Respiratory Physiology & Respiratory Function During Anesthesia
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Transcript of Respiratory Physiology & Respiratory Function During Anesthesia
1
RESPIRATORY PHYSIOLOGY & RESPIRATORY FUNCTION DURING
ANESTHESIA
Houman Teymourian M.D.Assistant professorDepartment of Anesthesiology and Critical Care, Shohada hospitalShahid Beheshti Medical University
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 volumes2. Active process: 1) local tissue derived products 2) alveolar gas concentrations 3)neural influences 4)humoral (hormonal)
Other nongravity- Determinants of compliance – resistance – volume - ventilation
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
ZONE 1
Collapse & Alveolar dead space
1) Ppa (SHOCK) 2)PA (Vt & peep )
Normally little or no zone 1 exists in the lung
5
ZONE 2
Waterfall,Weir,Sluice,Starling resistor Cyclic circulation Zone 1 - Zone 3
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
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
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
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
Non-gravitational Determinants of PVR & blood flow distribution
PASSIVE PROCESSES:1. Cardiac output: Pulmonary vascular system is high flow
and low pressure so : QT increases more than Ppa & PVR=Ppa/QT so: PVR decreases
2. Lung volumes: FRC is the volume in witch PVR is minimum , volume increase or decrease from FRC causes PVR increase:
Above FRC : Alveolar compression of small vessels (small vessel PVR)
Below FRC : 1) Mechanical tortuosity of vessels (passive)
2) Vasoconstriction (main mechanism) (active)
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
Local tissue derived products
From Endothelial – Smooth muscle1) NO : predominant endogenous vasodilator compound
L- Argenine NOS L-Citruline + NO
has small size , freely diffuses , increases cGMP in SM cells, dephosphorylates the myosin light chains vasodilatation
NOS :
1) cNOS (constitutive): Permenantly exists,
short bursts of NO ( ca , calmodulin) , keeps PVR low
2) iNOS (inducible) : Inflamation
large quantities & extended duration
13
Local tissue derived products
From Endothelial – Smooth muscle2) Endotheline: - ET-1 is the only endotheline that is made in
lungs (vasoconstriction)- ET receptors: 1) ET A vasoconstriction
2) ET B vasodilatation (NO, prostacyclyn)
- ET -1 Antagonists (Bosentan , sintaxsentan more
selective) are used in treatment of pulmonary hypertension complication: liver toxicity
14
Local tissue derived products
Vasoactive products:1) Adenosine Vasodilatation
2) NO Vasodilatation
3) Eicosanoids
a)PGI2 (Epoprostenol , Iloprost) Vasodilatation
b)Thromboxane A2 Vasoconstriction
c)Leukotriene B4 Vasoconstriction
4)Endotheline Vasoconstriction & Vasodilatation
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
16
CAUSES OF HPV
Alveolar hypoxia pulmonary vascular smooth muscle ETC change H2O2 (2nd messenger) Ca
Vasoconstriction Epithelial & smooth muscle derived products Hypercapnia Acidosis (metabolic & respiratory)
17
CLINICAL EFFECTS OF HPV
1. Life at high altitude (FIO2 Ppa zone1 zone2 PaO2 )
2. Hypoventilation – Atelectasis – Nitrogen ventilation (HPV Shunt )
3. Chronic lung disease (asthma-MS-COPD) administration of pulmonary vasodilator drugs (TNG-SNP-IPN)
Transpulmonary shunting PVR & PaO2
18
NEURAL EFFECT
1. Sympathetic system (1st five thoracic nerves+ branches of cervical ganglia & plexus arising from trachea) act mainly on 60 µm vessels ( α1 effect is predominant )
2. Parasympathetic system ( VAGUS nerve ) , NO-dependent , vasodilatation acetylcholine binds M3 muscarinic receptor Ca cNOS
3. NANC system NO-dependent vasodilatation using vasoactive intestinal peptide as neurotransmitter
19
HUMORAL EFFECTS
1. Vasodilator :histamine ( H1 on endothelium-H2 on smooth muscle) , adenosine , bradykinin , substance P ,
2. Vasoconstrictor :histamine (H1 on smooth muscle), neurokinin, angiotensin, serotonin,
3. Normalizer : ATP
