pulmonary ventilation, lungs perfusion, on exchange of respiratory gases and on capacity of blood to transport the oxygen Important mechanism of gas exchange in animals and human beings is air diffusion - from high concentration to lower concentration, but transportation by this way is possible only for 1 mm length. For further transportation convectional transportation is needed. Air molecules are transported trough respiratory ways and also blood transports them by means of convectional transportation. Thus Oxygen is transported from the environment to the tissues by the following sequence: 1. convectional transport till alveoli (ventilation), 2.Diffusion from alveoli to pulmonary capillaries, 3. Convectional transport of airs by blood to tissue capillaries. 4. Diffusion from capillaries to tissues. Carbon dioxide is being carried out from tissues on the contrary way. The main mechanisms of respiratory failure are the disturbances of ventilation, lungs perfusion, diffusion or their combinations. Ventilation, perfusion and exchange of the respiratory gases in the lungs are the primary functions of the cardiopulmonary system. Ventilation includes the mechanics of inspiration and the providing of atmospheric air to the alveoli, and the mechanics of expiration during which the air with decreased oxygen and increased carbon
dioxide levels is expired. Ventilation depends on many
factors neurogenic and chemical factors, respiratory muscles, the lung tissue, and the airways resistance to the airflow. The exchange of respiratory gases in the organism depends on oxygen diffusion from alveoli to the blood and then from the blood to the tissues. In this way, but vice versa carbon dioxide is eliminated from the body. The exchange of respiratory gases depends also on the integrity, thickness and area of the membrane which represents the site of the gas exchange. It further depends on the relative gradient of gases and their solubility on both sides of the membrane, on the affinity of hemoglobin to oxygen, and on the distribution of ventilation and perfusion. The perfusion of the lung represents the blood flow enabling the oxygen transport between alveoli and blood. Respiratory failure is a syndrome of inadequate gas exchange due to dysfunction of one or more essential components of the respiratory system: CNS or Brain Stem Chest wall (including pleura and diaphragm) Airways and Alveoli capillary units of Pulmonary circulation Nerves Pulmonary ventilation and its disorders Ventilation of the lungs is a complex of processes ensuring the transport of air into the lungs and the expiration of air enriched in carbon dioxide with low oxygen content.
During inspiration the thoracic cavity enlarges due to the
contraction of the respiratory muscles. The inspiration is an active process which depends on several factors. The expiration is a passive process, depending on relaxation of inspiratory muscles. The elastic properties of chest and lungs are important factors. The essence of lung ventilation is gas exchange between atmospheric and alveolar air. In this process, central neural system (respiratory centers located in medulla oblongata and pons), sensitive and motoric peripheral nerves, upper respiration ways, and lungs are involved. Lung ventilation disorder takes place at any of their dysfunction. Respiratory dysfunction related with the respiratory center disorders Respiratory centers located in medulla oblongata and pons (Pneumotaxic center) provide the certain depth, rate and rhythm of respiration. They permanently receive impulses from upper neural systems (brain bark, hypothalamus) and peripheral chemo-, baro-, mechano-, and thermo receptors. High temperature has significant meaning at high temperature respiration gets frequent as well as certain hormones (e.g. adrenalin and progesterone) increase lung ventilation. The excitation of respiratory center and lung ventilation is depended on CO2 tensity and PH of blood. Respiratory centre neurons react only on H+ ions, CO2 action is related with their capacity of H+ ions formation.
