Sravan abg ppt modified

Seminar on ABG
Presentor : Dr.
Sravan
Chair Person : Dr.
Vinathi

Extraction
 Blood is most commonly drawn from the radial
artery because it is
◦ easily accessible
◦ easily compressed to control bleeding
◦ less risk for occlusion.
 The femoral artery (or less often, the brachial
artery) is also used, especially during emergency
situations or with children.
 Blood can also be taken from an arterial catheter
already placed in one of these arteries.

 Samples drawn in plastic syringes should not be iced
and should always be analyzed within 30 minutes.

Parameters Of ABG
 pH
 PaO2
 PCo2
 Hco3-
 Sao2
 Lactate
 Anion Gap
 Electrolyte
s
 Glucose

The Key to Blood Gas Interpretation:
Four Equations, Three Physiologic
Processes
Equation Physiologic
Process
1) PaCO2 equation Alveolar ventilation
2) Alveolar gas equation Oxygenation
3) Oxygen content equation Oxygenation
4) Henderson-Hasselbalch equation Acid-base balance
These four equations, crucial to understanding and
interpreting arterial blood gas data, will provide the structure
for this slide presentation.

PaCO2 Equation: PaCO2 reflects ratio of metabolic
CO2 production to alveolar ventilation
VCO2 x 0.863 VCO2 = CO2 production
PaCO2 = ------------------- VA = VE – VD
VA VE = minute (total) ventilation (= resp. rate
x
tidal volume)
VD = dead space ventilation (= resp. rate x dead space volume
0.863 converts VCO2 and VA units to mm Hg
Condition State of
PaCO2 in blood alveolar ventilation
> 45 mm Hg Hypercapnia Hypoventilation
35 - 45 mm Hg Eucapnia Normal
ventilation
< 35 mm Hg Hypocapnia Hyperventilation

Hypercapnia (cont)
VCO2 x 0.863
PaCO2 = ------------------
VA VA = VE – VD
Inadequate VE leading to decreased VA and increased
PaCO2: sedative drug overdose; respiratory muscle
paralysis; central hypoventilation
Increased VD leading to decreased VA and increased
PaCO2: chronic obstructive pulmonary disease; severe
restrictive lung disease (with shallow, rapid breathing)

Dangers of Hypercapnia
Elevated PaCO2 poses a threat for three reasons:
1) An elevated PaCO2 will lower the PAO2 and as a
result will lower the PaO2.
(Alveolar gas equation)
2) An elevated PaCO2 will lower the pH
( Henderson-Hasselbalch equation).
3) The higher the baseline PaCO2, the greater it will
rise for a given fall in alveolar ventilation, e.g., a 1
L/min decrease in VA will raise PaCO2 a greater
amount when the baseline PaCO2 is 50 mm Hg than
when it is40 mmHg.

A-a Gradient
 FIO2 = 713 x O2%
 A-a gradient = PA O2 - PaO2
◦ Normal is 0-10 mm Hg
◦ 2.5 + 0.21 x age in years
 With higher inspired O2 concentrations, the A-a
gradient will also increase

Alveolar Gas Equation
PAO2 = PIO2 - 1.2 (PaCO2)*
Where PAO2 is the average alveolar PO2, and PIO2 is the
partial pressure of inspired oxygen in the trachea
PIO2 = FIO2 (PB – 47 mm Hg)
FIO2 is fraction of inspired oxygen and PB is the barometric
pressure. 47 mm Hg is the water vapor pressure at normal
body temperature.
* Note: This is the “abbreviated version” of the AG equation, suitable for most clinical purposes. In the longer
version, the multiplication factor “1.2” declines with increasing FIO2, reaching zero when 100% oxygen is inhaled. In
these exercises “1.2” is dropped when FIO2 is above 60%.

Alveolar Gas Equation
PAO2 = PIO2 - 1.2 (PaCO2)
where PIO2 = FIO2 (PB – 47 mm Hg)
Except in a temporary unsteady state, alveolar PO2 (PAO2) is always
higher than arterial PO2 (PaO2). As a result, whenever PAO2
decreases, PaO2 also decreases. Thus, from the AG equation:
If FIO2 and PB are constant, then as PaCO2 increases both PAO2
and PaO2 will decrease (hypercapnia causes hypoxemia).
If FIO2 decreases and PB and PaCO2 are constant, both PAO2 and
PaO2 will decrease (suffocation causes hypoxemia).
If PB decreases (e.g., with altitude), and PaCO2 and FIO2 are
constant, both PAO2 and PaO2 will decrease (mountain climbing
leads to hypoxemia).

PaO2-FiO2 ratio
 Normal PaO2/FiO2 is 300-500
 <250 indicates a clinically significant gas exchange
derangement

Hypoxemia
 Hypoventilation
 V/Q mismatch
 Right-Left shunting
 Diffusion impairment
 Reduced inspired oxygen tension

Right to Left Shunt
 Parenchymal diseases
leading to atelectasis or
alveolar flooding
(lobar pneumonia or
ARDS)
 Pathologic vascular
communications
(AVM or intracardiac
shunts)

Reduced inspired oxygen
delivery
 Delivery to tissue beds determined by arterial
oxygen content and cardiac output
 Oxygen content of blood is affected by level &
affinity state of hemoglobin
◦ Example is CO poisoning: reduction of arterial O2 content despite
normal PaO2 and Hgb caused by reduction in available O2 binding
sites on the Hgb molecule
 Tissue hypoxia may occur despite adequate
oxygen delivery
◦ CN poisoning causes interference with oxygen utilization by the
cellular cytochrome system, leading to cellular hypoxia

P(A-a)O2
P(A-a)O2 is the alveolar-arterial difference in partial
pressure of oxygen. It is commonly called the “A-a
gradient,” it results from gravity-related blood flow
changes within the lungs (normal ventilation-perfusion
imbalance).
PAO2 is always calculated based on FIO2, PaCO2, and
barometric pressure.
PaO2 is always measured on an arterial blood sample in
a “blood gas machine.”
Normal P(A-a)O2 ranges from @ 5 to 25 mm Hg
breathing room air (it increases with age).

