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Acid- Base Balance

Dr. Omar Mohamed Danfour
Senior Lecturer Specialist of Anesthesia & Intensive Care
(MSU-IMS-Anesthesia Department
Acids are H
+
donors.
Bases are H
+
acceptors, or give up OH
-
in solution.
Acids and bases can be:
Strong dissociate completely in solution
HCl, NaOH
Weak dissociate only partially in solution
Lactic acid, carbonic acid
2
PH = - log [H
+
]
H
+
is really a proton
If [H
+
] is high, the solution is acidic pH
If [H
+
] is low, the solution is basic or alkaline pH
pH Review
Acid Base -Basic Concepts
Hydrogen Ion [H
+
]

is tightly controlled
[H
+
]

is determined by the balance between PaCO
2

and serum HCO
3
(bicarbonate),
{normal ratio is 20 (Hco3) : 1(H2Co3)}
Henderson-Hasselbalch Equation
[H
+
] = 24 (PaCO
2
/ HCO
3
-
)
Normal Values
[H+] = 40 nEq/L
pH = 7.40 (7.35-7.45)
PaCO
2
= 40 mm Hg (35-45)
HCO
3
= 24 mEq/L (22-26)
< 6.8 or > 8.0 death occurs


3
[H
+
] pH

pH = 6.1 + log ([PaCO2] / [0.03 x HCO3-])
pH [H
+
] pH [H
+
]
7.80
7.75
16
18
7.30
7.25
50
56
7.70
7.65
20
22
7.20
7.15
63
71
7.60
7.55
25
28
7.10
7.00
79
89
7.50
7.45
32
35
6.95
6.90
100
112
7.40
7.35
40
45
6.85
6.80
141
159
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Keep It Simple
PaCO
2
= Acid
PaCO
2
= pH (Acidemia)
PaCO
2
= pH (Alkalemia)

HCO
3
= Base
HCO
3
= pH (Alkalemia)
HCO
3
= pH (Acidemia)

Acidosis: pH < 7.35
Respiratory PaCO

> 40 mmHg
Metabolic HCO
3
< 24 mEq/L

Alkalosis: pH > 7.45
Respiratory PaCO
2
< 40 mmHg
Metabolic HCO
3
>24 mEq/L




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6
The Body and pH
Simple Acid-Base Disorders
Type of Disorder pH PaCO
2
[HCO
3
]
Metabolic Acidosis

Metabolic Alkalosis

Acute Respiratory Acidosis

Chronic Respiratory Acidosis

Acute Respiratory Alkalosis

Chronic Respiratory Alkalosis


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Small changes in pH can produce major disturbances
Most enzymes function only with narrow pH ranges
Acid-base balance can also affect electrolytes (Na
+
,
K
+
, Ca
++
, Cl
-
)
Can also affect hormones
The body produces more acids than bases
Acids take in with foods
Acids produced by metabolism of lipids and
proteins
Cellular metabolism produces CO
2
.
CO
2
+ H
2
0 H
2
CO
3
H
+
+ HCO
3
-

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Control of Acids
1. Buffer systems
Take up H+ or release H+ as conditions change
Buffer pairs weak acid and a base
Exchange a strong acid or base for a weak one
Results in a much smaller pH change
CO
2
+ H
2
0 H
2
CO
3
H
+
+ HCO
3
-

Bicarbonate buffer
Sodium Bicarbonate (NaHCO
3
) and carbonic acid (H
2
CO
3
)
Maintain a 20:1 ratio : HCO
3
-
: H
2
CO
3
HCl strong Acid + NaHCO
3
weak Base H
2
CO
3 weak acid
+ NaCl
NaOH Sttrong base + H
2
CO
3 weak acid
NaHCO
3 weake base
+ H
2
O

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Phosphate buffer
Major intracellular buffer
H
+(acid)
+ HPO
4
2-
H
2
PO4
- (titratable acids eliminated in urine)
OH
-(Base)
+ H
2
PO
4
-acid
H
2
O + H
2
PO
4
2-
Protein Buffers
Hemoglobin is rich in histidine which is an effective
buffer from PH5.7 to 7.7.(Hb in RBCs in equilibrium
as a weak acid(HHB) and a potassium salt (KHb)
Carboxyl group gives up H
+

Amino Group accepts H
+
Side chains that can buffer H
+
are present on 27
amino acids.

