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RESPIRATORY PHYSIOLOGY &

RESPIRATORY FUNCTION DURING


ANESTHESIA
Houman Teymourian M.D.
Assistant professor
Department of Anesthesiology and Critical
Care, Shohada hospital
Shahid Beheshti Medical University

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Factors Dealing With Respiratory Function

 Gravity-Determined Distribution of Perfusion , ventilation


perfusion - ventilation- V/Q ratio
 Non-gravitational Determinants of PVR & blood flow
distribution
1. Passive process : cardiac out put – lung volumes
2. Active process: 1) local tissue derived products
2) alveolar gas concentrations
3)neural influences
4)humoral (hormonal)
 Other nongravity- Determinants of compliance – resistance –
volume - ventilation

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Gravity-Determined Distribution of
Perfusion , ventilation

 Perfusion
ZONE 1 ( Collapse ) PA>Ppa>Ppv
ZONE 2 (Waterfall ) Ppa>PA>Ppv
ZONE 3 (Distention ) Ppa>Ppv>PA
ZONE 4 (Interstitial pressure ) Ppa>Pisf>Ppv>PA

3
ZONE 1

 Collapse & Alveolar dead space


1) Ppa (SHOCK)

2)PA (Vt & peep )


 Normally little or no zone 1 exists in the lung

4
ZONE 2

 Waterfall,Weir,Sluice,Starling resistor
 Cycliccirculation
 Zone 1 - Zone 3

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ZONE 3

 Distention of vessels (gravity)


 Circulation is continuous & perfusion
pressure (Ppa-Ppv) is constant
 Proximal to distal increasing : transmural
distending pressure (Ppa-Ppl,Ppv-Ppl) ,
vessel radii , blood flow
 Vascular resistance decreases
 The most blood flow is in this zone

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ZONE 4

 Interstitial pressure
 Below the vertical level of left atrium
 Pisf > Ppv & perfusion is based on Ppa-Pisf
 Conditions resembling zone 4:
1. PVR : Volume overload, Emboli , mitral stenosis
2. Negative Ppl : vigorous breathing, airway
obstructions( most common: laryngospasm)
3. Rapid re expansion of lung

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VENTILATION

 PA is constant in the lung


 Ppl increases from apex to bottom (0.25
cmH2O Each cm)
 Density of lung is ¼ of water
 ∆P Is 7.5 cmH2O apex to bottom (30/4)
 Apical Alveoli are 4 fold bigger than the base
so most of the Vt goes to basilar alveoli

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Ventilation-Perfusion Ratio

 Both Ventilation (VA) and Blood flow (Q)


increase linearly with distance down the lung
 Blood flow increases more
( VA/Q <1 in the base)
 Base is hypoxic & hypercapnic
 Because of rapid co2 diffusion ∆P o2> ∆Pco2
apex to base ( 3 fold)

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Non-gravitational Determinants of
PVR & blood flow distribution

 PASSIVE PROCESSES:
 Cardiac output: Pulmonary vascular system is high
flow and low pressure so : QT increases more than
Ppa & PVR=Ppa/QT so: PVR decreases
 Lung volumes: FRC is the volume in witch PVR is
minimum , volume increase or decrease from FRC
causes PVR increase:
 Above FRC : Alveolar compression of small vessels
(small vessel PVR)
 Below FRC : 1) Mechanical tortuosity of vessels (passive)
2) Vasoconstriction (main mechanism) (active)

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Non-gravitational Determinants of
PVR & blood flow distribution

 ACTIVE PROCESSES:
1.local tissue derived products
2.alveolar gas concentrations
3.neural influences
4.humoral (hormonal)

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Local tissue derived products

 From Endothelial – Smooth muscle


1) NO : predominant endogenous vasodilator compound
L- Argenine NOS L-Citruline + NO
has small size , freely diffuses , increases cGMP in SM cells,
dephosphorylates the myosin light chains vasodilatation
NOS :
1) cNOS (constitutive): Permenantly exists,
short bursts of NO ( ca , calmodulin) , keeps PVR low
2) iNOS (inducible) : Inflamation
large quantities & extended duration

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Local tissue derived products
 From Endothelial – Smooth muscle
2) Endotheline:
- ET-1 is the only endotheline that is made in
lungs (vasoconstriction)
- ET receptors: 1) ET A vasoconstriction
2) ET B vasodilatation (NO, prostacyclyn)

- ET -1 Antagonists (Bosentan , sintaxsentan more


selective) are used in treatment of pulmonary hypertension
complication: liver toxicity

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Local tissue derived products

 Vasoactive products:
1) Adenosine Vasodilatation
2) NO Vasodilatation
3) Eicosanoids
a)PGI2 (Epoprostenol , Iloprost) Vasodilatation

b)Thromboxane A2 Vasoconstriction

c)Leukotriene B4 Vasoconstriction
4)Endotheline Vasoconstriction & Vasodilatation

