Arterial Blood Gas Interpretation
Lawrence Martin, MD, FACP, FCCP
Associate Professor of Medicine Case Western Reserve University School of Medicine, Cleveland firstname.lastname@example.org
Information in this slide presentation is adapted from All You Really Need to Know to Interpret Arterial Blood Gases (2nd ed.), by Lawrence Martin, MD, Lippincott, Williams, Wilkins
Normal Arterial Blood Gas Values*
pH PaCO2 PaO2 SaO2 HCO3¯ %MetHb %COHb Base excess CaO2
* At sea level, breathing ambient air ** Age-dependent
7.35 - 7.45 35 - 45 mm Hg 70 - 100 mm Hg ** 93 - 98% 22 - 26 mEq/L < 2.0% < 3.0% -2.0 to 2.0 mEq/L 16 - 22 ml O2/dl
The Key to Blood Gas Interpretation: Four Equations, Three Physiologic Processes
1) 2) 3) 4) PaCO2 equation Alveolar gas equation Oxygen content equation Henderson-Hasselbalch equation
Alveolar ventilation Oxygenation Oxygenation Acid-base balance
These four equations, crucial to understanding and interpreting arterial blood gas data, will provide the structure for this slide presentation.
863 converts VCO2 and VA units to mm Hg
> 45 mm Hg
Condition in blood
State of alveolar ventilation
35 .PaCO2 Equation: PaCO2 reflects ratio of metabolic CO2 production to alveolar ventilation
VCO2 x 0. rate x tidal volume) VD = dead space ventilation (= resp. rate x dead space volume 0.863 ------------------VA
VCO2 = CO2 production VA = VE – VD VE = minute (total) ventilation (= resp.45 mm Hg
< 35 mm Hg
Since alveolar ventilation (VA) equals total or minute ventilation (VE) minus dead space ventilation (VD). The PaCO2 equation shows that the only physiologic reason for elevated PaCO2 is inadequate alveolar ventilation (VA) for the amount of the body’s CO2 production (VCO2).Hypercapnia
VCO2 x 0. hypercapnia can arise from insufficient VE.863 -----------------VA
VA = VE – VD
Hypercapnia (elevated PaCO2) is a serious respiratory problem. increased VD.
. or a combination of both.
VCO2 x 0. respiratory muscle paralysis. central hypoventilation Examples of increased VD leading to decreased VA and increased PaCO2: chronic obstructive pulmonary disease. severe restrictive lung disease (with shallow. rapid breathing)
VA = VE – VD
Examples of inadequate VE leading to decreased VA and increased PaCO2: sedative drug overdose.
and effort cannot be reliably used to predict even a directional change in PaCO2. A patient without respiratory distress can have a high. (Even if VE is measured [respiratory rate x tidal volume]. which is what PaCO2 provides. normal.e. the dead space ventilation. or low PaCO2. i.) There is no predictable correlation between PaCO2 and the clinical picture. you cannot determine the amount of air going to dead space. A patient in respiratory distress can have a high. you cannot determine the VCO2/VA. respiratory rate.Clinical Assessment of Hypercapnia is Unreliable
The PaCO2 equation shows why PaCO2 cannot reliably be assessed clinically. normal. Since you never know the patient's VCO2 or VA. or low PaCO2. depth.
.. In a patient with possible respiratory disease.
e. 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.Dangers of Hypercapnia
Besides indicating a serious derangement in the respiratory system. elevated PaCO2 poses a threat for three reasons:
1) 2) An elevated PaCO2 will lower the PAO2 (see Alveolar gas equation). and as a result will lower the PaO2. An elevated PaCO2 will lower the pH (see Henderson-Hasselbalch equation). (See next slide)
. The higher the baseline PaCO2.g.. the greater it will rise for a given fall in alveolar ventilation.
.PCO2 vs. Alveolar Ventilation
The relationship is shown for metabolic carbon dioxide production rates of 200 ml/min and 300 ml/min (curved lines). (This situation is analogous to the progressively steeper rise in BUN as glomerular filtration rate declines. an increase in carbon dioxide production will result in an increase in PaCO2.) This graph also shows that if alveolar ventilation is fixed. A fixed decrease in alveolar ventilation (x-axis) in the hypercapnic patient will result in a greater rise in PaCO2 (y-axis) than the same VA change when PaCO2 is low or normal.
. What is the PaCO2 of a patient with respiratory rate 10/min. What is the PaCO2 of a patient with respiratory rate 24/min.
tidal volume 600 ml. dead space volume 150 ml. dead space volume 150 ml.PaCO2 and Alveolar Ventilation: Test Your Understanding
tidal volume 300 ml. CO2 production 200 ml/min? The patient shows some evidence of respiratory distress. CO2 production 300 ml/min? The patient shows some evidence of respiratory distress.
