arterial blood gas interpritation

Arterial Blood Gas InterpritationMark BromleyPGY-2

Why ABGs?

• Important clinical info

• Quick other labs (i.e. faster than a CBC)

• Fun to interpret

Why Not?• ABG analysis is not without drawbacks.

• It is painful!

• Complications• Local hematoma • Arterial dissection and thrombosis (rarely)

• Technically difficult, particularly in children and elderly patients, and several attempts may be required.

Normal ABG parameters

• pH 7.40

• PCO2 40 mmHg

• [HCO3] 24 mmol/l

• Anion Gap < 12

3 Processes

• Ventilation (CO2)

• Oxygenation (02)

• Acid-Base

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

PaCO2 Equation VCO2 x 0.863

PaCO2 = -----------------

VA

PaCO2 reflects ratio of metabolic CO2 production to alveolar ventilation

VCO2 = CO2 production

VA = VE – VD

VE = minute (total) ventilation

VD = dead space ventilation

0.863 converts units to mm Hg

PaCO2

VCO2

Ventilation

(0.863)=

PaCO2 Blood Alveolar Ventilation>45 mm Hg ------- Hypercapnia ----- Hypoventilation35 - 45 mm Hg –- Eucapnia ---------- Normal ventilation<35 mm Hg ------- Hypocapnia ------- Hyperventilation

PaCO2

CO2 production

Alveolar Ventilation

Hypercapnea

• The only physiologic reason for elevated PaCO2 is inadequate alveolar ventilation (VA) for the body’s CO2 production (VCO2)

• Hypercapnia can arise from insufficient total ventilation, increased dead space, or a combination of the two

Case

• 54 yr female presents with acute SOB

• Post colon resection for a malignant bowel obstruction

• Shortly after returning home from hospital she experienced sudden chest pain worse with inspiration.

Arterial Blood Gas Serum Chemistries Urine Tests

pH: 7.40

pO2 : 80 [Na+]: 136 mEq/L

pCO2: 20 mm Hg [Cl-]: 106 mEq/L

[HCO3-]: 15 mEq\L

Pulmonary Embolus

PaCO2CO2 production

(↑ ↑ ventilation) – (↑dead space)

Alveolar Gas Equation

PAO2 = PIO2 - 1.2 (PaCO2)Alveolar O2 = P Inspired O2 – Arterial CO2 PIO2 = FIO2 (PB – 47 mm Hg)

PIO2 = Inspired O2 (Barometric Pressure – 47 mm Hg)

water vapor pressure at normal body temperature

• This describes the factors that influence O2 in the alveoli

• Almost always,• Alveolar O2 is higher than Arterial O2

Alveolar O2 = P Inspired O2 – Arterial CO2 PIO2 = Inspired O2 (Barometric Pressure – 47mm Hg)

• Thus, when PAO2 ↓, PaO2 ↓

Why do I care?

• If everything else is constant…• as ↑PaCO2 both PAO2 and PaO2 will decrease

• (hypercapnia causes hypoxemia)

• as ↓FIO2 both PAO2 and PaO2 will decrease • (suffocation causes hypoxemia)

• as ↓PB (e.g., with altitude) both PAO2 and PaO2 will decrease • (mountain climbing causes hypoxemia)

P(A-a)O2

the “A-a gradient” • P(A-a)O2 is the alveolar-arterial difference in pO2• It results from gravity-related blood flow changes within

the lungs (normal ventilation-perfusion imbalance)

• PAO2 is always calculated• PaO2 is always measured

P(A-a)O2

the “A-a gradient”

• Normal P(A-a)O2 ranges from @ 5 to 25 mm Hg ORA • (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

• An ↑P(A-a)O2 signifies a problem within the lungs • Exception: right to left cardiac shunts

NON-RESPIRATORY P(A-a)O2

Cardiac 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

• 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 millions of alveolar-capillary units

• Virtually all lung disease lowers PaO2 via V-Q imbalance • i.e. asthma, pneumonia, atelectasis, pulm edema, COPD

• Diffusion barrier is seldom a major cause of low PaO2 • (it can lead to a low PaO2 during exercise)

Case VQ Mis-Match

Case

• 34 Male presents with HA

• Working out of town – sleeping in the shop

• Awoken at 2-3am by an alarm but went back to sleep

• Found by his foreman at about 9am

• Drove back to Calgary but had difficulty staying awake

GASArterial Blood Gas Serum Chemistries Other Tests

pH: 7.40 O2 sat: 97%

pO2: 80 mm Hg

pCO2: 38 mm Hg

[HCO3-]: 24 mEq\L

How much oxygen is in the blood?PaO2 vs. SaO2 vs. CaO2

• OXYGEN PRESSURE: PaO2

• 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

• 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)

• How much hemoglobin is there?

• OXYGEN CONTENT: CaO2

• CaO2 is the only value that incorporates the hemoglobin content (units ml O2/dl)

• Oxygen content can be measured directly or calculated by the oxygen content equation:

• CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)

• Is pO2 the best measure of oxygenation in this case?