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ALVEOLAR GASES

 Hypoxemia
 Causes localized pulmonary vessel vasoconstriction
(HPV)
 Causes systemic blood vessel vasodilatation
 HPV
 200 µm vessels near small bronchioles
 PSO2 : Oxygen tension at HPV stimulus site that is related to
PAO2 & PvO2 (PAO2 Has much greater effect)
 PSO2-HPV Response is sigmoid : 50% response at
PSO2=PAO2=PvO2=30 mmHg

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CAUSES OF HPV

 Alveolar
hypoxia pulmonary vascular
smooth muscle ETC change H2O2 (2 messenger) Ca
nd

Vasoconstriction
 Epithelial& smooth muscle derived products
 Hypercapnia
16  Acidosis (metabolic & respiratory)
CLINICAL EFFECTS OF HPV

 Life at high altitude (FIO2 Ppa zone1


zone2 PaO2 )
 Hypoventilation – Atelectasis – Nitrogen
ventilation (HPV Shunt )
 Chronic lung disease (asthma-MS-COPD)
administration of pulmonary vasodilator drugs (TNG-SNP-IPN)

Transpulmonary shunting PVR & PaO2

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NEURAL EFFECT

 Sympathetic system
(1st five thoracic nerves+ branches of cervical ganglia & plexus
arising from trachea) act mainly on 60 µm vessels ( α1 effect
is predominant )
 Parasympathetic system
( VAGUS nerve ) , NO-dependent , vasodilatation
acetylcholine binds M3 muscarinic receptor Ca cNOS
 NANC system NO-dependent vasodilatation using
vasoactive intestinal peptide as neurotransmitter

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HUMORAL EFFECTS

 Vasodilator :histamine ( H1 on endothelium-H2 on smooth muscle) ,


adenosine , bradykinin , substance P ,
 Vasoconstrictor :histamine (H1 on smooth muscle), neurokinin,
angiotensin, serotonin,
 Normalizer : ATP

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ALTERNATVE (NON ALVEOLAR)
PATHWAYS OF BLOOD
FLOW THROUGH THE LUNG

 FRC< CC Atelectasis Right to left shunting


 Normal shunting : 1- 3% of cardiac out put (plural &
bronchial circulation)

 Chronic bronchitis : 15% of cardiac out put


 PFO : 20-30% of individuals
 Any condition that causes right atrial pressure to be greater than left
atrial pressure may produce right to left shunting : pulmonary emboli,
COPD, CHF, PS, High peep, Emergence
 TEE is the most sensitive test for detecting PFO in anesthetized patients

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Other nongravitational Determinants
of compliance – resistance – volume
- ventilation
 COMPELIANCE C = ∆V/ ∆P
L/cm H2O

 1/CT=1/CL + 1/CCW
CT = CL X CCW/CL+CCW
 Normally , CL=CCW=0.2 SO CT= 0.1
 In clinic only CT can be measured
 CT 1) Dynamic ∆P/ peak pressure
2) Static ∆P/plateau pressure
 Peep must first subtracted from the peak or plateau pressure

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 LAPLACE expression : P = 2T / R
 T (surface tension)
 R( radius of curvature of the alveolus)
 Surfactant secreted by the intra alveolar type ║ T
lipoprotein

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Airway resistance

 R = ∆P/ ∆V
 R (Resistance) cmH2O/L/sec

 V ( airflow)
L/sec

 ∆P along the airway depends on the caliber


of the airway & pattern of airflow

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Patterns of airflow

 LAMINAR : Gas passes down a parallel sided tube at less than


a certain critical velocity ∆P = V X 8L X µ/πr4 µ is viscosity
 TURBULENT: when flow exceeds the critical velocity becomes
turbulent ∆P=V2 X p X f X L/4 πp2is
r5
density , f is friction
factor
 ORFICE : occurs at severe constrictions (kinked ETT, laryngospasm)
the pressure drop is proportional to the square of the flow

Laminar flow is confined to the airways below the main bronchi,


flow in trachea is turbulent , & orifice flow occurs at the larynx

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DIFFERENT REGIONAL LUNG TIME
CONSTANTS

‫זּ‬ =CT X R
 ‫( זּ‬time constant) is the time required to
complete 63% of an exponentially changing
function (2‫ = זּ‬87% ,3 ‫ =זּ‬95% ,4 ‫=זּ‬98%)

 CT = 0.1 ,R= 2 so ‫=זּ‬0.2 sec 4 ‫=זּ‬0.8 sec


 Time increases as resistance or compliance
increases

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Pathway of collateral ventilation

 Non gravitational
 Are designed to prevent hypoxia in neighboring
1. Interalveolar communications (kohn pores)
2. Distal bronchiolar to alveolar (lambert channels)
3. Respiratory bronchiole to terminal bronchiole (martin
channels)
4. Interlobar connections