Estimating A-a gradient:
Normal A-a gradient = (Age+10) / 4
 A-a increases 5 to 7 mmHg for every 10% increase
in FiO2

Predicted O2 (PaO2) = 109-0.43* age in
years
Average PaO2 95mmHg (range 85– 100 mmHg)

Physiologic Causes of Low PaO2
NON-RESPIRATORY P(A-a)O2
Cardiac right-to-left shunt Increased
Decreased PIO2 Normal
Low mixed venous oxygen content* Increased
RESPIRATORY P(A-a)O2
Pulmonary right-to-left shunt Increased
Ventilation-perfusion imbalance Increased
Diffusion barrier Increased
Hypoventilation (increased PaCO2) Normal

Oxygen Content
Neither the PaO2 nor the SaO2 tells how much oxygen is in the
blood.
CaO2 provides the oxygen content, (units = ml O2/dl)
calculated as:
CaO2 = quantity O2 bound + quantity O2 dissolved
to hemoglobin in plasma
CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)
1.34 ml O2 bound to each gm of Hb.
0.003 is solubility coefficient of oxygen in plasma

Acid/Base Balance
• The pH is a measurement of the acidity or alkalinity of
the blood.
• It is inversely proportional to the no. of (H+) in the
blood.
• The normal pH range is 7.35-7.45.

Calculation of pH
HCO
6.10 log 3
PaCO
0.03 2
pH

 

PaCO
    

3
2
24
HCO
H
Henderson-
Hesselbach
equation

Validation of ABG
The first part in ABG validation is:
 Determination of Hydrogen Ion Concentration by
using
PaCO
    

3
2
24
HCO
H
The second part of ABG validation is
• To confirm that for given hydrogen ions the pH is
correct.

Hydrogen ion concentration can be calculated
at a given pH by using this method
 At pH of 7.4 hydrogen ion concentration is 40
nmol/L
If pH < 7.4
For every 0.1 decrease in pH multiply hydrogen ion
concentration by 1.2 for example
 For pH 7.3 = 40 * 1.2
 For pH 7.2 = 40 * 1.2*1.2 and so on
If pH > 7.4
 For every 0.1 increase in pH multiply hydrogen ion
concentration by 0.8 for example
 For pH 7.5 = 40 * 0.8 For pH 7.6 = 40 * 0.8*0.8

pH in the Physiologic range
Relationship
between the pH
and H+
concentration (in
nanomol/L) in the
physiologic range

Acids and Bases
Acid : A substance that can “donate” H+ ion or when added
to solution raises H+ ion (i.e., lowers pH).
Base : A substance that can “accept” H+ ion or when added
to solution lowers H+ ion (i.e., raises pH).
(Definitions proposed by Bronsted)
H2CO3 <-> H+ + HCO3
–
HCl <-> H+ + Cl-
NH4
+ <-> H+ + NH3
H2PO4- <-> H+ + HPO4
2-
ACID BASE

Terminology
 Acidemia is present when blood pH <7.35.
 Alkalemia is present when blood pH >7.45.
 Metabolic
refers to disorders that result from a primary
alteration in [H+] or [HCO-].
3
 Respiratory
refers to disorders that result from a primary
alteration in PCO2 due to altered CO2 elimination.

Daily Acid Production
 Metabolism of
carbohydrates and fats → 15,000 mmol of CO2
CO2 + water → H2CO3 (weak acid)
CO2 removed via respiration.
 Noncarbonic acids derived from the metabolism of proteins.
Eg. Oxidation of sulfur-containing amino acids → H2SO4
1 meq/kg of non-volatile acid produced daily.
These H+ ions are excreted in the urine.
Non-Volatile Acids Volatile Acids
15,070 mmoles = 15,070 million nanomoles.

The ultimate pH of the body will
depend on ……..
 The amount of acid produced.
 The buffering capacity of the body.
 The rate of acid excretion by the lungs and kidneys.

At the end of the day, what would pH be if all
acid produced is retained in the body ?
pH
Initial H+
concentration
40 nanomoles/L
7.40
Daily H+
addition
15,070 ×106 nanomoles
Final H+
concentration
40 + {(15,070/42) ×106}
= 358 ×106 nanomoles/L 0.45
*Nanomole = one billionth of a mole.

Acid base balance
 Acid base homeostasis is essential for normal cellular
enzyme function.
 Arterial pH is maintained within a very narrow range
(7.35 and 7.45) by the interteraction of
Adjustment occurs within ….
1. Blood buffers ….seconds to minutes.
2. Lungs ….1 to 15 minutes.
3. Kidneys ….hours to days.

Buffering
 Buffers are chemical systems that either accept or
release H+, so that changes in the free H+ concentration
are minimized.
 Buffer, by themselves, do not remove acid/alkali from the
body.

