Arterial Blood Gases 2015

ARTERIAL BLOOD GASES
Interpretation of ABG
PROF/ TAGHRID SAID FARAG

ASS. PROF. OF CHEST DISEASES
Al-Azhar University
Faculty of Medicine for Girls
2015
Basic knowledge about ABG 2015
Page
Basic knowledge about Arterial Blood Gases 2
What are arterial blood gases (ABGs)? 2
What information arterial blood gases provide and what they do not 2
Technique for Sampling Arterial Blood 3
Why must arterial blood gas samples be obtained anaerobically? 4
Why are ABG samples transported on ice? 4
Why is heparin used in bl. gas syringes? 5
Are blood gas levels stable or are they variable in apparently stable patients? 5
What is meant by PaO2, SaO2 %, CaO2, DO2? 6
What are the forms of Oxygen in blood? 6
Oxygen content equation 7
Oxygen Delivery and Utilization= DO2 8
How does hypoxia differ from hypoxemia 9
Why can't VBG be used instead of ABGs 11
Alveolar Gas Equation 12
Calculation of alveolo-arterial O2 gradient (AaDO2) 14
Indices of Oxygenation 16
PaCO2 Equation 16
Interpretation of ABG 20
Calculation of alveolo arterial O2 gradient(AaDO2 23
Summary of assessment of oxygenation 25
Acid-base status 28
Test Your Understanding 35
(1) DR: TAGHRID SAID

Basic knowledge about Arterial Blood Gases
OBJECTIVE
It is important to understand
What information arterial blood gases provide and what they do not?
Indication & complication of ABG
Technique for Sampling Arterial Blood
Are blood gas levels stable or are they variable in apparently stable patients?
Why can't venous blood gases be used instead of ABGs?
It is essential to understand of the concepts of: - Partial pressure (tension),
Gas content.. and, Percent saturation.
How does hypoxia differ from hypoxemia?
What are arterial blood gases (ABGs)?
ABG define how well the lung is loading O2 into and removing CO2 from blood.
However, these are only the first and last steps in the gas transport system. (ABG)
sampling is still the most important pulmonary function test performed in
critically ill patient.
Why can't VBG be used instead of ABGs?
Difference bet. Arterial & Venous bl. Sample; Respir Care
37(8):913,1993
Arterial sample Venous sample
pH 7.35-7.45 7.35
PaO2 80 -100mmHg 38 - 42 mmHg
PaCO2 35 - 45 mmHg 44 - 48mmHg
(40 mmHg) (46 mmHg)
HCO3 22-26 mEq/L or 20-24 mEq/L
23-27 mEq/L
O2 sat. 95% or more 75%
ABG: Reflect lung function

VBG: Reflect
Tissue oxygenation
Tissue CO2 clearance

A low mixed venous PO2 (<35 mm Hg) reflects tissue hypoxia may be due to
1. Decreased oxygen delivery or
2. Increased tissue oxygen uptake
Venous PaO2 (38 - 42 mmHg) is typically much lower than arterial PaO2
(80 -100mmHg), and there is often little relationship between the two.
For example, the mixed venous PO2 may be low and the arterial PO2 may be
high if cardiac output is reduced, lung function is normal, and FiO2 is high.
Normally, the mixed venous PaCO2 (44 - 48mmHg) is only slightly greater than
the arterial PaCO2 (35 - 45 mmHg). However, venous PCO2 depends on blood
flow and, in cases of low blood flow (e.g., cardiac arrest), the mixed venous
PCO2 may be high even though the arterial PCO2 is normal or decreased.
What information ABG provide and what they do not?

ABG is the true PFT Evaluation of the ventilation, oxygenation & acid-base
status of the body which in turn provides information about functions of
the lungs, kidneys, heart & peripheral circulation
The determination of PaO2 and PaCO2 provides useful information about

the overall efficiency of external gas exchanges.
They do not assess how well O2 is being delivered to cells or the adequacy
of cellular function.
What is meant by PaO2, SaO2 %, CaO2 , DO2?

PaO2 Partial arterial oxygen pressure (oxygen tension)
PaCO2 Partial arterial carbon dioxide pressure (carbon dioxide tension)
SaO2 % arterial oxygen saturation
CaO2 arterial oxygen content
DO2 Oxygen delivery

What information arterial blood gases provide and what they do not?
1. The determination of PaO2 and PaCO2 provides useful information about
the overall efficiency of external gas exchanges.
2. They do not assess how well O2 is being delivered to cells or the adequacy
of cellular function.
Technique for Sampling Arterial Blood
Arterial blood is sampled either through:-
1. An indwelling arterial catheter ..or
2. Percutaneous arterial puncture.
1. An indwelling arterial catheter
Advantage: - avoidance the acute changes in ventilation that can result from
apprehension and pain associated with percutaneous puncture.
Indication: - for continuous blood pressure monitoring and the need for
frequent ABG samples or other laboratory assessments.
Complications associated with arterial catheters
Serious complications, although rare, include hge, vascular occlusion, and
infection.
Thrombus formation is avoided by use of a continuous irrigation system,
although the presence of heparin in the irrigation may not be necessary.
When blood is collected from arterial catheters, the irrigation solution
must be cleared from the connected tubing, which can cause considerable
blood loss if samples are collected frequently and blood conservation
procedures are not used
2. Percutaneous arterial puncture
Three anatomic sites are generally used for obtaining ABG samples:
1. Radial artery
2. Brachial artery
3. Femoral artery.

For several reasons, the radial artery is the preferred sampling site
1. Because of its superficial location at the wrist, easy to palpate and pain
from the puncture is lessened, in addition, no large veins lie in its
immediate vicinity.
2. Easy to compress by direct pressure, facilitating hemostasis when sampling
is complete.
3. The ulnar artery usually provides an adequate collateral circulation to the
hand in the rare instance of post sampling thrombosis of the radial artery
(commonly assessed using the modified Allen's test)
4. The radial artery (unlike the brachial artery) is far enough away from
nerves (e.g., the medial nerve) that damage to the nerve is unlikely.
5. The radial site is generally more aseptic than the femoral site
Technique for Sampling
ABG samples are drawn anaerobically into plastic or glass syringes coated with
heparin.
The sample either immediately analyzed or placed on ice
How can the complications of arterial puncture be avoided?
The risk of bleeding complications is increased with anticoagulant or
thrombolytic therapy; in these cases, pressure must be manually applied to
the puncture site until all signs of bleeding are absent (a minimum of 5-10
minutes).
The risk of pain is decreased by use of a 22- or 23-gauge needle, and a local
anesthetic (e.g lidocaine) can be used to lessen the pain associated with
arterial puncture.
Why must arterial blood gas samples be obtained anaerobically?
Because room air at sea level has a PO2150 mmHg & PCO2 zero mmHg, air
bubbles in the syringe will artificially increase PaO2 and reduce PaCO2 with a
resultant increase in pH.

Why are ABG samples transported on ice?

Metabolism by blood cells continues in the syringe until the sample is
analyzed, causing PaO2, PaCO2, & pH
The rate of change depends on the temp. of the sample and the elapsed time
before analysis.
This can be diminished by transport of the sample in ice-water slush unless
the sample is analyzed within 10 minutes.
The metabolic effects on the blood sample are caused primarily by the activity
of leukocytes.
In pts with leukocytosis > 100,000 cells/L, the PaO2 of the bl. sample may
decrease very quickly, which is called leukocyte larceny ( - ).
It may be impossible to accurately determine the PaO2 of pts in extreme
leukocytosis, and invivo methods (e.g., pulse oximetry) may be more reliable.
Why is heparin used in bl. gas syringes?
Coagulation of the blood sample must be avoided because clots interfere with
the function of the blood gas analyzer.
High conc. of heparin is acidic (pH less than 7) and lowers the pH of the
sample. If liquid heparin is used, its effects can be minimized by using only
enough to fill the dead volume of the needle and syringe.
Are blood gas levels stable or are they variable in apparently stable patients?
It is important not to react too strongly to a single blood gas result that differs
from previous results in an otherwise clinically stable patient.
ABG levels may vary considerably over brief 5-10 minute intervals in critically
ill mechanically ventilated patients who otherwise appear stable. Different
measured values may reflect physiologic alterations such as :-
Subtle changes in cardiopulmonary function .or
Patient re-positioning that alter distribution of blood flow to the lungs or
They may result from pre-analytic error.
Variability is greatest for PO2 and less for PCO2 & pH

-----XXXX Diagnostics-----
Blood Gas Report

328 03:44 Feb 5 2006
Pt ID 3245 / 00
Measured 37.0 0C Measured values

pH 7.452
pCO2
pO2
45.1
112.3
mm Hg
mm Hg
most important
Corrected 38.6 0C Temperature Correction :
pH 7.436
pCO2 47.6 mm Hg Is there any value to it ?
pO2 122.4 mm Hg
Calculated Data
HCO3 act 31.2 mmol / L Calculated Data :
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
Which are useful one?
O2 ct 15.8 mL / dl
O2 Sat 98.4 %
ct CO2 32.5 mmol / L
pO2 (A -a) 30.2 mm Hg
pO2 (a/A) 0.78 Entered Data :
Entered Data Important
Temp 38.6 0C
FiO2 30.0 %
ct Hb 10.5 gm/dl
ABG: values
Measured values:
pH (the negative log of hydrogen ion conc.)
PaO2 (partial pressure of oxygen )
PaCO2 ( partial pressure of carbon dioxide)
(CaO2) oxygen content
(COHb) carboxy Hb
Calculated values:
HCO3 (Serum bicarbonate)
BE (Base excess )
P(A-a)O2 (alveolar- arterial gradient )
(SaO2) oxygen saturation
Hb saturation with oxygen (O2Hb)
carboxyhemoglobin (COHb)
methemoglobin (metHb).