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2. Respiratory mechanisms
Exhalation of carbon dioxide
Powerful, but only works with volatile acids
Doesnt affect fixed acids like lactic acid
CO
2
+ H
2
0 H
2
CO
3
H
+
+ HCO
3
-
Body pH can be adjusted by changing rate and depth of
breathing
3. Kidney excretion
Can eliminate large amounts of acid
Can also excrete base
Can conserve and produce bicarb ions
Most effective regulator of pH
If kidneys fail, pH balance fails


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Buffers function almost
instantaneously (rapid)
Respiratory mechanisms take several
minutes to hours
Renal mechanisms may take several
hours to days
Rates of correction
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Acid-Base Imbalances
pH< 7.35 acidosis
pH > 7.45 alkalosis
The body response to acid-base imbalance is called
compensation
May be complete if brought back within normal
limits
Partial compensation if range is still outside normals
If underlying problem is metabolic, hyperventilation
or hypoventilation can help : respiratory
compensation.
If problem is respiratory, renal mechanisms can bring
about metabolic compensation

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Respiratory Acidosis
Carbonic acid excess caused by blood levels of CO
2

above 45 mm Hg.
Hypercapnia high levels of CO
2
in blood
Causes:
Chronic conditions:
Depression of respiratory center in brain that
controls breathing rate drugs or head trauma
Paralysis of respiratory or chest muscles
COPD, pneumonia & obesity

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CO
2
+ H
2
0 H
2
CO
3
H
+
+ HCO
3
-
Respiratory Acidosis
Acute conditons:
Adult Respiratory Distress Syndrome
Pulmonary edema
Pneumothorax
Pulmonary emboli
Aspiration pneumonia
Increased CO2 production (Malignant
hyperthermia & thyroid storm)
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Signs and Symptoms of Respiratory Acidosis
Breathlessness
Restlessness
Lethargy and disorientation
Tremors, convulsions, coma
Respiratory rate rapid, then gradually
depressed
Skin warm and flushed due to vasodilation
caused by excess CO
2

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Compensation for Respiratory Acidosis

This is accomplished via two mechanisms;
a) rapid cell buffering and
In this setting, carbonic acid (H
2
CO
3
) can only be
buffered by the limited intracellular buffers
(primarily hemoglobin and proteins).
H
2
CO
3
+ Hb- HHb + HCO
3
-

b) an increase in net acid excretion.
Kidneys eliminate hydrogen ion and retain
bicarbonate ion (Chronic state)

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Treatment of Respiratory Acidosis
Restore & improve alveolar ventilation
IV lactate solution (converted to bicarbonate ions
in the liver).
Treat underlying dysfunction or disease
e.g. pul odema, Res depression
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Respiratory Alkalosis
Carbonic acid deficit
pCO
2
less than 35 mm Hg (hypocapnea)
Most common acid-base imbalance
Primary cause is hyperventilation

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CO
2

+ H
2
0 H
2
CO
3
H
+
+ HCO
3
-
Respiratory Alkalosis
Conditions that stimulate respiratory center:
Oxygen deficiency at high altitudes
Pulmonary disease and Congestive heart failure caused
by hypoxia
Acute anxiety & pain
Fever, anemia
Early salicylate intoxication
Cirrhosis
Gram-negative sepsis
Iatrogenic (ventilator induced)

