tone
The walls of bronchi and bronchioles contain smooth muscle and they are innervated by the autonomic nervous system. In general, sympathetic discharge via Beta-2-adrenergic receptors causes the bronchi to dilate and parasympathetic discharge via the vagus nerves causes them to constrict.. It may be similar to the intrinsic enteric nervous system in the gastrointestinal tract and there is evidence that VIP (Vasoactive intestinal polypeptide) is the mediator secreted by its neurons.
The function of the bronchial muscles is still a matter of debate, but in general, they probably help to maintain an even distribution of ventilation. They also protect the bronchi during coughing. There is a circadian rhythm in bronchial tone, with maximal constriction at about and maximal dilatation at about Thats why the asthma attacks are more severe in the late night and early morning hours, pi–stimulants such as isoproterenol are effective in asthma because they mimic the effects of sympathetic stimulation. Cooling the airways causes bronchoconstriction, and exercise triggers asthmatic attacks because it lowers airway temperature.
Lung Volumes. The amount of air that moves into the lungs with each inspiration (or the amount that moves out, with each expiration) is called the tidal volume. The air inspired with a maximal inspiratory effort in excess of the tidal volume is the inspiratory reserve volume. The volume expelled by an active expiration effort after passive expiration is the expiratory reserve volume, and the air left in the lungs after a maximal expiratory effort is the residual volume. Normal values for these lung volumes, and names applied to combinations of them, are shown in Fig. 43-1.
1. Tidal volume (TV), 2. Inspiratory reserve volume (IRV). 3. Expiratory reserve volume (ERV). 4. Vital capacity (VC).
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Volume (L) |
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|
|
Men |
Women |
|
|
|
Vital capacity (VC) |
IRV |
3.3 |
1.9 |
Inspiratory capacity |
|
TV |
0.6 |
0.5 |
||
|
ERV |
1.0 |
0.7 |
Functional residual capacity |
|
|
RV |
1.2 |
1.1 |
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|
Total lung capacity |
|
|
|
|
Figure 43-1. Lung volume and some measurements related to the mechanics of breathing. The diagram at the upper right represent the excursions of a spirometer plotted against time.
The space in the conducting zone of the airways occupied by gas that does not exchange with blood in the pulmonary vessels is the respiratory dead space. The vital capacity, the greatest amount of air that can be expired after a maximal inspiratory effort, is frequently measured clinically as an index of pulmonary function. The fraction of the vital capacity expired in 1 second (timed vital capacity; also called forced expired volume in 1 second, or FEV I”) gives additional valuable information. The vital capacity may be normal but the timed vital capacity can be greatly reduced in diseases such as asthma, in which the resistance of the airways is increased due to bronchial constriction. The amount of air inspired per minute (pulmonary ventilation, respiratory minute volume) is normally about 6 L (500 ml/breath x 12 breaths/min). The maximal voluntary ventilation (MVV), or, as it was formerly called, the maximal breathing capacity, is the largest volume of gas that can be moved into and out of the lungs in 1 minute by voluntary effort. The normal MVV is 125-170 L/min.
Effects of Gravity on the Lung. Because of gravitational forces,the pressure gradient present. Intrapleural pressure at the bases of the lungs is 5 mm Hg greater than at the apexes. Consequently, the transmural pressure (the difference between intrapulmonary and intrapleural pressure) may become negative at the end of forced expiration, causing airways to close. For the same reason, more of the gas inspired during the first part of inspiration goes to the apexes than to the bases.
Gravity also affects the pressure in the pulmonary blood vessels. Dead Space& Uneven Ventilation. Since gaseous exchange in the respiratory system occurs only in the terminal portions of the airways, the gas that occupies the rest of the respiratory system is not available for gas exchange with pulmonary capillary blood. Thus, in a man who weighs 68 kg, only the first 350 ml of the 500 ml inspired with each breath at rest goes through gaseous exchange in the alveoli. Conversely, with each expiration, the first 150 ml expired is the gas that occupied the dead space, and only the last 350 ml is from the alveoli.
It is wise to distinguish between the anatomic dead space (respiratory system volume exclusive of Alveoli) and the total (physiologic) dead space (volume of gas which do not equilibrate with blood and air, e.g waste ventilation). In health, the 2 dead spaces are identical. In disease states that may be no exchange of gas between the alveoli and the blood, and some of the alveoli may be overventilated. The volume of gas ionperfused alveoli and any volume of air in the alveoli in excess of that necessary to arterialize the b1ood in the alveolar capillaries is part of the dead space (no equilibrating) gas volume. The anatomy dead space can be measured by analysis of the single breath N2 curves. From mid inspiration,the subject take a deep breath as possible of pure O2, then exhales steadily while the N2 content of the expired gas is continuously measured. The initial gas exhaled (phase I) is the gas that filled the dead space and that consequently contains no N2.
Alveolar Ventilation. Because of the dead space, the amount of air reaching the alveoli (alveolar ventilation) at a respiratory minute volume of 6 L/min is 500 minus 150 ml times 12 breath/min, or 4.2 L/min. because of the dead space, rapid, shallow respiration produces much less alveolar ventilation than slow, deep respiration at the same respiratory minute volume (Table 43-2).
Table 43-2. Effect of variations in respiratory rate and depth on alveolar ventilation.
|
Respiratory rate |
30/min |
10/min |
|
Tidal volume |
200 ml |
600ml |
|
Minute volume |
6 L |
6 L |
|
Alveolar, ventilation |
(200-150)x30 = 1500 ml |
(600-150)x10=4500ml |
TRANSPORT OF GASES.
The influence of cutting of vagal nerves on breathing. Fix a narcotized rat on the operation table. Make a longitudinal incision of skin on middle neck line, preparation the vagal nerve. Record the pneumogramme before and after cutting one and than both of vagal nerves. Draw the results in your reports. In conclusion explain the changes.
Unlike liquids, gases expand to fill the volume available to them, and the volume occupied by a given number of gas molecules at a given temperature and pressure is (ideally) the same regardless of the composition of the gas.
Therefore, the pressure exerted by any one gas in a mixture of gases (its partial pressure) is equal to the total pressure times the fraction of the total amount of gas it represents.
The composition of dry air is 20.98% O2, 0.04 CO2, 78.06% N2, and 0.92% other inert constituent such as argon and helium. The barometric pressure (pb) at sea level is 760 mm Hg (1 atmosphere). The partial pressure (indicated by the symbol P) of O2 in dry air is therefore 0.21 x 760, or 160 mm Hg at sea level. The partial pressure of N2 and the other inert gases is 0.79 x 760, or 600 mm Hg; and the P CO2 is 0.0004 x 760, or 0.3 mm Hg. The water vapor in the air in most climates reduces these percentages, and therefore the partial pressures, to a slight degree. Air equilibrated with water is saturated with water vapor and inspired air is saturated by the time it reaches the lungs. The P.H2O at body temperature (37 °C) is 47 mm Hg. Therefore, the partial pressures at sea level of the other gases in the air reaching the lungs are P O2 , 14′ mm Hg; P CO2 0-3 mm Hg; and P.N2 (including the other inert gases), 564 mm Hg.
Gas diffuses from areas of high pressure to area of low pressure, the rate of diffusion depending upon the concentration gradient and the nature of the barrier: between the 2 areas. When a mixture of gases is in contact with and permitted to equilibrate with a liquid each gas in the mixture dissolves in the liquid to an extent determined by its partial pressure and its solubility in the fluid. The partial pressure of a gas in a liquid is that pressure which in the gaseous phase in equilibrium with the liquid would produce the concentration of gas molecules found in the liquid.
GAS EXCHANGE IN THE LUNG
Composition of Alveolar Air. Oxygen continuously diffuses out of the gas in the alveoli (alveolar gas) into the bloodstream, and C02 continuously diffuses into the alveoli from the blood. In the steady state, inspired air mixes with the alveolar gas, replacing the O2 that has entered the blood and diluting the CO2 that has entered the alveoli. Part of this mixture is expired. The O2 content of the alveolar gas then falls and its CO2 content rises until the next inspiration. Since the volume of gas in the alveoli is about 2 L at the end of expiration (functional residual capacity, each 350-ml increment of inspired and expired air has relatively little effect on the P.O2 and P.CO2. Indeed, the composition of alveolar gas remains remarkably constant, not only at rest but also under a variety of other conditions
Sampling Alveolar Air . Theoretically, all but the first 150 ml expired with each expiration is alveolar air, but there is always some mixing at the interface between the dead space gas and the alveolar air. A later portion of expired air is therefore the portion taken for analysis. Using modern apparatus with a suitable automatic valve, it is possible to collect the last 10 ml expired during quiet breathing. The composition of alveolar gas is compared with that of inspired and expired air.
