Arterial Blood Gases

Respiratory Failure
Michael Lippmann, MD

Division of Pulmonary and Critical Care Medicine

Department of Internal Medicine
Respiratory System
 Lung
– Parenchyma
– Airways
 Bellows
– Respiratory control centers
– Peripheral nerves
– Muscles
– Chest wall
Role of Respiratory System
 Maintainoptimal levels of oxygen and pH in the
blood 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
Alveolar Gas Pressures
 Determinedby balance between delivery of
oxygen and carbon dioxide to the lung and their
removal
– Atmospheric air passes through airways where it is
fully saturated with water vapor and delivered to the
alveoli
– Oxygen is delivered to the alveoli by ventilation and
taken up by the hemoglobin in the blood perfusing the
lung
– Carbon dioxide is delivered to the alveoli by the blood
perfusing the lung and removed by ventilation
 . .
Effect of V/Q Ratio on Alveolar Gas

160 160
PO2 in alveolus
and capillary
140 140

120 120
PO2 or PCO2

100 100

80 80
Normal
60 range of 60
V/Q
40 ratios
PCO2 in alveolus 40
and capillary
20 20

.1 .2 .4 .6 .8 1 2 4 6 8 10
. .
Log V/Q ratios
Alveolar PCO2
. . .
PaCO2 = VCO2/(VE-VD)
Where:
PaCO2 = Arterial carbon dioxide tension
.
VCO = CO2 production by the body
. 2

.=
VE 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
Alveolar Gas Equation for Oxygen
PAO2 = FIO2(PB - PH2O) - PaCO2/R

Where:
FIO2 = Fraction inspired oxygen tension
PB = Barometric pressure (747 mm Hg)
PH2O = Partial pressure of water vapor (47 mm Hg)
PaCO2 = Arterial carbon dioxide tension
R = Respiratory equivalent (0.8)
Alveolar Gas Equation for Oxygen

PAO2 = FIO2(PB - PH2O) - PaCO2/R

 Balance between removal of oxygen from the alveolus by

perfusion, 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, which
removes oxygen and adds CO2 to the alveolus
Arterial Gas Pressures
 Determined by the average of gas contents of
blood leaving alveolo-capillary units
 Gas pressure ≠ gas content
 Pressure – index of the tendency of a gas
molecule to move
– Gas 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 a
given volume
Ideal Gas Law

PV = ηRT
P = pressure Pressure will increase with
V = volume of vessel  Increase in amount of gas

η = number of moles of gas  Decrease in volume of

container
R = universal gas constant
 Increase in temperature
T = absolute temperature
Henry’s Law
P = kC
 The solubility of a gas in a liquid is directly proportional
to the partial pressure of that gas above the liquid
– k is a temperature-dependent constant (769.2 L•atm/mol for
oxygen in water at 298° K)
– P is the partial pressure (atm)
– C is 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
Oxygen Content
 Oxygen is poorly soluble in plasma and is carried
by 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 (PaO2)
Oxyhemoglobin Dissociation Curve
100
Left-shifted (Increased affinity)
• decreased temp
80
• decreased 2-3 DPG
• increased pH Right-shifted (Decreased affinity)
60 • carbon monoxide • increased temp
SO2 %

• increased 2-3 DPG

• decreased pH
40

20

0 20 40 60 80 100 120
PO2
• Oxygen content = (1.34 ml x Hgb) SaO2
• Curve also represents relationship between
PO2 and oxygen content
Oxygen Content – PaO2 = 100

1.31 ml 1.31 ml
O2 O2 1.31 ml
O2
1.34 ml O2 x (16 g/dl Hgb) x 98% = 21 ml O2
1.31 ml
O2 1.31 ml 1.31 ml
1.31 ml
O2
O2 O2
+
1.31 ml
1.31 ml 1.31 ml 1.31 ml O2
O2 O2 O2 0.003 ml O2 (100) = .03 ml O2
1.31 ml
O2

