Transcript
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Arterial Blood GasesArterial Blood GasesRespiratory FailureRespiratory Failure
Michael Lippmann, MD
Division of Pulmonary and Critical Care Medicine
Department of Internal Medicine
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Respiratory SystemRespiratory System
LungParenchyma
Airways
BellowsRespiratory control centers
Peripheral nerves
Muscles
Chest wall
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Role of Respiratory SystemRole of Respiratory System
Maintain optimal levels of oxygen and pH in theblood despite variations in ambient conditions and
demand
pH maintained via control of arterial PCO2
Measurement of arterial blood gases evaluates
effectiveness of respiratory system in fulfilling its
role
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Alveolar Gas PressuresAlveolar Gas Pressures
Determined by balance between delivery ofoxygen and carbon dioxide to the lung and theirremovalAtmospheric air passes through airways where it is
fully saturated with water vapor and delivered to thealveoli
Oxygen is delivered to the alveoli by ventilation andtaken up by the hemoglobin in the blood perfusing thelung
Carbon dioxide is delivered to the alveoli by the bloodperfusing the lung and removed by ventilation
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Effect of V/Q Ratio on Alveolar GasEffect of V/Q Ratio on Alveolar Gas. .
Normal
range of
V/Q
ratios
.1 .2 .4 .6 .8 1 2 4 6 810
POPO22 in alveolusin alveolus
and capillary
and capillary
PCO2 in alveolus
and capillary
20
40
60
80
100
120
140
160
20
40
60
80
100
120
140
160
Log V/Q ratios. .
PO
2orP
CO
2
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Alveolar PCOAlveolar PCO22
PaCO2 = VCO2/(VE-VD)Where:
PaCO2 = Arterial carbon dioxide tension
VCO2 = CO2 production by the bodyVE= Minute ventilation
VD = Dead space ventilation
Therefore, arterial carbon dioxide tension will increase if:
there is an absolute decrease in bellows function
the bellows are unable to increase ventilation in proportion to
increased CO2 production or increased dead space
.
.
.
. . .
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Alveolar Gas Equation for OxygenAlveolar Gas Equation for Oxygen
PPAAOO22 = F= FIIOO22(P(PBB - P- PHH22OO) - P) - PaaCOCO22/R/R
Where:
FIO2= Fraction inspired oxygen tensionP
B= Barometric pressure (747 mm Hg)
PH2O
= Partial pressure of water vapor (47 mm Hg)
PaCO
2= Arterial carbon dioxide tension
R = Respiratory equivalent (0.8)
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Alveolar Gas Equation for OxygenAlveolar Gas Equation for Oxygen
Balance between removal of oxygen from the alveolus byperfusion, and the addition of oxygen to the alveolus by
ventilation determines alveolar O2 Calculates the PO2 of an alveolus with a specific ratio of
ventilation to perfusion The first part calculates the alveolar PO2 in the absence of any
perfusion
The second component corrects for effect of perfusion, whichremoves oxygen and adds CO2 to the alveolus
PPAAOO22 = FIO= FIO22(P(PBB - P- PHH22OO) - P) - PaaCOCO22/R/R
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Arterial Gas PressuresArterial Gas Pressures
Determined by the average of gas contents ofblood leaving alveolo-capillary units
Gas pressure gas content
Pressure index of the tendency of a gas
molecule to moveGas molecules move from areas of higher pressure to
those of lower pressure
Flow stops when pressure (not content) equilibrates
Content number of gas molecules contained in agiven volume
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Ideal Gas LawIdeal Gas Law
P = pressure
V = volume of vessel = number of moles of gas
R = universal gas constant
T = absolute temperature
Pressure will increase with
Increase in amount of gas Decrease in volume of
container
Increase in temperature
PV =PV = RTRT
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Henrys LawHenrys Law
P = kCP = kC The solubility of a gas in a liquid is directly proportional
to the partial pressure of that gas above the liquid
kis a temperature-dependent constant (769.2 Latm/mol for
oxygen in water at 298K)Pis the partial pressure (atm)
Cis the concentration of the dissolved gas in the liquid (mol/L)
The less soluble the gas (higher k) the lower the content for any
pressure
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Oxygen ContentOxygen Content
