Dr. Anwar Yusr
Consultant of Critical Care medicine
Egyptian fellowship of ICU
USTH
Indications for ABG
(1) Severe respiratory or metabolic disorders.
(2) Clinical features of hypoxia or hypercarbia
(3) Shock.
(4) Sepsis.
(5) Decreased cardiac output.
(6) Renal failure.
(7) Ideally any patient on oxygen therapy.
(9) ventilated patients.
 PaO2; the partial pressure of oxygen in arterial blood
 normal range breathing air > 75 mmHg on air (increases with FiO2)
 pH; the acidity or alkalinity of the blood, determined by the
concentration of hydrogen ions [H+]
 normal range 7.35 – 7.45
 PaCO2; the partial pressure of carbon dioxide in arterial blood
 normal range 35 – 45 mmHg
 Bicarbonate; a buffer, neutralises the effects of excess acid
 normal range 22 – 26 mmol L-1
 Base excess; a measure of the degree of excess acid or alkali
(base) in the blood
 normal range +2 to -2 mmol L-1
Terms used in arterial blood gas analysis
ABG: values
 pH 7.35-7.45
 PaCO2 35-45 mm Hg
 PaO2 80-100 mmHg**
 SaO2 93-98%
 HCO3
- 22-26 mEq/L
 Base excess -2.0 to 2.0 mEq/L
 %MetHb <2.0%
 %COHb <3.0%
 CaO2 16-22 ml O2/dl
* At sea level, breathing ambient air
** Age-dependent
“Normal ranges” difference between Labs
CENTRAL EQUATION OF ACID-BASE
PHYSIOLOGY
 Henderson Hasselbach Equation:
 where [ H+] is related to pH by
 To maintain a constant pH, PCO2/HCO3- ratio should
be constant.
 When one component of the PCO2/ [HCO3-] ratio is
altered, the compensatory response alters the other
component in the same direction to keep the
PCO2/[HCO3- ] ratio constant.
 [H+] in nEq/L = 24 x (PCO2 / [HCO3 -]
 [ H+] in nEq/L = 10 (9-pH)
Henderson-Hasselbalch
Equation
Base
HCO3
pH = pK + log --------- = 6.1 + log ---------
Acid H2CO3 + CO2
pK = the pH at which half of the compound is ionized = 6.1
Base= HCO3
Acid= Carbonic Acid= H2CO3 + pure dissolved CO2 = pCO2 (.03)
Acid-Base Equations
Bicarbonate-Carbonic Acid Buffer System
CO2 + H2O H2CO3 HCO3 + H
(carbonic anhydrase)
 at pH = 7.40 and pCO2 = 40: [HCO3] = 24
 Henderson-Hasselbalch Equation:
 pH = pK + log 10 [(HCO3)/(H2CO3 + CO2)]
(at normal) = 6.1 + log 10 (24/pCO2 x .03)
= 6.1 + log (24/1.2) = 6.1 + log 20 =
6.1 + 1.3 = 7.40
Bicarbonate-Carbonic acid
system HCO3- 24
pH= 6.1 + log ------------- ------ ---- log 20 = 1.3
pCO2 (.03) 1.2
HCO3- 12
pH= 6.1 + log ------------- ------ ---- log 10 = 1.0
pCO2 (.03) 1.2
 The normal ratio of HCO3 to H2CO3 is 20:1.
 The log of 20 is 1.3.
 If you cut the HCO3 in half to 12, the ratio is 10:1.
 The log of 10 is 1.0 .
 The pH thus decreased by 0.3.
 Whenever the ratio of HCO3 to H2CO3 is reduced by one-half,
the pH falls by 0.3.
pH
7.4
CO2 HCO3
-
Respiratory Component
(acid)
Metabolic Component
(base)
Arterial blood pH = 7.40
Venous Blood pH = 7.35
The Basic Relationship between PCO2
and Plasma pH
Animation: Relationship Between PCO2 and Plasma pH
PLAY
The Carbonic Acid-Bicarbonate
Buffer System
Compensatory response or regulation
of pH
By 3 mechanisms:
1. Chemical buffers:
 React instantly to compensate for the addition or
subtraction of H+ ions.
2. CO2 elimination:
 Controlled by the respiratory system.
 Change in pH result in change in PCO2 within minutes.
3. HCO3- elimination:
 Controlled by the kidneys.
 Change in pH result in change in HCO3.
 It takes hours to days and full compensation occurs in
2-5 days.
 75-80% HCO3 is absorbed in the proximal tubule.
Kidney tubules and pH Regulation
Correlating Chloride and Bicarbonate
 Tend to move in opposite directions.
 Metabolic Alkalosis:
 High Bicarbonate.
 Low Chloride.
 Metabolic Acidosis:
 Low Bicarbonate.
 Chloride Normal (Anion Gap) or High (non-AG).
 Chloride low if Na/Cl >1.4; high if Na/Cl < 1.27.
Low chloride is synonymous with metabolic alkalosis
(or compensation for chronic respiratory acidosis).
Even if pH is normal, low chloride means
alkalosis.
The Central Role of the Carbonic Acid-
Bicarbonate Buffer System in the Regulation
of Plasma pH
The Central Role of the Carbonic Acid-
Bicarbonate Buffer System in the Regulation
of Plasma pH
Compensation
 Compensation is rarely
complete Returns pH toward
normal.
 Compensation is not a secondary
acidosis or alkalosis.
 High altitude and pregnancy may
have full compensation—but it
takes time
 Acetazolamide hastens
compensation.
 Improves Mountain sickness.
Respiratory
Renal
Major causes are:
Depletion of bicarbonate reserve.
Inability to excrete hydrogen ions at
kidneys.
Production of large numbers of fixed /
organic acids.
Bicarbonate loss due to chronic diarrhea.
Metabolic acidosis
The Response to Metabolic Acidosis
Occurs when HCO3
- concentrations
become elevated.
Caused by repeated vomiting.
Metabolic alkalosis
Metabolic Alkalosis
Acid-Base: Tough Stuff?
It’s all in your mind
 7.53/15/80/12
 7.25/25/110/10
 6.88/32/100/7
 7.58/49/98/45
 7.30/40/156/19
 7.10/30/365/9
 7.72/28/95/37
 7.45/20/80/14
You are routinely
missing triple acid-
base disorders
Dr. Smith
Dr. Rock
Six step method
1) Identify any abnormality (is there acidemia or
alkalemia?).
2) Is the primary process metabolic or respiratory?
3) If the primary process is respiratory, is it acute
or chronic?
4) Is the compensation adequate?
5) Is there an AG?
6) Is there a mixed disorder?
Step 1 Identify the disorder
 Take a look at the pH, as it directs towards the
principal disorder.
< 7.35 Acidemia
>7.45 Alkalemia
7.35-
7.45
Normal
Mixed
disorder
Acidemia and Alkalemia vs.
acidosis and alkalosis
pH < 7.36 ([H+] > 44) is acidemia.
pH > 7.44 ([H+] < 36) is alkalemia.
mixed disorders of acidosis and
alkalosis may be neither acidemic
nor alkalemic.
e.g. 7.40/ 25/ pCO2/ 15
Step 2 RESPIRATORY or METABOLIC?
 IS PRIMARY DISTURBANCE RESPIRATORY OR
METABOLIC?
pH PCO2 or pH PCO2 METABOLIC
pH PCO2 or pH PCO2 RESPIRATORY
RULE- If either the pH or PCO2 is Normal, there is a
mixed metabolic and respiratory acid base disorder.
Step 4 Respiratory
Compensation
Metabolic Acidosis:
 Occurs rapidly.
 Hyperventilation.
 “Kussmaul Respirations”
 Deep > rapid (high tidal
volume).
 Is not Respiratory
Alkalosis.
Metabolic Alkalosis:
 Calculation not as
accurate
 Hypoventilation.
 Not Respiratory
Acidosis.
 Restricted by
hypoxemia.
