Tom and his group with great difficulty managed to climb the mountain, but before leaving they

had health checks including spirogram showed normal results and hemoglobin were also normal. After resting in place on the go, some members begin to experience hypoxia. The symptoms that they feel very different from the time of ride. Finally they decided to descend from a that height, because according to mountain climbing guide in reading, at high altitudes can occur that cause dyspnea hypoxia, decreased PCO2 and respiratory alkalosis. They do not know how the process. They finally decided to go down and after getting off them went to the doctor because some of them feel weak and dizzy. After the inspection is done, doctors recommend to check levels of hemoglobin, blood pH and PCO2. Tomi think what to do to climb the mountain with this examination.? He asked the doctor, "if shortness of breath can only happen because of climbing the mountain"? many other causes that can cause respiratory disorders "said the doctor.

Spirogram: graphic images of respiratory 2. Hypoxia: lack of O2 at the tissue situation 3. Dyspnea: heavy breathing 4. Respiratory alkalosis: the blood becomes alkaline because of rapid breathing and it causes the carbon dioxide levels to be low and the blood becomes alkaline 5. PCO2: partial pressure of carbon dioxide in the alveolar
1.

SCHEME
hypoxia Dyspnea, decrease in PCO2, respiratory alkal osis

Ventilation

Impaired ventilatio n contributing factor

alveoli

Lung

The principle of gas transportation

The mechanism of respiration regulation

Students are able to explain

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6.

Pulmonary ventilation. Alveolus ventilation. The principle of transport of the gas in blood. Respiratory control mechanism. Factor that causes ventilation disorders. The working principle spirometry.

The lungs can be expanded and contracted in two ways 1) By downward and upward movement of the diaphragm to lengthen or shorten the chest cavity. - during inspiration, contraction of the diagram pulls the lower surfaces of the lungs downward. - during expiration the diagram simply relaxes, and the elastic recoil of the lungs, chest wall, and abdominal structures compress the lungs and expels the air. 2) By elevation and depression of the ribs to increase and decrease the anteroposterior diameter of the chest cavity. - this method will expand the lungs in the natural resting position ,the ribs slant downward,thus allowing the sternum to fall backward toward the vertebral column. - the most important muscles that raise the rib cage the external intercostal but others that help are the:

1) sternocleidomastoid muscle which lift upward of the strenum. 2) anterior serrati which lift many of the ribs. 3) scaleni which lifts the first two ribs.
Pressures that cause the movement of air in and out of the lungs. 1. Pleural pressure pressure of the fluid in the thin space between the lungs pleura and chest wall pleura. 2. Alveolar pressure pressure of the air inside the lung alveoli. 3. Transpulmonary pressure the difference between the alveolar pressure and the pleural pressure. Compliance of the lungs That is the value at which the development of lung for each unit to increase the pressure of transpulmonery that determined by the lung elastic, elasticlung tissue caused by liquid surface tension which limits the inner wall of the alveoli.

Surfactant, surface tension, and collapse of the alveoli. a) Principle of surface tension. - When water forms a surface with air, the water molecules on the surface water has a very strong attraction to each other. - As a result, the water level is always attempting to contract. - This is what causes water to drip together, meaning there is a meeting of contractile membranes on the surface of the water molecules surrounding the drops. - This also happens on the inner surface of alveoli through the bronchi, and in doing so, also causes the alveoli trying to collapse. - Ultimately effect is causing the contraction of elastic around the elastic power of surface tension.

Surfactant and its effect on surface tension.

Surfactants are surface-active agents in water, which means that the surfactant is critical surface tension of water. Secreted by: alveolar epithelial cells type III, there are approximately 10% of the surface area of alveoli. These cells are granular, containing lipid inclusions that are secrete in the surfactant into the alveoli. Surfactant is a mixture of phospholipids, proteins, and ions. The most important substance is the phospholipid dipalmitoyl phosphatidylcholine, surfactant apoprotein and calcium ions. Normal fluid in the alveoli without surfactant: 50 dyne / cm. Fluid lining the alveoli with surfactant: 5-30 dyne / cm.

