Arterial Blood Gas Interpretation : Arterial Blood Gas Interpretation Dr Kuldeep A Dalal
Jaslok Hospital and Research Centre
Mumbai The Arterial Blood Gas Report : The Arterial Blood Gas Report Sample analysed within 15 minutes of collection.
Anticoagulated prior to transport
Measurement of pH or H+ ,pCO2 at 37oC with a glass electrode
Bicarbonate is derived from the pH & pCO2
pH = 7.4
H+ = 40nmol/L
pCO2 = 40 mm of Hg
HCO3- = 24 (22 – 26) mmol/L Analysing The Blood gas Report : Analysing The Blood gas Report Step 1:-
Step 1:- Check the validity of the report
Step 2:- Identify the most obvious disorder
Step 3:- Apply the formulae to determine whether compensation is adequate. If not a second disorder coexists.
Step 4:- Calculate the anion gap Normal Arterial Blood Gas Values* : Normal Arterial Blood Gas Values* pH 7.35-7.45
PaCO2 35-45 mm Hg
PaO2 70-100 mm Hg**
HCO3- 22-26 mEq/L
Base excess -2.0 to 2.0 mEq/L
CaO2 16-22 ml O2/dl
* At sea level, breathing ambient air
** Age-dependent The Key to Blood Gas Interpretation:4 Equations, 3 Physiologic Processes : The Key to Blood Gas Interpretation:4 Equations, 3 Physiologic Processes Equation Physiologic Process
1) PaCO2 equation Alveolar ventilation
2) Alveolar gas equation Oxygenation
3) Oxygen content equation Oxygenation
4) Henderson-Hasselbalch equation Acid-base balance Alveolar Gas Equation : Alveolar Gas Equation PAO2 = PIO2 - 1.2 (PaCO2)*
where PAO2 is the average alveolar PO2, 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. 47 mm Hg is the water vapor pressure at normal body temperature.
*Note: This is the ‘abbreviated version’ of the AG equation, suitable for most clinical purposes. In the longer version, the multiplication factor “1.2” declines with increasing FIO2, reaching zero when 100% oxygen is inhaled. In these exercises “1.2” is dropped when FIO2 is above 60%. Alveolar Gas EquationPAO2 = PIO2 - 1.2 (PaCO2)where PIO2 = FIO2 (PB – 47 mm Hg) : Alveolar Gas EquationPAO2 = PIO2 - 1.2 (PaCO2)where PIO2 = FIO2 (PB – 47 mm Hg) Except in a temporary unsteady state, alveolar PO2 (PAO2) is always higher than arterial PO2 (PaO2). As a result, whenever PAO2 decreases, PaO2 does as well. Thus, from the AG equation:
If FIO2 and PB are constant, then as PaCO2 increases both PAO2 and PaO2 will decrease (hypercapnia causes hypoxemia).
If FIO2 decreases and PB and PaCO2 are constant, both PAO2 and PaO2 will decrease (suffocation causes hypoxemia).
If PB decreases (e.g., with altitude), and PaCO2 and FIO2 are constant, both PAO2 and PaO2 will decrease (mountain climbing causes hypoxemia). Alveolar Gas Equation: Test your understanding : Alveolar Gas Equation: Test your understanding 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 Alveolar Gas Equation: Test your understanding - answers : Alveolar Gas Equation: Test your understanding - answers 1.a) PAO2 = 1.00(713) - 30 = 683 mm Hg
b) PAO2 = .21(713) - 1.2(50) = 90 mm Hg
c) PAO2 = .40(713) - 1.2(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 = .21(253 - 47) - 1.2(40) = - 5 mm Hg
b) PAO2 = 1.00(253 - 47) - 40 = 166 mm Hg
c) PAO2 = .21(253 - 47) - 1.2(10) = 31 mm Hg P(A-a)O2 : P(A-a)O2 P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen. It is commonly called the “A-a gradient,” though it does not actually result from an O2 pressure gradient in the lungs. Instead, it results from gravity-related blood flow changes within the lungs (normal ventilation-perfusion imbalance).
PAO2 is always calculated, based on FIO2, PaCO2 and barometric pressure.
PaO2 is always measured, on an arterial blood sample in a ‘blood gas machine’.
Normal P(A-a)O2 ranges from @ 5 to 25 mm Hg breathing room air (it increases with age). A higher than normal P(A-a)O2 means the lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries. Except for right to left cardiac shunts, an elevated P(A-a)O2 signifies some sort of problem within the lungs. Physiologic causes of low PaO2 : Physiologic causes of low PaO2 NON-RESPIRATORY P(A-a)O2Cardiac right to left shunt Increased
Decreased PIO2 NormalLow mixed venous oxygen content* Increased
RESPIRATORYPulmonary right to left shunt IncreasedVentilation-perfusion imbalance IncreasedDiffusion barrier IncreasedHypoventilation (increased PaCO2) Normal
*Unlikely to be clinically significant unless there is right to left shunting or ventilation-perfusion imbalance Ventilation-Perfusion imbalance : Ventilation-Perfusion imbalance A normal amount of ventilation-perfusion (V-Q) imbalance accounts for the normal P(A-a)O2.
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. Virtually all lung disease lowers PaO2 via V-Q imbalance, e.g., asthma, pneumonia, atelectasis, pulmonary edema, COPD.
Diffusion barrier is seldom a major cause of low PaO2 (it can lead to a low PaO2 during exercise). P(A-a)O2: Test your understanding : P(A-a)O2: Test your understanding 3. For each of the following scenarios, calculate the P(A-a)O2 using the abbreviated alveolar gas equation; assume PB = 760 mm Hg. Which of these patients is most likely to have lung disease? Do any of the values represent a measurement or recording error?
a) A 35-year-old man with PaCO2 50 mm Hg, PaO2 150 mm Hg, FIO2 .40.
b) A 44-year-old woman with PaCO2 75 mm Hg, PaO2 95 mm Hg, FIO2 0.28.
c) A young, anxious man with PaO2 120 mm Hg, PaCO2 15 mm Hg, FIO2 0.21.
d) A woman in the intensive care unit with PaO2 350 mm Hg, PaCO2 40 mm Hg, FIO2 0.80.
e) A man with PaO2 80 mm Hg, PaCO2 72 mm Hg, FIO2 0.21. P(A-a)O2: Test your understanding – Answers to #3 : P(A-a)O2: Test your understanding – Answers to #3 a) PAO2 = .40 (760 - 47) - 1.2(50) = 225 mm Hg; P(A-a)O2 = 225 - 150 = 75 mm
The P(A-a)O2 is elevated but actually within the expected range for supplemental oxygen at 40%, so the patient may or may not have a defect in gas exchange.