1.31 ml 1.31 ml
O2 O2 1.31 ml
1.31 ml O2
O2 .03 ml O2 Content = 21.03 ml/dl blood
O2
Oxygen Content – PaO2 = 40

1.00 ml 1.00 ml
O2 O2 1.00 ml
O2
1.34 ml O2 x (16 g/dl Hgb) x 75% = 16 ml O2
1.00 ml
O2 1.00 ml 1.00 ml
1.00 ml
O2
O2 O2
+
1.00 ml
1.00 ml 1.00 ml 1.00 ml O2
O2 O2 O2 0.003 ml O2 (40) = .012 ml O2
1.00 ml
O2

1.00 ml 1.00 ml
O2 O2 1.00 ml
1.00 ml O2
O2 .012 ml O2 Content = 16.012 ml/dl blood
O2
Oxygen Content – PaO2 = 600

1.34 ml 1.34 ml
O2 O2 1.34 ml
O2
1.34 ml O2 x (16 g/dl Hgb) x 100% = 21.4 ml O2
1.34 ml
O2 1.34 ml 1.34 ml
1.34 ml
O2
O2 O2
+
1.34 ml
1.34 ml 1.34 ml 1.34 ml O2
O2 O2 O2 0.003 ml O2 (600) = .18 ml O2
1.34 ml
O2

1.34 ml 1.34 ml
O2 O2 1.34 ml
1.34 ml O2
O2 .18 ml O2 Content = 21.58 ml/dl blood
O2
 Mixing
Equal volumes (100 cc) of blood mixed together
each with equal amounts of hemoglobin (16g/dl)

1.16 ml 1.16 ml
1.31 ml 1.31 ml 1.00 ml 1.00 ml 1.16 ml 1.16 ml O2 1.16 ml
O2 O2 O2 O2 O2 O2
O2 1.31 ml O2 1.00 ml
1.31 ml O2 1.00 ml O2 1.16 ml
1.16 ml 1.16 ml O2
O2 1.31 ml 1.31 ml O2 1.00 ml 1.00 ml O2 O2 1.16 ml 1.16 ml
1.31 ml O2 O2 1.00 ml O2 O2 1.16 ml 1.16 ml
1.16 ml O2 1.16 ml O2
O2 O2 O2 O2 O2
O2 1.16 ml

+
1.31 ml 1.00 ml 1.16 ml

= 1.16 ml 1.16 ml O2
1.31 ml 1.31 ml 1.31 ml O2 1.00 ml 1.00 ml 1.00 ml O2 O2 1.16 ml
O2 O2 O2 O2 O2 O2 O2 O2 O2
1.31 ml 1.00 ml 1.16 ml 1.16 ml 1.16 ml
1.16 ml O2 O2
O2 O2 O2
1.31 ml 1.00 ml 1.16 ml O2 1.16 ml
1.31 ml 1.00 ml 1.16 ml 1.16 ml
O2 O2 O2 O2
O2 1.31 ml O2 1.00 ml O2
1.16 ml O2
1.31 ml O2 1.00 ml O2
O2 O2 O2
1.16 ml 1.16 ml 1.16 ml 1.16 ml
O2 O2 O2 O2

PO2 = 100 PO2 = 40 PO2 = 54

SO2 = 98% SO2 = 75% SO2 = 86.5%
Content = 21 ml O2/100cc Content = 16 ml O2/100cc Content = 18.5 ml O2/100cc
 Mixing
Equal volumes (100 cc) of blood mixed together
each with equal amounts of hemoglobin (16g/dl)

1.17 ml 1.17 ml
1.34 ml 1.34 ml 1.00 ml 1.00 ml 1.17 ml 1.17 ml O2 1.17 ml
O2 O2 O2 O2 O2 O2
O2 1.34 ml O2 1.00 ml
1.34 ml O2 1.00 ml O2 1.17 ml
1.17 ml 1.17 ml O2
O2 1.34 ml 1.34 ml O2 1.00 ml 1.00 ml O2 O2 1.17 ml 1.17 ml
1.34 ml O2 O2 1.00 ml O2 O2 1.17 ml 1.17 ml
1.17 ml O2 1.17 ml O2
O2 O2 O2 O2 O2
O2 1.17 ml