If the patient's temperature is abnormal, the corrected values will differ from
those measured and reported by the blood gas analyzer.
Measured values should be considered and corrected values should be
discarded
Uncorrected pH & pCO2 are reliable reflections of in-vivo acid base status
Temperature correction of pH & pCO2 dont affect calculated bicarbonate
There is no scientific basis ... for applying temperature corrections to blood
gas measurements (Shapiro BA, OTCC, 1999).
pCO2 reference points at 37o C are well established as a reliable reflectors of
alveolar ventilation
Reliable data on DO2 and oxygen demand are unavailable at temperatures
other than 37o C
Bicarbonate is calculated on the basis of the Henderson equation: [H+] = 24
pCO2 / [HCO3-]
Standard Bicarbonate: Plasma HCO3 after equilibration to a PCO2 of 40 mm Hg

1. Reflects non-respiratory acid base change
2. Does not quantify the extent of the buffer base abnormality
3. Does not consider actual buffering capacity of blood
Base Excess: D base to normalize HCO3 (to 24) with PCO2 at 40 mm Hg

1. Reflects metabolic part of acid base D
2. No info. Over that derived from pH, PCO2 and HCO3
3. Misinterpreted in chronic or mixed disorders
SaO2) oxygen saturation: frequently measured by pulse oximetry

False elevations
o Carboxyhemoglobin and methemoglobin (until 85%) have similar absorption
spectrum as oxyhemoglobin; can be difficult to detect difference
o Fluoroescent lighting
False depression
o Tape
o Blue nail polish
o Dyes- indigo carmine, methylene blue

The Key to Blood Gas Interpretation

There are four equations, crucial to understanding and interpreting ABG data
which will be discussed later on:-
Four Equations, Three Physiologic Processes
Equation Physiologic Process
1. Oxygen content equation 1. Oxygenation
2. Alveolar gas equation 1. Oxygenation
3. PaCO2 equation 2. Alveolar ventilation
4. Henderson-Hasselbalch equation 3. Acid-base balance
Indications of ABG
1. Evaluation of the ventilation
2. Assessment of oxygenation
3. Assessment of acid-base status

Ventilation can be defined in terms of movement of a volume of air into
and out of the lungs, removing CO2 from the blood and providing O2.
Tidal volume (tidal ventilation) (VT) is the sum of alveolar volume (VA) and
dead space volume (VD)
VT=VA+VD
VA = VE VD
(VA): alveolar ventilation
(VE): = minute (total) ventilation (resp. rate x tidal volume)
(VD): dead space ventilation= (resp. rate x dead space volume)
Alveolar ventilation: The component that takes part in gas exchange
Assessment of alveolar ventilation is the key to determining whether a
patient is getting enough oxygen

Calculation of alveolar ventilation

VCO2 x 0.863
VA (L/min) = ---------------------------
PaCO2
VA=alveolar volume per unit of time corrected
to body temperature and pressure, saturated
with water (BTPS)
VCO2=carbon dioxide production by the body
(L/min) corrected to standard temperature and
pressure dry
863=conversion factor to express VA in L/min
BTPS
PACO2=partial pressure of alveolar carbon
dioxide (mm Hg, BTPS) which is essentially
equal to arterial carbon dioxide pressure
(PaCO2)
Alveolar ventilation is best defined in terms of ventilation of carbon
dioxide because diffusion of CO2 across the alveolo-capillary membrane is
more rapid than diffusion of O2, and the CO2 dissociation curve of blood is
linear over a wide range of alveolar ventilation
Changes in alveolar ventilation (VA) are accompanied by corresponding
linear changes in alveolar and thus PaCO2
PaCO2 Equation
PaCO2 reflects ratio of metabolic CO2 production to alveolar ventilation
VCO2 x 0.863
PaCO2 = ---------------------------
VA (Lmin)
The PaCO2 equation shows that the only physiologic reason for elevated PaCO2 is
inadequate alveolar ventilation (VA) for the amount of the bodys CO2
production (VCO2). Since alveolar ventilation (VA) equals total or minute
ventilation (VE) minus dead space ventilation (VD),
hypercapnia can arise from
1. Insufficient minute ventilation (VE)
2. Increased dead space ventilation (VD)
3. Or a combination of both

State of alveolar
PaCO2 Condition in blood
ventilation
> 45 mm Hg Hypercapnia Hypoventilation
35 - 45 mm Hg Eucapnia Normal ventilation
< 35 mm Hg Hypocapnia Hyperventilation
Dangers of Hypercapnia
Bodys CO2 production
PaCO2 -------------------------------------------------
Alveolar ventilation (VA) (Lmin)
Elevated PaCO2 poses serious derangement in the respiratory system for three
reasons:
1. An elevated PaCO2 will lower the PAO2 (Alveolar gas equation), and as a result
will lower the PaO2.
2. An elevated PaCO2 will lower the pH (Henderson-Hasselbalch equation).
The higher the baseline PaCO2, the greater it will rise for a given fall in
alveolar ventilation, e.g., a 1 L/min decrease in VA will raise PaCO2 a
greater amount when the baseline PaCO2 is 50 mm Hg than when it is 40
mm Hg.
A raised PaCO2 reflects reduced alveolar ventilation (type II respiratory failure).
Causes
inadequate minute ventilation (VE) (central or pump failure)leading to

decreased VA and increased PaCO2:i.e sedative drug overdose; respiratory
muscle paralysis; central hypoventilation
Increased dead space ventilation (VD) leading to decreased VA and

increased PaCO2: COPD(mismatch with perfusion giving a relative increase
in dead space ventilation and reduction in alveolar ventilation); severe
restrictive lung disease (with shallow, rapid breathing)

Test Your Understanding
1. What is the PaCO2 of a patient with respiratory rate 24/min, tidal volume 300
ml, dead space volume 150 ml, and CO2 production 300 ml/min? The patient
shows some evidence of respiratory distress.
2. What is the PaCO2 of a patient with respiratory rate 10/min, tidal volume 600
ml, dead space volume 150 ml, and CO2 production 200 ml/min? The patient
shows some evidence of respiratory distress.
3. A man with severe chronic obstructive pulmonary disease exercises on a

treadmill at 3 miles/hr. His rate of CO2 production increases by 50% but he is
unable to augment alveolar ventilation. If his resting PaCO2 is 40 mm Hg and
resting VCO2 is 200 ml/min, what will be his exercise PaCO2?
VCO2 x 0.863
PaCO2 = ---------------------------
VA (Lmin)
ANSWER
1) First, you must calculate the alveolar ventilation. Since minute ventilation
is 24 x 300 or 7.2 L/min, and dead space ventilation is 24 x 150 or 3.6
L/min, alveolar ventilation is 3.6 L/min. Then
300 ml/min x .863
PaCO2 = ----------------------- = 71.9 mm Hg
3.6 L/min
2) VA = VE VD = 10(600) 10 (150) = 6 - 1.5 = 4.5 L/min

200 ml/min x .863
PaCO2 = ---------------------- = 38.4 mm Hg
4.5 L/min
3) Exercise increases metabolic CO2 production. People with a normal

respiratory system are always able to augment alveolar ventilation to meet
or exceed the amount of VA necessary to excrete any increase in CO2

production. As in this example, patients with severe COPD or other forms

of chronic lung disease may not be able to increase their alveolar
ventilation, resulting in an increase in PaCO2. This patients resting alveolar
ventilation is
200 ml/min x 0.863

VA L/min = -----------------------------
PaCO2
200 ml/min x 0.863
VA = ----------------------------- = 4.32 L/min
40 mm Hg
Since CO2 production increased by 50% and alveolar ventilation not at all, His
exercise PaCO2 is
300 ml/min x .863
PaCO2 = -------------------------- = 59.9 mm Hg
4.32 L/min

Indications of ABG.cont.
3. Assessment of acid-base status
Assessment of oxygenation status includes:-
1. Is the pt hypoxemic or normoxemic
2. Assessment of level of hypoxemia (PaO2)
3. Oxygen content equation (CaO2: 16 - 22 ml O2/dl)
4. Alveolar gas equation: Calculation of alveolo-arterial O2 gradient(AaDO2)
5. lung injury score (If present)
What is the forms of Oxygen in blood? ? ?
Oxygen in blood exist in two forms
1) In physical solution (PaO2) i.e. dissolved in plasma & RBCs.
It is little in amount (0.3 cc/100 cc blood). So; it is not enough at all for
tissue oxygenation, but it is very important because its tension determine the
direction and rate of diffusion of O2 from or to blood.
NB: Tissue oxygenation which is about 225-250 cc/ min at rest
2) In chemical combination SaO2 % i.e. with hemoglobin.
Normally , blood contains about 15 gm %
Each gram of hemoglobin will bind 1.34 ml O2 when it is fully saturated
with O2, but blood in circulation is never fully saturated with O2 (Why).
Tissues need a requisite amount of oxygen molecules for metabolism.
Neither the PaO2 nor the SaO2 tells how much oxygen is in the blood.
O2 In physical sol. (PaO2) + O2 in chemical combination SaO2 % = Oxygen

Content (CaO2 mldl)

Oxygen content equation

CaO2 is calculated = quantity O2 bound + quantity O2 dissolved
to hemoglobin in plasma
CaO2 ml/dl = (Hb x 1.34 x SaO2) + (0.003 x PaO2)
CaO2Normally 16 - 22 ml /dl
Hb = hemoglobin in gm%
1.34 = ml O2 that can be bound to each gm of Hb
0.003 is solubility coefficient of oxygen in plasma
SaO2 is percent saturation of hemoglobin with oxygen
Normal SaO2 range in healthy adults (measured by pulse oximetry) of O2
Daytime healthy adults SaO2 96-98%
Transient dips in saturation are common during sleep (~84%)
(PaO2) is little in amount (0.3 cc/100 cc blood) & not enough at all for tissue
oxygenation, but it is very important?? ?
At an atmospheric pressure of 100 kPa (760mmHg) dry air contains: -
20.9% O2, 0.03% CO2 and 79.03% N2 (with minor contributions from other gases)
The approximate partial pressures for these

gases:-
The partial pressure of O2=
(Po2) is 0.21 760, or (160 mm Hg)
0.03 kpa (0.2mmHg) for CO2
79kpa (593mmHg) for N2
These partial pressures fall slightly in the

airways due to humidification & PO2 falls
further in the alveoli where O2 diffuses to
pulmonary capillary blood.