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
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
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
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
Patterns of airflow
LAMINAR : Gas passes down a parallel sided tube at less than a certain critical velocity = V X 8L X µ/πr4 µ is viscosity
TURBULENT: when flow exceeds the critical velocity becomes turbulent p is density , f is friction factor
ORFICE : occurs at severe constrictions (kinked ETT, laryngospasm) the pressure drop is proportional to the square of the flow
Laminar flow is confined to the airways below the main bronchi, flow in trachea is turbulent , & orifice flow occurs at the larynx
∆P
∆P=V2 X p X f X L/4 π2r5
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DIFFERENT REGIONAL LUNG TIME CONSTANTS
CT X R= ּז is the time required to (time constant) ּז
complete 63% of an exponentially changing function (2 98%=ּז 4 ,95%= ּז 3 ,87% = ּז )
CT = 0.1 ,R= 2 so 0.2=ּז sec 4 0.8=ּז sec Time increases as resistance or compliance
increases
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
WORK OF BREATHING
Work=force x distance, Force=pressure x area, Distance=volume/area So WORK = PRESSURE x VOLUME If R or C ,P , Work The metabolic cost of the work of breathing at rest is only 1-3% of the
total O2 consumption , and increases up to 50% in pulmonary disease Expiration is passive using potential energy that has been saved
during inspiration (awake) In anesthetized person with diffuse obstructive airway disease
resulting from the accumulation of secretions, elastic and airway resistive component of respiratory work would increase
For a constant minute volume , both deep , slow (elastic resistance ) & shallow , rapid (airway resistance ) breathing will increase work of breathing
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LUNG VOLUMES
FRC: the volume of gas in lung at end of normal expiration At FRC , There is no air flow & PA = ambient pressure Expansive chest wall elastic forces are exactly balanced by retractive lung
tissue elastic forces
ERV: is part of FRC, the volume of gas that can be consciously exhaled
RV: the minimum volume that remains after ERV
VC: ERV + IC
IC : VT+ IRV
TLC: VC+ RV
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LUNG VOLUMES
Volumes that can be measured by simple spirometry are VT , VC , IC , IRV ,ERV
TLC ,FRC & RV cannot be measured by spirometry
How to measure TLC ,FRC & RV :1. Nitrogen wash out2. Inert gas dilution3. Total body plethysmography
disparity between FRC in 2&3 is used to detect large nonventilating airtrapped blebs
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Airway closure & closing capacity
Ppl increases from top to the bottom and determines alveolar volume, ventilation & compliance
Gradients of Ppl may lead to airway closure and collapse
31
Airway closure in patients with normal lung
1. In normal resting end expiratory state (FRC) , the distending transpulmonary exceeds intrathoracic air passage transmural pressure and the airways remain patent
2. During the middle of normal inspiration ∆P increases and the airways remain patent
3. During the middle of normal expiration ,expiration is passive and PA is related to elastic recoil of the lung, airways remain patent
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4. During the middle of forced expiration , Ppl increases more than atmospheric pressure, in alveoli because of elastic recoil of alveolar septa, pressure is higher than Ppl, pressure drops down as air passes to the greater airways, and there be a place at which intraluminal pressure equals Ppl (EEP), down stream this point (small or large airways) air way closure will occur
Distal to 11th generation there is no cartilage=bronchioles Airway patency below this point is due to lung volume
above this point is due to intra thoracic pressure
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If lung volume decreases EPP goes downward (closer to alveolus ).