+
1.34 ml 1.00 ml 1.17 ml

= 1.17 ml 1.17 ml O2
1.34 ml 1.34 ml 1.34 ml O2 1.00 ml 1.00 ml 1.00 ml O2 O2 1.17 ml
O2 O2 O2 O2 O2 O2 O2 O2 O2
1.34 ml 1.00 ml 1.17 ml 1.17 ml 1.17 ml
1.17 ml O2 O2
O2 O2 O2
1.34 ml 1.00 ml 1.17 ml O2 1.17 ml
1.34 ml 1.00 ml 1.17 ml 1.17 ml
O2 O2 O2 O2
O2 1.34 ml O2 1.00 ml O2
1.17 ml O2
1.34 ml O2 1.00 ml O2
O2 O2 O2
1.17 ml 1.17 ml 1.17 ml 1.17 ml
O2 O2 O2 O2

PO2 = 600 PO2 = 40 PO2 = 57

SO2 = 100% SO2 = 75% SO2 = 87.5%
Content = 21.4 ml O2/100cc Content = 16 ml O2/100cc Content = 18.7 ml O2/100cc
West Two-Compartment Model -
Oxygen

. .
VA VA
. 2 l/min .
2 l/min VA
VA PO2 99 = .83
= .83 PO2 99
Q Q

99 SO
2.4 l/min 2 97
PO PO 2 .5
Blood 2 99
flow SO PO2 99 SO2 97.5
2 97.
2.4 l/min 5
• •
V/Q Mismatch - Oxygen

. .
VA VA
. 3.6 l/min 0.4 l/min .
VA VA
= 1.5 PO2 117 PO2 51.5 = .167
Q Q

2.4 l/min 51. 5 S O

PO 2 86
PO 2
Blood 2 11
7 PO2 64 SO2 92.1
flow SO
2 98.
2.4 l/min 2
Alveolar-arterial Gradient

Calculated alveolar O2 (PAO2) -

measured arterial O2 (PaO2)
A-a Gradient
. .
 Measures dispersion of V/Q ratios within the
lung
. .
 Normal lung has narrow range of V/Q ratios
 The greater the variability, the higher the A-a
gradient
A-a Gradient
 Clinically,can be used to assess underlying lung
function in patients with decreased PaCO2 or
receiving supplemental oxygen
– Arterial PO2 may 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
 PCO2 versus CO2 Content

60 60
CO2 content

40 55

20 50

0
20 40 60 80 40 50 60
PCO2
Deoygenated Oxygenated
blood blood
. .
V/Q Mismatch - Carbon Dioxide

PCO2 40 PCO2 40
100 ml/min 100 ml/min
CO2 production CO2 CO2
200 ml/min
low flo w PC
50% f 50% O
2 40
PCO2 46 PCO2 40

40
PCO 2
. .
V/Q Mismatch - Carbon Dioxide

100 ml/min 0 ml/min

CO2 production CO2 CO2
200 ml/min
low f low PC
50% f 50% O
2 46
PCO2 46 PCO2 43

40
PCO 2
 CO2 Elimination Must Equal CO2
Production

Options . .
 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)
Bicarbonate Buffer System
H2CO3 ⇔ H+ + HCO3-
weak acid conjugate
base

CO2 + H2O ⇔H2CO3 ⇔H+ + HCO3-

• 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 to

dissolved CO2. Dissolved CO2 in mmole =
0.03 x PCO2
Henderson-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 pK
 Also depends on the amount of buffer present
Henderson-Hasselbach Equation

[conjugate base ]
pH =pK + log
[ weak acid ]

For the bicarbonate system:

