Respiratory Physiology & Respiratory Function During Anesthesia | Exhalation | Vasodilation


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


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. 2.

Passive process : cardiac out put – lung volumes 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


Gravity-Determined Distribution of Perfusion , ventilation

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


 Collapse

& Alveolar dead space 1) Ppa (SHOCK) 2)PA (Vt & peep )  Normally little or no zone 1 exists in the lung


 Waterfall,Weir,Sluice,Starling  Cyclic


circulation  Zone 1 - 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

   

Interstitial pressure Below the vertical level of left atrium Pisf > Ppv & perfusion is based on Ppa-Pisf Conditions resembling zone 4:
1. 2.


PVR : Volume overload, Emboli , mitral stenosis Negative Ppl : vigorous breathing, airway obstructions( most common: laryngospasm) Rapid re expansion of lung


 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

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)

Non-gravitational Determinants of PVR & blood flow distribution


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)


Non-gravitational Determinants of PVR & blood flow distribution


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


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


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


Local tissue derived products

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

Vasodilatation Vasoconstriction

b)Thromboxane A2

c)Leukotriene B4 Vasoconstriction 4)Endotheline Vasoconstriction & Vasodilatation



 

Causes localized pulmonary vessel vasoconstriction (HPV) Causes systemic blood vessel vasodilatation 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

 


 Alveolar

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

 Epithelial


& smooth muscle derived products  Hypercapnia  Acidosis (metabolic & respiratory)

  

Life at high altitude (FIO2
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



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


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

  

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

Normalizer :



   

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


Other nongravitational Determinants of compliance – resistance – volume - ventilation


L/cm H2O

= ∆V/ ∆P

CT =
  


Normally , CL=CCW=0.2 SO CT= 0.1 In clinic only CT can be measured

∆P/ peak pressure 2) Static ∆P/plateau pressure Peep must first subtracted from the peak or plateau pressure
CT 1) Dynamic



expression :

P = 2T / R

 T (surface tension)  R( radius of curvature of the alveolus)  Surfactant
secreted by the intra alveolar type ║



Airway resistance
R = ∆P/ ∆V  R (Resistance)  V ( airflow)  ∆P along the airway depends on the caliber of the airway & pattern of airflow

cmH2O/L/sec L/sec


Patterns of airflow
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 factor p r5 ∆P=V2 X p X f X L/4 π2is density , f is friction


 TURBULENT: when flow exceeds the critical velocity becomes  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



=CT X R  ‫( זּ‬time constant) is the time required to complete 63% of an exponentially changing function (2‫)%89=זּ 4, %59 =זּ 3, %78 = זּ‬
 CT

= 0.1 ,R= 2 so ‫ 2.0=זּ‬sec 4 ‫ 8.0=זּ‬sec  Time increases as resistance or compliance increases

Pathway of collateral ventilation

Non gravitational
Are designed to prevent hypoxia in neighboring
1. 2. 3. 4.

Interalveolar communications (kohn pores) Distal bronchiolar to alveolar (lambert channels) Respiratory bronchiole to terminal bronchiole (martin channels) Interlobar connections


     

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



 

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


  

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 :
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


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


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


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


 If

lung volume decreases EPP goes downward (closer to alveolus ). RV small airways (<0.9mm) tend to close

 Near

 Airway

closure first happens in dependent lung regions (Ppl> Pintraluminal)


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


Closing Capacity


  

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


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


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


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. 2.

Anatomic dead space (airway) 2 cc/kg Alveolar dead space (zone 1- emboli) upright 60-80 cc supine VDphy = VDAna (VD Alv= 0)


      

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%


    

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


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


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


 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
O2 Supply = O2 available + 200 ml O2 /min/1000 ml blood O2 available = o2 reaches to tissues VO2 = 250 ml/min 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

 CaO2 = (1. 39 )(Hb)(SaO2) + (0.003)(PaO2)
 


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


Left shifted O2-Hb curve P50 < 27
– – – –

Right shifted O2-Hb curve P50 > 27
– – – – –

Alkalosis Hypothermia Abnormal & fatal Hb Decreased 2,3 DPG
old blood containing citrate , dextrose (adding phosphate minimizes changes)

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


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 )


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


Table 17- 4


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


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



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


CO2 transport in plasma
 

Acid carbonic (H2CO3 ) 7% Bicarbonate (HCO3 ) 80% Carbaminohemoglobin (Hb-CO2) 13%
carbonic anhydrase

CO2 transport in RBC

Using carbonic anhydrase

H2O + CO2


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


BOHR Effect

The effect of PCO2 & H+ on oxyhemoglobin dissociation curve Right shift : hypercapnia & acidosis Left shift : hypocapnia & alkalosis

 


