1. Anaesthesia & Respiratory System Dr Rob Stephens Consultant in Anaesthesia UCLH Hon Senior Lecturer UCL Thanks to Dr Roger Cordery

2. Positive Pressure Ventilation Dr Rob Stephens Consultant in Anaesthesia UCLH Hon Senior Lecturer UCL Thanks to Dr Roger Cordery

3. Anaesthesia & Respiratory System Dr Rob Stephens Consultant in Anaesthesia UCLH Hon Senior Lecturer UCL Thanks to Dr Roger Cordery

4. Anaesthesia & Respiratory System Dr Rob Stephens Consultant in Anaesthesia UCLH Hon Senior Lecturer UCL www.ucl.ac.uk/anaesthesia/people/stephens www.ucl.ac.uk/anaesthesia/people/stephens Google UCL Stephens talk on webpage above & supporting material robcmstephens[at]googlemail.com Thanks to Dr Roger Cordery

5. www.ucl.ac.uk/anaesthesia/people/stephens www.ucl.ac.uk/anaesthesia/people/stephens Google UCL Stephens

7. Contents Anatomy + Physiology revision What is Anaesthesia?- triad Anaesthesia effects… – airway – ‘respiratory depression’ – FRC – Hypoxaemia – after Anaesthesia Tips on the essay Break then Lecture 2: Positive Pressure Ventilation

8. Picture of Propofol/Thio ‘Lethal injection drug production ends in the US

9. Introduction Why learn?- intellectually interesting Practical – understand – prevent problems Practical – find new solutions Practical- pass exam!

10. Anatomy revision Upper Airway above the vocal cords Lower airway – below the vocal cords – Conducting vs gas exchange- different tissue types Muscles of respiration

11. Airway Airway is Lips/Nose to alveoli Upper Airway: lips/nose to vocal Cords Lower Airway: Vocal Cords down – Trachea – Conducting Airways – Respiratory Airways – gas exchange with capillaries R heart pulmonary artery capillaries vein L heart Pharynx

12. Lower Airway 23 divisions follow down from L +R main bronchus bronchi through to terminal bronchi bronchioles respiratory bronchioles alveolar ducts alveolar sacs or ‘alveoli’ 1-16 conduction of air 17-23 gas exchange

13. Anatomy Alveolus in detail – pulmonary capillary Image to show alveolus and bronchiole

14. Section to show the upper airway

15. CXR – carina, lungs, heart

16. Anatomy: Muscles of Respiration Upper airway muscles upper airway tone External IntercostalsInspiration DiaghramInspiration Internal IntercostalsForced Expiration Accessory musclesForced Inspiration Neck Accessory musclesForced Expiration Abdomen

18. Physiology revision Spirometry- basic volumes How we breathe spontaneously Compliance / elastance Deadspace and shunt V / Q ratios

19. 0 ml At Rest Inhale Exhale ~2500ml ~6000ml Physiology: Spirometry

20. Physiology: Volumes Tidal Volume, TV Functional Residual Capacity, FRC Volume in lungs at end Expiration not a fixed volume - conditions change FRC Residual Volume, RV Volume at end of a forced expiration Closing Volume, CV Volume in expiration when alveolar closure ‘collapse’ occurs Others

21. 0 ml At Rest Inhale Exhale ~2500ml ~6000ml Physiology: Closing Capacity ~40+ supine ~60+ standing

22. Normal breath inspiration animation, awake Diaghram contracts  Chest volume  Pleural pressure Pressure difference from lips to alveolus drives air into lungs ie air moves down pressure gradient to fill lungs -2cm H 2 0 -5cm H 2 0 Alveolar pressure falls -2cm H 2 0 Lung @ FRC= balance Physiology: Normal Spontaneous breath

23. Normal breath expiration animation, awake Diaghram relaxes Pleural / Chest volume  Pleural pressure rises Physiology: Normal Spontaneous breath Alveolar pressure rises to +1cm H 2 0 Air moves down pressure gradient out of lungs -5cm H20 +1cm H 2 0

