Arterial Blood GasArterial Blood Gas INTERPRETATIONINTERPRETATION

Manuel Antonio Ko, MDManuel Antonio Ko, MDSection of Pulmonary MedicineSection of Pulmonary Medicine

Department of Internal MedicineDepartment of Internal MedicineMakati Medical CenterMakati Medical Center

Objectives

Learn how to systematically interpret Arterial

Blood Gas results

Identify the different causes of abnormalities in

the ABG results

Problem solving exercises

Indications for Arterial Blood Gas Determination

• Evaluate Ventilatory, Oxygenation, Acid

Base and Oxygen carrying capacity of

blood

• Monitor severity and disease progression

• Quantify patient’s response to therapeutic intervention and or diagnostic evaluation

Respircare, 1992, 317

1. Determine Acid Base Status (Acidotic or Alkalotic – pH Levels)

2. Identify the cause of the Acid Base Imbalance (Respiratory or Metabolic)

3. Determine compensation

4. Identify the Presence of Hypoxemia Correction of Hypoxemia

5. Report Interpretation

Steps in ABG Interpretation

ABG Normal Values

Parameters Normal Values (Range)

pH 7.35 - 7.45

pO2 80 - 100 mmHg

pCO2 35 - 45 mmHg

HCO3- 22 - 26 mmol/l

Base excess -2 to +2 mmol/l

O2 Saturation 95 to 100 %

Fio2 as indicated

*a/A 0.8

* Not available in some ABG Machines

Neutral pH

7.47.35 7.45Acidosis AlkalosisNormal Range

H+ / H2CO3

CO2

HCO3

Normal

or

Compensated?

ABG Normal Values

Parameters Normal Values (Range)

pH 7.35 - 7.45

pO2 80 - 100 mmHg

pCO2 35 - 45 mmHg

HCO3- 22 - 26 mmol/l

Base excess -2 to +2 mmol/l

Base Excess – quick eye view of the adequacy of the buffer mechanism. If there is more than enough HCO3 to balance the pH (compensation)

Neutral pH

7.47.35 7.45

Acidosis Alkalosis

Normal Range

H+ / H2CO3

CO2

HCO3

Compensated

Uncompensated or Partly

Compensated

Uncompensated or Partly

Compensated

Increase PCO2

&/or

Decrease HCO3

Decrease PCO2

&/or

Increase HCO3

– Acute Respiratory Acidosis • PaCO2 increase by 10 mmHg decreases pH

0.08 • Bicarbonate increases 1 meq/L per 10 mmHg

PaCO2 rise

– Chronic Respiratory Acidosis • PaCO2 increase by 10 mmHg decreases pH

0.03 • Bicarbonate increases 4 meq/L per 10 mmHg

PaCO2 rise

Compensation

Acute Respiratory Acidosis Causes:

1. Central Nervous System Depression Sedative Medications (e.g. Benzodiazepines) Cerebrovascular Accident Head Trauma

2. Neuromuscular Disease Myasthenia Gravis Guillain-Barre Polio Muscular Dystrophy Hypokalemia

3. Impaired lung motion Pleural Effusion Pneumothorax Crush injury

Acute Respiratory Acidosis

Causes:

4. Acute airway obstruction Foreign Body Aspiration Tumor Laryngospasm (e.g. Croup, Epiglottitis) Bronchospasm (e.g. Asthma, COPD)

5. Acute Respiratory Disease Severe Pneumonia Pulmonary edema

Chronic Respiratory Acidosis

Causes:

Chronic Obstructive Pulmonary DiseasePickwickian Syndrome Chronic Neuromuscular Disease Thoracic cage limitation

• Kyphoscoliosis• Scleroderma

– Acute Respiratory Alkalosis • PaCO2 decreases by 10 mmHg increases pH by

0.08 • Bicarbonate decreases 2 meq/L per 10 mmHg

PaCO2 fall

– Chronic Respiratory Alkalosis • PaCO2 decrease by 10 mmHg increases pH by

0.03

• Bicarbonate decreases 4 meq/L per 10 mmHg PaCO2 fall

Compensation

Respiratory Alkalosis Causes:

1. Increased Central Respiratory Drive:

Anxiety CNS Infection Cerebrovascular AccidentBrain tumor Head Trauma Medications

(Salicylates, Nicotine, Aminophylline, Progesterone, Cathecolamines)

Fever Sepsis (especially with Gram Negative Bacteria) Pregnancy Liver failure, Cirrhosis or Hepatic Encephalopathy Hyperthyroidism

Respiratory Alkalosis Causes:

2. Increased Chemoreceptor Stimulation

Anemia Carbon Monoxide Poisoning Pulmonary edema Pneumonia Pulmonary Embolism High altitude (decreased FIO2) Restrictive lung disease (early)

3. Iatrogenic with Mechanical Ventilation

Metabolic Acidosis

– PaCO2 decreased

PaCO2 drops 1.2 mmHg per 1 meq/L bicarbonate fall

Calculated PaCO2 = 1.5 x HCO3 + 8 (+/- 2)

Measured PaCO2 discrepancy: respiratory disorder

Useful in High Anion Gap Metabolic Acidosis

Compensation

Elevated Anion Gap Acidosis

• Anion Gap Definition

– Difference between calculated serum anions and

cations

• Calculation

– AG = Serum Na – (Serum Cl + Serum HCO3)

• Interpretation

– Normal Anion Gap: 12 +/- 2 meq/L

Metabolic Acidosis

Elevated Anion Gap Acidosis (Mnemonic: "MUD PILERS") causes:

Methanol Intoxication Uremia Diabetic Ketoacidosis (DKA) or starvation ketosis Paraldehyde, Phenformin Isopropyl Alcohol, Isoniazid Lactic Acidosis Ethylene Glycol, ethyl alcohol Rhabdomyolysis Salicylates Other Causes: Hyperalbuminemia, administered anions

Metabolic Acidosis

Normal Anion Gap (Hyperchloremic Acidosis)

A.) Hypokalemia with Metabolic acidosis: 1. Diarrhea/ Vomiting2. Ureteral diversion

– Uretero-sigmoidostomy – Ileal bladder – Ileal ureter

3. Renal Tubular Acidosis (proximal or distal) *4. Mineralocorticoid Deficiency

– Angiotensin Deficiency: Liver Failure – ACE Inhibitor – Renin Deficiency

» Aging » Extracellular fluid volume expansion » Lead » Beta Blockers » Prostaglandin Inhibitor » Methyldopa

5. Carbonic Anhydrase Inhibitor – Acetazolamide – Mefenamic acid

6. Post-hypocapnia

Normal Anion Gap (Hyperchloremic Acidosis)

B.) (Hyperkalemic or normal Potassium) Metabolic Acidosis

1. Renal Failure (Early)*

2. Renal Disease* – SLE Interstitial Nephritis – Amyloidosis – Hydronephrosis – Sickle Cell Nephropathy

3. Acidifying agents – Ammonium Chloride – Calcium Chloride – Arginine

4. Sulfur toxicity

Metabolic Acidosis

Metabolic Alkalosis

Serum HCO3 increased » PaCO2 increased » PaCO2 rises 6 mmHg per 10 meq/L

bicarbonate rise » Expected PaCO2 = 0.7 x HCO3 + 20

(+/- 1.5) – discrepancy = Respiratory component

» Excess Anion Gap >30 mEq/L

Compensation

Metabolic Alkalosis

Causes: A. Low Urine Chloride <10 meq/L 1.Gastrointestinal causes

• Vomiting • Nasogastric suction • Chloride-wasting Diarrhea • Villous adenoma of colon

2. Renal Causes • Diuretic use (Urine Chloride <20 meq/L) • Poorly reabsorbable anion

– Carbenicillin

– Penicillin

– Sulfate

– Phsophate

• Post-Hypercapnia

Metabolic Alkalosis Causes:

A. Low Urine Chloride <10 meq/L 3.Exogenous alkali

• Sodium Bicarbonate (baking soda) • Sodium Citrate • Lactate • Gluconate • Acetate • Transfusion • Antacid

