No 44 COURSE FOR THE DIPLOMA IN AVIATION MEDICINE - PowerPoint PPT Presentation

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No 44 COURSE FOR THE DIPLOMA IN AVIATION MEDICINE
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No 44 COURSE FOR THE DIPLOMA IN AVIATION MEDICINE

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  1. No 44 COURSE FOR THE DIPLOMA IN AVIATION MEDICINE June 20th 2011 Revision Cardiovascular and Respiratory Physiology Earth’s Atmosphere Jane Ward MB ChB PhD

  2. Q. How low does PO2 need to be to give a large ventilatory response? • Q. As a person ascends to altitude in an unpressurised aircraft, how are his arterial PO2 and PCO2 affected: • if the subject failed to increase his ventilation (e.g. a carotid body resected subject who cannot sense the hypoxia)? • if ventilation increased in the normal way? • Is there any altitude at which the ventilatory response normalizes alveolar PO2 (i.e. returns it to the sea level value)?

  3. Ventilatory response to O2 60 50 40 Ventilation (litres per minute) 30 20 10 (mmHg) 120 60 0 (kPa) 0 4 8 12 16 Arterial PO2 acute exposure to 10,000 feet

  4. 16 120 kPa mmHg 100 80 Alveolar PO2 8 60 40 20 0 0 5.3 40 Alveolar PCO2 20 0 0 0 5000 10,000 15,000 20,000 25,000 feet Altitude 0 3,000 6,000 m Values if ventilation had not changed Mean values for 30 subjects exposed acutely to altitude 3000 0

  5. Two patients both have reduced arterial oxygen contents of 100 ml/l (instead of the normal 200 ml/l). In Mr A this is due to anaemia, in Mr C this is due to carbon monoxide poisoning. Q. Explain why Mr C is much sicker than Mr A. Q. Why does raising inspired oxygen concentration from 24% to 28% significantly improve the myocardial oxygen delivery in a patient with severe chronic obstructive pulmonary disease (COPD) but not in to a patient with angina? Q. Give an example of a condition or situation that increases arterial PO2 but is associated with symptoms of cerebral hypoxia.

  6. MI patient % sat COPD mmHg 0 5 10 15 20 kPa PO2

  7. Arterial PO2 vs arterial oxygen saturation Q. You are measuring arterial PO2 continuously (with an indwelling PO2 electrode) and oxygen saturation (with a pulse oximeter) in a patient. The patient stops breathing. Q. Describe the way in which arterial PO2 and O2 saturation will change during the apnoea.

  8. mmHg 100 kPa 13 arterial PO2 60 8 20 2.7 100% O2 saturation 50% stop breathing 30 seconds

  9. You are measuring alveolar PO2 continuously (with a fast response O2 meter sampling end-tidal gas) and oxygen saturation (with a pulse oximeter) in a pilot climbing from sea level to 40,000 in aircraft with its pressurisation accidentally switched off. Q. Describe the way in which arterial PO2 and O2 saturation will change as he ascends. Q. At roughly what altitude will he pass out if he fails to notice and take action? Steady fall in PO2 with increasing altitude, with rate of fall slowing a little as ventilation increases above about 10,000 feet. Little change in saturation until PO2 < 60 mmHg at around 10,000feet. Variable, depending on speed of ascent, activity, individual. The early balloonists lost consciousness at around 25,000-30,000 feet.

  10. Q. Could you give a reasonable estimate of arterial PO2 if you had an oxygen dissociation cure and a pulse oximeter oxygen saturation reading: • In a normal person at sea level? • In a severely hypoxic patient? No Yes

  11. 100 75 50 25 0 kPa 20 2 16 18 0 4 6 8 10 12 14 Oxygen saturation (%) PCO2 = 5.3 kPa (40 mmHg) pH = 7.4 Temperature = 37oC 0 50 100 mmHg 150 PO2 All measurements have some potential error If we are measuring oxygen saturation in a normal person at sea level: Large possible range of PO2 Small error in saturation So if the pulse oximeter read 96% there is a wide range of possible arterial PO2s