PAO2 = .28(713) - 1.2(75) = 200 - 90 = 110 mm Hg; P(A-a)O2 = 110 - 95 = 15 mm Hg
Despite severe hypoventilation, there is no evidence here for lung disease. Hypercapnia is most likely a result of disease elsewhere in the respiratory system, either the central nervous system or chest bellows.
c) PAO2 = .21(713) - 1.2(15) = 150 - 18 = 132 mm Hg; P(A-a)O2 = 132 - 120 = 12 mm Hg
Hyperventilation can easily raise PaO2 above 100 mm Hg when the lungs are normal, as in this case.
(continued) P(A-a)O2: Test your understanding – Answer to #3 (continued) : P(A-a)O2: Test your understanding – Answer to #3 (continued) d) PAO2 = .80 (713) - 40 = 530 mm Hg (Note that the factor 1.2 is dropped since FIO2 is above 60%)
P(A-a)O2 = 530 - 350 = 180 mm Hg
P(A-a)O2 is increased. Despite a very high PaO2, the lungs are not transferring oxygen normally.
e) PAO2 = .21 (713) - 1.2(72) = 150 - 86 = 64 mm Hg; P(A-a)O2 = 64 - 80 = -16 mm Hg
A negative P(A-a)O2 is incompatible with life (unless it is a transient unsteady state, such as sudden fall in FIO2 -- not the case here). In this example, negative P(A-a)O2 can be explained by any of the following: incorrect FIO2, incorrect blood gas measurement, or a reporting or transcription error. SaO2 and oxygen content : 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 + quantity O2 dissolved to hemoglobin in plasmaCaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)
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. : 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? : 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 co-oximeter 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 it is calculated from the PaO2 and the O2-dissociation 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. Carbon monoxide – an important cause of hypoxemia : Carbon monoxide – an important cause of hypoxemia Normal %COHb in the blood is 1-2%, from metabolism and small amount of ambient CO (higher in traffic-congested areas)
CO is colorless, odorless gas, a product of combustion; all smokers have excess CO in their blood, typically 5-10%.
CO binds @ 200x more avidly to hemoglobin than O2, effectively displacing O2 from the heme binding sites. CO is a major cause of poisoning deaths world-wide.
CO has a ‘double-whammy’ effect on oxygenation: 1) decreases SaO2 by the amount of %COHb present, and 2) shifts the O2-dissociation curve to the left, retarding unloading of oxygen to the tissues.
CO does not affect PaO2, only SaO2. To detect CO poisoning, SaO2 and/or COHb must be measured (requires co-oximeter). In the presence of excess CO, SaO2 (when measured) will be lower than expected from the PaO2. CO does not affect PaO2 – be aware! : CO does not affect PaO2 – be aware! Review the O2 dissociation curve shown on a previous slide. ‘X’ represents the 2nd set of blood gases for a patient who presented to the ER with headache and dyspnea.
His first blood gases showed PaO2 80 mm Hg, PaCO2 38 mm Hg, pH 7.43. SaO2 on this first set was calculated from the O2-dissociation curve at 97%, and oxygenation was judged normal.
He was sent out from the ER and returned a few hours later with mental confusion; this time both SaO2 and COHb were measured (SaO2 shown by ‘X’): PaO2 79 mm Hg, PaCO2 31 mm Hg, pH 7.36, SaO2 53%, carboxyhemoglobin 46%.
CO poisoning was missed on the first set of blood gases because SaO2 was not measured! Causes of Hypoxia A General Classification : Causes of Hypoxia A General Classification 1. Hypoxemia (=low PaO2 and/or low CaO2)
a. reduced PaO2 – usually from lung disease (most common physiologic mechanism: V-Q imbalance)
b. reduced SaO2 -- most commonly from reduced PaO2; other causes include carbon monoxide poisoning, methemoglobinemia, or rightward shift of the O2-dissociation curve
c. reduced hemoglobin content -- anemia
2. Reduced oxygen delivery to the tissues
a. reduced cardiac output -- shock, congestive heart failure
b. left to right systemic shunt (as may be seen in septic shock)
3. Decreased tissue oxygen uptake
a. mitochondrial poisoning (e.g., cyanide poisoning)
b. left-shifted hemoglobin dissociation curve (e.g., from acute alkalosis, excess CO, or abnormal hemoglobin structure) How much oxygen is in the blood, and is it adequate for the patient? PaO2 vs. SaO2 vs. CaO2 : How much oxygen is in the blood, and is it adequate for the patient? PaO2 vs. SaO2 vs. CaO2 The answer must be based on some oxygen value, but which one? Blood gases give us three different oxygen values: PaO2, SaO2, and CaO2 (oxygen content).
Of these three values, PaO2, or oxygen pressure, is the least helpful to answer the question about oxygen adequacy in the blood. The other two values -- SaO2 and CaO2 -- are more useful for this purpose. How much oxygen is in the blood?PaO2 vs. SaO2 vs. CaO2 : How much oxygen is in the blood?PaO2 vs. SaO2 vs. CaO2 OXYGEN PRESSURE: PaO2
Since PaO2 reflects only free oxygen molecules dissolved in plasma and not those bound to hemoglobin, PaO2 cannot tell us “how much” oxygen is in the blood; for that you need to know how much oxygen is also bound to hemoglobin, information given by the SaO2 and hemoglobin content.