The ultimate importance of pulmonary ventilation is to continually renew the air in the gas exchange areas of the lungs, where air is in proximity to the pulmonary blood. These areas include the alveoli, alveolar sacs, alveolar ducts, and respiratory bronchioles. The rate at which new air reaches these areas is called alveolar ventilation. Dead Space and Its Effect on Alveolar Ventilation. Some of the air a person breathes never reaches the gas exchange areas but simply fills respiratory passages where gas exchange does not occur, such as the nose, pharynx, and trachea. This air is called dead space air because it is not useful for gas exchange. On expiration, the air in the dead space is expired first, before any of the air from the alveoli reaches the atmosphere. Therefore, the dead space is very disadvantageous for removing the expiratory gases from the lungs.

Determination of dead space Anatomic dead space (VD) Approximately 1 ml/lb body weight in normal adult. Neural reflexes, traction or compression and pathologic changes can alter the anatomic dead space. Fowler's method - monitor expired [N2] after single breath of O2. Physiologic dead space Physiologic dead space = anatomic dead space plus alveolar dead space. Alveolar dead space - alveoli that are ventilated but not perfused. There is normally no alveolar dead space, so physiologic dead space equals anatomic dead space. Arterial PCO2 is normally equal to alveolar (end tidal) PCO2 When arterial PCO2 > alveolar PCO2, then alveolar dead space is present and physiologic dead space > anatomic dead space.

Rate of alveolar ventilation. Alveolar ventilation speed every time the breathing is: V A = Freq (V T - V D) V A: alveolar ventilation volume per minute Freq ': The frequency of respiratory minute V T: tidal volume V D: Volume of space and loss of physiological

1. 2.

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Oxygen is transported from the alveolar air to the red blood cells by diffusion across the alveolar-capillary barrier. The transit time for the red cells to pass through the approximately 1 mm long lung capillaries (3/4 s) is virtually always adequate for the haemoglobin to become fully saturated with the oxygen of the alveolar gas . A gas such as carbon monoxide (CO) that does not equilibrate across the alveolo-capillary barrier, such that its pressure gradient is maintained while the blood is still in transit through a pulmonary capillary, is purely diffusion limited, and is not dependent on the bloodflow per se (no perfusion limitation). The pulmonary transfer of O2 and CO2 is perfusion limited over a wide range of activity levels. Even though CO2 is 24-times more soluble in water and diffuses 20 times faster through water than does O2, the two gasses have essentially the same pulmonary equilibration times (which is 0.25 s when blood has passed one third of the way through the capillary at rest).

6) The equilibrium time is due to the small pressure gradient for CO2 and the time needed for conversion of bicarbonate and carbamino-compounds to dissolved CO2. Haemoglobin and the dissociation curve Oxygen is transported by haemoglobin, but also carbon dioxide (CO2) and hydrogen ions (H+) are being transported in the blood with a minimal pH change. Hb4(O2)4 + CO2 + H+ Hb4CO2(H+) + 4O2 According to Henrys Law the concentration of physically dissolved O2, [O2] is directly proportional, to its partial pressure in the blood. In the lungs, the concentration is high (due to the high partial pressure); hence the reaction is shifted to the left. This results in the release of CO2 and the oxygenation of haemoglobin. In the muscles, the [O2] is falling (due to mitochondrial consumption of O2); hence the reaction is shifted to the right, which results in uptake of carbon dioxide and the release of O2 and reduced haemoglobin.

The total CO2-concentration of blood rises with the PaCO2, and the CO2-dissociation curve is almost linear in the physiological range between 40 and 50 mmHg. In mixed venous blood the oxygen saturation (SO2) is 75% and the CO2-concentration is larger for a given PCO2 than in arterial blood. This is a general relationship called the Haldane effect: Oxyhaemoglobin is not able to bind as much CO2 as oxygen-free haemoglobin. The Haldane effect facilitates the release of carbon dioxide in the lungs. The reaction of oxygen with haemoglobin follows the law of mass action. The concentration of oxygen in physical solution is proportional to the oxygen partial pressure. Thus, the concentration of physically dissolved oxygen determines the relative amounts of haemoglobin and oxyhaemoglobin or the SO2, which varies from zero to 100%.

The reaction between protons and bicarbonate is shifted to the right when the H+-concentration rises: H+ + HCO3- H2CO3 * H2O + CO2. The last reaction is catalysed by carbonanhydrase (*). In fully oxygenated pulmonary blood, the oxygen concentration is approximately 200 ml STPD per l (SO2 = 1.0 or 100%) at an atmospheric oxygen partial pressure of 20 kPa and a PaO2 of 13.3 kPa . This fully oxygenated blood is mixed with venous blood that passes through the physiological shunt on its way to the left heart. Thus, the oxygen tension falls to 12.6 kPa (95 mmHg) in arterial blood from 13.3 kPa at the pulmonary capillaries and SaO2 is only 0.985. The solubility coefficient of oxygen is 0.022 ml STPD per ml per atmosphere. From the dissociation curve, SaO2 is read to be 0.985 .

