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RESPIRATORY PHYSIOLOGY & RESPIRATORY FUNCTION DURING

ANESTHESIA

Houman Teymourian M.D.Assistant professorDepartment of Anesthesiology and Critical Care, Shohada hospitalShahid 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 volumes2. 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

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ZONE 1

Collapse & Alveolar dead space

1) Ppa (SHOCK) 2)PA (Vt & peep )

Normally little or no zone 1 exists in the lung

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ZONE 2

Waterfall,Weir,Sluice,Starling resistor Cyclic circulation 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:1. Cardiac output: Pulmonary vascular system is high flow

and low pressure so : QT increases more than Ppa & PVR=Ppa/QT so: PVR decreases

2. 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 muscle1) 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 muscle2) 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 (2nd messenger) Ca

Vasoconstriction Epithelial & smooth muscle derived products Hypercapnia Acidosis (metabolic & respiratory)

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CLINICAL EFFECTS OF HPV

1. Life at high altitude (FIO2 Ppa zone1 zone2 PaO2 )

2. Hypoventilation – Atelectasis – Nitrogen ventilation (HPV Shunt )

3. Chronic lung disease (asthma-MS-COPD) administration of pulmonary vasodilator drugs (TNG-SNP-IPN)

Transpulmonary shunting PVR & PaO2

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NEURAL EFFECT

1. Sympathetic system (1st five thoracic nerves+ branches of cervical ganglia & plexus arising from trachea) act mainly on 60 µm vessels ( α1 effect is predominant )

2. Parasympathetic system ( VAGUS nerve ) , NO-dependent , vasodilatation acetylcholine binds M3 muscarinic receptor Ca cNOS

3. NANC system NO-dependent vasodilatation using vasoactive intestinal peptide as neurotransmitter

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HUMORAL EFFECTS

1. Vasodilator :histamine ( H1 on endothelium-H2 on smooth muscle) , adenosine , bradykinin , substance P ,

2. Vasoconstrictor :histamine (H1 on smooth muscle), neurokinin, angiotensin, serotonin,

3. 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 L/cm H2O= ∆V/ ∆P 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 = V X 8L X µ/πr4 µ is viscosity

TURBULENT: when flow exceeds the critical velocity becomes turbulent p is 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

∆P

∆P=V2 X p X f X L/4 π2r5

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DIFFERENT REGIONAL LUNG TIME CONSTANTS

CT X R= ּז is the time required to (time constant) ּז

complete 63% of an exponentially changing function (2 98%=ּז 4 ,95%= ּז 3 ,87% = ּז )

CT = 0.1 ,R= 2 so 0.2=ּז sec 4 0.8=ּז 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 out2. Inert gas dilution3. 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

1. In normal resting end expiratory state (FRC) , the distending transpulmonary exceeds intrathoracic air passage transmural pressure and the airways remain patent

2. During the middle of normal inspiration ∆P increases and the airways remain patent

3. 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 :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:1. Ventilation

2. Diffusion of o2 to blood

3. Chemical reaction of o2 with Hb

4. QT of arterial blood5. 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

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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

P50 < 27

– Alkalosis– Hypothermia– Abnormal & fatal Hb– Decreased 2,3 DPG old blood containing citrate ,

dextrose (adding phosphate minimizes

changes)

Right shifted O2-Hb curve P50 > 27

– Acidosis– Hyperthermia– Increased 2,3 DPG– Abnormal Hb– Inhaled anesthetics 1 MAC isoflurane shifts P50 to

right 2.6 + 0.07 or -0.07– 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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1. If VO2 remains constant and QT decreases the arteriovenous O2 content gradient must increase

2. 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:1. CO2 production parallels O2 consumption

2. 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 plasma1. Acid carbonic (H2CO3 ) 7%2. 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

Because of ΔP distal to proximal & arterial pulsation & 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

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The effect of a given anesthetic on respiratory function depends on :

1. The depth of general anesthesia

2. Preoperative respiratory function

3. Presence of special intraoperative anesthetic or surgical condition

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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 slow2. 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

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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

1. Anesthesia inhibits HPV (further shunting) ,decreases mucus velocity flow

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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

2. Hypoventilation3. Hyperventilation4. FRC decrease (supine position-induction of anesthesia-paralysis- light anesthesia- airway

resistant increase- excessive fluid administration- high inspired oxygen-secretion removal decrease)

