Abg Final
Abg Final
GASES
BASICS AND INTERPRETATION
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ABG
• ABG is a very useful diagnostic tool in our day to day practice.
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Acid-Base Physiology
• pH is the negative logarithm to the base 10 of the hydrogen ion
concentration in mmol/L
• pH = - log10[H+]
H2CO3
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• H+ = 24 x PCO2/HCO3- @ NKMishra 5
Regulation of pH
pH is maintained in narrow range by
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Regulation of arterial pH
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ROLE OF KIDNEY
It retains and regenerate HCO3- thereby regenerating the
body buffer with the net effect of eliminating the non-
volatile acid load
a. H+ secretion
1. Free urinary H+ - minimal contribution
2. Ammonia
3. Phosphorus
b. HCO3- reabsorption
1. Proximal tubule – 90%
2. Distal tubule -10%
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Applications of ABG
• To document respiratory failure and assess its severity.
• P(A-a)O2
• O2 content
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P(A-a)O2= PAO2- PaO2
HYPOXEMIA
Mild (60-80) mmHg
Moderate(40-60) mmHg
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Arterial Blood pH
7.35~7.45
6.8 7.8
7.4
Neutral
Academia Alkalemia
Acidosis? Alkalosis?
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TECHNIQUES of Sampling
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SAMPLE MANAGEMENT
• PaCO2 increases
• PaO2 decreases
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CAUTION
pH PaCO2 PaO2
Heparin ↓ ↓
Air Bubbles ↓ ↑
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Technical Errors
Risk of alteration of results with:
1)size of syringe/needle
2)vol of sample
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Parameters Excessive Heparin Air bubbles
pH ↓ or remain the same ↑
PCO2 ↓ ↓
PO2 May altered May altered
HbO2% sat May altered May altered
HbCO2% sat Will not altered Will not altered
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Technical Errors
WBC Counts
0.01 ml O2 consumed/dL/min
Marked increase in high TLC/plt counts : dec.pO2
Chilling / immediate analysis
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Site Selection
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45 DEGREE INSERTION
ANGLE FOR RADIAL
ARTERY
KK
60-90 DEGREE
INSERTION ANGLE FOR
BRACHAILARTERY
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Contraindication
• No absolute contraindications
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Site specific contraindication
Radial : Buergers disease
Raynauds
Absent Ulnar collateral circulation
AV dialysis shunt
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Arterial Venous
Pco2 35- 45 44 - 48
Po2 80 - 100 38 - 42
Hco3 24- 26 20 - 24
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A Stepwise
Approach
to Solving
Acid-Base
Disorders
Step 1: Assess the internal consistency of the values using the Henderseon-Hasselbach equation:
• [H+] = 24(PaCO2)
[HCO3-]
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If the pH and the [H+] are inconsistent, the ABG is probably not valid.
pH Approximate [H+]
(mmol/L)
7.00 100
7.05 89
7.10 79
7.15 71
7.20 63
7.25 56
7.30 50
7.35 45
7.40 40
7.45 35
7.50 32
7.55 28
7.60 25
7.65 22
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Step 2: Is there alkalemia or
acidemia present?
• pH < 7.35 acidemia
pH > 7.45 alkalemia
• This is usually the primary disorder
• Remember: an acidosis or alkalosis may be present even if the pH is in
the normal range (7.35 – 7.45)
• You will need to check the PaCO2, HCO3- and anion gap
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• Step 3: Is the disturbance respiratory or metabolic?
• What is the relationship between the direction of change in the pH and the
direction of change in the PaCO2?
• In primary respiratory disorders, the pH and PaCO2 change in opposite directions;
in metabolic disorders the pH and PaCO2 change in the same direction.
Acidosis Respiratory pH ↓ PaCO2 ↑ ROME
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• Step 4: Is there appropriate compensation for the primary disturbance?
• Usually, compensation does not return the pH to normal (7.35 – 7.45) except….?
If the observed compensation is not the expected compensation, it is likely that more than one acid-
base disorder is present.
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• Step 5: Calculate the anion gap (if a metabolic acidosis exists):
• AG= [Na+]-( [Cl-] + [HCO3-] )=12 ± 2
• In patients with hypoalbuminemia, the normal anion gap is lower than 12 meq/L; the “normal”
anion gap in patients with hypoalbuminemia is about 2.5 meq/L lower for each 1 gm/dL decrease
in the plasma albumin concentration (for example, a patient with a plasma albumin of 2.0 gm/dL
would be approximately 7 meq/L.)