Production of “new” bicarbonate linked to excretion of ammonium ions

Buffering
Illustration
Say 10 millimoles/L of H+ are produced
(= 10 × 106 nanomoles/L).
If unchecked, pH would decrease to <2.0 which is
fatal.
But, this acid load is bufferred by 10 mmoles/L
(=10 meq/L) of HCO3
–, producing CO2 and water.
Therefore, HCO3
– concentration decreases from 24
to 14.
Consequently pH decreases from 7.40 to 7.32,
which is within physiological range.

Buffering
Extracelular buffers (40 – 45%)
1.Bicarbonate/Carbon Dioxide buffer
system
2.Inorganic phosphates
3.Plasma proteins
Intracellular and Bone buffers (55 – 60%)
1.Proteins
2.Organic and inorganic phosphates
3.Hemoglobin
4.Bone

 Provides information on the physiological processes
that maintain pH homeostasis.
 Plays a pivotal role in diagnosis and management
of critically ill patients.
◦ Proper evaluation of ABG guides appropriate
diagnosis and, therefore, treatment.

An ABG Report
Parameters of importance Measured
pH
pCO2
Calculated
HCO3

Metabolic Acidosis
Primary Defect: Decrease in HCO3
 Accumulation of metabolic acids (non-carbonic)
caused by:
◦ Excess acid production which overwhelms renal capacity for
excretion. e.g. Diabetic ketoacidosis.
◦ Loss of alkali:
Leaves un-neutralized acid behind. e.g. Diarrhea.
◦ Renal excretory failure:
Normal total acid production in face of poor renal function.
e.g. Chronic renal failure.

Causes of Metabolic Acidosis
Acid Gain
1. L-lactic acid (= tissue hypoxia)
2. Ketoacids (= DKA, starvation)
3. D-lactic acid (= Low GI motility or altered GI
flora, eg. blind loop syndromes)
4. Intoxicants which are acids or become acids
 Methanol to formic acid
 Ethylene glycol to glyoxalic acid
 Paraldehyde to acetic acid
 Acetylsalicylic acid
 Toluene to hippuric acid
5. Renal Failure
Anion Gap =
Na – [Cl + HCO3]

Causes of Lactic Acidosis
 Type A
-Shock
- Acute severe hypoxia
- Acute severe anemia
 Type B
- Metformin
- Malignancy
- Thiamine deficiency
- Cyanide
- NRTI

Causes of Metabolic Acidosis
 Loss of NaHCO3
1. Loss via GI tract (diarrhea, ileus, fistula)
2. Loss in Urine (proximal RTA, acetazolamide)
3. Failure of kidneys to make new bicarbonate
(distal RTA)
4. Acid production and the excretion of its anion in
the urine without [H+] or [NH4
+] (Eg. Defective
renal reabsorption of betahydroxybutarate)

Metabolic acidosis
Compensatory Change

Sequential response to a H+ load, culminating in the restoration of
acid-base balance by the renal excretion of the excess H+
H+ Load
2 – 4 Hours
Minutes to
Hours
Intracellular
and bone
buffering
Respiratory
buffering by
lowering
PCO2
Extracellular
buffering by
HCO3
Increased
Renal H+
excretion
Hours to
Immediate days

Anion Gap
Unmeasured
Cation
Unmeasured
Anion

High Anion Gap Metabolic Acidosis
Example: 15 millimoles of organic acid added.
15 mEq of bicarbonate will be used up while buffering.

Normal Anion Gap Metabolic Acidosis
Example: 15 mEq of bicarbonate is lost.
Kidneys reclaim extra chloride to maintain electroneutrality.

High Anion Gap Met. Acidosis
 Ketoacidosis
 Lactic Acidosis
 Uremia
 Toxicity
◦ Salicylate
◦ Ethylene Glycol
◦ Methanol
◦ Paraldehyde
 Massive rhabdomyolysis
Anion Gap =
(Na – HCO3 – Cl)

Anion Gap
AG = [Na – (Cl + HCO3)]
 Increased unmeasured cation:
◦ Normally present cations
K+, Ca2+ , Mg2+
◦ Abnormal cations:
Lithium, IgG
 Decreased unmeasured anion:
◦ Hypoalbuminemia
 Lab Error:
◦ Hyponatremia due to viscous
serum
◦ Hyperchloremia in Bromide toxicity
◦ Random lab errors
 Decreased unmeasured cation:
◦ Decreased K, Ca, Mg
 Increased unmeasured anion:
◦ Organic:lactate, ketones
◦ Inorganic: PO42-, sulfates
◦ Hyperalbuminemia
◦ Exogenous anions: salicylates,
formate, penicillin, nitrate, etc.
◦ Incompletely idenitified: uremia,
paraldehyde, ehtylene glycol, HHS,
etc
 Lab Error:
◦ Falsely increased Na
◦ Falsely decreased Cl or HCO3

Pattern of Changes in Acid-Base Disorders
Primary
disorder
Initial
change
Compensatory
change
Metabolic
acidosis
↓ HCO3 ↓ PCO2

Metabolic Alkalosis
Primary Defect: Rise in HCO3
 from renal or extra-renal sources.
 Compensatory change:
◦ Tissues and RBC exchange intracellular H+
for extra-cellular Na+ and K+
◦ Hypoventilation and elevation of PaCO2
(Maximal PaCO2 rarely exceeds 55 mmHg)