 PCO2 seldom > 50-55.
pCO2=1.5 x HCO3 + 8 +/- 2
Winter’s formula
pCO2=0.9 x HCO3 + 15
Step 4 Metabolic
Compensation
Acute Hypercapnia:
HCO3 increases 1
mmol/L for each 10
mmHg increase in
PaCO2 >40
Chronic Hypercapnia:
HCO3 incr. 3.5 mmol/L
for each 10 mmHg
increase in PaCO2
>40
Acute Hypocapnia:
HCO3 decreases 2
mmol/L for every 10
mmHg decrease in
PaCO2 <40
Chronic Hypocapnia:
HCO3 decreases 5
mmol/L for every 10
mmHg decrease in
PaCO2 <40
CO2 + H2O H2CO3 H + HCO3
3 most important equations
so far
 Chronic resp. acidosis:
steady-state pCO2 is increased by 10 for
every 3.5 increase in HCO3.
 Acute metabolic acidosis:
 pCO2 = 1.5 x HCO3 + 8 (+/- 2)
 Acute metabolic alkalosis:
 pCO2 = 0.9 x HCO3 + 15
Step 5 Anion Gap
 Described by Gamble in 1939.
 Electroneutrality.
 Na+, Cl-, and HCO3 are measured ions
Na + UC = Cl + HCO3 + UA
UC = Sum of unmeasured cations
UA = Sum of unmeasured anions
Anion Gap
Anion Gap
Unmeasured Cations:
 Total 11 mEq/L
Potassium 4
Calcium 5
Magnesium 2
Unmeasured Anions:
 Total 23 mEq/L
Sulfates 1
Phosphates 2
Albumin 16
Lactic acid 1
Org. acids 3
Na + UC = Cl + HCO3 + UA
140 + 11 = 104 + 24 + 23
151 = 151
Anion Gap = Na - (Cl + HCO3)
Acid Base disorders
 Anion Gap: represent the unmeasured anions normally
present in plasma ( po4, SO4, Creatinine and proteins).
AG = (Na +k) - (CL+HCO3) = 16 ± 4 mEq/L
if K+ is not calculated= 12 mEq/L
Metabolic acidosis is conveniently divided into:
1. High anion–gap metabolic acidosis:  unmeasured anions 
 HCO3 lactic acidosis; ketoacidosis; drug poisonings (e.g., aspirin,
ethyelene glycol, methanol)
2. Normal anion–gap metabolic acidosis (hyperchloremic
metabolic acidosis)
 HCO3  compensatory  CL by the kidney.
Diarrhea; some kidney problems e.g., renal tubular
acidosis, interstitial nephritis, small bowel or pancreatic
drainage & fistula or Ureterosigmoidostomy.
Acid Base disorders
METABOLIC ALKALOSIS
 Chloride responsive (responds to NaCl or KCl therapy): diuretics;
Corticosteroids; gastric suctioning; vomiting.
 Chloride resistant: any hyperaldosterone state, e.g., Cushing's
syndrome; severe K+ depletion.
RESPIRATORY ACIDOSIS
 Central nervous system depression (e.g., drug overdose).
 Chest bellows dysfunction (e.g., Guillain-Barré syndrome, myasthenia
gravis).
 Disease of lungs and/or upper airway (e.g., chronic obstructive lung
disease, severe asthma attack, severe pulmonary edema).
RESPIRATORY ALKALOSIS
 Hypoxemia (includes altitude), Anxiety, Sepsis, Any acute
pulmonary insult e.g., pneumonia, mild asthma attack, early pulmonary
edema, pulmonary embolism.
Causes High AG Metabolic
Acidosis
 Methanol
 Uremia/Renal
Failure
 DKA
 Paraldehyde
 INH, Iron-lactate
 Lactic Acidosis:
 Has many etiologies.
 Cyanide, CO, Toluene, HS.
 Poor perfusion.
 Ethylene glycol.
 Salicylates:
 Methyl salicylate
o (Oil of wintergreen)
 Mg salicylate (Doan’s pills)
Levraut J et al. Int Care Med
23:417, 1997
MUDPILES
Metabolic Acidosis: Normal
AG
 Loss of HCO3:
Severe diarrhea.
Post-hypocapnia.
Ureteroileostomy.
Acetazolamide.
 Failure to excrete [H+]
Renal Tubular Acidosis
○ Types 1-4.
○ Toluene.
 Administration of [H+]
Ammonium chloride.
1. Loss of HCO3
2. Failure to excrete [H+]
3. Administration of [H+]
Decreased or Negative Anion
Gap
 Low protein most important:
Albumin has many unmeasured negative charges.
“Normal” anion gap (12) in cachectic person.
o Indicates anion gap metabolic acidosis.
2-2.5 mEq/liter drop in AG for every 1 g drop in
albumin.
 Other etiologies of low AG:
Low K, Mg, Ca, increased globulins (Mult. Myeloma),
Li, Br (bromism), I intoxication.
 Negative AG:
more unmeasured anions than unmeasured cations.
Bromide, Iodide, Multiple Myeloma.
Causes of metabolic
acidosis
Metabolic Acidosis—
Bad??
 Impaired cardiac contractility.
 Decreased threshold for VF.
 Decreased Hepatic and Renal perfusion.
 Increased Pulmonary Vasc resistance.
 Inability to respond to catecholamines.
 Vascular collapse.
 Increased Anion Gap.
 Normal Anion Gap (Hyperchloremic).
Reasons to Limit Bicarbonate
therapy
 Initially injected into 3 liter plasma volume.
 (not 5 liter blood volume because does not enter red cells).
 Theoretical, but probably does not happen:
 Increase intracellular acidosis.
 Will increase pCO2 and need for ventilation.
 N.S: 150mEq/l of Na, Bicarb: 1000mEq/l of Na.
 As much Na as 350 ml’s normal saline.
 like hypertonic saline: leads to Hypernatremia & Fluid overload.
 Extra bicarbonate can increase potassium
requirements, may increase hepatic production of
ketones, and may delay resolution of cerebral acidosis.
Base Deficit
Volume of distribution, extracellular fluid 0.3
L/kg
 = 0.3 x kg x (24 – HCO3) in mEq/l
one ampule of bicarb = 50 mEq/50 ml
 E.g.: 70 kg person with bicarb of 3
0.3 x 70 x 21 = 441 mEq
441mEq ÷ 50 mEq/ml/ampule = 9 Amps of bicarb
 Suppose you want to get the bicarb back to 6
0.3 x 70 x (6-3) = 63
63 mEq ÷ 50 mEq/ml/ampule = 1.25 Amps of
bicarb.
When to give
bicarbonate
Do NOT base it on pH.
Base it on HCO3 level < 6.
For low pH:
If bicarbonate < 6:
give bicarb 1-2 amps.
Recheck ABG.
If pCO2 > 1.5 (HCO3) + 8:
then ventilate better.
Step 6: Calculate Delta Gap
 Used only if there is Anion
Gap.
Delta gap = (actual AG – 12) + HCO3
 Adjusted HCO3 should be 24 (+_ 6) {18-30}
 If delta gap > 30 additional metabolic
alkalosis.
 If delta gap < 18 additional non-gap
metabolic acidosis.
 If delta gap 18 – 30 no additional
metabolic disorders.
Change in Anion Gap vs. HCO3
 In simple AG Metabolic Acidosis
decrease in plasma bicarbonate = increase in AG
Anion Gap
HCO3
 <1 = High anion gap & normal AG acidosis.
 1-2 = Pure anion gap metabolic acidosis.
 >2 = High anion gap acidosis with concurrent
metabolic alkalosis.
= 1
Six step method
1) Identify any abnormality (is there acidemia or
alkalemia?).
2) Is the primary process metabolic or respiratory.
3) If the primary process is respiratory, is it acute
or chronic?
4) Is the compensation adequate?
5) Is there an AG?
6) Is there a mixed disorder?
