![----- XXXX Diagnostics ------
Blood Gas Report
Measured37.0
o
C
pH 7.463
pCO2 44.4 mm Hg
pO2 113.2 mm Hg
Corrected38.6
o
C
Calculated Data
HCO3 act 31.1 mmol / L
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 CT 14.7 mL / dl
O2 Sat 98.3 %
t CO2 32.4 mmol / L
pO2 (A - a) 32.2 mm Hg
pO2 (a / A) 0.79
Entered Data
Temp 38.6 oC
ct Hb 10.5 g/dl
FiO2 30.0 %
Bicarbonate is calculated on the basis of the
Henderson equation:
[H
+
] = 24 pCO2 / [HCO3
-
]
Bicarbonate:](https://image.slidesharecdn.com/abgseminar-161019103518/85/Arterial-Blood-Gas-Interpretation-17-320.jpg)
![PaO2 (Partial pressure of arterial oxygen)
PaO2 is dependant upon Age, FiO2, Patm
As Age the expected PaO2
• PaO2 = 109 - [0.4 (Age)]
• Normal PaO2: 75-100 mmHg
As FiO2 the expected PaO2
• Alveolar Gas Equation:
• PAO2= (PB-P h2o) x FiO2- pCO2/R
O
X
Y
G
E
N
A
T
I
O
N
PAO2 = partial pressure of oxygen in alveolar gas, PB = barometric pressure
(760mmHg), Ph2o = water vapor pressure (47 mm Hg), FiO2 = fraction of
inspired oxygen, PCO2 = partial pressure of CO2 in the ABG, R = respiratory
quotient (0.8)](https://image.slidesharecdn.com/abgseminar-161019103518/85/Arterial-Blood-Gas-Interpretation-22-320.jpg)
![----- XXXX Diagnostics ------
Blood Gas Report
Measured37.0
o
C
pH 7.463
pCO2 44.4 mm Hg
pO2 113.2 mm Hg
Corrected38.6
o
C
Calculated Data
HCO3 act 31.1 mmol / L
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 CT 14.7 mL / dl
O2 Sat 98.3 %
t CO2 32.4 mmol / L
pO2 (A - a) 32.2 mm Hg
pO2 (a / A) 0.79
Entered Data
Temp 38.6 oC
ct Hb 10.5 g/dl
FiO2 30.0 %
Oxygenation:
O2 Content of blood:
Hb x O2 Sat x 1.34 + Dissolved O2 (given by
Pao2x0.003)
Useful in oxygen transport calculations
Derived from calculated saturation
Oxygen Saturation:
Ideally measured by co-oximetry
Calculated values may be error-prone
Alveolar / arterial gradient:
Hypoxemia causes differentiated by A-a Gradien
Estimate of normal A–a gradient <[age in years/4] + 4
An abnormally increased A–a gradient suggests :
• Defect in diffusion
• V/Q (ventilation/perfusion ratio) mismatch
• right-to-left shunt
Normal A-a Gradient:
• Hypoventilation
Neuromuscular disorders
Central nervous system disorder
• Low inspired FIO2 (e.g. high altitude)
Arterial / alveolar ratio:
Remains stable with change in FIO2
Low a/A (<0.6) = Shunt , V/Q mismatch, diffusion defect](https://image.slidesharecdn.com/abgseminar-161019103518/85/Arterial-Blood-Gas-Interpretation-25-320.jpg)
![Alveolar-arterial Difference
Inspired O2 = 21%= piO2 = (760-45) x .21=150 mmHg ( So at room air PiO2=150 mmHg)
O2
CO2
palvO2 = piO2 - pCO2 / RQ
= 150 - 40/0.8
= 150 – 50 = 100 mm Hg( Calculated)
partO2 = 90 mmHg (Measured)
(palvO2- partO2 )D = 10 mmHg (Normal= =<[age in years/4] + 4)](https://image.slidesharecdn.com/abgseminar-161019103518/85/Arterial-Blood-Gas-Interpretation-26-320.jpg)
![If the pH and the [H+] are inconsistent, the ABG is probably not valid.
[H+] = 24(PaCO2)
[HCO3-]
H+ ion (mmol/L) pH
100 7.00
79 7.10
63 7.20
50 7.30
45 7.35
40 7.40
35 7.45
32 7.50
25 7.60
STEP0: Is this ABG Authentic?](https://image.slidesharecdn.com/abgseminar-161019103518/85/Arterial-Blood-Gas-Interpretation-33-320.jpg)
![ADEQUATE COMPENSATION?STEP 4
IS THE COMPENSATORY RESPONSE ADEQUATE OR NOT?