24. Compliance = the volume Δ for a given pressure Δ A measure of ease of expansion ΔV / ΔP Normally ~ 200ml / 1 cm H 2 O for the chest 2 types: static & dynamic Elastance = the pressure Δ for a given volume Δ = the opposite of compliance The tendency to recoil to its original dimensions A measure of difficulty of expansion ΔP / ΔV eg blowing a very tight balloon Physiology: Compliance & Elastance

25. Chest, Lung, Thorax (= both together) Lung Elastin fibres in lung - cause recoil = collapse Alveolar surface tension - cause recoil Alveolar surface tension reduced by surfactant For the chest as a whole, it depends on Lungs and Chest Wall Diseases affect separately eg lung fibrosis, chest wall joint disease Physiology: Compliance & Elastance

26. Physiology: Deadspace and shunt Each part of the lung has Gas flow, V Blood flow, Q V/Q mismatching Deadspace = Ratio: V Normal/ Low Q That part of tidal volume that does not come into contact with perfused alveoli Shunt = Ratio: V low/ Normal Q That % of cardiac output bypasses ventilated alveoli Normally = 1-2% Ratio V/Q Perfect V/Q =1

27. Normal ‘Shunt’ Shunt % Blood not going through ventilated alveoli or blood going through unventilated alveoli Normal- 1-2% Pulmonary eg alveolar collapse, pus, secretions Cardiac eg ASD/VSD ‘hole in the heart’ (but mostly left to right…. due to L pressure> R pressures)

28. Normal ‘Shunt’ Air enters Alveolus Pulmonary capilary ‘Shunted’ blood 1-2% Blood in contact with ventilated alveolus Venous Arterial V Q ‘venous admixture’ Sa0 2 75% Sa0 2 ~100%

29. Increased Pulmonary Shunt Not much air enters Alveolus Pulmonary capilary ‘Shunted’ blood 1-2% Blood in contact with unventilated alveolus Venous Arterial V low V/Q = low Q normal Alveolus filled with pus or collapsed….. Sa0 2 75%

30. Pulmonary Hypoxic Vasoconstriction Less air enters Inflammatory exudate eg pus or fluid Arterial Venous Blood diverted away from hypoxic alveoli V low Q less V/Q = towards normal A method of normalising the V/Q ratio

31. Deadspace That part of tidal volume that does not come into contact with perfused alveoli Tidal volume = anatomical Pathological Alveolar volume ~400ml Deadspace volume ~ 200ml Conducting airways ie trachea and 1- 16= Anatomical deadspace

32. Deadspace Air enters Alveolus Pulmonary capilary ‘Shunted’ blood 1-2% Blood in contact with ventilated alveolus Venous Arterial V Q

33. Deadspace Air enters Alveolus Pulmonary capillary low flow eg bleeding or blocked ‘Shunted’ blood 1-2%  Blood in contact with ventilated alveolus Venous Arterial V Q V/  Q = Hi Classic anatomical = trachea!

34. Deadspace- Anatomical Trachea from L +R main bronchus bronchi through to terminal bronchi bronchioles respiratory bronchioles alveolar ducts alveolar sacs or ‘alveoli’ conduction of air Deadspace volume gas exchange Alveolar volume

35. Physiology: V/Q in lung Both V and Q increase down lung Q increases more than V down lung Another way to think about Q/V is ‘west zones’ V/Q ratios change down lung If patient supine (on back) V/Q changes front to back

36. Physiology: V/Q in lung

37. What is Anaesthesia? Reversable drug induced unconsciousness ‘Triad’ – Hypnosis, Analgesia, Neuromuscular Paralysis Induction, Maintainence, Emergence, (Recovery) Spontaneous vs Positive Pressure Ventilation See podcast ‘conduct of anaesthesia’ link from my website‘conduct of anaesthesia’

