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TERMINOLOGIES
ACID:- A chemical species that can act as a proton (H+)
donor
BASE:- A chemical species that can act as a proton (H+)
acceptor
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TERMINOLOGIES (contd)
WEAK ACID:- A substance that reversibly donates H+
and tends to have less of the effect on [H+]
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TERMINOLOGIES (contd)
ACIDOSIS:- Any pathologic process that tends to lower
pH
ALKALOSIS:- Any pathologic process that tends to
increase pH
METABOLIC DISORDER:- A disorder that primarily
affects [HCO3-]
RESPIRATORY DISORDER:- A disorder that primarily
affects PaCO2
SIMPLE ACID-BASE DISORDER:- The presence of only
one pathologic process
MIXED ACID-BASE DISORDER:- The presence of one
or more primary processes
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TERMINOLOGIES (contd)
ACIDEMIA & ALKALEMIA:- The net effect of all primary
processes and compensatory physiological responses on
arterial blood pH
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TERMINOLOGIES (contd)
ANION GAP:- The difference between the major
measured cations and the major measured anions
Anion Gap=[Na+] – ([Cl-] + [HCO3-])=7-14 mEq/L
DELTA ANION GAP:- The ratio of
(anion gap – 10)/( 24 - HCO3), assess increase in anion
gap relative to decrease in HCO3-
URINE ANION GAP:- The difference between the major
measured cations and the major measured anions in
urine
UAG = [Na+] + [K+] – [Cl-] = -20 to 0 mEq/L
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Compensatory mechanisms
Physiological responses to changes in [H+] is characterized by
Chemical buffers (immediate response)
Respiratory compensation
Renal compensation
Slower
More effective
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Compensatory mechanisms
Body Buffers
Buffers Sites
Bicarbonate (H2CO3/HCO3-) ECF
Hemoglobin (HbH/Hb-) Blood
Intracellular proteins (PrH/Pr-) ICF
Ammonia (NH3/NH4-) Urine
Phosphate (H2PO4-/HPO422-) Urine
Intracellular K+ ECF
Na+ & Ca2+ from bones Bone
(CaCO3,CaHPO4, NaHCO3)
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Basic concepts
Hydrogen ion concentration and pH
Hydrogen ion concentration is traditionally expressed by pH
which is a logarithmic function of the [H+]
pH=log 1/H+= -log[H+]
Normal pH of plasma range from 7.35 to 7.45
When hydrogen ion concentration increases, pH decreases
and vice versa
[H+]= 24 × (PCO2/HCO3)=40 at pH 0f 7.4
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Primary acid base disorders
Respiratory
When a change in PCO2 is responsible for a change in [H+]
Increase in PCO2 is respiratory acidosis
Decrease in PCO2 is respiratory alkalosis
Metabolic
When a change in HCO3 is responsible for a change in [H+]
Decrease in HCO3 is metabolic acidosis
Increase in HCO3 is metabolic alkalosis
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Secondary response
To limit the change in [H+] produced by primary acid base
disorders
Accomplished by changing the other component of the
PaCO2/HCO3 ratio in the same direction
Eg:
In primary respiratory acidosis where PCO2 is
increased,secondary response will involve an increase in HCO3
that will limit the change in [H+]
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Responses to metabolic Acid base
disorders
Involves change in minute ventilation that is mediated by
peripheral chemoreceptor located in the carotid body at the
carotid bifurcation in the neck
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Metabolic acidosis
Secondary response is increase in minute ventilation and
subsequent decrease in PaCO2
Response appears in 30-120 mins,can take 12-24hrs to complete
Change in PaCO2= 1.2 × change in HCO3
Expected PaCO2=40 –change in PaCO2
Anion gap calculation and Gap gap calculation
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Metabolic alkalosis
Secondary response is decrease in minute ventilation and
subsequent increase in PaCO2
Change in PaCO2= 0.7 × change in HCO3
Expected PaCO2= 40 + change in PaCO2
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Responses to respiratory acid base
disorders
Secondary response to changes in PaCO2 occurs in the
kidneys where HCO3 absorption in proximal tubes is
adjusted to produce appropriate change in plasma HCO3.
Renal response is relatively slow and can take 2-3 days so
respiratory acid base disorders are separated into acute and
chronic disorders
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Acute respiratory disorders
Acute changes in PaCO2 have small effect on plasma HCO3
For acute respiratory acidosis
Change in HCO3= 0.1 × change in PaCO2
Expected HCO3= 24 + change in HCO3
For acute respiratory alkalosis
Change in HCO3= 0.2 × change in PaCO2
Expected HCO3= 24- change in PaCO2
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Chronic respiratory disorders
Renal response to an increase in PaCO2 is an increase in
HCO3 reabsorption in the proximal renal tubules,which
raises the plasma HCO3 concentration.
Response to decrease in PaCO2 is decrease in renal HCO3
reabsorption which lowers plasma HCO3 concentration
Change in HCO3= 0.4 × change in PaCO2 for both acidosis
and alkalosis
For chronic respiratory acidosis
Expected HCO3= 24 + change in HCO3
For chronic respiratory alkalosis
Expected HCO3= 24- change in HCO3
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Stepwise approach to acid base
analysis
Stage 1: identify primary acid base disorder
PaCO2 and pH used to identify
Rule 1: if PaCO2 and/or pH is outside normal range,there is
an acid base disorder
Rule 2: if PaCO2 and pH are both abnormal,compare
directional change
2a: if PaCO2 and pH change in same direction,there is primary
metabolic acid base disorder
2b: if PaCO2 and pH change in opposite directions,there is
primary respiratory acid base disorder.
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Eg:
a case where arterial pH=7.2 and PaCO2=20.