Oxygen is poorly soluble in plasma and is carriedby hemoglobin
Oxygen capacity = 1.34 (ml O2/g Hgb) x
hemoglobin (g/dl)Oxygen content = (oxygen carrying capacity) x
(% oxygen saturation) + 0.003 ml/dl (PaO
2)
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Oxyhemoglobin Dissociation CurveOxyhemoglobin Dissociation Curve
Oxygen content = (1.34 ml x Hgb) SaO2 Curve also represents relationship between
PO2 and oxygen content
0
20
40
60
80
100
20 40 60 80 100 120
SO
2%
PO2
Left-shifted (Increased affinity) decreased temp decreased 2-3 DPG increased pH carbon monoxide
Right-shifted (Decreased affinity) increased temp
increased 2-3 DPG
decreased pH
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Oxygen ContentOxygen Content P PaaOO22 = 100= 100
1.34 ml O2
x (16 g/dl Hgb) x 98% = 21 ml O2
+
0.003 ml O2 (100) = .03 ml O2
1.31 ml
O2
1.31 mlO
2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 mlO
2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2 1.31 ml
O21.31 mlO
2
.03 ml
O2
O2 Content = 21.03 ml/dl blood
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Oxygen ContentOxygen Content P PaaOO22 = 40= 40
1.34 ml O2
x (16 g/dl Hgb) x 75% = 16 ml O2
+
0.003 ml O2 (40) = .012 ml O2
1.00 ml
O2
1.00 mlO
2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 mlO
2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2 1.00 ml
O21.00 mlO
2
.012 ml
O2
O2 Content = 16.012 ml/dl blood
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Oxygen ContentOxygen Content P PaaOO22 = 600= 600
1.34 ml O2
x (16 g/dl Hgb) x 100% = 21.4 ml O2
+
0.003 ml O2 (600) = .18 ml O2
1.34 ml
O2
1.34 mlO
2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 mlO2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2 1.34 ml
O21.34 mlO
2
.18 ml
O2
O2 Content = 21.58 ml/dl blood
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MixingMixingEqual volumes (100 cc) of blood mixed together
each with equal amounts of hemoglobin (16g/dl)
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2
1.31 ml
O2 1.31 ml
O21.31 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2 1.00 ml
O21.00 ml
O2
PO2 = 100
SO2 = 98%
Content = 21 ml O2/100cc
PO2 = 40
SO2 = 75%
Content = 16 ml O2/100cc
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
PO2 = 54
SO2 = 86.5%
Content = 18.5 ml O2/100cc
1.16 ml
O2
1.16 ml
O21.16 ml
O2
1.16 ml
O2
1.16 mlO2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
1.16 ml
O2
+ =
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MixingMixingEqual volumes (100 cc) of blood mixed together
each with equal amounts of hemoglobin (16g/dl)
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2
1.34 ml
O2 1.34 ml
O21.34 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2
1.00 ml
O2 1.00 ml
O21.00 ml
O2
PO2 = 600
SO2 = 100%
Content = 21.4 ml O2/100cc
PO2 = 40
SO2 = 75%
Content = 16 ml O2/100cc
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
PO2 = 57
SO2 = 87.5%
Content = 18.7 ml O2/100cc
1.17 ml
O2
1.17 ml
O21.17 ml
O2
1.17 ml
O2
1.17 mlO2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
1.17 ml
O2
+ =
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West Two-Compartment Model -West Two-Compartment Model -
OxygenOxygen
Bloodflow
2.4 l/min
2.4 l/min
VA2 l/min
PO2 99
VA2 l/min
PO2 99VAQ
= .83VAQ
= .83
P
O299SO
297.5
PO299
SO297.5
PO299 SO2 97.5
. .
. .
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V/Q Mismatch - OxygenV/Q Mismatch - Oxygen
Blood
flow
2.4 l/min
2.4 l/min
VA3.6 l/min
PO2 117
VA0.4 l/min
PO2 51.5VAQ
= 1.5VAQ
= .167
PO2117
SO298.2
PO251
.5 SO286
PO264 SO2 92.1
. .
..
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Alveolar-arterial GradientAlveolar-arterial Gradient
Calculated alveolar O2(P
AO
2) -
measured arterial O2 (PaO2)
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A-a GradientA-a Gradient
Measures dispersion of V/Q ratios within thelung
Normal lung has narrow range of V/Q ratios
The greater the variability, the higher the A-agradient
. .
. .
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A-a GradientA-a Gradient
Clinically, can be used to assess underlying lungfunction in patients with decreased P
aCO
2or
receiving supplemental oxygen
Arterial PO2may be normal or elevated despite the
presence of significant V/Q mismatch
In these situations the increased A-a gradient can
indicate significant underlying lung dysfunction
. .