METABOLIC DISORDER PCO2 expected
Metabolic acidosis: PaCO2(e)= (1.5 x [HCO3-]) +8± 2
Metabolic alkalosis:PaCO2(e)= (0.7 x [HCO3-])+ 21 + 2
PCO2measured ≠ PCO2expected MIXED DISORDER
RESPIRATORY DISORDER pHexpected (acute-chronic)
pHm ≠ pHe range MIXED DISORDER](https://image.slidesharecdn.com/abgseminar-161019103518/85/Arterial-Blood-Gas-Interpretation-39-320.jpg)
![CO EXISTANT METABOLIC
DISORDER – “Gap Gap”?
STEP 6
If an increased anion gap is present:
Assess the ratio of the change in the anion gap (∆AG ) to the
change in [HCO3-] (∆[HCO3-]): ∆AG/∆[HCO3-]
∆ Anion Gap = Measured AG – Normal AG
Measured AG – 12
∆ HCO3 = Normal HCO3 – Measured HCO3
24 – Measured HCO3
Ideally, ∆Anion Gap = ∆HCO3
For each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L
∆AG/D HCO3
- = 1 Pure High AG Met Acidosis
D AG/D HCO3
- > 1 Assoc Metabolic Alkalosis
D AG/D HCO3
- < 1 Assoc Non AG Met Acidosis](https://image.slidesharecdn.com/abgseminar-161019103518/85/Arterial-Blood-Gas-Interpretation-48-320.jpg)
![Question1.
A 45 year-old woman with a history of inhalant abuse presents to the
emergency room complaining of dyspnea. She has an SpO2 of 99% on room air
and is obviously tachypneic on exam with what appears to be Kussmaul’s
respirations. A room air arterial blood gas is performed and reveals: pH 6.95,
PCO2 9, PO2 128, HC3- 2. A chemistry panel revealed sodium of 130, chloride 98,
HCO3- 2.
Answer1.
The patient has a very low pH (acidemia)
The low pH in conjunction with the low bicarbonate tells us that the metabolic
acidosis is the primary process
The anion gap is elevated at 30[130-(98+2)]. This tells us that the patient has a
primary elevated anion gap metabolic acidosis.
Compensated as PaCO2 (e)=9-13(1.5x2+8+-2)
delta AG is 30-12 = 18
Delta AG/D HCO3
- < 1( 18/22) ,So there is an additional non-gap metabolic
acidosis as well.
Combined elevated anion gap and non-gap metabolic acidoses with
compensatory respiratory alkalosis.](https://image.slidesharecdn.com/abgseminar-161019103518/85/Arterial-Blood-Gas-Interpretation-54-320.jpg)
Uploaded byTauhid Iqbali
Arterial Blood Gas Interpretation
This document provides information about arterial blood gas (ABG) interpretation. It discusses the procedure and precautions for ABG sampling, how the body maintains acid-base balance through bicarbonate buffering and respiratory and renal regulation. It explains the anatomy of an ABG report, including measured, calculated and entered values. Key areas of interpretation are oxygenation parameters like PaO2, A-a gradient and oxygen saturation, as well as acid-base status through pH, PCO2 and bicarbonate levels. The document provides examples of interpreting ABG results to assess for respiratory and metabolic acid-base disorders.
More Related Content
Similar to Arterial Blood Gas Interpretation
Arterial Blood Gas Interpretation
- 1. Arterial Blood Gas Interpretation Dr.Tauhid Iqbali
- 2. OBJECTIVES ABG-Procedure and Precautions Maintainingacid-base balance in the body Working principle of ABG analyzer Anatomy of ABG report Interpretation of ABG Question and Answer stretch
- 3. ABG – Procedureand Precautions Site- (Ideally) Radial Artery Femoral Artery Ideally - Pre-heparinised ABG syringes - Syringe should be FLUSHED with 0.5ml of 1:1000 Heparin solution and emptied. DO NOT LEAVE EXCESSIVE HEPARIN IN THE SYRINGE HEPARIN DILUTIONAL HCO3 EFFECT PCO2 Only small 0.5ml Heparin for flushing and discard it Syringes must have > 50% blood. Use only 2ml or less syringe.
- 4. Ensure NoAir Bubbles. Syringe must be sealed immediately after withdrawing sample. – Contact with AIR BUBBLES Air bubble = PO2 150 mm Hg , PCO2 0 mm Hg Air Bubble + Blood = PO2 PCO2 ABG Syringe must be transported at the earliest to the laboratory for EARLY analysis via COLD CHAIN
- 5. Patients Body Temperatureaffects the values of PCO2 and HCO3. ABG Analyser is controlled for Normal Body temperatures Any change in body temp at the time of sampling leads to alteration in values detected by the electrodes Cell count PO2 ABG Sample should always be sent with relevant information regarding O2, FiO2 status and Temp.
- 6.