OXYGEN SATURATION: SaO2
The percentage of all the available heme binding sites saturated with oxygen is the hemoglobin oxygen saturation (in arterial blood, the SaO2). Note that SaO2 alone doesn’t reveal how much oxygen is in the blood; for that we also need to know the hemoglobin content.
OXYGEN CONTENT: CaO2
Tissues need a requisite amount of O2 molecules for metabolism. Neither the PaO2 nor the SaO2 provide information on the number of oxygen molecules, i.e., how much oxygen is in the blood. (Neither PaO2 nor SaO2 have units that denote any quantity.) Only CaO2 (units ml O2/dl) tells us how much oxygen is in the blood; this is because CaO2 is the only value that incorporates the hemoglobin content. Oxygen content can be measured directly or calculated by the oxygen content equation:
CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2) SaO2 and CaO2: test your understanding : SaO2 and CaO2: test your understanding Below are blood gas results from four pairs of patients. For each letter pair, state which patient, (1) or (2), is more hypoxemic. Units for hemoglobin content (Hb) are gm% and for PaO2 mm Hg.
a) (1) Hb 15, PaO2 100, pH 7.40, COHb 20%
(2) Hb 12, PaO2 100, pH 7.40, COHb 0
b) (1) Hb 15, PaO2 90, pH 7.20, COHb 5%
(2) Hb 15, PaO2 50, pH 7.40, COHb 0
c) (1) Hb 5, PaO2 60, pH 7.40, COHb 0
(2) Hb 15, PaO2 100, pH 7.40, COHb 20%
d) (1) Hb 10, PaO2 60, pH 7.30, COHb 10%
(2) Hb 15, PaO2 100, pH 7.40, COHb 15% SaO2 and CaO2: test your understanding - answers : SaO2 and CaO2: test your understanding - answers a) (1) CaO2 = .78 x 15 x 1.34 = 15.7 ml O2/dl
(2) CaO2 = .98 x 12 x 1.34 = 15.8 ml O2/dl
The oxygen contents are almost identical, and therefore neither patient is more hypoxemic. However, patient (1), with 20% CO, is more hypoxic than patient (2) because of the left-shift of the O2-dissociation curve caused by the excess CO.
b) (1) CaO2 = .87 x 15 x 1.34 = 17.5 ml O2/dl
(2) CaO2 = .85 x 15 x 1.34 = 17.1 ml O2/dl
A PaO2 of 90 mm Hg with pH of 7.20 gives an SaO2 of @ 92%; subtracting 5% COHb from this value gives a true SaO2 of 87%, used in the CaO2 calculation of patient (1). A PaO2 of 50 mm Hg with normal pH gives an SaO2 of 85%. Thus patient (2) is slightly more hypoxemic.
c) (1) CaO2 = .90 x 5 x .1.34 = 6.0 ml O2/dl
(2) CaO2 = .78 x 15 x 1.34 = 15.7 ml O2/dl
Patient (1) is more hypoxemic, because of severe anemia.
d) (1) CaO2 = .87 x 10 x .1.34 = 11.7 ml O2/dl
(2) CaO2 = .83 x 15 x 1.34 = 16.7 ml O2/dl
Patient (1) is more hypoxemic. Acid-Base Balance Henderson Hasselbalch Equation : Acid-Base Balance Henderson Hasselbalch Equation [HCO3-]
pH = pK + log ____
For teaching purposes, the H-H equation can be shortened to its basic relationships:
pH – _____ PaCO2 pH is inversely related to [H+]; a pH change of 1.00 represents a 10-fold change in [H+] : pH is inversely related to [H+]; a pH change of 1.00 represents a 10-fold change in [H+] pH [H+] in nanomoles/L
8.00 10 Acid base terminology : Acid base terminology Acidemia: blood pH < 7.35
Acidosis: a primary physiologic process that, occurring alone, tends to cause acidemia, e.g.: metabolic acidosis from decreased perfusion (lactic acidosis); respiratory acidosis from hypoventilation. If the patient also has an alkalosis at the same time, the resulting blood pH may be low, normal or high.
Alkalemia: blood pH > 7.45
Alkalosis: a primary physiologic process that, occurring alone, tends to cause alkalemia. Examples: metabolic alkalosis from excessive diuretic therapy; respiratory alkalosis from acute hyperventilation. If the patient also has an acidosis at the same time, the resulting blood pH may be high, normal or low. Acid base terminology (cont.) : Acid base terminology (cont.) Primary acid-base disorder: One of the four acid-base disturbances that is manifested by an initial change in HCO3- or PaCO2. They are: metabolic acidosis (MAc), metabolic alkalosis (MAlk), respiratory acidosis (RAc), and respiratory alkalosis (RAlk). If HCO3- changes first, the disorder is either MAc (reduced HCO3- and acidemia) or MAlk (elevated HCO3- and alkalemia). If PaCO2 changes first, the problem is either RAlk (reduced PaCO2 and alkalemia) or RAc (elevated PaCO2 and acidemia).
Compensation: The change in HCO3- or PaCO2 that results from the primary event. Compensatory changes are not classified by the terms used for the four primary acid-base disturbances. For example, a patient who hyperventilates (lowers PaCO2) solely as compensation for MAc does not have a RAlk, the latter being a primary disorder that, alone, would lead to alkalemia. In simple, uncomplicated MAc the patient will never develop alkalemia. Primary acid-base disorders- Respiratory alkalosis - : Primary acid-base disorders- Respiratory alkalosis - Respiratory alkalosis - A primary disorder where the first change is a lowering of PaCO2, resulting in an elevated pH. Compensation (bringing the pH back down toward normal) is a secondary lowering of bicarbonate (HCO3) by the kidneys; this reduction in HCO3- is not metabolic acidosis, since it is not a primary process.
Primary Event Compensatory Event
pH – ))))) pH – )))))
9PaCO2 9PaCO2 Primary acid-base disorders- Respiratory acidosis - : Primary acid-base disorders- Respiratory acidosis - Respiratory acidosis - A primary disorder where the first change is an elevation of PaCO2, resulting in decreased pH. Compensation (bringing pH back up toward normal) is a secondary retention of bicarbonate by the kidneys; this elevation of HCO3- is not metabolic alkalosis, since it is not a primary process.