2 L/min.6 L/min PaCO2 = 71.4 mm Hg 4.5 = 4.Answers
= 10(600) . Since
minute ventilation is 24 x 300 or 7.1.9 mm Hg
2. VA = VE .5 L/min
. First.863 PaCO2 = ---------------------. you must calculate the alveolar ventilation.6 L/min.863 PaCO2 = ----------------------3.10(150) = 6 . alveolar ventilation is 3.6 L/min.PaCO2 and Alveolar Ventilation: Test Your Understanding . Then
300 ml/min x . and dead space ventilation is 24 x 150 or 3.5 L/min
200 ml/min x .
If his resting PaCO2 is 40 mm Hg and resting VCO2 is 200 ml/min.PaCO2 and Alveolar Ventilation: Test Your Understanding
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. what will be his exercise PaCO2?
patients with severe COPD or other forms of chronic lung disease may not be able to increase their alveolar ventilation. Exercise increases metabolic CO2 production.863 -------------------------.PaCO2 and Alveolar Ventilation: Test Your Understanding .863 ----------------------. his exercise PaCO2 is 300 ml/min x . This patient’s resting alveolar ventilation is 200 ml/min x .32 L/min
.9 mm Hg 4.= 4. As in this example.= 59.32 L/min 40 mm Hg Since CO2 production increased by 50% and alveolar ventilation not at all. 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. resulting in an increase in PaCO2.Answer
* Note: This is the “abbreviated version” of the AG equation. reaching zero when 100% oxygen is inhaled.2” is dropped when FIO2 is above 60%.Alveolar Gas Equation
PAO2 = PIO2 . 47 mm Hg is the water vapor pressure at normal body temperature. the multiplication factor “1. and PIO2 is the partial pressure of inspired oxygen in the trachea
PIO2 = FIO2 (PB – 47 mm Hg)
FIO2 is fraction of inspired oxygen and PB is the barometric pressure.1. In these exercises “1.
Where PAO2 is the average alveolar PO2. In the longer version.2” declines with increasing FIO2. suitable for most clinical purposes.
and PaCO2 and FIO2 are constant. Thus. As a result. from the AG equation:
If FIO2 and PB are constant.2 (PaCO2)
where PIO2 = FIO2 (PB – 47 mm Hg)
Except in a temporary unsteady state. both PAO2 and PaO2 will decrease (mountain climbing leads to hypoxemia). alveolar PO2 (PAO2) is always higher than arterial PO2 (PaO2). If PB decreases (e.
. If FIO2 decreases and PB and PaCO2 are constant.1. PaO2 also decreases. both PAO2 and PaO2 will decrease (suffocation causes hypoxemia). then as PaCO2 increases both PAO2 and PaO2 will decrease (hypercapnia causes hypoxemia). with altitude). whenever PAO2 decreases..g.Alveolar Gas Equation
PAO2 = PIO2 .
PaCO2 = 50 mm Hg c) FIO2 = . Everest in the following circumstances? (Barometric pressure = 253 mm Hg)
a) FIO2 = .40. PaCO2 = 10 mm Hg
. PaCO2 = 30 mm Hg b) FIO2 = . PaCO2 = 40 mm Hg c) FIO2 = . What is the PAO2 at sea level in the following circumstances? (Barometric pressure = 760 mm Hg)
a) FIO2 = 1.
What is the PAO2 on the summit of Mt.Alveolar Gas Equation: Test Your Understanding
1.21. PaCO2 = 40 mm Hg b) FIO2 = 1.00. PaCO2 = 30 mm Hg
2 (30) = 249 mm Hg 2. In parts b and c.21 (253 . Again. using the barometric pressure of 253 mm Hg. a) PAO2 = 1.2 (40) = .00 (713) .47) .2 (10) = 31 mm Hg
.Alveolar Gas Equation: Test Your Understanding .1.2 (50) = 90 mm Hg c) PAO2 = .00.1. The PAO2 on the summit of Mt. the PaCO2 of 30 mm Hg is not multiplied by 1.2 since the FIO2 is 1.40 (713) .1.2.Answers
1. PaCO2 is multiplied by the factor 1.21 (713) . Everest is calculated just as at sea level.47) .40 = 166 mm Hg c) PAO2 = . In part a.00 (253 .5 mm Hg b) PAO2 = 1.30 = 683 mm Hg b) PAO2 = .47) . To calculate PAO2 the PaCO2 must be subtracted from the PIO2.21 (253 . a) PAO2 = .1. the barometric pressure is 760 mm Hg since the values are obtained at sea level.
Normal P(A-a)O2 ranges from @ 5 to 25 mm Hg breathing room air (it increases with age). an elevated P(A-a)O2 signifies some sort of problem within the lungs. Instead.
. and barometric pressure. Except for right to left cardiac shunts. It is commonly called the “A-a gradient.” though it does not actually result from an O2 pressure gradient in the lungs. it results from gravity-related blood flow changes within the lungs (normal ventilation-perfusion imbalance).P(A-a)O2
P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen.
PaO2 is always measured on an arterial blood sample in a “blood gas machine. A higher than normal P(A-a)O2 means the lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries. PAO2 is always calculated based on FIO2.
