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Pathophysiology of external breathing. Hypoxia. Reasons for respiratory dysfunction. Dysfunction of the respiratory neurons; Chest pathology Respiratory muscles and diaphragm pathology; Injure of pleura; Obstructive lung disease; Restrictive lung disease.
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Reasons for respiratory dysfunction • Dysfunction of the respiratory neurons; • Chest pathology • Respiratory muscles and diaphragm pathology; • Injure of pleura; • Obstructive lung disease; • Restrictive lung disease.
The pathological factors impair metabolism, structure and function of nerve cells. • They are hypoxia, hypoglycemia, toxic agents, inflammatory processes in the brain tissue, compression of the medulla, traumas, circulatory disorders in the brain.
Investigation of terminal breathing in experiment • 1 – normal breathing; • 2 – apneustic breathing after cutting both vagal nerves and brain between pneumotaxic and apneustic centers; • 3 – gasping after cutting under dorsal respiratory group; • 4 – an arrest of breathing after cutting medulla under respiratory neurons.
Pathological Patterns of Breathing • Eupnea - normal breathing movements • Bradypnea - decreased rate of breathing • Hyperpnea - increased breathing movement • Polypnea – increased rate and decreased depth of breathing • Apnea - arrested breathing • Periodic breathing • Terminal breathing • Asphyxia - inability to breathe
Bradypnea • Bradypnea– decreased rate of breathing, cased by lack of impulsation from respiratory neurons, that leads to hypoventilation. • Bradypnea is observed in hypertension (reflexes from carotid sinus baroreceptors), in increased ventilatory resistance, inhibition of respiratory neurons by hypoxia, effect of narcotic drugs to brain that decrease the sensitivity of the respiratory neurons to pH or CO2 in CSF, functional impaction of nervous system (neurosis, hysteria).
Hyperpnea • Hyperpnea - increased breathing movement. • Hyperpneais a result of intensive nerve or humoral stimulation of respiratory neuronal area (lack ofpO2in ihaled air, extra pCO2in ihaled air, anemia, acidosis).
Polypnoe • Polypnea – increased rate and decreased depth of breathing because of changed activity of respiratory neurons by reflex regulation. • Polypnea revealed in fever, functional impaction of nervous system (hysteria), injure of lungs (atelectasis, pneumonia, impaired perfusion), pain syndrome in body organs engaged in ventilatory function. • Polypneaaffects breathing in such a manner that ultimately sufficient O2 uptake and CO2 release can no longer be guaranteed.
Apnea • Apnea - an arrest of breathing lasting a few seconds. It is more likely in the presence of a metabolic alkalosis because decrease pCO2 in blood (after artificial lung ventilation), giving adrenalin in blood, inhibition of respiratory neurons (as a result of hypoxia, toxic effects, organic pathology of the brain) .
Periodic breathing • Cheyne–Stokes breathing is irregular. The depth of breathing periodically becomes gradually deeper and then gradually more shallow. It is caused by a delayed response of respiratory neurons to changes in blood gases resulting in an overshooting reaction. It occurs when there is hypoperfusion of the brain, or when breathing is regulated by a lack of oxygen (hypoxiaї, uremia, immature infants). • Biot breathing consists of a series of normal breaths interrupted by long pauses. It is an expression of damage to respiratory neurons. Gasping also signifies a marked disorder in the regulation of breathing (meningitis, encephalitis).
Terminal breathing • In terminal conditions the apneustic breathing and severe gasping are revealed. • Apneustic breathing consist of prolonged spastic inhales, interrupted by brief exhalations(impaired connections of apneustic, pneuvmotaxic centers and vagal nerve). • Severe gasping characterized by gradually decreased rate and depth of inhales because of arrest of resperatory neurons activity above dorsal and ventral respiratory group in medulla (in agony of death, terminal period of asphyxia).
Short wind • Short wind– increased breathing because of subjective feeling lack of air, when excitatory influences to respiratory neurons are more intensive, then pathological effects. • (in loss of diffusion area, lack of perfusion, inflammation and activation of reflexes from irritant receptors in pneumonia, decreased impulsation from baroreceptors in aorta and carotids in blood loss, shock; increased impulses from chemoreceptors in hypoxia, hypercapnia, acidosis, overstratching respiratory muscles because of decreased lung elastic recoil, obstruction of upper respiratory pathways.