Diffusion Capacity. Partial Pressures of O2 and CO2 in the body (normal, resting conditions): Alveoli: P.O2 = 100 mm Hg; P.CO2 = 40 mm Hg
Alveolar capillaries
Entering the alveolar capillaries P.O2 = 40 mm Hg (relatively low because this blood has just returned from the systemic circulation and has lost much of its oxygen); PCO2 = 46 mm Hg (relatively high because the blood returning from the systemic circulation has picked up carbon dioxide) (Figure 44-1).
Figure 1. Partial pressure and diffusion at the respiratory membrane.
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While in the alveolar capillaries, the diffusion of gasses occurs: oxygen diffuses from the alveoli into the blood and carbon dioxide from the blood into the alveoli. Leaving the alveolar capillaries: PO2 = 100 mm Hg; PCO2 = 40 mm Hg.
Blood leaving the alveolar capillaries returns to the left atrium and is pumped by the left ventricle into the systemic circulation. This blood travels through arteries& arterioles and into the systemic, or body, capillaries. As blood travels through arteries & arterioles, no gas exchange occurs.
Entering the systemic capillaries: PO2 = 100 mm Hg; PCO2 = 40 mm Hg.
Body cells (resting conditions): PO2 = 40 mm Hg; PCO2 = 46 mm Hg. Because of the differences in partial pressures of oxygen and carbon dioxide in the systemic capillaries and the body cells, oxygen diffuses from the blood and into the cells, while carbon dioxide diffuses from the cells into the blood. Leaving the systemic capillaries: PO2 = 40 mm Hg; PCO2 = 46 mm Hg. Blood leaving the systemic capillaries returns to the heart (right atrium) via venules and veins (and no gas exchange occurs while blood is in venules and veins). This blood is then pumped to the lungs (and the alveolar capillaries) by the right ventricle.
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Oxygen moves from the alveoli to the red blood cells along the short path. The PO2 of alveolar air is 100 mm Hg, whereas that in the venous blood in the pulmonary artery is 40 mm Hg (Fig. 44-2).
Figure 2. Partial pressure and diffusion at the tissue membrane.
There is no evidence that any process other than passive diffusion is involved in the movement of O2; into the blood along this pressure gradient. O2 dissolves in the plasma and enters the red blood cells, where it combines with hemoglobin. Diffusion into the blood must be very rapid, since the time for each milliliter of blood is in the capillaries is short. Nevertheless, O2 diffusion is adequate in health to raise the PO2; of the blood to 97 mm Hg, a value just under the alveolar PO2. This falls to 95 mm Hg in the aorta because of the physiologic shunt.
The diffusion capacity of the lungs for O2 is the amount of O2 that crosses the alveolar membrane per minute per mm Hg difference in PO2 between the alveolar gas and the blood in the pulmonary capillaries. Expressed in terms of STPD, it is normally about 20 ml/min/mm Hg at rest. As a result of capillary dilatation and an increase in the number of active capillaries, it rises to values of 65 or more during exercise. The diffusion capacity for O2 is decreased in diseases such as sarcoidosis and beryllium poisoning (berylliosis) that cause fibrosis of the alveolar walls and produce alveolar-capillary block.
Figure 3. Summary of PO2 and PCO2 values in air, lungs, blood, and tissues, graphed to emphasize the fact that both O2 and CO2 diffuse “downhill” along gradients of decreasing partial pressure.
The P.CO2 of venous blood is 46 mm Hg, whereas that of alveolar air is 40 mm Hg, and CO2 diffuses from the blood into the alveoli along this gradient. The PCO2 of blood leaving the lungs is 40 mm Hg. CO2 passes through all biologic membranes with ease, and the pulmonary diffusion capacity for CO2 is much greater than the capacity for O2. It is for this reason that CO2 retention is rarely a problem in patients with alveolar capillary block even when the reduction in diffusion capacity for O2 is severe.
The partial pressure gradients for O2 and CO2 have been plotted in graphic form in Fig 44-3 to emphasize that they are the key to gas movement and that O2 “flows downhill” from the air through the alveoli and blood into the tissues whereas CO2 ”flows downhill” from the tissues to the alveoli.
However, the amount of both of these gases transported to and from the tissues would be grossly inadequate if it were not that about 99% O2 which dissolves in the blood combines with the O2 carrying protein hemoglobin and that about 94% of the CO2 which dissolves enters into a series of reversible chemical reactions, which convert it into other compounds. The presence of hemoglobin increases the O2 carrying capacity of the blood 70-fold, and the reactions of CO2 increase the blood CO2 content 17-fold (Table 4).
Table 4. Gas content of blood.
|
Gas |
Ml/dl of blood containing |
|||
|
Arterial blood (PO2 |
Venous blood (PO2 |
|||
|
Dissolved |
Combined |
Dissolved |
Combined |
|
|
O2 |
0.23 |
19.5 |
0.12 |
15.1 |
|
CO2 |
2.62 |
46.4 |
2.98 |
49.7 |
|
N2 |
0.96 |
0 |
0.98 |
0 |
Oxygen Delivery to the Tissues. The O2 delivery system in the body consists of the lungs and the cardiovascular system. O2 delivery to a particular tissue depends on the amount of O2 entering the lungs, the adequacy of pulmonary gas exchange, the blood flow to the tissue, and the capacity of the blood to carry O2. The blood flow depends on the degree of constriction of the vascular bed in the tissue and the cardiac output. The amount of O2 in the blood is determined by the amount of dissolved O2, the amount of hemoglobin in the blood, and the affinity of the hemoglobin for O2.
OXYGEN TRANSPORT
Reaction of Hemoglobin & Oxygen. The dynamics of the reaction of hemoglobin with O2 make it a particularly suitable O2 carrier. Hemoglobin is a protein made up of 4 subunits, each of which contains a hem moiety attached to a polypeptide chain. Hem is a complex made up of porphyry and 1 atom of ferrous iron. Each of the 4 iron atoms can bind reversibly one O2 molecule. The iron stays in the ferrous state, so that the reaction is an oxygenation, not an oxidation. When hemoglobin takes up a small amount of O2, the R state is favored and additional uptake of O2 is facilitated. This is why the oxygen hemoglobin dissociation curve, the curve relating percentage saturation of the O2-carrying power of hemoglobin to the P.O2, has a characteristic sigmoid shape. Combination of the first hem in the Hb molecule with O2 increases the affinity of the second hem for O2, and oxygenation of the second increases the affinity of the third, etc, so that the affinity of Hb for the fourth O2 molecule is many times that for the first. When hemoglobin takes up O2, the 2/3 chains move closer together; when O2 is given up, they move further apart. This shift is essential for the shift in affinity for O2 to occur. When blood is equilibrated with 100% O2 (P.O2 = 760 mm Hg), the normal hemoglobin becomes 100% saturated. When fully saturated, each gram of hemoglobin contains 1.34 ml of O2. The hemoglobin concentration iormal blood is about 15 g/dl (14 g/dl in women and 16 g/dl in men). Therefore, 1 dl of blood contains 20.1 ml (1.34 ml x 15) of O2 bound to hemoglobin when the hemoglobin is 100% saturated. The amount of dissolved O2 is a linear function of the P.O2 (0.003 ml/dl blood/mm Hg PO2). In vivo, the hemoglobin in the blood at the ends of the pulmonary capillaries is about 97.5% saturated with O2 (PO2= 97 mm Hg). Because of a slight admixture with venous blood that bypasses the pulmonary capillary (“physiologic shunt”), the hemoglobin in systemic arterial blood is only 97% saturated. The arterial blood therefore contains a total of about 19.8 mL of O2 per deciliter: 0.29 ml in solution and 19.5 ml bound to hemoglobin. In venous blood at rest, the hemoglobin is 75% saturated, and the total O2 content is about 15.2 ml/dl.
Thus, at rest the tissues remove about 4.6 ml of O2 from each deciliter of blood passing through them (Table 44-4); 0.17 ml of this total represents O2 that was in solution in the blood, and the remainder represents O2 that was liberated from hemoglobin. In this way, 250 ml of O2 per minute is transported from the blood to the tissues at rest.
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Figure 5. Oxygen hemoglobin dissociation curve pH 7,40. temperature 380.
Factors Affecting the Affinity of Hemoglobin for Oxygen. Three important conditions affect the oxygen hemoglobin dissociation curve: the pH, the temperature, and the concentration of 2,3-diphosphoglycerate (DPG; 2,3-DPG). A rise in temperature or a fall in pH shifts the curve to the right (Fig 6).
When the curve is shifted in this direction, a higher P.O2; is required for hemoglobin to bind a given amount of O2. Conversely, a fall in temperature or a rise in pH shifts the curve to the left, and a lower P O2 is required to bind a given amount of O2. A convenient index of such shifts is the P50, the P O2 at which the hemoglobin is half saturated with O2; the higher the P50, the lower the affinity of hemoglobin for O2.
