ARTERIAL BLOOD GAS:

INTERPRETATION AND CLINICAL

IMPLICATIONS

BY – DR ANIL
Conditions Invalidating or Modifying ABG Results

• DELAYED ANALYSIS
Consumptiom of O2 & Production of CO2 continues after blood drawn
into syringe
Iced Sample maintains values for 1-2 hours
Uniced sample quickly becomes invalid
PaCO2  3-10 mmHg/hour
PaO2  at a rate related to initial value & dependent on Hb Sat
EFFECT OF TEMP ON RATE OF CHANGE IN ABG VALUES

37 C (Change 4 C (Change every

Parameter
every 10 min) 10 min)

 pH 0.01 0.001

 PCO2 1 mm Hg 0.1 mm Hg

 PO2 0.1 vol % 0.01 vol %

oEXCESSIVE HEPARIN
Dilutional effect on results  HCO3- & PaCO2
Syringe be emptied of heparin after flushing
Risk of alteration of results  with:
1. size of syringe/needle
2. vol of sample
25% lower values if 1ml sample taken in 10 ml syringe (0.25 ml heparin
in needle)
Syringes must be > 50% full with blood sample
HYPERVENTILATION OR BREATH HOLDING May lead to erroneous lab
results
 AIR BUBBLES

1. PO2 150 mmHg & PCO2 0 mm Hg in air bubble(R.A.)

2. Mixing with sample lead to  PaO2 &  PaCO2

3. Discard sample if excessive air bubbles

4. Seal with cork/cap imm after taking sample

 WBC COUNT

0.1 ml of O2 consumed/dL of blood in 10 min in pts with N TLC

Marked increase in pts with very high TLC/plt counts –
hence imm chilling/analysis essential
 TYPE OF SYRINGE

1. pH & PCO2 values unaffected

2. PO2 values drop more rapidly in plastic syringes (ONLY if PO2 > 400 mm
Hg)
3. Other adv of glass syringes:
Min friction of barrel with syringe wall
Usually no need to ‘pull back’ barrel – less chance of air bubbles
entering syringe
Small air bubbles adhere to sides of plastic syringes – difficult to expel
Though glass syringes preferred, differences usually not of clinical
significance  plastic syringes can be and continue to be used
 Approach to ABG Interpretation
 Assessment of the type of acid base disorder requires at a minimum 2 of the
following:
1) Arterial pH
2) pCO2
3) plasma HCO3-
 Complete analysis of an ABG requires:
1. pH
2. pO2
3. pCO2
4. HCO3-
5. O2 Sat BE/BD
Anion Gap (AG)
 AG
 HCO3-
 Arterial Oxygen Tension (PaO2)

 Normal value in healthy adult breathing room air at sea level  97

mm Hg.
  progressively with  age
 Dependant upon
1. FiO2
2. Patm
 Hypoxemia is PaO2 < 80 mm Hg at RA
• The expected Pao2 for a patient being given supplemental oxygen can
be roughly estimated by multiplying the actual delivered percentage
of O2 by 5, the “Five Times Rule.”
• Hg. For every 1000 ft (305 m) rise in altitude, barometric pressure
drops approximately 25 mm Hg, and the atmospheric partial pressure
of oxygen (Po2) drops about 5 mm Hg
 Inspired O2 – PaO2 Relationship

FIO2 (%) Predicted Min PaO2

(mm Hg)
30 150
40 200
50 250
80 400
100 500

If PaO2 < FIO2 x 5, pt probably hypoxemic at RA

 Venous Sample

• The person who has drawn the sample can tell if he has drawn a
pulsating blood’ OR blood under high pressure
• PaO2 < 40
• Partly mixed sample- Difficult to recognize
ARTERIAL VENOUS CENTRAL VENOUS

pH 7.38-7.42 7.36-7.39 7.37-7.40

paO2 80-100 38-42 50-54
pCO2 36-44 44-48 45-49
HCO3 22-26 20-24 22-26
SaO2 95-100 75 78
 DEFINITIONS AND TERMINOLOGY

3 Component Terminology –
I. Compensated/Uncompensated
II. Respiratory/Metabolic
III. Acidosis/Alkalosis
 ACIDEMIA – reduction in arterial pH (pH<7.35)
 ALKALEMIA – increase in arterial pH (pH>7.45)
 ACIDOSIS – presence of 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-
 Characteristics of  acid-base disorders