Case Continued

Arterial Blood Gas Serum Chemistries Other Tests

pH: 7.36 O2 sat: 97%

pO2: 79 mm Hg

pCO2: 31 mm Hg

SaO2: 53%

COHb: 46%

[HCO3-]: 24 mEq\L

• returned a few hours later with mental confusion

• this time both SaO2 and COHb were measured

• CO has a ‘double-whammy’ effect 1) decreases SaO2 by the amount of COHb present2) 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 • In the presence of excess CO, SaO2 will be

lower than expected from the PaO2

Carbon Monoxide • 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

• Normal %COHb in the blood is 1-2%, from metabolism and small amount of ambient CO • (higher in smokers and traffic-congested areas)

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 150, PaO2 100, pH 7.40, COHb 20%

(2) Hb 120, PaO2 100, pH 7.40, COHb 0

b) (1) Hb 150, PaO2 90, pH 7.20, COHb 5%

(2) Hb 150, PaO2 50, pH 7.40, COHb 0

SaO2 and CaO2: test your understandingAnswers

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 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.

Acid-Base

• Normal serum pH is between 7.36-7.44 • A pH outside 6.8 – 7.8 is incompatible with life• pH is maintained by 3 systems

1) Physiologic buffers2) Lungs3) Kidneys

• Disorders in any of these systems leads to alterations in blood pH

• Methanol poisoning example

Physiologic Buffers

• 1) Bicarbonate-carbonic acid • H+ + HCO3

- ↔ H2CO3 ↔ H2O + CO2

• 2) Blood protein buffers• Hemoglobin

• 3) Bone• Reservoir of bicarb and phosphate

Lungs• ∆ pH sensed by peripheral and central chemoreceptors

• Peripherally (carotid bodies)• Centrally (medulla oblongata)

• ↓ pH• Increased minute ventilation

• Lowers PaCO2

• ↑ pH • Decreased ventilatory effort

• Increases PaCO2

Kidneys• Not involved in acute compensation• After 6hrs of Alkalemia

• Excretion of HCO3-

• Retention of H+

• 6-12hrs Acidosis• Excretion of H+

• Retention of HCO3-

Terminology • Acidemia: blood pH < 7.35• Acidosis: a 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

Terminology

• Alkalemia: blood pH > 7.45• Alkalosis: a primary physiologic

process that, occurring alone, tends to cause alkalemia• i.e.: 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.

Terminology• Primary acid-base disorder: One of the four

acid-base disturbances that is manifested by an initial change in HCO3

- or PaCO2. • 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. • i.e. 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.

[ H+ ] x [ HCO3- ] k1 x H2CO3 k2 x [ CO2 ] x [ H2O ]k2 x [ CO2 ] x [ H2O ][ H+ ] x [ HCO3- ]

[ HCO3- ][ H+ ] X

Henderson without Hassel(balch)

X

Henderson without the Hassel(balch)

[ H+ ][ HCO3- ]

[CO2]

Henderson-Hasselbach

• Henderson's equation shows the relationship between [H+], [HCO3-], and PCO2

• It performs the same function as the more Henderson-Hasselbalch Equation

Acid-Base Disorders

• Respiratory disorders• Alter the serum PaCO2

• Metabolic disorders• Alter the serum HCO3

-

Thanks Marc!

Respiratory Disorders

• ACIDOSIS• Hypoventilation

• Pulmonary pathology• Airway obstruction• Decreased respiratory

drive

• ALKALOSIS• Hyperventilation

• CNS disease• Hypoxemia• Anxiety• Toxic states• Hepatic insufficiency• Assisted ventilation

Thanks Marc!

Metabolic Disorders

• ACIDOSIS

1) Wide gap metabolic acidosis

2) Non-AG metabolic acidosis

•ALKALOSIS

1) Saline responsive

2) Saline resistant

Thanks Marc!

Anion Gap Metabolic Acidosis

• Addition of Acids• or• Creation of Acids

• CAT MUDPILES• Carbon monoxide/cyanide• Alcohol/AKA• Toluene• Methanol• Uremia• DKA• Paraldehyde• INH/Iron• Lactic Acidosis• Ethylene glycol• Salicylates

Thanks Marc!

Normal AG Metabolic Acidosis

• Excessive loss of HCO3-

• OR

• Inability to excrete H+

• HARD UPS• Hyperalimentation/Hyperventilation• Acids/Addison’s/Acetazolamide• RTA• Diarrhea/Dehydration/ Diuretics• Uterosigmoidostomy• Pancreatic fistula or drainage• Saline (large amounts)

Thanks Marc!