Figure 6. Effect temperature and pH on hemoglobin dissociation curve.
The decrease in O2 affinity of hemoglobin when the pH of blood falls is called the Bohr effect and is closely related to the fact that deoxyhemoglobin binds H+ more actively than does oxyhemoglobin.
The pH of blood falls as its CO2 content increases , so that when the PCO2 rises, the curve shifts to the right and the P50 rises. Most of the unsaturation of hemoglobin that occurs in the tissues is secondary to the decline in the P O2, but an extra 1-2% unsaturation is due to the rise in P.CO2 and consequent shift of the dissociation curve to the right.
2,3-DPG is very plentiful in red cells. It is formed from 3-phosphoglyceraldehyde, which is a product of glycolysis via the Embden-Meyerhof pathway. It is a highly charged anion that binds to the Beta chains of deoxygenated hemoglobin but not to those of oxyhemoglobin. One mole of deoxygenated hemoglobin binds 1 mole of 2,3-DPG. In effect:
HbO2 + 2,3-DPG =Hb-2,3-DPG + O2
In this equilibrium, an increase in the concentration of 2,3-DPG shifts the reaction to the right, causing more O2 to be liberated. ATP binds to deoxygenated hemoglobin to a lesser extent, and some other organic phosphates bind to a minor degree.
Factors affecting the concentration of 2,3-DPG in the red cells include pH. Because acidosis inhibits red cell glycolysis, the 2,3-DPG concentration falls when the pH is low. Thyroid hormones, growth hormone, and androgens increase the concentration of 2,3-DPG and the P50.
Myoglobin. Myoglobin is an iron-containing pigment found in skeletal muscle. It resembles hemoglobin but binds one rather than 4 mol of O2 per mole. Its dissociation curve is a rectangular hyperbola rather than a sigmoid curve. Because its curve is to the left of the hemoglobin curve (Fig 44-5), it takes up O2 from hemoglobin in the blood.
It releases O2 only at low P.O2 values, but the P O2 in exercising muscle is close to zero. The myoglobin content is greatest in muscles specialized for sustained contraction.
Figure 44-5. Dissociation curve of hemoglobin and myoglobin at 380, pH 7,40.
The muscle blood supply is compressed during such contractions, and myoglobin may provide O2 when blood flow is cut off. There is also evidence that myoglobin facilitates the diffusion of O2 from the blood to the mitochondria, where the oxidative reactions occur.
· REGULATION OF RESPIRATION
· 2. Respiration is regulated by two mechanisms:Nervous or neural mechanismChemical mechanismNervous Mechanism: It involves respiratory centers, afferent and efferent nerves.Respiratory centers: The centres in the medulla oblongata and pons that collects sensory information about the level of oxygen and carbon dioxide in the blood and determines the signals to be sent to the respiratory muscles.Stimulation of these respiratory muscles provide respiratory movements which leads to alveolar ventilation.Respiratory centers are situated in the reticular formation of the brainstem and depending upon the situation in brainstem, the respiratory centers are classified into two groups:Medullary centersPontine centers
· 3. There are two centers in each group:Medullary Centers:Inspiratory centerExpiratory center Pontine Centers:Pneumotaxic centerApneustic center
· 4. Inspiratory center:Inspiratory center is situated in upper part of medulla oblongataThis center is also called dorsal group of respiratory neuronsIt is formed by nucleus of tractus solitariusFunction: it is concerned with inspiration. Expiratory center:It is situated in medulla oblongata anterior and lateral to the inspiratory centerIt is also called ventral group of respiratory neuronsIt is formed by neurons of nucleus ambiguous and nucleus retro ambiguous Function: this center is inactive during quiet breathing and inspiratory center is the active center, but during forced breathing or when the inspiratory center is inhibited it becomes active.
· 5. Pneumotaxic center:It is situated in upper Pons.It is formed by nucleus parabrachialis.Function: it controls medullary respiratory centers, particularly the inspiratory center through apneustic center. It always controls the activity of inspiratory center so that duration of inspiration is controlled.Apnuestic center:It is situated in lower Pons.Function: this center increases depth of inspiration by acting directly on the inspiratory center.
· 6. Nervous connections of respiratory centers:Afferent pathway:Respiratory center receive afferent impulses from different parts of the body according to movements of thoracic cage and lungs.From peripheral chemoreceptor and baroreceptor impulses are carried by glossopharyngeal and vagus nerves to respiratory center.Efferent pathway:Nerve fiber from respiratory center leaves the brain and descend in anterior part of lateral column of spinal cord.These nerve fibers terminate in the motor neurons in the anterior horn cells of the cervical and thoracic segments of spinal cord.From motor neurons two sets of nerve fiber arise which supplies particular muscle:Phrenic nerve fibers: supplies diaphragmThe intercostal nerve fibers: supplies intercostal muscles.
· 7. Factors affecting respiratory centers:Impulses from higher centers: impulses from higher center can stimulate or inhibit respiratory centers directly.Impulses from stretch receptors of lung:
· 8. Impulses from ‘J’ receptors of lungs: ‘J’ receptors are juxtacapillary receptors which are present in wall of the alveoli and have close contact with the pulmonary capillaries.These receptors get stimulated during conditions like pulmonary edema, pulmonary congestion, pneumonia as well as due to exposure of exogenous and endogenous chemicals like histamine, serotonin.Stimulation of ‘J’ receptor produces a reflex response called apnea.4) Impulses from irritant receptors of lungs:Irritant receptors are situated on the wall of bronchi and bronchioles of lungs.They got stimulated by harmful chemicals like ammonia and sulfur dioxide.Stimulation of irritant receptors produces reflex hyperventilation along with bronchospasm which prevents entry of harmful chemicals into the alveoli.
· 9. Impulses from Proprioceptors:Proprioceptors are the receptors which give response to the change in the position of different parts of the body.This receptors are situated in joints, muscles and tendons. They get stimulated during exercise and sends impulses to the cerebral cortex.Cerebral cortex in turn by activating medullary respiratory centres causes hyperventilation.6) Impulses from Thermoreceptors:Thermoreceptors give response to change in the body temperature.They are cutaneous receptors namely cold and warmthWhen this receptors get stimulated they send signals to cerebral cortexCerebral cortex in turn stimulates respiratory centres and causes hyperventilation.
· 10. Impulses from pain receptors:Pain receptors give response to pain stimulus.Like other receptors this receptors also send impulses to the cerebral cortex.Cerebral cortex in turn stimulates the respiratory centers ad causes hyperventilation.8) Cough reflex:This is a protective reflex caused by irritation of parts of the respiratory tract beyond nose like larynx, trachea and bronchi.Irritation of any of this part causes stimulation of vagus nerve and cough occurs.Cough begins with deep inspiration followed by forceful expiration with closed glottis.So the intrapleural pressure rises above
· 11. Sneezing reflex:It is also a protective reflex which occurs due to the irritation of nasal mucus membrane.During irritation of nasal mucus membrane, the olfactory receptors and trigeminal nerve endings present in the nasal mucosa are stimulated leading to sneezing.Sneezing starts with deep inspiration, followed by forceful expiratory effort with opened glottis and the irritants are expelled out of the respiratory tract.10) Deglutition reflex:During swallowing of the food, the respiration is arrested for a while.Temporary arrest of the respiration is called apnea and apnea which occurs during swallowing called swallowing apnea or deglutition apnea.This prevents entry of the food particles into the respiratory tract.
· 12. Chemical Mechanism:The chemical mechanism of the respiration is operated through the chemoreceptors.Chemoreceptors:They are the receptors which give response to change in the chemical constituents of blood like..HypoxiaHypercapneaIncreased hydrogen ions concentration (decreased blood pH)Chemoreceptors are classified into two groups:Central chemoreceptorsPeripheral chemoreceptors
· 13. Central chemoreceptorsThe chemoreceptors present in the brain are called central chemoreceptors.Situation:They are situated in deeper part of medulla oblongata, close to the dorsal group of neurons.This area is known as chemosensitivearea and neurons are called as chemoreceptors.They are in close contact with blood and CSF.Action:They are very sensitive to increase in hydrogen ion concentration.Hydrogen ion cannot cross the blood brain barrier and blood cerebrospinal fluid barrier.On the other hand if carbon dioxide increases in the blood as it is a gas it can cross both the barrier easily and after entering the brain it combines with water to form carbonic acid.As carbonic acid is unstable, it immediately dissociates into hydrogen and bicarbonate ions.The hydrogen ioow stimulates the central cemoreceptors which stimulates dorsal group of respiratory center (inspiratory group) and increase rate and force of breathing.