[ H C O3 ] m e ta b o li c
−

p H= 6.1 lo g

0.0 3 xP C O2 r e s p ir a to r y
Bicarbonate Buffer System
 The bicarbonate generated by the buffer pair does not
effectively buffer the change in H+ when PCO2 rises
CO2 + H2O ⇔H2CO3 ⇔H+ + HCO3-
– doubling the CO2 doubles [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 System
CO2 CO2

Open
(Ventilating)
PCO2 40 PCO2 40
System
+ 5 meq H+
Lung Lung

[HCO3-] = 24 mmole [HCO3-] = 19 mmole

0.03 x PCO2 = 1.2 mmole 0.03 x PCO2 = 1.2 mmole

pH = 6.1 + log (24/1.2) pH = 6.1 + log (19/1.2)

ph = 7.4 ph = 7.3
Bicarbonate Buffer System

CO2

Closed
(Non ventilating)
PCO2 40 PCO2 207 System
+ 5 meq H+
Lung Lung

[HCO3-] = 24 mmole [HCO3-] = 19 mmole

0.03 x PCO2 = 1.2 mmole 0.03 x PCO2 = 6.2 mmole

pH = 6.1 + log (24/1.2) pH = 6.1 + log (19/6.2)

ph = 7.4 ph = 6.59
Acid-Base Terminology
 Acidemia – blood pH < 7.36
 Alkalemia – blood pH > 7.44
 Hypocapnia – PaCO2 < 36 mmHg

 Hypercapnea – PaCO2 > 44 mmHg

 Hyperventilation – associated with hypocapnia
 Hypoventilation – associated with hypercapnea
 Tachypnia – high breathing rate
Acid-Base Terminology
 Respiratory acidosis
– A primary process associated with an increase in PaCO2
– Decreases pH
– Compensation through renal retention of bicarbonate
 Respiratory alkalosis
– A primary process associated with a decrease in PaCO2
– Increases pH
– Compensation through renal excretion of bicarbonate
Acid-Base Terminology
 Metabolic acidosis
– A primary process associated with a decrease in serum
bicarbonate
– Decreases pH
– Compensation through hyperventilation
 Metabolic alkalosis
– A primary process associated with an increase in serum
bicarbonate
– Increases pH
– Compensation through hypoventilation
Blood Gas Interpretation
 Normal values
– pH between 7.36 and 7.44
– PCO2 between 36 and 44 mmHg
– PO2 between 80 and 100 mmHg
Blood Gas Interpretation
 Establish relationship between pH and PCO2
– Primary 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 PCO2 discordant or change in pH is of a
greater magnitude than expected by change in PCO2
Blood Gas Interpretation
 pH 7.24, PCO2 60
– Reciprocal relationship between pH and PCO2
– Change in pH proportional to change in PCO2
– Acute respiratory acidosis

 pH 7.24, PCO2 80
– Reciprocal relationship between pH and PCO2
– Change in pH less than expected for elevation in PCO2
– Respiratory acidosis with partial metabolic
compensation (metabolic alkalosis)
Blood Gas Interpretation
 pH 7.24, PCO2 40
– Low pH with normal PCO2
– Metabolic acidosis

 pH 7.32, PCO2 30
– PCO2 and pH both low
– Metabolic acidosis with partial respiratory
compensation (respiratory alkalosis)
Acute Respiratory Failure
 Arterial carbon dioxide tension (PaCO2 ) greater
than 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
Bellows Failure - Etiologies
 Respiratory control centers
– drugs, infections, bleeding, trauma
 Peripheral nerves
– Guillain Barre syndrome, polio
 Muscles
– myotonic dystrophy, fatigue
 Chest wall
– kyphoscoliosis
Bellows Failure - Etiologies
 Respiratory control centers
– drugs, infections, bleeding, trauma
 Peripheral nerves
– Guillain Barre syndrome, polio
 Muscles
– myotonic dystrophy, fatigue
 Chest wall
– kyphoscoliosis
Ventilation vs. CO2

