Disturbances of Respiration and few.pptx

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1. Dr.Syam chandr nair Disturbances of Respiration

2. Tachypnea Bradypnea Polypnea Apnea Hyperpnea Hyperventilation Hypoventilation Dyspnea Periodic breathing

3. HYPOXIA Hypoxia is defined as reduced availability of oxygen to the tissues.

4. CLASSIFICATION AND CAUSES OF HYPOXIA 1. Oxygen tension in arterial blood 2. Oxygen carrying capacity of blood 3. Velocity of blood flow 4. Utilization of oxygen by the cells.

5. Hypoxic Hypoxia Causes i.Low oxygen tension in inspired (atmospheric) air, which does not provide enough oxygen ii.Respiratory disorders associated with decreased pulmonary ventilation, which does not allow intake of enough oxygen iii.Respiratory disorders associated with inadequate oxygenation in lungs, which does not allow diffusion of enough oxygen iv. Cardiac disorders, in which enough blood is not pumped to transport oxygen.

6. Anemic Hypoxia Characterized by the inability of blood to carry enough amount of oxygen. Oxygen availability is normal. i. Decreased number of RBCs ii. Decreased hemoglobin content in the blood iii. Formation of altered hemoglobin i v. Combination of hemoglobin with gases other than oxygen and carbon dioxide.

7. Stagnant Hypoxia decreased velocity of blood flow hypokinetic hypoxia. i. Congestive cardiac failure ii. Hemorrhage iii. Surgical shock i v. Vasospasm v. Thrombosis vi. Embolism.

8. Histotoxic Hypoxia inability of tissues to utilize oxygen. cyanide or sulfide poisoning Destruction of cellular oxidative enzymes and there is a complete paralysis of cytochrome oxidase system. Therefore even if oxygen is supplied, the tissues are not in a position to utilize it.

9. EFFECTS OF HYPOXIA Immediate Effects Hypoxia induces secretion of erythropoietin from kidney. Increase in rate and force of contraction of heart, cardiac output and blood pressure followed by reduction in the rate and force of contraction of heart. Cardiac output and blood pressure are also decreased. (d/t Reflex stimulation of cardiac and vasomotor centers) RR increases —-> CO2 decreases —-> Alkalemic blood Later, the respiration tends to be shallow and periodic. Finally, the rate and force of breathing are reduced to a great extent due to the failure of respiratory centers. Alkaline urine d/t release of erythropoietin from the juxtaglomerular apparatus Mild hypoxia produce sx similar to alcoholic intoxication. Severe cause sudden loss of consciousness. If not treated immediately, coma occurs, which leads to death.

10. Delayed Effects of Hypoxia Delayed effects appear depending upon the length and severity of the exposure to hypoxia. The person becomes highly irritable and develops the symptoms of mountain sickness, such as nausea vomiting depression weakness fatigue.

11. TREATMENT FOR HYPOXIA – OXYGEN THERAPY at one atmosphere (760 mm Hg), administration of pure oxygen is well tolerated by the patient for long hours. after 8 hours or more, lung tissues show fluid effusion and edema. Hyperbaric oxygen is the pure oxygen with high atmospheric pressure of 2 or more than 2 atmosphere. tolerated by the patient for about 5 hours. Efficacy :: Hypoxic Hypoxia > Anemic Hypoxia > Stagnant Hypoxia > Histotoxic Hypoxia Histotoxic hypoxia, the oxygen therapy is not useful at all.

12. OXYGEN TOXICITY (POISONING) occurs because of breathing pure oxygen with a high pressure of 2 to 3 atmosphere (hyperbaric oxygen) excess amount of oxygen is transported in plasma as dissolved form because oxygen carrying capacity of hemoglobin is limited to 1.34 mL/g. tracheobronchial irritation and pulmonary edema Metabolic rate increases in all the body tissues and the tissues are burnt out by excess heat Heat also destroys cytochrome system, leading to damage of tissues. hyperirritability —> increased muscular twitching, ringing in ears and dizziness. Finally, the toxicity results in convulsions, coma and death.

13. HYPERCAPNEA

14. Hypercapnea is the increased carbon dioxide content of blood. blockage of respiratory pathway, as in case of asphyxia. During hypercapnea, the respiratory centers are stimulated excessively. It leads to dyspnea. The pH of blood reduces and blood becomes acidic. associated with tachycardia and increas ed blood pressure. flushing of skin due to peripheral vasodilatation. headache, depression and laziness —-> muscular rigidity, fine tremors and generalized convulsions. Finally, giddiness and loss of consciousness occur.

15. HYPOCAPNEA

16. Hypocapnea is the decreased carbon dioxide content in blood. associated with hypoventilation. Also occurs after prolonged hyperventilation, because of washing out of excess carbon dioxide. Respiratory centers are depressed, leading to decreased rate and force of respiration. respiratory alkalosis. Calcium concentration decreases It causes tetany, which is characterized by neuromuscular hyperexcitability and carpopedal spasm. Dizziness, mental confusion, muscular twitching and loss of consciousness are the common features of hypocapnea.