COMPENSATORY
DISORDER PRIMARY RESPONSES RESPONSE

Metabolic
 [H+]  PH  HCO3-  pCO2
acidosis

Metabolic
 [H+]  PH  HCO3-  pCO2
alkalosis

Respiratory
 [H+]  PH  pCO2  HCO3-
acidosis

Respiratory
 [H+]  PH  pCO2  HCO3-
alkalosis
 Compensation

 In the presence of acidosis or alkalosis, regulatory mechanisms occur

which attempt to maintain the arterial pH in the physiologic range.
These processes result in the return of pH towards, but generally just
outside the normal range
 Disturbances in HCO3- (metabolic acidosis or alkalosis) result in
respiratory compensation while changes in CO2 (respiratory
acidosis/alkalosis) are counteracted by renal compensation
a. Renal compensation – kidneys adapt to alterations in pH by
changing the amount of HCO3- generated/excreted. Full renal
compensation takes 2-5 days
b. Respiratory compensation – alteration in ventilation allow
immediate compensation for metabolic acid-base disorders
 RENAL & RESPIRATORY COMPENSATIONS TO  ACID-
BASE DISTURBANCES
Disorder Prediction of
Compensation
Metabolic Paco2 = (1.5 X HC03-) + 8 士2 or
acidosis Paco, will ↓ 1 .25 mmHg per m mol/l ↓ in [HC03-]
or
Paco2 = [HC03-] + 15
Metabolic Paco, wi l l ↑ 0.75 mmHg per mmol/L ↑ in [HC03-] or
alkalosis Paco, will ↑ 6 mmHg per 10 mmol/L ↑ in [HC03-]
or
Paco2 = [HC03-] + 1 5
Respiratory alkalosis
Acute HCO3-] will ↓ 0.2 mmo1/L per mmHg ↓ in Paco2
Chronic [HCO3-] will ↓ 0.4 mmo1/L per mm Hg ↓ in Paco2

Respiratory acidosis
Acute [HCO3] will ↑ 0.1 mmo1/L per m m H g ↑ in Pac02
Chronic [HCO3-] will ↑ 0.4 mmo1/L per m m H g ↑in Paco2
 STEPWISE APPROACH TO ACID-BASE ANALYSIS

• Reference ranges for arterial pH, PCO2, and HCO3 are

• pH = 7.36 – 7.44
• PCO2 = 36 – 44 mm Hg
• HCO3 = 22 – 26 mEq/L
oStage I: Identify the Primary Acid-Base Disorder
• In the first stage of the approach, the PaCO2 and pH are used to
identify the primary acid-base disorder.
• Rule 1: If the PaCO2 and/or the pH is outside the normal range, there
is an acid-base disorder.
• Rule 2: If the PaCO2 and pH are both abnormal, compare the
directional change.

2a. If the PaCO2 and pH change in the same direction, there is a

primary metabolic acid-base disorder.
Ex – pH 7.1; HCO3 8 mEq/L; PaCO2 20mmHg ; Na 140 mEq; Cl 106mEq

2b. If the PaCO2 and pH change in opposite directions, there is a

primary respiratory acid-base disorder
Ex – pH 7.54; HCO3- 21mEq; PaCO2 21mmHg;
• Rule 3: If only the pH or PaCO2 is abnormal, the condition is a mixed
metabolic and respiratory disorder (i.e., equal and opposite disorders).