4. Cystic Fibrosis 5. Achlorhydria 6. Contraction alkalosis

Metabolic Alkalosis Causes: B. Normal or High Urine Chloride >20 meq/L

1. Hypertensive Patient a. Adrenal Disease

– Primary Hyperaldosteronism – Cushing's Syndrome (Pituitary, Adrenal or ectopic) – Liddle Syndrome

b. Exogenous steroids – Excess mineralocorticoid intake – Excess glucocorticoid intake – Excessive licorice intake – Carbenoxalone – Glycyrrhizic acid – Chewing Tobacco

2. Normotensive Patient 1. Bartter Syndrome or Gitelman Syndrome 2. Hypokalemia 3. Excessive alkali administration 4. Milk-Alkali Syndrome5. Refeeding alkalosis

Neutral pH

7.47.35 7.45

Acidosis Alkalosis

Normal Range

H+ / H2CO3

CO2

HCO3

Compensated

Uncompensated or Partly

Compensated

Uncompensated or Partly

Compensated

Increase PCO2

&/or

Decrease HCO3

Decrease PCO2

&/or

Increase HCO3

pH PaCO2 HCO3

Respiratory AcidosisRespiratory Acidosis

Uncompensated < 7.35 > 45 Normal Range

Partly Compensated < 7.35 > 45 > 26

Compensated Normal Range > 45 > 26

Respiratory AlkalosisRespiratory Alkalosis

Uncompensated > 7.45 < 35 Normal Range

Partly Compensated > 7.45 < 35 < 22

Compensated Normal Range < 35 < 22

Metabolic AcidosisMetabolic Acidosis

Uncompensated < 7.35 Normal Range < 22

Partly Compensated < 7.35 < 35 < 22

Compensated Normal Range < 35 < 22

Metabolic AlkalosisMetabolic Alkalosis

Uncompensated > 7.45 Normal Range > 26

Partly Compensated > 7.45 > 45 > 26

Compensated Normal Range > 45 > 26

* Uncompensated = acute

pH PaCO2 HCO3

Combined Acidosis<7.35 > 45 < 22

Combined Alkalosis>7.45 < 35 > 26

Oxygenation Status in ABG

Report

1. Adequate Oxygenation at Given FiO2

- Pa02 = 80 to 100 mmHg

2. Hypoxemia at a Given FiO2

- PaO2 < 80 mmHg

3. More Than Adequate Oxygenation at a Given FiO2

- PaO2 > 100 mm Hg

Respiratory Components in ABG

• PaO2 – Partial Pressure of Arterial Oxygen

- NV: 80-100mmHG

• PCO2 – Partial Pressure of Carbon Dioxide

- NV: 35-45 mmHg

• SaO2 – Oxygen Saturation in the Blood

The oxygen-hemoglobin dissociation curve plots the proportion of hemoglobin in its saturated form on the vertical axis against the prevailing oxygen tension on the horizontal axis. It is usually a sigmoid plot. Hemoglobin molecules can bind up to four oxygen molecules in a reversible way. Many factors influence the affinity of this binding and alter the shape of the curve including:

1.) pH2.) the concentration of 2,3-Diphosphoglycerate (2,3-DPG)3.) the type of hemoglobin molecules (adult vs fetal types)4.) the presence of poisons especially carbon monoxide

SaO2

Hypoxemia in ABG

• Inadequate oxygenation

• Pa02 < 80 at a given level of FiO2 - FiO2 (Fraction of Inspired O2)

- 21% at room air ( proportion of O2 in

the atmosphere )

Respiratory Failure

A. Type 1 – Hypoxemia without CO2 retention (Normal PCO2)

ex.: Pulmonary Edema, Pneumonia

B. Type 2 – There is CO2 retention (Increased PCO2)

ex.: Hypoventilation (reduced alveolar ventilation)

pump failure, airway obstruction, neuromuscular

weakness

C. Combined

1. Partial Pressure of Alveolar Oxygen

PAO2

2. Partial Pressure Difference between Alveolar and Arterial O2

A-aDO2

3. a/A Ratio (NV: 0.8)

a/A ratio

Determination of Hypoxemia

(Parameters)

PaO2 is generally lower than PAO2

- Physiologic shunt ( unoxygenated blood coming from the coronary arteries draining

into the Thebesian Veins and parts of the Bronchial Arteries both draining directly

into the Pulmonary Veins and bypassing the gas exchange mechanism of the lungs +

diffusion of O2 to the alveolar capillaries)

Widens when there is pulmonary shunting (Pneumonia, edema & etc.).