Step 6 Mixed Disorders
 Respiratory Acidosis
+ metabolic acidosis
+ metabolic alkalosis
+ metabolic acidosis and alkalosis (triple)
 Respiratory Alkalosis
+ metabolic acidosis
+ metabolic alkalosis
+ metabolic acidosis and alkalosis (triple)
Problem #1
 60 ys male presents to the ED from a nursing
home. You have no history other than he has
been breathing rapidly and is less responsive
than usual.
Na+ 123 Cl- 99 HCO3
- 5
pH 7.31 pCO2 10
Six Steps for Acid-Base Analysis
Step 1. Is there an acidemia or alkalemia?
Acidemia
Six Steps for Acid-Base Analysis
Step 2. Is the primary process metabolic
or respiratory?
pCO2 = 10 should drive pH ↑
HCO3
- = 5 should drive pH ↓
Six Steps for Acid-Base Analysis
Step 3:
If the primary process is respiratory, is it
acute or chronic?
Skip this step as primary process is metabolic!
Six Steps for Acid-Base Analysis
Step 4:
Is there an anion gap?
Na+ - Cl- - HCO3
- > 12?
123 - 99 - 5 = 19
Anion Gap Metabolic Acidosis
Six Steps for Acid-Base Analysis
Step 5:
Is the respiratory compensation adequate?
 Expected pCO2 range =
[1.5(measured HCO3
-)]+8+/- 2
[1.5 (5) +8] +/- 2 = [13.5 – 17.5]
pCO2 = 10
 Therefore it IS a respiratory alkalosis.
Six Steps for Acid-Base Analysis
Step 6:
Are there any other metabolic disturbances?
 Corrected HCO3
- =
(Measured HCO3
-) + (AG-12)
(5) + (19-12) = 12
 Since this does not correct bicarbonate back to
normal, there is a non anion gap acidosis.
1.Anion Gap Metabolic Acidosis.
2.Concurrent Respiratory Alkalosis.
3.non - anion gap met. acidosis.
Problem #2
 42 ys female has the flu for four days with
incessant vomiting. She presents to the ED
two days after stopping insulin due to no food
intake.
Na+ 130 Cl- 80 HCO3
- 10
pH 7.21 pCO2 25
Six Steps for Acid-Base Analysis
Step 1.
Is there an acidemia or alkalemia?
Acidemia
Six Steps for Acid-Base Analysis
Step 2.
Is the primary process metabolic or
respiratory?
pCO2 = 25 should drive pH ↑
HCO3
- = 10 should drive pH ↓
Six Steps for Acid-Base Analysis
Step 3:
If the primary process is respiratory, is
it acute or chronic?
Skip this step as primary process is metabolic!
Six Steps for Acid-Base Analysis
Step 4:
Is there an anion gap?
AG= Na+ - Cl- - HCO3
- > 12?
130 - 80 - 10 = 40!!
Anion Gap Metabolic Acidosis
Six Steps for Acid-Base Analysis
Step 5:
Is the respiratory compensation
adequate?
Expected pCO2 range =
[1.5(measured HCO3
-)]+8+/- 2
[1.5 (10) +8] +/- 2 = [21 - 25]
E.pCO2 = 25, therefore this is normal
respiratory compensation
Six Steps for Acid-Base Analysis
Step 6:
Are there any other metabolic disturbances?
 Corrected HCO3
- =
(Measured HCO3
-) + (AG-12)
(10) + (40-12) = 38
 Since this over corrects bicarbonate
there is a metabolic ALKALOSIS!!
1.Anion Gap Metabolic Acidosis.
2.Metabolic Alkalosis.
Problem #3
30 year old female BMT patient with neutropenic
fever has been receiving multiple antibiotics
including amphotericin B. You are called to the
bedside for her fevers, rigors, and dyspnea.
 Na+ 125 Cl- 100 HCO3
- 8
 pH 7.07 pCO2 28 K+ 2.5
Six Steps for Acid-Base Analysis
Step 1.
 Is there an acidemia or alkalemia?
Acidemia
Six Steps for Acid-Base Analysis
Step2:
 Is the primary process metabolic or
respiratory?
PCO2 = 28 should drive pH ↑
HCO3
- = 8 should drive pH ↓
Six Steps for Acid-Base Analysis
Step 3:
 If the primary process is respiratory, is it
acute or chronic?
Skip this step as primary process is metabolic!
Six Steps for Acid-Base Analysis
Step 4:
 Is there an anion gap?
Na+ - Cl- - HCO3
- > 12?
125 - 100 - 8 = 17
Anion Gap Metabolic Acidosis
Six Steps for Acid-Base Analysis
Step 5:
 Is the respiratory compensation adequate?
Expected pCO2 range =
[1.5(measured HCO3-)]+8+/- 2
[1.5 (8) +8] +/- 2 = [18-22]
pCO2 = 28, therefore this is a respiratory acidosis
even though the value is below 40!!
Six Steps for Acid-Base Analysis
Step 6:
Are there any other metabolic
disturbances?
Corrected HCO3
- =
(Measured HCO3
-) + (AG-12)
(8) + (17-12) = 13
 Since this is below the normal range after
correction,there is a non anion gap acidosis.
1.Anion Gap Metabolic Acidosis.
2.Concurrent Respiratory Acidosis.
3.non - anion gap met. acidosis.
Example 4
Case: 43 yo w f Brought by friends from convention.
Had been staggering, speaking incoherently,
swearing, yelling. Pt. was confused, agitated,
speaking jibberish. Brought to ED. Friends left.
110/70 128 R22 T 98
uncooperative, pretending to smoke cigarette o/w
exam negative except for dry MM Valium,
Cogentin, Haldol given
125/65/64/142 AG = 23 7.67/35/78/40
2.1/37/3.9
U/A, Etoh, U tox all neg. lactate 1.5
Resp. Alk. + Met. Alk. + (because of large
Case continued
To MICU
Pt. arrests. Monitor shows torsade. Pt. intubated and
CPR. Spontaneously back to NSR, now intubated,
unconscious, ventilated by bag, Pt. goes back into
torsade.
What immediate effective treatment was done?
bagging stopped! ---> torsade again spontan.
resolved
Pt. paralyzed, hypoventilated, and put on HCl drip.
Etiology was Alcoholic ketoacidosis with severe
vomiting elicited from later history.
Beware Severe Alkalemia
due to:
 Severe underlying pathology.
also:
General and Cerebral vasoconstrictor.
Shift of oxyhemoglobin dissociation.
Hypokalemia.
Increased SVR and decreased CO: Decreased
Contractility .
Cardiac arrhythmias refractory.
Seizures.
Severe Alkalosis/alkalemia
 HCO3 > 45.
 Be sure oxygenation OK.
 Avoid respiratory stimulation.
 Acetazolamide, 500 mg IV
Monitor K, Mg, PO4
 HCl infusion:
0.1M solution (100 mmol/L, 0.2 mmol/
kg/hour).
Central line.
Total dose = Δ HCO3 x kg x 0.5 (in mmoles).
Example 4
27 y.o man with polyuria and polydipsia for one
week, and intractable vomiting for 4 days.
Today he is critically ill with a temp. of 104 F.
pH 7.50 pCO2 26 pO2 100
150 100 50
3.8 20 1.8
650
AG= 30
Bicarb=24-20= 4
AG=30-12= 18
Na/Cl > 1.4
Mixed Acid-Base: Example
4
 Anion Gap Metabolic Acidosis.
 Concurrent Metabolic Alkalosis.
 Respiratory Alkalosis.
DKA
Vomiting
Sepsis
Example 5
25 y.o. woman admitted 6 hours ago with severe
DKA. Her initial pH was 6.9 with a pCO2 of 10,
and serum bicarb of 2.4. After insulin and NS
hydration, her lab values returned as follows…
140 110
10
AG= 20
Bicarb= 24-10= 14
AG= 20-12= 8
pH 7.25 pCO2 23
Mixed Acid-Base: Example 5
Anion Gap Metabolic Acidosis
Hyperchloremic Metabolic Acidosis.