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Alkalosis causes over excitability of the central and
peripheral nervous systems.
Numbness
Light headedness
It can cause :
Nervousness
muscle spasms or tetany
Convulsions
Loss of consciousness
Death
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Signs and Symptoms of Respiratory Alkalosis
Compensation of Respiratory Alkalosis
There are two mechanisms responsible for this
compensation to respiratory alkalosis;
1) Rapid cell buffering and
2) Decrease in net renal acid excretion.
hydrogen ions move from the cells into the extracellular
fluid, where they combine with [HCO
3
- to form carbonic
acid in the following reaction:
H+ + HCO
3
- H
2
CO
3
(CA)
In acute respiratory alkalosis, for every 10 mmHg decrease in the
PCO2, there is a 2meq/L decrease in the plasma HCO3-
concentration.
In chronic state renal compensation result in a 4 meq/L reduction in
plasma [HCO
3
-] for every 10 mmHg reduction in PCO2.
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Treatment of Respiratory Alkalosis
Treat underlying cause
Breathe into a paper bag ???

IV Chloride containing solution (hydrochloric acid,
arginine chloride & ammonium chloride), Cl
-
ions
replace lost bicarbonate ions
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Metabolic Acidosis
Bicarbonate deficit - blood concentrations of
bicarb drop below 22mEq/L
Occurs when pH falls below 7.35
Causes:
Loss of bicarbonate through diarrhea or renal
dysfunction
Accumulation of acids (lactic acid or ketones)
Failure of kidneys to excrete H+
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CO
2
+ H
2
0 H
2
CO
3
H
+
+ HCO
3
-
[H+] = 24 (PCO2 / [HCO3-])
Anion Gap Calculation
[Na
+
+ K
+
] [Cl + HCO3] (Normal = 12 + 2)
E.g :- Na 140, k 4 , CL 114, HCO3 18
(140 + 4) (114 + 18)
144 132 = 12 normal
E.g:- Na 140 , Cl 104, K 4.0, HCO3 10
(144) (114) = 30 = High anion gap
Two types of Metabolic Acidosis
High Anion Gap = net gain of acid
Normal anion gap = loss of bicarbonate
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High Anion Gap Differential
(MUDPILES)
Methanol
Uremia
DKA
Paraldehyde
Inborn
Errors
Lactic
Acidosis
Ethylene
Glycol
Salicylates
Normal Anion Gap
(USED CARP)
Ureterostomy
Small bowel fistula
Extra Chloride
Diarrhea
Carbonic anhydrase
inhibitors
Addisons disease
Renal tubular acidosis
Pancreatic fistulas
Treatment: Replace
Bicarbonate
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Symptoms of Metabolic Acidosis
Headache, lethargy
Nausea, vomiting, diarrhea
Coma
Death
Compensation for Metabolic Acidosis
Increased ventilation
Renal excretion of hydrogen ions if possible
K
+
exchanges with excess H
+
in ECF
( H
+
into cells, K
+
out of cells)



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CO
2
+ H
2
0 H
2
CO
3
H
+
+ HCO
3
-
Compensation
Respiratory compensation results in a 1.2 mmHg
reduction in PCO2 for every 1.0 meq/L reduction in
the plasma HCO3- concentration down to a
minimum PCO2 of 10 to 15mmHg.
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For example, if an acid load lowers the plasma HCO3-
concentration to 9 meq/L, then:
Degree of HCO3- reduction is 24 (optimal value) 9 =
15.
Therefore, PCO2 reduction should be 15 1.2 = 18.
Then PCO2 measured should be 40 (optimal value) 18
= 22mmHg.
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Treatment of Metabolic Acidosis
Treat the causes
Improve renal perfusion & acid excretion
NaHCO3, Dose = (weight Kg x base deficit x 0.3)
Ensure adequate ventilation

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Metabolic Alkalosis
Characterized by
Primary in HCO3 concentration greater than 26
mEq/L
Compensatory in PaCO2
Classified according to urinary chloride
Chloride responsive
Chloride resistant

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Metabolic Alkalosis
Chloride Responsive
Urine Cl
-
< 20 mEq/L
Causes
Volume Contraction:
Nasogastric suctioning, Gastric fistula
Vomiting , pyloric stenosis
Post Hypercapnia
Low chloride intake
Hypomagnesemia
Penicillin
Cystic fibrosis (sweat)
Alkali therapy (NaHCO3, Antacid abuse)
Chloride depletion (Diarrhoea & Diuretics