3a. If the PaCO2 is abnormal, the directional change in PaCO2 identifies the
type of respiratory disorder (e.g., high PaCO2 indicates a respiratory
acidosis), and the opposing metabolic disorder.
Example: Na+ 140; K+ 3.5; CI- 88; HC03- 42; AG 10; Paco2 67; pH 7.42 (COPD
on diuretics)

3b. If the pH is abnormal, the directional change in pH identifies the type of

metabolic disorder (e.g., low pH indicates a metabolic acidosis) and the
opposing respiratory disorder.
• Example: Na+ 140; K+ 4.0; CI- 102; HCO 18; AG 20; Paco2 38; pH 7.30
(severe pneumonia, pulmonary edema)
 Stage II: Evaluate the Secondary Responses

• The second stage of the approach is for cases where a primary acid-
base disorder has been identified in Stage I. (If a mixed acid-base
disorder was identified in Stage I, go directly to Stage III).
• The goal in Stage II is to determine if there is an additional acid-base
disorder.
• Rule 4: For a primary metabolic disorder, if the measured PaCO2 is
higher than expected, there is a secondary respiratory acidosis, and
• If the measured PaCO2 is less than expected, there is a secondary
respiratory alkalosis.

• Rule 5: For a primary respiratory disorder, a normal or near-normal

HCO3 indicates that the disorder is acute.
• Rule 6: For a primary respiratory disorder where the HCO3 is
abnormal, determine the expected HCO3 for a chronic respiratory
disorder.
ΔHCO3 = 0.4 × ΔPaCO2

• 6a. For a chronic respiratory acidosis, if the HCO3 is lower than

expected, there is an incomplete renal response, and if the HCO3 is
higher than expected, there is a secondary metabolic alkalosis.
Expected HCO3 = 24 + [0.4 × (current PaCO2 – 40)]

• 6b. For a chronic respiratory alkalosis, if the HCO3 is higher than

expected, there is an incomplete renal response, and if the HCO3 is
lower than expected, there is a secondary metabolic acidosis.
Expected HCO3 = 24 – [0.4 × (40 – current PaCO2)]
Stage III: Use The “Gaps” to Evaluate a Metabolic Acidosis

 AG traditionally used to assess acid-base status esp in D/D of met acidosis

  AG &  HCO3- used to assess mixed acid-base disorders

AG based on principle of electroneutrality:

 Total Serum Cations = Total Serum Anions
 Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4
+ Protein + Organic Acids)
 Na + UC = HCO3 + Cl + UA
 Na – (HCO3 + Cl) = UA – UC
 Na – (HCO3 + Cl) = AG
 Normal value of AG = 12 +/- 4 meq/L
 Revised N value AG = 8 +/- 4 meq/L
 Changes in methods of measurement of Na, Cl &
HCO3 and resultant shift of Cl value to higher range
 Limiting factors for AG

• Albumin is the principal unmeasured anion, and the principal determinant

of the anion gap.
• Albumin is a weak (i.e., poorly dissociated) acid that contributes about 3
mEq/L to the AG for each 1 g/dL of albumin in plasma (at a normal pH)
• A low albumin level in plasma will lower the AG, and this could mask the
presence of an unmeasured anion (e.g., lactate) that is contributing to a
metabolic acidosis.
• “corrected AG”(AGc) has been proposed to include the contribution of
albumin:
• AGc = AG + 2.5 × (4.5 – [albumin in g/dL])
 DRUGS –
• Lithium and polymyxin cause fall in AG ( UC) while
• carbenicillin cause  in AG (act as UA)
 Using the Anion Gap

Classification of Metabolic Acidosis with the Anion Gap (AG)

