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ABG INTERPRETATION

STEPWISE APPROACH
 Obtain clues from the clinical setting
 Determine primary disorder
 Check the compensatory response
 Calculate the anion gap
 Calculate the delta/deltas
 Identify specific etiologies for the acid-
base disorder
 Prescribe treatment
DETERMINE CLUES
FROM THE
CLINICAL SETTING
CLUES FROM
CLINICAL SETTING

HIGH ANION GAP METABOLIC ACIDOSIS


Ketoacidosis – dm, alcohol, starvation
INH, methanol, lactic acid
Renal failure
Hypotension
CLUES FROM
CLINICAL SETTING
NORMAL ANION GAP METABOLIC ACIDOSIS

Diarrhea
RTA
Interstitial nephritis
Early renal failure
Urinary tract obstruction
CLUES FROM
CLINICAL SETTING
METABOLIC ALKALOSIS
(urine Cl < 10 mEq/d)
Vomiting
Remote diuretic use
Post hypercapnea
Chronic diarrhea
Cystic fibrosis
CLUES FROM
CLINICAL SETTING
METABOLIC ALKALOSIS
(urine Cl > 10 mEq/d)
Bartter’s syndrome
Severe potassium depletion
Current diuretic use
Hypercalcemia
Hyperaldosteronism
Cushing’s syndrome
CLUES FROM
CLINICAL SETTING
RESPIRATORY ACIDOSIS
CHRONIC: COPD
ACUTE: pneumonia

RESPIRATORY ALKALOSIS
Hyperventilation
DETERMINE
THE
PRIMARY DISORDER
DETERMINE
PRIMARY DISORDER
 Check the trend of the pH, HCO3, pCO2
 The change that produces the pH is the
primary disorder

pH = 7.25 HCO3 = 12 pCO2 = 30

ACIDOSIS ACIDOSIS ALKALOSIS


METABOLIC ACIDOSIS
DETERMINE
PRIMARY DISORDER
 Check the trend of the pH, HCO3, pCO2
 The change that produces the pH is the
primary disorder

pH = 7.25 HCO3 = 28 pCO2 = 60

ACIDOSIS ALKALOSIS ACIDOSIS


RESPIRATORY ACIDOSIS
DETERMINE
PRIMARY DISORDER
 Check the trend of the pH, HCO3, pCO2
 The change that produces the pH is the
primary disorder

pH = 7.55 HCO3 = 19 pCO2 = 20

ALKALOSIS ACIDOSIS ALKALOSIS


RESPIRATORY ALKALOSIS
DETERMINE
PRIMARY DISORDER
 If the trend is the same, check the percent
difference
 The bigger %difference is the 10 disorder
(16-24)/24 = 0.33 (60-40)/40 = 0.5
pH = 7.25 HCO3 = 16 pCO2 = 60

ACIDOSIS ACIDOSIS ACIDOSIS


RESPIRATORY ACIDOSIS
DETERMINE
PRIMARY DISORDER
 If the trend is the same, check the percent
difference
 The bigger %difference is the 10 disorder
(38-24)/24 = 0.58 (30-40)/40 = 0.25
pH = 7.55 HCO3 = 38 pCO2 = 30