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WORK OF BREATHING
 Work=force x distance, Force=pressure x area, Distance=volume/area
 So WORK = PRESSURE x VOLUME
 If R or C ,P , Work
 The metabolic cost of the work of breathing at rest is only 1-3% of the
total O2 consumption , and increases up to 50% in pulmonary disease
 Expiration is passive using potential energy that has been saved
during inspiration (awake)
 In anesthetized person with diffuse obstructive airway disease resulting
from the accumulation of secretions, elastic and airway resistive
component of respiratory work would increase
 For a constant minute volume , both deep , slow (elastic resistance ) &
shallow , rapid (airway resistance ) breathing will increase work of
breathing

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LUNG VOLUMES

 FRC: the volume of gas in lung at end of normal expiration


 At FRC , There is no air flow & PA = ambient pressure
 Expansive chest wall elastic forces are exactly balanced by retractive lung
tissue elastic forces
 ERV: is part of FRC, the volume of gas that can be consciously exhaled
 RV: the minimum volume that remains after ERV
 VC: ERV + IC
 IC : VT+ IRV
 TLC: VC+ RV

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LUNG VOLUMES

 Volumes that can be measured by simple


spirometry are VT , VC , IC , IRV ,ERV
 TLC ,FRC & RV cannot be measured by spirometry
 How to measure TLC ,FRC & RV :
1. Nitrogen wash out
2. Inert gas dilution
3. Total body plethysmography

 disparity between FRC in 2&3 is used to detect


large nonventilating airtrapped blebs

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Airway closure & closing capacity

 Ppl increases from top to the bottom and


determines alveolar volume, ventilation &
compliance
 Gradients of Ppl may lead to airway closure
and collapse

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Airway closure in patients with normal
lung

 In normal resting end expiratory state (FRC) , the distending


transpulmonary exceeds intrathoracic air passage transmural
pressure and the airways remain patent

 During the middle of normal inspiration ∆P increases and the


airways remain patent

 During the middle of normal expiration ,expiration is passive


and PA is related to elastic recoil of the lung, airways remain
patent

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4. During the middle of forced expiration , Ppl increases more
than atmospheric pressure, in alveoli because of elastic recoil
of alveolar septa, pressure is higher than Ppl, pressure drops
down as air passes to the greater airways, and there be a
place at which intraluminal pressure equals Ppl (EEP), down
stream this point (small or large airways) air way closure will occur

 Distal to 11th generation there is no cartilage=bronchioles


 Airway patency below this point is due to lung volume
above this point is due to intra thoracic pressure

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 If
lung volume decreases EPP goes
downward (closer to alveolus ).

 Near RV small airways (<0.9mm) tend to close

 Airway closure first happens in dependent


lung regions (Ppl> Pintraluminal)

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Airway closure in patients with
abnormal lung

 EPP Is lower, airway closure occurs with lower gas flow, and
higher lung volume R ,Flow , Air way Radii
 Emphysema: Elastic recoil
 Epp is close to alveoli , transmural ∆p can become negative
 Epp is very near to point of collapse
 Bronchitis: Weak airway structure that may be closed with little
negative transmural ∆p
 Asthma: Bronchospasm narrow middle size airways
forced expiration closure
 Pulmonary Edema: peri brounchial & alveolar fluid cuffes
alveolus &bronchi FRC , CC
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Closing Capacity
 Spirogram: phase 1 :Exhale to RV
phase 2 :Inhale to TLC
phase 3 :Exhale to ERV
phase 4 :RV
 Measurement of CC : Using a tracer gas
 Phase 3 : constant concentration of tracer gas
 Phase 4 : sudden rise in tracer gas concentration
CC is the border between phase 4 & RV

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 CC: Is the amount of gas that must be in the lunges
to keep the small conducting airway open & is = RV+
CV
 CV: CV is the difference between the onset of phase
4 & RV
 CC : Smoking , obesity , aging , supine position
44 years CC = FRC in supine position
66 years CC = FRC in upright position

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Relationship Between FRC & CC
 CC >> FRC Atelectasis (CC > VT)
 CC > FRC Low VA/Q (CC is in VT) volume
dependent
 FRC > CC Normal
 IPPB In awake individual increases Inspiratory
time & increases VA/Q
 IPPB In anesthetized patients (Atelectasis in
dependent Area) patient’s lung will not be reserved
 If peep is added FRC FRC > CC no
closure

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Oxygen & carbon dioxide
transport
 Two thirds of each breath reaches alveoli
 The remaining third is termed physiologic or
total dead space VDphy = VDAna +VD Alv
 physiologic dead space:
1. Anatomic dead space (airway) 2 cc/kg
2. Alveolar dead space (zone 1- emboli)
upright 60-80 cc
supine VDphy = VDAna (VD Alv= 0)

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 Naturally Vco2 (co2 entering the alveoli) is equal to the co2
eliminated
 Vco2 = (VE)(FE co2)
 Expired gas = alveolar gas + VD gas
 So Vco2 = (VA)(FA co2)+(VD)(FI co2)
 Modified bohr equation :
VD/VT=(Pa co2 – PE co2) / Pa co2
 In a healthy adult VD/VT < 30%
 In COPD VD/VT > 60%