• If the anion gap is elevated, consider calculating the osmolal gap in compatible clinical situations.
• Elevation in AG is not explained by an obvious case (DKA, lactic acidosis, renal failure
• Toxic ingestion is suspected
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Table 2: Selected etiologies of respiratory acidosis
oAirway obstruction
- Upper
- Lower
o COPD
o asthma
o other obstructive lung disease
oCNS depression
oSleep disordered breathing (OSA or OHS)
oNeuromuscular impairment
oVentilatory restriction
oIncreased CO2 production: shivering, rigors, seizures, malignant hyperthermia,
hypermetabolism, increased intake of carbohydrates
oIncorrect mechanical ventilation settings
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Table 3: Selected etiologies of respiratory alkalosis
oCNS stimulation: fever, pain, fear, anxiety, CVA, cerebral
edema, brain trauma, brain tumor, CNS infection
oHypoxemia or hypoxia: lung disease, profound anemia, low
FiO2
oStimulation of chest receptors: pulmonary edema, pleural
effusion, pneumonia, pneumothorax, pulmonary embolus
oDrugs, hormones: salicylates, catecholamines,
medroxyprogesterone, progestins
oPregnancy, liver disease, sepsis, hyperthyroidism
oIncorrect mechanical ventilation settings
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Table 4: Selected causes of metabolic
alkalosis
oHypovolemia with Cl- depletion
o GI loss of H+
o Vomiting, gastric suction, villous
adenoma, diarrhea with chloride-rich
fluid
o Renal loss H+
o Loop and thiazide diuretics, post-
hypercapnia (especially after institution
of mechanical ventilation)
oHypervolemia, Cl- expansion
o Renal loss of H+: edematous states (heart
failure, cirrhosis, nephrotic syndrome),
hyperaldosteronism, hypercortisolism,
excess ACTH, exogenous steroids,
hyperreninemia, severe hypokalemia, renal
artery stenosis, bicarbonate administration
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Table 5: Selected etiologies of metabolic
oNormal anion gap: will have increase in [Cl-]
acidosis
oElevated anion gap: o GI loss of HCO3-
o Methanol intoxication o Diarrhea, ileostomy, proximal colostomy,
o Uremia ureteral diversion
o Diabetic ketoacidosisa, alcoholic o Renal loss of HCO3-
ketoacidosis, starvation ketoacidosis o proximal RTA
o Paraldehyde toxicity o carbonic anhydrase inhibitor
o Isoniazid (acetazolamide)
o Lactic acidosisa o Renal tubular disease
o Type A: tissue ischemia o ATN
o Type B: Altered cellular metabolism o Chronic renal disease
o Ethanolb or ethylene glycolb intoxication o Distal RTA
o Salicylate intoxication o Aldosterone inhibitors or absence
o NaCl infusion, TPN, NH4+ administration
a
Most common causes of metabolic acidosis with
an elevated anion gap
b
Frequently associated with an osmolal gap
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Table 6: Selected mixed and complex acid-base disturbances
Respiratory acidosis with pH in normal range •COPD with diuretics, vomiting, NG suction
metabolic alkalosis ↑ in PaCO2, •Severe hypokalemia
↑ in HCO3-
Metabolic acidosis with metabolic pH in normal range •Uremia or ketoacidosis with vomiting, NG suction,
alkalosis HCO3- normal diuretics, etc.
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ARTERIAL BLOOD GAS
MEASURES CALCULATES
• PaCO2 • Bicarbonate
• PaO2 • SaO2
• pH
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INTERPRETATION
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Normal Values
• pH - 7.35 - 7.45
• HCO3 - 22-26
• O2sat - 95-100%
• The BE (or base deficit) is defined as the amount of acid (or base) required
to be added to whole blood to achieve a pH of 7.4 at 37˚C and paCO2 of
40mmHg.