17. APNEA

18. Apnea is defined as the temporary arrest of breathing. Literally, apnea means absence of breathing. Arrest of breathing by voluntary effort is known as voluntary apnea or breath holding. At the end of voluntary apnea, the subject is forced to breathe, which is called the breaking point. It is because of the accumulation of carbon dioxide in blood, which stimulates the respiratory centers. Besides increased carbon dioxide content in blood, hypoxia and increased hydrogen ion concentration are also responsible for stimulation of respiratory centers. Apnea is always followed by hyperventilation.

19. Apnea is always followed by hyperventilation. Therefore CO2 is washed out, dec pCO2 leading to dec in stimulation of respiratory centers thereby ensues Apnea During Apnea —-> CO2 inc —-> respiratoty centre stimulates —-> respiration starts (full cycle) Deglutition apnea Vagal apnea : experimental apnea produced by the stimulation of vagus nerve in animals. Stimulation of vagus nerve causes apnea by inhibiting the inspiratory center. Adrenaline Apnea

20. CLINICAL CLASSIFICATION OF APNEA Obstructive sleep apnea Temporary stoppage of breathing that occurs repeatedly during sleep. It is also called sleep disordered breathing (SDB). It commonly affects overweight people. Major cause for sleep apnea is obstruction of upper respiratory tract by excess tissue growth in airway, like enlarged tonsils and large tongue. Characteristic feature of sleep apnea is loud snoring. Snoring without sleep apnea is called simple or primary snoring. Snoring with sleep apnea is dangerous and it may become life threatening.

21. Central Apnea Central apnea occurs due to brain disorders, especially when the respiratory centers are affected. It is seen in premature babies. Typical feature of central apnea is a short pause in between breathing. CLINICAL CLASSIFICATION OF APNEA

22. Mixed Apnea Mixed apnea is a combination of central and obstructive apnea. Seen in premature babies and in full-term born infants. Due to abnormal control of breathing due to immature or underdeveloped brain or respiratory system. CLINICAL CLASSIFICATION OF APNEA

23. HYPERVENTILATION HYPOVENTILATION DEFINITION increased pulmonary ventilation due to forced breathing.
both rate and force of breathing are increased decrease in pulmonary ventilation caused by decrease in rate or force of breathing. CONDITIONS exercise
Occurs when partial pressure of carbon dioxide (pCO2 ) is increased. administration of some drugs causing suppression of respiratory centres
Conditions causing partial paralysis of respiratory muscles EFFECTS Apnea
Cheyne-Stokes type of periodic breathing results in development of hypoxia along with hypercapnea.

24. Most common type of periodic breathing periodic breathing characterized by rhythmic hyperpnea and apnea. Physiological conditions when Cheyne-Stokes breathing occurs i.During deep sleep ii.In high altitude iii.After prolonged voluntary hyperventilation iv.During hibernation in animals v.In newborn babies vi.After severe muscular exercise. CHEYNE-STOKES BREATHING

25. Pathological conditions when Cheyne-Stokes breathing occurs i.During increased intracranial pressure ii.During advanced cardiac diseases, leading to cardiac failure iii. During advanced renal diseases, leading to uremia iv. Poisoning by narcotics v. In premature infants.

26. BIOT BREATHING Also characterised by period of apnea and hyperpnea. Waxing and waning of breathing is absent. It occurs in conditions involving nervous disorders due to lesions or injuries to brain. Only seen in pathological conditions

27. ASPHYXIA characterized by combination of hypoxia and hypercapnea, due to obstruction of air passage. All together, asphyxia extends only for 5 minutes. The person can survive only by timely help such as relieving the respiratory obstruction, good aeration, etc. 1. Stage of Hyperpnea Extends for about 1 minute. breathing becomes deep and rapid. due to the powerful stimulation of respiratory centers by excess of carbon dioxide. Hyperpnea is followed by dyspnea and cyanosis. Eyes become more prominent.

28. 2. Stage of Convulsions characterized mainly by convulsions (uncontrolled involuntary muscular contractions). Duration of this stage is less than 1 minute. Hypercapnea acts on brain and produces the following effects: i. Violent expiratory efforts ii. Generalized convulsions iii. Increase in heart rate iv. Increase in arterial blood pressure v. Loss of consciousness.

29. 3. Stage of Collapse lasts for about 3 minutes. Severe hypoxia produces the following effects during this stage: i. Depression of centers in brain and disappearance of convulsions ii. Development of respiratory gasping occurs. iii. Mydriasis iv. Bradycardia v. Loss of all reflexes. Duration between the gasps is gradually increased and finally death occurs.