Blood Gases, pH and Buffer Systems
BLOOD GASES
Oxygen and Gas Exchange
Oxygen and Carbon Dioxide
7 conditions necessary for adequate
tissue oxygenation:
Available atmospheric oxygen
Adequate ventilation
Gas exchange between lungs &
arterial blood
Loading of O2 onto hemoglobin
Adequate hemoglobin
Adequate transport
Release of O2 to tissue
Oxygen and Gas Exchange
(contd)
Oxygen and Carbon
Dioxide
Common factors influencing
amount of O2 that moves through
alveoli into blood & then to tissue:
Destruction of alveoli
Pulmonary edema
Airway blockage
Inadequate blood supply
Diffusion of CO2 and O2
Oxygen and Gas Exchange
(contd)
Oxygen Transport
Most O2 in arterial blood is transported to tissue
by hemoglobin.
Blood hemoglobin exists in one of four conditions:
1. Oxyhemoglobin (O2Hb): O2 reversibly
bound to hemoglobin
2. Deoxyhemoglobin (HHb): hemoglobin not
bound to O2 but capable of forming a bond when
O2 is available
3. Carboxyhemoglobin (COHb): hemoglobin
bound to CO
4. Methemoglobin (MetHb): hemoglobin
unable to bind O2 because iron (Fe) is in an
Oxygen and Gas Exchange
(contd)
Quantities Associated With Assessing
a Patients Oxygen Status
Oxygen saturation (SO2): ratio of O2 bound
to carrier protein, hemoglobin, compared with
total amount of hemoglobin capable of binding
to O2
Fractional oxyhemoglobin (FO2Hb): ratio of
concentration of oxyhemoglobin to
concentration of total hemoglobin (ctHb)
Trends in oxygen saturation: assessed by
transcutaneous, pulse oximetry (SpO2)
Oxygen content: total O2 in blood; sum of O2
bound to hemoglobin (O2Hb) & amount
dissolved in plasma (PO )
Oxygen and Gas Exchange
(contd)
HemoglobinOxygen
Dissociation
O2 must be released at tissues from its
carrier, hemoglobin.
Oxygen dissociates from adult (A1)
hemoglobin in characteristic fashion (Sshaped curve).
Shape of oxygen-dissociation curve &
affinity of hemoglobin for O2 are
affected by:
Hydrogen ion activity
PCO2 & CO levels
Body temperature
2,3-DPG
Measurement
Spectrophotometric Determination of
Oxygen Saturation
Actual percent oxyhemoglobin (O2Hb) can be
determined using cooximeter designed to measure
various hemoglobin species.
Each species has a characteristic absorbance curve.
Number of wavelengths incorporated into instrument
determines number of species that can be measured,
from 4 to hundreds.
4 most common hemoglobin species: HHb, O2Hb,
COHb, MetHb
Potential sources of error: faulty instrument
calibration & spectral-interfering substances
Measurement (contd)
Blood Gas Analyzers: pH, PCO2, and
PO2
Blood gas analyzers measure pH, PCO2, & PO2
with electrodes.
AMPEROMETRIC: Amount of current flow
indicates oxygen present (PO2).
POTENTIOMETRIC: Change in voltage indicates
analyte activity (PCO2, pH).
Cathode: 1) negative electrode; 2) site to which
cations tend to travel; 3) site at which
reduction occurs
Anode: 1) positive electrode; 2) site to which
anions tend to travel; 3) site at which oxidation
occurs
Electrochemical cell: formed when two opposite
electrodes are immersed in a liquid that will
conduct current
Measurement (contd)
Measurement of PO2
PO2 (Clarke) electrodes measure amount of
current flow in circuit related to amount of O 2
being reduced at cathode.
Sources of error: buildup of protein material on
surface of membrane, bacterial contamination
within measuring chamber
Continuous measurements for PO2 are possible
using transcutaneous electrodes placed directly
on skin.
Measurement
of pH and PCO2
Ion force measurement requires 2 electrodes & a
voltmeter.
Potential difference is related to concentration of
ion of interest by Nernst equation.
Measurement (contd)
Types of Electrochemical Sensors
Macroelectrode sensors: used in blood
gas instruments since beginning of clinical
measurement of blood gases
Microelectrodes: miniaturized
macroelectrodes
Thick and thin film technology: Sensors
are tiny wires embedded in printed circuit
Optical
Sensors
card that
are disposable.