Physiologic Causes of Low PaO2
Cardiac right-to-left shunt Decreased PIO2 Low mixed venous oxygen content*
Increased Normal Increased
Pulmonary right-to-left shunt Ventilation-perfusion imbalance Diffusion barrier Hypoventilation (increased PaCO2)
Increased Increased Increased Normal
* Unlikely to be clinically significant unless there is right-to-left shunting or ventilation-perfusion imbalance
atelectasis. pneumonia. COPD. asthma. e. Virtually all lung disease lowers PaO2 via V-Q imbalance.g.
A normal amount of ventilation-perfusion (V-Q) imbalance accounts for the normal P(A-a)O2. pulmonary edema.. By far the most common cause of low PaO2 is an abnormal degree of ventilation-perfusion imbalance within the hundreds of millions of alveolar-capillary units. Diffusion barrier is seldom a major cause of low PaO2 (it can lead to a low PaO2 during exercise).
FIO2 0. FIO2 . FIO2 0. PaCO2 15 mm Hg. e) A man with PaO2 80 mm Hg. PaCO2 40 mm Hg.40. calculate the P(A-a)O2
using the abbreviated alveolar gas equation. PaO2 150 mm Hg. FIO2 0. A 44-year-old woman with PaCO2 75 mm Hg. PaCO2 72 mm Hg. A woman in the intensive care unit with PaO2 350 mm Hg.28. FIO2 0. assume PB = 760 mm Hg.P(A-a)O2: Test Your Understanding
3. PaO2 95 mm Hg.21.21. A young. anxious man with PaO2 120 mm Hg. For each of the following scenarios.
.80. Which of these patients is most likely to have lung disease? Do any of the values represent a measurement or recording error?
a) b) c) d) A 35-year-old man with PaCO2 50 mm Hg.
either the central nervous system or chest bellows. P(A-a)O2 = 132 . Hypercapnia is most likely a result of disease elsewhere in the respiratory system. as in this case.2 (15) = 150 . P(A-a)O2 = 225 .95 = 15 mm Hg Despite severe hypoventilation.2 (75) = 200 .40 (760 .120 = 12 mm Hg Hyperventilation can easily raise PaO2 above 100 mm Hg when the lungs are normal.P(A-a)O2: Test Your Understanding Answers to #3
a) PAO2 = .28 (713) . (continued)
.90 = 110 mm Hg. P(A-a)O2 = 110 . PAO2 = .1. so the patient may or may not have a defect in gas exchange. PAO2 = .47) .2 (50) = 225 mm Hg.1.1.150 = 75 mm Hg The P(A-a)O22 is elevated but actually within the expected range for supplemental oxygen at 40%.21 (713) .18 = 132 mm Hg. there is no evidence here for lung disease.
40 = 530 mm Hg (Note that the factor 1.2 (72) = 150 .P(A-a)O2: Test Your Understanding Answers to #3 (cont)
d) PAO2 = . negative P(A-a)O2 can be explained by any of the following: incorrect FIO2.80 = -16 mm Hg A negative P(A-a)O2 is incompatible with life (unless it is a transient unsteady state. P(A-a)O2 = 64 .not the case here).80 (713) .2 is dropped since FIO2 is above 60%)
P(A-a)O2 = 530 .86 = 64 mm Hg.21 (713) .
. incorrect blood gas measurement. such as sudden fall in FIO2 -. or a reporting or transcription error.1. Despite a very high PaO2. the lungs are not transferring oxygen normally. e) PAO2 = .350 = 180 mm Hg
P(A-a)O2 is increased. In this example.
SaO2 and Oxygen Content
Tissues need a requisite amount of oxygen molecules for metabolism. Neither the PaO2 nor the SaO2 tells how much oxygen is in the blood. How much is provided by the oxygen content, CaO2 (units = ml O2/dl). CaO2 is calculated as: CaO2 = quantity O2 bound to hemoglobin + quantity O2 dissolved in plasma (.003 x PaO2)
CaO2 = (Hb x 1.34 x SaO2) +
Hb = hemoglobin in gm%; 1.34 = ml O2 that can be bound to each gm of Hb; SaO2 is percent saturation of hemoglobin with oxygen; .003 is solubility coefficient of oxygen in plasma: .003 ml dissolved O2/mm Hg PO2.
Oxygen Dissociation Curve: SaO2 vs. PaO2
Also shown are CaO2 vs. PaO2 for two different hemoglobin contents: 15 gm% and 10 gm%. CaO2 units are ml O2/dl. P50 is the PaO2 at which SaO2 is 50%. Point “X” is discussed on later slide.
SaO2 – Is it Calculated or Measured?
You always need to know this when confronted with blood gas data. SaO2 is measured in a “co-oximeter.” The traditional “blood gas machine“ measures only pH, PaCO2, and PaO2,, whereas the cooximeter measures SaO2, carboxyhemoglobin, methemoglobin, and hemoglobin content. Newer “blood gas” consoles incorporate a co-oximeter, and so offer the latter group of measurements as well as pH, PaCO2, and PaO2. You should always make sure the SaO2 is measured, not calculated. If SaO2 is calculated from PaO2 and the O2dissociation curve, it provides no new information and could be inaccurate - especially in states of CO intoxication or excess methemoglobin. CO and metHb do not affect PaO2, but do lower the SaO2.
from metabolism and small amount of ambient CO (higher in traffic-congested areas).
