Internal Respiration
Module F
Module F
• Chapter 9 – Assessment of
Hypoxemia and Shunting
• Chapter 10 – Treatment of
Hypoxemia and Shunting
• Chapter 11 – Hypoxia: Assessment
and Intervention
Objectives
At the conclusion of this session the participant will:
• Still be awake! This covers 3 chapters!
• Relax…most is a review and some will be covered in
Winter 09.
• Define oxygen extraction.
• Describe the effects of anaerobic metabolism.
• State the formula for calculating RQ.
• List the 5 causes of hypoxemia.
• State the effect of an increase or decrease in cardiac
output on the shunt fraction.
• List three methods, other than the shunt fraction, which
can be used to assess the degree of physiologic
shunting.
• State three ways to treat acute hypoxemia.
Objectives
• Define anemia.
• List three types of anemia and state the causes of
the defect.
• Describe the effect of anemia on the presence of
hypoxia.
• State the benefit, problems, and specific levels for
each of the following as it relates to it being an
indicator of cellular hypoxia:
• Lactate
• Mixed Venous Oxygenation
• Oxygen Consumption & Utilization
• Gastric Mucosal Acidosis
Internal Respiration
• Exchange of oxygen and carbon dioxide at
the cellular level.
• Some control by local vasculature.
• Increased distance from capillary to tissue will result
in decreased delivery.
• Some organs use more than others.
• Table 7-1 (p. 188).
• Note: % of blood flow is not equal to volume of
oxygen consumed.
Internal Respiration
• Normal metabolism exists when O2 is
consumed and CO2 is produced.
• Normal ratio of CO2 produced : O2 consumed
is 0.8:1 (200/250)
• Increased ratio with excess CHO utilization;
decreased with fat & ETOH.
• When insufficient oxygen is present,
anaerobic metabolism results.
• Less ATP produced.
• Lactic Acid is produced.
Adequacy and Efficiency of
Oxygen Delivery
• Adequacy: Is there sufficient oxygen present?
(Hint: Is hypoxemia present?)
• Causes of Hypoxemia
• Low PIO2
•
•
•
•
•
Hypoventilation
Absolute Shunts
Relative Shunts
Diffusion Defects
True or Absolute Deadspace (secondary mechanism)
• Efficiency: Is the PaO2 appropriate for the FIO2?
• If not…assume a shunt is present!
Effects of Cardiac Output on PaO2
• The normal decrease in PaO2 from alveolar
oxygen levels is due to the small mixing of
anatomically shunted blood (5%).
• This blood is venous in nature and has a PO2 the
same as the P O2.
• Four situations exist that can affect the PaO2:
• Decreased Cardiac Output with a Normal Shunt
• Increased Shunting with a Normal Cardiac Output
• Decreased Cardiac Output with an Increased Shunt
• Increased Cardiac Output with an Increased Shunt
The Normal Ventilation/Perfusion
Relationship
• Normal PAO2
• Normal PćO2
• Normal P
O2
• Normal CO
• Normal Oxygen
Consumption
• Normal PaO2
Decreased Cardiac Output with a
Normal Shunt
• P O2 decreases with a
decrease in cardiac
output because of an
increased oxygen
extraction (assuming
O2 doesn’t change).
• Any shunted blood will
have a reduced
P O2 .
• Because the amount of
shunted blood is so small,
the decrease in PaO2 isn’t
significant.
Increased Shunting with a
Normal Cardiac Output
• Example: ARDS
• Normal Cardiac
Output = Normal
P O2
• The problem here is
a significant increase
in intrapulmonary
shunt, meaning more
P O2 “contaminated”
blood entering the
pulmonary vein
(arterial system).
Decreased Cardiac Output with
an Increased Shunt
• Similar to the first
scenario, but here
there is an increased
intrapulmonary shunt.
• Example: ARDS with
an MI
• Reduced Cardiac
Output yields a
reduced P O2 (higher
extraction).
• More of that low P O2
blood is shunted in
the lungs, resulting in
a large reduction in
PaO2.
Increased Cardiac Output with an
Increased Shunt
• Normal physiologic
response to hypoxemia
is to increase heart rate
(peripheral
chemoreceptors) and
Cardiac Output.
• P O2 is increased (better
oxygen delivery).
• With an increased
intrapulmonary shunt,
however, there still is an
increased amount of
P O2 “contaminated”
blood entering the
system.
So What?
• Don’t always assume that an improvement or
deterioration in PaO2 is occurring solely because
of a change in pulmonary gas exchange.
• Suspect a change in cardiac output when an
abrupt, unexplained hypoxemia is observed in
critically ill patients.
• Also, consider other non-cardiac causes of
reduced P O2.
• Anemia
• Increased metabolism (fever)
• Maldistribution of systemic perfusion
Assessment of Hypoxemia
• Definition of “Hypoxemia”.
• Severity?
• Causes of Hypoxemia
• Differential Diagnosis of Hypoxemia
Abnormality
PaO2
PaCO2
Hypoventilation