Also widens when on supplemental oxygen ( more accurate when calculated at room air)

Minimal or no widening if the problem is pure hypoventilation

1

A-aO2Alveolar-Arterial Oxygen Tension Difference (PAO2 – PaO2)

PAO2 = 100 mmHg

Alveolar PO2

(PAO2)

Arterial PO2 (PaO2)Capillary PO2

PaO2 = 80-90mmHg (lower)

O2 Diffusion through the Capillaries + Physiologic

Shunt

A-aDO2

NORMAL

PAO2 = 100 mmHg

Alveolar PO2

(PAO2)

Arterial PO2 (PaO2)Capillary PO2

PaO2 = 50 mmHg (much lower)

O2 Diffusion through the Capillaries + Physiologic

Shunt + hypoxia

Widened A-aDO2

Disease

HYPOXEMIA

Type 1 Resp. Failure

PAO2 = inc. 300 mmHg

Alveolar PO2

(PAO2)

Arterial PO2 (PaO2)Capillary PO2

PaO2 = inc. 75 mmHg

( but slightly lower than normal)

O2 Diffusion through the Capillaries + Physiologic

Shunt + hypoxia

Widened A-aDO2

Disease

Supplemental O2

HYPOXEMIA

PAO2 already Decreased

PAO2 = 60mm.Hg

Alveolar PO2

Capillary PaO2

Hypoventilation

HYPOVENTILATION

Type 2 hypoxemia

Arterial PO2 (PaO2)

PaO2 = 50 mm Hg – No significant widening of the AaDO2

PACO2 = Decreased

Alveolar PCO2

(PACO2)

Arterial or Mixed Venous PCO2

(PaCO2/ PVCO2)Capillary PCO2

Increase PCO2

Airway Obstruction

Hypoventilation

HYPERCARBIA

1. Partial Pressure of Alveolar Oxygen

PAO2 = PiO2 – PCO2/0.8

(PiO2 = 713 X FiO2)

2. Partial Pressure Difference between Alveolar and Arterial O2

A-aD02 = PAO2 – PaO2

3. a/A Ratio (NV: 0.8)

a/A = PaO2/PAO2

Determination of Hypoxemia

Des. PaO2 / (a/A) + PCO2 / 0.8Desired FiO2 = ________________________

713

1. Desired PaO2 – 80 to 100 mmhg

2. (713) – Atmospheric pressure – water vapor pressure [ constant ]

3. PCO2 – Partial Pressure Carbon Dioxide

4. (0.8) – Respiratory Quotient ( volume of CO2 produced/ volume of O2 consumed ) [ constant ]

5. a/A – PaO2 (Arterial O2) / PAO2 (Alveolar O2)

O2 Correction

P/F Ratio

PaO2/ Fio2 (simple estimate)

• Indicates range of hypoxemia• P/F ratio > or equal 400 - Normal• P/F ratio < 400 - Hypoxemia

Giving O2 Supplement

• Supplemental O2 conversion

- LPM Oxygen = LPM x 4 + 20 ( Fi02)

ex: 2 (LPM O2) x 4 + 20 = 28% FiO2

(using O2 cannula, O2 mask)

(O2 supplementation is not provided by direct FiO2)

Conditions invalidating or modifying ABG ResultsConditions invalidating or modifying ABG Results

A. Large Air bubbles not expelled from sample:

PaO2 rises 0-30 mmHg PaCO2 may fall slightly

B. Fever or Hypothermia:

Patient temperature shifts oxy-hemoglobin curve

C. Hyperventilation or breath holding (due to anxiety):

Conditions invalidating or modifying ABG ResultsConditions invalidating or modifying ABG Results

D. Delayed analysis:

1. Iced Sample maintains values for 1-2 hours

2. Un-iced sample quickly becomes invalid

PaCO2 rises 3-10 mmHg/hour PaO2 falls at a rate related to initial value pH falls modestly