Use fluorescent dyes, into which sample
diffuses
Have been applied to indwelling blood gas
systems
Measurement (contd)
Calibration
pH & blood gas measurements are extremely
sensitive to temperature.
Electrode sample chamber must be maintained at
constant temperature.
pH electrode is calibrated with 2 buffer solutions,
traceable to standards prepared by NIST.
Two gas mixtures are used to calibrate for PCO2 &
PO2.
Most instruments are self-calibrating & are
programmed to indicate a calibration error if
electronic signal from electrode is inconsistent with
programmed expected value.
Measurement (contd)
Calculated Parameters
HCO2-: based on Henderson-Hasselbalch equation; can be
calculated when pH & PCO2 are known
Carbonic acid concentration: can be calculated using
solubility coefficient of CO2 in plasma at 37C
Total carbon dioxide content: bicarbonate plus dissolved
CO2 plus associated CO2 with proteins
Correction for Temperature
By convention, pH, PCO2, & PO2 are all measured at 37C.
If patients body temperature differs from 37C, blood gas
instrument can correct values; results at 37C should be
reported, too, however, for reference.
Quality Assurance
Preanalytic Considerations
Proper patient identification
Correct labeling of specimen & accurate info provided
Experienced, knowledgeable personnel
Proper collection & handling of blood gas specimens
Transport time
Analytic Assessments: QC &
Proficiency Testing
Surrogate liquid control materials, tonometry, duplicate assays,
non-surrogate QC
Interpretation of Results
The use of arterial samples for pH and blood gas studies is
recommended.
However, peripheral venous samples can be used if
pulmonary function or O2 transport is not being assessed.
Sources of error in the collection and handling of blood gas
specimens include:
the collection device
form and concentration of heparin used for anticoagulation
speed of syringe filling
maintenance of the anaerobic environment
mixing of the sample to ensure dissolution and distribution of the
heparin, and transport
storage time before analysis
the ideal collection device for arterial blood
sampling:
1- to 3-mL self-filling, plastic, disposable syringe, containing
the appropriate type and amount of anticoagulant.
Evacuated collection tubes are not
appropriate for blood gases.
Dry (lyophilized) and liquid heparin are
acceptable anticoagulants,
the liquid form is not recommended because excessive
amounts can dilute the sample and possibly contaminate the
sample if equilibrated with room air.
ACID AND BASES
17
pH Review
pH = - log [H+]
H+ is really a proton
Range is from 0 - 14
If [H+] is high, the solution is acidic;
pH < 7
If [H+] is low, the solution is basic or
alkaline ; pH > 7
18
19
20
Definitions: Acid, Base, Buffer
Acid: a substance that can yield a
hydrogen ion (H) or hydronium ion when
dissolved in water
Base: a substance that can yield
hydroxyl ions (OH-)
Dissociation constant (ionization
constant K value): describes relative
strengths of acids & bases
pK: negative log of ionization constant &
pH in which protonated & unprotonated
forms are present in equal concentrations
Buffer: combination of weak acid or
weak base & its salt; a system that
Acids are H+ donors.
Bases are H+ acceptors, or give up OHin solution.
Acids and bases can be:
Strong dissociate completely in solution
HCl, NaOH
HCl H+ + Cl NaOH Na + OH Weak dissociate only partially in solution
Lactic acid, carbonic acid
H2CO3 H+ + HCO3
H2CO3 H2O + CO2
22
The Body and pH
Homeostasis of pH is tightly
controlled
Extracellular fluid = 7.4
Blood = 7.35 7.45
< 6.8 or > 8.0 death occurs
23
AcidBase Balance
Maintenance of H+
Normal concentration of H in extracellular body fluid ranges
from 36 to 44 nmol/L, but body produces much greater
quantities of H.
Via lungs & kidneys, body controls & excretes H to maintain
pH homeostasis.
Normal Blood pH: 7.35-7.45
Acidosis:
a pH level below reference range (<7.35)
Alkalosis:
a pH level above reference range (>7.45)
25
Small changes in pH can produce
major disturbances
Most enzymes function only with narrow
pH ranges
Acid-base balance can also affect
electrolytes (Na+, K+, Cl-)
Can also affect hormones
26
The body produces more acids than
bases
Acids take in with foods
Acids produced by metabolism of lipids and
proteins
Cellular metabolism produces CO2.
CO2 + H20 H2CO3 H+ + HCO3-
27
Regulation of AcidBase Balance: Lungs and Kidneys
Lungs: Ventilation affects pH of
blood.
O2 is inspired & diffuses from alveoli into blood.