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PCOPCO22 versus COversus CO22 ContentContent
50
55
60
40 50 60
Deoygenated
bloodOxygenated
blood
0
20
40
60
20 40 60 80
CO
2con
ten
t
PCO2
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V/Q Mismatch - Carbon DioxideV/Q Mismatch - Carbon Dioxide
CO2 production
200 ml/min
PCO2 46
50%flow
PCO2 40
100 ml/minCO2
50%flow
PCO2 40
100 ml/minCO2
PCO240
PCO24
0
PCO2 40
. .
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V/Q Mismatch - Carbon DioxideV/Q Mismatch - Carbon Dioxide
CO2 production
200 ml/min
PCO2 46
50%flow
100 ml/min
CO2
50%flow
0 ml/min
CO2
PCO246
PCO240
PCO2 43
. .
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OptionsOptions
Increase blood flow to normal V/Q regions
Increase ventilation of normal V/Q regions (normal
ventilatory drive)
Increase arterial and mixed venous PCO2 (blunted
ventilatory drive)
. .
. .
COCO22 Elimination Must Equal COElimination Must Equal CO22ProductionProduction
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Bicarbonate Buffer SystemBicarbonate Buffer System
H2CO3H+
+ HCO3-
weak acid conjugate
base
Equilibrium is far to the left - there are 600 parts
of CO2 in solution for every part carbonic acid
Thus, carbonic acid component is equal todissolved CO2. Dissolved CO2 in mmole =
0.03 x PCO2
CO2 + H2OH2CO3H+ + HCO3-
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Henderson-Hasselbach EquationHenderson-Hasselbach Equation
Effectiveness of a buffer depends on its pK (pH at
which the buffer exists half as the weak acid and
half as the conjugate base). Buffering is optimal at
its pKAlso depends on the amount of buffer present
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Henderson-Hasselbach EquationHenderson-Hasselbach Equation
pH pKconjugate base
weak acid= + log
[ ]
[ ]
For the bicarbonate system:
p H= 6.1 l o g [H C O3 ] m e t a b o l i c0. 0 3xP C O
2
r e s p i r a t
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The bicarbonate generated by the buffer pair does not
effectively buffer the change in H+ when PCO2rises
CO2+ H
2OH
2CO
3H+ + HCO
3
-
doubling the CO2doubles [H+]
for every mole rise in [H+] there will be an identical rise in
[HCO3
-]
Thus [HCO3
-] will rise only 40 nanoequivalents, an
insignificant increase compared to usual concentration
Bicarbonate Buffer SystemBicarbonate Buffer System
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Bicarbonate Buffer SystemBicarbonate Buffer System
PCO2 40
[HCO3-] = 24 mmole
0.03 x PCO2 = 1.2 mmole
pH = 6.1 + log (24/1.2)
ph = 7.4
Lung
PCO2 40
[HCO3-] = 19 mmole
0.03 x PCO2 = 1.2 mmole
pH = 6.1 + log (19/1.2)
ph = 7.3
Lung
CO2 CO2
+ 5 meq H+
Open
(Ventilating)
System
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PCO2 40
[HCO3-] = 24 mmole
0.03 x PCO2 = 1.2 mmole
pH = 6.1 + log (24/1.2)
ph = 7.4
Lung
PCO2 207
[HCO3-] = 19 mmole
0.03 x PCO2 = 6.2 mmole
pH = 6.1 + log (19/6.2)
ph = 6.59
Lung
CO2
+ 5 meq H+
Bicarbonate Buffer SystemBicarbonate Buffer System
Closed
(Non ventilating)
System
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Acid-Base TerminologyAcid-Base Terminology
Acidemia blood pH < 7.36Alkalemia blood pH > 7.44
Hypocapnia PaCO2< 36 mmHg
Hypercapnea PaCO2 > 44 mmHgHyperventilation associated with hypocapnia
Hypoventilation associated with hypercapnea
Tachypnia high breathing rate
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Acid-Base TerminologyAcid-Base Terminology
Respiratory acidosisA primary process associated with an increase in P
aCO
2
Decreases pH
Compensation through renal retention of bicarbonate
Respiratory alkalosis
A primary process associated with a decrease in PaCO
2
Increases pH
Compensation through renal excretion of bicarbonate
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Acid-Base TerminologyAcid-Base Terminology
Metabolic acidosis
A primary process associated with a decrease in serumbicarbonate