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 Alveolar gas concentration = FI gas – out put/alveolar vent.
PA gas = FI gas + V gas / VA
 P dry Atmospheric = P wet Atmospheric – P H20
 713 = 760 – 47
 PA O2 = 713 X (FIO2 – VO2/VA)
 PA CO2=713 X (V co2 /VA) x 0.863
 Fresh gas flow < 4 lit/min PaCO2 ,PA O2

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Oxygen Transport

 Cardiopulmonary system has the ability to


increase function more than 30 folds
 Functional links in the oxygen transport chain:
 Ventilation
 Diffusion of o2 to blood
 Chemical reaction of o2 with Hb
 QT of arterial blood
 Distribution of blood to tissue and release of o2

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Oxygen-hemoglobin dissociation
curve

 Hb molecule consists of four heme molecule attached to a


globin molecule
 Each heme molecule consist of :
 glycine ,
 α-ketoglutaric acid
 Iron in ferrous form ( ++ )
 Hb is fully saturated by a PO2 of about 700 mm Hg
 This curve relates the saturation of Hb to PaO2
 PaO2 = 90 -100 SaO2=95-98
 PaO2 = 60 SaO2=90
 PVO2 = 40 SVO2 =75

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 O2 CONTENT : Amount of oxygen in 0.1 lit blood
 Oxygen is carried in solution in plasma 0.003 ml/mmHg/100 cc
 Theoretically 1 g of Hb can carry 1.39 ml of oxygen (1.31)
 O2 Supply = O2 available + 200 ml O2 /min/1000 ml blood
 O2 available = o2 reaches to tissues
 VO2 = 250 ml/min
 CaO2 = (1. 39 )(Hb)(SaO2) + (0.003)(PaO2)
 O2 Supply (transport) ml/100 cc = QT X CaO2
 SaO2= 40 O2 Supply=400 , O2 available =200 , VO2 = 250
Body Must increase QT or Hb
43
 In natural Po2 (75-100) The curve is relatively horizontal so
shifts of the curve have little effect on saturation

 P 50 : oxygen tension that make 50% of Hb saturated

 Normally P 50 is 26.7 mmHg

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 Left shifted O2-Hb curve  Right shifted O2-Hb
P50 < 27 curve P50 > 27
– Acidosis
– Alkalosis
– Hyperthermia
– Hypothermia
– Increased 2,3 DPG
– Abnormal & fatal Hb
– Abnormal Hb
– Decreased 2,3 DPG
old blood containing citrate ,
– Inhaled anesthetics
dextrose 1 MAC isoflurane shifts P50 to
(adding phosphate minimizes right 2.6 + 0.07 or -0.07
changes) – Narcotics have no effect
on the curve

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Effect of QS/QT on PaO2

 PAO2 is directly related to FIO2 in normal patients


 With a 50 % shunt of QT , increase in FIO2 results in
no increase in PAO2

so in this case treatment of hypoxemia is not
increasing the FIO2 , and is decreasing the
percentage of the shunt ( bronchoscopy , peep ,
positioning , antibiotics , suctioning , diuretics )

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Effect of QT on VO2 & CaO2

 CaO2 will decrease if VO2 increases or QT decreases


 In both conditions CVO2 is decreased because of more tissue o2
extraction
– Primarily: less O2 is available for blood & blood with lower CVO2 passes
trough the lung
– Secondarily: Mixture of this blood with oxygenated end-pulmonary
capillary blood (c’) decreases CaO2 (Qc’ =QT – QS)
 QS/QT = Cc’ O2 - CaO2 / Cc’ O2 - CVO2
 Decrease In CVO2 is > than CaO2 and the ratio is 2 to1 for 50% QS

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Table 17- 4

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FICK principle

 Fick principle is for calculation of VO2


1- O2 Consumption = O2 leaving the lung – O2 returning to the lung
 VO2 = (QT)(CaO2) –(QT)(CvO2) = QT(CaO2-CvO2)
 Normal C(a-v)O2= 5.5 ml O2/0.1 lit
 Normally VO2 = 0.27 L/min (5)(5.5)/(0.1)
2- O2 Consumption = O2 brought to the lung - O2 leaving the lung
 VO2 =VI(FIO2) - VE(FEO2) = VE( FIO2 – FEO2) (VI is considered equal to VE)
 Normally VO2 = 0.25 L/min (5)(0.21-0.16)
 PEO2 is measured from a sample of expired gas
 PEO2/dry atmospheric pressure(713) = FEO2

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 If VO2 remains constant and QT decreases the
arteriovenous O2 content gradient must increase
 QT decrease causes much larger and primary decrease in
CVO2 versus a smaller and secondary decrease in CaO2

 CVO2 & PVO2 are much more sensitive to QT


changes

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CARBON DIOXIDE TRANSPORT

 Circulating CO2 is a function of:


 CO2 production parallels O2 consumption
 CO2 elimination that depends on :
1) pulmonary blood flow
2) ventilation
 Respiratory quotient = V CO2 / V O2 Normally = 0.8
only 80% as much co2 produced as o2 is consumed
 It depends on structure of metabolic substrate that is used
 For Carbohydrates R = 1
 For fats R = 0.7