Absolute Shunt

N or 
Relative Shunt

N, , 
Diffusion Defect
N at
Rest, 
w/
exercise
N or 
RA P(A-a)O2
100% O2 P(A-a)O2
N
N
N
N at rest, with
exercise
N
Shunt Substitutes
• P(A-a)O2
• PaO2/PAO2
• PaO2/FIO2
PAO2
• PAO2 = [(PBARO - PH2O) x FIO2] –
(PaCO2/0.8)
• On FIO2 of less than 60%
• PAO2 = [(PBARO - PH2O) x FIO2] – PaCO2
• On FIO2 greater than 60%
• Normal Values:
• Room Air: 100 – 104 mm Hg
• 100% Oxygen: 600
P(A-a)O2
• Normal values is around 10 mm Hg on
room air.
• Values increase with increasing age and the
supine position.
• Normal values 25-65 mm Hg on 100%
• Difficult to use when FIO2 varies from 21
or 100%
• Normal values differ for each FIO2
• Limited value when using supplemental oxygen.
P(A-a)O2 on Room Air
• Normal A-a gradient on 21% is seen with:
• Pure hypoventilation
• High altitude
• Diffusion defect (patient at rest)
• Abnormal A-a gradient on 21% is seen
with
• Relative shunt
• Absolute shunt
P(A-a)O2 on 100%
• Relative Shunt will improve
• A-a gradient less than 300 mm Hg
• Absolute Shunt will not improve
• A-a gradient is greater than 300 mm Hg
Using P(A-a)O2 to Estimate
Shunt
• On 100% FIO2, a 1% shunt is estimated
for every 10 – 15 mm Hg P(A-a)O2
• Example: A-a gradient is 140 mm Hg
• 140 = 9.3%
15
140 = 14.0%
10
Using P(A-a)O2 to Estimate
Shunt
• Normal Shunt is 5%
• Add 5 % to the normal 5% shunt for every
100 mm Hg gradient; Example:
• 100 mm Hg – 10%
• 200 mm Hg – 15%
• 300 mm Hg – 20%
Shunt Equation
• Classic Shunt Equation
• “Gold Standard”
• Clinical Shunt Equation
• A shunt greater than or = 15% is significant
• Increased shunts will correlate with
• “White out on x-ray unless its cardiac in origin.
• Atelectasis, pneumonia, pulmonary edema, ARDS
Classic Shunt Equation

Q
s
CcO2  CaO2


100

Q t CcO2  Cv O2
• Where:
• CćO2= (1.34 x Hb x 1.0) + (PAO2 x .003)
• Assumes 100% saturation in the ideal alveolus
• Requires a Pulmonary Arterial Catheter
(BTFDC)
Clinical Shunt Equation