Decreases pH
Compensation through hyperventilation
Metabolic alkalosis
A primary process associated with an increase in serumbicarbonate
Increases pHCompensation through hypoventilation
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Blood Gas InterpretationBlood Gas Interpretation
Normal valuespH between 7.36 and 7.44
PCO2between 36 and 44 mmHg
PO2between 80 and 100 mmHg
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Blood Gas InterpretationBlood Gas Interpretation
Establish relationship between pH and PCO2Primary respiratory disorder
Inverse relationship between changes in pH and PCO2
In acute disorders reciprocal change of 0.08 in pH for every
change of 10 mmHg PCO2
Primary metabolic disorder
Changes in pH and PCO2discordant or change in pH is of a
greater magnitude than expected by change in PCO2
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Blood Gas InterpretationBlood Gas Interpretation
pH 7.24, PCO2 40Low pH with normal PCO2
Metabolic acidosis
pH 7.32, PCO2 30
PCO2 and pH both low
Metabolic acidosis with partial respiratory
compensation (respiratory alkalosis)
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Acute Respiratory FailureAcute Respiratory Failure
Arterial carbon dioxide tension (PaCO2) greaterthan 50 mm Hg concomitant with an arterial pH
less than 7.3
and/or
Arterial oxygen tension (PaO2) less than 50 mm
Hg when breathing room air at sea level
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Bellows Failure - EtiologiesBellows Failure - Etiologies
Respiratory control centersdrugs, infections, bleeding, trauma
Peripheral nerves
Guillain Barre syndrome, polio
Muscles
myotonic dystrophy, fatigue
Chest wall
kyphoscoliosis
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Bellows Failure - EtiologiesBellows Failure - Etiologies
Respiratory control centersdrugs, infections, bleeding, trauma
Peripheral nerves
Guillain Barre syndrome, polio
Muscles
myotonic dystrophy, fatigue
Chest wall
kyphoscoliosis
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Ventilation vs. COVentilation vs. CO22
21 3 4 5 6 7 8 9 10
20
40
60
80
100
120
Alveolar ventilation
PaC
O2
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Effects ofEffects ofHypercapneaHypercapnea
Decreased PaO2 proportional to rise in PaCO2 (A-agradient normal)
Acidemia (compensated by metabolic changes if
the increase is gradual)
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Lung FailureLung Failure
Characterized by hypoxemia with widened A-agradient
Hypercapnea not seen until later stages when
bellows failure supervenes
V/Q mismatch most common cause
easily corrected by supplemental oxygen
Intrapulmonary right-to-left shunting is refractory
to supplemental oxygen
. .
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Lung InfectionsLung Infections
Among the most common causes of V/Qmismatch
Upper airway or bronchial infections decreaseairflow to the distal alveoli
Infections of the distal airways and alveoli(pneumonia) disrupt or totally obstruct airflow toan area of the lung
Release of inflammatory mediators mayparadoxically increase the perfusion to these areasfurther lowering V/Q ratios
. .
. .
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Supplemental Oxygen in V/Q MismatchSupplemental Oxygen in V/Q Mismatch
Increasing the concentration of oxygen in inspiredair (FIO
2) increases P
AO
2
Increased PAO
2equilibrates with capillary blood
increasing PO2 and O2 content of blood leaving thealveolo-capillary unit
Blood with higher O2content mixes with blood
from other units and increases Pa
O2
A-a gradient remains elevated
. .
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ShuntShunt
Defined as areas of the lung where there isperfusion but no ventilation (V/Q ratio = 0)
Refractory to supplemental oxygen
Arterial oxygen tension dependant upon mixed
venous oxygen tension
. .