CO2 diffuses into alveoli from blood & is eliminated
via ventilation.
Result is minimal change in H concentration
between venous & arterial circulations.
Kidneys: regulate acidbase
balance by excreting acids or
bases
HCO3- is reclaimed from glomerular filtrate to
prevent excessive acid gain in blood from loss of
HCO3- in urine.
Control of Acids-Base Balance
1. Buffer systems
Take up H+ or release H+ as
conditions change
Buffer pairs weak acid and a
base
Exchange a strong acid or base
for a weak one
Results in a much smaller pH
change
29
Control of Acids
Bicarbonate buffer
Sodium Bicarbonate
(NaHCO3) and carbonic acid
(H2CO3)
Maintain a 20:1 ratio : HCO3- :
H2CO3
HCl + NaHCO3 H2CO3 +
NaCl
30
Control of Acids
Bicarbonate-carbonic acid
system
has low buffering capacity, but is still
important buffer for 3 reasons:
1. H2CO3 dissociates into CO2 and H2O,
allowing CO2 to be eliminated by lungs
and H as water.
2. Changes in CO2 modify ventilation
(respiration) rate.
3. HCO3- concentration can be altered
by kidneys.
31
Bicarbonate-Carbonic
Acid
CO2
+H2O
Carbon
Dioxide
Respiratory
component
H2CO3
Acidic
H+
+HCO3
Basic
Renal
Component
Control of Acids
Phosphate buffer
Major intracellular
buffer
H+ + HPO42- H2PO4 OH + H2PO4 H2O +
H2PO42-
33
Control of Acids
Protein Buffers
Includes hemoglobin, work in blood
and ISF
Carboxyl group gives up H+
Amino Group accepts H+
Side chains that can buffer H+ are
present on 27 amino acids.
34
Control of Acids
2. Respiratory mechanisms
Exhalation of carbon dioxide
Powerful, but only works with
volatile acids
Doesnt affect fixed acids like
lactic acid
CO2 + H20 H2CO3 H+ +
HCO3 Body pH can be adjusted by
changing rate and depth of
35
Control of Acids
3. Kidney excretion
Can eliminate large amounts
of acid
Can also excrete base
Can conserve and produce
bicarbonate ions
Most effective regulator of
pH
If kidneys fail, pH balance fails
36
Rates of correction
Buffers function almost
instantaneously.
Respiratory mechanisms take
several minutes to hours.
Renal mechanisms may take
several hours to days.
37
38
39
Homeostatic Regulators of
[H + ]
Chemical
Buffer System
1st to respond
Take < 1 sec.
Temporarily
tie up
excess acids
& bases
BicarbonateCarbonic
acid ,
Phosphate,
Protein buffer
systems
Respiratory
Mechanism
2nd to
respond
Takes 1-3
minutes
Respiratory
centre
involved
Removes CO2
& therefore
H2CO3
Renal
Mechanism
3rd to
respond but
most potent
Takes hours to
days
Kidneys
remove
metabolic
acids
Eg;
phosphoric,
uric & lactic
acids, ketone
bodies
Factors Effecting Balance
Age
especially infants
and the elderly
Gender and
Body Size
amount of fat
Environmental
Temperature
Lifestyle
stress
ACID-BASE IMBALANCE
43
Acid-Base Imbalances
pH< 7.35 acidosis
pH > 7.45 alkalosis
The body response to acid-base imbalance is called
compensation
May be complete if brought back within normal limits
Partial compensation if range is still outside norms.
44
Four Basic Types of
Imbalance
Respirat
ory
Acidosis
Metaboli
c
Acidosis
Respirat
ory
Alkalosis
Metaboli
c
Alkalosis
Compensation
If underlying problem is
metabolic, hyperventilation
or hypoventilation can help :
respiratory compensation.
If problem is respiratory, renal
mechanisms can bring about
metabolic compensation.
46
Acidosis
Principal effect of acidosis is depression of the CNS through in
synaptic transmission.
Generalized weakness
Deranged CNS function the greatest threat
Severe acidosis causes
Disorientation
coma
death
47
Alkalosis
Alkalosis causes over excitability of the central and
peripheral nervous systems.
Numbness
Lightheadedness
It can cause :
Nervousness
muscle spasms or tetany
Convulsions
Loss of consciousness
Death
48
49
Respiratory Acidosis
Carbonic acid excess caused by blood levels
of CO2 above 45 mm Hg.