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 CO2 transport in plasma
 Acid carbonic (H2CO3 ) 7%
-
 Bicarbonate (HCO3 ) 80%
 CO2 transport in RBC
 Carbaminohemoglobin (Hb-CO2) 13% Using carbonic anhydrase
 H2O + CO2 carbonic anhydrase H2CO3 in RBC
-
 99.9% of H2CO3 Is Rapidly transformed to H+ + HCO3
 Carbonic anhydrase contains zinc and moves reaction to right at a
rate of 1000 times faster than in plasma
+ _ _
 H is bufferd with Hb (HHb) ,HCO3 goes to the plasma and Cl
enters the cell , CO2 + HHb = HbCO2
 Solubility coefficient (α) of CO2 is 0.03 mmol/L

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BOHR Effect

 The effect of PCO2 & H+ on oxyhemoglobin


dissociation curve

 Right shift : hypercapnia & acidosis


 Left shift : hypocapnia & alkalosis

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HALDEN Effect

 Effect of oxygen on carboxyhemoglobin


dissociation curve

 Left shift Low PO2


 More CO2 uptake from tissues by blood
 Right shift High PO2
 More CO2 dissociates from blood in lungs

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Structure of alveolar septum

 Capillary blood is separated from alveolar gas by


these layers:
– Capillary endothelium
– Endothelial basement membrane
– Interstitial space
– Epithelial basement membrane
– Alveolar epithelium ( type I pneumocyte)
 On one side of alveolar septum (thick , upper – fluid & gas
exchanging side) there is connective tissue and interstitial space
 On the other side (thin , down- gas exchange only) basement
membranes are fused and there is a greatly restricted interstitial space

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 There are tight junctions on the epithelium of the
upper side (passage of fluid from interstitial space to alveolus)
 There are loose junction on the endothelium of the
upper side (passage of fluid from intravascular space to interstitial space)
 Pulmonary capillary permeability depends on the
size & number of loose junctions

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1. Interstitial space is between periarteriolar and
peribronchial connective tissue shit and between
epithelium & endothelium basement membrane in
alveolar septum
2. The space has a progressively negative distal to
proximal ΔP

 Negative ΔP increases brochi and arteries’ diameter

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Transcapillary-interstitial space fluid
movement

 ΔP distal to proximal & arterial pulsation &


Because of
lymphatic valves interstitial fluid flows from bronchi to
proximal

F = K [(PINSIDE – POUTSIDE) –(πINSIDE- πOUTSIDE)] (500 ml/day)


 K = capillary filtration coefficient ml/min/100 g
a product of surface area & the permeability per unit

P= capillary hydrostatic pressure (10 inside)
 Π = colloid oncotic pressure (26 inside in zone 2-3)

Proximal to zone 2 – 3 PINSIDE decreases and fluid is reabsorbed

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Respiratory function during anesthesia

 Oxygenatoin is impaired in most patients


during anesthesia (more in elderly-obese-smokers)

 Venus admixture (shunt) during anesthesia is


about 10% that closely correlates with the
degree of atelectasis

59
 The effect of a given anesthetic on
respiratory function depends on :
2. The depth of general anesthesia
3. Preoperative respiratory function
4. Presence of special intraoperative anesthetic or
surgical condition

60
Effect of depth of anesthesia on
respiratory pattern

 Less than MAC


may vary from excessive hyperventilation to breath holding
 1 MAC (light anesthesia)
regular pattern with larger VT than normal
 More deep
end inspiration pause (hitch) – active and prolong expiration
 More deep (moderate)
faster and more regular – shallow –no pause – I = E
 Deep
1. Narcotic- N2O : Deep and slow
2. Voletiles : rapid & shallow (panting)
 Very deep
all inhaled drugs : gasping-jerky respiration – paradoxical movement of chest-abdomen (only
diaphragmatic respiration) just like airway semi obstruction or partial paralysis

61
Effect of depth of anesthesia on
spontaneous minute ventilation

 VE decreases progressively as depth of anesthesia


increases
 ET CO2 increases as depth of anesthesia increases
 Increase of CO2 caused by halogenated anesthetics
(<1.24 MAC) enflurane > desflurane =isoflurane > sevoflurane > halothane
(>1.24 MAC) enflurane = desflurane > isoflurane > sevoflurane
 Ventilation response to CO2 increase is decreased
 Apneic threshold is increased

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EFFECT OF PREEXISTING RESPIRATORY
DISFUNCTION ON THE RESPIRATORY
EFFECT OF ANESTHESIA

 CC is very close to FRC in these patients


 anesthesia causes FRC to be decreased
 CC becomes greater than FRC ATELECTASIS and
SHUNT
1. Acute chest (infection) or systemic (sepsis-MT-CHF-CRF) disease
2. Heavy smokers
3. Emphysema & bronchitis
4. Obese people
5. Chest deformities
 Anesthesia inhibits HPV (further shunting) ,decreases mucus
velocity flow