High AG
Lactic Acidosis
Ketoacidosis
End-Stage Renal Failure
Methanol Ingestion
Ethylene Glycol Ingestion
Salicylate Toxicity
Normal AG
Diarrhea
Isotonic Saline Infusion
Early Renal Insufficiency
Renal Tubular Acidosis
Acetazolamide
Ureteroenterostomy
  AG -  HCO3- RELATIONSHIP
 used to assess mixed acid-base disorders in setting of high AG Met
Acidosis:
 AG/ HCO3- = 1  Pure High AG Met Acidosis
 AG/ HCO3- > 1  Assoc Metabolic Alkalosis
 AG/ HCO3- < 1  Assoc N AG Met Acidosis
 Based on assumption that for each 1 meq/L increase in AG, HCO3
will fall by 1 meq/L
• Management of a patient with diabetic ketoacidosis (DKA) is associated
with improvement in the blood glucose and the clinical condition of the
patient, but the acidosis persists
• DKA presents with a high AG metabolic acidosis,
• But the aggressive infusion of isotonic saline during the initial management
creates a hyperchloremic (normal AG) metabolic acidosis, which replaces
the high AG acidosis as the ketoacids are cleared.
• In this situation, the serum bicarbonate remains low, but the gap-gap ratio
falls below 1 as the acidosis switches from a high AG to a normal AG
acidosis
• Example: Na+ 1 35; K+ 3.0; CI- 110; HCO3- 10; AG 15; Paco2 =25; pH 7.20
( diarrhea and lactic acidosis, toluene toxicity, treatment of diabetic
ketoacidosis)
 Respiratory Acid-Base Disorders

• The secondary response to changes in PaCO2 occurs in the kidneys.

• Renal response is relatively slow, and can take 2 or 3 days to reach
completion.
• Because of the delay in the secondary response, respiratory acid-base
disorders are separated into acute and chronic disorders.
 Acute Respiratory Disorders

• Acute changes in PaCO2 have a small effect on the plasma HCO3, as

indicated in the following two equations .

• For acute respiratory acidosis: ΔHCO3 = 0.1 × ΔPaCO2

• For acute respiratory alkalosis: ΔHCO3 = 0.2 × ΔPaCO2

 Chronic Respiratory Disorders

• The renal response to an increase in PaCO2 is an increase in HCO3

reabsorption in the proximal renal tubules, which raises the plasma
HCO3 concentration.
• The response to a decrease in PaCO2 is a decrease in renal HCO3
reabsorption, which lowers the plasma HCO3 concentration.
• The magnitude of this response is similar, regardless of the directional
change in PaCO2,
• So the equation below applies to both chronic respiratory acidosis
and alkalosis.
ΔHCO3 = 0.4 × ΔPaCO2
• For chronic respiratory acidosis:
Expected HCO3 = 24 + [0.4 × (current PaCO2 – 40)]

• For chronic respiratory alkalosis:

Expected HCO3 = 24 – [0.4 × (40 – current PaCO2)]
 RESPIRATORY ALKALOSIS

Central nervous system Hypoxemia or tissue

Drugs or hormones
stimulation hypoxia

1. Pain
2. Anxiety, psychosis 1 . High altitude
3. Fever 2. Pneumonia, pulmonary
1 Pregnancy， progesterone
4. Cerebrovascular accident edema
2. Salicylates
5. Meningitis, encephalitis 3. Aspiration
3. Cardiac failure
6. Tumor 4. Severe anemia
7. Trauma
 Manifestations of Resp Alkalosis

• Acute reduction in Pco2 produces a reduction in [H+], resulting in an

increase in negative charge on anionic buffers.
• The now negatively charged proteins instead bind calcium, and if the
effect is sufficiently large, the reduction in ionized calcium produces
tetany (e.g., carpopedal spasm) and paresthesias.
• Hypocapnia also produces substantial reductions in cerebral blood
flow and results in reduced tissue oxygen delivery due to a leftward
shift in the oxygen-hemoglobin dissociation curve.
 Treatment of Respiratory Alkalosis