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Shunt and Mixed Venous OxygenShunt and Mixed Venous Oxygen
PO2
0
20
40
60
80
100
20 40 60 80 100 120
SO
2%
140 200 300 400 500 6000
20
40
60
80
100
20 40 60 80 100 120
SO
2%
140 200 300 400 500 600
PO2
Oxygenated Shunt Mixed
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ARDSARDS
A specific form of lung injury with diverse causescharacterized pathologically by diffuse alveolar
damage and pathophysiologically by a breakdown
in both the barrier and gas exchange function of
the lung, resulting in proteinaceous alveolaredema and hypoxemia
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Adult Respiratory DistressAdult Respiratory Distress
Syndrome (ARDS)Syndrome (ARDS)
Characterized physiologically by stiff, non-compliant lungs
and refractory hypoxemia due to shunt
Multiple possible etiologies cause diffuse damage to the
alveolo-capillary membrane resulting in increased vascularpermeability
Fluid accumulation in the alveolar and interstitial space
makes the lungs stiffer and inactivates surfactant causing
alveolar instability and collapse further reducing lungcompliance
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ARDS: Diagnostic CriteriaARDS: Diagnostic Criteria
Definitive
Diffuse bilateral alveolar edema
Increased lung vascular permeability
Diffuse alveolar damage at pathologic examination
OperationalDyspnea usually severe
Hypoxemia with PaO2 / FIO2 < 200
Bilateral radiographic infiltrates
Reduced respiratory system compliance
No evidence of cardiac etiology
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ARDS: CausesARDS: Causes
Direct Lung InjuryDirect Lung Injury
Common causes
Pneumonia
Aspiration of gastric contents
Less common causes Pulmonary contusion
Fat emboli
Near-drowning
Inhalational injury Reperfusion injury
Indirect Lung InjuryIndirect Lung Injury
Common causes
Sepsis
Severe trauma with shock
and multiple transfusions
Less common causes
Cardiopulmonary bypass
Drug overdose
Acute pancreatitis Transfusion of blood
products
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Pathophysiologic FeaturesPathophysiologic Features
Increased permeabilty of pulmonary vasculature
Loss of hypoxic vasoconstriction
Intrapulmonary right-to-left shunt
Increased pulmonary vascular resistance
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Consequences of IncreasedConsequences of Increased
PermeabilityPermeability
Formation of shunt
Increase in ventilation to non-flooded alveoli
Loss of complianceOverdistension of ventilated alveoli
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Lung ComplianceLung Compliance
Change in lung volume for any given change intranspulmonary pressure
Normally about 80-100 ml/cm H2O
Early in ARDS, compliance decreases because of
reduced volume of aeratable lung
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Lung Heterogeneity in ARDSLung Heterogeneity in ARDS
The lung in ARDS includes
Healthy tissue
Recruitable tissue
Diseased tissue
PEEP is used to open recruitable tissue and
maintain its patency throughout the inspiratory-
expiratory cycle
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ARDSARDS
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PEEP in ARDSPEEP in ARDS
Hypoxemia reversed through the use of positive
end expiratory pressure (PEEP)Prevents collapse of unstable alveoli allowing
them to participate in gas exchangeOpened alveoli positioned on a more compliant
portion of their pressure-volume curveDelivered tidal volume can be distributed to more
alveoli reducing over-distention of the previouslyventilated alveoli
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Lung RecruitmentLung Recruitment
Gattinoni et al. NEJM, 2006
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Effects of PEEP on ComplianceEffects of PEEP on Compliance
Pressure
Volume
{
{normal
ARDS
Alveolar
compliance
curve
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Protective VentilationProtective Ventilation
NEJM 2001;344:1986
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PEEP The Double Edged SwordPEEP The Double Edged Sword
Potential protective effects of PEEP
Reduction of shear stresses by preventing collapse of
alveoli
Reduction of high levels of FIO
2
Detrimental effects of PEEP
Decreased cardiac output
Overdistension of normal alveoli
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Oxygen TransportOxygen Transport
Danger ofhypoxemia (low arterial oxygentension) is that it will lead to insufficient
delivery of oxygen to the tissues (hypoxia)
leading to cellular dysfunction, lacticacidosis, and potential cell death
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Causes of HypoxiaCauses of Hypoxia
Reduced O2Delivery
Low cardiac output (heart failure, tamponade)
Low hemoglobin concentration (anemia)
Low arterial oxygen tension
Reduced O2 unloading in tissues High oxygen-hemoglobin affinity (alkalosis, reduced 2,3 DPG,
abnormal hemoglobin)
Impaired O2utilization in mitochondrion
Enzyme poisons (cyanide)
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Lung and Bellows FailureLung and Bellows Failure
Fatigue - the inability of a muscle to continue to
develop or maintain a predetermined force
When energy demands become excessive, fatigue
results and inspiratory muscles fail to generate or
sustain minute ventilation required to maintainnormal arterial carbon dioxide tension
Characteristics - elevated arterial PCO2, hypoxemia
