Respiratory adjustments in special conditions

1. Respiratory adjustmentsinspecial conditions By Dr. MB.Bhat..

2. In muscular exercise • In Heavy exercise body’s metabolism increases about 2000% above normal (compare to high fever it increases only about 100% above normal) • Energy store available in the body at this high level activities is only for 20 seconds. • For sustaining exercise extra fuel & O2 should be supplied by Respiration & CVS adjustments. • O2 consumption increases proportionaly to severity of exercise up to a maximum level

3. Increased O2 consumption during exercise is achieved by – Increased pulmonary ventilation Increased O2 diffusion capacity of lungs (from normal 250 to 4000ml/min) [same time CO2 diffusion capacity also increases from 200 to 8000ml/min)

4. Factors increasing pulmonary ventilation • In moderate exercise –by increased depth of respiration • In severe exercise –by increased depth & rate of respiration.

5. Effect of exercise on pulmonary ventilation

6. Pulmonary ventilation shows – With exercise -- Abrupt increase –during on-set of exercise (just before the exercise commence) Followed by a brief pause Graded increase –during exercise proportionate with grade of exercise Cessation of exercise – Abrupt slight decrease –immediately after cessation of exercise Followed by a brief pause Followed by graded decline to pre-exercise level

7. Abrupt increase with on-set of exercise due to stimulation of respiratory center by -- • Anticipatory response – Psychic stimuli coming from higher center (From limbic system) • Pyramidal tract impulses via some collaterals • Afferent impulses from proprioceptors of muscle, tendon & joints via collateral of dorsal column tracts (Lovan reflex)

8. The graded increase is due to stimulation of respiratory center by – Increase in temperature Increase sensitivity of the respiratory center to the CO2 (fluctuation of arterial PCO2 is increased even though the mean arterial PCO2 remain same) O2 (even though arterial PO2 in not decreased) Humeral effect (even though blood pH, PCO2 & PO2 remain constant during moderate exercise) Increase in plasma K+ level In vigorous exercise all the above + Lactic acid

9. Cessation of exercise • Abrupt decrease – due to stoppage of impulses bombarding respiratory center (but not coming back to basal level) • Graded decline – due to lactic acedemia -- due to O2 debt –last as long as 90 minutes • Magnitude of O2 debt – amount by which O2 exceeds basal consumption from the end of exertion until return to basal level

10. Extra O2 during this period is used for – Combine with muscle myoglobin Resynthesis of ATP & Phosphocreatine Removalof lactic acid Fate of lactic acid – 80% converted to glycogen in the liver 20% is metabolized to CO2 & water During strenuous exercise because of O2 debt the RQ rise to 2. After cessation because of repayment of O2 debt the RQ falls to 0.5

11. Hypoxia Oxygen deficiency at tissue level is known as hypoxia

12. Classification of hypoxia • Hypoxic hypoxia or Arterial hypoxia • Anemic hypoxia • Stagnant hypoxia or Ischemic hypoxia or Hypo kinetic hypoxia • Histotoxic hypoxia

14. Hypoxic hypoxia • Seen in -- • Physiological condition – High altitude (alveolar PO2 is decreased) • Pathological condition – Cardio-respiratory diseases (O2 diffusion capacity is decreased)

15. High altitude • Atmospheric pressure decreases in high altitude • Concentration of gases everywhere in the atmosphere is same • Whereas, partial pressure of the gas varies. • Also in the alveoli, the water vapor pressure is constant (47 mm Hg) • So PO2 in alveoli = ATP –47 X O2 concentration (20% or 0.2)

16. At 10,000ft (3000m) alveolar PO2 is 60 mm Hg –Hb saturation maybe normal At 12,000ft (3700m), mental irritability appears (first hypoxic symptom) At 18,000ft (5500m), hypoxic symptoms are severe At 20,000ft (6100m)consciousnes lost in 20 seconds & death occurs in 4 to 5 minutes (PO2 is only 20 mm Hg)

