Transcript Manuel Antonio Ko,MD 2008

Arterial Blood Gas
INTERPRETATION
Manuel Antonio Ko, MD
Section of Pulmonary Medicine
Department of Internal Medicine
Makati 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
Steps in ABG Interpretation
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
ABG Normal Values
Parameters
Normal Values (Range)
pH
7.35 - 7.45
pO2
80 - 100 mmHg
pCO2
35 - 45
HCO3-
22 - 26 mmol/l
Base excess
-2 to +2 mmol/l
O2 Saturation
95 to 100 %
Fio2
as indicated
*a/A
0.8
mmHg
* Not available in some ABG Machines
Neutral
pH
H+ / H2CO3
HCO3
CO2
Acidosis
7.35
7.4
Normal Range
Normal
or
Compensated?
7.45
Alkalosis
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
H+ / H2CO3
HCO3
CO2
7.35
7.4
7.45
Normal Range
Uncompensated
or Partly
Compensated
Acidosis
Compensated
Uncompensated
or Partly
Compensated
Alkalosis
Increase PCO2
Decrease PCO2
&/or
&/or
Decrease HCO3
Increase HCO3
Compensation
– 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
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 Disease
Pickwickian Syndrome
Chronic Neuromuscular Disease
Thoracic cage limitation
• Kyphoscoliosis
• Scleroderma
Compensation
– 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
Respiratory Alkalosis
Causes:
1. Increased Central Respiratory Drive:
Anxiety
CNS Infection
Cerebrovascular Accident
Brain 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
Compensation
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
Metabolic Acidosis
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
Normal Anion Gap (Hyperchloremic Acidosis)
A.) Hypokalemia with Metabolic acidosis:
1. Diarrhea/ Vomiting
2. 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
Metabolic Acidosis
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
Compensation
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
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 Syndrome
5. Refeeding alkalosis
Neutral
pH
H+ / H2CO3
HCO3
CO2
7.35
7.4
7.45
Normal Range
Uncompensated
or Partly
Compensated
Acidosis
Compensated
Uncompensated
or Partly
Compensated
Alkalosis
Increase PCO2
Decrease PCO2
&/or
&/or
Decrease HCO3
Increase HCO3
pH
PaCO2
HCO3
Uncompensated
< 7.35
> 45
Normal Range
Partly Compensated
< 7.35
> 45
> 26
Normal Range
> 45
> 26
Uncompensated
> 7.45
< 35
Normal Range
Partly Compensated
> 7.45
< 35
< 22
Normal Range
< 35
< 22
Uncompensated
< 7.35
Normal Range
< 22
Partly Compensated
< 7.35
< 35
< 22
Normal Range
< 35
< 22
Uncompensated
> 7.45
Normal Range
> 26
Partly Compensated
> 7.45
> 45
> 26
Normal Range
> 45
> 26
Respiratory Acidosis
Compensated
Respiratory Alkalosis
Compensated
Metabolic Acidosis
Compensated
Metabolic Alkalosis
Compensated
* Uncompensated = acute
pH
PaCO2
HCO3
Combined Acidosis
<7.35
> 45
< 22
Combined Alkalosis
>7.45
< 35
> 26
Oxygenation Status in ABG
Report
1.
2.
3.
Adequate Oxygenation at Given FiO2
- Pa02 = 80 to 100 mmHg
Hypoxemia at a Given FiO2
- PaO2 < 80 mmHg
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
SaO2
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.) pH
2.) the concentration of 2,3Diphosphoglycerate (2,3-DPG)
3.) the type of hemoglobin
molecules (adult vs fetal types)
4.) the presence of poisons
especially carbon monoxide
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
Determination of Hypoxemia
(Parameters)
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
A-aO2
Alveolar-Arterial Oxygen Tension Difference (PAO2 – PaO2)
 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
NORMAL
PAO2 = 100 mmHg
Alveolar
PO2
(PAO2)
Arterial PO2
(PaO2)
Capillary PO2
O2 Diffusion through the
Capillaries + Physiologic
Shunt
A-aDO2
PaO2 = 80-90mmHg
(lower)
HYPOXEMIA
Type 1 Resp.
Failure
PAO2 = 100 mmHg
Alveolar
PO2
(PAO2)
Disease
Arterial PO2
(PaO2)
Capillary PO2
O2 Diffusion through the
Capillaries + Physiologic
Shunt + hypoxia
Widened A-aDO2
PaO2 = 50 mmHg
(much lower)
HYPOXEMIA
PAO2 = inc. 300
mmHg
Supplemental O2
Alveolar
PO2
(PAO2)
Disease
Capillary PO2
Arterial PO2
(PaO2)
O2 Diffusion through the
Capillaries + Physiologic
Shunt + hypoxia
PaO2 = inc. 75 mmHg
Widened A-aDO2
( but slightly lower than normal)
HYPOVENTILATION
PAO2 already
Decreased
Type 2 hypoxemia
PAO2 = 60mm.Hg
Hypoventilation
Alveolar
PO2
Capillary PaO2
PaO2 = 50 mm Hg – No significant
widening of the AaDO2
Arterial PO2 (PaO2)
HYPERCARBIA
Airway
Obstruction
PACO2 = Decreased
Hypoventilation
Alveolar
PCO2
(PACO2)
Capillary PCO2
Increase PCO2
Arterial or Mixed
Venous PCO2
(PaCO2/ PVCO2)
Determination of Hypoxemia
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
O2 Correction
Desired FiO2
=
Des. PaO2 / (a/A) + PCO2 / 0.8
________________________
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)
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 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 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
Case 1
• 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
ABG and Labs Values
1. Interpret Acid Base Status?
pH
7.29
PCO2
50 mmHg
2. Determine if Hypoxemia
Exists ?
PaO2
59 mmHg
HCO3
17 mmol/L
BE
-3.5
FiO2
40%
SaO2
79%
3. Compute the a-AO2
gradient ?
4. Compute for the desired
FiO2 ?
5. Compute Anion Gap ?
6. Initial Diagnosis?
K
5.0
Na
132
Cl
95
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
Metabolic Acidosis
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
Interpretation
• Combined Respiratory and metabolic
Acidosis
• Inadequate Oxygenation at 40% FiO2
Case 2
• 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
ABG and Labs Values
1. Is this compatible with
the patient’s condition?
pH
7.34
PCO2
46 mmHg
2. Interpret?
PaO2
50 mmHg
HCO3
27 mmol/L
3. How do you confirm the
error ?
BE
+0.5
FiO2
21% room air
SaO2
80%
K
3.9
Na
137
Cl
97
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
PROBLEM
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?
ABG and Labs Values
1. Normal ?
pH
7.37
PCO2
49 mmHg
2. Compensated
Respiratory Alkalosis
PaO2
90 mmHg
HCO3
25 mmol/L
BE
+0.5
FiO2
21% room air
SaO2
97%
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