120

100

80
PaCO2

60

40

20

1 2 3 4 5 6 7 8 9 10
Alveolar ventilation
Effects of Hypercapnea
 Decreased PaO2 proportional to rise in PaCO2 (A-a
gradient normal)
 Acidemia (compensated by metabolic changes if
the increase is gradual)
Lung Failure
 Characterized by hypoxemia with widened A-a
gradient
 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
Lung Infections
. .
 Among the most common causes of V/Q
mismatch
 Upper airway or bronchial infections decrease
airflow to the distal alveoli
 Infections of the distal airways and alveoli
(pneumonia) disrupt or totally obstruct airflow to
an area of the lung
 Release of inflammatory mediators may
..
paradoxically increase the perfusion to these areas
further lowering V/Q ratios
 . .
Supplemental Oxygen in V/Q Mismatch
 Increasing the concentration of oxygen in inspired
air (FIO2) increases PAO2
 Increased PAO2 equilibrates with capillary blood
increasing PO2 and O2 content of blood leaving the
alveolo-capillary unit
 Blood with higher O2 content mixes with blood
from other units and increases PaO2
 A-a gradient remains elevated
Shunt
 Defined as areas of the lung where
. . there is
perfusion but no ventilation (V/Q ratio = 0)
 Refractory to supplemental oxygen
 Arterial oxygen tension dependant upon mixed
venous oxygen tension
 Shunt and Mixed Venous Oxygen

100
100

80
80
SO2 %

SO2 %
60
60

40
40

20
20

0 20 40 60 80 100 120 140 200 300 400 500 600

0 20 40 60 80 100 120 140 200 300 400 500 600
PO2 PO2

Oxygenated Shunt Mixed

ARDS
A specific form of lung injury with diverse causes
characterized pathologically by diffuse alveolar
damage and pathophysiologically by a breakdown
in both the barrier and gas exchange function of
the lung, resulting in proteinaceous alveolar
edema and hypoxemia
Adult Respiratory Distress
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 vascular
permeability
 Fluid accumulation in the alveolar and interstitial space
makes the lungs stiffer and inactivates surfactant causing
alveolar instability and collapse further reducing lung
compliance
ARDS: Diagnostic Criteria
 Definitive
– Diffuse bilateral alveolar edema
– Increased lung vascular permeability
– Diffuse alveolar damage at pathologic examination
 Operational
– Dyspnea – usually severe
– Hypoxemia with PaO2 / FIO2 < 200
– Bilateral radiographic infiltrates
– Reduced respiratory system compliance
– No evidence of cardiac etiology
ARDS: Causes
Direct Lung Injury Indirect Lung Injury
 Common causes  Common causes
– Pneumonia – Sepsis
– Aspiration of gastric contents – Severe trauma with shock
and multiple transfusions
 Less common causes
– Pulmonary contusion  Less common causes
– Fat emboli – Cardiopulmonary bypass
– Near-drowning – Drug overdose
– Inhalational injury – Acute pancreatitis
– Reperfusion injury – Transfusion of blood
products
Pathophysiologic Features
 Increased permeabilty of pulmonary vasculature

 Loss of hypoxic vasoconstriction

 Intrapulmonary right-to-left shunt

 Increased pulmonary vascular resistance

Consequences of Increased
Permeability
 Formation of shunt
 Increase in ventilation to non-flooded alveoli
– Loss of compliance
– Overdistension of ventilated alveoli
Lung Compliance
 Change in lung volume for any given change in
transpulmonary pressure

 Normally about 80-100 ml/cm H2O

 Earlyin ARDS, compliance decreases because of

reduced volume of aeratable lung
Lung 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
ARDS
PEEP in ARDS
 Hypoxemia reversed through the use of positive
end expiratory pressure (PEEP)
 Prevents collapse of unstable alveoli allowing
them to participate in gas exchange
 Opened alveoli positioned on a more compliant
portion of their pressure-volume curve
 Delivered tidal volume can be distributed to more
alveoli reducing over-distention of the previously
ventilated alveoli
Lung Recruitment

