Medicine related topics and vies

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.

7. 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.

8. 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.

9. 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.

11. 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.

12. 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.

13. 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.

14. 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.

15. HYPERCAPNEA

16. • 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.

17. HYPOCAPNEA

18. • 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.

19. APNEA

20. • 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.

21. • 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

22. 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.

23. 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

24. 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

25. 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.

27. • 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

29. • 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.

30. 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

31. 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.

32. • 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
Loss of consciousness.

33. • 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.