- 7. Acid Base Balance oH+ ion concentration in the body is precisely regulated o The body understands the importance of H+ and hence devised DEFENCES against any change in its concentration BICARBONATE BUFFER SYSTEM Acts in few seconds RESPIRATORY REGULATION Acts in few minutes RENAL REGULATION Acts in hours to days A C I D B A S E
- 8. Regulation of AcidBase 1. Bicarbonate Buffer System CO2 + H2O carbonic anhydrase H2CO3 H+ + HCO3 - In Acidosis - Acid = H+ H+ + HCO3 H2CO3 CO2 + H2O In Alkalosis - Alkali + Weak Acid = H2CO3 CO2 + H20 H2CO3 HCO3 - + H+ + ALKALI
- 9. 2. Respiratory Regulationof Acid Base Balance: H+ PaCO2 H+ PaCO2 ALVEOLAR VENTILATION ALVEOLAR VENTILATION
- 10. 3. Renal Regulationof Acid Base Balance: Kidneys control the acid-base balance by excreting either an acidic or a basic urine. This is achieved in the following ways: Reabsorption Secretion of H+ of HCO3 ions in tubules in blood and excretion • Proximal Convulated Tubules (85%) • Thick Ascending Limb of Loop of Henle (10%) • Distal Convulated Tubule • Collecting Tubules(5%)
- 11. Another mechanism bywhich the kidney controls the acid base balance is by the Combination of excess H+ ions in urine with AMMONIA and other buffers- A mechanism for generating NEW Bicarbonate ions In CKD, the dominant mechanism by which acid is eliminated by the Kidneys is excretion of NH4+ GLUTAMINE 2HCO3 - 2NH4 +REABSORBED EXCRETED + H+, Cl-
- 12. WORKING PRINCIPLE OF ABGANALYZIER
- 13. ABG ELECTRODES pH (SanzElectrode) Measures H+ ion concentration of sample against a known pH in a reference electrode, hence potential difference. Calibration with solutions of known pH (6.384 to 7.384). P CO2 (Severinghaus Electrode) CO2 reacts with solution to produce H+ higher CO2- more H+ higher P CO2 measured. P O2 (Clark Electrode) O2 diffuses across membrane producing an electrical current measured as P O2.
- 14. Measured Values Temperature Correction: Isthere any value to it? Calculated Data: Which are the useful ones? Entered Data: Derived from other sources The Anatomy of a Blood Gas Report
- 15. The Anatomy of aBlood Gas Report ----- XXXX Diagnostics ------ Blood Gas Report 248 05:36 Jul 22 2000 Pt ID 2570 / 00 Measured37.0 o C pH 7.463 pCO2 44.4 mm Hg pO2 113.2 mm Hg Corrected38.6 o C pH 7.439 pCO2 47.6 mm Hg pO2 123.5 mm Hg Calculated Data HCO3 act 31.1 mmol / L HCO3 std 30.5 mmol / L BE 6.6 mmol / L O2 CT 14.7 mL / dl O2 Sat 98.3 % ct CO2 32.4 mmol / L pO2 (A - a) 32.2 mm Hg pO2 (a / A) 0.79 Entered Data Temp 38.6 oC ct Hb 10.5 g/dl FiO2 30.0 % Measured Values Temperature Correction: Is there any value to it? Calculated Data: Which are the useful ones? Entered Data: Derived from other sources
- 16. Temperature Correction: “ Thereis no scientific basis ... for applying temperature corrections to blood gas measurements…” Shapiro BA, OTCC, 1999. Uncorrected pH & pCO2 are reliable reflections of in-vivo acid base status Temperature correction of pH & pCO2 do not affect calculated bicarbonate pCO2 reference points at 37 o C are well established as reliable reflectors of alveolar ventilation Reliable data on DO2 and oxygen demand are unavailable at temperatures other than 37 o C ----- XXXX Diagnostics ------ Blood Gas Report Measured37.0 o C pH 7.463 pCO2 44.4 mm Hg pO2 113.2 mm Hg Corrected38.6 o C pH 7.439 pCO2 47.6 mm Hg pO2 123.5 mm Hg Calculated Data HCO3 act 31.1 mmol / L HCO3 std 30.5 mmol / L BE 6.6 mmol / L O2 CT 14.7 mL / dl O2 Sat 98.3 % t CO2 32.4 mmol / L pO2 (A - a) 32.2 mm Hg pO2 (a / A) 0.79 Entered Data Temp 38.6 oC ct Hb 10.5 g/dl FiO2 30.0 %
- 17. ----- XXXX Diagnostics------ Blood Gas Report Measured37.0 o C pH 7.463 pCO2 44.4 mm Hg pO2 113.2 mm Hg Corrected38.6 o C Calculated Data HCO3 act 31.1 mmol / L HCO3 std 30.5 mmol / L BE 6.6 mmol / L O2 CT 14.7 mL / dl O2 Sat 98.3 % t CO2 32.4 mmol / L pO2 (A - a) 32.2 mm Hg pO2 (a / A) 0.79 Entered Data Temp 38.6 oC ct Hb 10.5 g/dl FiO2 30.0 % Bicarbonate is calculated on the basis of the Henderson equation: [H + ] = 24 pCO2 / [HCO3 - ] Bicarbonate:
- 18. ----- XXXX Diagnostics------ Blood Gas Report Measured37.0 o C pH 7.463 pCO2 44.4 mm Hg pO2 113.2 mm Hg Corrected38.6 o C Calculated Data HCO3 act 31.1 mmol / L HCO3 std 30.5 mmol / L BE 6.6 mmol / L O2 CT 14.7 mL / dl O2 Sat 98.3 % t CO2 32.4 mmol / L pO2 (A - a) 32.2 mm Hg pO2 (a / A) 0.79 Entered Data Temp 38.6 oC ct Hb 10.5 g/dl FiO2 30.0 % Standard Bicarbonate: Plasma HCO3 after equilibration to a PCO2 of 40 mm Hg : reflects non-respiratory acid base change : does not quantify the extent of the buffer base abnormality : does not consider actual buffering capacity of blood Base Excess: D base to normalise HCO3 (to 24) with PCO2 at 40 mm Hg (Sigaard-Andersen) : reflects metabolic part of acid base D : no info. over that derived from pH, pCO2 and HCO3 : Misinterpreted in chronic or mixed disorders
- 19. ----- XXXX Diagnostics------ Blood Gas Report Measured37.0 o C pH 7.463 pCO2 44.4 mm Hg pO2 113.2 mm Hg Corrected38.6 o C Calculated Data HCO3 act 31.1 mmol / L HCO3 std 30.5 mmol / L BE 6.6 mmol / L O2 CT 14.7 mL / dl O2 Sat 98.3 % t CO2 32.4 mmol / L pO2 (A - a) 32.2 mm Hg pO2 (a / A) 0.79 Entered Data Temp 38.6 oC ct Hb 10.5 g/dl FiO2 30.0 % Oxygenation Parameters: O2 Content of blood: Hb x O2 Sat x Const. + Dissolved O2 Oxygen Saturation: Alveolar / arterial gradient: Arterial / alveolar ratio:
- 20. Interpretation of ABG OXYGENATION ACID BASE
- 21.
- 22. PaO2 (Partial pressureof arterial oxygen) PaO2 is dependant upon Age, FiO2, Patm As Age the expected PaO2 • PaO2 = 109 - [0.4 (Age)] • Normal PaO2: 75-100 mmHg As FiO2 the expected PaO2 • Alveolar Gas Equation: • PAO2= (PB-P h2o) x FiO2- pCO2/R O X Y G E N A T I O N PAO2 = partial pressure of oxygen in alveolar gas, PB = barometric pressure (760mmHg), Ph2o = water vapor pressure (47 mm Hg), FiO2 = fraction of inspired oxygen, PCO2 = partial pressure of CO2 in the ABG, R = respiratory quotient (0.8)
- 23. PaO2 / FiO2ratio: Inspired Air FiO2 = 21% PiO2 = 150 mmHg PalvO2 = 100 mmHg PaO2 = 90 mmHg O2CO2 PaO2/FiO2 Ratio Inference >300 Normal <300 Acute Lung Injury <200 ARDS (along with other criteria)
- 24. PaO2/ FiO2 ratio( P:F Ratio ) Gives understanding that the patients OXYGENATION with respect to OXYGEN delivered is more important than simply the PO2 value. Example Patient 1 On Room Air Patient 2 On MV PO2 60 90 FiO2 21% (0.21) 50% (0.50) P:F Ratio 285 180
- 25. ----- XXXX Diagnostics------ Blood Gas Report Measured37.0 o C pH 7.463 pCO2 44.4 mm Hg pO2 113.2 mm Hg Corrected38.6 o C Calculated Data HCO3 act 31.1 mmol / L HCO3 std 30.5 mmol / L BE 6.6 mmol / L O2 CT 14.7 mL / dl O2 Sat 98.3 % t CO2 32.4 mmol / L pO2 (A - a) 32.2 mm Hg pO2 (a / A) 0.79 Entered Data Temp 38.6 oC ct Hb 10.5 g/dl FiO2 30.0 % Oxygenation: O2 Content of blood: Hb x O2 Sat x 1.34 + Dissolved O2 (given by Pao2x0.003) Useful in oxygen transport calculations Derived from calculated saturation Oxygen Saturation: Ideally measured by co-oximetry Calculated values may be error-prone Alveolar / arterial gradient: Hypoxemia causes differentiated by A-a Gradien Estimate of normal A–a gradient <[age in years/4] + 4 An abnormally increased A–a gradient suggests : • Defect in diffusion • V/Q (ventilation/perfusion ratio) mismatch • right-to-left shunt Normal A-a Gradient: • Hypoventilation Neuromuscular disorders Central nervous system disorder • Low inspired FIO2 (e.g. high altitude) Arterial / alveolar ratio: Remains stable with change in FIO2 Low a/A (<0.6) = Shunt , V/Q mismatch, diffusion defect
- 26. Alveolar-arterial Difference Inspired O2= 21%= piO2 = (760-45) x .21=150 mmHg ( So at room air PiO2=150 mmHg) O2 CO2 palvO2 = piO2 - pCO2 / RQ = 150 - 40/0.8 = 150 – 50 = 100 mm Hg( Calculated) partO2 = 90 mmHg (Measured) (palvO2- partO2 )D = 10 mmHg (Normal= =<[age in years/4] + 4)
- 27. Alveolar-arterial Difference O2 CO2 Oxygenation Failure(Type 1 Resp. Failure) piO2 = 150 pCO2 = 40 palvO2= 150 – 40/.8 =150-50 =100 pO2 = 45 (palvO2 - pO2) D = 100-45 = 55 Ventilation Failure (Type 2 Resp. Failure) piO2 = 150 pCO2 = 80 palvO2= 150-80/.8 =150-100 = 50 pO2 = 45 (palvO2 - pO2) D = 50-45 = 5
- 28.