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Metabolic Alkalosis
Chloride Unresponsive (resistant)
Mineralcorticoid excess e.g Hyperaldosteronism
Exogenous steroids, Cushings disease
Alkali Ingestion
Licorice ingestion
Too much wine
Tobacco chewers
Bartters Syndrome
Urine Cl
-

> 20 mEq/L
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Symptoms of Metabolic Alkalosis
Respiration slow and shallow
Hyperactive reflexes ; tetany
Often related to depletion of electrolytes
Dysrhythmias
Compensation for Metabolic Alkalosis
Alkalosis most commonly occurs with renal
dysfunction, so cant count on kidneys
Alkali load
Acid loss - vomiting
Respiratory compensation difficult
(hypoventilation limited by hypoxia)


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Compensation contn.
The development of alkalemia is sensed by central and
peripheral chemoreceptors, resulting in a reduction in the
rate of ventilation and a reduction in tidal volume and
thus an elevation in the pCO2.
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pCO2 rises 0.7 mmHg for every 1.0 meq/L increment in the
plasma [HCO3-].
For example, if an alkali load raises the the plasma HCO3-
concentration to 34 meq/L, then:
Degree of HCO3- elevation is 34 24 (optimal value)= 10.
Therefore, PCO2 elevation should be 0.7 10 = 7

Then PCO2 measured should be 40 (optimal value) +7 =
47mmHg.
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Treatment of Metabolic Alkalosis
Electrolytes to replace those lost
Treat underlying disorder
IV chloride containing solution e.g saline (Chloride
Responsive)
Aldosterone antagonist (Chloride resistant)

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Miscellaneous 1
Arterial pH is related to the ratio of PCO2 to HCO3,
both pulmonary & renal compensatory mechanism
are always such that PCO2 and HCO3 change in the
same direction.
the exception occurs when there is a mixed acid base
disorder. In that situation, multiple acid base
processes coexisting may lead to a normal pH or a
mixed picture especially when PCO2 & HCO3
moves in opposite direction
If the compensatory response is more or less than
expected, by definition a mixed acid-base disorder
exist.
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An Alternative Approach
An Alternative Approach that is rapid but perhaps less
precise is to correlate changes in Ph with changes in
CO2 or HCO3.
For a respiratory disturbance, every 10mmHg changes in
CO2 should change arterial PH by approximately 0.08 U in
the opposite direction.
During metabolic disturbance, every 6mEq change in HCO3
also changes arterial PH by 0,1 in the same direction.
If the change in pH exceed or is less than predicted, a
mixed acid-base disorder is likely to be present.
If the Arterial pH is relatively normal and the PCO
2
and/or
HCO
3
are abnormal, one can assume that a mixed
abnormality is present.

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Miscellaneous 2
The Delta Ratio (/)
Assessment of elevated anion gap metabolic
acidosis to determine if a mixed acid base
disorder is present.

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Delta ratio = Anion gap/ [HCO3-] or anion gap/ [HCO3-]

= Measured anion gap Normal anion gap
Normal [HCO3-] Measured [HCO3-]

= (AG 12)
(24 - [HCO3-])
Miscellaneous cont

Delta ratio

Assessment Guidelines

< 0.4

Hyperchloremic normal anion gap acidosis

< 1

High AG & normal AG acidosis

1 to 2

Pure Anion Gap Acidosis
Lactic acidosis: average value 1.6
DKA more likely to have a ratio closer to 1 due to urine
ketone loss


> 2

High AG acidosis and a concurrent metabolic alkalosis
or a pre-existing compensated respiratory acidosis
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Compensation
Primary Disorder Compensatory Mechanism
Metabolic acidosis Increased ventilation
Metabolic alkalosis Decreased ventilation
Respiratory acidosis Increased renal reabsorption of HCO
3
-

in the proximal tubule
Increased renal excretion of H in the
distal tubule
Respiratory alkalosis Decreased renal reabsorption of HCO
3
-

in the proximal tubule
Decreased renal excretion of H
+
in the
distal tubule
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Primary
disorder
Initial
chemical
change