 Effect

of oxygen on carboxyhemoglobin dissociation curve Left shift
 More

Low PO2 High PO2

CO2 uptake from tissues by blood CO2 dissociates from blood in lungs

 Right


 More


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) (thick , upper – fluid & gas

 On one side of alveolar septum  On the other side

exchanging side) there is connective tissue and interstitial space (thin , down- gas exchange only) basement

membranes are fused and there is a greatly restricted interstitial space


 

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




Interstitial space is between periarteriolar and peribronchial connective tissue shit and between epithelium & endothelium basement membrane in alveolar septum The space has a progressively negative distal to proximal ΔP Negative ΔP increases brochi and arteries’ diameter


Transcapillary-interstitial space fluid movement

ΔP distal to proximal & arterial pulsation & lymphatic valves interstitial fluid flows from bronchi to
Because of proximal


= 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


Respiratory function during anesthesia

 Oxygenatoin

is impaired in most patients during anesthesia (more in elderly-obese-smokers) admixture (shunt) during anesthesia is about 10% that closely correlates with the degree of atelectasis

 Venus


The effect of a given anesthetic on respiratory function depends on :
2. 3. 4.

The depth of general anesthesia Preoperative respiratory function Presence of special intraoperative anesthetic or surgical condition


Effect of depth of anesthesia on respiratory pattern
 

Less than MAC 1 MAC (light anesthesia)

may vary from excessive hyperventilation to breath holding

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


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


  


is very close to

FRC in these patients
to be decreased


CC becomes greater than FRC SHUNT
1. 2. 3. 4. 5.


Acute chest (infection) or systemic (sepsis-MT-CHF-CRF) disease Heavy smokers Emphysema & bronchitis Obese people Chest deformities

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


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


Mechanism of hypoxemia during anesthesia

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 Decreased QT & increased VO2 HPV inhibition Paralysis Right to left intra arterial shunting Specific diseases

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


1- Malfunction of equipment

Mechanical failure of anesthesia apparatus to deliver O2 to the patient
1. 2. 3.

Disconnection (Y piece) Failure of O2 supply system 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


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

- Decrease in VT causes hypoxemia in 2 way
Atelectasis 2. Decrease in over all V/Q ratio


3- Hyperventilation

Hypocapnic alkalosis may result in hypoxemia :
2. 3. 4. 5. 6.

QT decrease VO2 increase HPV inhibition Left shift of oxy-hemoglobin dissociation curve R increase & CL decrease


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


Causes of reduced FRC

Supine position:

FRC is reduced 0.5-1 lit
( diaphragm

displaced 4 cm cephalad ,pulmonary vascular congestion happens ) 


Induction of GA:


loss of inspiratory tone & increase in end expiratory tone (abdominal) Increases intra abdominal pressure , displaces diaphragm more cephalad and decreases FRC

Thoracic cage muscle tone change:

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

 

  


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


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


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


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. 2. 3. 4.

High FIO2 Low V/Q Long time exposure Low CVO2

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


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


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


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)


5. Decreased cardiac out put & increased VO2

 QT  QT

& VO2



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


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


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


8 . Right to left interatrial shunting
 

Patent foramen ovale Increased right side pressure

 Administration

of inhaled NO decrease PVR & functionally close the PFO


9 . Specific diseases :


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


complement mediated decreased QT- FRC-CL &



Hypercapnia :
2. 3. 4. 5.

Hypoventilation Increased dead space ventilation Increased CO2 production Inadvertent switching off of CO2 absorber



 Increased

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


Increased dead space ventilation
  4.

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

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


Increased CO2 production
 Any

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

Hyperthermia Shivering Light anesthesia Catecholamine release Hypertension Thyroid storm


Inadvertent switching off of CO2 absorber

 Occurrence
 Patient

of hypercapnia depends on:

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


     

Hyperventilation (most common) Decreased PEEP Increased Ppa Decreased VD ventilation Decreased rebreathing Decreased CO2 production :
hypothermia- deep anesthesia-hypotension


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


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)


Cardiovascular response to hypoxia
 Mild

hypoxia hypoxia

(SPO2>80%) , HR , SVR (SPO2<60%) , SV (80%>SPO2>60%)

Sympathetic activation BP

 Moderate  Severe

Local vasodilatation , HR


BP ,HR , Shock , VF , Asystole With preexisting hypotension even in mild hypoxemia shock can be developed


 

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


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)


 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


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

(Decrease in CL & ABG )

pulmonary edema pulmonary fibrosis

12 hour to few days few days to weeks


1. 2. 3.

Ventilation depression & hypercapnia Absorption atelactasis 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)



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)


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


 Cardiovascular
 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


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


    

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


 

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


 

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



 

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


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