Autonomic breathing system, no influence, working by itself. Metabolism increases when the needs of O2 by the cells increased. When metabolism increases, O2 to the cells will not be fulfilled if only depend on the autonomic work earlier. Control system: breathing pattern changed. Nervous system whose role is central nervous system, in areas of the brain stem,consists of the neurons in the brain stem,in dorsal ventral area, angustik. Area sends impulses: Dorsal begins inspiration. Ventral effects on breathing pattern,inspiration and expiration ca uses a deeper and stronger. Angustik inspiration becomes very long.

Respiration is affected by settings: a) the cerebral cortex that could affect the pattern of respiration. b) chemical substances: in the body there is kemoresptor sensitive to changes in the concentration of O2, CO2 and H + in the aorta, aortic arch and carotid arteries. c) Movement: changes accepted by proprioseptor movement. d) Reflexes Heuring Breur: keeping development and for optimal lu ng deflation. e) Other factors: blood pressure, emotions, temperature, pain, ani spinkter acti vity and respiratory tract irritation.

1. 2.

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Abnormalities radius alveoli Surfactant, a substance responsible for lowering the surface tension of pulmonary tuberculosis for not collapse. Impaired secretion of surfactant by alveolar type II granule cells can interfere with lung ventilation. Age

Spirometry (meaning the measuring of breath) is the most common of the Pulmonary Function Tests (PFTs), measuring lung function, specifically the measurement of the amount (volume) and/or speed (flow) of air that can be inhaled and exhaled. Spirometry is an important tool used for generating pneumotachographs which are helpful in assessing conditions such as asthma, pulmonary fibrosis, cystic fibrosis, and COPD. The spirometry test is performed using a device called a spirometer, which comes in several different varieties. Most spirometers display the following graphs, called spirograms: a volume-time curve, showing volume (liters) along the Y-axis and time (seconds) along the X-axis a flow-volume loop, which graphically depicts the rate of airflow on the Yaxis and the total volume inspired or expired on the X-axis

Procedure

The basic forced volume vital capacity (FVC) test varies slightly depending on the equipment used. Generally, the patient is asked to take the deepest breath they can, and then exhale into the sensor as hard as possible, for as long as possible, preferrably at least 6 seconds. It is sometimes directly followed by a rapid inhalation (inspiration), in particular when assessing possible upper airway obstruction. Sometimes, the test will be preceded by a period of quiet breathing in and out from the sensor (tidal volume), or the rapid breath in (forced inspiratory part) will come before the forced exhalation. During the test, soft nose clips may be used to prevent air escaping through the nose. Filter mouthpieces may be used to prevent the spread of microorganisms, particularly for inspiratory maneuvers.

Parameters
The most common parameters measured in spirometry are Vital capacity (VC), Forced vital capacity (FVC), Forced expiratory volume (FEV) at timed intervals of 0.5, 1.0 (FEV1), 2.0, and 3.0 seconds, Forced expiratory flow 2575% (FEF 2575) and Maximal voluntary ventilation (MVV). Forced Vital Capacity (FVC) Forced Vital Capacity (FVC) is the volume of air that can forcibly be blown out after full inspiration, measured in liters. FVC is the most basic maneuver in spirometry tests. Forced Expiratory Volume in 1 second (FEV1) Average values for FEV1 in healthy people depend mainly on sex and age, according to diagram at left. Values of between 80% and 120% of the average value is considered normal.

Tidal volume (TV) Tidal volume (TV) is the specific volume of air drawn into, and then expired out of, the lungs during normal tidal breathing. Total Lung Capacity (TLC) Total Lung Capacity (TLC) is the maximum volume of air present in the lungs. Maximum Voluntary Ventilation (MVV) Maximum Voluntary Ventilation (MVV) is a measure of the maximum amount of air that can be inhaled and exhaled within one minute. For the comfort of the patient this is done over a 15 second time period before being extrapolated to a value for one minute expressed as liters/minute. Average values for males and females are 140-180 and 80-120 liters per minute respectively.

 Fatimah

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