· 14. Peripheral chemoreceptors:Situation:The receptors are present in peripheral portions of the body that’s why called as peripheral chemoreceptors.Action:They are very sensitive to reduction in partial pressure of oxygen.Whenever, the partial pressure of oxygen decreases these chemoreceptors become activated and send impulses to inspiratory center and stimulate them.Thereby increases rate and force of respiration and rectifies the lack of oxygen.
NEURAL CONTROL OF BREATHING
Control Systems. Spontaneous respiration is produced by rhythmic discharge of the motor neurons that innervate the respiratory muscles. This discharge is totally dependent on nerve impulses from the brain; breathing stops if the spinal cord is transected above the origin of the premix nerves.
The pattern of motor stimuli during breathing can be divided into inspiratory and expiratory phases. Inspiration shows a sudden, ramped increase in motor discharge to the inspiratory muscles (including pharyngeal dilator muscles). Before the end of inspiration, there is a decline in motor discharge. Exhalation is usually silent, except at high minute ventilation rates.
The mechanism of generation of the ventilatory pattern is not completely understood, but involves the integration of neural signals by respiratory control centers in the medulla and pons. The nuclei known to be involved are divided into regions known as the following:
· medulla (reticular formation)
o ventral respiratory group (nucleus retroambigualis, nucleus ambigus, nucleus parambigualis and the pre-Bötzinger complex). The ventral respiratory group controls voluntary forced exhalation and acts to increase the force of inspiration.
o dorsal respiratory group (nucleus tractus solitarius). The dorsal respiratory group controls mostly inspiratory movements and their timing.
· pons
§ Coordinates transition between inhalation and exhalation
§ Sends inhibitory impulses to the inspiratory area
§ The pneumotaxic center is involved in fine tuning of respiration rate.
§ Coordinates transition between inhalation and exhalation
§ Sends stimulatory impulses to the inspiratory area – activates and prolongs inhalate (long deep breaths)
§ overridden by pneumotaxic control from the apneustic area to end inspiration
There is further integration in the anterior horn cells of the spinal cord.[citatioeeded]
Control of ventilatory pattern
Ventilation is normally controlled by the autonomic nervous system, with only limited voluntary override. An exception to this is Ondine’s curse, where autonomic control is lost.
Two separate neural mechanisms regulate respiration. One is responsible for voluntary control and the other for automatic control. The voluntary system is located in the cerebral cortex and sends impulses to the respiratory motor neurons via the corticospinal tracts. The automatic system is located in the pons and medulla, and the motor outflow from this system to the respiratory motor neurons is located in the lateral and ventral portions of the spinal cord.
The motor neurons to the expiratory muscles are inhibited when those supplying the inspiratory muscles are active, and vice versa. These reciprocal innervations are not due to spinal reflexes and in this regard differ from the reciprocal innervations of the limb flexors and extensors. Instead, impulses in descending pathways that excite agonists also inhibit antagonists, probably by exciting inhibitory interneurons.
Medullary Centers.Rhythmic discharge of neurons in the medulla oblongata produces automatic respiration. Respiratory neurons are of 2 types: those that discharge during inspiration (I neurons) and those that discharge during expiration (E neurons). Many of these discharge at increasing frequencies during inspiration, in the case of I neurons, or during expiration, in the case of E neurons. Some discharge at decreasing frequencies, and some discharge at the same high rate during inspiration or expiration. I neurons are actively inhibited during expiration, E neurons durin
g inspiration.
The area in the medulla that is concerned with respiration has classically been called the respiratory center, but there are actually 2 groups of respiratory neurons (Fig 45-1). The dorsal group of neurons near the nucleus of the tracts solitaries is the source of rhythmic drive to the centra lateral premix motor neurons. These neurons also project to and drive the ventral group. This group has 2 divisions. The cranial division is made up of neurons in the nucleus ambiguous that innervate the ipsilateral accessory muscles of respiration, principally via the vagus nerves. The caudal division is made up of neurons in the nucleus retroambigualis that provide the inspiratory and expiratory drive to the motor neurons supplying the intercostal muscles. The paths from these neurons to expiratory motor neurons are crossed, but those to inspiratory motor neurons are both crossed and uncrossed.
Pontine & Vagal Influences. The rhythmic discharge of the neurons in the respiratory center is spontaneous, but it is modified by centers in the pons and by afferents in the vagus nerves from receptors in the lungs. The interactions of these components can be analyzed by evaluating the results of the experiments summarized diagrammatically in Fig .
Complete transaction of the brain stem below the medulla (section D in Fig ) stops all respiration. When all of the cranial nerves (including the vagi) are cut and the brain stem is transected above the pons (section A in Fig 45-1), regular breathing continues. However, when an additional transaction is made in the inferior portion of the pons (section B in Fig 45-1), the inspiratory neurons discharge continuously and there is a sustained contraction of the inspiratory muscles. This arrest of respiration in inspiration is called apneusis. The area in the pons that prevents apneusis is called the pneumotaxic center and is located in the nucleus parabrachialis. The area in the caudal pons responsible for apneusis is called the apneustic center.
Figure. Respiratory neurons in the brain stem. Dorsal view of brain stem; cerebellum removed. The effects of transecting the brain stem at various levels are also shown. The spirometer tracing at the right indicate the depth and rate of breathing, and the letters identify the level transaction. DRG, dorsal group of respiratory neurons; VRG, ventral group of respiratory neurons; NPBL, nucleus parabrachialis (pneumotaxic center); APC, apneustic center; 4th vent, fourth ventricle; IC, inferior colliculus, CP, middle cerebellar pedumcle. (Modified reproduced, with permission, from Mitchell R A, Berger A: State of the art. Review of neural regulation of raspiration/ am. Rev Respir. Dis. 1975;111-206.)
When the brain stem is transected in the inferior portion of the pons and the vagus nerves are left intact, regular respiration continues. In an apneustic animal, stimulation of the proximal stump of one of the cut vagi produces, after a moderate latent period, a relatively prolonged inhibition of inspiratory neuron discharge. There are stretch receptors in the lung parenchyma that relay to the medulla via afferents in the vagi, and rapid inflation of the lung inhibits inspiratory discharge (Hering-Breuer reflex). Thus, stretching of the lungs during inspiration reflexly inhibits inspiratory drive, reinforcing the action of the pneumotaxic center in producing intermittency of inspiratory neuron discharge. This is why the depth of inspiration is increased after vagotomy in otherwise intact experimental animals, although breathing continues as long as the pneumotaxic center is intact.
When all pontine tissue is separated from the medulla (section C in Fig 45-1), respiration continues whether or not the vagi are intact. This respiration is somewhat irregular and gasping, but it is rhythmic. Its occurrence demonstrates that the respiratory center neurons are capable of spontaneous rhythmic discharge.
The precise physiologic role of the pontine respiratory areas is uncertain, but they apparently make the rhythmic discharge of the medullary neurons smooth and regular. It appears that there are topically discharging neurons in the apneustic center which drive inspiratory neurons in the medulla, and these neurons are intermittently inhibited by impulses in afferents from the pneumotaxic center and vagal afferents.
REGULATION OF RESPIRATORY CENTER ACTIVITY
Ventilatory rate (minute volume) is tightly controlled and determined primarily by blood levels of carbon dioxide as determined by metabolic rate. Blood levels of oxygen become important in hypoxia. These levels are sensed by chemoreceptors in the medulla oblongata for pH, and the carotid and aortic bodies for oxygen and carbon dioxide. Afferent neurons from the carotid bodies and aortic bodies are via the glossopharyngeal nerve (CN IX) and the vagus nerve (CN X), respectively.
Levels of CO2 rise in the blood when the metabolic use of O2 is increased beyond the capacity of the lungs to expel CO2. CO2 is stored largely in the blood as bicarbonate (HCO3–) ions, by conversion first to carbonic acid (H2CO3), by the enzyme carbonic anhydrase, and then by disassociation of this acid to H+ and HCO3–. Build-up of CO2 therefore causes an equivalent build-up of the disassociated hydrogen ion, which, by definition, decreases the pH of the blood.
During moderate exercise, ventilation increases in proportion to metabolic production of carbon dioxide. During strenuous exercise, ventilation increases more than needed to compensate for carbon dioxide production. Increased glycolysis facilitates release of protons from ATP and metabolites lower pH and thus increase breathing.
Mechanical stimulation of the lungs can trigger certain reflexes as discovered in animal studies. In humans, these seem to be more important ieonates and ventilated patients, but of little relevance in health. The tone of respiratory muscle is believed to be modulated by muscle spindles via a reflex arc involving the spinal cord.
Drugs can greatly influence the control of respiration. Opioids and anaesthetic drugs tend to depress ventilation, especially with regards to carbon dioxide response. Stimulants such as amphetamines can cause hyperventilation.
Pregnancy tends to increase ventilation (lowering plasma carbon dioxide tension below normal values). This is due to increased progesterone levels and results in enhanced gas exchange in the placenta.