• Resp alkalosis by itself not a cause of resp failure unless work of

increased breathing not sustained by resp muscles
• Rx underlying cause
• Usually extent of alkalemia produced not dangerous.
• Admn of O2 if hypoxaemia
• If pH>7.55 pt may be sedated/anesthetised/ paralysed and/or put on
MV.
 RESPIRATORY ACIDOSIS

Central Airway Parenchyma Neuromuscular

1.Drugs 1. Obstruction 1 . Emphysema 1. Poliomyelitis

(anesthetics， 2. Asthma 2. Pneumoconiosis 2. Kyphoscoliosis
morphine, 3. Bronchitis 3. Myasthenia
sedatives) 4. Adult respiratory 4. Muscular
distress syndrome dystrophies
2. Stroke 5 . Barotrauma

3. 1nfection
 Manifestations of Resp Acidosis

 NEUROMUSCULAR: Related to cerebral A

vasodilatation &  Cerebral BF
1.Anxiety
2.Asterixis
3.Lethargy, Stupor, Coma
4.Delirium
5.Seizures
6.Headache
7.Papilledema
8.Focal Paresis
9.Tremors, myoclonus
 Treatment of Respiratory Acidosis

• Ensure adequate oxygenation - care to avoid inadequate

oxygenation while preventing worsening of hypercapnia due to
supression of hypoxemic resp drive
• Correct underlying disorder if possible
• Alkali (HCO3) therapy rarely in ac and never in ch resp acidosis  only
if acidemia directly inhibiting cardiac functions
 METABOLIC ACIDOSIS

• Pathophysiology
• 1. HCO3 loss
a. Renal
b. GIT
2.Decreased renal acid secretion –
3.Increased production of non-volatile acids
a. Ketoacids
b. Lactate
c. Poisons
d. Exogenous acids
 Causes of High AG Met Acidosis

Lactic acidosis Toxins

Ethylene glycol
Ketoacidosis Methanol
Diabetic Salicylates
Alcoholic Propylene glycol
Starvation Pyroglutamic acid (5-oxoproline)

Renal failure (acute and chronic)

 Causes of N AG Met Acidosis

• Gastrointestinal bicarbonate loss – Diarrhea

• Renal acidosis
A. Hypokalemia
1 . Proximal RTA (type 2)
Drug-induced: acetazolamide, topiramate
2. Distal (classic) RTA (type 1 )
Drug induced: amphotericin ß
• B. Hyperkalemia
1 . Generalized distal nephron dysfunction (type 4 RTA)
 Manifestations of Met Acidosis

• Cardiovascular
Impaired cardiac contractility
Arteriolar dilatation
Increased pul vascular resistance
Fall in C.O.,ABP & hepatic and renal BF
Sensitization to reentrant arrhythmias & reduction in threshold
of VFib
Attenuation of cardiovascular responsiveness to catecholamines
 Respiratory
Hyperventilation
 strength of respiratory muscles & muscle fatigue
Dyspnea
 Metabolic
Increased metabolic demands
Insulin resistance
Inhibition of anaerobic glycolysis
 Cerebral
Inhibition of metabolism and cell vol regulation
Mental status changes
 Treatment of Met Acidosis

When to treat
•Severe acidemia  Effect on Cardiac function most imp factor for pt
survival since rarely lethal in absence of cardiac dysfunction.
•Contractile force of LV  as pH  from 7.4 to 7.2
•However when pH < 7.2, profound reduction in cardiac function
occurs and LV pressure falls by 15-30%
•Most recommendations favour use of base when pH < 7.15-7.2 or
HCO3 < 8-10 meq/L
 How to treat?