The excitation of respiratory center and consequently lung
ventilation decreases at central neural system impairment (brain blood vessels sclerosis and spasm, hemorrhage, brain compression, intoxications). Chemoreceptors involved in respiratory regulation react mainly on oxygen tensity decrease in blood; In this case ventilation is increased. Vegetative neural system is very important: by symphatic prevalence bronches are dilated, and excess parasyphatic impulses cause bronchospasm. Sensitive termination of vagus nerve play important role at normal and pathologic conditions; at inspiration alveoli are stretched, sensitive receptors are irritated that reflectively causes expiration (HeringBreuer reflex). E.g. at inflammation acid exudates increase sensitivity of stretching receptors and inspiration ends earlier therefore superficial respiration develops. Ventilation disorders related with Chest wall dysfunctions (including pleura and diaphragm). Obstruction in upper respiratory ways cause respiratory failure of obstructive type (foreign body, tumor, laryngospasm. Lower respiratory ways obstruction (e.g. bronches or bronchioles obstruction with vomited masses, water, and mucus.) also cause obstructive type of respiratory failure. Ventilation disorders at lung respiratory surface decrease are characterized by severe decrease of external respiration of restrictive type. The lung stretching capacity decrease restricts alveolis ability to
enlarge that can be met at pneumonia, minor circle
dam, at emphysema, fibrosis, some toxic impairments. Important role plays deficiency of surfactant substance that resists lung atelectasis via decrease of surface tension in alveoli. Forms of ventilation disorders are: hyperventilation, hypoventilation. Physiologic or compensative hyperventilation (e.g. at exercise) is an organisms reaction to excessive demand for oxygen and is being stopped when the cause is eliminated. Pathologic hyperventilation develops at respiratory centre excitation during brain and its membranes inflammation. Prolonged and severe hyperventilation causes hypocapnia and alkalosis that inhibits respiratory centre and cause hypoventilation. Respiration act changes Normally a man breathe without any effort paying no attention to the process, this condition is called respiratory comfort - eupnoea. Bradypnoea is a rare breathing. This reflex decreasing breathing rate may be observed at increased arterial pressure (reflex from he baroreceptors of aortic arch and carotidal sinus), at hyperoxia. Polipnoea or tachipnoea is frequent superficial respiration. Tachipnoea occurs when there is
increased stimulation of pneomotaxic centres or
excessive inactivation of their inhibiting factors. Hyperpnoea or deep and frequent breathing develops e.g. at mountain disease because of oxygen partial pressure decrease. At this time excess CO2 is eliminated that cause hypocapnia, alkalosis, respiratory arrhythmia and rarely stopping of breathing. Apnea is an absence of breathing but usually this is temporary respiratory stand still.
Dyspnoea is a ventilation disorder together with
feeling of breathing difficulty. Inspirational (prolonged inspiration phase) and expirational dyspnoea (expiration process disorder) are classified. Periodic breathing it is a breath rhythm disorder when breaths are separated by intervals of apnea (no breathing). As opposed to normal breathing which is usually regular. Following types of breath disorders are observed: Cheyne-Stokes respirations, Biots Breathing, Kussmaul respirations. . Cheyne-Stokes respirations are a phase, or cyclic, type of breathing in response to hypercapnia in the system. The cycle starts with a smooth increase, in the rate and depth of respirations followed by a gradual
smooth decrease, in the rate and depth of respirations
ending in a short period of apnea that can last from 15 to 60 seconds. Then the cycle repeats itself. Cheyne Stokes respirations result from any condition that slows the blood flow to the brain stem because it slows impulses sending information to the respiratory center. An injury of the brain above the brain stem will also contribute to the development of Cheyne-Stokes respirations. Causes include CNS dysfunction, cardiac failure with low cardiac output, sleep, hypoxia, profound hypocapnia. Biots Breathing is irregular respirations with irregular periods of apnea. There is no cyclic nature to them as in Cheyne-Stokes breathing. Breaths are generally of equal depth (also distinguishing them from CheyneStokes). It may be seen with respiratory depression and brain damage at the level of the medulla. Kussmaul respirations, or hyperpnoea, are deep, rapid respiration with no end-expiratory pause and indicate the body is trying to compensate for severe metabolic acidosis (blow off the excess carbon dioxide in the system) or after strenuous exercise. They have an increased rate and no expiratory pause. In other words there is no stopping between inhaling and exhaling. It is seen in profound metabolic acidosis, i.e. diabetic ketoacidosis.