1. 1
RESPIRATORY PHYSIOLOGY &
RESPIRATORY FUNCTION DURING
ANESTHESIA
Houman Teymourian M.D.
Assistant professor
Department of Anesthesiology and Critical
Care, Shohada hospital
Shahid Beheshti Medical University
2. 2
Factors Dealing With Respiratory Function
Gravity-Determined Distribution of Perfusion , ventilation
perfusion - ventilation- V/Q ratio
Non-gravitational Determinants of PVR & blood flow
distribution
1. Passive process : cardiac out put – lung volumes
2. Active process: 1) local tissue derived products
2) alveolar gas concentrations
3)neural influences
4)humoral (hormonal)
Other nongravity- Determinants of compliance – resistance –
volume - ventilation
3. 3
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
4. 4
ZONE 1
Collapse & Alveolar dead space
1) Ppa (SHOCK)
2)PA (Vt & peep )
Normally little or no zone 1 exists in the lung
6. 6
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
7. 7
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
8. 8
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
9. 9
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)
10. 10
Non-gravitational Determinants of
PVR & blood flow distribution
PASSIVE PROCESSES:
Cardiac output: Pulmonary vascular system is high
flow and low pressure so : QT increases more than
Ppa & PVR=Ppa/QT so: PVR decreases
Lung volumes: FRC is the volume in witch PVR is
minimum , volume increase or decrease from FRC
causes PVR increase:
Above FRC : Alveolar compression of small vessels
(small vessel PVR)
Below FRC : 1) Mechanical tortuosity of vessels (passive)
2) Vasoconstriction (main mechanism) (active)
11. 11
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)
12. 12
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
13. 13
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
15. 15
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
17. 17
CLINICAL EFFECTS OF HPV
Life at high altitude (FIO2 Ppa zone1
zone2 PaO2 )
Hypoventilation – Atelectasis – Nitrogen
ventilation (HPV Shunt )
Chronic lung disease (asthma-MS-COPD)
administration of pulmonary vasodilator drugs (TNG-SNP-IPN)
Transpulmonary shunting PVR & PaO2
18. 18
NEURAL EFFECT
Sympathetic system
(1st
five thoracic nerves+ branches of cervical ganglia & plexus
arising from trachea) act mainly on 60 µm vessels ( α1 effect
is predominant )
Parasympathetic system
( VAGUS nerve ) , NO-dependent , vasodilatation
acetylcholine binds M3 muscarinic receptor Ca cNOS
NANC system NO-dependent vasodilatation using
vasoactive intestinal peptide as neurotransmitter
19. 19
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
20. 20
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
21. 21
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
22. 22
LAPLACE expression : P = 2T / R
T (surface tension)
R( radius of curvature of the alveolus)
Surfactant secreted by the intra alveolar type ║ T
lipoprotein
23. 23
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
24. 24
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
25. 25
DIFFERENT REGIONAL LUNG TIME
CONSTANTS
זּ =CT X R
זּ (time constant) is the time required to
complete 63% of an exponentially changing
function (2זּ = 87% ,3 =זּ 95% ,4 =זּ98%)
CT = 0.1 ,R= 2 so =זּ0.2 sec 4 =זּ0.8 sec
Time increases as resistance or compliance
increases
26. 26
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
27. 27
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
28. 28
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
29. 29
LUNG VOLUMES
Volumes that can be measured by simple
spirometry are VT , VC , IC , IRV ,ERV
TLC ,FRC & RV cannot be measured by spirometry
How to measure TLC ,FRC & RV :
1. Nitrogen wash out
2. Inert gas dilution
3. Total body plethysmography
disparity between FRC in 2&3 is used to detect
large nonventilating airtrapped blebs
30. 30
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
31. 31
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
32. 32
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
33. 33
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)
34. 34
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
35. 35
Closing Capacity
Spirogram: phase 1 :Exhale to RV
phase 2 :Inhale to TLC
phase 3 :Exhale to ERV
phase 4 :RV
Measurement of CC : Using a tracer gas
Phase 3 : constant concentration of tracer gas
Phase 4 : sudden rise in tracer gas concentration
CC is the border between phase 4 & RV
36. 36
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