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STEP -6 : Calculate anion gap
1. pH
↓ ↓ Metabolic Acidosis
↑ ↓ Respiratory Alkalosis
- Delta ratio
4. Compensation
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ANION GAP (AG)
• Normal value 8 – 12
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UNADJUSTED AG ADJUSTED AG
Decreased 4.7 %
Decreased 26.7 %
Normal 22.0 %
Normal 36.4 %
Normal 62.6 %
Increased 26.3 %
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Case 0
• pH 7.28
• PaCO2 27 mm Hg
• PaO2 105 mm Hg
• H+ 70 mmhg
• Na+ 134 mmol/L
• K+ 3.7 mmol/L
• Cl- 109 mmol/L
• HCO3- 13 mmol/L
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CASE 1
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CASE 1
• pH 7.28
• PaCO2 27 mm Hg
• PaO2 105 mm Hg
• H+ 50 mmhg
• Na+ 134 mmol/L
• K+ 3.7 mmol/L
ANION GAP = 12
• Cl- 109 mmol/L
• HCO3- 13 mmol/L
↓ ↓ Metabolic Acidosis
↓ ↑ Respiratory Acidosis
↑ ↓ Respiratory Alkalosis
4. Compensation
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COMPENSATION
PaCO2 = 1.5 x HCO3- + 8 ± 2
PaCO2 = 1.5 x 13 + 8 ± 2
PaCO2 = 19.5 + 8 ± 2
PaCO2 = 27.5 ± 2
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CASE 1
1. pH: ↓
NON-ANION GAP
2. PCO2: ↓
METABOLIC ACIDOSIS
- Delta ratio
ADEQUATE
COMPENSATION
4. Compensation
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NON-ANION GAP ACIDOSIS
• NAG Acidosis:
• Hyperchloremic: Net
Bicarbonate loss
Diarrhea RTA
NAG M.Acidosis NAG M.Acidosis
• Two main different routes UAG= Neg UAG= Positive
K+= dec K+= Inc
• GI: diarrhea, fistulas
• Renal: RTAs, drugs
• What is used to differentiate?
Urine AG = Na+ + K+ - Cl-
UAG = Negative normally bcz CL- content is high in urine.
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DIARRHEA
DIARRHEA
RTA
CONTROL
RTA
DIARRHEA
RTA
CONTROL
CONTROL
[Na ] + [K ] + [NH
+ +
4
+
?
] + [UC] ≈ [Cl ] +
-
[HCO3-] + [UA]
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HOW TO USE IT
NORMAL RESPONSE TO ACIDOSIS IF KIDNEYS UNABLE TO EXCRETE H+
NH4 +
Cl - NH4+
Cl
-
UAG < 0
UAG > 0
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NON ANION GAP ACIDOSIS
RENAL
GASTROINTESTINAL - Hypokalemic
- Diarrhea * Proximal RTA (type 2)
- External pancreatic or bowel * Distal RTA (type 1)
drainage
- Ureterosigmoidostomy * Drugs: Acetazolamide, Amphotericin B
- Drugs - Hyperkalemic
* Calcium Chloride * Type 4 RTA
* Magnesium Sulfate * Mineralocorticoid deficiency
* Cholestyramine * Tubulointerstitial disease
* Ammonium excretion defect
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URINE ANION
GAP
NEGATIVE POSITIVE
Gastrointestinal
Diarrhea URINE pH > 5.5
Small bowel / pancreatic Type I RTA
drainage
IATROGENIC
URINE pH < 5.5
Parenteral nutrition
Saline
Low K+
Anion exchange resins Type II RTA
High K+
Aldosterone deficiency
Type IV RTA
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CASE 2
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CASE 2
• pH 7.30
• PaCO2 34 mm Hg
• PaO2 235 mm Hg
• H+ 48 mmhg
↓ ↓ Metabolic Acidosis
↓ ↑ Respiratory Acidosis
↑ ↓ Respiratory Alkalosis
4. Compensation
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DELTA RATIO
• Delta ratio = Δ anion gap / Δ bicarbonate
Actual AG – 12
Delta Ratio =
24 – HCO3-
22 – 12 12
Delta Ratio = = = 1.7
24 – 17 7
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Δ AG (↑AG-12)
Delta Ratio = ------------- = -----------------
Δ HCO3- (24-↓HCO3)
1 (0.8-1.5)
Δ RATIO
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CASE 2
1. pH: ↓
ANION GAP
2. PCO2: ↓
METABOLIC ACIDOSIS
4. Compensation
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COMPENSATION
PaCO2 = 1.5 x HCO3- + 8 ± 2
PaCO2 = 1.5 x 17 + 8 ± 2
PaCO2 = 25.5 + 8 ± 2
PaCO2 = 33.5 ± 2
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CASE 2
1. pH: ↓
ANION GAP
2. PCO2: ↓
METABOLIC ACIDOSIS
U remia
P araldehyde, paracetamol
L actic Acidosis
S alicylates
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CASE 3
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CASE 3
• pH 7.24
• PaCO2 60 mm Hg
• PaO2 158 mm Hg
RESPIRATORY
2. PCO2: ↑
ACIDOSIS
pH PaCO2 Disorder
↓ ↓ Metabolic Acidosis
↑ ↑ Metabolic Alkalosis
↓ ↑ Respiratory Acidosis
↑ ↓ Respiratory Alkalosis
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RESPIRATORY DISORDERS
Δ pH 0.08 0.03
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ACUTE OR CHRONIC?