5. Decreased QT & increased VO26. HPV inhibition7. Paralysis8. Right to left intra arterial shunting9. 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 system3. Wrong cylinder

air way pressure monitoring & FIO2 analyzer will detect most of the causes

Mechanical failure of tracheal tube1. Esophageal intubation2. Disconnection low pressure3. 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 way1. Atelectasis

2. Decrease in over all V/Q ratio

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3- Hyperventilation

Hypocapnic alkalosis may result in hypoxemia :

1. QT decrease

2. VO2 increase

3. HPV inhibition

4. Left shift of oxy-hemoglobin dissociation curve

5. R increase & CL decrease

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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

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Causes of reduced FRC

1. Supine position: FRC is reduced 0.5-1 lit ( diaphragm is displaced 4 cm cephalad ,pulmonary vascular congestion happens )

2. 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

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Causes of reduced FRC

3. 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

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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

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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

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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

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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)

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Causes of reduced FRC

8 . Surgical position:1. Supine : FRC

2. Trendelenburg: FRC 3. Steep trendelenburg: FRC most of the lung is zone3-4

4. Lateral decubitus : FRC in dependent lung and FRC in un dependent lung (overall FRC )

5. Lithotomy & Kidney : FRC more than supine

6. Prone : FRC

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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

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Causes of reduced FRC

10. Decreased removal of secretion: Increasing viscosity & slowing mucocilliary clearance

1. Tracheal tube (low or high pressure cuffs any place in trachea)

2. High FIO2

3. Low moisture

4. Low temperature <42°

5. Halogenated anesthetics (does not stop)

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5. Decreased cardiac out put & increased VO2

QT & VO2 CVO2 CaO2

QT decrease : MI , Hypovolemia VO2 increase : sympathetic activity,

hyperthermia, shivering

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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

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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

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8 . Right to left interatrial shunting

Patent foramen ovale Increased right side pressure

Administration of inhaled NO decrease PVR

& functionally close the PFO

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9 . Specific diseases :

1. Emboli: severe increase in Ppa right to left transpulmonary shunting (PFO-opened arteriovenous anastomoses) Edema inhibition of HPV - dead space ventilation & hypoventilation

2. ARDS : complement mediated decreased QT- FRC-CL & hypoxemia

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MECHANISM OF HYPER & HYPOCAPNIA DURING ANESTHESIA

Hypercapnia :

1. Hypoventilation

2. Increased dead space ventilation

3. Increased CO2 production

4. Inadvertent switching off of CO2 absorber

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HYPOVENTILATION

Increased airway resistance Decreased respiratory drive Decreased compliance (position)

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Increased dead space ventilation

1. Decreased Ppa (hypotension) zone 1 increased alveolar dead space

2. vascular obliteration (emboli – clamping - aging)

dead space is increased with aging VD/VT= 33+ age/3

3. 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

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Increased CO2 production

Any reason causes increase in O2 consumption ( VO2 ) will increase CO2 production

– Hyperthermia– Shivering– Light anesthesia– Catecholamine release– Hypertension– Thyroid storm

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Inadvertent switching off of CO2 absorber

Occurrence of hypercapnia depends on: Patient ventilatory responsiveness Fresh gas flow Circle system design cO2 production

High fresh gas flow (>5lit /min) minimize this problem with almost all systems for almost all patients

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hypocapnia

1. Hyperventilation (most common)

2. Decreased PEEP

3. Increased Ppa

4. Decreased VD ventilation

5. Decreased rebreathing6. Decreased CO2 production :

hypothermia- deep anesthesia-hypotension

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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

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Cardiovascular response to hypoxia

1. Reflex (neural & humoral)

2. Direct effect

The reflex effect occurs first and are excitatory and vasoconstrictory (general)

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

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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

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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

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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)

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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

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Symptoms & complications

1. Respiratory distress (mild irritation in the area of carina and coughing)

2. Pain 3. Severe dyspnea 12 hour

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

4. Tracheobronchitis (Decrease in CL & ABG )

5. pulmonary edema 12 hour to few days

6. pulmonary fibrosis few days to weeks

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7. Ventilation depression & hypercapnia8. Absorption atelactasis9. 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)

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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)

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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

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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

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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

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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

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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

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Hypocapnia

Mostly is due to hyperventilation Causes QT decrease in tree ways

1. Increase in intra thoracic pressure

2. Withdrawal of sympathetic activity

3. Increase in PH & So decrease in Ca++

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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