17. Hypoxic symptoms at high altitude • Less severe hypoxic symptoms – • Acute mountain sickness -- • Many individuals first arrive at high altitude develop “transient mountain sickness” –acute mountain sickness • The syndrome develops 8 to 24 hours after arrival & last 4 to 8 days • Symptoms of acute mountain sickness are – • Mental symptoms --Irritability, mental aberrations such as impaired judgment, dis-orientation, excitement, drowsiness, loss of sense of time, loss of sensibility, • Other systemic symptoms -- dulled pain & headache, breathlessness, dizziness, insomnia, fatigue, Cheyne-Stoke breathing is common during sleep • –anorexia, nausea, vomiting, tachycardia, palpitation, retinal hemorrhage (after healing no visual defect);

18. Severe hypoxic symptoms – 1. Hypertension (proportionate to severity of chemoreceptor drive) 2. High-altitude cerebral edema –due to low PO2 –arteriolar dilation –increase capillary pressure –increase transudation of fluid into brain tissue Due to Cerebral edema – ataxia, disorientation, in extreme case coma & death

19. 3. High-altitude pulmonary edema –is a patchy edema of lungs due to pulmonary hypertension (due to low PO2), Left atrial pressure is normal Cough with pink frothy sputum Increased pulmonary capillary pressure along with polycythemia cause increased right heart work & right ventricular hypertrophy.

20. Chronic mountain sickness(Monge’s disease) • Disease of long term residents at high altitude • These people develop –manifestation of superimposed pulmonary disease with -- • Fatigue, reduced exercise tolerance, severe hypoxemia & polycythemia

21. Acclimatization (Increase altitude tolerance)Compensatory mechanisms develop over a period of time to tolerate high altitude • ‘Mechanisms are – • Hyperventilation –due to hypoxic action through peripheral chemoreceptor • Increased sensitivity to CO2(after 4 days) —due to --outward movement of HCO3 from ; --active transport of H+ ions into CSF; --development of lactic acidosis in the brain All these decrease pH in CSF that stimulate respiration through central chemoreceptor

22. 3. Polycythemia – dueto erythropoietin (within 2 to 3 days) –due to hypoxia –sustain as long as stay in high altitude Others – Increase number of capillaries in peripheral tissues Increase mitochondria Increase cytochrome oxidase in the tissue Increase myoglobin level Increase MBC (up to 200L/min) as air is less dense Kidney secrete alkaline urine

23. Hypoxic hypoxia in pathological condition • Lung failure (or) Gas-exchange failure – • Pulmonary fibrosis • V/Q imbalance –Shunt –Congenital heart diseases –Tetralogy of Fallot (Blue baby) –Right to left shunt • Pump failure (or) Ventilation failure – • Respiratory muscles fatigue • Mechanical defects cause atelectasis • Depression of respiratory center –by morphine & other drugs

24. Atelectasis –Collapse of the alveoli • Causes – • Surfactant deficiency • Obstruction of bronchus & bronchioles –alveoli beyond point of obstruction collapse –leading to more negative intrapleural pressure –pulls mediastinum towards affected side • Pneumothorax –air in the interstitial space –intrapleural pressure equal to atmospheric pressure –Push the mediastinum towards normal side

25. Asthma • Obstructive type of respiratory disease • Due to air way obstruction – due to • Air way hypersensitivity –due to –Allergy • Attack usually occurs in morning & also during exercise • Treatment – • β2 adrenergic agonists • Administration of steroids

26. Emphysema • Obstructive type of respiratory disease • Degenerative potentially fatal disease • Lungs are voluminous & inelastic with widespread destruction of alveolar walls & pulmonary capillaries • Most common cause heavy cigarette smoking • Smoking increase PAM which attracts leucocytes –which release protease enzymes & O2 free radicals –destroy lung tissues • Smoking also decrease α1antitrypsin –which destroy protease enzymes