Hypercapnia high levels of CO2 in blood
pH < 7.35, PaCO2 > 45mm Hg
Hypoventilation
50
Respiratory Acidosis
Causes:
Lung disorders, such as emphysema,
chronic bronchitis, severe asthma,
pneumonia, or pulmonary edema
Sleep-disordered breathing
Diseases of the nerves or muscles of the
chest that impair breathing, such as
Guillain-Barr syndrome or amyotrophic
lateral sclerosis, myasthenia gravis
Overdose of drugs such as alcohol, opioids,
and strong sedative
Sepsis or burns
Respiratory Acidosis
Acute conditons:
Adult Respiratory Distress Syndrome
Pulmonary edema
Pneumothorax
Chronic conditions:
Depression of respiratory center in brain that
controls breathing rate drugs or head trauma
Paralysis of respiratory or chest muscles
Emphysema
52
Compensation for Respiratory
Acidosis
Kidneys eliminate
hydrogen ion and retain
bicarbonate ion
53
Signs and Symptoms of
Respiratory Acidosis
Breathlessness
Restlessness
Lethargy and
disorientation
Tremors,
convulsions,
coma
Respiratory rate
rapid, then
gradually
depressed
Skin warm and
flushed due to
vasodilation
caused by
excess CO2
Dyspnea,
Disorientation or
coma
Headache and
drowsiness
Hyperkalemia or
Hypoxemia
54
Treatment of Respiratory
Acidosis
Restore
ventilation
IV lactate
solution
Treat
underlying
dysfunction
or disease
55
56
Respiratory Alkalosis
Carbonic acid deficit
pCO2 less than 35 mm Hg
(hypocapnea)
Most common acid-base imbalance
Primary cause is hyperventilation
pH > 7.45;PaCO2< 35 mm Hg
57
Respiratory Alkalosis
Causes:
Pain, Fear, Stress, Anxiety
High altitude residence
Pregnancy
Anaemia
Hysterical hyperventilation syndrome
Brain injury
Hyperthyroidism
Respiratory Alkalosis
Conditions that stimulate respiratory
center:
Oxygen deficiency at high altitudes
Pulmonary disease and Congestive heart
failure caused by hypoxia
Acute anxiety
Fever, anemia
Early salicylate intoxication
Cirrhosis
Gram-negative sepsis
59
Signs and Symptoms of
Respiratory Alkalosis
Tachypnea
Complaints of
SOB, chest
pain
Numbness
,tingling or
weakness of
extremities
Lightheadedness
Difficult
concentrating,
tremors,
blurred vision
60
Compensation of Respiratory
Alkalosis
Kidneys conserve
hydrogen ion.
Excrete bicarbonate
ion.
61
Treatment of Respiratory
Alkalosis
Treat underlying
cause
Breathe into a
paper bag
IV Chloride
containing
solution Cl- ions
replace lost
bicarbonate ions
62
63
Metabolic Acidosis
Bicarbonate deficit - blood concentrations of bicarb drop
below 22mEq/L
pH < 7.38; HCO3-< 22 mEq/L
Acid accumulation from increased acid production or acid
ingestion; decreased acid excretion; or GI or renal
HCO3loss.
Metabolic acidoses are categorized as high(hyperchloremic)
or normal anion gap based on the presence or absence of
unmeasured anions in serum.
64
High anion gap
acidosis:(most common )
Ketoacidosis (Diabetes, Chronic
alcoholism, Undernutrition, Fasting)
Lactic acidosis
Renal failure
Toxic ingestions (Alcohol, Methylene
glycol, Methanol)
65
Causes:
Loss of bicarbonate
through diarrhea or
renal dysfunction
Accumulation of acids
(lactic acid or ketones)
Failure of kidneys to
excrete H+
66
Symptoms of Metabolic
Acidosis
Headache, lethargy
Nausea, vomiting,
diarrhea
Coma
Death
Kussmauls
respiration (slow and
deep)
Lethargy, confusion,
headache, weakness
Hypotension and
shock, ventricular
arrhythmias; and
coma.