ALKALOSIS ALKALOSIS ALKALOSIS


METABOLIC ALKALOSIS
CHECK THE
COMPENSATORY RESPONSE
COMPENSATORY
RESPONSE
HENDERSEN-HASSELBACH EQUATION

24 x pCO2
H = ----------------
HCO3

Metabolic or Respiratory Acidosis


COMPENSATORY
RESPONSE
HENDERSEN-HASSELBACH EQUATION

24 x pCO2
H = ----------------
HCO3

Metabolic or Respiratory Alkalosis


COMPENSATORY
RESPONSE

METABOLIC ACIDOSIS
 pCO2 = HCO3 x 1.2 + 2

HCO3 =12 pCO2 =14.4 – 40 = 25.6

HCO3 =7 pCO2 =20.4 – 40 = 19.6


COMPENSATORY
RESPONSE

METABOLIC ALKALOSIS
 pCO2 =  HCO3 x 0.7 + 2

HCO3 =35 pCO2 =7.7 + 40 = 47.7

HCO3 =40 pCO2 =11.2 + 40 = 51.2


COMPENSATORY
RESPONSE

ACUTE RESPIRATORY ACIDOSIS


 HCO3 = pCO2 x 0.1

pCO3 =55 HCO3 =1.5 + 24 = 25.5

pCO3 =80 HCO3 =4 + 24 = 28


COMPENSATORY
RESPONSE

CHRONIC RESPIRATORY ACIDOSIS


 HCO3 = pCO2 x 0.35

pCO3 =55 HCO3 =5.25 + 24 = 29.25

pCO3 =80 HCO3 =14 + 24 = 38


COMPENSATORY
RESPONSE

RESPIRATORY ALKALOSIS
 HCO3 = pCO2 x 0.2

pCO3 =25 HCO3 =3 - 24 = 21

pCO3 =32 HCO3 =1.6 - 24 = 22.4


CALCULATE THE
ANION GAP
ANION GAP
Na – (HCO3 + Cl) = 12 + 4

Na = 135 HCO3 = 15
Cl = 97 RBS = 100 mg%

AG = 135 – 112 = 23
ANION GAP
Na – (HCO3 + Cl) = 12 + 4

Na = 135 HCO3 = 15
Cl = 97 RBS = 500 mg%

Corrected Na = Na + RBS mg% -100 x 1.6


100

AG = 135 + 6.4 – 112 = 29.4


CHECK THE DELTA / DELTA
DELTA - DELTA
 If with high AG metabolic acidosis
AG
 HCO3
 If with normal AG metabolic acidosis
Cl
HCO3
A high AG always indicates the presence
of a HAG metabolic acidosis
DELTA - DELTA

/ = 1 Simple NAG metabolic


acidosis

/ > 1 HAGMA/NAGMA +


meta alk

HAGMA+NAGMA
/ < 1
CASE 1
56F with vomiting and diarrhea 3 days ago
despite intake of loperamide. Her last
urine output was 12 hours ago.

PE showed BP = 80/60, HR = 110, RR = 28.


There is poor skin turgor.
CASE 1
serum Na = 130 pH = 7.30
K = 2.5 pCO2 = 30
Cl = 105 HCO3 = 15
BUN = 15 pO2 = 90
crea = 177
RBS = 100
BCR = BUN / crea x 247.6 = 21 PRE-RENAL
CASE 1
serum Na = 130 pH = 7.30
K = 2.5 pCO2 = 30
Cl = 105 HCO3 = 15
BUN = 15 pO2 = 90
crea = 177
RBS = 100
pH = acidosis, pCO2 =alk, Metabolic
HCO3 = acidosis Acidosis
CASE 1
serum Na = 130 pH = 7.30
K = 2.5 pCO2 = 30
Cl = 105 HCO3 = 15
BUN = 15 pO2 = 90
crea = 177
RBS = 100 Compensated
pCO2 = 9 x 1.2 = 10.8 Metabolic
Acidosis
CASE 1
serum Na = 130 pH = 7.30
K = 2.5 pCO2 = 30
Cl = 105 HCO3 = 15
BUN = 15 pO2 = 90
crea = 177
RBS = 100
AG= 130 – (105+15) = 10 NAGMA
CASE 1
serum Na = 130 pH = 7.30
K = 2.5 pCO2 = 30
Cl = 105 HCO3 = 15
BUN = 15 pO2 = 90
crea = 177
RBS = 100
/= (105-100)/(24-15) = NAGMA +
0.56 HAGMA
CASE 1
56F with vomiting and diarrhea 3 days ago
despite intake of loperamide. Her last urine
output was 12 hours ago.

PE showed BP = 80/60, HR = 110, RR = 28.


There is poor skin turgor.
pH 7.30, HCO3=15, pCO2=30, Na=130 K=2.5

How will you correct the acid base disorder?


CASE 1

1) Hydrate
2) Hydrate + IV NaHCO3
3) Hydrate + oral NaHCO3
4) Hydrate + correct hypokalemia

How will you correct the acid base disorder?