Pattern of Changes in Acid-Base
Disorders
Primary
disorder
Initial
change
Compensatory
change
Metabolic
acidosis
↓ HCO3 ↓ PCO2
Metabolic
alkalosis
↑ HCO3 ↑ PCO2

Metabolic Alkalosis – Pathogenesis
Generation
 Loss of hydrogen ion from upper GI tract
(vomiting) or urine (diuretics)
 Addition of alkali – administration of bicarbonate
or its precursors (citrate, lactate, etc.)
Maintenance
• Volume/chloride depletion
• Hypokalemia
• Aldosterone excess

Metabolic Alkalosis – Causes
Saline Responsive
Urine Chloride (<10 mEq/L)
Saline Resistant
Urine Chloride (>20 mEq/L)
ECF Volume Depletion
Vomiting/Gastric Suction
Diuretics
Hypercapnia correction
Hypertensive (Normal
or increased ECF)
Hyperaldosteronism
Cushing syndrome
No ECF Vol. Depletion
NaHCO3 infusion
Multiple transfusions
Normo/Hypotensive
Bartter’s syndrome
Severe K depletion

Metabolic Alkalosis – Clinical Features

Metabolic Alkalosis – Clinical Features
 CNS:
◦ Increased neuromuscular excitability leading to
paresthesia, light headache, and carpopedal spasm
 CVS:
◦ Hypotension, cardiac arrhythmias
 Other:
◦ Weakness, muscle cramps, postural dizziness
◦ Muscle weakness and polyuria due to hypokalemia
 Respiratory:
◦ Compensatory hypoventilation may lead to hypoxia
symptoms in patients with pre-existing lung disease

D/D of Metabolic Alkalosis
Urine
Electrolyte
Saline
Sensitive
Saline
Resistant
Cl < 10 mEq/L
(unless on diuretics)
> 20 mEq/L
Na < 20 mEq/L
(unless recent
vomiting)
> 20 mEq/L
K May be high
if high distal
Na
(diuretics or recent
vomiting)
Usually high
as
aldosterone
is acting

Metabolic Alkalosis – Treatment
Treat underlying cause
 Saline reponsive
◦ Normal saline with KCl or Isolyte-G
◦ H2 inhibitors or PPI
◦ In diuretic induced, dose reduction, KCl
suplementation, spironolactone
◦ Discontinue exogenous sources of alkali (bicarbonate,
RL, acetate, citrate)
◦ When pH > 7.65, may administer 0.1 N HCl via central
veins
◦ Dialysis
 Saline Resistant – Treat the cause.
Spironolactone, K correction and Na restriction.

Respiratory Acidosis
Primary Defect: Rise in PCO2
 Decrease in pulmonary clearance of CO2
 Compensatory Change:
◦ Acute (<24 hrs): Buffering by tissue and RBC to
increase HCO3. Rarely more than 4 mEq
◦ Chronic (>72 hrs): Stimulation of renal tubular
secretion of H+ thus synthesizing more HCO3. Chloride
is lost along with NH4+

Respiratory Acidosis – Causes
 CNS Depression
◦ Drugs (anaesthesia, sedatives), infection, stroke
 Neuromuscular impairment
◦ Myopathy, Myasthenia gravis, polymyositis, hypokalemia
 Ventilation restriction
◦ Rib fracture, pneumothorax, hemothorax
 Airway
◦ Asthma, obstruction
 Alveolar diseases
◦ COPD, pulmonary edema, ARDS, pneumonitis
 Miscellaneous
◦ Obesity, Hypoventilation

Response to an increase in PCO2
Increased PCO2
Hours to Days
10 to 30
minutes
Increased
Renal H+
Excretion
Intracellular
Buffering

Respiratory Acidosis – Treatment
 Acute
◦ Treat the cause.
◦ Bronchodilators.
◦ Mechanical ventilation.
◦ Antibiotics
 Chronic
◦ Oxygen -long term supplemental.
◦ Nasal continuous positive airway pressure.
◦ Improving respiratory muscle function.
◦ Drugs- Progesterone, Doxapram, Almitrine,
Acetazolamide, Methyphenidate and Caffeine.

Respiratory Alkalosis
Primary Defect: Decrease in PCO2
 Compensatory Change:
◦ Acute (<24 hrs): Buffering by tissue and RBC
to lower HCO3. Rarely to less than 18 mEq/L
◦ Chronic (>72 hrs): Impairs kidney's ability to
excrete acid thus lowering HCO3. If more than
2 weeks, pH may return to normal.

Respiratory Alkalosis – Causes
 Hypoxemia
◦ Pneumonia, interstitial diseases, pulm emboli, edema, etc.
◦ CHF
◦ Severe anemia
◦ High altitude resisdence
 Direct stimulation of the medullary respiratory
center
◦ Psychogenic/voluntary
◦ Pain
◦ Pregnacy
◦ Hepatic failure
◦ Gram Negative sepsis
◦ Salicylate toxicity
◦ Rapid correction of metabolic acidosis
◦ Neurological – CVA, trauma, tumors, infections, etc.
 Mechanical Ventilation (overtreatment)

Respiratory Alkalosis – Treatment
 Treat the cause
 Does not need treatment unless pH > 7.50
 Relief of hypoxia.
 Rebreathing into a non compliant bag as
long as hyperventilation exists.
 Treatment of anxiety.