Respiratory alkalosis
Mixed Acid-Base: Example 6
72 y.o. man with a h/o PUD has been vomiting for 2
weeks. Vitals on presentation: P 140, BP 60/P
pH 7.40 pCO2 40 pO2 300 (FiO2 50%), HCO3 = 24
150 86 100
2.6 24 2.5
AG=150-110= 40
Bicarb=24-24= 0
AG= 40-12= 28
Mixed Acid-Base: Example 6
 Anion Gap Metabolic Acidosis (Shock)
 Metabolic Alkalosis (Vomiting)
Normal ABG does not
equal normal
patient….
Dr. Smith
Test Case #1
An 80 year old man has been confused and c/o
SOB for one week. He also has a hearing
problem and has seen 3 ENT docs in the past
month. Family denies medications.
pH 7.53 pCO2 15 pO2 80 HCO3 12
140 108
3.0 13
120 Diagnosis?
AG = 140 - 121 = 19
Test Case #1
Anion Gap= 140-(108+13)= 19,
 Δ AG = 7
 Δ Bicarb= 24-13= 11
E.pCO2= 1.5 (12) + 8= 26 (compared/w 15)
Patient is Alkalemic (pH= 7.53) indicating a
Superimposed Respiratory Alkalosis
Dx: Metabolic Acidosis and Respiratory Alkalosis
Test Case # 2
23 year old AIDS patient c/o weakness and
prolonged severe diarrhea. He appears
markedly dehydrated.
pH 7.25 pCO2 25 pO2 110 HCO3 11
151 129 60
2.0 12 2.0 Diagnosis?
Test Case # 2
 Anion Gap= 151-(129 + 11)= 11 (normal)
 The patient is Acidemic (pH 7.25)
 Respiratory compensation normal?
1.5 (HCO3) + 8 plus or minus 2
1.5 (11) + 8= 24.5 (compare with 25)
Dx: Uncomplicated Non-AG Metabolic
Acidosis
Test Case #3
45 y.o. alcoholic man has been vomiting for 3
days. Vitals: BP 100/70, P 110. Intern
administered Valium 30 mg for tremulousness.
pH 7.30 pCO2 40
145 96
3.0 19
Serum Ketones +
Diagnosis?
Test Case #3
 Anion Gap= 145- (96 + 19)= 30
 Δ Bicarb= 24-19= 5
 Δ AG= 30-12= 18
 Change in AG >> Change in Bicarb
 Superimposed Metabolic Alkalosis
 Respiratory compensation?
1.5 x (19) + 8= 36 (compared with pCO2=40)
Test Case #3
 Anion Gap Metabolic Acidosis (AKA)
 Metabolic Alkalosis (Persistent Vomiting)
 Mild Respiratory Acidosis (Oversedation)
Test Case #4
A 22 y.o. diabetic man has been vomiting for
several days. He appears ill and dehydrated.
His ABG reveals 7.40/ 40/ 100 on room air.
His labs are below. The resident states he
does not have DKA because the ABG is
normal. Is the resident correct?
130 76
3.0 24
800
Test Case #4
 The resident is NOT correct; Sorry admit
MICU
 Anion gap= 130- (76 + 24)= 30
 Δ Bicarb= 24-24= 0
 Δ AG= 30-12= 18
 Change in AG >>> Change in Bicarb
Dx: Anion Gap Metabolic Acidosis (DKA)
Metabolic Alkalosis (Vomiting)
Test Case #5
33 y.o. woman c/o leg pain and SOB which
started suddenly yesterday.
pH 7.45 pCO2 20 pO2 80
140 116
4.0 14
Diagnosis?
Test Case #5
 Anion gap=
140- (116 + 14)= 10
Dx: Respiratory Alkalosis (PE) with
Compensation
Absolute
contraindications
1. An abnormal modified Allen's test.
2. Local infection, thrombus, or distorted anatomy at
the puncture site (eg, previous surgical
interventions, congenital or acquired
malformations, burns, aneurysm, stent,
arteriovenous fistula, vascular graft)
3. Severe peripheral vascular disease of the artery
selected for sampling
4. Active Raynaud syndrome (particularly sampling
at the radial site)
Relative Contraindications
 Supra therapeutic coagulopathy and infusion of
thrombolytic agents (eg, during streptokinase or
tissue plasminogen activator infusion) are relative
contraindications to arterial needle stick.
we suggest avoiding repeated arterial needle
sticks when the international normalized ratio is
≥3 and/or the activated partial thromboplastin
time is ≥100 seconds
Relative Contraindications
 Similarly, arterial needle stick and catheterization
can be performed in patients with
thrombocytopenia a platelet count >50 x 109/L,
but is generally avoided in those whose count is
≤30 x 109/L. For those with counts between 30
and 50 x 109/L limited needle stick sampling is
sometimes performed, when necessary, with
increased compression time.
 A platelet count <50 x 109/L is generally a
contraindication to arterial catheter insertion.
How are ABG done?
 Site: Radial artery (Brachial, femoral arteries)
 non-dominant hand / good Ulnar artery blood flow/ adequate
pressure following sampling.
 Positioning of wrist: hyperextended + good support
under wrist.
 Syringe & Needles: low resistance / heparinized /
small/ blood “pulse” /  Arterial cannula.
 Lignocaine 1% ? Repeated sampling / pain induced
hyperventilation.
 Complications: Pain, hematoma, air/blood emboli,
infection, vascular trauma/occlusion, arterial spasm.
Delayed Analysis
Consumption of O2 & Production of CO2
continues after blood drawn.
 Iced Sample maintains values for 1-2 hours.
 Uniced sample quickly becomes invalid within 15
-20 minutes.
 PaCO2  3-10 mmHg/hour.
 Pao2 
 pH  d/t lactic acidosis generated by glycolysis
in R.B.C.
FEVER OR HYPOTHERMIA
1. Most ABG analyzers report data at N body temp.
2. If severe hyper/hypothermia, values of pH &
PCO2 at 37 C can be significantly differ from pt’s
actual values.
3. Changes in PO2 values with temp also
predictable.
Hansen JE, Clinics in Chest Med 10(2), 1989 227-237
 If Pt.’s temp < 37C
Substract 5 mmHg Po2, 2 mmHg Pco2 and Add
0.012 pH per 1C decrease of temperature.
AIR BUBBLES:
1. PO2 150 mmHg & PCO2 0 mm Hg in air bubble(R.A).
2. Mixing with sample, lead to  PaO2 &  PaCO2.
 To avoid air bubble, sample drawn very slowly and
preferabily in glass syringe.
Steady State:
Sampling should done during steady state after change
in oxygen therapy or ventilator parameter.
Steady state is achieved usually within 3-10 minutes.
Leucocytosis :
  pH and Po2 ; and  Pco2.
 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.
EXCESSIVE HEPARIN:
 Dilutional effect on results  HCO3
- & PaCO2
 Only .05 ml heperin required for 1 ml blood.
 So syringe be emptied of heparin after flushing or only
dead space volume is sufficient or dry heperin should
be used.
Summary of important points
 Acidosis/Alkalosis are metabolic states ≠ acidemia/alkalemia.
 Doubling or halving the pCO2:HCO3 ratio changes pH by 0.3.
 Bicarbonate therapy based on bicarb ≤ 6, not Ph.
 Low pH with bicarb > 6 needs Rx with ventilation.
 Know the anion gap and MUDPILES.
 Anion Gap > 18 is metabolic acidosis.
 no matter what the pH, pCO2, or bicarb.
 Normal Na/Cl ratio is 1.33 (140/105)
 Na/Cl ratio > 1.4 is metabolic alkalosis (e.g. 140/99)
○ (or compensation for respiratory acidosis)
 Na/Cl < 1.3 is hyperchloremic acidosis (e.g., 140/111)
○ (or compensation for resp alkalosis)
 Winter’s formula: pCO2 should be = 1.5 x HCO3 + 8
“Understanding ABG is not
magic but an art learned by
continued practice”
Acid base and ABG interpretation in  ICU

Acid base and ABG interpretation in ICU

  • 1.