63
Effect of special intraoperative condition on
the respiratory effects of anesthesia

 Surgical positioning ,massive blood loss, surgical


retraction on the lung will decrease QT , May cause
hypoventilation & FRC reduction

 All of these conditions will magnify respiratory depressant effect


of any anesthetic

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Mechanism of hypoxemia during
anesthesia

1. Malfunction of equipment
 Mechanical failure of anesthesia apparatus to deliver O2 to the patient
 Mechanical failure of tracheal tube
 Hypoventilation
 Hyperventilation
 FRC decrease (supine position-induction of anesthesia-paralysis- light anesthesia- airway
resistant increase- excessive fluid administration- high inspired oxygen-secretion removal decrease)
 Decreased QT & increased VO2
 HPV inhibition
 Paralysis
 Right to left intra arterial shunting
 Specific diseases

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1- Malfunction of equipment

 Mechanical failure of anesthesia apparatus to


deliver O2 to the patient
1. Disconnection (Y piece)
2. Failure of O2 supply system
3. Wrong cylinder
air way pressure monitoring & FIO2 analyzer will detect most of the causes
 Mechanical failure of tracheal tube
 Esophageal intubation
 Disconnection low pressure
 Others (kincking- secretions-ruptured cuff) R increases & hypo ventilation
occurs endo bronchial intubation = hypoventilation+shunt
30 ° trendelenburg = endo bronchial intubation

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2- Hypoventilation

- VT is reduced under GA :
1. Increased work of breathing
2. Decreased drive of breathing

- Decrease in VT causes hypoxemia in 2 way


1. Atelectasis
2. Decrease in over all V/Q ratio

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3- Hyperventilation

 Hypocapnic alkalosis may result in hypoxemia :

2. QT decrease
3. VO2 increase
4. HPV inhibition
5. Left shift of oxy-hemoglobin dissociation curve
6. R increase & CL decrease

68
4- Decrease in FRC
 Induction of general anesthesia decreases FRC
15 – 20 %
 So CL is decreased
 MAX decrease is within the first few minutes
 FRC decrease in awake patients is very slightly
during controlled ventilation
 FRC is inversely related to BMI
 FRC decrease continues into the post operative
period
 Application of peep may restore FRC to normal

69
Causes of reduced FRC

 Supine position: FRC is reduced 0.5-1 lit


( diaphragm is
displaced 4 cm cephalad ,pulmonary vascular
congestion happens )
 Induction of GA:
Thoracic cage muscle tone change:
loss of
inspiratory tone & increase in end expiratory tone
(abdominal) Increases intra abdominal pressure ,
displaces diaphragm more cephalad and
decreases FRC
70
Causes of reduced FRC

 Paralysis : diaphragm separates two compartments of


high different hydrostatic gradients. Abdomen(1 cmH2O/cm)
and thorax (0.25 cmH2O/cm)

 In upright position there is no trans diaphragmatic pressure


gradient
 In supine higher trans diaphragmatic gradient must be generated
toward dependent parts of diaphragm to keep abdominal contents
out of thorax
 In un paralyzed this tension is developed by 1)diaphragmatic
passive stretch 2)neurally mediated active contracture
 In paralyzed diaphragmatic motion is more cephalad
 Pressure on diaphragm In un paralyzed by an increased expiratory
muscle tone = pressure caused by the weight of abdominal contents
In paralyzed
71
Causes of reduced FRC

4. Light anesthesia & active expiration


 general anesthesia increases expiratory muscle tone but this is not
coordinated (spontaneous ventilation in contrast )
 Light general anesthesia : forceful active expiration – raises intra
thoracic pressure – collapse may occur
 In a normal subject collapse may occur during a max forced expiration
and is responsible for wheeze on both awake and anesthetized
patients
 Use of sub atmospheric expiratory pressure in paralyzed can cause
air way closure, gas trapping, & decrease in FRC

72
Causes of reduced FRC

5. Increased airway resistance :


 Over all reduction of all components of lung volumes
 Reduced airway caliber increased resistance collapse
 FRC decreases 0.8 lit in supine position, 0.4 lit because of
induction of anesthesia volume , resistance
 Tracheal tube increases resistance
(reduces size of the trachea 30-50%)
 Respiratory apparatus increases resistance
 ETT + Respiratory apparatus Imposes an additional work of
breathing 2-3 times normal

73
Causes of reduced FRC

6. Supine position, immobility, excessive


intravenous fluid administration:
 Dependent areas below the heart (zone3-4) are susceptible
to edema

 After long time being immobile in supine position with excess


volume administration in nondependent areas this will happen
too (5 hour or more)
 Changing position every hour is beneficial

74
Causes of reduced FRC

7 .High inspired oxygen concentration and


absorption atelectasis:
 Administration of FIO2>30% turns Low V/Q areas (1/10 to 1/100) to
shunt (atelectasis)
 As O2 increases, PAO2 raises , net flow of gas into blood exceeds
the inspired gas , the lung unit becomes progressive smaller &
collapse occurs if
1. High FIO2
2. Low V/Q
3. Long time exposure
4. Low CVO2