38. Anaesthesia Timeline Preoperative Induction: Analgesia & IV hypnotic Maintain: Analgesia & Volatile Hypnotic Emergence: Analgesia Only Recovery Patient can be paralysed vs not= Needs ventilation vs spontaneously breathing

39. Anaesthesia Hypnosis = Unconsciousness – Gas eg Halothane, Sevoflurane – Intravenous eg Propofol, Thiopentone Analgesia = Pain Relief – Different types: ‘ladder’, systemic vs other Neuromuscular paralysis – Nicotinic Acetylcholine Receptor Antagonist

40. Anaesthetic Machine Delivers Precise Volatile Anaesthetic Agents Carrier Gas Other stuff Picture of anaesthesia machine

41. Detail of anaesthesia machine

42. Volatile or Inhalational Anaesthetic Agents Eg Sevoflurane -A halogenated ether -with a carrier gas -ie air/N 2 0 Hypnosis Picture of Sevoflurane bottle

43. Intravenous- pictures

44. Analgesia = Pain relief Systemic: not limited to one part of the body pictures

45. Analgesia = Pain relief Systemic: not limited to one part of the body Simple eg Paracetamol Non Steroidal Anti-Inflammatory Drugs eg Ibuprofen Opiods weak eg Codeine strong eg Morphine, Fentanyl Others Ketamine, N 2 O, gabapentin…..

46. Analgesia = Pain relief Regional: limited to one part of the body images

47. Neuromuscular Paralysis Nicotinic AcetylCholine Channel @ NMJ Non-competitive Suxamethonium Competitive All Others eg Atracurium Different properties Different length of action Paralyse Respiratory muscles Apnoea – ie no breathing Need to ‘Ventilate’ images

48. Respiratory effects of Anaesthesia airway ‘respiratory depression’ Functional Residual Capacity, FRC Hypoxaemia

49. Respiratory effects of Anaesthesia airway ‘respiratory depression’ Functional Residual Capacity, FRC Hypoxaemia

50. Anaesthesia Airway Upper: loss of muscular tone eg oropharynx Upper: tongue falls posteriorly ie back

51. images

52. Anaesthesia Airway Upper: loss of muscular tone eg oropharynx Upper: tongue falls posteriorly ie back Need to keep it open to allow airflow! “Airway obstruction’ = no airflow Keep Airway open: – Airway manoeuvres (chin lift etc) – Airway devices- above vs blow cords – Above eg, gudel, LMA – Below - Into trachea = intubation, paralysis

53. Anaesthesia Airway Equipment images

54. Laryngeal Mask Airway

55. Video of LMA insertion

56. Image to show how LMS sits In the airway above the vocal cords

57. Respiratory effects of Anaesthesia airway ‘respiratory depression’ Functional Residual Capacity, FRC Hypoxaemia

58. Anaesthesia ‘respiratory depression’ CO 2 and O 2 response curves of volatiles Opioids Respiratory depression …..is opposed by surgical stimulation No cough – good and bad – Caused by all 3 types of drug – Forced expiration: expands lungs, clears secretions – Allows pt to tolerate airway tubes…eg LMA

59. V L/min Arterial CO 2 kPa Increasing concentration of volatile Awake Volatiles  response to CO 2 Anaesthesia ‘respiratory depression’ 5.3 9 7

60. Volatiles reduce minute ventilation Unstimulated volatiles – Reduce V tidal and therefore V minute – Make you less responsive to the effects of CO 2 – ie slope is more flat = the normal increase in ventilation that occurs when CO 2 rises is reduced Anaesthesia ‘respiratory depression’

61. Volatiles  response to hypoxaemia PaO 2 kPa Awake High concentration Low concentration 813 5 Anaesthesia ‘respiratory depression’ V L/min

62. Opioids Opioids = a drug acting on Opioid receptor Morphine, Fentanyl Act in CNS, PNS, GI Reduced respiratory rate, increase tidal volume, but still increase PaCO 2 Suppress cough

63. Opioids Video to show opioid induced low respiratory rate

64. Respiratory effects of Anaesthesia airway ‘respiratory depression’ Functional Residual Capacity, FRC Hypoxaemia

65. Anaesthesia FRC Why important?- closing Volume and O 2 store Why would it change? FRC is decreased by 16-20% by Anaesthesia – Falls rapidly (seconds to minutes). – FRC remains low for 1-2 days Weak but significant correlation with age Less FRC reduction if patient is in the sitting position but most operations aren’t done sitting!