The diffusion of a gas across membrane occurs from the higher tension (=
Pressure) to lower tension regardless of the amount of gas present on either side.
Therefore, O2 pass from Alveoli (PAO2 100 mmHg) Arterial blood (PaO2 90
mmHg) tissue (PO2 40 mmHg) venous
blood (PO2 40 mmHg)
Dashed line represents the approximate
intracellular anaerobic threshold
Also CO2 pass from tissue to arterial blood and

from venous blood to alveoli
Oxygen Delivery and Utilization= DO2
the eventual goal of tissue oxygenation
requires transport of O2 from the lungs to the
peripheral tissues and organs
(Tissue oxygenation): Transport of oxygen from atmospheric air to tissue

mitochondria (the ultimate sites of oxygen utilization) requires the integrated
function of:-
1) Pulmonary system
Determine PaO2
2) CVS
Determine COP
Determine blood flow
3) Hematological system
Determine Hb concentration

DO2 (Total O2 delivery ml/min) = COP X CaO2 X 10
DO2 (Total O2 delivery ml/min) = COP X (Hb x 1.34 x SaO2) + (0.003 x PaO2) X 10
So; Oxygen delivery (DO2) to the periphery is determined by:

1) Oxygen content of arterial blood (CaO2 ml/dl)
2) Cardiac output (COP L/m)
How does hypoxia differ from hypoxemia?
HYPOXEMIA refers to decreased oxygen delivery from the atmosphere to the
blood. Hypoxemia is defined by a PaO2 of less than 80 mm Hg in a person
breathing room air at sea level.
CAUSES OF HYPOXEMIA
1. Decreased effective parometric pressure: high altitude
2. Hypoventilation: Respiratory center depression, neuromuscular disease, or
respiratory failure
3. Shunt: Pulmonary (e.g., atelectasis, pneumonia, pulmonary edema, or acute
respiratory distress syndrome) or cardiac (i.e., patent foramen ovale)
4. V/Q mismatch: Airway secretions or bronchospasm
5. Diffusion defect: Pulmonary fibrosis, emphysema, or pulmonary resection
It is important to recognize that hypoxemia may occur without hypoxia, and
vice versa.
HYPOXIA
Refers to decreased oxygen delivery to the tissues below physiological levels
despite adequate perfusion of the tissue by blood.
Tissue hypoxia develops whenever oxygen delivery is inadequate to meet
metabolic demands

CAUSES OF HYPOXIA
1. Hypoxemic hypoxia: Lower-than-normal PaO2 (hypoxemia)
2. Anemic hypoxia: Decreased RBCs cell count, or decreased release of oxygen
from hemoglobin to the tissues i.e carboxyhemoglobin, methemoglobin, or
hemoglobinopathy or sulph-Hb
3. Stagnant hypoxia: Decreased cardiac output or decreased local perfusion
4. Histotoxic hypoxia: Cyanide poisoning
Arterial blood venous blood
PO2 O2 CONTENT PO2 O2 CONTENT
Hypoxic hypoxia Decreased Decreased Decreased Decreased

Normal Decreased Decreased Decreased
Anemic hypoxia
Normal Normal Decreased Decreased
Stagnant hypoxia
Normal Normal Increased Increased
Histotoxic hypoxia
Alveolar Gas Equation

The alveolar gas equation is used to calculate the average alveolar PO2 (PAO2)
PAO2= PIO2 (1.25 X PaCO2)
PAO2= (EBP X FiO2) (1.25 X PaCO2)
PAO2: is the average alveolar PO2
PIO2: is the partial pressure of inspired oxygen in the trachea
FIO2: is fraction of inspired oxygen
(EBP): is the effective barometric pressure.
(EBP): is the difference bet. Barometric pressure & water vapor pressure at
body temp (47 mm Hg at 37C) = 760 - 47=713.

Pt . On room air breathing FiO2 = 0.21So;

PAO2 = (713 X 0.21) (1.25 X PaCO2) =
PAO2 = [150 (1.25 X PaCO2)]
Pt on FiO2
PAO2 = [(EBP X FiO2) (1.25 X PaCO2)]
The alveolar PO2 (PAO2) is always higher than arterial PO2 (PaO2). As a result,
whenever PAO2 decreases, PaO2 also decreases. Thus, from the AG equation:
1) If FIO2 and EBP are constant, then as PaCO2 increases both PAO2 and PaO2
will decrease (hypercapnia causes hypoxemia).
2) If FIO2 decreases and EBP and PaCO2 are constant, both PAO2 and PaO2 will
decrease (suffocation causes hypoxemia).
3) If EBP decreases (e.g., with altitude), and PaCO2 and FIO2 are constant,
both PAO2 and PaO2 will decrease (mountain climbing leads to
hypoxemia).
1. What is the PAO2 at sea level in the following circumstances? (Barometric

pressure = 760 mm Hg)
a) FIO2 = 1.00, PaCO2 = 30 mm Hg

b) FIO2 = .21, PaCO2 = 50 mm Hg
c) FIO2 = .40, PaCO2 = 30 mm Hg
2. What is the PAO2 on the summit of Mt. Everest in the following circumstances?
(Barometric pressure = 253 mm Hg)
a) FIO2 = .21, PaCO2 = 40 mm Hg
b) FIO2 = 1.00, PaCO2 = 40 mm Hg
c) FIO2 = .21, PaCO2 = 10 mm Hg

ANSWER
1. To calculate PAO2 the PaCO2 must be subtracted from the PIO2. Again, the
barometric pressure is 760 mm Hg since the values are obtained at sea level.
EBP=760-47=713
PAO2= PIO2 (1.25 X PaCO2)

On room air PAO2 = [150 (1.25 X PaCO2)]
The PaCO2 of 30 mm Hg is not multiplied by 1.25 since the FIO2 is 1.00
In parts b and c, PaCO2 is multiplied by the factor 1.25
a) PAO2 = 1.00 (713) - 30 = 683 mm Hg
b) PAO2 = 0.21 (713) - 1.25 (50) = 90 mm Hg
c) PAO2 = 0.40 (713) - 1.25 (30) = 249 mm Hg
2. The PAO2 on the summit of Mt. Everest is calculated just as at sea level, using
the barometric pressure of 253 mm Hg.
a) PAO2 = 0 .21 (253 - 47) - 1.25 (40) = - 6.74 mm Hg
b) PAO2 = 1.00 (253 - 47) - 40 = 193 mm Hg
c) PAO2 = 0.21 (253 - 47) - 1.25 (10) = 31 mm Hg
The modified alveolar gas equation is used to calculate the PAO2 & then:-
Calculation of alveolo-arterial O2 gradient (AaDO2)
The alveolar-arterial O2 gradient (AaDO2), which is the difference between the

calculated PaO2 (PAO2)& the measured PaO2:
AaDO2 = PAO2 PaO2
Pt on room air
AaDO2 = [150 (1.25 X PaCO2)] PaO2
Pt on FiO2
AaDO2 = [(EBP X FiO2) (1.25 X PaCO2)] PaO2

Can the PaO2 normally be more than 100 mm Hg or less than 75 mm Hg?
A. Can the PaO2 normally more than 100 mm Hg?

The PaO2 can never be greater than (PAO2). The modified alveolar gas
equation is used to calculate the PAO2:
PAO2=(EBP X FiO2) (1.25 X PaCO2)
(EBP) is the effective barometric pressure.
EBP is the difference bet. barometric pressure & water vapor pressure at body
temp (47 mm Hg at 37C) = 760- 47=713.
For an individual breathing room air (FiO2 0.21) at sea level (barometric
pressure = 760 mm Hg) with a normal PaCO2 (40 mm Hg), SO;
PAO2= (713 X 0.21) (1.25 X 40) = 149.73 - 50 = 100 mm Hg.
Considering the alveolar-to arterial (A-a) gradient of 5-10 mm Hg, the
measured PaO2 would be 90-95 mm Hg.
PaO2 will be > 100 mm Hg with
1. Hyperbaric conditions (e.g., patients treated with hyperbaric oxygen).
2. PaO2 also increases with an increase in FiO2. The alveolar gas equation
predicts that the PAO2 will be 675 mm Hg when 100% oxygen is breathed at
sea level; thus, the PaO2 is normally > 600 mm Hg when FiO2 is 1.0
Can the PaO2 normally be less than 75 mm Hg?
The alveolar gas equation predicts that the PaO2 will be <100 mmHg if:-
1. The barometric pressure is <760 mm Hg (at an altitude at which ambient
barometric pressure is 650 mm Hg). Thus, the normal PaO2 is lower at higher
altitudes e.g the PaO2 is 75 mm Hg

Indices of Oxygenation
1) AaDO2 = PAO2 PaO2

2) Lung injury score
Normal Value:
patients < 60 y. > 400
patients > 60 y expected P/F = 400 [(age in years 60) x 5]
Actual P/F Ratio < expected = hypoxemic
Actual P/F Ratio > expected = normoxemic
1. Acute lung injury (ALI): PaO2/FIO2 300 mm Hg or less,
2. ARDS: PaO2/FIO2 200 mmHg

1. Type of blood Sample
2. Assessment of oxygenation status includes:-
a) Is the pt hypoxemic or normoxemic
b) Assessment of level of hypoxemia (PaO2)
c) Oxygen content equation (CaO2: 16 - 22 ml O2/dl)
d) Alveolar gas equation: Calculation of alveolo-arterial O2
gradient(AaDO2)
e) lung injury score (If present)
3. Assessment of acid base status
Difference bet. Arterial & Venous bl. sample
Respir Care 37(8):913,1993
Arterial sample Venous sample
pH 7.35-7.45 7.35
PaO2 80 -100mmHg 38 - 42 mmHg
PaCO2 35 - 45 mmHg 44 - 48mmHg
(40 mmHg) (46 mmHg)
HCO3 22-26 mEq/L or 20-24 mEq/L
23-27 mEq/L
O2 sat. 95% or more 75%
BE The base excess indicates the amount of excess or insufficient
level of bicarbonate in the system.
Normal + 3 mmol/L
Relatively balanced + 5 mmol/L
Significant imbalance: + 10 mmol/L
Remember:- A negative BE indicates a base deficit in the blood
CaO 16 - 22 ml O2/dl
2
%MetHb < 2.0%
%COHb < 3.0%
Na+ 135 148 mEq/L
K+ 3.5 5.5 mEq/L
Cl- 95 -105 mEq/L

1. Type of blood Sample.
a) Arterial bl sample (N: SaO2 95% or more)

b) Venous bl sample (SaO2 75% or less)
c) Blood sample (SaO2 more than 75%) for clinical correlation
Arterial bl sample . Or
Mixed Venous bl sample
2. Assessment of oxygenation Is the pt hypoxemic or normoxemic?
a) Assessment of level of hypoxemia
o PaO2 ( N 80 -100 mmHg) for person who breathing room air
o Hypoxemia is defined by a PaO2 of less than 80 mm Hg in a person
breathing room air at sea level.
Mild hypoxemia PaO2 60 79 mmHg
Moderate hypoxemia (RF) PaO2 40 59 mmHg
Severe hypoxemia (RF) PaO2 les than 40 mmHg
NB: - At any age, PaO2 < 40 mmHg indicates severe hypoxemia.