Q
s
P A  a O2  .003


Q t P A  a O2  .003  CaO2  Cv O2 
• Requires a Pulmonary Arterial Catheter
(BTFDC)
• Only accurate at lower FIO2
PaO2 /PAO2 (a-A ratio)
• Normal value is greater than 75% on any
FIO2
• Example: 100/104 = 96%
• 96% of oxygen is diffusing across the A-C
membrane
PaO2/FIO2 ratio
•
•
•
•
Normal value is 400 – 500
Example: 100 mm Hg/.21 = 476
Value between 200 – 300 = ALI
Value less than 200 = ARDS
• Values less than 200 correlate with a shunt of
greater than 20%
Treatment of Hypoxemia
• Increase FIO2
• Increase MAP
• PEEP, Inspiratory Time, Vt
• Body Positioning
• Prone Positioning
• Lateral decubitus (good lung down)
• Good bronchial hygiene
• Suction, bronchodilators, CPT/Flutter/PEP
Oxygen Administration
• Treat hypoxemia/Hypoxia
• Decrease the work of breathing
• Decrease the work of the heart
Hazards of Oxygen Therapy
•
•
•
•
Absorption atelectasis
Oxygen Toxicity
Retinopathy of prematurity
Oxygen induced hypoventilation in COPD
• Look for oxygen levels above 60 mm Hg and
a rising PaCO2
• Evaluate FIO2 patient is receiving
• Patient symptomatic: sleepy, lethargic
Hyperoxemia
• PaO2 greater than 100 mm Hg
• Usually undesirable
• Very little oxygen content is gained
• A PaO2 above 130 mm Hg indicates the
patient is breathing supplemental oxygen.
• Hyperoxemia is indicated in COHb%.
Hyperoxemia
• SpO2% of 100% means the PaO2 could be
between 100 mm Hg & 600 mm Hg
• Very dangerous in infants
Oxygen Administration in
Chronic Hypercapnia
• PaO2 will increase 3 mm Hg for each 1%
increase in FIO2
• Keep PaO2 around 60 mm Hg
• FIO2 = 60 - PaO2 on room air
3
Example
• You are asked to draw an ABG on a
CO2 retainer. The PaO2 is 39 mmHg on
21%
Where should the FIO2 be set?
FiO2 = 60 - 39 = 7% Add to 21%
3
• Set FIO2 at 28%
Calculating the maximal PaO2
for any given FIO2
• The PaO2 on room air during
hyperventilation may go up to 130 mm Hg
• A PaO2 more than 5 times the % of oxygen
is suspicious.
•
•
•
•
30
40
50
60
x
x
x
x
5
5
5
5
=
=
=
=
150
200
250
300
Problem
• pH 7.32, PaCO2 48, PaO2 200, FIO2 .30
• PAO2 = 760 – 47 x 0.30 – 48/.8
= 154 mm Hg
• Can’t have a PaO2 greater than PAO2, so…
• Either the FIO2 was not recorded accurately
• Lab error (air bubble)
Evaluating FIO2
• High flow devices may not be delivering
the FIO2 that is set
• If the patient’s total flowrate is exceeding the
flow from the oxygen delivery device, the FIO2
will decrease
• Water in the aerosol tubing will increase FIO2
• High flow oxygen delivery systems should
be analyzed
Analyze High Flow Systems
• Polarographic (battery and electrolyte
solution)
• Galvanic (fuel cell)
• Troubleshooting: If analyzer is not
reading the FIO2 within + 2% then:
• Calibrate analyzer first
• Change fuel cell (galvanic) or
• Change battery/electrolyte level
(polarographic)
Correlating ABG to the Patients
Condition
• A patient who looks good but has bad
ABG
• Suspect a lab error
• Venous blood gas sample
• COPD (high PaCO2 and HCO3-)
Correlating ABG to the
Patients Condition
• A patient who looks and feels bad but
ABG are good.
• CO poisoning, MetHB%
• Tissue hypoxia
• Anemic hypoxia
• Histotoxic hypoxia
• Circulatory hypoxia
• Pulmonary embolism – high Vd/Vt ratio and
high E
Analyzing an ABG
• On 21%, add PaCO2 and PaO2 to see if
greater than 150.
• If one of the three acid base parameters
is abnormal, there is an error.
• pH 7.58, PaCO2 40, HCO3- 24
• PaO2 cannot be greater than PAO2 on any
FIO2.
Analyzing an ABG
• Know normal venous values and
suspect when a venous sample may
have been drawn
• Inaccurate FIO2
• Improperly recorded
• Patients total flow exceeds flow from
delivery device
• FIO2 recorded from low flow system
• Water in the aerosol tubing
Objectives
• Define anemia.
• List three types of anemia and state the
causes of the defect.
• Describe the effect of anemia on the
presence of hypoxia.
• State the benefit, problems, and specific
levels for each of the following as it relates
to it being an indicator of cellular hypoxia:
•
•
•
•
Lactate
Mixed Venous Oxygenation
Oxygen Consumption & Utilization
Gastric Mucosal Acidosis
Hypoxia
• Definition: Reduced oxygen levels at the
tissue.
• No “best” index for assessing tissue
oxygenation.
• Begin assessment by assessing the
components of oxygen delivery:
•
•
•
•
Dissolved Oxygen
Bound Oxygen
Hemoglobin
Cardiac Output (This will be covered in RSPT 2420)
• Then look at markers of the effects of possible
tissue hypoxia.
Types of Hypoxia
•
•
•
•
Hypoxemic Hypoxia