66. 0 ml At Rest Inhale Exhale ~2500ml ~6000ml Physiology: Closing Volume

67. 0 ml At Rest Inhale Exhale ~2500ml ~6000ml Physiology: Closing Volume

68. What causes these changes? 1.Cephalad (to brain) movement of the diaphragm 2.Loss of inspiratory muscle tone 3.Reduced cross sectional rib cage area 4. Gas trapping behind closed airways Anaesthesia FRC

69. Respiratory effects of Anaesthesia airway ‘respiratory depression’ FRC Hypoxaemia

70. Anaesthesia Hypoxaemia Hypoxaemia – Low blood oxygen level FRC changes- Closing Vol,  collapse/atelectasis and shunt Position also effects eg legs/laparoscopy/head down - Tidal volume Hypovolaemia/vasodilation increases deadspace, – V/low Q areas ….mismatch PHVC reduced by volatiles – increases V/Q mismatch No cough/ yawn ?-collapse/secretions Apnoea/Airway obstruction- no 0 2 in no CO 2 out!

71. Hypoxaemia: Atelectasis Atelectasis = the lack of gas exchange within alveoli, due to alveolar collapse or fluid consolidation

72. CT scan of Diaphragm during awake spontaneous breathing

73. CT scan of Diaphragm during anaesthesia: Atelectasis

74. After Anaesthesia Some changes persist – Collapse/Atelectasis abnormal 1-2 days – FRC abnormal 1-2 days – CO 2 and O 2 responses normal in hours – V/Q mis-smatch – PHVC (reduces V/Q mismatch) Some new changes happen – Wound pain causing hypoventilation – Drug overdose causing hypoventilation – Pneumonia, cough supression, PE, LVF etc

75. Summary 1 Airway – conducting and respiratory Physiology V/Q different as you go down lung Extreme – no blood flow (Deadspace) Extreme – no ventilation (Shunt) Anaesthesia – Hypnosis, Analgesia, Paralysis

76. Summary 2 Anaesthesia effects due to drugs! – Upper airway obstruction – Respiratory ‘depression’ – Hypoxaemia – collapse (FRC/Closing volume) = ‘shunt’ -  pulmonary blood flow - deadspace -PHVC drugs

79. Further reading http://en.wikipedia.org/wiki/Respiratory_physiology Articles and Podcast on my webpage Pulmonary Physiology and Pathophysiology: an integrated, case-based approach John West mostly free on google books

80. Writing the essay Break the answer down into parts Lots of space Graphs and diagrams, labelled- colour? Underline important parts Headline each paragraph with a statement? – ‘GA causes V/Q mismatch Don’t just write dense text

81. Revision Aids When answering question on Anaesthesia or IPPV – Lung volumes – Normal airway pressures / mechanics of breathing – Upper airway – Lower airway – Compliance/Resistance – V, Q and V/Q match /mis-match (?West zones) – Causes of hypoxaemia +/- hypercapnia – Muscle tone (upper airway + respiration) – Respiratory drive – CVS effects – Drug effects (Hypnosis/Analgesia/paralysis) – Other bleeding, position, age, sleep, pathology

82. MCQ 1 Shunt is..??? AThat part of tidal volume that does not come into contact with perfused alveoli B% Blood not going through ventilated alveoli

83. MCQ 2 Pulmonary Embolus (blood clot stopping blood flowing through part of the lungs) AIs an example of a shunt BIs an example of deadspace C can cause hypoxia

84. Qn3 List as many causes of hypoxia under anaesthesia as you can