Академический Документы
Профессиональный Документы
Культура Документы
1
Factors Dealing With Respiratory Function
2
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
3
ZONE 1
4
ZONE 2
Waterfall,Weir,Sluice,Starling resistor
Cycliccirculation
Zone 1 - Zone 3
5
ZONE 3
6
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
7
VENTILATION
8
Ventilation-Perfusion Ratio
9
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)
10
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)
11
Local tissue derived products
12
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)
13
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
14
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
15
CAUSES OF HPV
Alveolar
hypoxia pulmonary vascular
smooth muscle ETC change H2O2 (2 messenger) Ca
nd
Vasoconstriction
Epithelial& smooth muscle derived products
Hypercapnia
16 Acidosis (metabolic & respiratory)
CLINICAL EFFECTS OF HPV
17
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
18
HUMORAL EFFECTS
19
ALTERNATVE (NON ALVEOLAR)
PATHWAYS OF BLOOD
FLOW THROUGH THE LUNG
20
Other nongravitational Determinants
of compliance – resistance – volume
- ventilation
COMPELIANCE C = ∆V/ ∆P
L/cm H2O
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
21
LAPLACE expression : P = 2T / R
T (surface tension)
R( radius of curvature of the alveolus)
Surfactant secreted by the intra alveolar type ║ T
lipoprotein
22
Airway resistance
R = ∆P/ ∆V
R (Resistance) cmH2O/L/sec
V ( airflow)
L/sec
23
Patterns of airflow
24
DIFFERENT REGIONAL LUNG TIME
CONSTANTS
זּ =CT X R
( זּtime constant) is the time required to
complete 63% of an exponentially changing
function (2 = זּ87% ,3 =זּ95% ,4 =זּ98%)
25
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
26
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
27
LUNG VOLUMES
28
LUNG VOLUMES
29
Airway closure & closing capacity
30
Airway closure in patients with normal
lung
31
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
32
If
lung volume decreases EPP goes
downward (closer to alveolus ).
33
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
34
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
35
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
36
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
37
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)
38
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%
39
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
40
Oxygen Transport
41
Oxygen-hemoglobin dissociation
curve
42
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
43
In natural Po2 (75-100) The curve is relatively horizontal so
shifts of the curve have little effect on saturation
44
Left shifted O2-Hb curve Right shifted O2-Hb
P50 < 27 curve P50 > 27
– Acidosis
– Alkalosis
– Hyperthermia
– Hypothermia
– Increased 2,3 DPG
– Abnormal & fatal Hb
– Abnormal Hb
– Decreased 2,3 DPG
old blood containing citrate ,
– Inhaled anesthetics
dextrose 1 MAC isoflurane shifts P50 to
(adding phosphate minimizes right 2.6 + 0.07 or -0.07
changes) – Narcotics have no effect
on the curve
45
Effect of QS/QT on PaO2
46
Effect of QT on VO2 & CaO2
47
Table 17- 4
48
FICK principle
49
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
50
CARBON DIOXIDE TRANSPORT
51
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
52
BOHR Effect
53
HALDEN Effect
54
Structure of alveolar septum
55
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
56
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
57
Transcapillary-interstitial space fluid
movement
58
Respiratory function during anesthesia
59
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
60
Effect of depth of anesthesia on
respiratory pattern
61
Effect of depth of anesthesia on
spontaneous minute ventilation
62
EFFECT OF PREEXISTING RESPIRATORY
DISFUNCTION ON THE RESPIRATORY
EFFECT OF ANESTHESIA
63
Effect of special intraoperative condition on
the respiratory effects of anesthesia
64
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
65
1- Malfunction of equipment
66
2- Hypoventilation
- VT is reduced under GA :
1. Increased work of breathing
2. Decreased drive of breathing
67
3- Hyperventilation
2. QT decrease
3. VO2 increase
4. HPV inhibition
5. Left shift of oxy-hemoglobin dissociation curve
6. R increase & CL decrease
68
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
69
Causes of reduced FRC
72
Causes of reduced FRC
73
Causes of reduced FRC
74
Causes of reduced FRC
75
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
76
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
77
Causes of reduced FRC
78
5. Decreased cardiac out put &
increased VO2
QT decrease : MI , Hypovolemia
VO2 increase : sympathetic activity,
hyperthermia, shivering
79
6 . Inhibition of HPV
80
7 . Paralysis
81
8 . Right to left interatrial shunting
82
9 . Specific diseases :
83
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
84
HYPOVENTILATION
Increasedairway resistance
Decreased respiratory drive
Decreased compliance (position)
85
Increased dead space ventilation
86
Increased CO2 production
87
Inadvertent switching off of CO2
absorber
88
hypocapnia
89
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
90
Cardiovascular response to hypoxia
91
Cardiovascular response to hypoxia
92
Hypoxia can induce arrhythmia :
arrhythmias are usually ventricular (UF,MFPVC-VT-VF)
93
Other Important effects
94
Hyperoxia
95
Symptoms & complications
1. Respiratory distress
(mild irritation in the area of carina and coughing)
Pain
Severe dyspnea 12 hour
96
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)
97
ENZIMATIC & METABOLIC CHANGES
98
Therapeutic effect
99
Hypercapnia
Cardiovascular system:
Direct: cardiovascular depression
Indirect: activation of sympathoadrenal system
100
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
101
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
102
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
103
Hypocapnia
104
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
105