Ventilation is temporarily modified by voluntary acts and complex reflexes such as sneezing, straining, burping, coughing and vomiting.
Receptors play important roles in the regulation of respiration; central and peripheral chemoreceptors, and mechanoreceptors.
· Central chemoreceptors of the central nervous system, located on the ventrolateral medullary surface, are sensitive to the pH of their environment.[1][2]
· Peripheral chemoreceptors act most importantly to detect variation of the oxygen in the arterial blood, in addition to detecting arterial carbon dioxide and pH.
· Mechanoreceptors are located in the airways and parenchyma, and are responsible for a variety of reflex responses. These include:
o The Hering-Breuer reflex that terminates inspiration to prevent over inflation of the lungs, and the reflex responses of coughing, airway constriction, and hyperventilation.
o The upper airway receptors are responsible for reflex responses such as, sneezing, coughing, closure of glottis, and hiccups.
o The spinal cord reflex responses include the activation of additional respiratory muscles as compensation, gasping response, hypoventilation, and an increase in breathing frequency and volume.
o The nasopulmonary and nasothoracic reflexes regulate the mechanism of breathing through deepening the inhale. Triggered by the flow of the air, the pressure of the air in the nose, and the quality of the air, impulses from the nasal mucosa are transmitted by the trigeminal nerve to the breathing centres in the brainstem, and the generated response is transmitted to the bronchi, the intercostal muscles and the diaphragm.
In addition to involuntary control of respiration by the respiratory center, respiration can be affected by conditions such as emotional state, via input from the limbic system, or temperature, via the hypothalamus. Voluntary control of respiration is provided via the cerebral cortex, although chemoreceptor reflex is capable of overriding conscious control.
A rise in the P.CO2 or H+ concentration of arterial blood or a drop in its P.O2 increases the level of respiratory neuron activity, and changes in the opposite direction have a slight inhibitory effect. The effects of variations in blood chemistry on ventilation are mediated via respiratory chemoreceptors – receptor cells in the medulla and the carotid and aortic bodies sensitive to changes in the chemistry of the blood which initiate impulses that stimulate the respiratory center.
Superimposed on this basic chemical control of respiration, other afferents provide nonchemical controls for the fine adjustments that affect breathing in particular situations held constant, the effects of excess in the blood are combated, and the P.O2; is raised when it falls to a potentially dangerous level. (Table 2).
The respiratory minute volume is proportionate to the metabolic rate, but the link between metabolism and ventilation is CO2, not O2. The receptors in the carotid and aortic bodies are stimulated by a rise in the P CO2 or H+ concentration of arterial blood or a decline in its PO2. After denervation of the carotid chemoreceptors, the response to a drop in PO2; is abolished; the predominant effect of hypoxia after denervation of the carotid bodies is a direct depression of the respiratory center.
Table 2. Stimuli affecting the respiratory center
|
Chemical control |
|
|
CO2 |
Via CSF H+ concentration |
|
O2 |
Via carotid and aortic bodies |
|
H+ |
|
|
Nonchemical control |
|
|
Afferents from proprioceptors |
|
|
Afferents from pharynx, trachea, and bronchi for sneezing, coughing, and swolowing |
|
|
Vagal afferents from inflation and deflation receptors |
|
|
Afferents from baroreceptors: arterial, ventricular, pulmonary |
|
The response to changes in arterial blood H+ concentration in the pH 7.3-7.5 range is also abolished, although larger changes exert some effect. The response to changes in arterial P.CO2 is affected only slightly; it is reduced no more than 30-35%.
Carotid & Aortic Bodies.There is a carotid body near the carotid bifurcation on each side, and there are usually 2 or more aortic bodies near the arch of the aorta. Each carotid and aortic body (glomus) contains islands of 2 types of cells, type I and type II cells, surrounded by fenestrated sinusoidal capillaries.
NONCHEMICAL INFLUENCES ON RESPIRATION
Afferents from “Higher Centers”.
There are afferents from the neocortex to the motor neurons innervating the respiratory muscles, and even though breathing is not usually a conscious event, both inspiration and expiration are under voluntary control. Pain and emotional stimuli affect respiration, so there must also be afferents from the limbic system and hypothalamus.
Since voluntary and automatic control of respiration is separate, automatic control is sometimes disrupted without loss of voluntary control. The clinical condition that results has been called Ondine’s curse. In German legend, Ondine was a water nymph who had an unfaithful mortal lover. The king of the water nymphs punished the lover by casting a curse upon him that took away all his automatic functions. In this state, he could stay alive only by staying awake and remembering to breathe. He eventually fell asleep from sheer exhaustion and his respiration stopped. Patients with this intriguing condition generally have disease processes that compress the medulla or bulbar poliomyelitis. The condition has also been inadvertently produced in patients who have been subjected to bilateral anterolateral cervical cordotomy for pain. This cuts the pathways that bring about automatic respiration while leaving the voluntary efferent pathways in the corticospinal and rubrospinal tracts intact.
Afferents from Proprioceptors. Carefully controlled experiments have shown that active and passive movements of joints stimulate respiration, presumably because impulses in afferent pathways from proprioceptors in muscles, tendons, and joints stimulate the inspiratory neuron. This effect probably helps increase ventilation during exercise.
Responses to Irritation of the Air Passages. Sneezing and coughing are reflex responses to irritation of receptors in the mucosa of the large respiratory passages. Irritation of the walls of the trachea or large bronchi produces coughing, which begins with a deep inspiration followed by forced expiration against a closed glottis. This increases intrapleural pressure to
Other Pulmonary Receptors. The vagally mediated inhibition of inspiration produced by inflation of the lung has been mentioned above. The response is due to stimulation of stretch receptors located in the smooth muscle of the airways. Pulmonary deflation receptors that trigger inflation have also been described, and the expiratory and inspiratory reflex responses to pulmonary inflation and deflation, respectively, have been known as the Hering-Breuer reflexes. However, the deflation receptors respond better to pulmonary congestion and embolization, producing shallow, rapid breathing, and they have come to be called J receptors instead, because of their juxtacapillary location. There are also lung irritant receptors located between the epithelial cells in the bronchi and bronchioles. When stimulated, they initiate hyperventilation and bronchoconstriction, but their function iormal breathing is not known.
Respiratory Components of Other Visceral Reflexes.
The respiratory adjustments during vomiting, swallowing and gagging; inhibition of respiration and closure of the glottis during these activities not only prevent the aspiration of food or vomitus into the trachea but, in the case of vomiting, fix the chest so that contraction of the abdominal muscles increases the intra-abdominal pressure. Similar glottis closure and inhibition of respiration occur during voluntary and involuntary straining.
Hiccup is a spasmodic contraction of the diaphragm that produces an inspiration during which the glottis suddenly closes. The glottis closure is responsible for the characteristic sensation and sound. Yawning is a peculiar “infectious” respiratory act the physiologic basis and significance of which are uncertain. However, under ventilated alveoli have a tendency to collapse, and it has been suggested that the deep inspiration and stretching open them alveoli and prevent the development of atelectasis. Yawning also increases venous return to the heart.
Respiratory Effects of Baroreceptor Stimulation. Afferent fibers from the baroreceptors in the carotid sinuses, aortic arch, atria, and ventricles relay to the respiratory center as well as the vasomotor and cardioinhibitory centers in the medulla. Impulses in them inhibit respiration, but the inhibitory effect is slight and of little physiologic importance. The hyperventilation in shock is due to chemoreceptor stimulation caused by acidosis and hypoxia secondary to local stagnation of blood flow and is not baroreceptor mediated. The activity of the inspiratory neurons affects the blood pressure and heart rate and activity in the vasomotor center and the cardiac centers in the medulla may have minor effects on respiration.
Effect of irritant receptors in the airways.
Airway receptors. that may have some relevance to the effect of anesthetics include laryngeal and pulmonary irritant receptors and pulmonary stretch receptors. These receptors play an important role in the regulation of breathing patterns, laryngeal and pulmonary defense mechanisms, and bronchomotor tone. Irritant receptors are situated between airway epithelial cells and may mediate rapid reflex responses such as coughing, laryngospasm, bronchoconstriction, and mucus secretion following the induction of general anesthesia, abrupt increases in the inspired concentration of volatile anesthetics, and sudden mechanical deformation of the laryngotracheobronchial system.