27. Features of Emphysema • Barrel-shaped chest • Work of breathing (both inspiration & expiration is laboured) • Compliance (normal o.25 to 0.9L/mm Hg) • FRC (normal 3L to 8L) • FVC duration (normal 4 to 8second) • FEV1 (normal 3.2L to 0.75L) • Physiological dead space (doubled) • Physiological shunt • O2 diffusion capacity (1/5th)

28. 9. Arterial PO2 (even goes to 50 mm Hg) 10. Arterial PCO2 (goes up to 60 mm Hg) 11. Hb saturation (only 80 to 85%) 12. Plasma HCO3 (compensatory acidosis) 13. Polycythemia (due to hypoxia) 14. Pulmonary hyperventilation 15. Right ventricular hypertrophy (Cor Pulmonale) Here respiratory drive is due to hypoxia. So O2 treatment is not recommended

29. Anemic hypoxia • Seen in • Anemia –only in severe anemia; where Hb deficiency is marked (because in hypoxic condition increase 2,3-DPG level shift O2 dissociation curve to right) • Carbon-monoxide poisoning

30. Stagnant hypoxia • Due to slowing of circulation • Local –vasoconstriction due to cold or obstruction to venous outflow; & peripheral circulatory failure • General – cardiac failure

31. Histotoxic hypoxia • Seen in cyanide poisoning • Cyanide inhibit cytochrome oxidase & other iron containing enzymes • Treatment –Administration of methylene blue or nitrates (oxidizing agents) • –oxidized Hb to methemoglobin which react with cyanide to form cyanmethemoglobin, a non-toxic compound • Hyperbaric O2 therapy is useful

32. Cyanosis • Bluish coloration of skin, nail beds, ear lobe, lips, fingers & mucus membrane due to presence of HHb >5gm/dl • Local cyanosis or Peripheral cyanosis – seen in stagnant hypoxia due to exposure of cold, circulatory failure • Signs –patients may be cold & blue, peripheral pulses difficult to feel • Central cyanosis – seen in hypoxic hypoxia • Signs –patients extremities are warm & pulsatile, rapid blood flow, increase heart rate & pulse pressure and vasodilation

33. Before cyanosis readily apparent; the Hb saturation of O2 must fall below 80% & PO2 45 mm Hg. Cyanosis does not occur in – Anemic hypoxia –due to low Hb content CO poisoning –COHb is cheery red Histotoxic hypoxia –O2 utilization is less so HHb is also less High circulatory level of methemoglobin also produce discoloration of skin similar to cyanosis

34. O2 therapy • Useful in treatment of • Hypoxic hypoxia (except in shunt condition) • Cyanosis • Only limited value in treatment of – • Anemic, Stagnant & Histotoxic hypoxia

35. Hyperbaric oxygen therapy • Exposure of O2 with high pressure • Advantage –markedly increase dissolved O2 content in blood • Used in treatment of – • CO poisoning, Cyanide poisoning, Congenital cardiac disease (right to left shunt) • Gas gangrene • Very severe blood loss anemia • Diabetic leg ulcers & other wounds that are slow to heal • Rescue of skin flaps & grafts in which circulation is marginal, • Primary treatment for decompression sickness & air embolism • Radiation induced tissue injury

36. Oxygen toxicity • Due to production of superoxide anions (O2—)—oxygen free radicals & H2O2, also – due to decrease surfactant production & lung macrophages in high PO2. • Safe level –gas mixture contain O2 <80% (can administer even 24 hours for years) • When gas mixture contain O2 >80% to 100% (& 2 to 3 ATP) –can tolerate only up to 5 hours (Hyperbaric O2 treatment) • When above administered >8 hours –respiratory irritation, sub-sternal distress, nasal congestion, sore throat & coughing