Rx Undelying Cause
HCO3- Therapy
 Aim to bring up pH to 7.2 & HCO3-  10 meq/L
 Qty of HCO3 admn calculated:
0.5 x LBW (kg) x HCO3 Deficity (meq/L)
 METABOLIC ALKALOSIS

Pathophysiology
• Metabolic alkalosis results from gain of bicarbonate or loss of acid
• Metabolic alkalosis is typically classified as chloride-sensitive and chloride-
insensitive.
• Conditions that result in chloride loss
• Tend to reduce serum chloride concentration and extracellular volume
• Reduction in extracellular volume increases mineralocorticoid activity,
which enhances sodium reabsorption and potassium and hydrogen ion
secretion in the distal tubule, which in turn enhance bicarbonate
generation.
• The resulting increase in serum [HCO3–] eventually exceeds the tubule’s
maximum ability to reabsorb filtered bicarbonate.
• The resulting urine is alkaline
• It is largely free of chloride (<10 mEq/L).
• The result is hypokalemic, hypochloremic alkalosis that responds to normal
saline.

• Chloride-insensitive metabolic alkalosis

• Usually associated with normovolemia or hypervolemia and often include
hypertension.
• These diseases usually cause excess mineralocorticoid activity, resulting in
the same pathophysiologic cascade described above.
• Urine chloride is generally normal or elevated (>10 mEq/L) and the
alkalosis cannot be reversed with normal saline
• Conditions that result in chloride loss, such as
1. Vomiting (which also causes acid loss),
2. diarrhea,
3. diuretic therapy, and
4. Chloride wasting diseases (e.g., cystic fibrosis and chloride-wasting
enteropathy.
• Conditions producing “chloride-unresponsive alkalosis” and
hypertension include
1. renal artery stenosis,
2. renin-secreting tumors,
3. adrenal hyperplasia,
4. hyperaldosteronism,
5. Cushing’s syndrome,
6. Liddle’s syndrome, and
7. exogenous mineralocorticoids (e.g., licorice, fludrocortisone).

• Chloride-unresponsive alkalosis caused by

1. Bartter’s and Gitelman’s syndromes is usually associated with
normotension.
 Evaluation of Met Alkalosis

 Urinary Cl- & K+ measurements before therapy useful diagnostically.

 Low urinary chloride (<10 mEq/L) seen in alkalotic states where Cl-
depletion predominates (except cause is use of chloruretic diuretic)
 Remains low until Cl- repletion nearly complete.
 Urinary K+ conc of >30 mEq/L with  S. K+ suggests renal K+
wasting due to:
1. Intrinsic renal defect
2. Diuretics
3. High circulating aldosterone
 Urinary K+ conc of <20 mEq/L with  S. K+ suggests extrarenal K+
loss.
 Manifestations of Met Alkalosis

 Cardiovascular
Arteriolar constriction
Reduction in Coronary BF/Anginal threshold
Predisposition to refractory SV & V arrhythmias
(esp if pH > 7.6)
Respiratory - Hypoventilation (Compensatory) 
Hypercapnia/Hypoxemia
 Metabolic
Stimulation of anaerobic glycolysis & organic acid production
Reduction plasma ionized Calcium conc
Hypokalemia (secondary to cellular shifts)
Hypomagnesemia & Hypophosphatemia
 Cerebral
Reduction in Cerebral BF  mental status changes
(stupor, lethargy & delirium)
N-M irritability (related to low ionized plasma Ca)
 Tetany, Hyperreflexia, Seizures
 Treatment of Metabolic Alkalosis

• Rx underlying cause resp for vol/Cl- depletion

• Isotonic NaCl appropriate therapy  simultaneously corrects both deficits
• Acetazolamide produces significant bicarbonaturia and is effective in the
treatment of metabolic alkalosis,
• If alkalosis is severe ([HCO3 –] >45 mmol/L) and associated with serious
signs or symptoms not responsive to supportive care, the use of
intravenous hydrochloric acid should be considered.
• Dose = (Δ[HCO3–]) ∗ 0.5 weight, in kg)
• 0.1 normal solution (100 mmol/L) should be used,
• Infused ideally at 0.1 mmol/kg/h
 CASE 1

• George Kent is a 54 year old widower with a history of chronic

obstructive pulmonary disease and was rushed to the emergency
department with increasing shortness of breath, pyrexia. Upon
examination, crackles and wheezes can be heard in the lower lobes;
he has a tachycardia and a bounding pulse.
• Measurement of arterial blood gas shows pH 7.3, PaCO2 68 mm Hg,
HCO3 28 mmol/L, and PaO2 60 mm Hg. How would you interpret
this?