Metabolic Alkalosis

• Saline Responsive

• Vomit → lose HCl

• Kidneys try to hang on to H+

• …excrete Na+ instead

• Until, dehydration kicks in → Renin/Aldo

• If we rehydrate we allow the kidneys to work

Saline Responsive

• Vomiting/Gastric Suction

• Diuretics

• Ion-deficient baby formula

• Colonic adenomas (HCl)

• Saline shuts off Renin/Angiotensin/Aldo

Saline Non-Responsive

• Higher up in the cascade• Primary aldosteronism• Exogenous steroids• Adenocarcinoma• Bartter’s Syndrome• Cushing’s disease• Ectopic ACTH

Mixed Acid-Base Disorders• In chronically ill respiratory patients• In renal failure

Metabolic Compensation for Respiratory Disorders

• Compensation PaCO2 : HCO3-

• Acute Resp Acidosis 10:1

• Acute Resp Alkalosis 10:2

• Chronic Resp Acidosis 10:3

• Chronic Resp Alkalosis 10:4

Respiratory Compensation for Metabolic Disorders

• Compensation PaCO2 : HCO3-

• Metabolic Acidosis 1:1

• Metabolic Alkalosis 1: 0.75

“The Corey Slovis approach to

acid-base abnormalities”

Thanks again Marc!

Slovis 6-step approach to ABG

1) Check the numbers

2) Apply the ABG rules

3) Calculate the AG

4) If Acidosis apply the rule of 15 (+/- 2)

5) If Acidosis apply the delta gap (+/- 4)

6) Check the osmolar gap

Check the numbers

• Know your normal values

• Does the blood gas make sense?

• Are there any immediate hints to the diagnosis

The ABG rules

• 1) Is it an Acidosis or Alkalosis• Look at the pH

• 2) Is it Respiratory or Metabolic• Metabolic = pCO2 + pH ∆ in same direction

• Resp = pCO2 + pH ∆ in opposite direction

• 3) Is it a pure respiratory acidosis?

• ↑pCO2 : ↓pH = 1:1

Calculate the AG

• Na – [HCO3 + Cl]

• Normal = 5-12

• Upper limit of normal is 15

What is the Anion Gap?

Cations Anions

Cations Anions

What is the Anion Gap?

Na+ Cl-

HCO3-

K+AcetateHipurate

Mg++Ca++ Lactate

Cations Anions

What elevates the Gap?

Na+

Cl-

HCO3-

K+AcetateHipurateMg++Ca++Lactate

Cations Anions

What lowers the Gap?

Na+ Cl-

HCO3-

K+

Mg++Ca++ Lactatelithium

• Our blood is neutral

• ↑AG = unmeasured cations

• ↓AG = unmeasured anions

Rule of 15

• HCO3 + 15 = pCO2 and pH (last 2 digits)

• Used in acidosis• Derived from Henderson Hasselbalch equation• It predicts what resp compensation will do to the

pCO2 and the pH

• If the Rule is broken then another process other than just resp compensation exists

Rule of 15

• Creates a new set point for the pCO2

• pCO2 appropriate = normal compensation

• pCO2 too low = superimposed primary resp alkalosis

• pCO2 too high = superimposed primary resp acidosis

• Note: as HCO3 falls below 10 you need to use the formula

• HCO3 x 1.5 + 8 = expected pCO2

Examples of rule of 15

• 1) HCO3=20, pCO2=35 pH= 7.35• Pure wide gap metabolic acidosis with an

appropriate 2ndary resp alkalosis

• 2) HCO3=10, pCO2=20 pH= 7.32• pCO2 is too low. Superimposed primary resp

alkalosis

• 3) HCO3=10, pCO2=32 pH= 7.14• pCO2 is too high. Superimposed primary resp

acidosis

Delta Gap

• Checks for “hidden” metabolic process• Based on the 1:1 concept that

↑AG = ↓HCO3

• Upper limit of AG = 15• Normal HCO3 = 24

• Bicarb too high = metabolic alkalosis• Bicarb too low = Non-gap metabolic

acidosis

What is the Delta Gap?

• Looks for other metabolic processes in an elevated AG acidosis

• What happens in an isolated AG acidosis?

• Acid is added → Anion + H+

• H+ + HCO3- ↔ H2CO3 ↔ H2O + CO2

• → Anion + H2O + CO2

• ↑AG = ↓HCO3

• Bicarb too high = metabolic alkalosis• Bicarb too low = Non-gap metabolic acidosis

Examples of delta gap

• AG=22 HCO3=17• ∆AG = 7 and ∆HCO3 = 7 • No hidden process

• AG=24 HCO3=8• ∆AG = 9 and ∆HCO3 = 16• Bicarb too low = additional non-gap MAc

• AG=28 HCO3=20• ∆AG = 13 and ∆HCO3 = 4• Bicarb too high = additional MAlk

Osmolar Gap

• 2Na + BUN + Glucose = calculated gap

• OG = Measured – calculated

• Upper limit of normal is ~10

• If higher consider toxic alcohols

• Remember with EtOH• 2Na + BUN + Glucose + [1.25 x EtOH]

Case 1

20 F presents with lethargy, polydipsia and polyuria

Arterial Blood Gas Lytes Urine Tests

pH: 7.24 Na+: 130 mEq/L pH: 5.0

pCO2: 24 mm Hg K+: 4.5 mEq/L

HCO3-: 10 mEq/L Cl-: 94 mEq/L

Glucose: 32