FIO2>50% Can produce atelectasis solely (therapeutic-measurement)

75
Causes of reduced FRC

8 . Surgical position:
– Supine : FRC
– Trendelenburg: FRC
– Steep trendelenburg: FRC most of the lung is zone3-4
– Lateral decubitus : FRC in dependent lung and
FRC in un dependent lung (overall FRC )
– Lithotomy & Kidney : FRC more than supine
– Prone : FRC

76
Causes of reduced FRC

9 .Ventilation pattern:
Rapid shallow breathing is a regular feature of
anesthesia FRC &CL promote atelectasis.
 Probable cause is increasing surface tension
 This can be prevented by
 Periodic large mechanical inspiration
 Spontaneous sigh
 Peep

77
Causes of reduced FRC

10. Decreased removal of secretion:


Increasing viscosity & slowing mucocilliary clearance
 Tracheal tube (low or high pressure cuffs any place in trachea)
 High FIO2
 Low moisture
 Low temperature <42°
 Halogenated anesthetics (does not stop)

78
5. Decreased cardiac out put &
increased VO2

 QT & VO2 CVO2 CaO2

 QT decrease : MI , Hypovolemia
 VO2 increase : sympathetic activity,
hyperthermia, shivering

79
6 . Inhibition of HPV

 Normally PAO2 Decrease will cause HPV


 Pulmonary circulation is poorly endowed with
smooth muscle
 Any condition that causes Ppa increase may cause
HPV decrease
 Direct: nitroprusside ,TNG, Isoproterenol ,inhaled
anesthetics, hypocapnia
 Indirect: MS , fluid overload, high fio2 ,
hypothermia ,emboli, vasoactive drugs, lung
disease

80
7 . Paralysis

 Normally Dependent or posterior part of diaphragm in supine


position is the part that has lesser radius and more muscle and
therefore contracts more effectively ( more ventilation)
 Dependent lung has the most perfusion
 Most perfusion in most ventilated area
 In paralyzed patients : nondependent or anterior part of
diaphragm moves most (passive movement)
 Dependent lung has the most perfusion
 Most perfusion in least ventilated area

81
8 . Right to left interatrial shunting

 Patent foramen ovale


 Increased right side pressure

 Administration of inhaled NO decrease PVR


& functionally close the PFO

82
9 . Specific diseases :

 Emboli: severe increase in Ppa right to left transpulmonary


shunting (PFO-opened arteriovenous anastomoses) Edema
inhibition of HPV - dead space ventilation & hypoventilation

 ARDS : complement mediated decreased QT- FRC-CL &


hypoxemia

83
MECHANISM OF HYPER &
HYPOCAPNIA DURING ANESTHESIA

 Hypercapnia :

2. Hypoventilation
3. Increased dead space ventilation
4. Increased CO2 production
5. Inadvertent switching off of CO2 absorber

84
HYPOVENTILATION

 Increasedairway resistance
 Decreased respiratory drive
 Decreased compliance (position)

85
Increased dead space ventilation

 Decreased Ppa (hypotension) zone 1


increased alveolar dead space
 vascular obliteration (emboli – clamping - aging)
dead space is increased with aging VD/VT= 33+ age/3
4. The anesthesia apparatus
 Increase in anatomic dead space from 33% to 46% in intubated
subject , & to 64% in mask ventilated subject
 Rebreathing : is increased
1) spontaneous ventilation A D C B
2) controlled ventilation D B C A
 No rebreathing occurs In E system (ayer’s T-piece) with enough
fresh gas flow & expiratory time

86
Increased CO2 production

 Anyreason causes increase in O2


consumption ( VO2 ) will increase CO2
production
– Hyperthermia
– Shivering
– Light anesthesia
– Catecholamine release
– Hypertension
– Thyroid storm

87
Inadvertent switching off of CO2
absorber

 Occurrence of hypercapnia depends on:


 Patient ventilatory responsiveness
 Fresh gas flow
 Circle system design
 cO2 production

 Highfresh gas flow (>5lit /min) minimize this


problem with almost all systems for almost all
patients

88
hypocapnia

 Hyperventilation (most common)


 Decreased PEEP
 Increased Ppa
 Decreased VD ventilation
 Decreased rebreathing
 Decreased CO2 production :
hypothermia- deep anesthesia-hypotension

89
Physiologic effect of abnormalities in
respiratory gases

 Hypoxia
 The essential feature of hypoxia is cessation of
oxidative phosphorylation when mitochondrial
PO2 falls below a critical level
 Anaerobic production of energy is insufficient and produces
+
H & LACTATE which are not easily excreted and will accumulate

 The Most susceptible organ to hypoxia is the brain in an


awake patient and the heart in an anesthetized patient and the
spinal cord in aortic surgery

90
Cardiovascular response to hypoxia

 Reflex (neural & humoral)


 Direct effect

 The reflex effect occurs first and are excitatory


and vasoconstrictory (general)
 The direct effect is inhibitory and vasodilatory
and occur late (local)