Circulatory (Stagnant) Hypoxia
Anemic Hypoxia
Histotoxic Hypoxia
Oxygenation Indices
• Dissolved Oxygen as an index of hypoxia.
• Not very useful
• Pretty good bet hypoxia is present with severe hypoxemia
• Be careful at extremes!
• Keep PaO2 above 60 mm Hg.
• Combined Oxygen (SaO2) as an index of
hypoxia.
• Make sure how you know HOW it is reported
• SaO2 with nomogram, 2-wavelength oximetry, CO-Oximetry,
Pulse Oximetry
• Better than PaO2, but has its faults.
• Abnormal species of hemoglobin
• Insensitive in telling deterioration or at high PaO2 levels.
Anemia
• RBC:
• 5 million/mm3 in men; 4.5 million/mm3 in
women.
• Hemoglobin
• 15 g% in men, 13 to14 g% in women.
• Anemia defined as a reduction in the
amount of circulating RBC or hemoglobin.
• Hematocrit (formed elements in blood)
• 47% in men, 42% in women.
• Too low is bad; too high is bad.
Types of Anemia
• Presence of anemia means one of two things:
• Decrease in production of RBC or Hb
• Bone Marrow Failure (Aplastic Anemia)
• Usually due to chemical or physical agent (normocytic)
• Inadequate Hemoglobin synthesis
• Iron deficiency 2° chronic blood loss or pregnancy (microcytic)
• Pagophagia: Ice chip craving
• Thalassemias – genetic disorder (microcytic)
• Inadequate RBC formation
• Folic Acid deficiency: Green vegetables & alcoholics (macrocytic)
• B12 deficiency: Pernicious anemia 2° lack of intrinsic factor
(macrocytic)
• RBC & Hb are being lost or destroyed at an accelerated rate.
• Blood loss
• Acute bleeding (normocytic)
• Excessive hemolysis
• Sickle cell disease
Analyzing FIO2
• Always correlate ABG to patients
condition.
• When drawing from an A-line, always
remove all heparin from the lines – this
means withdrawing 3-5 cc and discarding.
• Understand the relationship of increased
metabolism with leukocytosis (leukemia).
Anemia and Hypoxia
• Mild anemia (10 g%) usually won’t cause
hypoxia
• 25% extraction
• Cardiac output reserves (acute)
• Changes in levels of 2,3 DPG (cardiac)
• Probably significant with Hb < 6 g%
• Transfuse when Hb levels fall below 7 g%
Key Indicators of Hypoxia
•
•
•
•
•
Lactate
Mixed Venous Oxygen
Oxygen Consumption/Oxygen Extraction
Gastric Tonometry
Vital Organ Function
Lactate
• Immediate response to a reduced oxygen
delivery is the onset of anaerobic metabolism.
•
•
•
•
Glycolysis: Pyruvate reduction to lactate.
Normal lactate is 0.9 to 1.9 mM/L or 8 to 17 mg/dL
Metabolic Acidosis + hypoxemia + CO = Hypoxia
Increase in mortality at levels above 2.5 mM/L; 90% at
levels above 8 mM/L
• Problem is lactate elevation is not linear (not a good
early predictor)
• Reduction is by liver. Poor perfusion/Liver failure worsens
prognosis.
• Cyanide poisoning (Histotoxic hypoxia) should be
suspected with high lactates and no increase in HbCO
with smoke inhalation.
Mixed Venous Oxygenation
• Requires a pulmonary artery catheter.
• Assessment of oxygen supply vs. demand
• S O2: Continuous vs. Spot Check
• Normal 75%
• Decreased with increased O2, decreased SaO2, decreased Hb or
decreased CO.
• P
O2: Average
end-capillary driving pressure.
• Usefulness depends on distribution of cardiac output.
• Decreases are associated with decreased supply or increased
demands.
• Increases are associated with reduced utilization (NOT
ALWAYS A GOOD THING!)
Oxygen Uptake and Utilization
• Normal oxygen uptake (consumption) by the
tissue remains constant despite changes in
cardiac output because of huge reserve (25%
normal extraction).
• Hypoxia is present when O2del falls below 8 to 10
ml/kg/min.
• Covert Hypoxia: Normally, increasing oxygen
delivery is not needed; in some situations (MOF
secondary to ARDS, septic shock, ARF). The
cause is suspected to be an altered oxygen
utilization.
Gastric Tonometry
• Blood shunting to key organs
occurs with reduced oxygen
supply at the expense of non-vital
organ systems (GI tract).
• If hypoxic crisis is present, GI
involvement will be a primary
source.
• The mixing of gases to a point of
equilibration is called tonometry.
• Use of a specialized catheter with
a balloon can measure the
gastric carbon dioxide and infer
gastric blood flow.
Sublingual Tissue PCO2
• Improvement on gastric
tonometry.
• Uses CO2 sensor in
“temperature” like probe.
• Results within 60 seconds.
Vital Organ Function
• If compensatory mechanisms are intact,
the presence of these compensatory
mechanisms may be an indication that
hypoxia is present.
•
•
•
•
Urine output
Mental status
Skin coolness
Great toe temperature