Pattern of Changes in Acid-Base Disorders
Primary
disorder
Initial
change
Compensatory
change
Metabolic
acidosis
↓ HCO3 ↓ PCO2
Metabolic
alkalosis
↑ HCO3 ↑ PCO2
Respiratory
acidosis
↑ PCO2 ↑ HCO3
Respiratory
alkalosis
↓ PCO2 ↓ HCO3

The Boston Approach
to
Acid-Base Disorders

5-Steps in the Evaluation of
Systemic Acid Base Disorders
1. Comprehensive history and physical
examination.
2. Evaluate simultaneously performed ABG &
serum electrolytes.
3. Identification of the dominant disorder.
4. Calculation of compensation.
5. Calculate the anion gap and the Δ.
1.Anion Gap
2.ΔAG
3.Δ Bicarbonate

Step 3:
Identification of the dominant disorder
Primary
disorder
pH Initial
change
Compensatory
change
Metabolic
acidosis
↓ ↓ HCO3 ↓ PCO2
Metabolic
alkalosis
↑ ↑ HCO3 ↑ PCO2

Step 3:
Identification of the dominant disorder
pH HCO3 PCO2
Dominant
(Primary) disorder
↓ ↓ ↓ Metabolic acidosis
↑ ↑ ↑ Metabolic
alkalosis
↓ ↑ ↑ Respiratory
acidosis
↑ ↓ ↓ Respiratory
alkalosis

Dictums in ABG Analysis
 pH and Primary parameter change in the
same direction suggests a metabolic
problem
 pH and Primary parameter change in the
opposite direction suggests a respiratory
problem

What is the Magnitude of
Compensation?

Compensation Formula Simplified
1.2
0.7
0.1 0.3
0.2 0.5
Acute Chronic
Metabolic
Acidosis
Alkalosis
Acidosis
Respiratory
Alkalosis

Step 4. Check if the compensatory
response is appropriate or not.
If the compensation is not appropriate,
suspect a second (and perhaps a triple)
acid-base disorder.

Step 4:
Calculation of compensation
Disorder pH Primary
change
Compensatory
Response
Equation
Metabolic
Acidosis
-]  PCO2 ΔPCO2  1.2  ΔHCO3
  [HCO3
Metabolic
Alkalosis
-]  PCO2 ΔPCO2  0.7  ΔHCO3
  [HCO3
Respiratory
Acidosis
-] Acute:
  PCO2  [HCO3
-  0.1  ΔPCO2
Chronic:
ΔHCO3
-  0.3  ΔPCO2
ΔHCO3
Respiratory
Alkalosis
-] Acute:
  PCO2  [HCO3
-  0.2  ΔPCO2
Chronic:
ΔHCO3
-  0.5  ΔPCO2
ΔHCO3
Note: The formula calculates the change in the compensatory parameter.

Step 5: Calculate the “gaps”
Anion gap = Na+ − [Cl− + HCO3
−]
Δ AG = Anion gap − 12
Δ HCO3 = 24 − HCO3
Δ AG = Δ HCO3
−, then Pure high AG Met. Acidosis
Δ AG > Δ HCO3
−, then High AG Met Acidosis + Met. Alkalosis
Δ AG < Δ HCO3
−, then High AG Met Acidosis + HCMA
Note:
Add Δ AG to measured HCO3
− to obtain
bicarbonate level that would have existed IF the
high AG metabolic acidosis were to be absent,
i.e., “Pre-existing Bicarbonate.”
 e existing Bicarb
Delta AG




Current Bicarb
Pr _ _
_
_









Delta AG / Delta HCO3 Ratio
 Ratio 1-2 : High anion gap acidosis
 Ratio > 2 : HAG acidosis and metabolic
alkalosis
 Ratio < 1 : HAG acidosis and NAG acidosis
: DKA with ketone excretion
: CKD with anion excretion but H+
retention

Dictums in ABG Analysis
1. Primary change & Compensatory change always
occur in the same direction.
2. pH and Primary parameter change in the same
direction suggests a metabolic problem.
pH and Primary parameter change in the opposite
direction suggests a respiratory problem.
3. Renal and pulmonary compensatory mechanisms
return pH toward but rarely to normal.
Corollary:
A normal pH in the presence of changes in PCO2 or
HCO3 suggets a mixed acid-base disorder.

Normal Values for Major Acid-Base variables
pH H+
nanoEq/L
 S Na = 135 – 145 mEq/L
 S K = 3.5 – 5.5 mEq/L
 S Cl = 97 – 110 mEq/L
PaCO2
mmHg
HCO3
–
mEq/L
Arterial 7.37 – 7.43 37 – 43 36 – 44 22 – 26
Venous 7.32 – 7.38 42 – 48 42 – 50 23 – 27

Common clinical states and associated acid-base disorders
Clinical state Acid-base disorder
Renal failure Metabolic acidosis
Vomiting Metabolic alkalosis
Severe diarrhea Metabolic acidosis
Cirrhosis Respiratory alkalosis
Hypotension Metabolic acidosis
COPD Respiratory acidosis
Sepsis Respiratory alkalosis, metabolic acidosis
Pulmonary embolus Respiratory alkalosis
Pregnancy Respiratory alkalosis
Diuretic use Metabolic alkalosis

Clues to Mixed Acid-Base Disorders
 Normal pH (with the exception of chronic
respiratory alkalosis)
 PCO2 and HCO3 deviating in opposite
directions
 pH change in the opposite direction of a
known primary (dominant) acid-base
disorder

