Respiratory Physiology & Respiratory Function During Anesthesia

RESPIRATORY PHYSIOLOGY & RESPIRATORY FUNCTION DURING ANESTHESIA 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
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
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

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

ZONE 2
Waterfall,Weir,Sluice,Starling resistor
Cyclic circulation
Zone 1 - Zone 3

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

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

VENTILATION
PA is constant in the lung
Ppl increases from apex to bottom (0.25 cmH 2 O Each cm)
Density of lung is ¼ of water
∆P Is 7.5 cmH 2 O 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 co 2 diffusion ∆P o 2 > ∆Pco 2 apex to base ( 3 fold)

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)

ACTIVE PROCESSES:
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

From Endothelial – Smooth muscle
2) Endotheline:
- E T-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

Vasoactive products:
1) Adenosine Vasodilatation
2) NO Vasodilatation
3) Eicosanoids
a)PGI 2 (Epoprostenol , Iloprost) Vasodilatation
b)Thromboxane A 2 Vasoconstriction
c)Leukotriene B 4 Vasoconstriction
4)Endotheline Vasoconstriction & Vasodilatation

ALVEOLAR GASES
Hypoxemia
Causes localized pulmonary vessel vasoconstriction (HPV)
Causes systemic blood vessel vasodilatation
HPV
200 µm vessels near small bronchioles
PSO 2 : 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

CAUSES OF HPV
Alveolar hypoxia pulmonary vascular smooth muscle ETC change H2O2 (2 nd messenger) Ca
Vasoconstriction
Epithelial & smooth muscle derived products
Hypercapnia
Acidosis (metabolic & respiratory)

CLINICAL EFFECTS OF HPV
Life at high altitude ( FIO2 Ppa zone1 zone2 PaO 2 )
Hypoventilation – Atelectasis – Nitrogen ventilation (HPV Shunt )
Chronic lung disease (asthma-MS-COPD) administration of pulmonary vasodilator drugs (TNG-SNP-IPN)
Transpulmonary shunting PVR & PaO 2

NEURAL EFFECT
Sympathetic system (1 st five thoracic nerves+ branches of cervical ganglia & plexus arising from trachea) act mainly on 60 µm vessels ( α 1 effect is predominant )
Parasympathetic system ( VAGUS nerve ) , NO-dependent , vasodilatation acetylcholine binds M 3 muscarinic receptor Ca cNOS
NANC system NO-dependent vasodilatation using vasoactive intestinal peptide as neurotransmitter

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

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

Other nongravitational Determinants of compliance – resistance – volume - ventilation
COMPELIANCE C L/cm H2O = ∆V/ ∆P
1/C T =1/C L + 1/C CW C T = C L X C CW /C L +C CW
Normally , C L =C CW =0.2 SO C T = 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

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

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

Patterns of airflow
LAMINAR : Gas passes down a parallel sided tube at less than a certain critical velocity = V X 8L X µ/ π r 4 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= V 2 X p X f X L/4 π 2 r 5

DIFFERENT REGIONAL LUNG TIME CONSTANTS
זּ =C T X R
זּ (time constant) is the time required to complete 63% of an exponentially changing function (2 זּ = 87% , 3 זּ = 95% , 4 זּ =98% )
CT = 0.1 ,R= 2 so זּ =0.2 sec 4 זּ =0.8 sec
Time increases as resistance or compliance increases

Pathway of collateral ventilation
Non gravitational
Are designed to prevent hypoxia in neighboring
Interalveolar communications (kohn pores)
Distal bronchiolar to alveolar (lambert channels)
Respiratory bronchiole to terminal bronchiole (martin channels)
Interlobar connections

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

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

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 :
Nitrogen wash out
Inert gas dilution
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 11 th 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 ).
Near RV small airways (<0.9mm) tend to close
Airway closure first happens in dependent lung regions (Ppl> P intraluminal )

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
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

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 VD phy = VD Ana +VD Alv
physiologic dead space:
Anatomic dead space (airway) 2 cc/kg
Alveolar dead space (zone 1- emboli)
upright 60-80 cc
supine VD phy = VD Ana (VD Alv= 0 )

Naturally Vco 2 (co 2 entering the alveoli) is equal to the co 2 eliminated
Vco 2 = (VE)(FE co 2 )
Expired gas = alveolar gas + VD gas
So Vco 2 = (VA)(FA co 2 )+(VD)(FI co 2 )
Modified bohr equation : VD/VT=(Pa co 2 – PE co 2) / Pa co 2
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 H 2 0
713 = 760 – 47
PA O 2 = 713 X (FIO 2 – VO 2 /VA)
PA CO 2 =713 X (V co 2 /VA ) x 0.863
Fresh gas flow < 4 lit/min PaCO 2 ,PA O 2