Chronic acidemia
causes bone
demineralization
disorders (rickets,
osteomalacia,
osteopenia
Nausea and
Vomiting
67
Compensation for Metabolic
Acidosis
Increased
ventilation
Renal
excretion
of
hydrogen
ions if
possible
K+
exchanges
with
excess H+
in ECF
( H+ into
cells, K+
out of
cells)
68
Treatment of Metabolic
Acidosis
IV lactate solution
Hemodialysis is required for renal failure and
sometimes for ethylene glycol, methanol, and
salicylate poisoning
NaHCO3is clearly indicated only in certain
circumstances (normal anion gap)
69
70
Metabolic Alkalosis
Bicarbonate excess concentration in blood is
greater than 26 mEq/L
pH> 7.45; [HCO3-] > 26
mEq/L
body loses too much acid or
gains too much base
71
Causes:
Excess vomiting = loss of stomach acid
Excessive use of alkaline drugs
Certain diuretics
Endocrine disorders
Heavy ingestion of antacids
Severe dehydration
Overactive adrenal gland (cushings
syndrome)
Adenoma of the colon
72
Compensation for Metabolic
Alkalosis
Alkalosis most commonly
occurs with renal dysfunction,
so cant count on kidneys
Respiratory compensation
difficult hypoventilation
limited by hypoxia
73
Symptoms of Metabolic
Alkalosis
Respiration
slow and
shallow
Hyperactive
reflexes ;
tetany
Often related
to depletion of
electrolytes
Atrial
tachycardia
Dysrhythmias,
dizziness,
irritability
Muscle
twitching,
muscle cramps
Prolonged
contraction and
spasms of
muscles
(tetany)
Hypoventilatio
n
(compensatory
)
Paresthesia,
numbness,
tingling of
extremities
74
Treatment of Metabolic
Alkalosis
Electrolytes to replace
those lost
IV chloride containing
solution
Treat underlying disorder
75
76
DIAGNOSIS OF ACID-BASE
IMBALANCES
78
INTERPRETATION OF BLOOD GASES
Step 1:
Determine if the numbers fit.
The right side of the equation should be within
about 10% of the left side.
If the numbers do not fit, you need to obtain
another ABG
INTERPRETATION OF BLOOD GASES
Step 2:
determine if an acidemia (pH
<7.37)
or an alkalemia (pH >7.44) is
present.
Step 3: Identify the primary
disturbance as metabolic or
respiratory.
For example: if acidemia is
present:
Check the pCO2:
Reference Range: 35-45 mm Hg
If the pCO2 >45 mm Hg (respiratory
acidosis)
Check the HCO3-:
Reference Range: 22 -26 mEq/L
If the [HCO3 -] <22 mmol/L (metabolic
acidosis)
if alkalemia is present:
Check the pCO2:
Reference Range: 35-45 mm Hg
If the pCO2 <35 mm Hg (respiratory alkalosis),
Check the HCO3-:
Reference Range: 22 -26 mEq/L
If the [HCO3 -] >26 mmol/L (metabolic
alkalosis)
83
In other words, identify which component, respiratory
or metabolic, is altered in the same direction as the
pH abnormality.
If both components act in the same direction (eg,
both respiratory [pCO2 > 44 mm Hg] and metabolic
[HCO3 - <22 mmol/L] acidosis are present), then this
is a mixed acid-base problem.
The primary disturbance will be the one that varies
from normal the greatest, that is, with a [HCO3 -] = 6
mmol/L and pCO2 = 50 mm Hg, the primary
disturbance would be a metabolic acidosis, the [HCO3
-] is about one-quarter normal, whereas the increase
in pCO2 is only 25%.
84
Step 4:
Calculate the anion gap.
Anion gap = Na+ - (Cl- + HCO3 -).
Normal anion gap is 8-12 mmol.
Step 5:
If the anion gap is elevated
Then compare the changes from normal
between the anion gap and [HCO3 -].
If the change in the anion gap is greater
than the change in the [HCO3 -] from
normal, then a metabolic alkalosis is present
in addition to a gap metabolic acidosis.
If the change in the anion gap is less than
the change in the [HCO3 -] from normal,
then a non gap metabolic acidosis is present
in addition to a gap metabolic acidosis.
METABOLIC ACIDOSIS: DIAGNOSIS AND
TREATMENT
Metabolic acidosis represents an
increase in acid in body fluids .
Reflected by a decrease in [HCO3 -]
and a compensatory decrease in
pCO2.
Anion Gap Acidosis:
Anion gap >12 mmol/L; caused by a
decrease in [HCO3 -]
balanced by an increase in an
unmeasured acid ion from either
endogenous production or exogenous
ingestion (normochloremic
acidosis).