Respiratory failure has been defined as:- a PaO2, measured at rest at sea level,
of less than 8kPa (60mmHg) or a PaCO2 above 6.5 kPa (49 mmHg)
Acceptable lower limits for PaO2 (at see level) can be determined by the following:-
1. For person in sitting position
PaO2 = 104.2 (0.27 age) mmHg
e.g pt. 45 y old the acceptable lower limits for PaO2 at room air in sitting position
= 104.2 (0.27 45) = 104.2 12.15= 92.05 mmHg
e.g pt. 85 y old the acceptable lower limits for PaO2 at room air in sitting position
= 104.2 (0.27 85) = 104.2 22.95= 81.25 mmHg
2. For person in supine position
PaO2 = 103.5 (0.42 age) 4 mmHg

e.g Same pt. 45 y old the acceptable lower limits for PaO2 at room air in supine
position = 103.5 (0.42 45) 4 = 103.5 18.9= 84.6 4 mmHg
e.g Same pt. 85 y old the acceptable lower limits for PaO2 at room air in supine
position = 103.5 (0.42 85) = 103.5 35.7 = 67.8 4 mmHg
In general the acceptable lower limits for PaO2 for

1) Patients < 60 y
PO2 = 100 + 20
2) Patients > 60 y
PO2 = 100 (years > 60)
For each year > 60 subtract 1 mmHg for limits of mild & moderate hypoxemia.
Patients on O2 therapy (FiO2 more than 21%)

1. Corrected hypoxemia: 80 120 mmHg
2. Uncorrected hypoxemia: PaO2 less than acceptable lower limits ( 80 mmHg)
3. Excessively corrected hypoxemia: PaO2 greater than 120 mmHg
FiO2 to PaO2 Relationship in Normal Lungs
FiO2 x 500 = PaO2 (mmHg)

0.30 > 150
0.40 > 200
0.50 > 250
0.80 > 400
1.00 > 500 (pt < 60 y)
Calculation of alveolo arterial O2 gradient(AaDO2)
The alveolar-arterial O2 gradient (AaDO2), which is the difference between the
calculated PaO2 (PAO2)& the measured PaO2:
AaDO2 = PAO2 PaO2
Pt on room air
AaDO2 = [150 (1.25 X PaCO2)] PaO2
Pt on FiO2
AaDO2 = [(EBP X FiO2) (1.25 X PaCO2)] PaO2

AaDO2 increases with age

AaDO2 = [4 + age/4] or.. AaDO2 = age X 0.3
The upper limits of normal AaDO2 nearly 20 mmHg for 30- 40 year &
30 mmHg for 50-70 y of age (other literature 15, 25)
During ideal gas exchange, blood flow and ventilation would perfectly match each
other, resulting in no alveolar-arterial PO2 difference. However, even in normal
lungs;
a) Not all alveoli are ventilated and perfused perfectly.
b) Some alveoli are under ventilated while others are over ventilated.
c) Similarly, for known alveolar ventilation, some units are underperfused
while others are overperfused.
The optimally ventilated alveoli that are not perfused well are called high V/Q
units (acting like dead space)
And alveoli that are optimally perfused but not adequately ventilated are
called low V/Q units (acting like a shunt).
AaDO2 measure all factors that impair the equilibrium of arterial bl. with
alveolar gas
AaDO2 helps to determine whether the lung parenchyma is functioning

normally or not ; so AaDO2 is critical for evaluation of causes of hypoxemia
AaDO2 should be calculated hypoxemic or normoxemic subject because it is

possible to have normal PaO2 with widened AaDO2, which indicating the
presence of a disorder impairing normal oxygenation of blood (lung
parenchymal disorders).
If AaDO2 is normal & the patient is hypoxemic, PaCO2 is elevated, then

Alveolar hypoventilation is the cause of the hypoxemia which means that the
lungs themselves are working normally & that pt. has problem in ventilatory
drive or neuromuscular disease.

AaDO2 calculation is particularly useful in patients with a drug overdose who

hypoventilate but also may have components of chemical or bacterial
aspiration pneumonia or atelectasis
Causes of hypoxemia
With normal AaDO2 With widened AaDO2
1. Decreased barometric 1. Shunt= refractory hypoxemia (FiO2 100%)
pressure ( EBP) &PO2 Pulmonary (e.g., atelectasis,
high altitude pneumonia, pulmonary edema, or
ARDS)
2. Alveolar Hypoventilation
(causes of type 2 RF) Or cardiac (ASD)
Resp center depression, Or vascular (Liver diseases)
neuromuscular disease 2. V/Q mismatch: Airway secretions or

bronchospasm
respiratory failure
3. Diffusion defect:
airway diseases
DPLD, emphysema, or pul resection
O2
O2
B (acting like a C (acting like

A shunt). dead space)

Summary of assessment of oxygenation

1. Date & time of sample, on room air or on FiO2 , at sea level
2. Arterial bl sample (SaO2 .), or Venous bl sample (SaO2 75% or less) or Mixed
Venous bl sample
3. Assessment of level of hypoxemia
PaO2 ( mmHg) ( N 80 -100 mmHg) Mild or Moderate (RF) or
Severe hypoxemia (RF)
PaCO2 ( mmHg) ( N 35-45 mmHg) Hypercapnia or Eucapnia or

Hypocapnia
Type 1 or type 11 RF or just respiratory insufficiency or normal
If the pt. on FiO2 corrected , or uncorrected or Excessively corrected

hypoxemia
4. Calculation of alveolo arterial O2 gradient(AaDO2)
Hypoxemia With normal AaDO2 DD (all causes of Alveolar

Hypoventilation )
Hypoxemia With widened AaDO2 DD (Shunt, or V/Q mismatch, or

Diffusion defect)
NB : The minimal elevation in PaO2 with 100% O2 indicates that a shunt is

the major cause of the hypoxemia


SaO2 PaO2 PaCO2
Room air 90% 45 mm Hg 30 mm Hg
1)
(100% O2) 93% 65 mm Hg 32 mm Hg
2)
(100% O2) 96% 560 mm Hg 32 mm Hg
3)

4)
5) Room air 87% 30 mm Hg 60 mm Hg

Answers
1) Arterial bl sample (SaO2 90%)
PaO2 ( 45 mmHg) ( N 80 -100 mmHg) Moderate hypoxemia (RF)
PaCO2 ( 30 mmHg) ( N 35-45 mmHg) Hypocapnia
Type 1 RF
pt. on FiO2 0.1 PaO2 ( 65 mmHg) uncorrected hypoxemia
Calculation of alveolo arterial O2 gradient(AaDO2)
On room air, the pts AaDo2 = 67.5 mm Hg, which is elevated.
Hypoxemia With widened AaDO2 DD (Shunt, or V/Q mismatch, or

Diffusion defect). The minimal elevation in PaO2 with 100% O2 indicates
that a shunt is the major cause of the hypoxemia.
2) Identical to Problem 1, except that the dramatic increase in PaO2 with 100%
O2 indicates that ventilation-perfusion mismatch is the major cause of the
hypoxemia.
3) Even though PaO2 appears normal, AaDo2 is elevated to 37 mm Hg, indicating

the presence of a disorder impairing normal oxygenation of blood.
4) Arterial bl sample (SaO2 90%)
PaO2 ( 65 mmHg) ( N 80 -100 mmHg) Mild hypoxemia
PaCO2 ( 60 mmHg) ( N 35-45 mmHg) Hypercapnia
AaDo2 = 10 mm Hg, indicating that hypoxemia is due to hypoventilation
Respiratory insufficiency with alveolar hypoventilation for DD.
5) As in Problem 4. AaDo2 is elevated (to 45 mm Hg), indicating that both either

ventilation perfusion mismatch or shunting (most likely the former) are
responsible for the hypoxemia.

ACID-BASE STATUS
Measured values from ABG include PaO2, PaCO2 and pH, not serum HCO3.
Therefore, must either measure serum HCO3 (as part of serum electrolyte values)
or use a value calculated from Pco2 and pH according to the Henderson
Hasselbalch equation. Look at the pH value to determine the net disturbance in
acid-base balance.
Clinical Terminology
1. Acidemia means pH < 7.35

2. Alkalemia means pH > 7.45
3. Acidosis means HCO3- < 22 mmol/L & BD > 5 mmol/L
4. Alkalosis means HCO3- > 26 mmol/L & BE > 5 mmol/L
5. Ventilatory failure (respiratory acidosis) means PaCO2 > 45 mm Hg
a) Acute ventilatory failure (respiratory acidosis) means PaCO2 > 45
mmHg & pH < 7.35
b) Chronic ventilatory failure (respiratory acidosis) means PaCO2 > 45
mmHg & pH 7.36 - 7.44
6. Alveolar hyperventilation (respiratory alkalosis) means PaCO2 < 35 mmHg
a) Acute alveolar hyperventilation (respiratory alkalosis) means PaCO2 <
35 mmHg & pH > 7.45
b) Chronic alveolar hyperventilation (respiratory alkalosis) means PaCO2
< 35 mmHg & pH 7.36 -7.44

Simple Rules for the Interpretation of Acid Base status

Step (1) pH normal or acidemia, or alkalemia
Step (2) is the primary disorder respiratory or metabolic disorder?
Step (3) for primary respiratory disorder is it acute or chronic?
Step (4) for primary metabolic disorder is respiratory system compensated

correctly or not?
Step (5) for primary metabolic acidosis, there is an increased anion gap?
Step (6) for an increased anion gap metabolic acidosis, are there any other
derangement
Mantra
MC 1 for 1
MK 10 for 7
1
4
2
5
Metabolic Acidosis: 1 HCO3 from normal(24) => 1 PCO2 from normal(40)
Metabolic Alkalosis: 10 HCO3 => 7 PCO2
Acute Resp Acid: 10 PCO2 = 1 HCO3
Chronic Resp Acid: 10 PCO2 = 4 HCO3
Acute Resp Alk: 10 PCO2 => 2 HCO3
Chronic Resp Alk: 10 PCO2 => 5 HCO3
These are the relationships that the mantra refers to. They are not
mathematically derived formulas. Rather, they reflect the way in which
human physiology predictably responds to acid-base perturbations. They are
empiric observations, and, combined with a few other rules, they help you
understand whether the patient has a single, double, or even triple acid-base
disorder.

Step (1) pH normal or acidemia, or alkalemia

A normal pH (approximately 7.357.45) indicates normal acid-base status or
Fully Compensated balancing problems.
If the pH is outside the range of 7.35-7.45, the condition is uncompensated
only partially compensated.
Remember, neither buffer system has the ability to overcompensate!
pH
Abnormal (or )
Step (2) Identify the primary acid base disorder

a) If the pH value moves in the same direction for the PCO2 change i.e ( pH
with PCO2; or pH with PCO2), then a metabolic disorder is the primary
disorder.
b) If the pH value move in opposite direction for the PCO2 change i.e ( pH
with PCO2; or pH with PCO2), then the respiratory disorder is the
primary disturbance.
c) Combined
Respiratory Acidosis & Metabolic Acidosis
Respiratory Alkalosis & Metabolic Alkalosis
d) Mixed (Partly compensated or sub-acute)

Respiratory Acidosis & Metabolic Alkalosis
Respiratory Alkalosis & Metabolic Acidosis

pH in the opposite direction of CO2

1ry disorder
Respiratory or combined or mixed
Chorionic (Compensated) Combined

(Acute) Uncompensated
Alkalosis Acidosis Alkalosis Acidosis Combined Combined Acidosis
Alkalosis
pH in the same direction of CO2

1ry disorder
Metabolic
Compensated Uncompensated Partially compensated

(Mixed)
Alkalosis Acidosis Alkalosis Acidosis Alkalosis Acidosis
34 DR: TAGHRID SAID