37. 37
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
38. 38
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)
39. 39
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%
40. 40
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
41. 41
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
42. 42
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
43. 43
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
44. 44
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
45. 45
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
46. 46
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 )
47. 47
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
49. 49
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
50. 50
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
51. 51
CARBON DIOXIDE TRANSPORT
Circulating CO2 is a function of:
CO2 production parallels O2 consumption
CO2 elimination that depends on :
1) pulmonary blood flow
2) ventilation
Respiratory quotient = V CO2 / V O2 Normally = 0.8
only 80% as much co2 produced as o2 is consumed
It depends on structure of metabolic substrate that is used
For Carbohydrates R = 1
For fats R = 0.7
52. 52
CO2 transport in plasma
Acid carbonic (H2CO3 ) 7%
Bicarbonate (HCO3
-
) 80%
CO2 transport in RBC
Carbaminohemoglobin (Hb-CO2) 13% Using carbonic anhydrase
H2O + CO2 carbonic anhydrase H2CO3 in RBC
99.9% of H2CO3 Is Rapidly transformed to H
+
+ HCO3
-
Carbonic anhydrase contains zinc and moves reaction to right at a
rate of 1000 times faster than in plasma
H
+
is bufferd with Hb (HHb) ,HCO3
_
goes to the plasma and Cl
_
enters the cell , CO2 + HHb = HbCO2
Solubility coefficient (α) of CO2 is 0.03 mmol/L
53. 53
BOHR Effect
The effect of PCO2 & H
+
on oxyhemoglobin
dissociation curve
Right shift : hypercapnia & acidosis
Left shift : hypocapnia & alkalosis
54. 54
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
55. 55
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
56. 56
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
57. 57
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
58. 58
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
59. 59
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
60. 60
The effect of a given anesthetic on
respiratory function depends on :
2. The depth of general anesthesia
3. Preoperative respiratory function
4. Presence of special intraoperative anesthetic or
surgical condition
61. 61
Effect of depth of anesthesia on
respiratory pattern
Less than MAC
may vary from excessive hyperventilation to breath holding
1 MAC (light anesthesia)
regular pattern with larger VT than normal
More deep
end inspiration pause (hitch) – active and prolong expiration
More deep (moderate)
faster and more regular – shallow –no pause – I = E
Deep
1. Narcotic- N2O : Deep and slow
2. Voletiles : rapid & shallow (panting)
Very deep
all inhaled drugs : gasping-jerky respiration – paradoxical movement of chest-abdomen (only
diaphragmatic respiration) just like airway semi obstruction or partial paralysis
62. 62
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
63. 63
EFFECT OF PREEXISTING RESPIRATORY
DISFUNCTION ON THE RESPIRATORY
EFFECT OF ANESTHESIA
CC is very close to FRC in these patients
anesthesia causes FRC to be decreased
CC becomes greater than FRC ATELECTASIS and
SHUNT
1. Acute chest (infection) or systemic (sepsis-MT-CHF-CRF) disease
2. Heavy smokers
3. Emphysema & bronchitis
4. Obese people
5. Chest deformities
Anesthesia inhibits HPV (further shunting) ,decreases mucus
velocity flow
64. 64
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
65. 65
Mechanism of hypoxemia during
anesthesia
1. Malfunction of equipment
Mechanical failure of anesthesia apparatus to deliver O2 to the patient
Mechanical failure of tracheal tube
Hypoventilation
Hyperventilation
FRC decrease (supine position-induction of anesthesia-paralysis- light anesthesia- airway
resistant increase- excessive fluid administration- high inspired oxygen-secretion removal decrease)
Decreased QT & increased VO2
HPV inhibition
Paralysis
Right to left intra arterial shunting
Specific diseases
66. 66
1- Malfunction of equipment
Mechanical failure of anesthesia apparatus to
deliver O2 to the patient
1. Disconnection (Y piece)
2. Failure of O2 supply system
3. Wrong cylinder
air way pressure monitoring & FIO2 analyzer will detect most of the causes
Mechanical failure of tracheal tube
Esophageal intubation