Compensatory

response
Compensatory

Mechanism
Expected level of
compensation
Metabolic
Acidosis
HCO3- PCO2 Hyperventilation
PCO2 = (1.5 [HCO3-]) + 8
2
PCO2 = 1.2 [HCO3-]
Metabolic
Alkalosis
HCO3- PCO2 Hypoventilation
PCO2 = (0.9 [HCO3-]) + 16
2
PCO2 = 0.7 [HCO3-]
Respiratory
Acidosis
PCO2 HCO3-
Acute
Intracellular Buffering
(hemoglobin,
intracellular proteins)
[HCO3-] = 1 mEq/L for every
10 mm Hg PCO2
Chronic
Generation of new
HCO3- due to the
increased excretion of
ammonium.
[HCO3-] = 3.5 mEq/L for every
10 mm Hg PCO2
Respiratory
Alkalosis
PCO2 HCO3-
Acute Intracellular Buffering
[HCO3-] = 2 mEq/L for every
10 mm Hg PCO2
Chronic
Decreased
reabsorption of HCO3-,
decreased excretion of
ammonium
[HCO3-] =4 mEq/L for every 10
mm Hg PCO2
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Acidemia (PH<7.35)
PCO2
High
Normal
Or low
Normal
or high
Incompatible
[HCO3]
[HCO3]
High Normal
Low
Low
Chronic
respiratory
acidosis
Acute
respiratory
acidosis
Mixed
respiratory
and metabolic
acidosis
Metabolic
acidosis
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Plasma [HCO3]
Anion gap
Normal Increased
High anion gap
metabolic acidosis
Plasma [K]
Low
Normal
High
Hypokalemic
hyperchloremic
metabolic acidosis
Respiratory
alkalosis
Hyperkalemic
hyperchloremic
metabolic acidosis
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Alkalemia (PH>7.45)
PCO2
Low High\Normal
Normal
or
Low
Incompatible
High
Normal
[HCO3]
Low
High
[HCO3]
Mixed
respiratory and
metabolic
alkalosis
Acute
respiratory
alkalosis
Chronic
respiratory
alkalosis
Metabolic
alkalosis
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Plasma [HCO3]
Metabolic alkalosis Respiratory acidosis
Spot urine [Cl]
>20mmol\L
<20mmol\L
Saline
unresponsive
metabolic
alkalosis
Saline responsive
metabolic
alkalosis
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Example
A patient is in intensive care because he suffered
a severe myocardial infarction 3 days ago. The lab
reports the following values from an arterial
blood sample:
pH 7.3
HCO3- = 20 mEq / L ( 22 - 26)
pCO2 = 32 mm Hg (35 - 45)

Diagnosis
Metabolic acidosis
With partial compensation

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CASE 1
A 44 year old moderately dehydrated man was
admitted with a two day history of acute
severe diarrhea. Electrolyte results: Na+ 134,
K+ 2.9, Cl- 108, HCO3- 16,
Urea 31, Cr 1.5.

ABG: pH 7.31 pCO2 33 mmHg
HCO3 16 pO2 93 mmHg
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CASE 2
A 22 year old female with type I DM, presents to the
emergency department with a 1 day history of nausea,
vomiting, polyuria, polydypsia and vague abdominal pain.
P.E. noted for deep sighing breathing, orthostatic
hypotension, and dry mucous membranes.
Labs: Na 132 , K 6.0, Cl 93, HCO3- 11 glucose 720, Urea 38,
Cr 2.6.
UA: pH 5, SG 1.010, ketones negative, glucose positive .
Plasma ketones trace.
ABG: pH 7.27 HCO3- 10 PCO2 23
What is the acid base disorder?
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CASE 3
A 70 year old man
with history of CHF
presents with
increased shortness
of breath and leg
swelling.
ABG: pH 7.24, PCO2
60 mmHg, PO2 52
HCO3- 27
What is the acid
base disorder?

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