INDICATIONS FOR
HCO3 THERAPY

 pH < 7.2 and HCO3 < 5 – 10 mmHg


 When there is inadequate ventilatory
compensation
 Elderly on beta blockers in severe acidosis with
compromised cardiac function
 Concurrent severe AG and NAGMA
 Severe acidosis with renal failure or intoxication
COMPLICATIONS OF
HCO3 THERAPY
 Volume overload
 Hypernatremia NaHCO3 50 ml = 45 mEq Na
 Hyperosmolarity
NaHCO3 gr X tab = 7 mEq Na
 Hypokalemia
 Intracellular acidosis
 Causes overshoot alkalosis
 Stimulates organic acid production
  tissue O2 delivery
POTASSIUM CORRECTION
 K deficit = (3.5 – K)/0.27 x 100
 Give ½ of the deficit in 24 hours

K deficit = (3.5 – 2.5)/0.27 x 100 = 370

1 cc oral KCL = 1.33 mEq K


1 potassium durule = 10 mEq K
CASE 2
30M with epilepsy has a grand mal seizure.
Labs showed:
pH = 7.14 Na = 140
pCO2= 45 K=4
HCO3 = 17 Cl = 98

%pCO2 =13, %HCO3 = 29 Metabolic


Acidosis
CASE 2
30M with epilepsy has a grand mal seizure.
Labs showed:
pH = 7.14 Na = 140
pCO2= 45 K=4
HCO3 = 17 Cl = 98

Metabolic &
pCO2 =7 x 1.2 = 8.4 Respiratory
Acidosis
CASE 2
30M with epilepsy has a grand mal seizure.
Labs showed:
pH = 7.14 Na = 140
pCO2= 45 K=4
HCO3 = 17 Cl = 98

AG = 140 – (98+17) = 25 HAGMA +


RAc
CASE 2
30M with epilepsy has a grand mal seizure.
Labs showed:
pH = 7.14 Na = 140
pCO2= 45 K=4
HCO3 = 17 Cl = 98

/= (25-12)/(24-17) = 1.9 HAGMA +


MAlk + RAc
CASE 2
30M with epilepsy has a grand mal seizure.
Labs showed:
pH = 7.14 Na = 140
pCO2= 45 K=4
HCO3 = 17 Cl = 98

How will you correct the acid base disorder?


CASE 2
1) IV NaHCO3 using HCO3 deficit
2) oral NaHCO3 at 1 mEq/kg/day
3) intubate
4) no treatment

How will you correct the acid base disorder?


CASE 2
HCO3 DEFICIT = (D –A) x 0.5 x kg BW

HCO3 deficit = (18 – 17) x 0.5 x 60 = 30

As HCO3  < 5-10, the dHCO3 = 15 - 18


Vd increases; hence
Maintenance 1 mEq/day
use 0.7 to 0.1

How
Give ½ will you correct
as bolus and thethe acid½base
other disorder?
as drip in 24 hrs
PRINCIPLES OF
HCO3 THERAPY
LACTIC ACIDOSIS

 Primary effort should be improving O2 delivery


 Use NaCO3 only when HCO3 < 5 mmol/L
 In states of  CO, raising the CO will have
more impact on the pH
 In cases of low alveolar ventilation, 
ventilation to lower the tissue pCO2
PRINCIPLES OF
HCO3 THERAPY
KETOACIDOSIS
 Rate of H+ production is slow; NaHCO3 tx may
just provoke severe hypokalemia
 Should be given if…
1) severe hyperkalemia despite insulin
2) HCO3 < 5 mmol/L
3) worsening acidemia inspite of insulin
CASE 3
19F, fashion model, is surprised to find her
K=2.7 mmol/L because she was
normokalemic 6 months ago. She admits
to being on a diet of fruit and vegetables
but denies vomiting and the use of
diuretics or laxatives. She is
asymptomatic. BP = 90/55 with subtle
signs of volume contraction.
CASE 3 Plasma Urine
serum Na 138 63
K 2.7 34
Cl 96 0
HCO3 30 0
pH 7.45 5.6
pCO2 45

pH = alk, pCO2 =acidosis Metabolic


HCO3 = alkalosis Alkalosis
CASE 3 Plasma Urine
serum Na 138 63
K 2.7 34
Cl 96 0
HCO3 30 0
pH 7.45 5.6
pCO2 45
Compensated
pCO2 = 6 x 0.7 = 4.2 Metabolic
Alkalosis
CASE 3 Plasma Urine
serum Na 138 63
K 2.7 34
Cl 96 0
HCO3 30 0
pH 7.45 5.6
pCO2 45

AG= 138 – (96+30) = 12 NAG


CASE 3 Plasma Urine
serum Na 138 63
K 2.7 34
Cl 96 0
HCO3 30 0
pH 7.45 5.6
pCO2 45

What is the cause of the acid base disorder?