Slow-adapting pulmonary stretch receptors, located within small airway smooth muscle (high concentratioear the carina), respond to stretching or changes in lung volume. Increases in lung volume increase afferent nerve traffic via the vagus nerve to the respiratory control center, thereby inhibiting further inspiration (the Hering-Breuer reflex). This limitation of inspiration elicited by pulmonary stretch receptors may determine the relationship between tidal volume and respiratory frequency, but unlike in animals, the Hering-Breuer reflex cannot be demonstrated in the awake resting human during normal tidal volume breathing. The alteration in ventilatory pattern by anesthetics has been attributed to sensitization of pulmonary stretch receptors, leading to lower tidal volumes and tachypnea. The presence of volatile anesthetics increased vagal afferent discharge at varying lung volumes in decerebrate cats (i.e., sensitization of pulmonary stretch receptors), but little evidence exists of such a mechanism in humans. There is evidence in the cat that halothane-induced tachypnea is primarily a suprapontine effect, but the mechanism of production of tachypnea with decreased tidal volume in anesthetized humans remains unclear.
The direct effects of halothane, isoflurane, and enflurane on pulmonary and laryngeal irritant receptors and on tracheobronchial slow-adapting stretch receptors have been investigated in spontaneously breathing and vagotomized, paralyzed dogs. All three volatile anesthetics increase the activity of laryngeal irritant receptors and inhibit pulmonary irritant receptors. In addition, the volatile anesthetics elevate the excitation threshold and increase the sensitivity of low-threshold stretch receptors. The inspiratory activity was augmented while the end-expiratory activity was greatly attenuated. The clinical implications of these findings have yet to be determined, but these anesthetic-induced changes may in part relate to effects on reducing bronchomotor tone.
It has been suggested that general anesthesia may result in posterior tongue displacement, producing upper airway obstruction; however, several recent studies do not confirm this. Anteroposterior displacement of upper airway structures occurs with changes in head position that are in the same direction as that of the mandible. In addition, general anesthesia and paralysis may widen the dimensions of the larynx, but the nasopharyngeal airway decreases in size. Volatile anesthetics produce a greater depression of the upper airway electromyogram or nerve activity as compared to that of the diaphragm in intact anesthetized, spontaneously breathing cats and in paralyzed, ventilated, vagotomized cats. The extent to which this depression of upper airway motoneuron activity is a result of an anesthetic-induced inhibition of the reticular activating system is unknown.
The epithelium of the trachea, bronchi, and bronchioles is supplied with sensory nerve endings that are stimulated by irritants that enter the respiratory airways. These cause coughing and sneezing. They possibly also cause bronchial constriction in such diseases as asthma and emphysema.
Function of Lung “J” Receptors. A few sensory nerve endings occur in the alveolar walls in Juxtaposition to the pulmonary capillaries, from whence comes the name “J” receptors. They are stimulated when irritant chemicals are injected into the pulmonary blood, and they are also excited when the pulmonary capillaries become engorged with blood or when pulmonary edema occurs in such conditions as congestive heart failure. Though the functional role of the J receptors is not known, their excitation perhaps does give the person a feeling of dyspnea.
Limitation of Inspiration by Lung Inflation Signals – the Hering-Breuer Inflation Reflex
This is a reflex triggered to prevent over-inflation of the lungs. Pulmonary stretch receptors present in the smooth muscle of the airways respond to excessive stretching of the lung during large inspirations.
Once activated, they send action potentials through large myelinated fibers of the paired vagus nerves to the inspiratory area in the medulla and apneustic area of the pons. In response, the inspiratory area is inhibited directly and the apneustic area is inhibited from activating the inspiratory area. This inhibits inspiration, allowing expiration to occur.
The Hering–Breuer inflation reflex ought not be confused with the deflation reflex discovered by the same individuals, Hering and Breuer. The majority of this page discusses the inflation reflex; the deflation reflex is considered separately at the end.
The Hering–Breuer inflation reflex, named for Josef Breuer and Ewald Hering, is a reflex triggered to prevent over-inflation of the lungs. Pulmonary stretch receptors present in the smooth muscle of the airways respond to excessive stretching of the lung during large inspirations.
Once activated, they send action potentials through large myelinated fibers[4] of the paired vagus nerves to the inspiratory area in the medulla and apneustic center of the pons. In response, the inspiratory area is inhibited directly and the apneustic center is inhibited from activating the inspiratory area. This inhibits inspiration, allowing expiration to occur.
The Hering–Breuer inflation reflex ought not be confused with the deflation reflex discovered by the same individuals, Hering and Breuer. The majority of this page discusses the inflation reflex; the deflation reflex is considered separately at the end.
Located in the walls of the bronchi and bronchioles throughout the lungs are stretch receptors that transmit signals through the vagi into the dorsal respiratory group of neurons when the lungs become overstretched. These signals affect inspiration in much the same way as signals from the pneumotaxic center; that is, they limit the duration of inspiration (Figure 45-3).
Therefore, when the lungs become overly inflated, the stretch receptors activate an appropriate feedback response that “switches off” the inspiratory ramp and thus limits further inspiration. This is called the Hering-Breuer inflation reflex. This reflex also increases the rate of respiration because of the reduced period of inspiration, the same as is true for signals from the pneumotoxic center.
Figure 3. Effect of vagal stimulation (between arrows) on discharge rate in phrenic nerve fibers in an “isolated inspiratory center preparation.” The cat had been prepared by cutting both vagi and transecting the medulla at the caudal border of the pons, this cutting off the pneumotaxic center. In A, the continuous discharge of the inspiratory neurons is shown. In B and C, stimulation of the proximal stump of one vagus produces, after a considerable latent period, inhibition of inspiratory discharge. The animal exhales when the inspiratory discharge stops, as is shown by the record of respiratory excursions (upper line in B and C; inspiration upward).
However, in human beings, the Hering-Breuer reflex probably is not activated until the tidal volume increases to greater than approximately
EFFECTS OF EXERCISE
We breathe oxygen into the body from the atmosphere. While this oxygen does not itself contain useable energy, it is the key that unlocks the energy stored in previously-ingested food. As the energy demands of the contracting muscles change during exercise, so must their energy and oxygen provision. But oxygen comprises only 21% of the atmospheric air; one therefore needs to inhale a volume of air each minute which is at least five times the volume of oxygen which is being absorbed out of the lungs by the body.
Lung ventilation — the volume breathed in and out per minute — however, is not five times that of the rate of oxygen utilization for metabolism, rather, it is twenty-five times. This is because most of the oxygen is breathed back into the atmosphere during expiration: only 20% or so of the inspired oxygen is actually taken up by the blood coursing through the lungs en route to the cells.
The air taken into the lungs does not all reach the gas-exchange regions (the alveoli). Airways that conduct air to the alveoli do not themselves take part in this exchange: only the volume of air that gets beyond this dead space into the alveoli contributes to the gas exchange. Consequently the alveolar ventilation is less than the total ventilation — and this is the volume which provides the oxygen to be taken up into the body.
The alveolar oxygen concentration, and its equivalent oxygen pressure, is determined by the balance between the supply of oxygen to the alveoli and the demand for its uptake into the blood: the alveolar ventilation per minute and the oxygen consumption per minute. The alveolar oxygen pressure in turn establishes the oxygen pressure in the arterial blood, which is normally maintained at, or close to, a constant level during exercise, the same level as when at rest, despite the body’s oxygen consumption increasing more than 10-fold. This can only be achieved if the alveolar ventilation increases proportionally. Normally it does so, increasing so that it maintains a ratio of about twenty times the oxygen uptake rate, for moderate exercise, with the ratio for total ventilation being about twenty five.
While this characterizes the ventilatioeeded to maintain the level of oxygen in the arterial oxygen, it may or may not be appropriate for the other vital breathing requirement during exercise — the defence of blood and tissue acidity.
The exercise-induced challenge to the body’s acidity levels has two different origins. Firstly, foodstuffs that serve as energy sources for exercise (carbohydrates and fats) are composed entirely of hydrogen, carbon, and oxygen atoms. During the progressive metabolic fragmentation of food molecules, hydrogen atoms are stripped away, to link with oxygen, yielding energy.
For example, for glucose:
C6H 12O6 + 6O2 → 6H2O + 6CO2
This leaves the carbon and oxygen to be vented into the atmosphere as carbon dioxide. As the body’s carbon dioxide production from this source is normally approximately equal to its oxygen consumption during exercise, the same level of ventilation can serve both purposes: intake and exhaust. However, if ventilation does not increase sufficiently during exercise, the oxygen level will fall in the blood and tissues, and the carbon dioxide level will rise. Such an increase in carbon dioxide would increase blood and tissue acidity.