Primary Event Compensatory Event
HCO3- 8 HCO3-
9pH – ))))) 9pH – )))))
8PaCO2 8PaCO2 Primary Acid-Base Disorders - Metabolic acidosis - : Primary Acid-Base Disorders - Metabolic acidosis - Metabolic Acidosis - A primary acid-base disorder where the first change is a lowering of HCO3-, resulting in decreased pH. 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.
Primary Event Compensatory Event
9pH – ))))) 9pH – )))))
PaCO2 9PaCO2 Primary Acid-Base Disorders - Metabolic alkalosis - : Primary Acid-Base Disorders - Metabolic alkalosis - Metabolic alkalosis - A primary acid-base disorder where the first change is an elevation of HCO3-, resulting in increased pH. 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 acid-base disorders.
Primary Event Compensatory Event
8pH – ))))) 8pH – )))))
PaCO2 8PaCO2 Anion Gap : Anion Gap Metabolic acidosis is conveniently divided into elevated and normal anion gap (AG) acidosis. AG is calculated as
AG = Na+ - (Cl- + CO2)
Note: CO2 in this equation is the “total CO2” measured in the chemistry lab as part of routine serum electrolytes, and consists mostly of bicarbonate. Normal AG is typically 12 ± 4 mEq/L. If AG is calculated using K+, the normal AG is 16 ± 4 mEq/L. Normal values for AG may vary among labs, so one should always refer to local normal values before making clinical decisions based on the AG. Metabolic Acid-Base Disorders -- Some clinical causes -- : Metabolic Acid-Base Disorders -- Some clinical causes -- METABOLIC ACIDOSIS 9HCO3- & 9pH
Increased anion gap
lactic acidosis; ketoacidosis; drug poisonings (e.g., aspirin, ethyelene glycol, methanol)
Normal anion gap
diarrhea; some kidney problems, e.g., renal tubular acidosis, intersititial nephritis
METABOLIC ALKALOSIS 8HCO3- & 8pH
Chloride responsive (responds to NaCl or KCl therapy): contraction alkalosis, diuretics; corticosteroids; gastric suctioning; vomiting
Chloride resistant: any hyperaldosterone state, e.g., Cushings’s syndrome; Bartter’s syndrome; severe K+ depletion Respiratory Acid-Base Disorders -- Some clinical causes -- : Respiratory Acid-Base Disorders -- Some clinical causes -- RESPIRATORY ACIDOSIS 8PaCO2 & 9pH
Central nervous system depression (e.g., drug overdose)
Chest bellows dysfunction (e.g., Guillain-Barré syndrome, myasthenia gravis) Disease of lungs and/or upper airway (e.g., chronic obstructive lung disease, severe asthma attack, severe pulmonary edema)
RESPIRATORY ALKALOSIS 9PaCO2 & 8 pH
Hypoxemia (includes altitude)
Any acute pulmonary insult, e.g., pneumonia, mild asthma attack, early pulmonary edema, pulmonary embolism Mixed Acid-base disorders are common : Mixed Acid-base disorders are common In chronically ill respiratory patients, mixed disorders are probably more common than single disorders, e.g., RAc + MAlk, RAc + Mac, Ralk + MAlk.
In renal failure (and other patients) combined MAlk + MAc is also encountered.
Always be on lookout for mixed acid-base disorders. They can be missed! Tips to diagnosing mixed acid-base disorders : Tips to diagnosing mixed acid-base disorders TIP 1. Don’t interpret any blood gas data for acid-base diagnosis without closely examining the serum electrolytes: Na+, K+, Cl- and CO2.
A serum CO2 out of the normal range always represents some type of acid-base disorder (barring lab or transcription error).
High serum CO2 indicates metabolic alkalosis &/or bicarbonate retention as compensation for respiratory acidosis
Low serum CO2 indicates metabolic acidosis &/or bicarbonate excretion as compensation for respiratory alkalosis
Note that serum CO2 may be normal in the presence of two or more acid-base disorders. Tips to diagnosing mixed acid-base disorders (cont.) : Tips to diagnosing mixed acid-base disorders (cont.) TIP 2 . Single acid-base disorders do not lead to normal blood pH. Although pH can end up in the normal range (7.35 - 7.45) with a mild single disorder, a truly normal pH with distinctly abnormal HCO3- and PaCO2 invariably suggests two or more primary disorders.
Example: pH 7.40, PaCO2 20 mm Hg, HCO3- 12 mEq/L, in a patient with sepsis. Normal pH results from two co-existing and unstable acid-base disorders: acute respiratory alkalosis and metabolic acidosis. Tips to diagnosing mixed acid-base disorders (cont.) : Tips to diagnosing mixed acid-base disorders (cont.) TIP 3. Simplified rules predict the pH and HCO3- for a given change in PaCO2. If the pH or HCO3- is higher or lower than expected for the change in PaCO2, the patient probably has a metabolic acid-base disorder as well.
The next slide shows expected changes in pH and HCO3- (in mEq/L) for a 10 mm Hg change in PaCO2 resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis). Expected changes in pH and HCO3- for a 10 mm Hg change in PaCO2 resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis). : Expected changes in pH and HCO3- for a 10 mm Hg change in PaCO2 resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis). ACUTE CHRONIC
pH 9 by 0.07 pH 9 by 0.03
HCO3- 8 by 1* HCO3- 8 by 3-4
pH 8 by 0.08 pH 8 by 0.03
HCO3- 9 by 2 HCO3- 9 by 5
*Units for HCO3- are mEq/L Predicted changes in HCO3- for a directional change in PaCO2 can help uncover mixed acid-base disorders. : Predicted changes in HCO3- for a directional change in PaCO2 can help uncover mixed acid-base disorders. a) A normal or slightly low HCO3- in the presence of hypercapnia suggests a concomitant metabolic acidosis, e.g., pH 7.27, PaCO2 50 mm Hg, HCO3- 22 mEq/L. Based on the rule for increase in HCO3- with hypercapnia, it should be at least 25 mEq/L in this example; that it is only 22 mEq/L suggests a concomitant metabolic acidosis.