CASE 3
1) diuretic intake
2) surreptitious vomiting
3) diuretic intake
4) Bartter’s syndrome
5) Adrenal tumor
6) nonreabsorbable anion
How
What
should
is the
her
cause
acid-base
of the disorder
acid basebedisorder?
managed?
CASE 3

1) correct hypokalemia
2) hydrate with NSS
3) administer acidyfing agent
4) give carbonic anhydrase inhibitor

How should her acid-base disorder be managed?


MANAGEMENT OF
METABOLIC ALKALOSIS
 Chloride repletion
 Potassium repletion
 Tx hypermineralocorticoidism
 Dialysis
 Carbonic anhydrase inhibitors
 Acidyfing agents
 HCl, NH4Cl
INDICATIONS OF HCl
 pH > 7.55 and HCO3 > 35 with
contraindications for NaCl or KCl use
 Immediate correction of metabolic
alkalosis in the presence of hepatic
encephalopathy, cardiac arrhythmias,
digitalis intoxication
 When initial response to NaCl, KCl, or
acetalozamide is too slow or too little
USE OF HCl
 HCL requirement = (A – D) x 0.5 x kg BW
 0.1 – 0.2 N HCl solution = 100 – 200 mEq
 Do not exceed 0.2 mEq/kg/hour of HCl

HCO3 = 70 HCl = 1,380 mEq


wt = 60 kg
CASE 4
73M with long standing COPD (pCO2 stable
at 52-58 mmHg), cor pulmonale, and
peripheral edema had been taking
furosemide for 6 months. Five days ago,
he had anorexia, malaise, and productive
cough. He continued his medications until
he developed nausea. Later he was
found disoriented and somnolent
CASE 4
PE: BP 110/70, HR 110, RR 24, T=40
respiratory distress
prolonged expiratory phase
postural drop in BP
drowsy, disoriented
scattered rhonchi and rales BLFs
distant heart sounds
trace pitting edema
CASE 4 admission after 48
serum Na hrs 136 139
K 3.2 3.9
Cl 78 86
HCO3 40 38
pH 7.33 7.42
pCO2 78 61
pO2 43 56
pH = acidosis  Respiratory
pCO2 =acidosis, HCO3 = alk Acidosis
Respiratory Acidosis & M. Alkalosis
CASE 4 admission after 48
serum Na hrs 136 139
K 3.2 3.9
Cl 78 86
HCO3 40 38
pH 7.33 7.42
pCO2 78 61
pO2 43 56
HCO3 = 24 +
HCO3 = (55-40) x 0.35 = 5.25 5.25 + 2.3 =
HCO3 = (78-55) x 0.1 = 2.3 31.55
CASE 4 admission after 48
serum Na hrs 136 139
K 3.2 3.9
Cl 78 86
HCO3 40 38
pH 7.33 7.42
pCO2 78 61
pO2 43 56

How should this patient be managed?


CASE 4

1) intubation and mechanical ventilation


2) low flow oxygenation by nasal prong
3) oxygen by face mask
4) sodium bicarbonate infusion with KCl

How should this patient be managed?


MANAGEMENT OF
RESPIRATORY ACIDOSIS
 Correct underlying cause for
hypoventilation
  effective alveolar ventilation 
intubate, mechanically ventilate
 Antagonize sedative drugs
 Stimulate respiration (e.g. progesterone)
 Correct metabolic alkalosis
CASE 5
42M, alcoholic, brought to the ER
intoxicated. He was found at Rizal park in
a pool of vomitus. PE showed unkempt
and incoherent patient with a markedly
contracted ECF volume. T=390 C with
crackles on the RULF.
CASE 5
serum Na = 130 pH = 7.53
K = 2.9 pCO2 = 25
Cl = 80 HCO3 = 20
BUN = 12 pO2 = 60
crea = 120 alb = 38
RBS = 15 mmol/L

BCR = (12/120) x 247.6 = 24.76 PRE-RENAL


CASE 5
serum Na = 130 pH = 7.53
K = 2.9 pCO2 = 25
Cl = 80 HCO3 = 20
BUN = 12 pO2 = 60
crea = 120 alb = 38
RBS = 15 mmol/L

