Acute Respiratory Failure 2010

8/8/2019 Acute Respiratory Failure 2010

1/87

Arterial Blood GasesArterial Blood GasesRespiratory FailureRespiratory Failure

Michael Lippmann, MD

Division of Pulmonary and Critical Care Medicine

Department of Internal Medicine


2/87

Respiratory SystemRespiratory System

LungParenchyma

Airways

BellowsRespiratory control centers

Peripheral nerves

Muscles

Chest wall


3/87

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


4/87

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


5/87

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


6/87

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

.

.

.

. . .


7/87

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)


8/87

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


9/87

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


10/87

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


11/87

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


12/87

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)


13/87

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


14/87

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


15/87


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



16/87


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



17/87

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%


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

+ =


18/87

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%


PO2 = 40

SO2 = 75%


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%


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

+ =


19/87

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

. .

. .


20/87

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

. .

..


21/87

Alveolar-arterial GradientAlveolar-arterial Gradient

Calculated alveolar O2(P

AO

2) -

measured arterial O2 (PaO2)


22/87

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

. .

. .


23/87

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

. .


24/87

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


25/87

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

. .


26/87

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

. .


27/87

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


28/87

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-


29/87

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


30/87

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


31/87

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



32/87


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


33/87

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+


Closed

(Non ventilating)

System


34/87

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


35/87


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


36/87


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


37/87

Blood Gas InterpretationBlood Gas Interpretation

Normal valuespH between 7.36 and 7.44

PCO2between 36 and 44 mmHg

PO2between 80 and 100 mmHg


38/87


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


39/87


40/87


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)


41/87

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


42/87

Bellows Failure - EtiologiesBellows Failure - Etiologies

Respiratory control centersdrugs, infections, bleeding, trauma

Peripheral nerves

Guillain Barre syndrome, polio

Muscles

myotonic dystrophy, fatigue

Chest wall

kyphoscoliosis


43/87

Bellows Failure - EtiologiesBellows Failure - Etiologies

Respiratory control centersdrugs, infections, bleeding, trauma

Peripheral nerves

Guillain Barre syndrome, polio

Muscles

myotonic dystrophy, fatigue

Chest wall

kyphoscoliosis


44/87

Ventilation vs. COVentilation vs. CO22

21 3 4 5 6 7 8 9 10

20

40

60

80

100

120

Alveolar ventilation

PaC

O2


45/87

Effects ofEffects ofHypercapneaHypercapnea

Decreased PaO2 proportional to rise in PaCO2 (A-agradient normal)

Acidemia (compensated by metabolic changes if

the increase is gradual)


46/87

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

. .


47/87

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

. .

. .


48/87

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

. .


49/87

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

. .


50/87

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


51/87

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


52/87

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


53/87

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


54/87

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


55/87

Pathophysiologic FeaturesPathophysiologic Features

Increased permeabilty of pulmonary vasculature

Loss of hypoxic vasoconstriction

Intrapulmonary right-to-left shunt

Increased pulmonary vascular resistance


56/87

Consequences of IncreasedConsequences of Increased

PermeabilityPermeability

Formation of shunt

Increase in ventilation to non-flooded alveoli

Loss of complianceOverdistension of ventilated alveoli


57/87

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


58/87

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


59/87

ARDSARDS


60/87

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


61/87

Lung RecruitmentLung Recruitment

Gattinoni et al. NEJM, 2006


62/87

Effects of PEEP on ComplianceEffects of PEEP on Compliance

Pressure

Volume

{

{normal

ARDS

Alveolar

compliance

curve


63/87

Protective VentilationProtective Ventilation

NEJM 2001;344:1986


64/87

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


65/87

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


66/87

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)


67/87

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


68/87

Respiratory MusclesRespiratory Muscles


69/87

Diaphragmatic InsertionsDiaphragmatic Insertions

Di h ti O i t tiDi h ti O i t ti


70/87

Diaphragmatic OrientationDiaphragmatic Orientation

Di h ti O i t tiDi h ti O i t ti


71/87

Diaphragmatic OrientationDiaphragmatic Orientation

fW k f B thi


72/87

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


73/87

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


74/87

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


75/87

LaPlaces LawLaPlaces Law

P=2Tr

Where:

P = pressure

T = tension

r = radius of curvature

P ti I dP ti I d


76/87

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


77/87

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


78/87

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


79/87

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



80/87


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



81/87


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


82/87

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


83/87

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


84/87

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


85/87

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. .


86/87

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

. .


87/87

Documents

Acute Respiratory Failure 2010