Nomenclature pH PCO2 HCO3 BE

Respiratory acidosis
Uncompensated (acute) N N
Partially compensated (subacute or mixed )
Compensated (chronic) N
Respiratory alkalosis
Uncompensated (acute) N N
Partially compensated (subacute or mixed )
Metabolic acidosis
Uncompensated (acute) N
Partially compensated (sub-acute or mixed )
Metabolic alkalosis
Uncompensated (acute) N
Partially compensated (sub-acute or mixed )
Combined
Respiratory Acidosis & Metabolic Acidosis
Respiratory Alkalosis & Metabolic Alkalosis
Mixed (partially compensated )

Respiratory Acidosis & Metabolic Alkalosis
Respiratory Alkalosis & Metabolic Acidosis
35 DR: TAGHRID SAID

Step (3) Evaluate compensatory response & level of compensation

A. For the primary respiratory disorder is it acute or chronic?
If there is primary resp. acidosis or alkalosis: calculate the expected pH:
1. For respiratory acidosis:
1. if the PH < expected for the acute condition secondary metabolic
acidosis
2. If the PH > expected for the chronic condition secondary
metabolic alkalosis.
2. For respiratory alkalosis:
1. If the PH > expected for the acute condition secondary
2. If the PH < expected for the chronic condition secondary

metabolic acidosis.
3. If measured PH is between the expected PH for the acute and
chronic partially compensated respiratory acidosis or alkalosis
B. For the primary metabolic disorder (acidosis or alkalosis): calculate
expected PaCO2:
1. For primary metabolic acidosis:
The physiological response to metabolic acidosis is hyperventilation, with
a resulting compensatory drop in PCO2 according to "Winter's formula":
Expected PCO2 in metabolic acidosis = 1.5 x HCO3 + 8 (range: 2)
If measured PCO2 > expected PCO2 secondary respiratory acidosis.
This may occur, for instance, when respiratory depressants like morphine
or fentanyl are administered to the patient to reduce pain.
2. For primary metabolic alkalosis:
The response to metabolic alkalosis is hypoventilation, with a resulting
increase in PCO2 according to the following formula:
Expected PCO2 in metabolic alkalosis = 0.7 x HCO3 + 20 mmHg (range: 5)
If measured PCO2< expected PCO2 secondary respiratory alkalosis.
36 DR: TAGHRID SAID

The expected change in pH can be estimated with the following equations

Acute respiratory acidosis Acute respiratory alkalosis
expected pH = 7.40 0.008 X (PaCO240)
ex. PCO2 = 60 ex. PCO2 = 20
expected pH = 7.40 0.008 X (60 40) expected pH = 7.40 0.008 X (20 40)
= 7.24 = 7.56
expected HCO3-= 24 + 0.1 (PaCO240) expected HCO3-= 24 + 0.2 (PaCO240)
HCO3-increases 0.1 1 meq/L per 10 HCO3- decreases 0 - 2 meq/L per 10
mmHg PCO2 increase mmHg PCO2 decrease
Chronic respiratory acidosis: Chronic respiratory alkalosis
expected pH = 7.40 0.003 X (PaCO240)
ex. PCO2 = 60 ex. PCO2 = 20
pH = 0.003 x (60 40) = 0.06 pH = 0.003 x (20 40) = 0.06
expected pH = 7.40 0.06 = 7.34 Expected pH = 7.40 + 0.06 = 7. 46
expected HCO3-= 24 + 0.4 (PaCO240) expected HCO3-= 24 + 0.5 (PaCO240)
HCO3- increases 1-3.5 meq/L per 10 HCO3- decreases 2-5 meq/L per 10
mmHg PCO2 increase mmHg PCO2 decrease
Expected PCO2 in metabolic acidosis = 1.5 x HCO3 + 8 (range: 2)

Expected PCO2 in metabolic alkalosis = 0.7 x HCO3 + 20 mmHg (range: 5)
Expected compensation for acid base disturbance
Respiratory acidosis HCO3 = 0.10 PaCO2 (acute)
HCO3 = 0.35 PaCO2 (chronic)
Respiratory alkalosis HCO3 = 0.2 PaCO2 (acute)
HCO3 = 0.5 PaCO2 (chronic)
Metabolic acidosis PaCO2= 1.2 HCO3
Metabolic alkalosis PaCO2= 0.9 HCO3
37 DR: TAGHRID SAID


pH=7.35, PCO2=60, HCO3=32
Parameter Value Normal Analysis
pH: 7.35 7.35-7.45 pH is within normal (fully compensated)
-
[HCO3 ]: 32 mEq/L 22-26 mEq/L HCO3- conc. is high (metabolic alkalosis)
PaCO2: 60 mmHg 35-45 mmHg CO2 tension is high (respiratory acidosis)
The pH is at the low end of normal (toward the acidotic side) because the body
generally doesn't overcompensate, the acidotic factor is the primary
So; the pH value move in opposite direction for the PCO2 change i.e ( pH with
PCO2), then the respiratory disorder is the primary disturbance.
Is it an ACUTE or CHRONIC respiratory acidosis? The pCO2 is up by 20 and
according to the mnemonic"
For Acute Resp Acid: 10 PCO2 = 1 HCO3
For Chronic Resp Acid: 10 PCO2 = 4 HCO3
Here the HCO3 has risen by 8 (4 for every 10 rise in pCO2).
Diagnosis
Chronic respiratory acidosis, as the full renal response to retain HCO3 has
occurred.
pH=7.25, PCO2=60, HCO3=26
pH: 7.25 7.35-7.45 pH is low: Acidemia
-
[HCO3 ]: 26 mEq/L 22-26 mEq/L HCO3- within normal
The pH is low: Acidemia, the pH value move in opposite direction for the PCO2
change i.e respiratory disorder is the primary disturbance.
Here the HCO3 has risen by 2 (1 for every 10 rise in pCO2).
Diagnosis: - acute respiratory acidosis (the kidneys have not had any time to
respond).
38 DR: TAGHRID SAID

pH=7.30, PCO2=60, HCO3=29

-
The pH is low: Acidemia, the pH value move in opposite direction for the PCO2
change i.e then the respiratory disorder is the primary disturbance.
Here the HCO3 has risen by (5). The HCO3 is in between what would be
predicted for an acute and chronic respiratory acidosis. The most reasonable
explanation for this is that the patient has both conditions: chronic respiratory
acidosis upon which an acute respiratory acidosis is superimposed.
Diagnosis :- This is commonly referred to as acute on top of chronic respiratory
acidosis.
pH = 7.33, PCO2=30, HCO3=15

[HCO3-]: 15 mEq/L 22-26 mEq/L HCO3- concentration is low
(metabolic acidosis)
PaCO2: 30 mmHg 35-45 mmHg CO2 tension is low (respiratory
alkalosis)
The pH and CO2 levels are both in the same direction, so the primary mechanism
is a metabolic acidosis. The mnemonic predicts that
For Metabolic Acidosis: 1 HCO3 => 1 PCO2
The HCO3 is decreased by 9, the PCO2 is decreased by 10 (close enough), so
this is a metabolic acidosis, with respiratory alkalosis is compensatory, but the
pH is not within normal limits, so it is only partially effective.
Diagnosis
metabolic acidosis with partial compensatory respiratory alkalosis
39 DR: TAGHRID SAID

pH=7.22, PCO2=38, HCO3=15

PaCO2: 38 mmHg 35-45 mmHg CO2 tension is normal
The patient is acidemic, so the primary mechanism is a metabolic acidosis. The
HCO3 is down by 9; so the pCO2 should be down by 9. The pCO2 is only down
by 2, reflecting an inappropriate respiratory response to the acidosis. Since the
respiratory response is blunted, this represents a COMBINED metabolic and
respiratory acidosis.
Diagnosis
Met and Resp acidosis or
Uncompensated Met Acidosis
pH=7.38, PCO2=28, HCO3=16

pH: 7.38 7.35-7.45 pH is within normal (fully compansated)
-
[HCO3 ]: 16 mEq/L 22-26 mEq/L HCO3- concentration is low (metabolic
acidosis)
PaCO2: 28 mmHg 35-45 mmHg CO2 tension is low (respiratory alkalosis)
The pH is normal (toward the acidotic side) Because the body generally doesn't
overcompensate, the acidotic factor is the primary; The HCO3 is down by 8, so the
pCO2 should be down by 8. Since the pCO2 is down by 12, the patient is blowing
off more CO2 than is physiologically predicted. Here, there is a metabolic acidosis,
fully compensated by respiratory alkalosis
diagnosis:
Met Acid with Resp alkalosis or
Overcompensated Met acidosis
40 DR: TAGHRID SAID

pH =7.47, PCO2=47, HCO3=34

pH: 7.47 7.35-7.45 pH is high: Alkalemia
-
PaCO2: 47mmHg 35-45 mmHg CO2 tension is high (respiratory acidosis)
The pH and CO2 levels are both in the same direction, so the primary mechanism is a
metabolic Alkalosis. The mnemonic predicts that
Metabolic Alkalosis: 10 HCO3 => 7 PCO
The HCO3 is increased by 10, the pCO2 is increased by 7 (close enough), so

this is a metabolic alkalosis, with respiratory acidosis is compensatory, but
the pH is not within normal limits, so it is only partially effective.
Diagnosis metabolic alkalosis
pH=7.45, PCO2=25, HCO3=17

-
[HCO3 ]: 17mEq/L 22-26 mEq/L HCO3- conc. is low (metabolic acidosis)
PaCO2: 25mmHg 35-45 mmHg CO2 tension is low (respiratory alkalosis)
The pH is at the high end of normal (toward the alkalotic side) because the body
generally doesn't overcompensate, so the primary process is respiratory in
origin.
Is it an ACUTE or CHRONIC respiratory alkalosis? According to the mnemonic,
for every 10 that the pCO2 is down, the HCO3 should decrease by 2 in an acute
alkalosis and by 5 in a chronic alkalosis. The PCO2 is down by 15, and the HCO3
is down by 7, which is what would be predicted for a CHRONIC respiratory
alkalosis (Prediction = down 7.5). This is thus a chronic respiratory alkalosis (the
kidneys have had time to make a full response). This is seen when humans
chronically hyperventilate, as when they live at high altitude.
Diagnosis
chronic respiratory alkalosis
41 DR: TAGHRID SAID

pH=7.51, PCO2=42, HCO3=34

pH: 7.51 7.35-7.45 pH is high: Alkalemia
-
PaCO2: 42mmHg 35-45 mmHg CO2 tension is normal
The patient is alkalemic, therefore the primary problem is an alkalosis.
According to the mnemonic, for every 10 elevation in the HCO3, the pCO2
should rise by 7. It is only up by 2, so the patient is breathing off more CO2
that expected for the degree of alkalosis.
Diagnosis metabolic alkalosis and Respiratory alkalosis
pH=7.42, PCO2=52, HCO3=34