CO does not affect PaO2. only SaO2. a product of combustion. all smokers have excess CO in their blood. typically 5 -10%. CO has a “double-whammy” effect on oxygenation: 1) decreases SaO2 by the percentage of COHb present. In the presence of excess CO.
CO binds 200x more avidly to hemoglobin than O2. and 2) shifts the O2dissociation curve to the left. odorless gas. retarding unloading of oxygen to the tissues.
CO is colorless. SaO2 (when measured) will be lower than expected from the PaO2.
.2%. SaO2 and/or COHb must be measured (requires co-oximeter). CO is a major cause of poisoning deaths world-wide. effectively displacing O2 from the heme binding sites. To detect CO poisoning.Carbon Monoxide – An Important Cause of Hypoxemia
Normal percentage of COHb in the blood is 1 .
CO poisoning was missed on the first set of blood gases because SaO2 was not measured!
. carboxyhemoglobin 46%. pH 7. SaO2 on this first set was calculated from the O2dissociation curve as 97%. His first blood gases showed PaO2 80 mm Hg. “X” represents the 2nd set of blood gases for a patient who presented to the ER with headache and dyspnea. this time both SaO2 and COHb were measured (SaO2 shown by “X”): PaO2 79 mm Hg. He was sent out from the ER and returned a few hours later with mental confusion. PaCO2 31 mm Hg.CO Does Not Affect PaO2 – Be Aware!
Review the O2 dissociation curve shown on a previous slide. pH 7.43.36. SaO2 53%. PaCO2 38 mm Hg. and oxygenation was judged normal.
methemoglobinemia. reduced hemoglobin content – anemia a. left-shifted hemoglobin dissociation curve (e. other causes include carbon monoxide poisoning.. from acute alkalosis. excess CO. reduced SaO2 – most commonly from reduced PaO2. mitochondrial poisoning (e. Reduced oxygen delivery to the tissues
3. Decreased tissue oxygen uptake
a.. congestive heart failure b.Causes of Hypoxia
A General Classification
1. reduced cardiac output – shock.g. or rightward shift of the O2-dissociation curve c.g. left-to-right systemic shunt (as may be seen in septic shock)
2. cyanide poisoning) b. reduced PaO2 – usually from lung disease (most common physiologic mechanism: V-Q imbalance) b. or abnormal hemoglobin structure)
. Hypoxemia (= low PaO2 and/or low CaO2)
SaO2. and CaO2 (oxygen content). and is it adequate for the patient?
PaO2 vs. SaO2 vs.
. or oxygen pressure. The other two values . is the least helpful to answer the question about oxygen adequacy in the blood.How much oxygen is in the blood.are more useful for this purpose.SaO2 and CaO2 .
Of these three values. CaO2
The answer must be based on some oxygen value. PaO2. but which one? Blood gases give us three different oxygen values: PaO2.
) Only CaO2 (units ml O2/dl) tells us how much oxygen is in the blood.
OXYGEN SATURATION: SaO2
The percentage of all the available heme binding sites saturated with oxygen is the hemoglobin oxygen saturation (in arterial blood.e. this is because CaO2 is the only value that incorporates the hemoglobin content. Neither the PaO2 nor the SaO2 provide information on the number of oxygen molecules.. the SaO2). (Neither PaO2 nor SaO2 have units that denote any quantity.How much oxygen is in the blood?
PaO2 vs. Note that SaO2 alone doesn’t reveal how much oxygen is in the blood.003 x PaO2)
OXYGEN CONTENT: CaO2
Tissues need a requisite amount of O2 molecules for metabolism. CaO2
OXYGEN PRESSURE: PaO2
Since PaO2 reflects only free oxygen molecules dissolved in plasma and not those bound to hemoglobin. for that we also need to know the hemoglobin content. PaO2 cannot tell us “how much” oxygen is in the blood. i. for that you need to know how much oxygen is also bound to hemoglobin. how much oxygen is in the blood.34 x SaO2) + (. information given by the SaO2 and hemoglobin content. Oxygen content can be measured directly or calculated by the oxygen content equation: CaO2 = (Hb x 1. SaO2 vs.
. PaO2 60.40.SaO2 and CaO2: Test Your Understanding
Below are blood gas results from four pairs of patients. COHb 20% Hb 12. pH 7. COHb 20% Hb 10. COHb 5%
Hb 15. PaO2 100. state which patient.30. (1) or (2). PaO2 90. pH 188.8.131.52. pH 7. is more hypoxemic.20. PaO2 60. pH 7. COHb 10% Hb 15. PaO2 100.40. Units for hemoglobin content (Hb) are gm% and for PaO2 mm Hg. COHb 0
Hb 15. COHb 0 Hb 15. For each letter pair. pH 7.
a) (1) (2) Hb 15. PaO2 50. pH 7. PaO2 100.40. pH 7. COHb 0 Hb 5. PaO2 100. pH 7.