- 29. Definitions and Terminology ACIDOSIS: Presenceof a process which tends to pH by virtue of gain of H + or loss of HCO3 - ALKALOSIS: Presence of a process which tends to pH by virtue of loss of H+ or gain of HCO3 - If these changes, change pH, suffix ‘emia’ is added ACIDEMIA : Reduction in arterial pH (pH<7.35) ALKALEMIA : Increase in arterial pH (pH>7.45)
- 30. Simple Acid BaseDisorder/ Primary Acid Base disorder A single primary process of acidosis or alkalosis due to an initial change in PCO2 and HCO3 Compensation The normal response of the respiratory system or kidneys to change in pH induced by a primary acid-base disorder Note: The Compensatory responses to a primary Acid Base disturbance are never enough to correct the change in pH , they only act to reduce the severity Mixed Acid Base Disorder Presence of more than one acid base disorder simultaneously
- 31.
- 32. STEP 0 • Isthis ABG Authentic? STEP 1 • ACIDEMIA or ALKALEMIA? STEP 2 • RESPIRATORY or METABOLIC? STEP 3 • If Respiratory – ACUTE or CHRONIC? STEP 4 • Is COMPENSATION adequate? STEP 5 • If METABOLIC – ANION GAP? STEP 6 • If High gap Metabolic Acidosis– GAP GAP?
- 33. If the pHand the [H+] are inconsistent, the ABG is probably not valid. [H+] = 24(PaCO2) [HCO3-] H+ ion (mmol/L) pH 100 7.00 79 7.10 63 7.20 50 7.30 45 7.35 40 7.40 35 7.45 32 7.50 25 7.60 STEP0: Is this ABG Authentic?
- 34. Look at pH <7.35: acidemia >7.45 : alkalemia NOTE – An acid base abnormality is present even if either the pH or PCO2 are Normal. ACIDEMIA OR ALKALEMIA?STEP 1
- 35. PRIMARY DISORDER PRIMARY RESPONSES COMPENSATORY RESPONSESH+ion pH Primary Conc. Defect Metabolic Acidosis H+ pH HCO3 PCO2 Alveolar Hyperventilation Metabolic Alkalosis H+ pH HCO3 PCO2 Alveolar Hypoventilation Respiratory Acidosis H+ pH PCO2 HCO3 Respiratory Alkalosis H+ pH PCO2 HCO3 RESPIRATORY or METABOLIC?STEP 2 RULE- If either the pH or PCO2 is Normal, there is a mixed metabolic and respiratory acid base disorder.
- 36. IF RESPIRATORY, ISIT ACUTE OR CHRONIC? oAcute respiratory disorder : ∆pH(e-acute) = 0.008x ∆Pco2 oChronic respiratory disorder : ∆pH(e-chronic)= 0.003x ∆pCO2 oCompare, pHmeasured (pHm) v/s pHexpected (pHe) Respiratory acidosis: pH(e-chronic)=7.40–0.008( PCO2-40) pH(e-acute)=7.40–0.003(PCO2-40) Respiratory alkalosis: pH(e-chronic)=7.40+0.008(40-PCO2) pH(e-acute)=7.40+0.003(40-PCO2) IF RESPIRATORY- ACUTE/CHRONIC?STEP 3 pH(m) = pH(e- acute) pH(m) = between pH(e- acute) & pH(e- chronic) pH(m) = pH(e-chronic) ACUTE RESPIRATORY DISORDER PARTIALLY COMPENSATED CHRONIC RESPIRATORY DISORDER
- 37. ----- XXXX Diagnostics------ Blood Gas Report Measured 37.0 o C pH 7.301 pCO2 76.2 mm Hg pO2 45.5 mm Hg Calculated Data HCO3 act 36.1 mmol / L O2 Sat 78 % pO2 (A - a) 9.5 mm Hg D pO2 (a / A) 0.83 Entered Data FiO2 21 % Case 1 60 year old male smoker with progressive respiratory distress and somnolence. D CO2 =76-40=36 Ac D pH = 36/10 x0.08=0.29 Exp Acute pH = 7.40-0.29=7.11 Chronic D pH= 36/10 x0.03=0.10 Exp Chr pH = 7.40-0.10=7.30 Chronic resp. acidosis pH <7.35 ; acidemia pCO2 >45; respiratory acidemia Hypoxia Normal A-a gradient Due to hypoventilation