Near RV small airways (<0.9mm) tend to close
Airway closure first happens in dependent lung regions (Ppl> Pintraluminal)
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
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
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
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
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
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
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
Oxygen Transport
Cardiopulmonary system has the ability to increase function more than 30 folds
Functional links in the oxygen transport chain:1. Ventilation
2. Diffusion of o2 to blood
3. Chemical reaction of o2 with Hb
4. QT of arterial blood5. Distribution of blood to tissue and release of o2
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
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
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
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
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
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
48
Table 17- 4
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
1. If VO2 remains constant and QT decreases the arteriovenous O2 content gradient must increase
2. QT decrease causes much larger and primary decrease in CVO2 versus a smaller and secondary decrease in CaO2
CVO2 & PVO2 are much more sensitive to QT changes
51
CARBON DIOXIDE TRANSPORT
Circulating CO2 is a function of:1. CO2 production parallels O2 consumption
2. CO2 elimination that depends on : 1) pulmonary blood flow
2) ventilation
Respiratory quotient = V CO2 / V O2 Normally = 0.8 only 80% as much co2 produced as o2 is consumed
It depends on structure of metabolic substrate that is used For Carbohydrates R = 1 For fats R = 0.7
52
CO2 transport in plasma1. Acid carbonic (H2CO3 ) 7%2. Bicarbonate (HCO3-) 80%
CO2 transport in RBC Carbaminohemoglobin (Hb-CO2) 13% Using carbonic anhydrase
H2O + CO2 carbonic anhydrase H2CO3 in RBC
99.9% of H2CO3 Is Rapidly transformed to H+ + HCO3-
Carbonic anhydrase contains zinc and moves reaction to right at a rate of 1000 times faster than in plasma
H+ is bufferd with Hb (HHb) ,HCO3
_ goes to the plasma and Cl
_
enters the cell , CO2 + HHb = HbCO2 Solubility coefficient (α) of CO2 is 0.03 mmol/L
53
BOHR Effect
The effect of PCO2 & H+ on oxyhemoglobin dissociation curve
Right shift : hypercapnia & acidosis Left shift : hypocapnia & alkalosis
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
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
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
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
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
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
The effect of a given anesthetic on respiratory function depends on :
1. The depth of general anesthesia
2. Preoperative respiratory function
3. Presence of special intraoperative anesthetic or surgical condition
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 slow2. Voletiles : rapid & shallow (panting)
Very deep all inhaled drugs : gasping-jerky respiration – paradoxical movement of chest-abdomen (only
diaphragmatic respiration) just like airway semi obstruction or partial paralysis
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
EFFECT OF PREEXISTING RESPIRATORY DISFUNCTION ON THE RESPIRATORY EFFECT OF ANESTHESIA
CC is very close to FRC in these patients
anesthesia causes FRC to be decreased
CC becomes greater than FRC ATELECTASIS and SHUNT
1. Acute chest (infection) or systemic (sepsis-MT-CHF-CRF) disease
2. Heavy smokers
3. Emphysema & bronchitis
4. Obese people
5. Chest deformities
1. Anesthesia inhibits HPV (further shunting) ,decreases mucus velocity flow
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
Mechanism of hypoxemia during anesthesia
1. Malfunction of equipment Mechanical failure of anesthesia apparatus to deliver O2 to the patient Mechanical failure of tracheal tube
2. Hypoventilation3. Hyperventilation4. FRC decrease (supine position-induction of anesthesia-paralysis- light anesthesia- airway
resistant increase- excessive fluid administration- high inspired oxygen-secretion removal decrease)
5. Decreased QT & increased VO26. HPV inhibition7. Paralysis8. Right to left intra arterial shunting9. Specific diseases
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 system3. Wrong cylinder
air way pressure monitoring & FIO2 analyzer will detect most of the causes
Mechanical failure of tracheal tube1. Esophageal intubation2. Disconnection low pressure3. Others (kincking- secretions-ruptured cuff) R increases & hypo ventilation
occurs endo bronchial intubation = hypoventilation+shunt 30 ° trendelenburg = endo bronchial intubation
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 way1. Atelectasis
2. Decrease in over all V/Q ratio
68
3- Hyperventilation
Hypocapnic alkalosis may result in hypoxemia :
1. QT decrease
2. VO2 increase
3. HPV inhibition
4. Left shift of oxy-hemoglobin dissociation curve
5. R increase & CL decrease
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
Causes of reduced FRC
1. Supine position: FRC is reduced 0.5-1 lit ( diaphragm is displaced 4 cm cephalad ,pulmonary vascular congestion happens )