Thus patient (2) is slightly more hypoxemic.87 x 15 x 1.SaO2 and CaO2: Test Your Understanding .83 x 15 x 1.85 x 15 x 1. used in the CaO2 calculation of patient (1). subtracting 5% COHb from this value gives a true SaO2 of 87%.34 = 15. because of severe anemia. patient (1).
.78 x 15 x 1.34 = 6.20 gives an SaO2 of @ 92%.
(1) CaO2 = .5 ml O2/dl (2) CaO2 = . However.7 ml O2/dl (2) CaO2 = .87 x 10 x .78 x 15 x 1.34 = 11. A PaO2 of 50 mm Hg with normal pH gives an SaO2 of 85%.0 ml O2/dl (2) CaO2 = .8 ml O2/dl
The oxygen contents are almost identical.34 = 16.34 = 15.90 x 5 x .7 ml O2/dl
Patient (1) is more hypoxemic. is more hypoxic than patient (2) because of the left-shift of the O2-dissociation curve caused by the excess CO.7 ml O2/dl (2) CaO2 = .1.34 = 15.7 ml O2/dl
Patient (1) is more hypoxemic.1. and therefore neither patient is more hypoxemic.34 = 17.Answers
a) (1) CaO2 = .
(1) CaO2 = .34 = 17.1 ml O2/dl
A PaO2 of 90 mm Hg with pH of 7.98 x 12 x 1.
(1) CaO2 = . with 20% CO.
pH = pK + log
For teaching purposes. the H-H equation can be shortened to its basic relationships:
HCO3pH ~ --------PaCO2
[H+] in nanomoles/L
100 80 50 40 30 20 10
.00 7. a pH change of 1.pH is inversely related to [H+].70 8.10 7.52 7.40 7.00 represents a 10-fold change in [H+]
normal. or high. Alkalemia: blood pH > 7. If the patient also has an alkalosis at the same time.45 Alkalosis: a primary physiologic process that. tends to cause alkalemia.35 Acidosis: a primary physiologic process that. occurring alone. Examples: metabolic alkalosis from excessive diuretic therapy.Acid-base Terminology
Acidemia: blood pH < 7. tends to cause acidemia. Examples: metabolic acidosis from decreased perfusion (lactic acidosis). the resulting blood pH may be low. If the patient also has an acidosis at the same time. respiratory alkalosis from acute hyperventilation. the resulting blood pH may be high. normal. respiratory acidosis from hypoventilation. or low. occurring alone.
the disorder is either MAc (reduced HCO3and acidemia) or MAlk (elevated HCO3.)
Primary acid-base disorder: One of the four acid-base disturbances that is manifested by an initial change in HCO3.or PaCO2 that results from the primary event. uncomplicated MAc the patient will never develop alkalemia. would lead to alkalemia. the latter being a primary disorder that. Compensatory changes are not classified by the terms used for the four primary acid-base disturbances. For example. metabolic alkalosis (MAlk). If PaCO2 changes first. They are: metabolic acidosis (MAc).
Compensation: The change in HCO3. a patient who hyperventilates (lowers PaCO2) solely as compensation for MAc does not have a RAlk. alone.and alkalemia). and respiratory alkalosis (RAlk).Acid-base Terminology (cont. the problem is either RAlk (reduced PaCO2 and alkalemia) or RAc (elevated PaCO2 and acidemia). If HCO3. respiratory acidosis (RAc).changes first. In simple.
this reduction in HCO3.A primary disorder where the first change is a lowering of PaCO2. since it is not a primary process.
Primary Event HCO3↑ pH ~ ------↓ PaCO2 Compensatory Event
↑ pH ~ -------↓ PaCO2
.Primary Acid-base Disorders: Respiratory Alkalosis
Respiratory alkalosis . Compensation (bringing the pH back down toward normal) is a secondary lowering of bicarbonate (HCO3) by the kidneys.is not metabolic acidosis. resulting in an elevated pH.
Primary Acid-base Disorders: Respiratory Acidosis
Respiratory acidosis .is not metabolic alkalosis since it is not a primary process. resulting in decreased pH.A primary disorder where the first change is an elevation of PaCO2. this elevation of HCO3.
Primary Event HCO3↓ pH ~ --------↑PaCO2 Compensatory Event
↓ pH ~ --------↑ PaCO2
. Compensation (bringing pH back up toward normal) is a secondary retention of bicarbonate by the kidneys.
resulting in decreased pH.
Primary Event ↓ HCO3↓ pH ~ -----------PaCO2 Compensatory Event ↓HCO3↓ pH ~ -----------↓ PaCO2
. Compensation (bringing pH back up toward normal) is a secondary hyperventilation. this lowering of PaCO2 is not respiratory alkalosis since it is not a primary process.A primary acid-base disorder where the first change is a lowering of HCO3-.Primary Acid-base Disorders: Metabolic Acidosis
Metabolic acidosis .