- 38. ----- XXXX Diagnostics------ Blood Gas Report Measured 37.0 o C pH 7. 232 pCO2 60.1 mm Hg pO2 66.3 mm Hg Calculated Data HCO3 act 24.5 mmol / L O2 Sat 92 % pO2 (A - a) mm Hg D pO2 (a / A) Entered Data FiO2 30 % Case 2 18-year-old male asthmatic; 3 days of cough, dyspnea and orthopnea not responding to usual bronchodilators. O/E: Respiratory distress; suprasternal and intercostal retraction; tired looking; on 4 L NC. D CO2 = 60 - 40 = 20 Expect Acute D pH = 20/10x0.08= 0.16 Expect Ac pH = 7.40 - 0.16 = 7.24 Acute resp. acidosis pH <7.35 ; acidemia pCO2 >45; respiratory acidemia Hypoxemia piO2 = (760-45)x.3=214.5 / palvO2 = 214-60/.8=129 129-66= 63 Oxygenation failure
- 39. ADEQUATE COMPENSATION?STEP 4 ISTHE COMPENSATORY RESPONSE ADEQUATE OR NOT? METABOLIC DISORDER PCO2 expected Metabolic acidosis: PaCO2(e)= (1.5 x [HCO3-]) +8± 2 Metabolic alkalosis:PaCO2(e)= (0.7 x [HCO3-])+ 21 + 2 PCO2measured ≠ PCO2expected MIXED DISORDER RESPIRATORY DISORDER pHexpected (acute-chronic) pHm ≠ pHe range MIXED DISORDER
- 40. CASE 1 Mr. Shamshuddin,62/M, Nagina k/c/o COPD Breathlessness, progressively increased, aggravated on exertion, 2 days Chronic smoker O/E RS- B/L expiratory rhonchi 22/7/11 7:30 am pH 7.20 PCO2 92 mmHg PO2 76 mmHg Actual HCO3 21.00 mmol/l SO2 89 FiO2 37%
- 41. STEP 1– ACIDEMIA STEP 2 – pH PCO2 Respiratory STEP 3 – pH expected pH acute = 7.40 – 0.008(92-40) 7.40 – 0.008(52) 6.984 pH chronic = 7.40 – 0.003(92- 40) 7.244 pH b/w 6.98 to 7.244 Primary Respiratory Acidosis, partially compensated
- 42. METABOLIC ACIDOSIS- ANION GAP? STEP5 IN METABOLIC ACIDOSIS WHAT IS THE ANION GAP? ANION GAP(AG) = Na – (HCO3 + Cl) Normal Value = 12 + 4 ( 8- 16 Meq/l) Adjusted Anion Gap = Observed AG +2.5(4.5- S.Albumin) 50% in S. Albumin 75% in Anion Gap !!! Metabolic Acidosis High Anion Gap Metabolic Acidosis Normal Anion Gap Acidosis
- 43. Anion Gap AG basedon principle of electroneutrality: Total Serum Cations = Total Serum Anions M cations + U cations = M anions + U anions Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4 + Protein + Organic Acids) Na + UC = HCO3 + Cl + UA But in Blood there is a relative abundance of Anions, hence Anions > Cations Na – (HCO3 + Cl) = UA – UC Na – (HCO3 + Cl) = Anion Gap
- 44. CASE 3 Mr.Dharam Dutt,63/M, Bijnor k/c/o CRF(conservativeRx) Breathlessness Decreased Urine Otpt. 2days Vomiting 10-15 O/E No pedal edema, dehydration + RS – B/L A/E Normal 31/7/11 11:30pm pH 7.18 PCO2 21.00 PO2 90 Actual HCO3 7.80 Base Excess -18.80 SO2 95 Na 140.6 Chloride 102 T.Protein 6 Albumin 2.4
- 45. STEP 1– ACIDEMIA STEP 2 – pH PCO2 METABOLIC STEP 4 – PCO2expected PCO2exp = (1.5 x HCO3)+8+2 (1.5X7.80)+8+2 19.7+2= 17.7 – 21.7 STEP5 – ANION GAP = Na – (HCO3 +Cl) = 140.6-(7.80+102) = 30.8 AG corrected for albumin = 30.8+5.25 AG = 36.05 HIGH AG Met. Acidosis
- 46. High Anion GapMetabolic Acidosis M U D P I L E S METHANOL UREMIA - ARF/CRF DIABETIC KETOACIDOSIS & other KETOSIS PARALDEHYDE, PROPYLENE GLYCOL ISONIAZIDE, IRON LACTIC ACIDOSIS ETHANOL, ETHYLENE GLYCOL SALICYLATE