Here both are reduced indicating primary metabolic disorder
and as pH is acidic, diagnosis is primary metabolic acidosis
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Rule 3: if only pH or PaCO2 is abnormal, condition is mixed
metabolic and respiratory disorder.
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Eg:
a case where pH 7.38 and PaCO2 55mmHg.
Only PaCO2 is abnormal, so there is mixed disorder.
As PaCO2 is elevated indicating respiratory acidosis and so the
metabolic disorder must be metabolic alkalosis
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Stage 2: Evaluate the secondary response
Goal is to determine if there is an additional acid base disorder
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Eg: case where PaCO2 =23,pH=7.32 and HCO3=16.
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Rule 5: for a primary respiratory disorder, a normal or near
normal HCO3 indicates that the disorder is acute
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Eg: patient with PaCO2 23 mm Hg and pH of 7.54 and HCO3
38.
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Stage 3: use Gaps to evaluate metabolic acidosis
Helps to identify underlying cause of acidosis
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The Anion Gap….
By the law of electroneutrality,
Unmeasured anions + measured anions = unmeasured
cations + measured cations,
Unmeasured anions – unmeasured cations = measured
cations – measured anions,
Anion Gap = [Na +] – ([Cl -] + [HCO3-])
Normal value = 7 – 14 mEq/L
Unmeasured anions = plasma proteins, SO42-, PO42- and
organic anions
Unmeasured cations = K+, Ca2+, Mg2+
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The Anion Gap….
Plasma albumin accounts for the largest fraction of the
anion gap (11 mEq/L)
Adjusted AG = observed AG + 2.5 x (4.5 - measured
albumin in g/dl)
Any process that increases “unmeasured anions” or
decreases “unmeasured cations” will increase the anion
gap and vice versa
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Increased Anion Gap
Increased production of nonvolatile acids
Ketoacidosis
Uremia
Salycilate toxicity
Sepsis
Methanol poisoning
Ethanol poisoning
Lactic acidosis
Ethylene glycol poisoning
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Normal Anion Gap (Hyperchloremic)
Increased GI losses of HCO3-
Diarrhoea
Anion exchange resin (cholestyramine)
Ingestion of CaCl2. MgCl2
Fistulae (pancreatic, billiary or small bowel)
Increased renal losses of HCO3-
Renal tubular acidosis
Carbonic anhydrase inhibitors
Hypoaldesteronism
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Normal Anion Gap (Hyperchloremic)
Dilutional
Large amount of HCO3- free fluids
Total parentral nutrition
Increased intake of chloride containing acids
Ammonium chloride
Lysine hydrochloride
Arginine hydrochloride
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Urine Anion Gap
Useful in evaluation of non anion gap metabolic acidosis
to r/o non renal loss of HCO3
UAG = Unmeasured anions – unmeasured cations
= measured cations – measured anions
= [Na +] + [K +] – [Cl -] = -20 to 0 mEq/L
The predominant unmeasured urine cations = NH4+
Large negative urine anion gap = metabolic acidosis with
intact renal acidification (diarrhoea)
Positive urine anion gap = metabolic acidosis with
impaired renal acidification (RTA)
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The Delta Anion Gap
Used to detect additional acid-base disorders in patients
with high anion gap metabolic acidosis
Assess in anion gap relative to in HCO3 -
Delta anion gap = (anion gap – 10) / ( 24 - HCO3)
Normal value = 1
Value <1 = HCO3- has decreased out of proportion to the
elevation of anion gap and suggests the presence of
nonanion gap metaboic acidosis
Value >1 = the anion gap has increased out of proportion
to the rise in HCO3- and suggests the presence of a
concommitant metabolic alkalosis
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Example
A 42 yr old man brought to the ER after he was found
lying in an alley with an empty liquor bottle near by.
P=110/m,BP=120/80mmHg,RR=28/m,T=98.6ºF. The patient was
unresponsive. Pupils were minimally reactive to light, and
fundoscopic exam was normal. Bibasilar crackles were noted.
His deep tendon reflexes were brisk and symmetric, and
plantar reflexes were normal. His history suggested ingestion of
a toxin, some of which are associated with acid-base disorders.
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The patient’s lab reports were as follows:
Arterial blood gas pH=7.1
PaCO2= 35mmHg
PaO2=90mmHg at room air
Na+= 145mEq/L
Cl- =97mEq/L
HCO3- =12mEq/L
Blood urea nitrogen=30mg%
Creatinine=1.5mg%
Glucose = 110mg%
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Test the accuracy of the data
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[H+]=24 × PCO2/HCO3=70
Then,
For every 0.1 decrease in pH,multiply H+ sequentially by
1.25. In our case,40×1.25 ×1.25 ×1.25=78
For every 0.1 increase in pH,multiply H+ sequencially by
0.8
Comparing both which is close,so test is valid.
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Identify primary disorder
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Both pH(7.1) & PaCO2 (35mmHg) has decreased, the
primary disorder is metabolic acidosis
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Calculation of the expected compensation
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Decrease in PaCO2 = 1.2 × (24 – 12) = 14.4 mmHg
Expected PaCO2 = 40 –14 = 26 mmHg
Measured PaCO2 = 35 mmHg
concomitant respiratory acidosis is present
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Calculate the gaps
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The anion gap = 145 - 97 – 12 = 36 mEq/L
High anion gap metabolic acidosis
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In summary, this patient has a complex triple acid base
disorder:
high anion gap metabolic aciosis secondary to toxic
ingestion (methanol or ethylene glycol), respiratory
acidosis & metabolic alkalosis, probably as a result of
vomiting
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Reference Paul Marino’s ‘the ICU Book’
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Thankyou
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