Δ 2x10 = 20 Δ10 PaCO2 ACUTE CHRONIC
• PaCO2 = 60
Δ 2x0.08 =0.16
• pH = 7.24 Δ pH 0.08 0.03
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CASE 3
1. pH: ↓
ACUTE
2. PCO2: ↑ RESPIRATORY
ACIDOSIS
3. Anion Gap: Normal
- Delta Ratio
4. Compensation
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HCO3 ??? -
ACIDOSIS ALKALOSIS
ACUTE
1 2
Δ 10 PaCO2
CHRONIC
4 5
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CASE 3
• pH 7.24
Δ 2x10=20
• PaCO2 60 mm Hg
Δ1
• HCO3 -
25 mmol/L
ACIDOSIS ALKALOSIS
ACUTE 1 2
Δ 10 PaCO2
CHRONIC
4 5
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CASE 3
1. pH: ↓
ACUTE
2. PCO2: ↑ RESPIRATORY
ACIDOSIS
3. Anion Gap: Normal
- Delta Ratio
ADEQUATE
4. Compensation COMPENSATION
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CASE 4
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CASE 4
• pH 7.33
• PaCO2 60 mm Hg
• PaO2 158 mm Hg
RESPIRATORY
2. PCO2: ↑
ACIDOSIS
pH PaCO2 Disorder
↓ ↓ Metabolic Acidosis
↑ ↑ Metabolic Alkalosis
↓ ↑ Respiratory Acidosis
↑ ↓ Respiratory Alkalosis
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RESPIRATORY DISORDERS
Δ pH 0.08 0.03
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ACUTE OR CHRONIC?
Δ 2x10=20 Δ10 PaCO2 ACUTE CHRONIC
• PaCO2 = 60
Δ2x0.03= 0.06
• pH = 7.33 Δ pH 0.08 0.03
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CASE 4
1. pH: ↓
CHRONIC
2. PCO2: ↑ RESPIRATORY
ACIDOSIS
3. Anion Gap: Normal
- Delta Ratio
4. Compensation
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CASE 4
• pH 7.33 ↑2 x 10 = 20
• PaCO2 60 mm Hg
↑2x4=8
• HCO3 -
32 mmol/L
ACIDOSIS ALKALOSIS
ACUTE 1 2
Δ 10 PaCO2
CHRONIC
4 5
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CASE 4
1. pH: ↓
CHRONIC
2. PCO2: ↑ RESPIRATORY
ACIDOSIS
3. Anion Gap: Normal
- Delta Ratio
ADEQUATE
4. Compensation COMPENSATION
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CASE 5
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CASE 5
• pH 7.47
• PaCO2 45 mm Hg
• PaO2 146 mm Hg
2. PCO2: ↑
METABOLIC
ALKALOSIS
3. Anion Gap: Normal pH PaCO2 Disorder
↓ ↓ Metabolic Acidosis
↓ ↑ Respiratory Acidosis
↑ ↓ Respiratory Alkalosis
4. Compensation
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COMPENSATION
PaCO2 = 0.7 x HCO3- + 21 ± 2
PaCO2 = 0.7 x 33 + 21 ± 2
PaCO2 = 23.1 + 21 ± 2
PaCO2 = 44.1 ± 2
2. PCO2: ↑
METABOLIC
ALKALOSIS
3. Anion Gap: Normal
- Delta Ratio
ADEQUATE
COMPENSATION
4. Compensation
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METABOLIC ALKALOSIS
• Decreased H+ concentration
• Chloride responsive
• Chloride resistant
CHLORIDE
CHLORIDE RESISTANT
RESPONSIVE
Laxative abuse
Gastric fluid loss Severe K+ depletion
Diuretics Diuretic abuse
Post hypercapnia Bartter or Gitelman Syndrome
Villous adenoma Primary aldosteronism
Congenital chloridorrhea Adrenal Hyperplasia
Cushing syndrome
↓ ↓ Metabolic Acidosis
↓ ↑ Respiratory Acidosis
↑ ↓ Respiratory Alkalosis
4. Compensation
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DELTA RATIO
• Delta ratio = Δ anion gap / Δ bicarbonate
Actual AG – 12
Delta Ratio =
24 – HCO3-
21 – 12 9