↑ HCO3↑ pH ~ ------------
↑HCO3↑ pH ~ --------↑
.Primary Acid-base Disorders: Metabolic Alkalosis
Metabolic alkalosis . resulting in increased pH.A primary acid-base disorder where the first change is an elevation of HCO3-. Compensation is a secondary hypoventilation (increased PaCO2). which is not respiratory acidosis since it is not a primary process. Compensation for metabolic alkalosis (attempting to bring pH back down toward normal) is less predictable than for the other three acidbase disorders.
Normal values for AG may vary among labs.Anion Gap
Metabolic acidosis is conveniently divided into elevated and normal anion gap (AG) acidosis. AG is calculated as AG = Na+ .(Cl. the normal AG is 16 ± 4 mEq/L. so one should always refer to local normal values before making clinical decisions based on the AG.+ CO2)
Note: CO2 in this equation is the “total CO2” measured in the chemistry lab as part of routine serum electrolytes. If AG is calculated using K+. Normal AG is typically 12 ± 4 mEq/L.
. and consists mostly of bicarbonate.
some kidney problems (e. renal tubular acidosis.& ↓ pH
. ketoacidosis.. diuretics. corticosteroids. drug poisonings (e.. severe K+ depletion)
. vomiting Chloride resistant: any hyperaldosterone state (e.g. Cushing’s syndrome.& ↑ pH
Chloride responsive (responds to NaCl or KCl therapy): contraction alkalosis. aspirin..g.Increased anion gap • lactic acidosis. methanol) . interstitial nephritis)
↑ HCO3.Metabolic Acid-base Disorders: Some Clinical Causes
METABOLIC ACIDOSIS ↓HCO3. Bartter’s syndrome. gastric suctioning.Normal anion gap • diarrhea.g. ethylene glycol.
.Respiratory Acid-base Disorders: Some Clinical Causes
RESPIRATORY ACIDOSIS ↑PaCO2 & ↓ pH
Central nervous system depression (e. severe asthma attack. severe pulmonary edema)
↓PaCO2 & ↑ pH
Hypoxemia (includes altitude) Anxiety Sepsis Any acute pulmonary insult (e. mild asthma attack. pulmonary embolism)
.g.g...g.g.. drug overdose) Chest bellows dysfunction (e. myasthenia gravis) Disease of lungs and/or upper airway (e. chronic obstructive lung disease. Guillain-Barré syndrome. early pulmonary edema. pneumonia.
RAc + MAlk.. In renal failure (and other conditions) combined MAlk + MAc is also encountered.g. They can be missed!
. mixed disorders are probably more common than single disorders. Always be on the lookout for mixed acid-base disorders.Mixed Acid-base Disorders are Common
In chronically ill respiratory patients. RAc + Mac. e. Ralk + MAlk.
• Low-serum CO2 indicates metabolic acidosis &/or bicarbonate excretion as compensation for respiratory alkalosis.
• A serum CO2 out of the normal range always represents some type of acid-base disorder (barring lab or transcription error).Tips to Diagnosing Mixed Acid-base Disorders
TIP 1. and CO2. Cl-. • Note that serum CO2 may be normal in the presence of two or more acid-base disorders. Do not interpret any blood gas data for acid-base diagnosis without closely examining the serum electrolytes: Na+. K+. • High-serum CO2 indicates metabolic alkalosis &/or bicarbonate retention as compensation for respiratory acidosis.
45) with a single mild acid-base disorder.Tips to Diagnosing Mixed Acid-base Disorders (cont.12 mEq/L in a patient with sepsis. Single acid-base disorders do not lead to normal blood pH.
.35 .and PaCO2 invariably suggests two or more primary disorders. HCO3.
Example: pH 7.7. Normal pH results from two co-existing and unstable acid-base disorders . PaCO2 20 mm Hg. a truly normal pH with distinctly abnormal HCO3.40. Although pH can end up in the normal range (7.acute respiratory alkalosis and metabolic acidosis.)
for a given change in PaCO2.
.(in mEq/L) for a 10-mm Hg change in PaCO2 resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis). The next slide shows expected changes in pH and HCO3. If the pH or HCO3.is higher or lower than expected for the change in PaCO2.Tips to Diagnosing Mixed Acid-base Disorders (cont)
TIP 3. Simplified rules predict the pH and HCO3. the patient probably has a metabolic acid-base disorder as well.
for a 10-mm Hg change in PaCO2 resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis):
pH ↓ by 0.07 HCO3.↓ by 5
* Units for HCO3.4
pH ↑ by 0.↓ by 2 pH ↑ by 0.08 HCO3.Expected changes in pH and HCO3.are mEq/L
.↑ by 3 .↑ by 1*
pH ↓ by 0.03 HCO3.03 HCO3.