b) A normal or slightly elevated HCO3- in the presence of hypocapnia suggests a concomitant metabolic alkalosis, e.g., pH 7.56, PaCO2 30 mm Hg, HCO3- 26 mEq/L. Based on the rule for decrease in HCO3 with hypocapnia, it should be at least 23 mEq/L in this example; that it is 26 mEq/L suggests a concomitant metabolic alkalosis. Tips to diagnosing mixed acid-base disorders (cont.) : Tips to diagnosing mixed acid-base disorders (cont.) TIP 4. In maximally-compensated metabolic acidosis, the numerical value of PaCO2 should be the same (or close to) the last two digits of arterial pH. This observation reflects the formula for expected respiratory compensation in metabolic acidosis:
Expected PaCO2 = [1.5 x serum CO2] + (8 ± 2)
In contrast, compensation for metabolic alkalosis (by increase in PaCO2) is highly variable, and in some cases there may be no or minimal compensation. Acid-base disorders: test your understanding : Acid-base disorders: test your understanding 1. A patient’s arterial blood gas shows pH of 7.14, PaCO2 of 70 mm Hg, and HCO3- of 23 mEq/L. How would you describe the likely acid-base disorder(s)?
2. A 45-year-old man comes to hospital complaining of dyspnea for three days. Arterial blood gas reveals pH 7.35, PaCO2 60 mm Hg, PaO2 57 mm Hg, HCO3- 31 mEq/L. How would you characterize his acid-base status? Acid-base disorders: test your understanding - answers : Acid-base disorders: test your understanding - answers 1. Acute elevation of PaCO2 leads to reduced pH, i.e., an acute respiratory acidosis. However, 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), pH falls about 0.07 units. Because this patient's pH is down 0.26, or 0.05 more than expected for a 30 mm Hg increase in PaCO2, there must be an additional, metabolic problem. Also, note that with acute CO2 retention of this degree, the HCO3- should be elevated 3 mEq/L. Thus a low-normal HCO3- with increased PaCO2 is another way to uncover an additional, metabolic disorder. Decreased perfusion leading to mild lactic acidosis would explain the metabolic component.
2. PaCO2 and HCO3- are elevated, but HCO3- is elevated more than would be expected from acute respiratory acidosis. Since the patient has been dyspneic for several days it is fair to assume a chronic acid-base disorder. Most likely this patient has a chronic or partially compensated respiratory acidosis. Without electrolyte data and more history, you cannot diagnose an accompanying metabolic disorder. Acid-base disorders: test your understanding : Acid-base disorders: test your understanding 3. State whether each of the following statements is true or false.
a) Metabolic acidosis is always present when the measured serum CO2 changes acutely from 24 to 21 mEq/L.
b) In acute respiratory acidosis, bicarbonate initially rises because of the reaction of CO2 with water and the resultant formation of H2CO3.
c) If pH and PaCO2 are both above normal, the calculated bicarbonate must also be above normal.
d) An abnormal serum CO2 value always indicates an acid-base disorder of some type.
e) The compensation for chronic elevation of PaCO2 is renal excretion of bicarbonate.
f) A normal pH with abnormal HCO3- or PaCO2 suggests the presence of two or more acid-base disorders.
g) A normal serum CO2 value indicates there is no acid-base disorder.
h) Normal arterial blood gas values rule out the presence of an acid-base disorder. Acid-base disorders: test your understanding - answers : Acid-base disorders: test your understanding - answers 3. a) false
g) false Summary ) Clinical and laboratory approach to acid-base diagnosis : Summary ) Clinical and laboratory approach to acid-base diagnosis Determine existence of acid-base disorder from arterial blood gas and/or serum electrolyte measurements. Check serum CO2; if abnormal there is an acid-base disorder. If the anion gap is significantly increased there is a metabolic acidosis.
Examine pH, PaCO2 and HCO3- for the obvious primary acid-base disorder, and for deviations that indicate mixed acid-base disorders (TIPS 2 through 4). Summary ) Clinical and laboratory approach to acid-base diagnosis (cont.) : Summary ) Clinical and laboratory approach to acid-base diagnosis (cont.) Use a full clinical assessment (history, physical exam, other lab data including previous arterial blood gases and serum electrolytes) to explain each acid-base disorder. Remember that co-existing clinical conditions may lead to opposing acid-disorders, so that pH can be high when there is an obvious acidosis, or low when there is an obvious alkalosis.
Treat the underlying clinical condition(s); this will usually suffice to correct most acid-base disorders. If there is concern that acidemia or alkalemia is life-threatening, aim toward correcting pH into the range of 7.30-7.52 ([H+] = 50-30 nM/L).
Clinical judgment should always apply Arterial Blood Gases – test your overall understanding : Arterial Blood Gases – test your overall understanding Case 1. A 55-year-old man is evaluated in the pulmonary lab for shortness of breath. His regular medications include a diuretic for hypertension and one aspirin a day. He smokes a pack of cigarettes a day.
FIO2 .21 HCO3- 30 mEq/L
pH 7.53 %COHb 7.8%
PaCO2 37 mm Hg Hb 14 gm%
PaO2 62 mm Hg CaO2 16.5 ml O2
How would you characterize his state of oxygenation, ventilation and acid-base balance? Arterial Blood Gases – test your overall understanding : Arterial Blood Gases – test your overall understanding Case 1 - Discussion.
OXYGENATION: The PaO2 and SaO2 are both reduced on room air. Since P(A-a)O2 is elevated (approximately 43 mm Hg), the low PaO2 can be attributed to V-Q imbalance, i.e., a pulmonary problem. SaO2 is reduced, in part from the low PaO2 but mainly from elevated carboxyhemoglobin, which in turn can be attributed to cigarettes. The arterial oxygen content is adequate.
VENTILATION: Adequate for the patient's level of CO2 production; the patient is neither hyper- nor hypo- ventilating.