Delta Ratio = = = 9
24 – 23 1
Δ RATIO
4. Compensation
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COMPENSATION
PaCO2 = 1.5 x HCO3- + 8 ± 2
PaCO2 = 1.5 x 23 + 8 ± 2
PaCO2 = 34.5 + 8 ± 2
PaCO2 = 42.5 ± 2
• PH: 7.4
• PCO2: 30
• HCO3:25
• AG: 30
• M. AC(Alcoholic Ketoacidosis)
• with M.Alk(Vomiting)
• with R. Alk( Hyperventilation due to hepatic dysfxn or alcohol withdrawal)
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SUMMARY
↓ ↑ Respiratory Acidosis
Δ RATIO
3. Anion Gap
< 0.8 0.8 - 1.5 > 1.5
- Delta ratio Anion Gap metabolic Anion Gap metabolic
acidosis acidosis
Anion Gap metabolic
acidosis
4. Compensation Non anion gap acidosis Metabolic alkalosis
Δ pH 0.08 0.03
2. PaCO2
3. Anion Gap
ACIDOSIS ALKALOSIS
- Delta ratio
ACUTE 1 2
4. Compensation
Δ 10 PaCO2
CHRONIC
4 5
Thank you!!
ABG results
pH 7.31
PCO₂ 10
HCO₃ 5
Na 123
K 5
Cl 99
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Stepwise interpretation
1. At pH 7.3 H+ conc. Should be ≈50nmol/L
• Calculated H+ = 24 × 10/5 = 24 × 2 = 48
• Both values corroborate, hence result is valid.
2. pH is 7.3, i.e Acidosis
3. HCO₃ value has gone down, primary process is
metabolic
4. Respiratory compensation:
• Calculated PCO₂ = (1.5 × 5)+8 ± 2 = 13.5 to 17.5
• Partially compensated M.Acidosis a/w respiratory
alkalosis :- Mixed disorder
ABG results
pH 7.42
PCO₂ 67
HCO₃ 42
Na 140
K 3.5
Cl 88
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• pH is normal; but PCO₂ & HCO₃ both are increased.
• Change in PCO₂ is 67-40 = 27
• Expected rise in HCO₃ should be 27 × 0.4 = 10.8
• Expected HCO₃ = 24+10.8 ≈ 35
• Actual HCO₃ = 42
• AG = 12 (N)
• Mixed disorder, both respiratory acidosis & metabolic
alkalosis.
ABG results
pH 7.42
PCO₂ 40
HCO₃ 25
Na 140
K 3.0
Cl 95
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• pH, PCO₂, HCO₃ all WNL
• AG = 23 (↑)
• Delta gap = 13 – 1 = 12 (↑)
• AG >> HCO3–
ABG results
pH 7.3
PCO₂ 38
HCO₃ 16
Na 136
K 4
Cl 102
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• pH 7.3 = Acidosis
• HCO₃ is low ; primary disorder is metabolic acidosis
• Expected PCO₂ = (1.5 × 16) + 8 = 32
• Calculated PCO₂ < estimated PCO₂
• AG = 22
• Delta gap = (10-8) = 2
• Mixed disorder with metabolic acidosis & respiratory
acidosis
4. Renal Failure
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5. Rhabdomyolsis @ NKMishra 145
CAUSES OF NORMAL ANION GAP
METABOLIC ACIDOSIS
1. HCO3 loss:
GIT Diarrhoea
Pancreatic or biliary drainage
Urinary diversions (ureterosigmoidostomy)
3. Misc:
Acid Administration (NH4Cl)
Hyperalimentation
Cholestyramine Cl
HCl therapy (Rx of severe met alkalosis)
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METABOLIC ALKALOSIS
GI LOSS: Vomiting
Gastric Aspiration
Villous adenoma
4. MIXED/UNKNOWN MECHANISMS:
Drugs – Salicylates Nicotine
Progesterone Thyroid hormone
Catecholamines
Xanthines (Aminophylline & related compounds)
Cirrhosis
Gram –ve Sepsis
Pregnancy
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Heat exposure @ NKMishra 157
• ABG is a very useful diagnostic tool for our day to day
practice.