Is a VBG just as good as an
ABG?
Risk with ABG
◦ Significant pain
◦ Hematoma
◦ Aneurysm formation
◦ Thrombosis or
embolization
◦ Needlestick injuries .
Advantages with ABG
◦ PaO2
◦ Arterial
Oxyhemoglobin
saturation (SaO2)

 Brandenburg and Dire investigated 66 patients (DKA) .
An ABG and VBG were subsequently drawn. 44 pts
had acidosis with arterial pH less than 7.35.
 Among these cases, the mean difference between
arterial and venous pH values was 0.02 (range 0.0 to
0.11) with a Pearson’s correlation coefficient (r) of
0.9689
 This study concludes that venous blood gas
measurements accurately demonstrated the degree of
acidosis in patients with DKA.

 Lactate
In 2000, Lavary et al studied 375 patients and
compared arterial and venous lactates and showed
that there was no significant difference between
the two
 Recent study in 2002 investigated whether venous
pCO2 and pH could be used to screen for
significant hypercarbia ,
the authors stated that a venous pCO2 of
44mmHg had a sensitivity for detection of
hypercarbia of 100% and a specificity of 57%, thus
making it an effective screening test for hypercarbia

Comparing Electrolytes
In ABG & Biochem Lab Analyser

Case Scenarios in
Acid-Base Disorders

Case 1
 A 15 yr old juvenile diabetic presents with abdominal
pain, vomiting, fever & tiredness for 1 day. He had
stopped taking insulin 3 days ago. Examination
revealed tachycardia, BP- 100/60, signs of
dehydration. Abdominal examination was normal.
 ABG:
pH 7.31
PaCO2 26 mmHg
HCO3 12 mEq/L
PaO2 92 mm Hg
Serum Electrolytes:
Na 140 mEq/L
K 5.0 mEq/L
Cl 100 mEq/L
 Evaluate the acid-base disturbance(s)?

Case 1: Solution
 Dominant disorder is Metabolic Acidosis
 Compensation formula:
Δ PaCO2 = 1.2 × Δ HCO3
= 1.2 × 12
= 14.4
PaCO2 = 40 – 14 = 26
Compensation is appropriate.
 Anion Gap = 140 – (100 + 12)
= 28
AG is high.
pH 7.31
PaCO2 26
HCO3 12
PaO2 92
Na 140
K 5.0
Cl 100

Case 1: Solution
 Δ AG = 28 – 12
= 16
 Δ HCO3 = 24 – 12
= 12
-
 Δ AG > Δ HCO3
 Final Diagnosis:
pH 7.31
PaCO2 26
HCO3 12
PaO2 92
Na 140
K 5.0
Cl 100
High AG Met. Acidosis + Met. Alkalosis

Case 2
 A 24 yr old boy presents with continuous vomiting of
3 days duration, mental confusion, giddiness, and
tiredness for 1 day.
 Examination revealed tachycardia, hypotension and
dehydration.
 ABG
pH 7.50
PaCO2 48
HCO3 32
PaO2 90
Serum Electrolytes:
Na 139
K 3.9
Cl 85

Case 2: Solution
 Dominant disorder is Metabolic Alkalosis
= 0.7 × 8
= 5.6
PaCO2 = 40 + 6 = 46
 Anion Gap = 139 – (85 + 32)
= 22
AG is high.
pH 7.50
PaCO2 48
HCO3 32
PaO2 90
Na 139
K 3.9
Cl 85

Case 2: Solution
 Δ AG = 22 – 12
= 10
 High AG metabolic acidosis
pH 7.50
PaCO2 48
HCO3 32
PaO2 90
Na 139
K 3.9
Cl 85
Metabolic Alkalosis + High AG Met. Acidosis

Case 3: Varieties of Metabolic Acidosis
Patient A B C
ECF volume Low Low Normal
Glucose 600 120 120
pH 7.20 7.20 7.20
Na 140 140 140
Cl 103 118 118
HCO- 10 10 10
3
AG 27 12 12
Ketones 4+ 0 0
High-AG
Met.
Acidosis
Non-AG
Met.
Acidosis
Non-AG
Met.
Acidosis

Renal handling of Hydrogen in
Metabolic Acidosis
 In the setting of metabolic acidosis, normal kidneys try to
increase H+ excretion by increasing titratable acidity and
ammonia. The latter is excreted as NH+.
4
 When NH4
+ is excreted, it also causes increased
chloride loss, to maintain electrical neutrality.
 Chloride loss, therefore, will be in excess of Na and K.
 Urine Anion-Gap = Na + K – Cl
 In metabolic acidosis, if Urine anion gap is negative, it
suggests that the kidneys are excreting H+ effectively.

Urine Electrolytes in Metabolic
Acidosis
Patient A B C
U. Na 10 50
U. K 14 47
U. Cl 74 28
Urine AG –50 +69
Dx: Diarrhea RTA
Urine Anion Gap = (U. Na + U. K – U. Cl)
In Normal anion gap Metabolic Acidosis,
Positive Urine AG suggests distal Renal Tubular Acidosis
Negative Urine AG suggests non-renal cause for Metabolic Acidosis.