with an increased A-a gradient
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Respiratory MusclesRespiratory Muscles
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Diaphragmatic InsertionsDiaphragmatic Insertions
Di h ti O i t tiDi h ti O i t ti
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Diaphragmatic OrientationDiaphragmatic Orientation
Di h ti O i t tiDi h ti O i t ti
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Diaphragmatic OrientationDiaphragmatic Orientation
fW k f B thi
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Work of BreathingWork of Breathing
Force required to move air into and out of alveoli
per unit time
Determinants
Compliance of the lung
Resistance of the airways
Minute ventilation
Frequency and tidal volume
I i t M l St thI i t M l St th
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Inspiratory Muscle StrengthInspiratory Muscle Strength
AtrophyNeuromuscular disease
Nutritional status
Oxygen deliveryLung volume
M h i l I di t i COPDM h i l I di t i COPD
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Mechanical Impediments in COPDMechanical Impediments in COPD
Thoracic cage
elastic recoil
directed inwards
Shortened
muscle fibers
Decreased
diaphragmatic
curvature
Medial orientation
of diaphragmatic fibers
Decreased zone
of apposition
Horizontal ribs
L Pl LL Pl L
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LaPlaces LawLaPlaces Law
P=2Tr
Where:
P = pressure
T = tension
r = radius of curvature
P ti I dP ti I d
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Pressure-time IndexPressure-time Index
0
0.5
1
0 10.5
Fatigue
Criticalzone
Duratio
n
(TI
/T
tot
)
Force (Pdi / Pdi max )
TI = Inspiratory time
Ttot = Inspiratory + expiratory timePdi = Pressure generated by diaphragm
Pdimax = Maximum pressure diaphragm can generate
DD
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DyspneaDyspnea
An uncomfortable awareness of breathing
Corresponds to several factors
increased ventilatory drive
length-tension inappropriateness
pulmonary arterial or venous hypertension
hypoxemia and hypercapnea
cortical influences including depression and anxiety
fF t I fl i D
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DYSPNEA
Cortical influences
(depression, anxiety)
Length-tension
inappropriateness
Respiratory
drive
Vagal
reflexes
Pulmonary edema
Pulmonary
hypertension
Ventilatorydrive
PaO2
PaCO2 pH
Respiratory muscle
weakness or fatigue
Neuromuscular
disease
Malnutrition
Impediment to
breathing
Hyperinflation
Airway
obstruction
COPDAsthma
Factors Influencing DyspneaFactors Influencing Dyspnea
Chronic COChronic CO RetentionRetention
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Chronic COChronic CO22 RetentionRetention
Seen most commonly in patients with high
inspiratory work loads (chronic bronchitis or
obesity)
May help reduce the work of breathing and
prevent acute diaphragmatic fatigue
Chronic COChronic CO RetentionRetention
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Chronic COChronic CO22 RetentionRetention
In order to maintain a constant level of arterial PCO2, a
person must excrete the same amount of carbon dioxide
as the body produces each minute
The amount of carbon dioxide excreted is determined by
the amount delivered to the alveolus by the blood vs. thealveolar ventilation
Blood with elevated PCO2delivers more CO
2to the
alveolus so each breath can excrete more at the same
alveolar ventilation
Chronic COChronic CO RetentionRetention
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Chronic COChronic CO22 RetentionRetention
Drawbacks
worsening hypoxemia through decrease in alveolar
oxygen tensions
acidosis (will have renal compensation)
Response of Respiratory Drive to COResponse of Respiratory Drive to CO
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Response of Respiratory Drive to COResponse of Respiratory Drive to CO22
40 50 60 70 80 90
10
20
PaCO2
P0.1
(mm
Hg
)
Normocapnic COPD
Normal
Hypercapnic COPD
Ch i H d OCh i H d O
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Chronic Hypercapnea and OxygenChronic Hypercapnea and Oxygen
TherapyTherapy Patients with chronic hypercapnea and hypoxemia will
often have further increases in arterial PCO2when given
supplemental oxygen
Etiologies decreased minute ventilation
increased V/Q mismatch
Haldane effect
. .
D d Mi t V til tiDecreased Minute Ventilation
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Decreased Minute VentilationDecreased Minute Ventilation
Long postulated that patients are dependent onhypoxic drive to maintain ventilation
Supplemental oxygen felt to improve hypoxemia,
decreasing driveStudies have not confirmed this to be a factor
.. ..V/Q Mi t h
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Increases in alveolar PO2from the supplemental
oxygen decrease hypoxic vasoconstriction of
vessels supplying poorly ventilated alveoli
Increases in perfusion to alveolus are initially not
matched by increases in ventilation causingworsening V/Q ratios
V/Q MismatchV/Q Mismatch
..
/QV/Q Mi t h. .
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V/Q MismatchV/Q Mismatch
Decreasing V/Q ratio increases the PCO2of the
blood leaving the alveolocapillary unit
Normal individuals compensate for this increase
by increasing minute ventilation
Patients with preexisting hypercapnea do not
increase their ventilation to compensate
. .
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