Based on the rule for decrease in HCO3.in the presence of hypocapnia suggests a concomitant metabolic alkalosis. it should be at least 25 mEq/L in this example. pH 7. PaCO2 30 mm Hg. it should be at least 23 mEq/L in this example.in the presence of hypercapnia suggests a concomitant metabolic acidosis. that it is only 22 mEq/L suggests a concomitant metabolic acidosis. HCO3.22 mEq/L.27.26 mEq/L.Predicted changes in HCO3. PaCO2 50 mm Hg.with hypocapnia..g.
a) A normal or slightly low HCO3. HCO3. e. that it is 26 mEq/L suggests a concomitant metabolic alkalosis. Based on the rule for increase in HCO3.g.56.with hypercapnia.for a directional change in PaCO2 can help uncover mixed acid-base disorders. pH 7. A normal or slightly elevated HCO3. e.
and in some cases there may be no or minimal compensation.Tips to Diagnosing Mixed Acid-base Disorders (cont.5 x serum CO2] + (8 ± 2)
In contrast. the numerical value of PaCO2 should be the same (or close to) as the last two digits of arterial pH.)
. This observation reflects the formula for expected respiratory compensation in metabolic acidosis: Expected PaCO2 = [1. In maximally-compensated metabolic acidosis. compensation for metabolic alkalosis (by increase in PaCO2) is highly variable.
Arterial blood gas reveals pH 7.of 23 mEq/L.Acid-base Disorders: Test Your Understanding
1. PaCO2 of 70 mm Hg. HCO3.14. and HCO3. A patient’s arterial blood gas shows pH of 7. How would you characterize his acid-base status?
.35. How would you describe the likely acid-base disorder(s)? 2. PaO2 57 mm Hg. A 45-year-old man comes to the hospital complaining of dyspnea for three days. PaCO2 60 mm Hg.31 mEq/L.
but HCO3.are elevated.Acid-base Disorders: Test Your Understanding . there must be an additional metabolic problem..with increased PaCO2 is another way to uncover an additional metabolic disorder. Most likely this patient has a chronic or partially compensated respiratory acidosis.is elevated more than would be expected from acute respiratory acidosis.should be elevated 3 mEq/L. Also note that with acute CO2 retention of this degree. Because this patient's pH is down 0. Decreased perfusion leading to mild lactic acidosis would explain the metabolic component. Thus a low-normal HCO3. you cannot diagnose an accompanying metabolic disorder.
.05 more than expected for a 30-mm Hg increase in PaCO2. or 0.07 units. Since the patient has been dyspneic for several days it is fair to assume a chronic acid-base disorder. However. pH falls about 0.
2. an acute respiratory acidosis. Without electrolyte data and more history. i.Answers
1. is the problem only acute respiratory acidosis or is there some additional process? For every 10-mm Hg rise in PaCO2 (before any renal compensation). the HCO3. Acute elevation of PaCO2 leads to reduced pH.26. PaCO2 and HCO3.e.
If pH and PaCO2 are both above normal. A normal serum CO2 value indicates there is no acid-base disorder. Normal arterial blood gas values rule out the presence of an acid-base disorder. State whether each of the following statements is true or false. the calculated bicarbonate must also be above normal.
a) b) c) d) Metabolic acidosis is always present when the measured serum CO2 changes acutely from 24 to 21 mEq/L.Acid-base Disorders: Test Your Understanding
3. In acute respiratory acidosis.
.or PaCO2 suggests the presence of two or more acidbase disorders. bicarbonate initially rises because of the reaction of CO2 with water and the resultant formation of H2CO3.
f) g) h)
The compensation for chronic elevation of PaCO2 is renal excretion of bicarbonate. An abnormal serum CO2 value always indicates an acid-base disorder of some type.
A normal pH with abnormal HCO3.
3. a) false
b) true c) true d) true e) false f) true g) false
.Acid-base Disorders: Test Your Understanding .
there is an acid-base disorder. if abnormal. If the anion gap is significantly increased. Examine pH. Check serum CO2. PaCO2.for the obvious primary acidbase disorder and for deviations that indicate mixed acid-base disorders (TIPS 2 through 4). there is a metabolic acidosis.
.Summary: Clinical and Laboratory Approach to Acid-base Diagnosis
Determine existence of acid-base disorder from arterial blood gas and/or serum electrolyte measurements. and HCO3.
Summary: Clinical and Laboratory Approach to Acid-base Diagnosis (cont. aim toward correcting pH into the range of 7. physical exam.7.30 . Remember that co-existing clinical conditions may lead to opposing acidbase disorders. this will usually suffice to correct most acid-base disorders. so that pH can be high when there is an obvious acidosis or low when there is an obvious alkalosis.
Clinical judgment should always apply
. If there is concern that acidemia or alkalemia is life-threatening.)
Use a full clinical assessment (history.52 ([H+] = 50-30 nM/L). other lab data including previous arterial blood gases and serum electrolytes) to explain each acid-base disorder. Treat the underlying clinical condition(s).
Arterial Blood Gases: Test Your Overall Understanding
Case 1. and acid-base balance?
.21 7. His regular medications include a diuretic for hypertension and one aspirin a day. He smokes a pack of cigarettes a day. ventilation.53 37 mm Hg 62 mm Hg 87% HCO3%COHb Hb CaO2 30 mEq/L 7.8% 14 gm% 16.5 ml O2/dl
How would you characterize his state of oxygenation.