E. Excessive Heparin:

1. Dilutional effect on results

2. Decreases bicarbonate and PaCO2

• 65 year old male, seen at the ER, diagnosed case of Chronic Renal Failure presently undergoing Hemodialysis. He was placed on Multivent Mask at 40% FiO2. Chest X-ray shows Increase Broncho-vascular markings with concomitant interstitial and alveolar infiltrates on the Right Lower Lobe

PPE:• T= 37.8, RR: 26, BP: 90/60, CR: 115• Pale skin and Diaphoretic• Use of accessory muscle and abdominal breathing pattern

observed• fine crackles on the right lower lung fields with expiratory

wheezes all over • bipedal edema noted

Case 1

ABG and Labs Values

pH 7.29

PCO2 50 mmHg

PaO2 59 mmHg

HCO3 17 mmol/L

BE -3.5

FiO2 40%

SaO2 79%

K 5.0

Na 132

Cl 95

1. Interpret Acid Base Status?

2. Determine if Hypoxemia Exists ?

3. Compute the a-AO2 gradient ?

4. Compute for the desired FiO2 ?

5. Compute Anion Gap ?

6. Initial Diagnosis?

7. What are your immediate plans for the patient ?

pH PaCO2 HCO3

Combined Acidosis<7.35 > 45 < 22

Combined Alkalosis>7.45 < 35 > 26

Acute Respiratory Acidosis

Causes:

4. Acute airway obstruction Foreign Body Aspiration Tumor Laryngospasm (e.g. Croup, Epiglottitis) Bronchospasm (e.g. Asthma, COPD)

5. Acute Respiratory Disease

Severe Pneumonia Pulmonary Edema

Elevated Anion Gap Acidosis

• Anion Gap Definition

– Difference between calculated serum anions and

cations

• Calculation

– AG = Serum Na – (Serum Cl + Serum HCO3)

• Interpretation

– Normal Anion Gap: 12 +/- 2 meq/L

Metabolic Acidosis

Elevated Anion Gap Acidosis (Mnemonic: "MUD PILERS") causes:

Methanol Intoxication

Uremia Diabetic Ketoacidosis (DKA) or starvation ketosis Paraldehyde, Phenformin Isopropyl Alcohol, Isoniazid Lactic Acidosis Ethylene Glycol, ethyl alcohol Rhabdomyolysis Salicylates Other Causes: Hyperalbuminemia, administered anions

Metabolic Acidosis

Interpretation

• Combined Respiratory and metabolic Acidosis

• Inadequate Oxygenation at 40% FiO2

• 25 year old female, seen at the ER, diagnosed case of Asthma, who complained of difficulty of breathing 2 days ago but apparently she is feeling much better now after inhaling bronchodilators. Past Medical History is unremarkable except for Asthma. She went to the ER because of persistent coughing. Chest X-ray is normal

PPE: • T= 36.8, RR: 14, BP:110/70, CR: 70• Her breath sounds are clear• She refuses to receive supplemental oxygen• Someone, for some reason, ordered an ABG and the results showed

Case 2

ABG and Labs Values

pH 7.34

PCO2 46 mmHg

PaO2 50 mmHg

HCO3 27 mmol/L

BE +0.5

FiO2 21% room air

SaO2 80%

K 3.9

Na 137

Cl 97

1. Is this compatible with the patient’s condition?

2. Interpret?

3. How do you confirm the error ?

Problem

• Compensated Respiratory Acidosis with hypoxemia at room air (21% FiO2)

• Determine O2 sat by Pulse Oximeter

• SaO2 = SpO2 +/- 4% (difference)

• Probably Mixed Venous Blood Sample obtained

ABG and Labs Values

pH 7.37

PCO2 49 mmHg

PaO2 90 mmHg

HCO3 26 mmol/L

BE +0.5

FiO2 21% room air

SaO2 97%

1. Interpret?

PROBLEM

ABG and Labs Values

pH 7.37

PCO2 49 mmHg

PaO2 90 mmHg

HCO3 25 mmol/L

BE +0.5

FiO2 21% room air

SaO2 97%

1. Normal ?

2. Compensated Respiratory Alkalosis

3. Consider PCO2 levels instead ?(directly measured over HCO3 which is only estimated by machine calculation)

4. Have sample repeated (Consider Error) ?

THANK YOU

for your attention