The body’s acidity is determined by the concentration of hydrogen ions [H+] — the positively-charged protons which form the nuclei of the smallest of all atoms. An increase in carbon dioxide in body fluids increases the concentration of [H+]. For [H+] to be stabilized in the arterial blood leaving the lungs, the carbon dioxide level needs to be regulated by exhaling the carbon dioxide at a rate equivalent to its production rate
Normally, for moderate exercise, ventilation does indeed increase in proportion to the increased metabolic rate, thereby maintaining arterial blood levels of both oxygen and carbon dioxide (and hence [H+]) at, or close to, resting levels. This control is mediated through an interaction of neural and blood-borne mechanisms. The neural mechanisms which lead to muscle contraction also simultaneously signal the breathing control centres of the brain; these receive neural information from the contracting muscles as well. If the resulting drive to breathe is not appropriate, then an ‘error’ in the arterial oxygen, carbon dioxide, and [H+] levels is sensed by chemoreceptors which ‘sample’ the blood in the carotid arteries perfusing the brain. This provides the ‘fine tuning’ of the control system.The second challenge to arterial [H+] stability occurs only at higher work rates, where the energy demands cannot be met entirely through aerobic (i.e. oxygen-linked) metabolism. At these work rates the aerobic transfer of energy is supplemented by degradation of carbohydrates to lactic acid — present in the form of a lactate ion [L–] and [H+]. This component is anaerobic metabolism (it utilizes no oxygen). The fitter the subject, the higher the work rate at which it begins to contribute (see figure). The resulting increase in [H+] has a number of deleterious effects on exercise tolerance: impaired muscle contraction; perception of limb fatigue; and ‘shortness of breath’.
As exercise continues at this high intensity, the body’s acidity level can only be maintained (or its increase constrained) if the carbon dioxide-related component of the acidity is reduced. The body therefore ‘compensates’ by increasing ventilation proportionally more relative to carbon dioxide production. This reduces alveolar and arterial carbon dioxide levels (see figure) as a result of the increased carbon dioxide ‘washout’. Clearly, the greater the amount of carbon dioxide ‘washed out’ under these conditions, the less will be the increase in acidity for any given level of lactic acid production.
The additional drive to breathe which is linked to the increased lactic acid levels is thought to result predominantly from the effects of the [H+] (and other mediators such as potassium ions released from the active muscles) stimulating the carotid chemoreceptors. Neither hydrogen ions nor potassium ions readily cross the blood-brain barrier, so they do not stimulate the other chemoreceptors on the surface of the brain stem (which in other circumstances also influence ventilation).The increase in ventilation during exercise could, theoretically, be accomplished by an infinite variety of depths (tidal volumes) and number (breathing frequency) of breaths per minute. Very deep and slow breathing requires extra effort because the thorax, and the lungs in particular, become very stiff at high volumes. Rapid shallow breathing, on the other hand, mostly ventilates the dead space. The spontaneously-chosen pattern is typically the one which most effectively combines low breathing effort with a high fraction of the breaths reaching the alveoli. Consequently, most people initially increase ventilation predominantly by increasing tidal volume up to a certain optimal maximum; higher ventilatory demands are then achieved predominantly by increasing breathing frequency. In many sporting events, however (e.g. swimming, rowing, and even running), athletes must, or choose to, link the duration of each breath to the cadence of their limb motions.
Profiles of response of ventilation and arterial lactate and carbon dioxide levels to exercise that progressively increases to the limit of the subject’s tolerance. The dashed line represents a subject of normal fitness, the solid line represents an athlete capable of achieving higher levels of oxygen consumption. The solid circle and the open circle represents the levels at which the subjects begin to increase their lactic acid production. Maximum possible ventilation shows the highest level that can be achieved by these subjects
Physical training or increased fitness does little to improve the lung as a mechanical pump or gas exchanger, unlike the beneficial effects of exercise on skeletal muscles and the heart. Luckily, however, the limits of operation of the lungs normally far exceed the demands placed upon them. For example, at maximum levels of exercise, not only is full blood oxygenation maintained iormal subjects, but also ventilation has not reached a maximum: it can be increased further by volitional effort (see figure). Elite athletes may be different in this regard. The unusually high metabolic rates they can achieve require unusually high levels of ventilation and of blood flow through the lungs. Those athletes who have not been graced by their genetic make-up to have large lungs with large airways (allowing high levels of airflow), and large capillary volumes (allowing the high cardiac output of rapidly-flowing blood to be exposed to the gas-exchange surface at the alveoli long enough for oxygenation to be completed), can show a component of ‘pulmonary limitation’ to exercise. This is manifest, only at a very high work rates, by airflow rate reaching a limiting maximum, and by a reduction in arterial oxygenation — but only in those without the appropriate genetically-superior lung structure.
Normal individuals also experience ‘shortness of breath’ (dyspnoea) during exercise. This is quite modest at low work rates — except when the carotid chemoreceptors are sensitized, such as during sojourns at high altitude. At high work rates the dyspnoea is usually more marked and sustained. There is a narrow range of work rates — high but usually sustainable for long periods — for which dyspnoea develops but which then subsides as the exercise continues. This relief of dyspnoea has been termed second wind. This proves difficult to reproduce in the laboratory; consequently its mechanisms are poorly understood. Reduction in the lactic acid-related drive to breathe, as aerobic mechanisms catch up with the high-energy demands, is likely to be contributory.
Many cardiovascular and respiratory mechanisms must operate in an integrated fashion if the O2 needs of the active tissues are to be met and the extra CO2 and heat removed from the body during exercise. An increase in ventilation provides extra O2, eliminates some of the heat, and excretes extra CO2; circulatory changes increase muscle blood flow while maintaining an adequate circulation in the rest of the body, and there is an increase in the extraction of O2 from the blood in muscle.
Changes in Ventilation
During exercise, the amount of O2 entering the blood in the lungs is increased because the amount of O2 added to each unit of blood and the pulmonary blood flow per minute are increased. The PO2 of blood flowing into the pulmonary capillaries falls from 40mm Hg to
Figure 1.Relation between work load, blood lactic acid, and O2 uptake. I-VI, increasing work loads produced by increasing the speed and grade of treadmill on which the subjects worked.
The total amount of O2 entering the blood therefore increases from 250 ml/min at rest to values as high as 4000 ml/min. The amount of CO2 removed from each unit of blood is increased, and CO2 excretion increases from 200 ml/min to as much as 8000 ml/min. The increase in O2 uptakes is proportionate to work load up to a maximum. Above this maximum, O2 consumption levels off and the blood lactic acid level rises precipitously.
The lactic acid comes from muscles in which aerobic resynthesis of energy stores cannot keep pace with their utilization and an oxygen debt is being incurred.
There is an abrupt increase in ventilation with the onset of exercise, followed by a further, more gradual increase .
With moderate exercise, the increase is due mostly to an increase in the depth of respiration; this is accompanied by an increase in the respiratory rate when the exercise is more strenuous.
Figure 2. Change in ventilation during exercise.
There is an abrupt decrease in ventilation when exercise ceases, followed by a more gradual decline to preexercise values. The abrupt increase at the start of exercise is presumably due to psychic stimuli and afferent impulses from proprioceptors in muscles, tendons, and joints. The more gradual increase is presumably humeral even though arterial pH, P.CO2 and P.O2 remain constant during moderate exercise. The increase in ventilation is proportionate to the increase in O2 consumption, but the mechanisms responsible for the stimulation of respiration are still the subject of much debate. The increase in body temperature may play a role. In addition, it may be that the sensitivity of the respiratory center to CO2 is increased or that the respiratory fluctuations in arterial P.CO2 increase so that, even though the mean arterial P.CO2 does not rise, it is C02 that is responsible for the increase in ventilation. O2 also seems to play some role despite the lack of a decrease in arterial P.O2 since, during the performance of a given amount of work, the increase in ventilation while breathing 100% O2 is 10-20% less than the increase while breathing air .
Thus, it currently appears that a number of different factors combine to produce the increase in ventilation seen during moderate exercise.
When exercise becomes more severe, buffering of the increased amounts of lactic acid that are produced liberates more CO2, and this further increases ventilation.
Figure 3. Effect of 100% O2 on ventilation during work at various levels on the bicycle ergometer.
With increased production of acid, the increases in ventilation and CO2 production remain proportionate, so alveolar and arterial CO2 change relatively little (isocapnic buffering). The additional increase in ventilation produced by the acidosis is dependent on the carotid bodies and does not occur if they are removed.
The respiratory rate after exercise does not reach basal levels until the O2 debt is repaid. This may take as long as 90 minutes. The stimulus to ventilation after exercise is not the arterial PCO2, which is normal or low, or the arterial PO2, which is normal or high, but the elevated arterial H+ concentration due to the lactic acidemia. The magnitude of the O2 debt is the amount by which O2 consumption exceeds basal consumption from the end of exertion until the O2 consumption has returned to preexercise basal levels. Because of the extra CO2 produced by the buffering of lactic acid during strenuous exercise, the R rises, reaching 1.5-2.0. After exertion, while, the O2 debt is being repaid, the R falls to 0.5 or less.