FIO2 pH PaCO2 PaO2 SaO2 . A 55-year-old man is evaluated in the pulmonary lab for
shortness of breath.
. the low PaO2 can be attributed to V-Q imbalance.nor hypo-ventilating.
VENTILATION: Adequate for the patient's level of CO2 production.
most likely related to the patient's diuretic. Since
P(A-a)O2 is elevated (approximately 43 mm Hg). in part from the low PaO2 but mainly from elevated carboxyhemoglobin.e. his serum K+ should be checked for hypokalemia.suggest a state of metabolic alkalosis.Arterial Blood Gases: Test Your Overall Understanding
Case 1 . SaO2 is reduced. The arterial oxygen content is adequate..Discussion OXYGENATION: The PaO2 and SaO2 are both reduced on room air. a pulmonary problem.
ACID-BASE: Elevated pH and HCO3. the
patient is neither hyper. i. which in turn can be attributed to cigarettes.
He is breathing oxygen through a nasal cannula at 3 l/min. dyspneic.2 ml O2/dl
How would you characterize his state of oxygenation. ventilation.40 20 mm Hg 1. He was recovering but has just become diaphoretic.0% 80 mm Hg 95% 13. A 46-year-old man has been in the hospital two days with pneumonia.3 gm% 12 mEq/L 17. and acid-base balance?
pH PaCO2 %COHb PaO2 SaO2 Hb HCO3CaO2 7.Arterial Blood Gases: Test Your Overall Understanding
Case 2. and hypotensive.
The oxygen content is adequate. If these changes are of sudden onset.
. and points to significant V-Q imbalance.
ACID-BASE: Normal pH with very low bicarbonate and PaCO2 indicates
combined respiratory alkalosis and metabolic acidosis.
VENTILATION: PaCO2 is half normal and indicates marked
hyperventilation.Arterial Blood Gases: Test Your Overall Understanding
Case 2 .Discussion
OXYGENATION: The PaO2 is lower than expected for someone
hyperventilating to this degree and receiving supplemental oxygen. especially in someone with a documented infection. the diagnosis of sepsis should be strongly considered.
and acid-base balance?
.Arterial Blood Gases: Test Your Overall Understanding
FIO2 pH PaCO2 %COHb PaO2 SaO2 Hb HCO3CaO2 .19 65 mm Hg 1. A 58-year-old woman is being evaluated in the emergency department for acute dyspnea.3 ml O2/dl
How would you characterize her state of oxygenation. ventilation.1 gm% 24 mEq/L 18.21 7.1% 45 mm Hg 90% 15.
is lower than expected from acute respiratory acidosis alone.
. the calculated HCO3.Arterial Blood Gases: Test Your Overall Understanding
Case 3 .Discussion
OXYGENATION: The patient's PaO2 is reduced for two reasons hypercapnia and V-Q imbalance .
VENTILATION: The patient is hypoventilating.the latter apparent from an elevated P(Aa)O2 (approximately 27 mm Hg). ACID-BASE: pH and PaCO2 are suggestive of acute respiratory acidosis
plus metabolic acidosis.
Arterial Blood Gases: Test Your Overall Understanding
Case 4. His respiratory rate is 38/min and he is using accessory breathing muscles.1 mEq/L 100 mEq/L 24 mEq/L
How would you characterize his state of oxygenation. ventilation.
FIO2 pH PaCO2 PaO2 SaO2 HCO3%COHb Hb CaO2 .1% 13 gm% 15.90 7. A 23-year-old man is being evaluated in the emergency room for severe pneumonia. and acid-base balance?
.29 55 mm Hg 47 mm Hg 86% 23 mEq/L 2.8 ml O2/dl Na+ K+ ClCO2 154 mEq/L 4.
indicating severe ventilation-perfusion imbalance. indicating a primary process that is increasing it. However. The patient is hypoventilating despite the presence of tachypnea. and metabolic alkalosis.
The low pH. indicating significant dead-pace ventilation.all point to combined acute respiratory acidosis and metabolic acidosis. metabolic acidosis. possibly from lactic acidosis. This is a dangerous situation that suggests the need for mechanical ventilation. The cause of the alkalosis is as yet undetermined. i. his serum CO2 should be much lower. high PaCO2. and slightly low calculated HCO3. to reflect buffering of the increased acid.. his serum CO2 is near normal.e. In summary: this patient has respiratory acidosis. Anion gap is elevated to 30 mEq/L indicating a clinically significant anion gap (AG) acidosis.Discussion OXYGENATION: VENTILATION:
The PaO2 and SaO2 are both markedly reduced on 90% inspired oxygen.Arterial Blood Gases: Test Your Overall Understanding
Case 4 .
. a metabolic alkalosis in addition to a metabolic acidosis. With an of AG of 30 mEq/L.
Arterial Blood Gas Interpretation
Lawrence Martin. FACP.email@example.com
. Cleveland larry. FCCP
Associate Professor of Medicine Case Western Reserve University School of Medicine. MD.