    Dr. Anwar Yusr Consultantof Critical Care medicine Egyptian fellowship of ICU USTH
  • 2.
    Indications for ABG (1)Severe respiratory or metabolic disorders. (2) Clinical features of hypoxia or hypercarbia (3) Shock. (4) Sepsis. (5) Decreased cardiac output. (6) Renal failure. (7) Ideally any patient on oxygen therapy. (9) ventilated patients.
  • 3.
     PaO2; thepartial pressure of oxygen in arterial blood  normal range breathing air > 75 mmHg on air (increases with FiO2)  pH; the acidity or alkalinity of the blood, determined by the concentration of hydrogen ions [H+]  normal range 7.35 – 7.45  PaCO2; the partial pressure of carbon dioxide in arterial blood  normal range 35 – 45 mmHg  Bicarbonate; a buffer, neutralises the effects of excess acid  normal range 22 – 26 mmol L-1  Base excess; a measure of the degree of excess acid or alkali (base) in the blood  normal range +2 to -2 mmol L-1 Terms used in arterial blood gas analysis
  • 4.
    ABG: values  pH7.35-7.45  PaCO2 35-45 mm Hg  PaO2 80-100 mmHg**  SaO2 93-98%  HCO3 - 22-26 mEq/L  Base excess -2.0 to 2.0 mEq/L  %MetHb <2.0%  %COHb <3.0%  CaO2 16-22 ml O2/dl * At sea level, breathing ambient air ** Age-dependent “Normal ranges” difference between Labs
  • 6.
    CENTRAL EQUATION OFACID-BASE PHYSIOLOGY  Henderson Hasselbach Equation:  where [ H+] is related to pH by  To maintain a constant pH, PCO2/HCO3- ratio should be constant.  When one component of the PCO2/ [HCO3-] ratio is altered, the compensatory response alters the other component in the same direction to keep the PCO2/[HCO3- ] ratio constant.  [H+] in nEq/L = 24 x (PCO2 / [HCO3 -]  [ H+] in nEq/L = 10 (9-pH)
  • 7.
    Henderson-Hasselbalch Equation Base HCO3 pH = pK+ log --------- = 6.1 + log --------- Acid H2CO3 + CO2 pK = the pH at which half of the compound is ionized = 6.1 Base= HCO3 Acid= Carbonic Acid= H2CO3 + pure dissolved CO2 = pCO2 (.03) Acid-Base Equations
  • 8.
    Bicarbonate-Carbonic Acid BufferSystem CO2 + H2O H2CO3 HCO3 + H (carbonic anhydrase)  at pH = 7.40 and pCO2 = 40: [HCO3] = 24  Henderson-Hasselbalch Equation:  pH = pK + log 10 [(HCO3)/(H2CO3 + CO2)] (at normal) = 6.1 + log 10 (24/pCO2 x .03) = 6.1 + log (24/1.2) = 6.1 + log 20 = 6.1 + 1.3 = 7.40
  • 9.
    Bicarbonate-Carbonic acid system HCO3-24 pH= 6.1 + log ------------- ------ ---- log 20 = 1.3 pCO2 (.03) 1.2 HCO3- 12 pH= 6.1 + log ------------- ------ ---- log 10 = 1.0 pCO2 (.03) 1.2  The normal ratio of HCO3 to H2CO3 is 20:1.  The log of 20 is 1.3.  If you cut the HCO3 in half to 12, the ratio is 10:1.  The log of 10 is 1.0 .  The pH thus decreased by 0.3.  Whenever the ratio of HCO3 to H2CO3 is reduced by one-half, the pH falls by 0.3.
  • 10.
    pH 7.4 CO2 HCO3 - Respiratory Component (acid) MetabolicComponent (base) Arterial blood pH = 7.40 Venous Blood pH = 7.35
  • 11.
    The Basic Relationshipbetween PCO2 and Plasma pH Animation: Relationship Between PCO2 and Plasma pH PLAY
  • 12.
  • 13.
    Compensatory response orregulation of pH By 3 mechanisms: 1. Chemical buffers:  React instantly to compensate for the addition or subtraction of H+ ions. 2. CO2 elimination:  Controlled by the respiratory system.  Change in pH result in change in PCO2 within minutes. 3. HCO3- elimination:  Controlled by the kidneys.  Change in pH result in change in HCO3.  It takes hours to days and full compensation occurs in 2-5 days.
  • 15.
     75-80% HCO3is absorbed in the proximal tubule.
  • 16.
    Kidney tubules andpH Regulation
  • 17.
    Correlating Chloride andBicarbonate  Tend to move in opposite directions.  Metabolic Alkalosis:  High Bicarbonate.  Low Chloride.  Metabolic Acidosis:  Low Bicarbonate.  Chloride Normal (Anion Gap) or High (non-AG).  Chloride low if Na/Cl >1.4; high if Na/Cl < 1.27. Low chloride is synonymous with metabolic alkalosis (or compensation for chronic respiratory acidosis). Even if pH is normal, low chloride means alkalosis.
  • 18.
    The Central Roleof the Carbonic Acid- Bicarbonate Buffer System in the Regulation of Plasma pH
  • 19.
    The Central Roleof the Carbonic Acid- Bicarbonate Buffer System in the Regulation of Plasma pH
  • 21.
    Compensation  Compensation israrely complete Returns pH toward normal.  Compensation is not a secondary acidosis or alkalosis.  High altitude and pregnancy may have full compensation—but it takes time  Acetazolamide hastens compensation.  Improves Mountain sickness. Respiratory Renal
  • 25.
    Major causes are: Depletionof bicarbonate reserve. Inability to excrete hydrogen ions at kidneys. Production of large numbers of fixed / organic acids. Bicarbonate loss due to chronic diarrhea. Metabolic acidosis
  • 26.
    The Response toMetabolic Acidosis
  • 27.
    Occurs when HCO3 -concentrations become elevated. Caused by repeated vomiting. Metabolic alkalosis
  • 28.
  • 29.
    Acid-Base: Tough Stuff? It’sall in your mind  7.53/15/80/12  7.25/25/110/10  6.88/32/100/7  7.58/49/98/45  7.30/40/156/19  7.10/30/365/9  7.72/28/95/37  7.45/20/80/14 You are routinely missing triple acid- base disorders Dr. Smith Dr. Rock
  • 30.
    Six step method 1)Identify any abnormality (is there acidemia or alkalemia?). 2) Is the primary process metabolic or respiratory? 3) If the primary process is respiratory, is it acute or chronic? 4) Is the compensation adequate? 5) Is there an AG? 6) Is there a mixed disorder?
  • 31.
    Step 1 Identifythe disorder  Take a look at the pH, as it directs towards the principal disorder. < 7.35 Acidemia >7.45 Alkalemia 7.35- 7.45 Normal Mixed disorder
  • 32.
    Acidemia and Alkalemiavs. acidosis and alkalosis pH < 7.36 ([H+] > 44) is acidemia. pH > 7.44 ([H+] < 36) is alkalemia. mixed disorders of acidosis and alkalosis may be neither acidemic nor alkalemic. e.g. 7.40/ 25/ pCO2/ 15
  • 33.
    Step 2 RESPIRATORYor METABOLIC?  IS PRIMARY DISTURBANCE RESPIRATORY OR METABOLIC? pH PCO2 or pH PCO2 METABOLIC pH PCO2 or pH PCO2 RESPIRATORY RULE- If either the pH or PCO2 is Normal, there is a mixed metabolic and respiratory acid base disorder.
  • 34.
    Step 4 Respiratory Compensation MetabolicAcidosis:  Occurs rapidly.  Hyperventilation.  “Kussmaul Respirations”  Deep > rapid (high tidal volume).  Is not Respiratory Alkalosis. Metabolic Alkalosis:  Calculation not as accurate  Hypoventilation.  Not Respiratory Acidosis.  Restricted by hypoxemia.  PCO2 seldom > 50-55. pCO2=1.5 x HCO3 + 8 +/- 2 Winter’s formula pCO2=0.9 x HCO3 + 15
  • 35.