- 47. Non Anion GapMetabolic Acidosis U S E D C R A P URETEROENTEROSTOMIES SMALL BOWEL FISTULA EXCESS CHLORIDE DIARRHOEA CARBONIC ANHYDRASE INHIBITOR RTA ADDISSION’S DISEASE PANCREATOENTEROSTOMIES
- 48. CO EXISTANT METABOLIC DISORDER– “Gap Gap”? STEP 6 If an increased anion gap is present: Assess the ratio of the change in the anion gap (∆AG ) to the change in [HCO3-] (∆[HCO3-]): ∆AG/∆[HCO3-] ∆ Anion Gap = Measured AG – Normal AG Measured AG – 12 ∆ HCO3 = Normal HCO3 – Measured HCO3 24 – Measured HCO3 Ideally, ∆Anion Gap = ∆HCO3 For each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L ∆AG/D HCO3 - = 1 Pure High AG Met Acidosis D AG/D HCO3 - > 1 Assoc Metabolic Alkalosis D AG/D HCO3 - < 1 Assoc Non AG Met Acidosis
- 49. CASE 4 Mr.Dharam Dutt,63/M, Bijnor k/c/o CRF(conservativeRx) Breathlessness Decreased Urine Otpt. 2days Vomiting 10-15 O/E No pedal edema, dehydration + RS – B/L A/E Normal 31/7/11 11:30pm pH 7.18 PCO2 21.00 PO2 90 Actual HCO3 7.80 Base Excess -18.80 SO2 95 Na 140.6 Chloride 102 T.Protein 6 Albumin 2.4
- 50. STEP 1– ACIDEMIA STEP 2 – pH PCO2 METABOLIC STEP 4 – PCO2expected PCO2exp = (1.5 x HCO3)+8+2 (1.5X7.80)+8+2 19.7+2= 17.7 – 21.7 COMPENSATED STEP5 – ANION GAP = Na – (HCO3 +Cl) = 140.6-(7.80+102) = 30.8 AG corrected for albumin = 30.8+5.25 AG = 36.05 HIGH AG Met. Acidosis
- 51. STEP 6– GAP GAP = (AG-12)/(24-HCO3) = 36.05-12/24-7.80 = 24.05/16.2 = 1.48 Gap/gap > 1 = add. Metabolic alkalosis ∆sis – Primary Metabolic Acidosis,High Anion Gap, compensated Cause- CRF -Add. Metabolic Alkalosis Cause - ? Vomiting
- 52. Normal AG= 12;D Gap = 16 - 12 = 4 Normal HCO3=24;DHCO3 = 24 -14 = 10 D AG/D HCO3 - < 1(4/10) Indicates additional non-gap Met.acidosis ----- XXXX Diagnostics ------ Blood Gas Report Measured 37.0 o C pH 7.236 pCO2 34 mm Hg pO2 110.5 mm Hg Calculated Data HCO3 act 14 mmol / L O2 Sat % pO2 (A - a) mm Hg D pO2 (a / A) Entered Data FiO2 21.0 % Case 5 28 year old diabetic with respiratory distress fatigue and loss of appetite. pH <7.35 ; acidemia HCO3 <22; metabolic acidemia Limits: Expected pCO2 = (1.5 x HCO3)+8 + 2 = (1.5 x 14)+ 8 + 2 = 29 + 2 = 27 to 31 Met. Acidosis + Resp. acidosis If Na = 130, Cl = 100 Anion Gap = 130 - (100 + 14) = 130 - 114= 16
- 54. Question1. A 45 year-oldwoman with a history of inhalant abuse presents to the emergency room complaining of dyspnea. She has an SpO2 of 99% on room air and is obviously tachypneic on exam with what appears to be Kussmaul’s respirations. A room air arterial blood gas is performed and reveals: pH 6.95, PCO2 9, PO2 128, HC3- 2. A chemistry panel revealed sodium of 130, chloride 98, HCO3- 2. Answer1. The patient has a very low pH (acidemia) The low pH in conjunction with the low bicarbonate tells us that the metabolic acidosis is the primary process The anion gap is elevated at 30[130-(98+2)]. This tells us that the patient has a primary elevated anion gap metabolic acidosis. Compensated as PaCO2 (e)=9-13(1.5x2+8+-2) delta AG is 30-12 = 18 Delta AG/D HCO3 - < 1( 18/22) ,So there is an additional non-gap metabolic acidosis as well. Combined elevated anion gap and non-gap metabolic acidoses with compensatory respiratory alkalosis.