  12. If we are measuring arterial PO2 in a normal person at sea level: 100 75 50 25 0 kPa 20 2 16 18 0 4 6 8 10 12 14 Oxygen saturation (%) PCO2 = 5.3 kPa (40 mmHg) pH = 7.4 Temperature = 37oC 0 50 100 mmHg 150 PO2 Small error in PO2 Little effect on saturation So if arterial PO2 was 96 mmHg (12.8 kPa) we can be fairly confident that the oxygen saturation is fairly close to 97%

  13. 100 75 50 25 0 kPa 20 2 16 18 0 4 6 8 10 12 14 Oxygen saturation (%) PCO2 = 5.3 kPa (40 mmHg) pH = 7.4 Temperature = 37oC 0 50 100 mmHg 150 PO2 Q. In a hypoxic person (P < 8 kPa) with an oxygen dissociation curve could you reasonably predict PO2 from saturation or saturation from PaO2? Yes, on the steep part of the dissociation cure=ve PO2 predicts saturation quite well and saturation predicts PO2 quite well.

  14. Different situations and conditions affect the arterial partial pressure of oxygen (PaO2), arterial O2 saturation (O2 sat) and arterial O2 content (O2 cont) differently. Compared to a normal person at sea level: PaO2 : N O2 sat: N O2 cont: N State how are these things affected by the following situations or conditions: E.g. Low (L), Slightly L, high (H), normal (N) ….

  15. 1. Mild hypoxia with normal blood. E.g. mild respiratory depression or skiing in the Alps. PaO2: O2 sat: O2 cont: 2. Polycythaemia RubraVera PaO2: O2 sat: O2 cont: 3. Severe hypoxia with normal blood.E.g. marked hypoventilation in a patient with a head injury or at very high altitude. PaO2: O2 sat: O2 cont: 4. Polycythaemia and hypoxia. E.g chronic respiratory diseases esp. severe COPD. Or a normal person whose has lived in the Himalayas for several weeks. The polycythaemia is a response to chronic hypoxia. PaO2: O2 sat: O2 cont: L slightly L slightly L N N H L L L L L L or N or H

  16. 6. Anaemia with a normal respiratory system. PaO2: O2 sat: O2 cont: 7. Anaemia with the patient breathing oxygen enriched air. PaO2: O2 sat: O2 cont: 8. Carbon monoxide poisoning. PaO2: O2 sat: O2 cont: N N L H N L N (usually) L L

  17. 1 Q. How would (a) arterial PO2 and (b) oxygen saturation by pulse oximetry be affected in a patient with carbon monoxide poisoning? PaO2is unaffected by CO poisoning. (FIO2 normal; PaO2 only affected when ill enough for ventilation to be depressed.) (b) The pulse oximeter is based on colour of haemoglobin. Hand of person who died of CO poisoning. The simple pulse oximeter will give a falsely high O2saturation. c.f. low oxygenated Hb, high deoxygenated Hb where it correctly records low oxygen saturation

  18. Q. List the special features of the cerebral circulation: • High blood flow for weight. • Total flow relatively constant (but does fall on standing). Local flow increases with neuronal activity. • Good autoregulation • Very sensitive to changes in PCO2 and PO2. • Hyperventilation lowers PCO2 and can give such marked cerebral vasoconstriction that oxygen delivery becomes inadequate despite raised PaO2.

  19. Autoregulation: maintenance of a fairly constant blood flow in the face of changes in perfusion pressure F = DP/R immediate after a few minutes Cerebral blood flow (ml/min/100g tissue) Perfusion Pressure (arterial – venous pressure)

  20. Q. Where are the arterial baroreceptors? Q. What are the main reflex cardiovascular effect of stimulating the arterial baroreceptors by increasing arterial BP? Carotid sinus Aortic arch and coronary arterial

  21. Arterial baroreceptor reflex  firing carotid sinus and aortic arch baroreceptors glossopharyngeal and vagus nerves Brainstem (NTS)  BP   sympathetic parasympathetic sympathetic blood vessels heart vasodilatation venodilatation heart rate contractility BP NTS = Nucleus of the tractus solitarius

  22. Q. What is/are the important differences between the carotid sinus and the aortic arch baroreceptor reflexes?

  23. Aortic baroreceptors: less sensitive to pulse pressure. The aortic baroreceptor reflex may have a relatively stronger effect on heart rate than on vascular resistance and the carotid baroreflex the other way round 75 mmHg 95 mmHg On standing aortic baroreceptors remain at heart level but carotid sinus is now about 25 cm above the heart. On standing, even if heart level pressure unchanged, carotid sinus pressure falls  carotid baroreceptor firing falls but aortic baroreceptor firing unchanged 95 mmHg

  24. Q. What mechanism(s) help to both: 1. to reduce foot swelling with prolonged standing and 2. to minimize the all in cardiac output with prolonged standing?