Case 4
 A 50 yr old man presented with history of
progressive dyspnoea with wheezing for 4 days.
 He also had fever, cough with yellowish
expectoration.
 He had increased sleepiness for 1 day.
 On examination, he was tachypnoeic, pulse-
100/min bounding, BP-160/96, central cyanosis
+, drowsy, asterixis +, RS – B/L extensive
wheezing +.
 CXR- hyperinflated lung fields with tubular heart.

Case 4: Laboratory data
 ABG:
pH 7.30
PaCO2 60 mmHg
HCO3 28 mEq/L
PaO2 68 mm Hg
 Serum Electrolytes:
Na 136 mEq/L
K 4.5 mEq/L
Cl 98 mEq/L

Case 4: Solution
 Dominant disorder is Respiratory Acidosis
Δ HCO3 = 0.3 × Δ PaCO2
= 0.3 × 20
= 6
HCO3 = 24 + 6 = 30
 Anion Gap = 138 – (98 + 28)
= 10
AG is normal.
pH 7.30
PaCO2 60
HCO3 28
PaO2 68
Na 136
K 4.5
Cl 98

Case 5
 20 year old girl presented with complaints of
difficulty in breathing and upper abdominal
discomfort for the past 1 hr.
 On examination, vitals normal, patient
hyperventilating, RS – normal, Abdomen – normal.

Case 5: Laboratory data
 ABG:
pH 7.50
PaCO2 25 mmHg
HCO3 21 mEq/L
PaO2 100 mm Hg
 Serum Electrolytes:
Na 137 mEq/L
K 3.9 mEq/L
Cl 99 mEq/L
Calcium 9.0 mEq/L

Case 5: Solution
 Dominant disorder is Respiratory Alkalosis
= 0.2 × 15
= 3
HCO3 = 24 – 3 = 21
 Anion Gap = 137 – (99 + 21)
= 17
pH 7.50
PaCO2 25
HCO3 21
PaO2 100
Na 137
K 3.9
Cl 99
Calcium 9.0
AG is slightly high which can be seen in
respiratory alkalosis.

Case 6
For each of the following sets of arterial blood gas
values, what is (are) the likely acid-base disorder(s)?
pH PaCO2 HCO3 Acid-Base status
7.28 50 23 respiratory acidosis and
metabolic acidosis
7.50 33 25 respiratory alkalosis
and metabolic alkalosis
7.23 34 14 metabolic acidosis and
respiratory acidosis

Case 7
 Explain the acid-base status of a 35-year-old man with
history of chronic renal failure treated with high dose
diuretics admitted to hospital with pneumonia and the
following lab values:
ABG Serum Electrolytes
pH 7.52 Na+ 145 mEq/L
PaCO2 30 mm Hg K+ 2.9 mEq/L
PaO2 62 mm Hg Cl- 98 mEq/L
HCO3
- 21 mEq/L

Case 7: Solution
 Dominant disorder is Respiratory Alkalosis
= 0.2 × 10
= 2
HCO3 = 24 – 2 = 22
 Anion Gap = 145 – (98 + 21)
= 26
pH 7.52
PaCO2 30
HCO3 21
PaO2 62
Na 145
K 2.9
Cl 98
AG is very high suggestive of metabolic
acidosis.

Case 7: Solution
 Δ AG = 26 – 12
= 14
 Δ HCO3 = 24 – 21
= 3
 Δ AG > Δ HCO3
-
High AG Met Acidosis + Met. Alkalosis
Respiratory Alkalosis +
High AG Metabolic Acidosis +
Metabolic Alkalosis
pH 7.52
PaCO2 30
HCO3 21
PaO2 62
Na 145
K 2.9
Cl 98

Case 8
The following values are found in a 65-year-old patient.
Evaluate this patient's acid-base status?
ABG Serum Chemistry
pH 7.51 Na + 155 mEq/L
PaCO50 mm Hg K+ 5.5 mEq/L
2 HCO- 39 mEq/L Cl- 90 mEq/L
3
CO2 40 mEq/L
BUN 121 mg/dl
Glucose 77 mg/dl

Case 8: Solution
 Dominant disorder is Metabolic Alkalosis
= 0.7 × 16
= 11.2
PaCO2 = 40 + 11 = 51
 Anion Gap = 155 – (90 + 40)
= 25
AG is high.
pH 7.51
PaCO2 50
HCO3 40
PaO2 62
Na 155
K 5.5
Cl 90
BUN 121

Case 8: Solution
 Δ AG = 25 – 12
= 13
 High AG metabolic acidosis
Metabolic Alkalosis +
pH 7.51
PaCO2 50
HCO3 40
PaO2 62
Na 155
K 5.5
Cl 90
BUN 121
High AG Metabolic Acidosis

Case 9
 A 52-year-old woman has been mechanically ventilated
for two days following a drug overdose. Her arterial blood
gas values and electrolytes, stable for the past 12 hours,
show:
ABG Serum Chemistry
pH 7.45 Na + 142 mEq/L
Cl- 100 mEq/L
HCO3- 18 mEq/L

Case 9: Solution
 Dominant disorder is Chronic Respiratory
Alkalosis
= 0.5 × 15
= 7.5
HCO3 = 24 – 8 = 16
 Anion Gap = 142 – (100 + 18)
= 24
pH 7.45
PaCO2 25
HCO3 18
Na 142
K 4.0
Cl 100
AG is very high suggestive of metabolic
acidosis.