- 55. Question2. A 45 year-oldman with a history of very severe COPD (FEV1~ 1.0L, < 25% predicted) and chronic carbon dioxide retention (Baseline PCO2 58) presents to the emergency room complaining of worsening dyspnea and an increase in the frequency and purulence of his sputum production over the past 2 days. His oxygen saturation is 78% on room air. Before he is placed on supplemental oxygen, a room air arterial blood gas is drawn and reveals: pH 7.25, PCO2 68, PO2 48, HCO3-31. Answer2. The patient has a low pH (acidemia) The combination of the low pH and the high PCO2 tells us that the respiratory acidosis is the primary process. pH(e-acute)=7.2 and pH(e-chronic)=7.3 (If pH(m) = between pH(e- acute) & pH(e- chronic) - partially compensated metabolic alkalosis. The alveolar-arterial oxygen difference is 17 mmHg(As ABG is taken before placing him on supplemental oxygen, So PiO2 will be 150 and RQ will be 0.8). palvO2= piO2 - pCO2 / RQ= 150-68/0.8=65 , And A-a gradient= palvO2 –PaO2=65-48=17 This value is elevated, suggesting that the hypoxemia is due to either shunt or areas of low V/Q (the more likely explanation in a patient with COPD) and cannot be explained by hypoventilation alone. Primary respiratory acidosis with partially compensated metabolic alkalosis with hypoxemia due to either shunt or V/Q mismatch.
- 56.
- 57. for not becomingcomatose!
Editor's Notes
- #3 I would like to thank my mentor of this seminar dr. sushil pathak sir for providing insight and for inspiring and helping us to dig dipper into abg interpretation
- #19 Base excess is defined as the amount of strong acid that must be added to each liter of fully oxygenated blood to return the pH to 7.40 at a temperature of 37°C and a pCO2 of 40 mmHg. A base deficit (i.e., a negative base excess) can be correspondingly defined in terms of the amount of strong base that must be added. actual base excess is that present in the blood, while standard base excess is the value when the hemoglobin is at 5 g/dl. The latter gives a better view of the base excess of the entire extracellular fluid. A typical reference range for base excess is −2 to +2 mEq/L More negative values of base excess may indicate: Lactic acidosis Ketoacidosis Ingestion of acids Cardiopulmonary collapse Shock More positive values of base excess may indicate: Loss of buffer base Hemorrhage Diarrhea Ingestion of alkali
- #23 PO2 (partial pressure of oxygen) reflects the amount of oxygen gas dissolved in the blood. It primarily measures the effectiveness of the lungs in pulling oxygen into the blood stream from the atmosphere. Elevated pO2 levels are associated with: Increased oxygen levels in the inhaled air Polycythemia Decreased PO2 levels are associated with: Decreased oxygen levels in the inhaled air Anemia Heart decompensation Chronic obstructive pulmonary disease Restrictive pulmonary disease Hypoventilation
- #24 ARDS:acute, meaning onset over 1 week or less, bilateral opacities consistent with pulmonary edema, PF ratio <300mmHg with a minimum of 5 cmH20 PEEP (or CPAP) .“must not be fully explained by cardiac failure or fluid overload. ARDS Severity PaO2/FiO2* Mild 200 – 300 Moderate 100 – 200 Severe < 100
- #26 Interpretation: Hypoxemia causes differentiated by A-a Gradient Increased A-a Gradient Right to Left Intrapulmonary Shunt (due to fluid filled alveoli) Congestive Heart Failure Adult Respiratory Distress Syndrome (ARDS) Lobar Pneumonia V/Q Mismatch (due to lung dead space) Pulmonary Embolism Atelectasis Pneumonia Obstructive Lung Disease (e.g. Asthma, COPD) Pneumothorax Alveolar hypoventilation Interstitial Lung Disease Normal A-a Gradient Hypoventilation Neuromuscular disorders Central nervous system disorder Low inspired FIO2 (e.g. high altitude)
- #28 Type 1 respiratory failure is defined as a low level of oxygen in the blood (hypoxemia) without an increased level of carbon dioxide in the blood (hypercapnia) PaO2 decreased (< 60 mmHg (8.0 kPa)) PaCO2 normal or decreased (<50 mmHg (6.7 kPa)) PA-aO2 increased Type 2 respiratory failure is defined as Hypoxemia (PaO2 <8kPa) with hypercapnia (PaCO2 >6.0kPa) PaO2 decreased (< 60 mmHg (8.0 kPa)) PaCO2 increased (> 50 mmHg (6.7 kPa)) PA-aO2 normal pH decreased Causes:Increased airways resistance (chronic obstructive pulmonary disease, asthma, suffocation) Reduced breathing effort (drug effects, brain stem lesion, extreme obesity) A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis) Neuromuscular problems (Guillain–Barré syndrome,[2] motor neuron disease) Deformed (kyphoscoliosis), rigid (ankylosing spondylitis), or flail chest.[2]
- #37 Respiratory acidosis: Acute-Increase in [HCO3-]= ∆ PaCO2/10 +-3 Chronic-Increase in [HCO3-]=3.5(∆PaCO2/10) Respiratory alkalosis: Acute-Decrease in [HCO3-]= 2(∆ PaCO2/10) Chronic-Decrease in [HCO3-] = 5(∆ PaCO2/10) to 7(∆ PaCO2/10)
- #39 Oxygenation Failure