• pCO2↑
• pH ↓
• For acute respiratory acidosis: ΔHCO3 = 0.1 × ΔPaCO2
=2.8
• Expected HCO3 = 24+2.8 = 26.8

• The patient has respiratory acidosis (raised carbon dioxide) resulting

from an acute exacerbation of chronic obstructive pulmonary disease.
 CASE 2

• An elementary student, was rushed to the hospital due to vomiting

and a decreased level of consciousness. The patient displays slow and
deep (Kussmaul breathing), and he is lethargic and irritable in
response to stimulation. He appears to be dehydrated—his eyes are
sunken and mucous membranes are dry—and he has a two week
history of polydipsia, polyuria, and weight loss.
• Measurement of arterial blood gas shows pH 7.0, PaO2 90 mm Hg,
PaCO2 23 mm Hg, and HCO3 12 mmol/L; other results are Na+ 126
mmol/L, K+ 5 mmol/L, and Cl- 95 mmol/L. What is your assessment?
• pH↓ pCO↓ = primary metabolic acidosis
• Expected pC02 = (1.5 * 12) + 8 +/- 2
= 24+/-2
• AG = 19
• High AG metabolic acidosis
• The student was diagnosed having diabetes mellitus. The results show
that he has metabolic acidosis (low HCO3 -) with respiratory
compensation (low CO2).
 CASE 3
• Na+ 140; K+ 3; Cl- 95; HCO3- 25; paCO2 40; pH 7.42;

• This is seeming normal set of values until the anion gap is calculated
• AG = 140- (95+25) = 20
• ∆ AG = 10
• ∆ HCO3 = 1
• METABOLIC ACIDOSIS AND METABOLIC ALKALOSIS
• CASE-These lab values are from a patient with chronic renal failure(causing
the metabolic acidosis) who began vomiting (metabolic alkalosis).

• The acute alkalosis of vomiting offset the chronic acidosis of renal failure
and hence the pH is normal.
 CASE 4

• PH-7.50,Pco2-20mmHg,bicarb-15 mmol.,sodium-145,chloride-100mmol.
• The pH is high ,the pco2 is low ,bicarb is low and increased anion gap.
• The primary abnormality is low pco2 and pH is high the patient is in
respiratory alkalosis.
• Compensation expected HCO3 = 24-(0.2* [40-20])=20
• Concamitant metabolic acidosis is present.
• Anion gap is 30(I,e > 10) and excess anion gap is 20
• ∆HCO3 = 24-15= 9
• ∆AG/∆HCO3 > 1
• RESPIRATORY ALKALOSIS,METABOLIC ACIDOSIS , METABOLIC
ALKALOSIS

• CASE-This person had h/o vomiting(metabolic alkalosis),evidence of

ketoacidosis(metabolic acidosis) and bacterial pneumonia(respiratory
alkalosis).
 CASE 5
• A 22yr old woman took an overdose of propoxyphene. She arrived
actively seizing in the emergency department. The following lab
studies were obtained on arrival. Ph 7.10, pco2 32mmhg, hco3-
9meq/l. Na 140meq/l, K-3.4meq/l, Cl 106meq/l.

• Calculate AG: 140-(106+9)=25

• Calculate the expected Pco2= 1.5*9+8=21.5

• Calculate the delta AG: 25-10=15

• Diagnosis : AG met acidosis ( d/t seizure lactic acidosis)

• Acute resp acidosis ( opoid toxicity)

THANK YOU