Changes in the Tissues
During exercise, the contracting muscles use more O2 and the tissue PO2; falls nearly to zero. More O2 diffuses from the blood, the blood PO2; of the blood in the muscles drops and more O2 is removed from hemoglobin. Because the capillary bed is dilated and many previously closed capillaries are open, the mean distance from the blood to the tissue cells is greatly decreased; this facilitates the movement of O2 from blood to cells.
The oxygen hemoglobin dissociation curve is steep in the PO2; range below
Hypoxia.
Hypoxia is O2 deficiencies at the tissue level. It is a more correct term than anoxia, there rarely being no O2 at all left in the tissues.
Traditionally, hypoxia has been divided into 4 types. Numerous other classifications are currently in use, but the 4-type system still has considerable utility if the definitions of the terms are kept clearly in mind. The 4 categories are as follows: (1) hypoxic hypoxia (anoxic anoxia), in which the PO2 of the arterial blood is reduced; (2) anemic hypoxia, in which the arterial P.O2 is normal but the amount of hemoglobin available to carry O2 is reduced; (3) stagnant or ischemic hypoxia, in which the blood flow to a tissue is so low that adequate O2 is not delivered to it despite a normal PO2; and hemoglobin concentration; and (4) histotoxic hypoxia, in which the amount of O2 delivered to a tissue is adequate but, because of the action of a toxic agent, the tissue cells cannot make use of the O2 supplied to them.
Effects of Hypoxia
The effects of stagnant hypoxia depend upon the tissue affected. In hypoxic hypoxia and the other generalized forms of hypoxia, the brain is affected first. A sudden drop in the inspired P.O2 to less than
by alcohol: impaired judgment, drowsiness, dulled pain sensibility, excitement, disorientation, loss of time sense, and headache. Other symptoms include anorexia, nausea, vomiting, tachycardia, and, when the hypoxia is severe, hypertension. The rate of ventilation is increased in proportion to the severity of the hypoxia of the carotid chemoreceptor cells.
Respiratory Stimulation
Dyspnea is by definition difficult or labored breathing in which the subject is conscious of shortness of breath; hyperpnea is the general term for an increase in the rate or depth of breathing regardless of the patient’s subjective sensations. Tachypnea is rapid, shallow breathing. In general, a normal individual is not conscious of respiration until ventilation is doubled, and breathing is not uncomfortable (ie, the dyspnea point is not reached) until ventilation is tripled or quadrupled. Whether or not a given level of ventilation is uncomfortable also depends upon the respiratory reserve. This factor is taken into account in the dyspneic index.
Effects of Decreased Barometric Pressure
The composition of air stays the same, but the total barometric pressure falls with increasing altitude. Therefore, the PO2 also falls. At
Hypoxic Symptoms Breathing Air/
There are a number of compensatory mechanisms that operate over a period of time to increase altitude tolerance (acclimatization), but in unacclimatized subjects, mental symptoms such as irritability appeared about
Hypoxic Symptoms Breathing Oxygen. The total atmospheric pressure becomes the limiting factor in altitude tolerance when breathing 100% O2. The partial pressure of water vapor in the alveolar air is constant at
However, an artificial atmosphere can be created around an individual; in a pressurized suit or cabin supplied with O2 and a system to remove CO2, it is possible to ascend to any altitude and to live in the vacuum of interplanetary space.
At
Delayed Effects of High Altitude.
Many individuals, when they first arrive at a high altitude, develop transient “mountain sickness”. This syndrome develops 8-24 hours after arrival at altitude and lasts 4-8 days. It is characterized by headache irritability, insomnia, breathlessness, nausea and vomiting. Its cause is unknown, but the symptoms are reduced or prevented if alkalosis is reduced by procedures such as treatment with acetazolamide.
High altitude pulmonary edema and cerebral edema are serious forms of mountain sickness. Pulmonary edema is prone to occur in individuals who ascend quickly to altitudes above
Acclimatization.
Acclimatization to altitude is due to the operation of a variety of compensatory mechanisms. The respiratory alkalosis produced by the hyperventilation shifts the oxygen hemoglobin dissociation curve to the left, but there is a concomitant increase in red blood cell 2,3-DPG, which tends to decrease the O2 affinity of hemoglobin. The decrease in O2 affinities makes more O2 available to the tissues. However, it should be noted that the value of the increase in P50 is lost at very high altitudes, because when the arterial PO2 is markedly reduced, the decreased O2 affinity also interferes with O2 uptake by hemoglobin in the lungs.
The initial ventilatory response to increased altitude is relatively small, because the alkalosis tends to counteract the stimulating effect of hypoxia. However, there is a steady increase in ventilation over the next 4 days because the active transport of H+ into CSF, or possibly a developing lactic acidosis in the brain, causes a fall in CSF pH that increases the response to hypoxia. After 4 days, the ventilatory response begins to decline slowly, but it takes years of residence at higher altitudes for it to decline to the initial level. Associated with this decline is a gradual desensitization to the stimulatory effects of hypoxia.
Erythropoietin secretion increases promptly on ascent to high altitude and then falls somewhat over the following 4 days as the ventilatory response increases and the arterial PO2 rises. The increase in circulating red blood cells triggered by the erythropoietin begins in 2-3 days and is sustained as long as the individual remains at high altitude.
There are also compensatory changes in the tissues. The mitochondria, which are the site of oxidative reactions, increase iumber, and there is an increase in myoglobin that facilitates the movement of O2 in the tissues. There is also an increase in the tissue content of cytochrome oxidase.
The effectiveness of the acclimatization processes is indicated by the fact that in the Andes and
1. Mechanism of the first breath of child consists of:
irritation of central chemoreceptors by increasing CO2 tension
irritation of peripheral chemoreceptors by increasing CO2 tension
irritation of central chemoreceptor by lack of oxygen (hypoxia)
Gering-Brayer’s reflex
irritation of inspiratory neurons by afferent influences from thermo receptors of skin
2. What is the breathing frequency of newborn child?
14-16/min. a) 12-14/min. b) 18-20/min. c) 10-12/min. d) 25-30/min
1. Indicate three mechanisms of height acclimatization that are advantageous from the physiological point of view.
2. After previous hyperventilation time of being under water increases for 1-2 min. Why?
3. Two persons were examined. After a slight physical load it was determined that first one has breathing frequency (BF) of 16/min, volume of dead space of 150 ml, breath volume of 600 ml. The second one has BF of 24/min, volume of dead space of 150 ml, breath volume of 400 ml. What can you say about level of training of these people?
Hyperventilation, polycytaemia, increasing of quantity of capillaries in tissues, changes of intracellular activity of oxygenates enzymes.
During hyperventilation, as a result of decreasing of pCO2 and increasing of pO2 in alveolar air, some time is needed to reach the basic level of pCO2 and pO2 in alveolar air, when the person will stop breathing delay.
The first person has more effective breath because his active inhale (AI) is bigger while their respiratory minute volumes are equal. That’s why the first one is trained better.
Analysis of spirogram of persons of different age groups.
You have to determine BF, lung volume and capacity of lungs according to spirogram, given by the teacher. Put results into the table.
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Breathing frequency |
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Tidal volume |
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Inspiratory reserve volume |
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Expiratory reserve volume |
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Respiratory minute volume |
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Vital capacity |
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Influence of physical loads on human breathing
After five minutes of adaptation, on the device ПА 5-01, determine tidal volume, breathing frequency, respiratory minute volume. Then after 20 squats with the hands ahead of your trunk repeat the experiment in tree minutes. Put the results into the table.
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Breathing indices |
Before physical exercises |
After physical exercises |
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Breathing frequency |
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Tidal volume |
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Respiratory minute volume |
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TEMPERATURE REGULATION
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The human body has the remarkable capacity for regulating its core temperature somewhere between The external heat transfer mechanisms are radiation, conduction and convection and evaporation of perspiration. The process is far more than the passive operation of these heat transfer mechanisms, however. The body takes a very active role in temperature regulation. |
The temperature of the body is regulated by neural feedback mechanisms which operate primarily through the hypothalmus. The hypothalmus contains not only the control mechanisms, but also the key temperature sensors. Under control of these mechanisms, sweating begins almost precisely at a skin temperature of
· Vasoconstriction to decrease the flow of heat to the skin.
· Cessation of sweating.
· Shivering to increase heat production in the muscles.
· Secretion of norepinephrine, epinephrine, and thyroxine to increase heat production
· In lower animals, the erection of the hairs and fur to increase insulation.
Age Factors Very young and very old people are limited in their ability to regulate body temperature when exposed to environmental extremes. A newborn infant’s body temperature decreases if the infant is exposed to a cool environment for a long period. Elderly people also are not able to produce enough heat to maintain body temperature in a cool environment. With regard to overheating in these age groups, heat loss mechanisms are not fully developed in the newborn. The elderly do not lose as much heat from their skin as do younger people. Both groups should be protected from extreme temperatures.