Disconnection low pressure
Others (kincking- secretions-ruptured cuff) R increases & hypo ventilation
occurs endo bronchial intubation = hypoventilation+shunt
30 ° trendelenburg = endo bronchial intubation
67. 67
2- Hypoventilation
- VT is reduced under GA :
1. Increased work of breathing
2. Decreased drive of breathing
- Decrease in VT causes hypoxemia in 2 way
1. Atelectasis
2. Decrease in over all V/Q ratio
68. 68
3- Hyperventilation
Hypocapnic alkalosis may result in hypoxemia :
2. QT decrease
3. VO2 increase
4. HPV inhibition
5. Left shift of oxy-hemoglobin dissociation curve
6. R increase & CL decrease
69. 69
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
70. 70
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
71. 71
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
72. 72
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
73. 73
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
74. 74
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
75. 75
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)
76. 76
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
77. 77
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
78. 78
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)
80. 80
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
81. 81
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
82. 82
8 . Right to left interatrial shunting
Patent foramen ovale
Increased right side pressure
Administration of inhaled NO decrease PVR
& functionally close the PFO
83. 83
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
84. 84
MECHANISM OF HYPER &
HYPOCAPNIA DURING ANESTHESIA
Hypercapnia :
2. Hypoventilation
3. Increased dead space ventilation
4. Increased CO2 production
5. Inadvertent switching off of CO2 absorber
86. 86
Increased dead space ventilation
Decreased Ppa (hypotension) zone 1
increased alveolar dead space
vascular obliteration (emboli – clamping - aging)
dead space is increased with aging VD/VT= 33+ age/3
4. The anesthesia apparatus
Increase in anatomic dead space from 33% to 46% in intubated
subject , & to 64% in mask ventilated subject
Rebreathing : is increased
1) spontaneous ventilation A D C B
2) controlled ventilation D B C A
No rebreathing occurs In E system (ayer’s T-piece) with enough
fresh gas flow & expiratory time
87. 87
Increased CO2 production
Any reason causes increase in O2
consumption ( VO2 ) will increase CO2
production
– Hyperthermia
– Shivering
– Light anesthesia
– Catecholamine release
– Hypertension
– Thyroid storm
88. 88
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
89. 89
hypocapnia
Hyperventilation (most common)
Decreased PEEP
Increased Ppa
Decreased VD ventilation
Decreased rebreathing
Decreased CO2 production :
hypothermia- deep anesthesia-hypotension
90. 90
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
91. 91
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)
92. 92
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
93. 93
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
94. 94
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)
95. 95
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
96. 96
Symptoms & complications
1. Respiratory distress
(mild irritation in the area of carina and coughing)
Pain
Severe dyspnea 12 hour
(paroxysmal coughing- decreased VC) recovery : 12-24 hour
Tracheobronchitis
(Decrease in CL & ABG )
pulmonary edema 12 hour to few days
pulmonary fibrosis few days to weeks
97. 97
1. Ventilation depression & hypercapnia
2. Absorption atelactasis
3. Retrolental fibroplasia
abnormal proliferation of immature retinal vasculature in pre matures
extremely premature infants are more susceptible :
1 )less than 1 kg birth weight
2) less than 28 weeks’ gestation
3)PaO2 > 80 for more than 3 hour in an infant gestation+life age<44
week
In presence of PDA arterial blood sample should be taken from right
radial artery ( umbelical & lower extermities have lower O2)
98. 98
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)
99. 99
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
100. 100
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
101. 101
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
102. 102
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
103. 103
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
104. 104
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
++
105. 105
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