37. When exposed above >24 to 48 hours –cause lung damage, pulmonary edema, diminished vital capacity (due to absorption atelectasis), due CNS effect convulsion preceded by nausea, ringing in the ear & twitching of face In children – Bronchopulmonary dysplasia, Retrolental fibroplasia –formation of opaque vascular tissue in eyes (retinopathy of pre maturity)

38. Hypercapnea • Occurs in – • Various forms of pump failure • Febrile state –For each 1oC rise in temperature, the CO2 production by 13% • High carbohydrate food intake • Symptoms of large excess of CO2 in blood –CO2 narcosis – Depression of CNS –leads to confusion, diminished sensory activity, in extreme case –coma, respiratory depression & death

39. Hypocapnia • Occurs due to hyperventilation • Leads to – • Alkalosis • Vasoconstriction • Reduction in Cerebral blood flow (by 30%) • Cerebral ischemia –cause dizziness & parenthesis

40. Asphyxia • Existence of acute hypercapnia & hypoxia together due to closed airway breathing • Leads to improper aeration of blood • Occur in – • Drowning • Hanging • Pneumothorax

41. Effect of asphyxia • Stage 1 –Stage of hyperpnoea – • duration 1 min • Features – • Rate & depth of respiration increased • Respiratory efforts are Violent • Dyspnea results • Initially both inspiratory & expiratory movements are increased • Later expiratory movements are more pronounced • Unconsciousness marked end of this stage • Cause –due to hypercapnea

42. Stage 2 –Stage of central excitation – duration 1 to 2 minutes Expiratory movements are still more pronounced with each expiration, the whole body enters into convulsion Saliva secretion & vomiting occurs Blood pH decreases –acidosis (accumulation of lactic acid due to convulsion) Increased wide spread sympathetic stimulation Signs of central excitations appear – such as Increase heart rate & BP; Pupillary constriction (myosis) Exaggeration of reflexes Cause –hypercapnia, hypoxia & acidosis

43. Stage 3 –Stage of central depression - Duration 2 to 3 minutes Expiratory convulsion ceased Replaced by slow deep spasmodic inspiration –individuals stretches out & open mouth wide as if gasping for breath (gasping type of breathing) Signs of central depression appear – Pupillary dilation (mydriasis) Abolition of reflexes Decreased HR & BP and vasodilation

44. As this stage is progressed interval between successive gasping longer Cause –direct hypoxic effect on respiratory & other brain centers which is depressive. Asphyxiated victim can still be saved by artificial respiration Victim may develop ventricular fibrillation due to hypoxic myocardial damage & high circulatory catecholamine If artificial respiration is not started – At the end of 4 to 5 minutes of stage 3, the victim dies.

45. Periodic breathing • When breathing is non-rhythmic & irregular, it is said to be periodic breathing • Two types • Cheyne-Stoke breathing –Regularly irregular type of periodic breathing • Biot’s breathing –Irregularly irregular type of periodic breathing

46. Physiological High altitude After hyperventilation In deep sleep In anesthetic condition Quite commonin healthy infants Pathological Congestive heart failure Uremia Elevating intracranial pressure Cheyne-Stoke breathingOccurrence of waxing & waning type of respiration with a period of apnea in between last for few seconds to few minutes & then the cycle repeats

48. Biot’s breathing • Varying breathing time alternate with apnoeic periods of different lengths • Transition from periods of activity to apnea & back are abrupt • Occurs only in pathological conditions affect CNS –such as meningitis

49. Dyspnea • Difficulty in breathing; where breathing becomes consciousness • Causes – • Reflex stimulation of respiratory centers either through central or peripheral or both chemoreceptors. • Hypersensitivity of the Hering-Breuer reflex • Hypoxic conditions • Restriction of the action of the diaphragm or inter-costal

50. Acidosis Increased metabolism Nervous conditions such as emotional disturbance, neurasthenia, hysteria, encephalitis, cerebral tumor, cerebral hemorrhage or cerebral edema Various pulmonary diseases Cardiac Dyspnea –mitral stenosis