2. Induction of GA: Thoracic cage muscle tone change: loss of inspiratory tone & increase in end expiratory tone (abdominal) Increases intra abdominal pressure , displaces diaphragm more cephalad and decreases FRC
71
Causes of reduced FRC
3. Paralysis : diaphragm separates two compartments of high different hydrostatic gradients. Abdomen(1 cmH2O/cm) and thorax (0.25 cmH2O/cm)
In upright position there is no trans diaphragmatic pressure gradient In supine higher trans diaphragmatic gradient must be generated
toward dependent parts of diaphragm to keep abdominal contents out of thorax
In un paralyzed this tension is developed by 1)diaphragmatic passive stretch 2)neurally mediated active contracture
In paralyzed diaphragmatic motion is more cephalad Pressure on diaphragm In un paralyzed by an increased expiratory
muscle tone = pressure caused by the weight of abdominal contents In paralyzed
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
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
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
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
Causes of reduced FRC
8 . Surgical position:1. Supine : FRC
2. Trendelenburg: FRC 3. Steep trendelenburg: FRC most of the lung is zone3-4
4. Lateral decubitus : FRC in dependent lung and FRC in un dependent lung (overall FRC )
5. Lithotomy & Kidney : FRC more than supine
6. Prone : FRC
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
Causes of reduced FRC
10. Decreased removal of secretion: Increasing viscosity & slowing mucocilliary clearance
1. Tracheal tube (low or high pressure cuffs any place in trachea)
2. High FIO2
3. Low moisture
4. Low temperature <42°
5. Halogenated anesthetics (does not stop)
79
5. Decreased cardiac out put & increased VO2
QT & VO2 CVO2 CaO2
QT decrease : MI , Hypovolemia VO2 increase : sympathetic activity,
hyperthermia, shivering
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
7 . Paralysis
Normally Dependent or posterior part of diaphragm in supine position is the part that has lesser radius and more muscle and therefore contracts more effectively ( more ventilation)
Dependent lung has the most perfusion Most perfusion in most ventilated area In paralyzed patients : nondependent or anterior part of
diaphragm moves most (passive movement) Dependent lung has the most perfusion Most perfusion in least ventilated area
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8 . Right to left interatrial shunting
Patent foramen ovale Increased right side pressure
Administration of inhaled NO decrease PVR
& functionally close the PFO
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9 . Specific diseases :
1. Emboli: severe increase in Ppa right to left transpulmonary shunting (PFO-opened arteriovenous anastomoses) Edema inhibition of HPV - dead space ventilation & hypoventilation
2. ARDS : complement mediated decreased QT- FRC-CL & hypoxemia
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MECHANISM OF HYPER & HYPOCAPNIA DURING ANESTHESIA
Hypercapnia :
1. Hypoventilation
2. Increased dead space ventilation
3. Increased CO2 production
4. Inadvertent switching off of CO2 absorber
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HYPOVENTILATION
Increased airway resistance Decreased respiratory drive Decreased compliance (position)
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Increased dead space ventilation
1. Decreased Ppa (hypotension) zone 1 increased alveolar dead space
2. vascular obliteration (emboli – clamping - aging)
dead space is increased with aging VD/VT= 33+ age/3
3. The anesthesia apparatus Increase in anatomic dead space from 33% to 46% in intubated
subject , & to 64% in mask ventilated subject Rebreathing : is increased 1) spontaneous ventilation A D C B 2) controlled ventilation D B C A No rebreathing occurs In E system (ayer’s T-piece) with enough
fresh gas flow & expiratory time
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Increased CO2 production
Any reason causes increase in O2 consumption ( VO2 ) will increase CO2 production
– Hyperthermia– Shivering– Light anesthesia– Catecholamine release– Hypertension– Thyroid storm
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Inadvertent switching off of CO2 absorber
Occurrence of hypercapnia depends on: Patient ventilatory responsiveness Fresh gas flow Circle system design cO2 production
High fresh gas flow (>5lit /min) minimize this problem with almost all systems for almost all patients
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hypocapnia
1. Hyperventilation (most common)
2. Decreased PEEP
3. Increased Ppa
4. Decreased VD ventilation
5. Decreased rebreathing6. Decreased CO2 production :
hypothermia- deep anesthesia-hypotension
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Physiologic effect of abnormalities in respiratory gases
Hypoxia The essential feature of hypoxia is cessation of
oxidative phosphorylation when mitochondrial PO2 falls below a critical level
Anaerobic production of energy is insufficient and produces H+ & LACTATE which are not easily excreted and will accumulate
The Most susceptible organ to hypoxia is the brain in an awake patient and the heart in an anesthetized patient and the spinal cord in aortic surgery
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Cardiovascular response to hypoxia
1. Reflex (neural & humoral)
2. Direct effect