Gattinoni et al. NEJM, 2006

Effects of PEEP on Compliance

Alveolar
Volume

compliance
curve

normal
Pressure
{

ARDS
 Protective Ventilation

NEJM 2001;344:1986
PEEP – The Double Edged Sword
 Potential protective effects of PEEP
– Reduction of shear stresses by preventing collapse of
alveoli
– Reduction of high levels of FIO2
 Detrimental effects of PEEP
– Decreased cardiac output
– Overdistension of normal alveoli
Oxygen Transport

• Danger of hypoxemia (low arterial oxygen

tension) is that it will lead to insufficient
delivery of oxygen to the tissues (hypoxia)
leading to cellular dysfunction, lactic
acidosis, and potential cell death
Causes of Hypoxia
 Reduced O2 Delivery
– 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 O2 utilization in mitochondrion
– Enzyme poisons (cyanide)
Lung 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 maintain
normal arterial carbon dioxide tension
 Characteristics - elevated arterial PCO2, hypoxemia
with an increased A-a gradient
Respiratory Muscles
Diaphragmatic Insertions
Diaphragmatic Orientation
Diaphragmatic Orientation
Work 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
Inspiratory Muscle Strength
 Atrophy
 Neuromuscular disease
 Nutritional status
 Oxygen delivery
 Lung volume
Mechanical Impediments in COPD

Thoracic cage
elastic recoil Horizontal ribs
directed inwards

Decreased zone
of apposition

Decreased
Shortened diaphragmatic Medial orientation
muscle fibers curvature of diaphragmatic fibers
LaPlace’s Law

2T
P= r
Where:
P = pressure
T = tension
r = radius of curvature
 Pressure-time Index
TI = Inspiratory time
1 Ttot = Inspiratory + expiratory time
Pdi = Pressure generated by diaphragm
Pdimax = Maximum pressure diaphragm can generate

Fatigue
Duration
(TI / Ttot )

0.5

Critical
z one
0
0 0.5 1
Force (Pdi / Pdi max )
Dyspnea
 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
Factors Influencing Dyspnea
Pulmonary edema ↓ PaO2
Ventilatory ↑ PaCO2
drive ↓ pH
Vagal
reflexes

Respiratory
Pulmonary drive
hypertension Neuromuscular Malnutrition
disease

DYSPNEA Respiratory muscle

weakness or fatigue Airway
obstruction

Cortical influences Length-tension Impediment to

(depression, anxiety) inappropriateness breathing

Hyperinflation COPD
Asthma
Chronic CO2 Retention
 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 CO2 Retention
 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. the
alveolar ventilation
 Blood with elevated PCO2 delivers more CO2 to the
alveolus so each breath can excrete more at the same
alveolar ventilation
Chronic CO2 Retention
 Drawbacks
– worsening hypoxemia through decrease in alveolar
oxygen tensions
– acidosis (will have renal compensation)
Response of Respiratory Drive to CO2

20 Normocapnic COPD

Normal
P0.1 (mm Hg)

Hypercapnic COPD
10

40 50 60 70 80 90

PaCO2
Chronic Hypercapnea and Oxygen
Therapy
 Patientswith chronic hypercapnea and hypoxemia will
often have further increases in arterial PCO2 when given
supplemental oxygen
 Etiologies
– decreased minute
. . ventilation
– increased V/Q mismatch
– Haldane effect
Decreased Minute Ventilation

 Long postulated that patients are dependent on

hypoxic drive to maintain ventilation
 Supplemental oxygen felt to improve hypoxemia,
decreasing drive
 Studies have not confirmed this to be a factor
. .
V/Q Mismatch
 Increases in alveolar PO2 from 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 causing
worsening V/Q ratios
. .
V/Q Mismatch
. .
 Decreasing V/Q ratio increases the PCO2 of 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
Haldane Effect
 Oxygenated hemoglobin has a lower affinity for
carbon dioxide than deoxygenated
 For the same CO2 content, oxygenated blood will
have a higher PCO2 than poorly oxygenated blood