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

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

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

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

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

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

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

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

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

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

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

Anatomy Alveolus in detail – pulmonary capillary Bronchiole Alveolus

Anatomy: Muscles of Respiration Upper airway muscles upper airway tone External Intercostals Inspiration Diaghram Inspiration Internal Intercostals Forced Expiration Accessory muscles Forced Inspiration Neck Accessory muscles Forced Expiration Abdomen

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

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

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

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

Physiology: Normal Spontaneous breath Normal breath inspiration animation, awake Lung @ FRC= balance Diaghram contracts -2cm H20 Chest volume Pleural pressure Pressure difference from lips to alveolus drives air into lungs ie air moves down pressure gradient to fill lungs -5cm H20 Alveolar pressure falls -2cm H20

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

Physiology: Compliance & Elastance Compliance = the volume Δ for a given pressure Δ A measure of ease of expansion ΔV / ΔP Normally ~ 200ml / 1 cm H2O 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 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: 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

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)

with ventilated alveolus Normal ‘Shunt’ V Air enters Alveolus Pulmonary capilary Blood in contact with ventilated alveolus Sa02~100% Q Sa0275% ‘Shunted’ blood 1-2% Arterial Venous ‘venous admixture’

Increased Pulmonary Shunt Not much air enters Alveolus V low Alveolus filled with pus or collapsed….. V/Q = low Pulmonary capilary Blood in contact with unventilated alveolus Sa0275% Q normal Sa0275% ‘Shunted’ blood 1-2% Arterial Venous

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

Deadspace That part of tidal volume that does not come into contact with perfused alveoli Anatomical Tidal volume Pathological Physiological – Deadspace volume ~ 200ml Conducting airways ie trachea and 1-16= Anatomical deadspace Alveolar volume ~400ml that part of the alveolar ventilation that goes to un-perfused or poorly perfused alveoli

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

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

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

Physiology: V/Q in lung Both V and Q increase down lung Q increases more than V down lung V/Q ratios change down lung If patient supine (on back) V/Q changes front to back Another way to think about V& Q is ‘West zones’ 1-3

Physiology: V/Q in lung

So far… Anatomy – Upper / lower airway Physiology – Mechanics Conducting ie deadspace vs Respiratory ie gas exchange Volumes / FRC Physiology – Mechanics Compliance, Elastance Blood Flow (Q) and Ventilation (V) – extremes – Shunt, Deadspace, West Zones

What is Anaesthesia? Reversable drug-induced unconsciousness ‘Triad’ Hypnosis, Analgesia, Neuromuscular Paralysis Induction, Maintainence, Emergence, (Recovery) Spontaneous vs Positive Pressure Ventilation See podcast ‘an intro to anaesthesia’ link from my page and article an intro to anaesthesia

Anaesthesia Timeline Preoperative Induction: Analgesia & IV hypnotic +/- paralysis Maintain: Analgesia & Volatile Hypnotic +/- paralysis Emergence: Analgesia Only +/- reversal of paralysis Recovery: Analgesia Only , residual effects Patient can be paralysed vs not= Needs ventilation vs spontaneously breathing

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

Anaesthetic Machine Delivers Precise Volatile Anaesthetic Agents Carrier Gas Other stuff

Hypnosis Volatile or Inhalational Anaesthetic Agents Eg Sevoflurane A halogenated ether with a carrier gas ie air/N20

Intravenous

Analgesia = Pain relief Systemic: not limited to one part of the body Regional: limited to one part of the body

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, N2O, gabapentin…..

Analgesia = Pain relief Regional: limited to one region or part of the body

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’

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

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

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

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

Anaesthesia Airway Equipment

Laryngeal Mask Airway

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

Anaesthesia ‘respiratory depression’ CO2 and O2 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

Anaesthesia ‘respiratory depression’ Volatiles  response to CO2 Awake Increasing concentration of volatile V L/min 5.3 7 9 Arterial CO2 kPa

Volatiles reduce minute ventilation Anaesthesia ‘respiratory depression’ Volatiles reduce minute ventilation Unstimulated volatiles Reduce Vtidal and therefore V minute Make you less responsive to the effects of CO2 ie slope is more flat = the normal increase in ventilation that occurs when CO2 rises is reduced

Volatiles response to hypoxaemia Anaesthesia ‘respiratory depression’ Volatiles response to hypoxaemia V L/min Awake Low concentration High concentration 5 8 13 PaO2 kPa

Opioids Opioids = a drug acting on Opioid receptors Morphine, Fentanyl Act in CNS, PNS, GI Reduced respiratory rate, increase tidal volume, but still increase PaCO2 as  V Suppress cough

Opioids

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

Anaesthesia FRC Why important?- closing Volume and O2 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!

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

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

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

Respiratory effects of Anaesthesia airway ‘respiratory depression’ FRC Hypoxaemia

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 02 in no CO2 out!

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

CT scan of Diaphragm during awake spontaneous breathing

CT scan of Diaphragm during anaesthesia: Atelectasis

After Anaesthesia Some changes persist Some new changes happen Collapse/Atelectasis abnormal 1-2 days FRC abnormal 1-2 days CO2 and O2 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

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

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

Further reading Many articles and a Podcast on my webpage Pulmonary Physiology and Pathophysiology: an integrated, case-based approach John West mostly free on google books

Lets have a break

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

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

End Thanks – Part 2 Positive Pressure Ventilation next