    Step 4 Metabolic Compensation AcuteHypercapnia: HCO3 increases 1 mmol/L for each 10 mmHg increase in PaCO2 >40 Chronic Hypercapnia: HCO3 incr. 3.5 mmol/L for each 10 mmHg increase in PaCO2 >40 Acute Hypocapnia: HCO3 decreases 2 mmol/L for every 10 mmHg decrease in PaCO2 <40 Chronic Hypocapnia: HCO3 decreases 5 mmol/L for every 10 mmHg decrease in PaCO2 <40 CO2 + H2O H2CO3 H + HCO3
  • 36.
    3 most importantequations so far  Chronic resp. acidosis: steady-state pCO2 is increased by 10 for every 3.5 increase in HCO3.  Acute metabolic acidosis:  pCO2 = 1.5 x HCO3 + 8 (+/- 2)  Acute metabolic alkalosis:  pCO2 = 0.9 x HCO3 + 15
  • 37.
    Step 5 AnionGap  Described by Gamble in 1939.  Electroneutrality.  Na+, Cl-, and HCO3 are measured ions Na + UC = Cl + HCO3 + UA UC = Sum of unmeasured cations UA = Sum of unmeasured anions Anion Gap
  • 38.
    Anion Gap Unmeasured Cations: Total 11 mEq/L Potassium 4 Calcium 5 Magnesium 2 Unmeasured Anions:  Total 23 mEq/L Sulfates 1 Phosphates 2 Albumin 16 Lactic acid 1 Org. acids 3 Na + UC = Cl + HCO3 + UA 140 + 11 = 104 + 24 + 23 151 = 151 Anion Gap = Na - (Cl + HCO3)
  • 40.
    Acid Base disorders Anion Gap: represent the unmeasured anions normally present in plasma ( po4, SO4, Creatinine and proteins). AG = (Na +k) - (CL+HCO3) = 16 ± 4 mEq/L if K+ is not calculated= 12 mEq/L Metabolic acidosis is conveniently divided into: 1. High anion–gap metabolic acidosis:  unmeasured anions   HCO3 lactic acidosis; ketoacidosis; drug poisonings (e.g., aspirin, ethyelene glycol, methanol) 2. Normal anion–gap metabolic acidosis (hyperchloremic metabolic acidosis)  HCO3  compensatory  CL by the kidney. Diarrhea; some kidney problems e.g., renal tubular acidosis, interstitial nephritis, small bowel or pancreatic drainage & fistula or Ureterosigmoidostomy.
  • 41.
    Acid Base disorders METABOLICALKALOSIS  Chloride responsive (responds to NaCl or KCl therapy): diuretics; Corticosteroids; gastric suctioning; vomiting.  Chloride resistant: any hyperaldosterone state, e.g., Cushing's syndrome; severe K+ depletion. RESPIRATORY ACIDOSIS  Central nervous system depression (e.g., drug overdose).  Chest bellows dysfunction (e.g., Guillain-Barré syndrome, myasthenia gravis).  Disease of lungs and/or upper airway (e.g., chronic obstructive lung disease, severe asthma attack, severe pulmonary edema). RESPIRATORY ALKALOSIS  Hypoxemia (includes altitude), Anxiety, Sepsis, Any acute pulmonary insult e.g., pneumonia, mild asthma attack, early pulmonary edema, pulmonary embolism.
  • 43.
    Causes High AGMetabolic Acidosis  Methanol  Uremia/Renal Failure  DKA  Paraldehyde  INH, Iron-lactate  Lactic Acidosis:  Has many etiologies.  Cyanide, CO, Toluene, HS.  Poor perfusion.  Ethylene glycol.  Salicylates:  Methyl salicylate o (Oil of wintergreen)  Mg salicylate (Doan’s pills) Levraut J et al. Int Care Med 23:417, 1997 MUDPILES
  • 45.
    Metabolic Acidosis: Normal AG Loss of HCO3: Severe diarrhea. Post-hypocapnia. Ureteroileostomy. Acetazolamide.  Failure to excrete [H+] Renal Tubular Acidosis ○ Types 1-4. ○ Toluene.  Administration of [H+] Ammonium chloride. 1. Loss of HCO3 2. Failure to excrete [H+] 3. Administration of [H+]
  • 47.
    Decreased or NegativeAnion Gap  Low protein most important: Albumin has many unmeasured negative charges. “Normal” anion gap (12) in cachectic person. o Indicates anion gap metabolic acidosis. 2-2.5 mEq/liter drop in AG for every 1 g drop in albumin.  Other etiologies of low AG: Low K, Mg, Ca, increased globulins (Mult. Myeloma), Li, Br (bromism), I intoxication.  Negative AG: more unmeasured anions than unmeasured cations. Bromide, Iodide, Multiple Myeloma.
  • 48.
  • 49.
    Metabolic Acidosis— Bad??  Impairedcardiac contractility.  Decreased threshold for VF.  Decreased Hepatic and Renal perfusion.  Increased Pulmonary Vasc resistance.  Inability to respond to catecholamines.  Vascular collapse.  Increased Anion Gap.  Normal Anion Gap (Hyperchloremic).
  • 50.
    Reasons to LimitBicarbonate therapy  Initially injected into 3 liter plasma volume.  (not 5 liter blood volume because does not enter red cells).  Theoretical, but probably does not happen:  Increase intracellular acidosis.  Will increase pCO2 and need for ventilation.  N.S: 150mEq/l of Na, Bicarb: 1000mEq/l of Na.  As much Na as 350 ml’s normal saline.  like hypertonic saline: leads to Hypernatremia & Fluid overload.  Extra bicarbonate can increase potassium requirements, may increase hepatic production of ketones, and may delay resolution of cerebral acidosis.
  • 52.
    Base Deficit Volume ofdistribution, extracellular fluid 0.3 L/kg  = 0.3 x kg x (24 – HCO3) in mEq/l one ampule of bicarb = 50 mEq/50 ml  E.g.: 70 kg person with bicarb of 3 0.3 x 70 x 21 = 441 mEq 441mEq ÷ 50 mEq/ml/ampule = 9 Amps of bicarb  Suppose you want to get the bicarb back to 6 0.3 x 70 x (6-3) = 63 63 mEq ÷ 50 mEq/ml/ampule = 1.25 Amps of bicarb.
  • 53.
    When to give bicarbonate DoNOT base it on pH. Base it on HCO3 level < 6. For low pH: If bicarbonate < 6: give bicarb 1-2 amps. Recheck ABG. If pCO2 > 1.5 (HCO3) + 8: then ventilate better.
  • 56.
    Step 6: CalculateDelta Gap  Used only if there is Anion Gap. Delta gap = (actual AG – 12) + HCO3  Adjusted HCO3 should be 24 (+_ 6) {18-30}  If delta gap > 30 additional metabolic alkalosis.  If delta gap < 18 additional non-gap metabolic acidosis.  If delta gap 18 – 30 no additional metabolic disorders.
  • 57.
    Change in AnionGap vs. HCO3  In simple AG Metabolic Acidosis decrease in plasma bicarbonate = increase in AG Anion Gap HCO3  <1 = High anion gap & normal AG acidosis.  1-2 = Pure anion gap metabolic acidosis.  >2 = High anion gap acidosis with concurrent metabolic alkalosis. = 1
  • 58.
    Six step method 1)Identify any abnormality (is there acidemia or alkalemia?). 2) Is the primary process metabolic or respiratory. 3) If the primary process is respiratory, is it acute or chronic? 4) Is the compensation adequate? 5) Is there an AG? 6) Is there a mixed disorder?
  • 59.
    Step 6 MixedDisorders  Respiratory Acidosis + metabolic acidosis + metabolic alkalosis + metabolic acidosis and alkalosis (triple)  Respiratory Alkalosis + metabolic acidosis + metabolic alkalosis + metabolic acidosis and alkalosis (triple)
  • 60.