ACID-BASE: Elevated pH and HCO3- suggest a state of metabolic alkalosis, most likely related to the patient's diuretic; his serum K+ should be checked for hypokalemia. Arterial Blood Gases – test your overall understanding : Arterial Blood Gases – test your overall understanding Case 2. A 46-year-old man has been in the hospital two days, with pneumonia. He was recovering but has just become diaphoretic, dyspneic and hypotensive. He is breathing oxygen through a nasal cannula at 3 l/min.
PaCO2 20 mm Hg
PaO2 80 mm Hg
Hb 13.3 gm%
HCO3- 12 mEq/L
CaO2 17.2 ml O2
How would you characterize his state of oxygenation, ventilation and acid-base balance? Arterial Blood Gases – test your overall understanding : 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, and points to significant V-Q imbalance. The oxygen content is adequate.
VENTILATION: PaCO2 is half normal and indicates marked hyperventilation.
ACID-BASE: Normal pH with very low bicarbonate and PaCO2 indicates combined respiratory alkalosis and metabolic acidosis. If these changes are of sudden onset the diagnosis of sepsis should be strongly considered, especially in someone with a documented infection. Arterial Blood Gases – test your overall understanding : Arterial Blood Gases – test your overall understanding Case 3. A 58-year-old woman is being evaluated in the emergency department for acute dyspnea.
PaCO2 65 mm Hg
PaO2 45 mm Hg
Hb 15.1 gm%
HCO3- 24 mEq/L
CaO2 18.3 ml O2
How would you characterize her state of oxygenation, ventilation and acid-base balance? Arterial Blood Gases – test your overall understanding : 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, the latter apparent from an elevated P(A-a)O2 (approximately 27 mm Hg).
VENTILATION: The patient is hypoventilating.
ACID-BASE: pH and PaCO2 are suggestive of acute respiratory acidosis plus metabolic acidosis; the calculated HCO3- is lower than expected from acute respiratory acidosis alone.
. Arterial Blood Gases – test your overall understanding : Arterial Blood Gases – test your overall understanding Case 4. A 23-year-old man is being evaluated in the emergency room for severe pneumonia. His respiratory rate is 38/min and he is using accessory breathing muscles.
FIO2 .90 Na+ 154 mEq/L
pH 7.29 K+ 4.1 mEq/L
PaCO2 55 mm Hg Cl- 100 mEq/L
PaO2 47 mm Hg CO2 24 mEq/L
HCO3- 23 mEq/L
Hb 13 gm%
CaO2 15.8 ml O2
How would you characterize his state of oxygenation, ventilation and acid-base balance? Arterial Blood Gases – test your overall understanding : Arterial Blood Gases – test your overall understanding Case 4 - Discussion.
OXYGENATION: The PaO2 and SaO2 are both markedly reduced on 90% inspired oxygen, indicating severe ventilation-perfusion imbalance.
VENTILATION: The patient is hypoventilating despite the presence of tachypnea, indicating significant dead space ventilation. This is a dangerous situation that suggests the need for mechanical ventilation.
ACID-BASE: The low pH, high PaCO2 and slightly low calculated HCO3- all point to combined acute respiratory acidosis and metabolic acidosis. Anion gap is elevated to 30 mEq/L indicating a clinically significant anion gap (AG) acidosis, possibly from lactic acidosis. With an of AG of 30 mEq/L his serum CO2 should be much lower, to reflect buffering of the increased acid. However, his serum CO2 is near normal, indicating a primary process that is increasing it, i.e., a metabolic alkalosis in addition to a metabolic acidosis. The cause of the alkalosis is as yet undetermined. In summary this patient has respiratory acidosis, metabolic acidosis and metabolic alkalosis. Body Acid Production : Body Acid Production * Accidental or purposeful ingestion, ^ Increased in Pathological conditions Buffering Mechanisms in the Body : Buffering Mechanisms in the Body Physicochemical Buffering
CO2/HCO3- buffering system
Biochemical Buffering (metabolism driven)
Plasmalemmal Acid –base flux
Na+ H+ exchangers
Cl- HCO3- exchangers Whole Blood Buffering : Whole Blood Buffering Slide 61: Role of the kidney in Acid base Homeostasis Net acid excretion = Titratable acid + NH4+ - HCO3- 4000 mmol 50 -100 mmol Compensatory Responses : Compensatory Responses Opposes & limits the effect of the primary change of an acid base disturbance on the plasma H+ ion concentration.
Are never complete.
Have well defined limits & a characteristic time course.
Affect the component not involved in the primary change. Estimating Hydrogen ion conc from pH : Estimating Hydrogen ion conc from pH Identifying the Obvious Disorder : Identifying the Obvious Disorder Checking the Compensation : Checking the Compensation Metabolic Acidosis:- pCO2 = 1.5 X HCO3- + 8
Metabolic Alkalosis:- pCO2 = 40 + 0.7 X HCO3- deficit
Acute: HCO3- increases by 1 meq/L for every 10 mm
rise in pCO2
Chronic: HCO3- increases by 3.5 meq/L for every 10
mm rise in pCO2
Acute: HCO3- decreases by 2meq/L for every 10 mm drop in
Chronic: HCO3- decreases by 5meq/L for every 10 mm drop in
pCO2 CASE 1 : CASE 1 A 38 yr. Old male with c/o breathlessness and decreased urine output.
The ABG on room air is as follows-
ABG :pH 7.351
pCO2 22.8 mmHg
pO2 108 mmHg
HCO3 10 mmol/l
S Electrolytes: 135/6.2/104 Solution : Solution Step 1 – H+ ion concentration = 24 X 22.8/10 = 47, which agrees with the pH value of 7.35.
Step 2 – pH = 7.35, HCO3 = 10, therefore metabolic acidosis.
Step 3 – pCO2 = 1.5 X 10 + 8 = 23, which is the same as the measured value of 22.8.