Acute deficiency of breathing • Acute deficiency of breathing develops in some minutes to hours and progressing rapidly. • The main pathological mechanisms are hypoxemia, hypercapnia, acidosis, central nerve control disturbances. Acute deficiency of breathing can result in coma.
Chronicle deficiency of breathing • Chronicle deficiency of breathing is characterized by gradual enhance of hypoxemia and hypercapnia. • Pathological disturbances in chronicle deficiency of breathing are less intensive, than in acute deficiency of breathing due to activation of compensatory mechanisms.
Damage to the chest • Thecontaminationofairinthepleuralcavityiscalledpneumothorax (opened, closed,valvular). • If air can enter the pleural cavity and go out by place of trauma, this is opened pneumothorax. • In case of shift the damaged tissues the air cannot go out the pleural cavity and closed pneumothorax develops. • When mild tissues in the place of trauma permit entering of air and prevent outflow of air from the pleural cavity, the valvular pneumothorax develops.
Damage of the respiratory muscles • Damage of motoneurons of spinal cord that control respiratory muscles may occur due to inflammatory and degenerative processes (with amyotrophic lateral sclerosis, poliomyelitis, syringomyelia), due to intoxication (strychnine, tetanus toxin). • Violation of the conduction impulses in the peripheral nerves that supply respiratory muscles can occur because of inflammation, vitamin deficiency, trauma. Diaphragmatic nerve lesion leads to paralysis of the diaphragm, which manifests its paradoxical movements according to changes in pressure in the chest cavity - at the inhalation diaphragm rises, at the exhale – gets plant. Violation of neuromuscular transmission of impulses occurs in myasthenia, botulism, introduction of muscle relaxants. In all these cases, the ventilation function get disturbed.
Whenobstructiverespiratoryinsufficiency, airwaycanbebrokenduetotheirnarrow, leadingtoincreasedresistancetoairmovement (wheninhaledforensicparticles, thickeningofthewallsofairwaysduetoinflammation, musclespasmofthelarynx, bronchialcompressionduetoswelling, inflammation, enlargedthyroidgland .)
Emphysema • In emphysema the lungs lose their elasticity and stretch considerably with less transpulmonary pressure, so there is lack of pressure from within bronchioles - their clearance decreases, increases resistance to air movement, difficult breath. • Exhalation becomes active due to decreased elasticity of the lungs, the pressure increases and bronchioles collapse, so alveoli are filled with residual air.
Pathology of the lung in end-stage cystic fibrosis Key features are: • the widespread mucus impaction of airways and bronchiectasis (U); • small cysts (C); • hemorrhagic pneumonia in lower lobe.
Atelectasis • Atelectasis caused by airway obstruction and absorption of air from the involved lung area on the left and by compression of lung tissue on the right.
Atelectasis • The right lung of an infant (left side of photo) is pale and expanded by air, whereas the left lung is collapsed.
Asphyxia • The first stage is characterized by deep and rapid breathing with a predominance of inspiratory phase (inspiratory dyspnea).• In the second stage begins a gradual decline in respiration rate against the background of deep respiratory movements. Phase exhalation prevails over the inspiratory phase (expiratory dyspnea).• In the third stage of the frequency and depth of respiratory movements decreased steadily up to a complete stop breathing. After a short term of absent respiration (preterminal pause) several rare deep respiratory movements are observed (terminal or agonic, breathing).• Stimulation of breathing at the beginning of asphyxia associated with direct and reflex excitation of carbon dioxide and respiratory center hipoksemichnoyu blood. With the growth inhibition of hypoxic brain come the respiratory center and complete paralysis of its functions. The appearance of terminal respiration explained by the excitation of neurons of the caudal medulla oblongata.
Obstruction of larynx leads to hypoxia А – normal larynx; В – Obstruction of larynx from edema caused by croup.