-
PaCO2: 52mmHg 35-45 mmHg CO2 tension is high (respiratory acidosis)
The pH is at the high end of normal (toward the alkalotic side) because the body
generally doesn't overcompensate, so the primary process is and alkalosis. The
HCO3 is up by 10, so the pCO2 should be up by 7. The pCO2 is up by 12,
reflecting more of a respiratory suppression than expected for this degree of
alkalosis.
Diagnosis metabolic alkalosis and Respiratory acidosis
42 DR: TAGHRID SAID

Interpretation Quiz
CASE (1)
pH [HCO3-] PaCO2
7.55 26 mEq/L 27 mmHg
Primary mechanism Compensatory Level of

mechanism compensation
1. all within normal limits 1. none present 1. none (or N/A)
2. metabolic acidosis 2. metabolic acidosis 2. incomplete
3. metabolic alkalosis 3. metabolic alkalosis 3. complete
4. respiratory acidosis 4. respiratory acidosis
5. respiratory alkalosis 5. respiratory alkalosis
6. metabolic and respiratory
acidosis
alkalosis
CASE (2)
pH [HCO3-] PaCO2
7.25 25 mEq/L 49 mmHg

5. respiratory alkalosis 5. respiratory
6. metabolic and respiratory acidosis alkalosis
alkalosis
43 DR: TAGHRID SAID

CASE (3)
pH [HCO3-] PaCO2
7.37 19 mEq/L 29 mmHg

acidosis
alkalosis
CASE (4)
pH [HCO3-] PaCO2
7.31 20 mEq/L 46 mmHg

acidosis
alkalosis
44 DR: TAGHRID SAID

CASE (5)
pH [HCO3-] PaCO2
7.33 29 mEq/L 47 mmHg
Compensatory Level of
Primary mechanism mechanism compensation

alkalosis
acidosis
alkalosis
CASE (6)
pH [HCO3-] PaCO2
7.52 26 mEq/L 29 mmHg

6. metabolic and resp. acidosis
alkalosis
45 DR: TAGHRID SAID

CASE (7)
pH [HCO3-] PaCO2
7.36 20 mEq/L 30 mmHg


acidosis
alkalosis
CASE (8)
pH [HCO3-] PaCO2
7.31 18 mEq/L 55 mmHg


6. metabolic and respiratory alkalosis
acidosis
alkalosis
46 DR: TAGHRID SAID

CASE (9)
pH [HCO3-] PaCO2
7.32 26 mEq/L 54 mmHg


6. metabolic and respiratory alkalosis
acidosis
alkalosis
47 DR: TAGHRID SAID

CASE (1)
Parameter Value Normals Analysis

pH: 7.55 7.35-7.45 pH is high: Patient is (still) alkalotic
-
[HCO3 ]: 26 22-26 HCO3- concentration is normal
mEq/L mEq/L
PaCO2: 27 35-45 CO2 tension is low (respiratory alkalosis)
mmHg mmHg
The pH and CO2 levels are both alkalotic, so the primary mechanism is a
respiratory alkalosis. The pH is high, so there is no indication of metabolic
compensation.
CASE (2)

pH: 7.25 7.35-7.45 pH is low: Patient is (still) acidotic
-
[HCO3 ]: 25 22-26 HCO3- concentration is normal
mEq/L mEq/L
PaCO2: 49 35-45 CO2 tension is high (respiratory acidosis)
mmHg mmHg
The pH and CO2 levels are both acidotic, so the primary mechanism is a
respiratory acidosis. There is no indication of metabolic compensation.
CASE (3)

pH: 7.37 7.35-7.45 pH is normal
-
[HCO3 ]: 19 22-26 HCO3- concentration is low (metabolic
mEq/L mEq/L acidosis)
PaCO2: 29 35-45 CO2 tension is low (respiratory alkalosis)
mmHg mmHg
The pH is at the low end of normal (toward the acidotic side), but the
bicarbonate and CO2 levels indicate something abnormal is happening. Because
the body generally doesn't overcompensate, the acidotic factor is the primary
culprit. Here, there is a metabolic acidosis, fully compensated by respiratory
alkalosis.
48 DR: TAGHRID SAID

CASE (4)

PaCO2: 46 mmHg 35-45 mmHg CO2 tension is high (respiratory
acidosis)
All levels are acidotic, so the metabolic and respiratory systems are contributing
to the acidosis. There is no compensation present here.
CASE (5)

[HCO3-]: 29 mEq/L 22-26 mEq/L HCO3- concentration is high
(metabolic alkalosis)
acidosis)
respiratory acidosis. The metabolic alkalosis is compensatory, but the pH is not
within normal limits, so it is only partially effective.
CASE (6)

pH: 7.52 7.35-7.45 pH is high: Patient is (still) alkalotic
[HCO3-]: 26 mEq/L 22-26 mEq/L HCO3- concentration is normal
alkalosis)
The pH and CO2 levels are both alkalotic, so the primary mechanism is a
respiratory alkalosis. The pH is high, so there is no indication of metabolic
compensation.
49 DR: TAGHRID SAID

CASE (7)

pH: 7.36 7.35-7.45 pH is normal
alkalosis)
The pH is at the low end of normal (toward the acidotic side), but the
bicarbonate and CO2 levels indicate something abnormal is happening. Because
the body generally doesn't overcompensate, the acidotic factor is the primary
culprit. Here, there is a metabolic acidosis, fully compensated by respiratory
alkalosis.
CASE (8)

acidosis)
All levels are acidotic, so the metabolic and respiratory systems are contributing
to the acidosis. There is no compensation present here.
CASE (9)

[HCO3-]: 26 mEq/L 22-26 mEq/L HCO3- concentration is normal
acidosis)
respiratory acidosis. There is no indication of metabolic compensation.
50 DR: TAGHRID SAID

pH PaO2 PaCO2
1) Room air 7.30 110 mm Hg 20 mm Hg
1) Mixed acid-base disorder with a primary metabolic acidosis complicated by a

primary respiratory alkalosis. Pco2 is too low to represent just compensation
for the metabolic acidosis, indicating the presence of a respiratory alkalosis
as well. AaDo2 = 15 mm Hg, the upper limit of normal for a young adult.
2) The simplest explanation of the acid-base status is a compensated metabolic

alkalosis. However, this pattern probably is seen more commonly with a
mixed acid-base disorder consisting of a compensated respiratory acidosis
complicated by a superimposed primary metabolic alkalosis. AaDo2 _ 35 mm
Hg. Therefore hypoxemia is due partly to hypoventilation but mostly to
ventilation-perfusion mismatch or shunt, probably the former.
3) Something is wrong because AaDo2 is negative (-15 mm Hg). Several possible

explanations are as follows:
a) The patient was receiving supplemental O2
b) A laboratory error was made
c) The blood was not collected or transported properly under anaerobic
conditions.
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Respiratory acidosis can be acute or chronic

In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the
reference range (> 45 mm Hg) with an accompanying aciademia (pH <7.35).
In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of
the reference range, with a normal or near-normal pH secondary to renal
compensation and an elevated serum HCO3 value (>30 mm Hg).
Acute resp acidosis is present when an abrupt failure of ventilation occurs .
1. Respiratory center depression by cerebral disease (eg, trauma encephalitis,
brainstem disease), primary alveolar hypoventilation or drugs (eg, narcotics,
barbiturates, benzo-diazepines, other CNS depressants).
2. Neuromuscular diseases
Amyotrophic lateral sclerosis , Diaphragm dysfunction and paralysis
Guillain-Barr syndrome, Myasthenia gravis, Muscular dystrophy
3. Chest wall disorders
Severe kyphoscoliosis , Status post thoracoplasty, Flail chest
Less commonly, ankylosing spondylitis, pectus excavatum, or pectus
carinatum
4. Airway obstruction COPD, Emphysema, severe asthma , chronic bronchitis
5. Obesity-hypoventilation syndrome (ie, pickwickian syndrome).
6. Obstructive sleep apnea
7. Excessive CO2 production
TPN
Sepsis
Severe burns
NaHCO3 administration
8. Other lung and airway diseases - Laryngeal and tracheal stenosis
9. Lung-protective ventilation in ARDS.
10. Extreme ventilation-perfusion mismatch
11. Exhaustion
12. Inadequate MV
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Management
Increasing ventilation will correct respiratory acidosis. The method for achieving
this will vary with the cause of hypoventilation. If the patient is unstable, manual
ventilation with a bagmask is indicated until the underlying problem can be
addressed. After stabilization, rapidly resolvable causes are addressed
immediately. Causes that can be treated rapidly include pneumothorax, pain,
and CNS depression related to medications. If the cause cannot be readily
resolved, the patient may require mechanical ventilation while treatment is
rendered. Although patients with hypoventilation often require supplemental
oxygen, it is important to remember that oxygen alone will not correct the
problem.
Respiratory Alkalosis
Primary central disorders
Hyperventilation syndrome, anxiety
Cerebrovascular disease
Meningitis, encephalitis
Pulmonary disease
Interstitial fibrosis
Pneumonia
Pulmonary embolism
Pulmonary edema (some patients)
Hypoxia
Septicemia, hypotension
Hepatic failure
Drugs
Salicylates
Nicotine
Xanthines
Progestational hormones
53 DR: TAGHRID SAID
High altitude
Mechanical ventilators
Management
Treatment of respiratory alkalosis centers on resolving the underlying problem.
Patients presenting with respiratory alkalosis have dramatically increased work
of breathing and must be monitored closely for respiratory muscle fatigue.
When the respiratory muscles become exhausted, acute respiratory failure may
ensue.
Selected mixed and complex acid-base disturbances
Disorder Characteristics Selected situations
Respiratory acidosis in pH 4) Cardiac arrest
with metabolic acidosis in HCO3 5) Intoxications
in PaCO2 6) Multi-organ failure
(combined)
Respiratory alkalosis in pH 1. Cirrhosis with diuretics
with metabolic alkalosis in HCO3- 2. Pregnancy with vomiting
in PaCO2 3. Over ventilation of COPD
(combined)
Resp. acidosis with pH normal 1. COPD with diuretics, vomiting,
metabolic alkalosis in PaCO2, NG suction
in HCO3- 2. Severe hypokalemia
(Mixed)
Respiratory alkalosis pH normal 1. Sepsis
with metabolic acidosis in PaCO2 2. Salicylate toxicity
in HCO3 3. Renal failure with CHF or pn.
(Mixed) 4. Advanced liver disease
pH normal
Metabolic acidosis with HCO3- normal Uremia or ketoacidosis with
metabolic alkalosis vomiting, NG suction, diuretics.
54 DR: TAGHRID SAID