  25. valves Mechanisms limiting increase in capillary pressure in the foot: a. skeletal muscle pumping - aids venous return to the heart may lower foot venous pressure to 20-30 mmHg.

  26. Foot venous pressures standing and with walking 120 80 Venous pressure in foot (cm H2O) 40 0 Time (s) From Levick JR, An introduction to cardiovascular physiology. 4th edition Arnold

  27. Normal response to 20 minutes of head up tilt in a young adult (no faint). Note: there is actually small increase in BP - the %increase in TPR is greater than the %fall in CO.

  28. Q. What factors determine the oxygen delivery to a tissue?

  29. Oxygen Delivery • Oxygen delivery to a tissue (ml/min) = • arterial oxygen content (ml/ml) xblood flow to the tissue (ml/min) • Arterial oxygen content depends on: • the arterial PO2 • the haemoglobin concentration • the proportion of oxygen binding sites available for oxygen binding (reduced by CO and methaemoglobin) • the affinity of the haemoglobin for oxygen (e.g. [H+], PCO2, temp, 2,3 DPG concentration) • Blood flow to a tissue depends on blood pressure and vascular resistance.

  30. There are 5 mechanisms which can lead to arterial hypoxia, low PaO2. Of these, only hypoventilation inevitably leads to a high arterial PCO2. Air or alveolar gas with normal PO2 Air or alveolar gas with reduced PO2 Deoxygenated blood (‘mixed venous’or right-sided) Normal, fully oxygenated blood Incompletely oxygenated blood Mechanisms 3, 4 and 5 increase the A-a PO2 gradient.

  31. Q. Apart from the oxygen delivered to a tissue, what else affects the oxygen consumption of a tissue? Oxygen consumption of a tissue (ml/min) = oxygen delivery (ml/min)) x oxygen extraction (ml O2/ ml blood) Oxygen extraction is affected by capillary density, tissue oedema, the affinity of haemoglobin for oxygen. If the tissue cells cannot use oxygen (e.g. cyanide or sepsis poisoning the mitochondria) oxygen extraction is also reduced.

  32. Cells furthest from a capillary are exposed to a lower tissue PO2 than cells near the capillary. These areas (critical zones or lethal corners) are vulnerable if capillary PO2 falls.

  33. Q. What is normal alveolar PO2 at sea level? Q. What is usually considered to the highest altitude at which most people will show only minor physical and psychometric deficit when breathing air? Q.* What will their alveolar PO2 be at this altitude? Above this altitude the raising FIO2 above the usual 0.21 (21%) can be used to compensate for the low barometric pressure. Q. What is the maximum altitude at which a normal sea level alveolar PO2 can be achieved by breathing 100% Oxygen? Q. What is the maximum altitude at which the alveolar PO2 in Q* can be achieved by breathing 100% Oxygen at ambient pressure? Approx 103 mmHg, 13.3 kPa Approx 10,000 feet Approx 55 mmHg, 7.5 kPa Approx 33,700 feet Approx 40,000 feet

  34. Campbell & Bagshaw, 2002

  35. In plane A a pilot in an unpressurised aircraft lying at 40,000 feet loses his oxygen supply and starts breathing ambient air. In Plane B, the pilot is breathing cabin air pressurised to 8,000 feet when there is a sudden decompression caused by a large hole (door sized) suddenly deveolping in the fuselage. The pilot of which plane is likely to be adversely affected most quickly?

  36. Loss of oxygen supply: 25,000 feet breathing O2 enriched air 25,000 feet breathing air O2 O2 PAO2 falls progressively to 30 mmHg PAO2 = 103 mmHg 95 103 103 40 40 RA LA RA LA RV RV LV LV PAO2 falls at a rate which depends on alveolar ventilation. Note as PO2 falls to 30 mmHg O2 moves from blood to alveolus.