Oxygen Transport
Cardiopulmonary system has the ability to increase function more than 30 folds
Functional links in the oxygen transport chain :
Ventilation
Diffusion of o 2 to blood
Chemical reaction of o 2 with Hb
QT of arterial blood
Distribution of blood to tissue and release of o 2

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 PO 2 of about 700 mm Hg
This curve relates the saturation of Hb to PaO 2
PaO 2 = 90 -100 SaO 2 =95-98
PaO 2 = 60 SaO 2 =90
PVO 2 = 40 SVO 2 =75

O 2 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)
O 2 Supply = O 2 available + 200 ml O 2 /min/1000 ml blood
O 2 available = o 2 reaches to tissues
VO 2 = 250 ml/min
C a O2 = (1. 39 )(Hb)(SaO 2 ) + (0.003)(PaO 2 )
O 2 Supply (transport) ml/100 cc = QT X Ca O 2
SaO 2= 40 O 2 Supply=400 , O 2 available =200 , VO 2 = 250
Body Must increase QT or Hb

In natural Po 2 (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 O 2 -Hb curve
P50 < 27
Alkalosis
Hypothermia
Abnormal & fatal Hb
Decreased 2,3 DPG
old blood containing citrate , dextrose
(adding phosphate minimizes changes)
Right shifted O 2 -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

Effect of QS/QT on PaO 2
PAO 2 is directly related to FIO 2 in normal patients
With a 50 % shunt of QT , increase in FIO 2 results in no increase in PAO 2
so in this case treatment of hypoxemia is not increasing the FIO 2 , and is decreasing the percentage of the shunt ( bronchoscopy , peep , positioning , antibiotics , suctioning , diuretics )

Effect of QT on VO 2 & CaO 2
CaO 2 will decrease if VO 2 increases or QT decreases
In both conditions CVO 2 is decreased because of more tissue o 2 extraction
Primarily : less O 2 is available for blood & blood with lower CVO 2 passes trough the lung
Secondarily : Mixture of this blood with oxygenated end-pulmonary capillary blood (c’) decreases CaO 2 (Qc’ =QT – QS)
QS/QT = Cc’ O 2 - CaO 2 / Cc’ O 2 - CVO 2
Decrease In CVO 2 is > than CaO 2 and the ratio is 2 to1 for 50% QS

Table 17- 4

FICK principle
Fick principle is for calculation of VO 2
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 VO 2 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

CARBON DIOXIDE TRANSPORT
Circulating CO 2 is a function of:
CO 2 produc tion parallels O2 consumption
CO 2 e limination that depends on : 1) pulmonary blood flow
2) ventilation
Respiratory quotient = V CO 2 / V O 2 Normally = 0.8 only 80% as much co 2 produced as o 2 is consumed
It depends on structure of metabolic substrate that is used
For Carbohydrates R = 1
For fats R = 0.7

CO 2 transport in plasma
Acid carbonic (H2CO3 ) 7%
Bicarbonate (HCO3 - ) 80%
CO 2 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

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

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

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

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 Δ P
Negative Δ P increases brochi and arteries’ diameter

Transcapillary-interstitial space fluid movement
Because of Δ P distal to proximal & arterial pulsation & lymphatic valves interstitial fluid flows from bronchi to proximal
F = K [(P INSIDE – P OUTSIDE ) –( π INSIDE - π OUTSIDE )] (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 P INSIDE decreases and fluid is reabsorbed

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

The effect of a given anesthetic on respiratory function depends on :
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
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
Narcotic- N2O : Deep and slow
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

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
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 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

1- Malfunction of equipment
Mechanical failure of anesthesia apparatus to deliver O2 to the patient
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
Decreased drive of breathing
- Decrease in VT causes hypoxemia in 2 way
Atelectasis
Decrease in over all V/Q ratio

3- Hyperventilation
Hypocapnic alkalosis may result in hypoxemia :
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 C L 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 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

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

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

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

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

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
High FIO2
Low V/Q
Long time exposure
Low CVO2
FIO2>50% Can produce atelectasis solely (therapeutic-measurement)

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

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

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 & VO2 CVO2 CaO2
QT 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 :
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

MECHANISM OF HYPER & HYPOCAPNIA DURING ANESTHESIA
Hypercapnia :
Hypoventilation
Increased dead space ventilation
Increased CO2 production
Inadvertent switching off of CO2 absorber

HYPOVENTILATION
Increased airway resistance
Decreased respiratory drive
Decreased compliance (position)

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
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 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

hypocapnia
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 (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

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)

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
No changes has been observed after administration of 50% O2 for long period

Symptoms & complications
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

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)

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)

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

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

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

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 ++

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

Respiratory Physiology & Respiratory Function During Anesthesia

by Dang Thanh Tuan

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