Base excess/deficit
Base Ecxess(BE): the base required to titrate a blood sample to pH 7.4 at
40 mmHg PaCO2 and 37 C.
BE = HCO3 at pH 7.4 - 24
BE = [HCO3 measured 10 (7.4 pH measured)] - 24
Normal value= 2.5 mmole/L
It measures the amount of metabolic acid or base added to ECF.
PH change of 0.1unit = base(HCO3) change of 7meq /l
Using base excess for bicarbonate therapy:
HCO3= 0.1 -BE wt in kg (ignoring minus sign)
Also HCO3= 0.1 wt (24 - HCO3)
However it cannot specify or quantify the type and amount of added acids.
Blood with large buffering capacity: significant changes in acid content with
little change in free H+ concentrations (pH)
Acidemia or alkalemia: i.e buffering capacity > potential for pH change from
any given change in H+ content
Buffering capacity depends on: [HCO3-]; RBC mass; other factors
Base excess/deficit= (measured pH predicted pH) x 100 x 2/3
1. Normal metabolic acid-base status: + 3 mmol/L
2. Relatively balanced metabolic acid-base status 5 mmol/L
3. Clinically significant imbalance: + 10 mmol/L
Metabolic Acidosis Anion Gap
Artificial disparity between major plasma cations & anions that are
routinely measured
Anion Gap = major plasma cations major plasma anions
Anion Gap = [Na+] [(Cl-) + (HCO3-)] =12 + 2 (normal)
Minor cations: K+, Ca++

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Minor anions: phosphates, sulfates, organic anions
Anion gap acidosis it is process of increases minor anions
ex. lactatemia, ketonemia, renal failure, excessive organic salt treatment,

dehydration, ingestion (salicylates, methanol, ethylene glycol, paraldehyde)
~ process which decreases minor cations rare!
Non-anion gap acidosis : associated with increased plasma Cl- that has replaced
HCO3-
~ ex. GIT loss of HCO3- (diarrhea), renal wasting of HCO3- (RTA), ingestion
of acids, parenteral hyperalimentation, carbonic anhydrase inhibitors
Selected etiologies of metabolic acidosis
o Elevated anion gap :

o Methanol intoxication
o Uremia
a
o Diabetic ketoacidosis , alcoholic ketoacidosis, starvation ketoacidosis
o Paraldehyde toxicity
o Isoniazid
a
o Lactic acidosis
Type A: tissue ischemia
Type B: Altered cellular metabolism
b b
o Ethanol or ethylene glycol intoxication
o Salicylate intoxication
o Most common causes of metabolic acidosis with an elevated anion gap
o Frequently associated with an osmolal gap
o Normal anion gap: will have increase in [Cl-]

o GI loss of HCO3-
Diarrhea, ileostomy, proximal colostomy, ureteral diversion
o Renal loss of HCO3-
proximal RTA
carbonic anhydrase inhibitor (acetazolamide)
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o Renal tubular disease

ATN
Chronic renal disease
Distal RTA
Aldosterone inhibitors or absence
NaCl infusion, TPN, NH4+ administration
These are the processes that classically make up the differential diagnosis of
an elevated anion gap metabolic acidosis. The mnemonic KUSEMALE may or
may not be helpful
Additional RuThe HCO3 normally falls 1 for every 1 increase in anion gap, with
the exception of sepsis.
This is a critical relationship for interpreting complex acid-base disorders.
Sometimes called the delta-delta, any elevation in the anion gap above 12
should result in a commensurate drop in the HCO3.
The Anions of Sepsis HPLC studies have failed to identify the anions
responsible for the AG in sepsis.
Lactate accounts for a portion.
H+ is likely from ATP hydrolysis which drives the fall in bicarbonate and is
not coupled to lactate production.
Sepsis is an exception to this rule, and the reasons for this remain poorly
understood.
What Lowers Anion Gap? Hypoalbuminemia
Lithium
Myeloma
Since albumin is the major unmeasured anion, when its levels are low, the
anion gap decreases. In fact this relationship is predictable: for every
1g/dl that albumin is decreased below 4.0 g/dl, the anion gap should
decrease by 2.5mmol/L. Therefore the upper limit of the anion gap for a
patient with a serum albumin of 2.0 would be 12 (2.5 X 2) = 7 Lithium is
an unmeasured cation. Just as unmeasured anions increase the anion
gap, unmeasured cations decrease it. Halide intoxication is rare but can
57 DR: TAGHRID SAID

lead to spectacularly elevated serum chloride levels and a huge negative

anion gap. Bromide is the most common halide to cause this syndrome.
In multiple myeloma there are elevated levels of abnormal paraproteins.
Unlike albumin, however, these paraproteins are positively charged, and
thus, like lithium, are unmeasured cations that lower the anion gap.
pH = 7.20, HCO3=10, PCO2=25
Na=140, Cl=110
diagnosis
The pH is low so the patient is acidemic. The HCO3 is low, so this is a
metabolic acidosis. The anion gap is 20, so this is an anion gap metabolic
acidosis. We know from the mnemonic that a fall of one by the HCO3
should result in a fall in 1 by the pCO2. As the HCO3 is down 14 and the
pCO2 is down 15, the respiratory response is appropriate. We also know
that the anion gap is elevated by 8, so the HCO3 should be down by 8.
Since 24 8 = 16, and the HCO3 is actually all the was down to 10, there
MUST also be a NON-GAP metabolic acidosis present. diagnosis
AG Met acid and
Non-AG met acid
DDx of NonAG Met Acid
USED CARSUreterosigmoidostomy / Fistulae
Saline
Early Renal Failure
Diarrhea
CAI
AAs
RTA
Supplements
The differential diagnosis is non-anion gap (normal anion gap) metabolic
acidosis is remeberd by an actual mnemonic! CAI refers to carbonic
anhydrase inhibitors such as acetazolamide. Interestingly, chronic adrenal
insufficiency (another CAI) can also result in a mild, non-gap metabolic
acidosis. AAs refers to amino acids as with TPN, an uncommon problem in
the modern era of close monitoring. Supplements refers to herbals that
patients sometimes take that may have this effect.
58 DR: TAGHRID SAID
Urine Anion GapUAG = Na+ + K+ - Cl-

largely reflects NH4+ and therefore is usually negative due to renal
ammoniagenesis
In non-AG metabolic acidosis, a negative UAG implies extra-renal cause of
the disorder.
If positive, renal ammoniagenesis is likely impaired.
The urinary anion gap is used to distinguish whether the cause of a non-
gap metabolic acidosis is due to a renal or extra-renal defect. A negative
urinary anion gap reflects a non-renal cause such a high distal GI tract
losses. pH = 7.35, HCO3=19, PCO2=35
Na=140, Cl=100
The pH shows the patient to be acidemic and the HCO3 is low, indicating a
metabolic acidosis. The HCO3 and the pCO2 are both down by 5, so the
respiratory response is appropriate. The anion gap is 21, hence elevated
by 9. By the delta-delta rule, the HCO3 should also be down by 9, but it
is only down by 5. diagnosis AG
metabolic acidosis and metabolic alkalosis
Hence there must be a competing metabolic alkalosis.
pH = 7.31, HCO3=15, PCO2=30
Na=138, Cl=112
diagnosis
Thus you have diagnosed a TRIPLE ACID-BASE disorder.
pH = 7.38, HCO3=14, PCO2=23
Na=138, Cl=95
The pH is just slightly acidemic, and the HCO3 is low so this is a metabolic
acidosis. The HCO3 is down by 10, so the pCO2 should be also down by
10.. It is down by 17, so there is a respiratory alkalosis present. The anion
gap is 29, hence elevated by 17, so there is an elevated anion gap acidosis.
By the delta-delta rule, the HCO3 should also be down by 17. It is only
down by 10, so there must be a metabolic alkalosis present as well.
diagnosis AG metabolic acidosis
and metabolic alkalosis and respiratory alkalosis
VOILA! Another triple acid-base disorder deciphered.
pH = 7.40, HCO3=24, PCO2=40
59 DR: TAGHRID SAID

Na=140, Cl=96
diagnosisThe pH is normal, as are the HCO3 and pCO2. BUT, the anion gap is
20, elevated by 8. Thus there is a metabolic acidosis present. According to
the delta-delta rule, the HCO3 should be down by 8. IT is not so there has
to be an offsetting metabolic alkalosis present to result in the normal HCO3.
diagnosis AG metabolic acidosis and
Metabolic alkalosis A double acid-base disorder that is invisible
unless you calculate the anion gap.
pH = 7.40, HCO3=24, PCO2=40
Na=140, Cl=104
OK everything looks normal here even the anion gap, which is 12.
pH = 7.40, HCO3=24, PCO2=40
Na=140, Cl=104, albumin=1.1
Oops. We know that the upper level of the normal range for the anion
gap drops by 2.5 for every 1g/dl drop in albumin from 4.0. Thus the upper
level of the anion gap for this patient would be 12 (3 x 2.5) = 4.5. Thus
the anion gap of 12 represents an elevation of 7.5, and the HCO3 should
be down by that amount. As in the last example, this implies the
presence of an offsetting metabolic alkalosis.
For every 1.0 g/dl that the serum albumin is below 4.0, the upper limit of
the anion gap is decreased by 2.5
Normal upper limit = 12
Alb 3.0 upper limit = 9.5
Alb 2.0 upper limit = 7.0
Alb 1.9 upper limit = 4.5Oops. We know that the upper level of the normal
range for the anion gap drops by 2.5 for every 1g/dl drop in albumin from
4.0. Thus the upper level of the anion gap for this patient would be 12 (3 x
2.5) = 4.5. Thus the anion gap of 12 represents an elevation of 7.5, and the
HCO3 should be down by that amount. As in the last example, this implies
the presence of an offsetting metabolic alkalosis.
pH = 7.40, HCO3=24, PCO2=40
Na=140, Cl=104, albumin=1.1
60 DR: TAGHRID SAID

Oops. We know that the upper level of the normal range for the anion
gap drops by 2.5 for every 1g/dl drop in albumin from 4.0. Thus the upper
level of the anion gap for this patient would be 12 (3 x 2.5) = 4.5. Thus
the anion gap of 12 represents an elevation of 7.5, and the HCO3 should
be down by that amount. As in the last example, this implies the
presence of an offsetting metabolic alkalosis.
Diagnosis: Anion Gap Metabolic
Acidosis Metabolic Alkalosis
Another invisible disorder uncovered with careful analysis for the patients
lab values.
Dogmatic StatementYou cannot interpret arterial blood gases without
looking at the electrolytesBe sure to check the albumin as well.
Summary Metabolic Acidosis: 1 HCO3 => 1 PCO2
Metabolic : 10 HCO3 => 7 PCO2
Acute Resp Acid: 10 PCO2 = 1 HCO3
Chronic Resp Acid: 10 PCO2 = 4 HCO3
Acute Resp Alk: 10 PCO2 => 2 HCO3
Chronic Resp Alk: 10 PCO2 => 5 HCO3
But dont forget to check the anion gap and the serum albumin!
61 DR: TAGHRID SAID