Non anion Gap Acidosis:
Anion gap = 8-12 mmol/L; caused by a decrease in [HCO3 -]
balanced by an increase in chloride (hyperchloremic
acidosis). Renal tubular acidosis is a type of non gap
acidosis
The anion gap is helpful in identifying metabolic gap
acidosis, non gap acidosis, mixed metabolic gap and non
gap acidosis. If an elevated anion gap is present, a closer
look at the anion gap and the bicarbonate helps
differentiate among
(a) a pure metabolic gap acidosis
(b) a metabolic non gap acidosis
(c) mixed metabolic gap and non gap acidosis, and
(d) a metabolic gap acidosis and metabolic alkalosis.
Compensations for Metabolic Disturbances
Metabolic acidosis
pCO2 = 1.5 x HCO3 + 8 ( 2)
Metabolic alkalosis
pCO2 increases by 7 for every 10
mEq increases in HCO3
Compensations for Respiratory Acidosis
Acute respiratory acidosis
HCO3 increases by 1 for every 10
mm increases in pCO2
Chronic respiratory
acidosis
HCO3 increases by 3 for every 10
mm increases in pCO2
Compensations for Respiratory Alkalosis
Acute respiratory alkalosis
HCO3 decreases by 2 for every 10
mm decrease in pCO2
Chronic respiratory
alkalosis
HCO3 decreases by 4 for every 10
mm decrease in pCO2
Clinical Example 1
72 y/o male, COPD with acute
exacerbation
Ref. range
Under O2 2L/min
pH
7.35-7.45
pH 7.44
pCO2
35-45 mm Hg
PCO2 54
pHCO3
2-26 mEq/L
PO2 60
HCO3 36
INTERPRETATION
Metabolic alkalosis with respiratory
compensation
Mixed respiratory acidosis
96
Clinical Example 2
30 y/o male, sudden onset dyspnea
Room air
pH 7.33
Ref. range
PCO2 24 pH
7.35-7.45
PO2 111 pCO2
35-45 mm Hg
HCO3 12
pHCO3
2-26 mEq/L
INTERPRETATION
Metabolic acidosis
Respiratory compensation
Normal A-a O2 gradient
O2: hyperventilation
98
Clinical Example 3
70 y/o male, acute hemoptysis and
dyspnea
Room air
Ref. range
pH 7.50
pH
7.35-7.45
PCO2 31
pCO2
35-45 mm Hg
PO2 88
pHCO3
2-26 mEq/L
HCO3 24
INTERPRETATION
Respiratory alkalosis
Not been renal compensated yet
Normal PO2, but A-a O2 gradient
100
Clinical Example 4
18 y/o female, chest tightness and
dyspnea for 4 hrs
RR 28/min, distressed, widespread
wheezing
O2 mask 6L/min
Ref. range
pH 7.31
PCO2 49 pH
7.35-7.45
PO2 115 pCO2
35-45 mm Hg
HCO3 26
pHCO3
2-26 mEq/L
INTERPRETATION
Respiratory acidosis
Normal bicarbonate acute
May have problems with oxygenation
102
Clinical Example 5
37 y/o female, mild asthma history
Wheezes for 3 weeks, increasing chest tightness
and dyspnea for 24 hrs, call for ambulance with
Oxygen use
RR 18/min, anxious and distressed
Room air
Ref. range
pH 7.37
PCO2 43 pH
7.35-7.45
PO2 97
35-45 mm Hg
HCO3 27 pCO2
pHCO3
2-26 mEq/L
INTERPRETATION
Normal?
r/o CO2 retention
Low A-a O2: Oxygen use in the
ambulance
104
Clinical Example 6
19 y/o male, Duchenne muscular
dystrophy on wheelchair for 7 yrs
No previous respiratory problems but
frequent UTI
Room air
pH 7.21
Ref. range
PCO2 81
pH
7.35-7.45
PO2 44
35-45 mm Hg
HCO3 36 pCO2
pHCO3
2-26 mEq/L
INTERPRETATION
Respiratory acidosis
Metabolic compensation
Normal A-a O2 pure ventilatory
failure
106
Clinical Example 7
57 y/o male, smoker, one week URI then 36 hrs productive
cough, fever and dyspnea
RR 36/min, distressed, CXR: RLL pneumonia
pH 7.33
PCO2 27
PO2 51
HCO3 22
Ref. range
2L/min
pH 7.34 pH
PCO2 32
PO2 58 pCO2
HCO3 24
pHCO3
10L/min mask
7.35-7.45
35-45 mm Hg
2-26 mEq/L
INTERPRETATION
Early metabolic acidosis
Severe hypoxemic respiratory failure
Intra-pulmonary shunting
108