91
Cardiovascular response to hypoxia

 Mild hypoxia (SPO2>80%)


Sympathetic activation BP , HR , SV
 Moderate hypoxia (80%>SPO2>60%)
Local vasodilatation , HR , SVR
 Severe hypoxia (SPO2<60%)
BP ,HR , Shock , VF , Asystole
 With preexisting hypotension even in mild hypoxemia
shock can be developed

92
 Hypoxia can induce arrhythmia :
 arrhythmias are usually ventricular (UF,MFPVC-VT-VF)

 Direct : decrease in heart’s O2 supply


 Tachycardia : increase demand
 Increase SVR : increase after load and therefore demand
 Decrease SVR : decrease supply

 The level of hypoxemia that will cause cardiac arrhythmias


varies case to case

93
Other Important effects

 Hypoxemia causes CBF to increase even at


the presence of hypocapnia
 Ventilation will be stimulated
 Ppa is increased
 Chronic hypoxia leads to an increase in Hb &
2,3 DPG .(right shift in curve)

94
Hyperoxia

 Exposure to high O2 tension clearly cause


pulmonary damage in healthy individuals
 Dose-Time toxicity :

100% O2 is not allowed for more than 12 hours


80% O2 is not allowed for more than 24 hours
60% O2 is not allowed for more than 36 hours
 No changes has been observed after administration of 50% O2 for
long period

95
Symptoms & complications

1. Respiratory distress
(mild irritation in the area of carina and coughing)
 Pain
 Severe dyspnea 12 hour

(paroxysmal coughing- decreased VC) recovery : 12-24 hour


 Tracheobronchitis
(Decrease in CL & ABG )
 pulmonary edema 12 hour to few days

 pulmonary fibrosis few days to weeks

96
1. Ventilation depression & hypercapnia
2. Absorption atelactasis
3. Retrolental fibroplasia
abnormal proliferation of immature retinal vasculature in pre matures
extremely premature infants are more susceptible :
1 )less than 1 kg birth weight
2) less than 28 weeks’ gestation
3)PaO2 > 80 for more than 3 hour in an infant gestation+life age<44
week
 In presence of PDA arterial blood sample should be taken from right
radial artery ( umbelical & lower extermities have lower O2)

97
ENZIMATIC & METABOLIC CHANGES

 Enzymes particularly those with sulfhydryl groups,


are inactivated by O2 derived free radicals

 Inflamatory mediators then are released from


neutrophils that will damage epithelium &
endothelium & surfactant systems

 Most acute toxic effect is convulsion(>2 atm)

98
Therapeutic effect

 Clearance of gas loculi in the body may be


greatly accelerated by the inhalation of 100%
O2
 It creates a large nitrogen gradient from loculi
to blood so the size of loculi diminishes
– Intestinal obstruction
– Air embolus
– Pneumopritoneum
– Pneumocephalus
– pneumothorax

99
Hypercapnia

 Cardiovascular system:
 Direct: cardiovascular depression
 Indirect: activation of sympathoadrenal system

– Indirect effect may be equal,more or less than


direct effect
– Cathecholamine level during anesthesia is equal
to the level in awake patients

100
 Hypercapnia just like hypoxia may cause increase
myocardial demand (tachycardia, early hypertension) and
decrease supply (tachycardia, late hypotension)
 Hypercapnia induced arrhythmias
– are sirous during anesthesia in contrast of awake patients
– all voletiles decrease QT interval torsades de pointes & VF
– With halothane arrhythmias frequently occur above a PaCO2
arrhythmic threshold that is constant for a particular patient

101
 Max stimulatory respiratory effect is at a PCO2 about
100
 Further increase causes right-shift in PCO2
ventilation-response curve
 Anesthetic drugs cause a right-shift in PCO2
ventilation-response curve
 CO2 narcosis occurs when PCO2 rises to more than
90-120 mm Hg
 30% CO2 is sufficient for production of anesthesia
and causes total flattening of EEG

102
 It causes bronchodilatation
 In constant N concentration any increase in CO2 can cause
decrease in O2
 It shifts the oxyhemoglobin dissociation curve to right &
increase tissue oxygenation
 Chronic hypercapnia increases resorption of bicarbonate and
metabolic alkalosis
+
 It causes K leakage from cell to plasma (Mostly from liver from
glucose metabolism due to increased catecholamines )
 Oculocephalic reflex is more common

103
Hypocapnia

 Mostly is due to hyperventilation


 Causes QT decrease in tree ways
 Increase in intra thoracic pressure
 Withdrawal of sympathetic activity
++
 Increase in PH & So decrease in Ca

104
 Alkalosis shifts oxy-Hb curve to left so Hb affinity to
O2 increases & tissue oxygenation decreases
 Whole body VO2 is increased because of increase
in PH
 PCO2 = 20 30% Increase in VO2
 HPV is inhibited & CL is decreased , and
bronchoconstriction is produced VA/Q abnormalities

 Passive hypocapnia promotes apnea

105