Case 9: Solution
 Δ AG = 24 – 12
= 12
 Δ HCO3 = 24 –18
= 6
 Δ AG > Δ HCO3
-
High AG Met Acidosis + Met. Alkalosis
Chronic Respiratory Alkalosis +
High AG Metabolic Acidosis +
? Metabolic Alkalosis

Case 10
 An 18-year-old college student is admitted to the
ICU for an acute asthma attack, after not
responding to treatment received in the Casualty
department. ABG values (on room air) show: pH
7.46, PaCO2 25 mm Hg, HCO3- 17 mEq/L, PaO2
55 mm Hg, SaO2 87%. Her peak expiratory flow
rate is 95 L/min (25% of predicted value).
 Asthma medication is continued. Two hours later
she becomes more tired and peak flow is < 60
L/minute. Blood gas values (on 40% oxygen) now
show: pH 7.20, PaCO2 52 mm Hg, HCO3- 20
mEq/L, PaO2 65 mm Hg. At this point intubation
and mechanical ventilation are considered. What is
her acid-base status?

Case 10 Solution
 Initial status:
◦ chronic respiratory alkalosis, resulting from
several days of hyperventilation (pH almost
normal)
 When her asthamatic condition has
worsened, she has acutely hypoventilated.
 The second set of blood gas values reflects
acute respiratory acidosis on top of a
chronic respiratory alkalosis.

Case 11
A 21 year old male with progressive renal insufficiency is
admitted with abdominal cramping. He had congenital
obstructive uropathy with creation of ileal loop for
diversion. On admission,
ABG Serum Chemistry
pH 7.20 Na + 140 mEq/L
Cl- 110 mEq/L
HCO3- 10 mEq/L

Case 11: Solution
 Dominant disorder is Metabolic Acidosis
= 1.2 × 14
= 16.8
PaCO2 = 40 – 17 = 23
 Anion Gap = 140 – (110 + 10)
= 20
High anion-gap metabolic acidosis.
pH 7.20
PaCO2 24
HCO3 10
Na 140
K 5.6
Cl 110

Case 11: Solution
 Δ AG = 20 – 12
= 8
 Δ HCO3 = 24 –10
= 14
 Δ AG < Δ HCO3
-
pH 7.20
PaCO2 24
HCO3 10
Na 140
K 5.6
Cl 110
High AG Met Acidosis + Normal-AG Met. Acidosis
Mixed Metabolic Acidosis

Case 12
 A 45 year old female with
hypertension was treated
with low salt diet and
diuretics. BP 135/85.
Otherwise normal.
See initial lab values.
 She developed profound
water diarrhea, nausea and
weakness.
 On exam, HR = 96, T=100.6
F, BP 115/70. Abdominal
tenderness with guarding on
palpation.
Paramete
r
Initial
Subse
quent
Na 137 138
K+ 3.1 2.8
Cl- 90 102
HCO3 35 25
pH 7.51 7.42
PaCO2 47 39

Case 12: Solution
 Initally, dominant disorder is Metabolic Alkalosis
= 0.7 × 11
= 7.7
PaCO2 = 40 + 8 = 48
 Anion Gap = 137 – (90 + 35)
= 12
AG is normal.
pH 7.51
PaCO2 47
HCO3 35
Na 137
K 3.1
Cl 90

Case 12: Solution
 Subsequently, she has developed
pH HCO3 PaCO2
↓ ↓ ↓
pH 7.51  7.42
PaCO2 47  39
HCO3 35  25
Na 137  138
K 3.1  2.8
Cl 90  102

Case 12: Solution
 Subsequently, she has developed
pH HCO3 PaCO2
↓ ↓ ↓ Metabolic acidosis
The decrease in bicarbonate is almost same as
the rise in chloride.
Metabolic Alkalosis +
Hyperchloremic (non-AG) Metabolic Acidosis

Case 13
 A patient with salicylate overdose.
pH = 7.45
PCO2 = 20 mmHg
HCO3 = 13 mEq/L
 Dominant disorder: Respiratory alkalosis
 Appropriate Compensation would have been
HCO3 of 20 (24 – 4)
 Lower than expected HCO3 suggests presence of
metabolic acidosis as well.

Case 14
 A 55 year old female with DM Nephropathy was admitted
with acute LV failure and hyperkalemia. ST-T changes
and increased troponin noted.
 Hemodialysis was initiated.
 CAG revealed near normal coronaries.
 She was about to be discharged home when she
developed sudden cardiorespiratory arrest.
 CPR and ACLS begun and after about 8 mins cardiac
rhythm returned.
 She was transferred to ICU and placed on ventilator at
about 1 PM.

Case 14 (continued): ABG & Ventilator settings
Parameter 1 PM 2 PM 6 PM 8 PM
pH 6.99 7.24 7.52 7.54
PO2 162 73 274 131
PaCO2 49 33 17 20
HCO3 12 14 13 16
Base Excess –20 –12 –6 –3
Ventilator settings
Mode CMV CMV CMV CMV
Rate 20 20 20 16
Tidal volume 400 400 500 500
FIO2 100% 80% 80% 60%
Action Taken
Sod. Bicarb
3 amps.
Increase
Tidal vol.
Decrease
Rate
Decr. Rate &
Ch. To SIMV

“Life is a struggle,
not against sin,
not against the Money Power,
not against malicious animal
magnetism ,
but against hydrogen ions."
H.L. MENCKEN

Sravan abg ppt modified

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (20)

Similar to Sravan abg ppt modified

Similar to Sravan abg ppt modified (20)

Sravan abg ppt modified