  37. Altitude atmosphere cabin 40000 8000 65 PAO2 tracheal PO2 108 A rapid decompression can cause a much faster fall in alveolar and arterial PO2 40000 rapid change to 40000 20 15

  38. Q. How quickly does the pilot need to breath oxygen after a sudden decompression at 40,000 feet? Q. What determines how likely he is to lose consciousness?

  39. At A ‘cabin’ (or hypobaric chamber) altitude from 8000 to 40,000 feet in 1.6 seconds A * ** * 2 seconds after time 0 ** 8 seconds after time 0 If area under critical line > 140 mmHg.sec consciousness will almost certainly be lost

  40. Typical times of useful consciousness (TUC) in a healthy resting subject. The values are much more variable at the lower altitudes. TUC is very much reduced by even light exercise. Altitude Feet Metres Progressive Hypoxia: Rapid As when inspired oxygen Decompression changed to air 25,000 7,620 3-6 minutes 2-3 minutes 30,000 9,140 1.5-3 minutes 0.5-1.5 minutes 35,000 10, 670 45-75 seconds 25-35 seconds 40,000 12,190 25 seconds 18 seconds

  41. Q. What are the symptoms and signs of hypoxia? Q. What factors affect an individual’s susceptibility to hypoxia? Q. What are the symptoms and signs of hyperventilation?

  42. Symptoms and signs of acute hypobaric hypoxia • personality change • lack of insight and judgment • loss of self-criticism • euphoria • loss of memory • mental incoordination • muscular incordination • sensory loss • cyanosis • hyperventilation specific symptoms (see later) • clouding of consciousness • loss of consciousness • death

  43. Factors affecting the susceptibility to hypoxia Altitude Length of time of the exposure Exercise Cold Illness Fatigue Drugs/Alcohol Smoking (carbon monoxide)

  44. Hypocapnia = low PaCO2 due to hyperventilation (caused by: anxiety, pain, low PaO2, acidosis, excessive mechanical ventilation) symptoms: dizziness visual disturbances pins and needles esp. hands stiff muscles, tetany and feet mechanisms: low PaCO2 cerebral vasoconstriction  cerebral hypoxia low PaCO2 alkalosis  plasma [Ca2+]  nerve and muscle excitability

  45. Hyperventilation Alveolar ventilation is increased relative to CO2 production. PACO2 (and PaCO2) CO2 production alveolar ventilation Normal PaCO2 = 40 mmHg, 5.3 kPa PaCO2 < 25 mmHg: significant fall in psychomotor performance lightheadedness/dizziness, anxiety, tingling (lips, fingers, toes) <20 mmHg - muscle spasms in hands and feet (carpopedal spasm) and face <10-15 mmHg - clouding of consciousness, unconsciousness whole body muscle spasms

  46. Neurological effects Below 10,000 feet: little effect on well-learned tasks (PAO2 ≈ 55mmHg slightly impaired performance novel tasks O2 sat ≈ 87%) reduced night vision 10,000 - 15,000 feet: with increasing altitude / hypoxia difficulties (PAO2 ≈ 55 - 45mmHg in more complex tasks (as tested by choice- O2 sat 87 - 80%) reaction time), first then simpler tasks (tested by pursuit-meter tasks) e.g.: 12,000 feet 10% fall in ability to air speed, heading etc 15,000 feet 20-30% increasing problems with memory, drowsiness, judgement also reduced muscle coordination

  47. 15,000 - 20,000 feet: headaches, dizziness, somnolence, euphoria, (PAO2 55 - 45mmHg fatigue, air hunger O2 sat 80 - 65%) 20,000 - 23,000 feet: confusion and dizziness occurs within a few (PAO2 29 - 22mmHg minutes of exposure and total incapacitation O2 sat 65 - 60 %) and loss of consciousness occurs rapidly after this. Loss of consciousness - affected by both arterial PO2 and cerebral blood flow and therefore arterial PCO2. Occurs when jugular venous PO2 falls to 17-19 mmHg which occurs when arterial PO2 is 20-40 mmHg. (can occur as low as 16,000 feet)