    Problem #1  60ys male presents to the ED from a nursing home. You have no history other than he has been breathing rapidly and is less responsive than usual. Na+ 123 Cl- 99 HCO3 - 5 pH 7.31 pCO2 10
  • 61.
    Six Steps forAcid-Base Analysis Step 1. Is there an acidemia or alkalemia? Acidemia
  • 62.
    Six Steps forAcid-Base Analysis Step 2. Is the primary process metabolic or respiratory? pCO2 = 10 should drive pH ↑ HCO3 - = 5 should drive pH ↓
  • 63.
    Six Steps forAcid-Base Analysis Step 3: If the primary process is respiratory, is it acute or chronic? Skip this step as primary process is metabolic!
  • 64.
    Six Steps forAcid-Base Analysis Step 4: Is there an anion gap? Na+ - Cl- - HCO3 - > 12? 123 - 99 - 5 = 19 Anion Gap Metabolic Acidosis
  • 65.
    Six Steps forAcid-Base Analysis Step 5: Is the respiratory compensation adequate?  Expected pCO2 range = [1.5(measured HCO3 -)]+8+/- 2 [1.5 (5) +8] +/- 2 = [13.5 – 17.5] pCO2 = 10  Therefore it IS a respiratory alkalosis.
  • 66.
    Six Steps forAcid-Base Analysis Step 6: Are there any other metabolic disturbances?  Corrected HCO3 - = (Measured HCO3 -) + (AG-12) (5) + (19-12) = 12  Since this does not correct bicarbonate back to normal, there is a non anion gap acidosis. 1.Anion Gap Metabolic Acidosis. 2.Concurrent Respiratory Alkalosis. 3.non - anion gap met. acidosis.
  • 67.
    Problem #2  42ys female has the flu for four days with incessant vomiting. She presents to the ED two days after stopping insulin due to no food intake. Na+ 130 Cl- 80 HCO3 - 10 pH 7.21 pCO2 25
  • 68.
    Six Steps forAcid-Base Analysis Step 1. Is there an acidemia or alkalemia? Acidemia
  • 69.
    Six Steps forAcid-Base Analysis Step 2. Is the primary process metabolic or respiratory? pCO2 = 25 should drive pH ↑ HCO3 - = 10 should drive pH ↓
  • 70.
    Six Steps forAcid-Base Analysis Step 3: If the primary process is respiratory, is it acute or chronic? Skip this step as primary process is metabolic!
  • 71.
    Six Steps forAcid-Base Analysis Step 4: Is there an anion gap? AG= Na+ - Cl- - HCO3 - > 12? 130 - 80 - 10 = 40!! Anion Gap Metabolic Acidosis
  • 72.
    Six Steps forAcid-Base Analysis Step 5: Is the respiratory compensation adequate? Expected pCO2 range = [1.5(measured HCO3 -)]+8+/- 2 [1.5 (10) +8] +/- 2 = [21 - 25] E.pCO2 = 25, therefore this is normal respiratory compensation
  • 73.
    Six Steps forAcid-Base Analysis Step 6: Are there any other metabolic disturbances?  Corrected HCO3 - = (Measured HCO3 -) + (AG-12) (10) + (40-12) = 38  Since this over corrects bicarbonate there is a metabolic ALKALOSIS!! 1.Anion Gap Metabolic Acidosis. 2.Metabolic Alkalosis.
  • 74.
    Problem #3 30 yearold female BMT patient with neutropenic fever has been receiving multiple antibiotics including amphotericin B. You are called to the bedside for her fevers, rigors, and dyspnea.  Na+ 125 Cl- 100 HCO3 - 8  pH 7.07 pCO2 28 K+ 2.5
  • 75.
    Six Steps forAcid-Base Analysis Step 1.  Is there an acidemia or alkalemia? Acidemia
  • 76.
    Six Steps forAcid-Base Analysis Step2:  Is the primary process metabolic or respiratory? PCO2 = 28 should drive pH ↑ HCO3 - = 8 should drive pH ↓
  • 77.
    Six Steps forAcid-Base Analysis Step 3:  If the primary process is respiratory, is it acute or chronic? Skip this step as primary process is metabolic!
  • 78.
    Six Steps forAcid-Base Analysis Step 4:  Is there an anion gap? Na+ - Cl- - HCO3 - > 12? 125 - 100 - 8 = 17 Anion Gap Metabolic Acidosis
  • 79.
    Six Steps forAcid-Base Analysis Step 5:  Is the respiratory compensation adequate? Expected pCO2 range = [1.5(measured HCO3-)]+8+/- 2 [1.5 (8) +8] +/- 2 = [18-22] pCO2 = 28, therefore this is a respiratory acidosis even though the value is below 40!!
  • 80.
    Six Steps forAcid-Base Analysis Step 6: Are there any other metabolic disturbances? Corrected HCO3 - = (Measured HCO3 -) + (AG-12) (8) + (17-12) = 13  Since this is below the normal range after correction,there is a non anion gap acidosis. 1.Anion Gap Metabolic Acidosis. 2.Concurrent Respiratory Acidosis. 3.non - anion gap met. acidosis.
  • 81.
    Example 4 Case: 43yo w f Brought by friends from convention. Had been staggering, speaking incoherently, swearing, yelling. Pt. was confused, agitated, speaking jibberish. Brought to ED. Friends left. 110/70 128 R22 T 98 uncooperative, pretending to smoke cigarette o/w exam negative except for dry MM Valium, Cogentin, Haldol given 125/65/64/142 AG = 23 7.67/35/78/40 2.1/37/3.9 U/A, Etoh, U tox all neg. lactate 1.5 Resp. Alk. + Met. Alk. + (because of large
  • 82.
    Case continued To MICU Pt.arrests. Monitor shows torsade. Pt. intubated and CPR. Spontaneously back to NSR, now intubated, unconscious, ventilated by bag, Pt. goes back into torsade. What immediate effective treatment was done? bagging stopped! ---> torsade again spontan. resolved Pt. paralyzed, hypoventilated, and put on HCl drip. Etiology was Alcoholic ketoacidosis with severe vomiting elicited from later history.
  • 83.
    Beware Severe Alkalemia dueto:  Severe underlying pathology. also: General and Cerebral vasoconstrictor. Shift of oxyhemoglobin dissociation. Hypokalemia. Increased SVR and decreased CO: Decreased Contractility . Cardiac arrhythmias refractory. Seizures.
  • 84.
    Severe Alkalosis/alkalemia  HCO3> 45.  Be sure oxygenation OK.  Avoid respiratory stimulation.  Acetazolamide, 500 mg IV Monitor K, Mg, PO4  HCl infusion: 0.1M solution (100 mmol/L, 0.2 mmol/ kg/hour). Central line. Total dose = Δ HCO3 x kg x 0.5 (in mmoles).
  • 85.
    Example 4 27 y.oman with polyuria and polydipsia for one week, and intractable vomiting for 4 days. Today he is critically ill with a temp. of 104 F. pH 7.50 pCO2 26 pO2 100 150 100 50 3.8 20 1.8 650 AG= 30 Bicarb=24-20= 4 AG=30-12= 18 Na/Cl > 1.4
  • 86.
    Mixed Acid-Base: Example 4 Anion Gap Metabolic Acidosis.  Concurrent Metabolic Alkalosis.  Respiratory Alkalosis. DKA Vomiting Sepsis
  • 87.
    Example 5 25 y.o.woman admitted 6 hours ago with severe DKA. Her initial pH was 6.9 with a pCO2 of 10, and serum bicarb of 2.4. After insulin and NS hydration, her lab values returned as follows… 140 110 10 AG= 20 Bicarb= 24-10= 14 AG= 20-12= 8 pH 7.25 pCO2 23
  • 88.
    Mixed Acid-Base: Example5 Anion Gap Metabolic Acidosis Hyperchloremic Metabolic Acidosis. Respiratory alkalosis
  • 89.