The reflex effect occurs first and are excitatory and vasoconstrictory (general)
The direct effect is inhibitory and vasodilatory and occur late (local)
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Cardiovascular response to hypoxia
Mild hypoxia (SPO2>80%)
Sympathetic activation BP , HR , SV
Moderate hypoxia (80%>SPO2>60%)
Local vasodilatation , HR , SVR
Severe hypoxia (SPO2<60%)
BP ,HR , Shock , VF , Asystole With preexisting hypotension even in mild hypoxemia
shock can be developed
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Hypoxia can induce arrhythmia : arrhythmias are usually ventricular (UF,MFPVC-VT-VF)
Direct : decrease in heart’s O2 supply Tachycardia : increase demand Increase SVR : increase after load and therefore demand Decrease SVR : decrease supply
The level of hypoxemia that will cause cardiac arrhythmias
varies case to case
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Other Important effects
Hypoxemia causes CBF to increase even at the presence of hypocapnia
Ventilation will be stimulated Ppa is increased Chronic hypoxia leads to an increase in Hb &
2,3 DPG .(right shift in curve)
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Hyperoxia
Exposure to high O2 tension clearly cause pulmonary damage in healthy individuals
Dose-Time toxicity : 100% O2 is not allowed for more than 12 hours
80% O2 is not allowed for more than 24 hours
60% O2 is not allowed for more than 36 hours No changes has been observed after administration of 50% O2 for
long period
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Symptoms & complications
1. Respiratory distress (mild irritation in the area of carina and coughing)
2. Pain 3. Severe dyspnea 12 hour
(paroxysmal coughing- decreased VC) recovery : 12-24 hour
4. Tracheobronchitis (Decrease in CL & ABG )
5. pulmonary edema 12 hour to few days
6. pulmonary fibrosis few days to weeks
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7. Ventilation depression & hypercapnia8. Absorption atelactasis9. Retrolental fibroplasia
abnormal proliferation of immature retinal vasculature in pre matures
extremely premature infants are more susceptible : 1 )less than 1 kg birth weight 2) less than 28 weeks’ gestation 3)PaO2 > 80 for more than 3 hour in an infant gestation+life age<44
week In presence of PDA arterial blood sample should be taken from right
radial artery ( umbelical & lower extermities have lower O2)
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ENZIMATIC & METABOLIC CHANGES
Enzymes particularly those with sulfhydryl groups, are inactivated by O2 derived free radicals
Inflamatory mediators then are released from
neutrophils that will damage epithelium & endothelium & surfactant systems
Most acute toxic effect is convulsion(>2 atm)
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Therapeutic effect
Clearance of gas loculi in the body may be greatly accelerated by the inhalation of 100% O2
It creates a large nitrogen gradient from loculi to blood so the size of loculi diminishes
– Intestinal obstruction– Air embolus– Pneumopritoneum– Pneumocephalus– pneumothorax
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Hypercapnia
Cardiovascular system: Direct: cardiovascular depression Indirect: activation of sympathoadrenal system
– Indirect effect may be equal,more or less than direct effect
– Cathecholamine level during anesthesia is equal to the level in awake patients
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Hypercapnia just like hypoxia may cause increase myocardial demand (tachycardia, early hypertension) and
decrease supply (tachycardia, late hypotension)
Hypercapnia induced arrhythmias – are sirous during anesthesia in contrast of awake patients– all voletiles decrease QT interval torsades de pointes & VF– With halothane arrhythmias frequently occur above a PaCO2
arrhythmic threshold that is constant for a particular patient
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Max stimulatory respiratory effect is at a PCO2 about 100
Further increase causes right-shift in PCO2 ventilation-response curve
Anesthetic drugs cause a right-shift in PCO2 ventilation-response curve
CO2 narcosis occurs when PCO2 rises to more than 90-120 mm Hg
30% CO2 is sufficient for production of anesthesia and causes total flattening of EEG
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It causes bronchodilatation In constant N concentration any increase in CO2 can cause
decrease in O2 It shifts the oxyhemoglobin dissociation curve to right &
increase tissue oxygenation Chronic hypercapnia increases resorption of bicarbonate and
metabolic alkalosis It causes K+ leakage from cell to plasma (Mostly from liver from
glucose metabolism due to increased catecholamines )
Oculocephalic reflex is more common
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Hypocapnia
Mostly is due to hyperventilation Causes QT decrease in tree ways
1. Increase in intra thoracic pressure
2. Withdrawal of sympathetic activity
3. Increase in PH & So decrease in Ca++
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Alkalosis shifts oxy-Hb curve to left so Hb affinity to O2 increases & tissue oxygenation decreases
Whole body VO2 is increased because of increase in PH
PCO2 = 20 30% Increase in VO2 HPV is inhibited & CL is decreased , and
bronchoconstriction is produced VA/Q abnormalities
Passive hypocapnia promotes apnea