%pCO2 =38, %HCO3 = 18 Respiratory


Alkalosis
CASE 5
serum Na = 130 pH = 7.53
K = 2.9 pCO2 = 25
Cl = 80 HCO3 = 20
BUN = 12 pO2 = 60
crea = 120 alb = 38
RBS = 15 mmol/L
Compensated
HCO3 = (40-25) x 0.2 = 3 Respiratory
Alkalosis
CASE 5
serum Na = 130 pH = 7.53
K = 2.9 pCO2 = 25
Cl = 80 HCO3 = 20
BUN = 12 pO2 = 60
crea = 120 alb = 38
RBS = 15 mmol/L
HAGMA +
AG = 130 – (80 + 20) = 30 RAlk
CASE 5
serum Na = 130 pH = 7.53
K = 2.9 pCO2 = 25
Cl = 80 HCO3 = 20
BUN = 12 pO2 = 60
crea = 120 alb = 38
RBS = 15 mmol/L

What are the causes of his acid base


disturbance?
CASE 5

1) aspiration pneumonia
2) alcohol ketoacidosis
3) vomiting

What are the causes of his acid base


disturbance?
MANAGEMENT OF
RESPIRATORY ALKALOSIS
 Correct underlying cause of
hyperventilation
 Rebreathe carbon dioxide
 Mechanical control of ventilation
 increase dead space
 decrease back up rate
 decrease tidal volume
 paralyze respiratory muscles
QUESTIONS?
Thank You
ACID BASE PHYSIOLOGY
by:
ROMMEL S. GAMBOA, M.D.
ACID BASE PHYSIOLOGY

 maintenance of constant blood pH


 physiologic buffers
 renal system
 respiratory system
BUFFERS
1. Extracellular buffers
a. HCO3-
major extracellular buffer
b. PO4-
minor extracellular buffer
2. Intracellular buffers
a. Organic phosphates (AMP. ADP, ATP,
2,3DPG)
b. Proteins (hemoglobin [major intracellular],
DeoxyHgb, oxyHgb, imidazole and α-amino
groups.
HENDERSON-HASSELBALCH
EQUATION

 is used to calculate pH
 pH = pK + log [A-]/[HA-]
pH = log of 10 [H]
pK = log 10 equilibrium constant
[A-] = base form of the buffer
[HA] = acid form of the buffer
Techniques of obtaining a sample
 Materials
 The patient is seated or lying down
 The wrist should be extended
approximately30 degrees
 A definite pulse should be palpated
 The site should be cleansed with 70%
isopropyl alcohol
 The radial artery should again be palpated
while holding the heparinized syringe much
like a pencil or dart with the opposite hand.
Techniques of obtaining a sample
 The needle is then inserted opposite the
blood flow at 45-degree angle or less with
the bevel turned upward.
 After a 3-4 ml of sample is withdrawn, a
sterile cotton is applied over the puncture
site. Digital pressure should be applied for
at least 5 minutes.
 The specimen must be placed on ice and
transported within 15 minutes at 4ºC and
tested immediately
NORMAL BLOOD GAS VALUES

pH pCO2 pO2 HCO3 BE Hgb O2Sat

Hi 7.45 45 100 26 +2 18 100


Lo 7.35 35 80 22 -2 12 90
TWO ORGAN SYSTEM INVOLED
IN ACID-BASE PHYSIOLOGY

 Respiratory System
 Renal System
BLOOD GAS ANALYZERS
 determine acid-base balance through the
measurement of partial pressure of
oxygen, carbon dioxide and pH.
 Bicarbonate and other parameters are
calculated from previously mentioned
measurements
METABOLIC ACIDOSIS
 increase in arterial [H+]
 decrease in arterial [HCO3]
 respiratory compensation –
hyperventilation (Kussmaul breathing)
 renal compensation - ↑ excretion of H+ as
titratable acid and NH4; ↑ reabsorption of
HCO3
METABOLIC ALKALOSIS
 decrease in arterial H+
 ↑ HCO3 because of loss of H+ e.g.
vomiting when H+ is lost from the stomach
 respiratory compensation: hypoventilation
 renal compensation: ↑ excretion of HCO3
RESPIRATORY ACIDOSIS
 caused by primary decrease in respiratory
rate and retention of CO2
 ↑ in H+ and HCO3 by mass action
 no respiratory compensation
 renal compensation: ↑ excretion of H+ and
NH4
 ↑ reabsorption of HCO3
RESPIRATORY ALKALOSIS
 caused by primary increase in respiratory
rate and loss of CO2
 ↓ H+ and HCO3 by mass action
 no respiratory compensation
 renal compensation: ↓ excretion of H+ and
NH4
 ↓ reabsorption of HCO3