    Mixed Acid-Base: Example6 72 y.o. man with a h/o PUD has been vomiting for 2 weeks. Vitals on presentation: P 140, BP 60/P pH 7.40 pCO2 40 pO2 300 (FiO2 50%), HCO3 = 24 150 86 100 2.6 24 2.5 AG=150-110= 40 Bicarb=24-24= 0 AG= 40-12= 28
  • 90.
    Mixed Acid-Base: Example6  Anion Gap Metabolic Acidosis (Shock)  Metabolic Alkalosis (Vomiting) Normal ABG does not equal normal patient…. Dr. Smith
  • 91.
    Test Case #1 An80 year old man has been confused and c/o SOB for one week. He also has a hearing problem and has seen 3 ENT docs in the past month. Family denies medications. pH 7.53 pCO2 15 pO2 80 HCO3 12 140 108 3.0 13 120 Diagnosis? AG = 140 - 121 = 19
  • 92.
    Test Case #1 AnionGap= 140-(108+13)= 19,  Δ AG = 7  Δ Bicarb= 24-13= 11 E.pCO2= 1.5 (12) + 8= 26 (compared/w 15) Patient is Alkalemic (pH= 7.53) indicating a Superimposed Respiratory Alkalosis Dx: Metabolic Acidosis and Respiratory Alkalosis
  • 93.
    Test Case #2 23 year old AIDS patient c/o weakness and prolonged severe diarrhea. He appears markedly dehydrated. pH 7.25 pCO2 25 pO2 110 HCO3 11 151 129 60 2.0 12 2.0 Diagnosis?
  • 94.
    Test Case #2  Anion Gap= 151-(129 + 11)= 11 (normal)  The patient is Acidemic (pH 7.25)  Respiratory compensation normal? 1.5 (HCO3) + 8 plus or minus 2 1.5 (11) + 8= 24.5 (compare with 25) Dx: Uncomplicated Non-AG Metabolic Acidosis
  • 95.
    Test Case #3 45y.o. alcoholic man has been vomiting for 3 days. Vitals: BP 100/70, P 110. Intern administered Valium 30 mg for tremulousness. pH 7.30 pCO2 40 145 96 3.0 19 Serum Ketones + Diagnosis?
  • 96.
    Test Case #3 Anion Gap= 145- (96 + 19)= 30  Δ Bicarb= 24-19= 5  Δ AG= 30-12= 18  Change in AG >> Change in Bicarb  Superimposed Metabolic Alkalosis  Respiratory compensation? 1.5 x (19) + 8= 36 (compared with pCO2=40)
  • 97.
    Test Case #3 Anion Gap Metabolic Acidosis (AKA)  Metabolic Alkalosis (Persistent Vomiting)  Mild Respiratory Acidosis (Oversedation)
  • 98.
    Test Case #4 A22 y.o. diabetic man has been vomiting for several days. He appears ill and dehydrated. His ABG reveals 7.40/ 40/ 100 on room air. His labs are below. The resident states he does not have DKA because the ABG is normal. Is the resident correct? 130 76 3.0 24 800
  • 99.
    Test Case #4 The resident is NOT correct; Sorry admit MICU  Anion gap= 130- (76 + 24)= 30  Δ Bicarb= 24-24= 0  Δ AG= 30-12= 18  Change in AG >>> Change in Bicarb Dx: Anion Gap Metabolic Acidosis (DKA) Metabolic Alkalosis (Vomiting)
  • 100.
    Test Case #5 33y.o. woman c/o leg pain and SOB which started suddenly yesterday. pH 7.45 pCO2 20 pO2 80 140 116 4.0 14 Diagnosis?
  • 101.
    Test Case #5 Anion gap= 140- (116 + 14)= 10 Dx: Respiratory Alkalosis (PE) with Compensation
  • 102.
    Absolute contraindications 1. An abnormalmodified Allen's test. 2. Local infection, thrombus, or distorted anatomy at the puncture site (eg, previous surgical interventions, congenital or acquired malformations, burns, aneurysm, stent, arteriovenous fistula, vascular graft) 3. Severe peripheral vascular disease of the artery selected for sampling 4. Active Raynaud syndrome (particularly sampling at the radial site)
  • 103.
    Relative Contraindications  Supratherapeutic coagulopathy and infusion of thrombolytic agents (eg, during streptokinase or tissue plasminogen activator infusion) are relative contraindications to arterial needle stick. we suggest avoiding repeated arterial needle sticks when the international normalized ratio is ≥3 and/or the activated partial thromboplastin time is ≥100 seconds
  • 104.
    Relative Contraindications  Similarly,arterial needle stick and catheterization can be performed in patients with thrombocytopenia a platelet count >50 x 109/L, but is generally avoided in those whose count is ≤30 x 109/L. For those with counts between 30 and 50 x 109/L limited needle stick sampling is sometimes performed, when necessary, with increased compression time.  A platelet count <50 x 109/L is generally a contraindication to arterial catheter insertion.
  • 105.
    How are ABGdone?  Site: Radial artery (Brachial, femoral arteries)  non-dominant hand / good Ulnar artery blood flow/ adequate pressure following sampling.  Positioning of wrist: hyperextended + good support under wrist.  Syringe & Needles: low resistance / heparinized / small/ blood “pulse” /  Arterial cannula.  Lignocaine 1% ? Repeated sampling / pain induced hyperventilation.  Complications: Pain, hematoma, air/blood emboli, infection, vascular trauma/occlusion, arterial spasm.
  • 107.
    Delayed Analysis Consumption ofO2 & Production of CO2 continues after blood drawn.  Iced Sample maintains values for 1-2 hours.  Uniced sample quickly becomes invalid within 15 -20 minutes.  PaCO2  3-10 mmHg/hour.  Pao2   pH  d/t lactic acidosis generated by glycolysis in R.B.C.
  • 108.
    FEVER OR HYPOTHERMIA 1.Most ABG analyzers report data at N body temp. 2. If severe hyper/hypothermia, values of pH & PCO2 at 37 C can be significantly differ from pt’s actual values. 3. Changes in PO2 values with temp also predictable. Hansen JE, Clinics in Chest Med 10(2), 1989 227-237  If Pt.’s temp < 37C Substract 5 mmHg Po2, 2 mmHg Pco2 and Add 0.012 pH per 1C decrease of temperature.
  • 109.
    AIR BUBBLES: 1. PO2150 mmHg & PCO2 0 mm Hg in air bubble(R.A). 2. Mixing with sample, lead to  PaO2 &  PaCO2.  To avoid air bubble, sample drawn very slowly and preferabily in glass syringe. Steady State: Sampling should done during steady state after change in oxygen therapy or ventilator parameter. Steady state is achieved usually within 3-10 minutes.
  • 110.
    Leucocytosis :  pH and Po2 ; and  Pco2.  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. EXCESSIVE HEPARIN:  Dilutional effect on results  HCO3 - & PaCO2  Only .05 ml heperin required for 1 ml blood.  So syringe be emptied of heparin after flushing or only dead space volume is sufficient or dry heperin should be used.
  • 111.
    Summary of importantpoints  Acidosis/Alkalosis are metabolic states ≠ acidemia/alkalemia.  Doubling or halving the pCO2:HCO3 ratio changes pH by 0.3.  Bicarbonate therapy based on bicarb ≤ 6, not Ph.  Low pH with bicarb > 6 needs Rx with ventilation.  Know the anion gap and MUDPILES.  Anion Gap > 18 is metabolic acidosis.  no matter what the pH, pCO2, or bicarb.  Normal Na/Cl ratio is 1.33 (140/105)  Na/Cl ratio > 1.4 is metabolic alkalosis (e.g. 140/99) ○ (or compensation for respiratory acidosis)  Na/Cl < 1.3 is hyperchloremic acidosis (e.g., 140/111) ○ (or compensation for resp alkalosis)  Winter’s formula: pCO2 should be = 1.5 x HCO3 + 8
  • 112.
    “Understanding ABG isnot magic but an art learned by continued practice”