When a primary respiratory disorder is present:-
1. If the process is acute; the pH value should change approximately 0.08 units for
each 10 mm Hg change in Pco2.
2. If the process is chronic, the kidneys compensate (by retaining or losing HCO3)
and blunt the pH change in response to any change in Pco2.
3. The resulting change in pH when the respiratory disorder is chronic is slightly

different for acidosis versus alkalosis.
1. With a chronic respiratory acidosis, the expected pH decrease is

approximately 0.03 for each 10 mm Hg increase in Pco2.
2. With a chronic respiratory alkalosis, the expected pH increase is

approximately 0.02 for each 10 mm Hg decrease in Pco2.
4. If the pH value does not move in the appropriate direction for the Pco2 change,
then a metabolic disorder is the primary disorder.
5. An alkalotic pH (7.44) indicates the presence of :-
a) a primary respiratory alkalosis

b) a metabolic alkalosis
c) or both.
6. An acidotic pH (7.36) indicates the presence of:-
a. a primary respiratory acidosis
b. a metabolic acidosis
c. Or both.
7. Look at Pco2.
a. A high Pco2 (44) indicates that a respiratory acidosis is present
62 DR: TAGHRID SAID

b. A low Pco.2 (36) indicates that a respiratory alkalosis is present.
3. A low pH value with a low Pco2 indicates a primary metabolic acidosis with
respiratory compensation.
4. A high pH value with a high Pco2 can indicate a primary metabolic alkalosis
with secondary suppression of respiratory drive.
5. However, in many patients the latter pattern of a high pH value with a high
Pco2 often represents a complex acid-base disturbance, such as a chronic
compensated respiratory acidosis with a superimposed primary metabolic
alkalosis (e.g., as a result of diuretics, vomiting, or nasogastric suction).
6. To determine whether there has been appropriate respiratory compensation

for a primary metabolic disorder, a rough guideline is that Pco2 should
approximate the last two digits of the pH value.
7. For example, a Pco2 of 25 mm Hg accompanying a pH value of 7.25 indicates

appropriate respiratory compensation for a primary metabolic acidosis.
8. However, the degree of compensatory hyperventilation (i.e., lowering of

Pco2) for a metabolic acidosis tends to be more predictable than the degree
of compensatory hypoventilation (i.e., CO2 retention) accompanying a
Causes of Metabolic Alkalosis
1. Hypokalemia*
2. Ingestion of large amounts of alkali or licorice
3. Gastric fluid loss: Vomiting, NG suctioning*
4. Hyperaldosteronism 20 to nonadrenal factors
Bartters syndrome
Inadequate renal perfusion
diuretics (inhibiting NaCl reabsorption)*
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5. Bicarbonate administration
Sodium bicarbonate overcorrection

Blood transfusion
6. Adrenocortical hypersecretion (e.g tumor)
7. Steroids*
8. Eucapnic ventilation posthypercapnia
64 DR: TAGHRID SAID

Summary of assessment of acid base status

A. Identify the primary acid base disorder
1. If PH is normal normal acid base status or fully compensated
a) If the PH is normal, the direction of change of pH identifies the disorder
acidosis pH7.4 Alkalosis
2. If PH &PaCO2, are both abnormal, compare the direction:
a) If both change in the same direction primary metabolic disorder
b) If both change in the opposite direction primary respiratory disorder
B. Evaluate compensatory response
3. If there is primary metabolic acidosis: calculate expected PaCO2:
If measured > predicted secondary respiratory acidosis.
If measured < predicted secondary respiratory alkalosis.
4. If there is respiratory acidosis or alkalosis: calculate the PH:
If measured PH is between the expected PH for the acute and chronic
partially compensated respiratory acidosis or alkalosis
8. For respiratory acidosis:
1. if the PH < expected for the acute condition secondary
metabolic acidosis
2. If the PH > expected for the chronic condition secondary
9. For respiratory alkalosis:
10.If the PH > expected for the acute condition secondary metabolic
alkalosis.
11.If the PH < expected for the chronic condition secondary metabolic
acidosis.
5. Evaluate metabolic acidosis:
Estimate the AG: help to identify the cause of MA
Estimate the GAP GAP: help to identify mixed metabolic disorders
65 DR: TAGHRID SAID

1. A 78 year old woman with a history of HTN, A fib, DM, and COPD presents
with severe abdominal pain. On examination she has diffuse severe
tenderness throughout the abdomen, mild wheezes and the following vital
signs:
HR 110 bpm, RR 22/min, T37C, BP 105/70 mmHg Oxygen Saturation of

93% on RA
A blood gas is obtained with a lactate
VBG 7.20/29/33 HCO3 12 Lactate 9
What should you do?
A. Repeat the lactate as an arterial sample
B. Empirically start a bicarbonate drip
C. Intubate for respiratory failure
D. Repeat the sample as arterial, presume a severe lactic

acidemia is present
2. A 30 year old male with a CD4 of 8 presents with dyspnea on exertion. An

ABG is attempted, but the sample obtained is not pulsating and is likely to be
venous.
VBG results are 7.38/35/40 HCO3 23
What should you do?

A. Start empiric corticosteroid therapy
B. Repeat the gas as an arterial sample
C. Send a lactate, urine for ketones, and a repeat chemistry
D. Correct pCO2 by adding a correction factor of 7 mmHg
66 DR: TAGHRID SAID

3. A 29 year old female is struck by a car while crossing the street. She is awake
and alert with normal vital signs and oxygen saturation and a large bruise
across her right flank.
An IV line is placed. Should she get a complete gas or just a lactate? If so,
venous or arterial?
4. A 26 year old male with a history of insulin requiring diabetes presents with
abdominal pain, vomiting once, and polydipsia. He has missed one day of
medication. His glucose is 487 mg/dL
He is mildly tachycardic, RR 24, afebrile, with clear lungs and a soft

abdomen
What should you do?

a. Send an ABG and lactate as he may have a triple acid-base disorder
b. Obtain a urine for ketones, VBG with electrolytes, and repeat as
ABG if necessary
c. Obtain an ABG as he is tachypneic and may have an A-a gradient
d. Correct a venous pH by 0.05 upwards to obtain arterial value
5. An 8 week old male presents in respiratory distress after 2 days of cough and
nasal congestion with poor feeding. His oxygen saturation is 88% on room
air. His lungs sound clear.
What should you do?

a) Presume methemoglobinemia and empirically treat
b) Obtain an arterial sample for MetHgb
c) Consider congenital right to left shunt, sepsis, pneumonia, or
methemoglobinemia and send capillary blood gas
d) Consider broad differential, administer oxygen, obtain cultures, venous
metHgb if no response to oxygen, and ABG
67 DR: TAGHRID SAID

Conclusions
Venous lactate and co-oximetry are clinically valuable alternatives to

arterial samples
paO2 is inadequately assessed with venous sampling
Extremely acidemic venous pH will likely predict severe arterial acidemia
A normal venous pH is likely to exclude severe arterial pH abnormalities
No single equation has been validated to predict arterial from venous

sampling
All decisions must be made with regards to the clinical context of the
patient and whether management would be potentially affected.
68 DR: TAGHRID SAID

References
1. Bowers, B., (2009). Arterial Blood Gas Analysis: An Easy Learning Guide.
Primary Health Care, 19 (7), 11.
2. Coggon, J.M. (2008). Arterial blood gas analysis 1: understanding ABG

reports. Nursing Times, 104 (18), 28-9.
3. Coggon, J.M.(2008). Arterial blood gas analysis: 2: compensatory

mechanisms. Nursing Times, 104 (19), 24-5.
4. Dunford, F. (2009). Book reviews. Arterial blood gas analysis: an easy learning
guide. New Zealand Journal of Physiotherapy, 37 (2), 97.
5. Greaney, B. (2008). Book mark. Arterial blood gas analysis: an easy learning
guide. Emergency Nurse, 16 (7), 6.
6. Lawes, R. (2009). Body out of balance: understanding metabolic acidosis and

alkalosis. Nursing, 39 (11), 50-4.
7. Lynch, F. (2009). Arterial blood gas analysis: implications for nursing.

Paediatric Nursing, 21 (1), 41-4.
8. Palange, P., Ferrazza, A.M.(2009). A simplified approach to the interpretation

of arterial blood gas analysis. Breathe, 6 (1), 15-22
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Arterial Blood Gases 2015

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ARTERIAL BLOOD GASES

PROF/ TAGHRID SAID FARAG

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Basic knowledge about Arterial Blood Gases

ABG: Reflect lung function

(2) DR: TAGHRID SAID

What information ABG provide and what they do not?

The determination of PaO2 and PaCO2 provides useful information about

What is meant by PaO2, SaO2 %, CaO2 , DO2?

(3) DR: TAGHRID SAID

(4) DR: TAGHRID SAID

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Why are ABG samples transported on ice?

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Blood Gas Report

Measured 37.0 0C Measured values

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Standard Bicarbonate: Plasma HCO3 after equilibration to a PCO2 of 40 mm Hg

Base Excess: D base to normalize HCO3 (to 24) with PCO2 at 40 mm Hg

SaO2) oxygen saturation: frequently measured by pulse oximetry

(8) DR: TAGHRID SAID

The Key to Blood Gas Interpretation

1. Oxygen content equation 1. Oxygenation

2. Alveolar gas equation 1. Oxygenation

3. PaCO2 equation 2. Alveolar ventilation

4. Henderson-Hasselbalch equation 3. Acid-base balance

1. Evaluation of the ventilation

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Calculation of alveolar ventilation

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2. An elevated PaCO2 will lower the pH (Henderson-Hasselbalch equation).

A raised PaCO2 reflects reduced alveolar ventilation (type II respiratory failure).

inadequate minute ventilation (VE) (central or pump failure)leading to

Increased dead space ventilation (VD) leading to decreased VA and

(11) DR: TAGHRID SAID

Test Your Understanding

3. A man with severe chronic obstructive pulmonary disease exercises on a

2) VA = VE VD = 10(600) 10 (150) = 6 - 1.5 = 4.5 L/min

3) Exercise increases metabolic CO2 production. People with a normal

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production. As in this example, patients with severe COPD or other forms

200 ml/min x 0.863

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O2 In physical sol. (PaO2) + O2 in chemical combination SaO2 % = Oxygen

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Oxygen content equation

The approximate partial pressures for these

These partial pressures fall slightly in the

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Also CO2 pass from tissue to arterial blood and

(Tissue oxygenation): Transport of oxygen from atmospheric air to tissue

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DO2 (Total O2 delivery ml/min) = COP X CaO2 X 10

So; Oxygen delivery (DO2) to the periphery is determined by:

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Arterial blood venous blood

PO2 O2 CONTENT PO2 O2 CONTENT

Hypoxic hypoxia Decreased Decreased Decreased Decreased

Alveolar Gas Equation

(18) DR: TAGHRID SAID

Pt . On room air breathing FiO2 = 0.21So;

1. What is the PAO2 at sea level in the following circumstances? (Barometric

a) FIO2 = 1.00, PaCO2 = 30 mm Hg

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