Hence we have an adequate compensation for a simple metabolic acidosis CASE 2 : CASE 2 A 24 yr old woman entered the ED with a broken ankle. She appeared to be in exquisite pain and severely upset.Her vitals were stable,RR: 30 and room air blood gas values were:
ABG :pH 7.55
pCO2 27 mmHg
pO2 105 mmHg
HCO3 23 mmol/l
S Electrolytes: 132/3.8/100 Solution : Solution Step 1 – H+ ion conc = 24 X 27 / 23 = 27.2, which agrees fairly reasonably with the pH of 7.55.
Step 2 - pH = 7.55, pCO2 = 27, therefore the patient has respiratory alkalosis.
Step 3 Expected value for HCO3 = 24 – 2.6 = 21.4, which is close to to the measured value of 23.
Hence the compensation is adequate and this patient has an partially compensated acute respiratory alkalosis. CASE 3 : CASE 3 A 78 yr old man with a long history of symptomatic COPD entered the hospital with a severe LRTI. He was alert and cooperative save the breathlessness.
ABG :pH 7.25
pCO2 90 mmHg
HCO3 38 mmol/l
S Electrolytes: 132/4.6/102 Solution : Solution Step 1 – H+ ion conc = 24 X 90 / 38 = 56, which agrees perfectly with the pH of 7.25.
Step 2 - pH = 7.25, pCO2 = 90, therefore the patient has respiratory acidosis.
Step 3 Expected value for HCO3 = 24 +17.5 = 41.5, which is close to to the measured value of 38.
Hence the compensation is slightly inadequate and this patient has a partially compensated chronic respiratory acidosis. CASE 4 : CASE 4 70 yr. old male, 45 kg, k/c/o motor neuron disease, admitted with h/o cough,fever and breathlessness x 4 days, drowsiness x 1 day
O/E obtunded, P: 110/min, BP:80 systolic, SpO2: 88% ,
RR 32/min, accessory muscles +, AE b/l decreased,
ABG :pH 7.123
pCO2 72 mmHg
pO2 56 mmHg
HCO3 32 mmol/l
What is your diagnosis and interpretation of the blood gas?
How will you manage this patient? Solution : Solution Step 1 – H+ ion conc = 24 X 72 / 32 = 54, which is vastly different from the pH of 7.123.
This ABG is invalid and should not be analysed any further. CASE 4- The next day : CASE 4- The next day ABG :pH 7.679 ventilator settings
pCO2 25 mmHg pressure control 18
pO2 198.4 mmHg PEEP 5
HCO3 30 mmol/l TV 600ml
O2sat 99.8% Min.ventilation 12 l/m
S. electrolytes: 134/2.0 FiO2 0.6
interpretation of the report.
What do you think happened and how would you correct it? Solution : Solution Step 1 – H+ ion conc = 24 X 25 / 30 = 20, which agrees well with the pH of 7.67.
pH = 7.67, pCO2 = 25, hence the patient has respiratory alkalosis,
However the bicarbonate is 30 and therefore there is no compensation, so the patient has a metabolic alkalosis as well.
The expected HCO3 should have been 24 – 1.5 = 22.5, which has not been achieved in the short time duration.
Hence the patient has a mixed acute respiratory and chronic metabolic alkalosis Case 5 : Case 5 A patient with recurrent episodes of small bowel obstruction presents with severe abdominal pain & vomiting. HR = 116/min. BP = 82/54, Urine ketones – negative.
ABG – pH = 7.33, pO2= 76, pCO2 = 35, HCO3- = 18, O2 sat = 96%,
Na+ = 142, K+ = 5.6, Cl- = 89, Ca++ = 10.5. Solution : Solution Step1:- pH = 7.33, HCO3- = 18- Metabolic Acidosis.
Step2:- pCO2 by compensation = 1.5 X 18 + 8 = 35.
Compensation adequate- No respiratory disorder.
Anion gap = 142 – (91 +18) = 33.
Starting HCO3- = 24 - 21 = 3
Actual HCO3- = 18, hence a metabolic alkalosis exists despite the low HCO3-
Therefore a metabolic alkalosis coexists.
This is a mixed disorder. Case 6 : Case 6 A 50 year old woman admitted to hospital with protracted abdominal pain, nausea, & vomiting. Abdominal X-rays revealed an ileus, which resolved with nasogastric suction & IV fluids. Abdominal pain which had initially resolved has now returned. She now has a temperature of 101.6 & BP has fallen from 130/86 to 86/52. Abdomen is very tender & no bowel sounds are present.
Na+ = 140 meq/L, K+ = 4.5, Cl- = 80, HCO3- = 25
pH=7.40, pO2= 100, pCO2 = 40, O2 sat =98%.
What is your diagnosis Solution. : Solution. pH, pCO2 & HCO3- are all normal
Anion gap = 140-(80+25) = 35.
Severe anion gap metabolic acidosis is present
Likely cause:- Lactic acidosis secondary to bowel ischemia and shock.
Change in anion gap = 23
Change in HCO3- = 24 - 23/1.5= 8 = starting HCO3-.
Actual HCO3- = 25.
Therefore masking metabolic alkalosis exists
Probable cause:- Vomiting & nasogastric suction. Case 7 : Case 7 A 17 year old boy with grade IV vesico-ureteric reflux was operated for ureteric reimplantation.
Pre-op BUL = 68, S. Creat = 2.6mg%, Ser Elec 134/4.3, Hb = 7.8, TLC = 8500/mm3, P70 L28 E2.
Intra-operative course smooth, 1 unit packed cells transfused.
Post -op day 3 developed abdominal pain, vomiting & distension
Bowel sounds poor, X-ray abdomen - multiple air fluid levels.
Nasogastric tube inserted , patient kept NBM on IV fluids 500 ml of DNS & RL 6 hrly.
Post op day 4- developed high grade fever , & decreased urine o/p.
Ascitic tap done - protein = 100mg%, LDH = 137, Creat = 3.9, cells = 24/mm3, all polymorhs
Urine & ascitic fluid sent for c/s- fluids decreased to 12 hrly. Slide 81: Day 5 - developed hypotension with BP = 90 systolic. Tachypnoeic .
Had developed a wound gape.
Urine o/p was 700 ml, RTA = 900 ml.