Violation of ventilation-perfusion ratio • To maintain the gas composition of blood it is important to not only the absolute value of alveolar ventilation, but the proper balance between ventilation and perfusion lung. The amount of blood flowing through the lungs for 1 min, equal to 4.5-5 liters, approximately corresponds to the value cardiac output.• The optimal ratio of alveolar ventilation and perfusion lung is 0.8 (4 l/ 5 l). It may vary upward or downward. In both cases, normal blood gas composition can not provide.• The predominance of ventilation pressure of oxygen in the alveoli in blood is sufficient, but blood carry out too much carbon dioxide (hipokapniya). If, however, ventilation is slower than perfusion, hypoxemia and hypercapnia occur.
Hypoxia Hypoxia occurs when O2 transport from ambient air to the cell is impaired. There may be several causes: • In exogenous (hypoxic) hypoxia the hypoventilation reduces the diffusion gradient to venous blood and thus impairs O2uptake. • In respiratory (hypoxic) hypoxia reduced diffusing capacity prevents equilibration of gas concentrations in alveoli and capillary blood. • In hemic hypoxia reduced O2 uptake capacity of the blood. • In circulativehypoxia circulatory failure impairs O2 transport in the cardiovascular system. • In hystotoxic(tissue) hypoxia the tissue diffusion is impaired.
The damage of nervous system by hypoxia • In the early stages of hypoxia structural changes in nerve tissue are reversible. If to continue hypoxia, the structure and function of neurones will be disturbed. Neurons of the cerebral cortex live without oxygen for no longer than 5-6 min, even under normal conditions they are on the verge of hypoxia.• The narrowing of the vessels at cerebral atherosclerosis causes atrophy and glial sclerosis in brain substance, which is expressed clinically senile forgetfulness.•The neurons of the cerebellum are damaged easily. More stable and breathing vasomotor centers, they can withstand a complete cessation of blood supply for 30 min. Spinal cord saves hours of livelihoods during hypoxia. As a result of inhibition of the respiratory center appears periodic breathing.
Myocardial injury during hypoxia • Second place for sensitivity to hypoxia has the heart. On the contraction of the muscle fibers spent half the energy generated by them, as hypoxia, accompanied by an energy deficit, dramatically reduces myocardial contractile function. In addition, an excess of calcium in cardiac myocites retards their relaxation, shortens diastole and further reduces their contractile ability.• Conductive system of the heart as a whole more resistant to hypoxia, compared with the contractile myocardium. Resistance is increasing its divisions from the base to the apex of the heart. The most enduring Purkinje cells, which provided energy primarily due to oxygen-free glycolysis. The sharp decrease in myocardial blood supply leads to dystrophic and necrotic changes, life-threatening.
Compensatory reactions during hypoxia • Breathing • Haemodynamic • Hemic • Tissue
Respiratory compensatory reactions (bronchial asthma) There is shortness of breath pochaschenym and depth, resulting in inhibition of the respiratory center appears periodic breathing
Haemodynamic compensatory reactions • tachycardia; • increase in stroke volume of blood due to the action of adrenaline on cardiac beta-adrenoreceptors; • increase in cardiac output; • acceleration of blood flow; • peripheral vascular constriction and vasodilatation in vital organs, i.e. centralization of blood circulation, redistribution of blood to the heart, brain, lung, while limiting the blood supply to muscles, intestines, skin, spleen.
Hemic compensatory reaction • The blood reactions primarily increase the oxygen capacity of blood. For hypoxia characteristic polycythaemia, i.e. increasing the number of erythrocytes per unit volume of blood. Initially, this occurs due to release of erythrocytes from the depot, which perform the function of capillaries of the skin, liver, spleen, lungs. Normally there are up to 45% of blood.• If prolonged hypoxia, stimulated erythropoiesis in red bone marrow. This condition stimulates erythropoietin, secreted mostly by the kidneys. They act on erythropoietic cells and make them proliferate and differentiate into mature erythrocytes. At the same time increases the synthesis of haemoglobin, and charge it to each erythrocyte becomes larger. In addition, the increased affinity of haemoglobin for oxygen in the lungs and decreases - in the tissues.
Tissue compensatory reaction Reactions of tissue type are aimed:• to reduce the need for oxygen (decrease in basal metabolism),• maximum utilization of oxygen from the blood (respiratory chain enzyme activation),• obtain energy in anoxic processes (activation of glycolysis).