Still had intestinal obstruction,
BUL = 123, Creat = 3.7mg%, Ser Elec = 123/3.6
ABG showed pH = 7.10, pCO2 = 21, HCO3- = 10
Dopamine started. IV Sodabicarb 100ml stat & 50 ml to each drip added.
Antibiotic changed from Cefotaxime to Ceftazidime. Slide 82: Day 6 - Patient was transferred to KEMH
O/E - P =110/min, BP = 70 systolic.
Unhealthy looking abdominal wound with greenish slough.
CVS & RS - NAD.
BUL = 95, Creat = 3.1mg%
ABG - pH = 7.41, pCO2 = 24.5 mm of Hg, pO2 = 88mm of Hg, HCO3- = 14.2 meq/L Ser Na+ = 134meq/L, K+ = 4.3 meq/L Ser Cl- = 90 meq/L Solution to Case 7 : Solution to Case 7 Step 1 - Check the ABG for validity
H+ ion conc = 39 acc to the pH
Using the Henderson equation , H+ ion conc = 42, a reasonably close value hence the ABG is valid.
The anion gap is 134 - 90 - 14.2 = 29.8meq/L
Hence a severe metabolic acidosis exists despite the normal pH.
Possible cause - Sepsis & Renal Failure
Check the compensation- pCO2 = 14 X 1.5 + 8 = 29
The actual pCO2 = 24.5, which is lower.
Hence a second disorder - a respiratory alkalosis exists.
Possible cause - Hyperventilation from fever .
Final Step - Calculate starting Bicarbonate = 24 - 17.6 = 6.4.
Actual Bicarbonate is 14.2, hence a metabolic alkalosis coexists.
Possible cause - Nasogastric sution & volume depletion Case 2 : Case 2 A patient presents with a temperature of 102oF & BP of 80/50 He is diaphoretic, vomiting & tachypnoeic & his urinalysis shows numerous WBCs & bacteria Urine ketones are negative on dipstick.
ABG:- pH = 7.65, pCO2 30mm, pO2 = 54, HCO3- = 32meq/L, O2sat = 93%. Na+ = 128, K+ = 4.1, Cl- = 66. Solution : Solution Step 1:H+ = 24 X 30/32 = 22.5 (ABG valid)
pH = 7.65, HCO3- = 32.- Metabolic Alkalosis
Step2 :- pCO2 = 40 + 8 X 0.7 = 45.6
Actual pCO2 = 30.
Therefore Respiratory Alkalosis coexists.
Anion gap= 128 –(66+32) = 30.
Therefore severe anion gap acidosis coexists!
Starting HCO3- = 24 – 18 = 6
Actual HCO3- = 32, hence a mixed metabolic acidosis & alkalosis are present.
This is a triple disorder. PaCO2 equation: PaCO2 reflects ratio of metabolic CO2 production to alveolar ventilation : PaCO2 equation: PaCO2 reflects ratio of metabolic CO2 production to alveolar ventilation VCO2 x 0.863 VCO2 = CO2 production
PaCO2 = ------------------ VA = VE – VD
VA VE = minute (total) ventilation
VD = dead space ventilation 0.863 converts units to mm Hg
Condition State of
PaCO2 in blood alveolar ventilation
>45 mm Hg Hypercapnia Hypoventilation
35 - 45 mm Hg Eucapnia Normal ventilation
<35 mm Hg Hypocapnia Hyperventilation Hypercapnia : Hypercapnia VCO2 x 0.863
PaCO2 = ------------------
Hypercapnia (elevated PaCO2) is a serious respiratory problem. 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). Since alveolar ventilation (VA) equals total or minute ventilation (VE) minus dead space ventilation (VD), hypercapnia can arise from insufficient VE, increased VD, or a combination. Hypercapnia (continued) : Hypercapnia (continued) VCO2 x 0.863
PaCO2 = ------------------
VA VA = VE – VD
Examples of inadequate VE leading to decreased VA and increased PaCO2: sedative drug overdose; 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) Clinical assessment of hypercapnia is unreliable : Clinical assessment of hypercapnia is unreliable The PaCO2 equation shows why PaCO2 cannot reliably be assessed clinically. Since you never know the patient's VCO2 or VA, you cannot determine the VCO2/VA, which is what PaCO2 provides. (Even if tidal volume is measured, you can’t determine the amount of air going to dead space.)
There is no predictable correlation between PaCO2 and the clinical picture. In a patient with possible respiratory disease, respiratory rate, depth, and effort cannot be reliably used to predict even a directional change in PaCO2. A patient in respiratory distress can have a high, normal, or low PaCO2. A patient without respiratory distress can have a high, normal, or low PaCO2. Dangers of hypercapnia : Dangers of hypercapnia Besides indicating a serious derangement in the respiratory system, elevated PaCO2 poses a threat for three reasons:
1) An elevated PaCO2 will lower the PAO2 (see Alveolar gas equation), and as a result lower the PaO2.
2) An elevated PaCO2 will lower the pH (see Henderson-Hasselbalch equation).
3) 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. (See next slide) PCO2 vs. 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). 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. (This situation is analogous to the progressively steeper rise in BUN as glomerular filtration rate declines.)This graph also shows that, if alveolar ventilation is fixed, an increase in carbon dioxide production will result in an increase in PaCO2. PaCO2 and alveolar ventilation: Test your understanding : PaCO2 and alveolar ventilation: 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, 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, CO2 production 200 ml/min? The patient shows some evidence of respiratory distress. PaCO2 and alveolar ventilation: Test your understanding - answers : PaCO2 and alveolar ventilation: Test your understanding - answers 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 = )))))))))))))))))
PaCO2 = 71.9 mm Hg
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 PaCO2 and alveolar ventilation: Test your understanding : 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. If his resting PaCO2 is 40 mm Hg and resting VCO2 is 200 ml/min, what will be his exercise PaCO2? PaCO2 and alveolar ventilation: Test your understanding - answer : PaCO2 and alveolar ventilation: Test your understanding - answer 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 patient’s resting alveolar ventilation is
200 ml/min x .863
)))))))))))) = 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
))))))))))))) = 59.9 mm Hg