Download Acid-base balance

Acid Base Balance
Dr. M. A. Maleque Molla,
FRCP(Ed), FRCPCH
October 22, 2014
Pre review Q 1
 What is the normal range for arterial
blood pH?
A. 7.38 – 7.46
7.40 – 7.52
C. 7.35 – 7.45
D. 7.45-7.55
B.
Answer C
Q2
What 2 extracellular substances work together to
regulate pH?
A. Sodium bicarbonate & carbonic acid
B. Carbonic acid & bicarbonate
C. Acetic acid & carbonic acid
D. Hydrochloric acid & bicarbonate
Answer-B
Q3
 Defining an acid & a base, based on the
choices below, which statement is true?
Acids accept H+ ions & bases release H+ ions
B. Acids release hydrogen (H+) ions & bases accept
H+ ions
C. Acids accept H+ ions & bases accept H+ ions
D. Acid release H+ & Base Release H+
A.
 Answer: B
Q4
 Buffering is a normal body mechanism that
occurs rapidly in response to acid-base
disturbances in order to prevent changes in
what?
A.
B.
C.
D.
HCO3
H2CO3
H+
CO2
 Answer: C
Acid Base Balance
Terminology & Definitions:
 Acid - Any substance that can donate proton (H+) e.g.
H2CO3, NH3, HCL,
● Base- Any substance that can accept proton e.g.
HCO3,PO4, protein
● Acidemia- pH< normal range(7.35-7.45). i.e. H+ in the
blood above normal range
● Alkalemia-pH>normal (7.35-7.45). i.e. H+ in the blood
less than normal range
● An acidosis & alkalossis is a pathologic process that
causes an increase or decrease in the hydrogen ion
concentration,
Terminology & Definitions
 pH-Negative log of the hydrogen ion concentration
 pH= pK + log([base]/[acid])
 Represents the hydrogen concentration
● Neutral pH is 7 at temp 250 C, 6.8 at 370C (Water)
● Normal pH of body fluids:
 Arterial blood is 7.4 (7.35-7.45)
 Venous blood and interstitial fluid is 7.35
 Intracellular fluid pH 7.0
 Acidosis -Blood pH <7.35
 Alkalosis- Blood pH > than 7.45
● pH compatible with life 6.8-7.8
Terminology & Definitions
 Buffers are substances that attenuate the change in pH
that occurs when acids or bases are added to the body.
 Physiologic buffers: are weak acid and or of a weak
base and its salt:
 bicarbonate-carbonic acid buffering system,
 intracellular protein buffers,
 phosphate buffers in the bone
 What does Buffer do?
Buffers protect the body against major changes in pH, by
binding or releasing the hydrogen ions(H+)
Acid-Base Balance
 Acid-base balance: a normal balance between production and
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excretion of acid or alkali by the body, resulting in a stable
concentration of H+ in body fluids
An adult normally produces 1-2 mEq/kg/24 hr of hydrogen ions.
Children produce 2-3 mEq/kg/24 hr of hydrogen ions.
The 3 principal sources of hydrogen ions:
 Dietary protein metabolism,
 Incomplete metabolism of carbohydrates and fat,
 losses of bicarbonate in the stool
In order to maintain acid-base homeostasis, acid production
must balance the neutralization or excretion.
Why acid-base balance?
 Regulation of normal pH is necessary because;
 Cellular enzymes and other metabolic processes,
function optimally at normal pH.
 Chronic derangements in acid-base status may
interfere with normal growth and development
 Acute, severe changes in pH can be fatal.
How acid-base balance regulates?
 Body strictly maintains pH in a range from 7.35-7.45
 Control of normal acid-base balance depends on;
Lungs( Respiratory system).
2. Kidneys, (Renal System).
3. Intracellular and extracellular buffers.
1.
1. Respiratory Control mechanisms on pH
 Works within minutes to control pH- maximal in 12-24
hours
 Major source of acid in the body is CO2
 CO2 react with water produce 12,500 mEq of H+ daily
CO2+ H2O = H2CO3= H+ + HCO3 Excess CO2 & H+ in the blood act directly on respiratory
centers in the brain increase rate & depth of respiration
 H+ stimulates respiratory center ↑ the respirations
eliminate CO2
 In case of alkalosis(pH>7.45), respiratory center is
inhibited and there is retention of CO2
2. Renal Control Mechanisms on pH
 Kidney takes several hours to days to act & restore pH
to, or close to normal
 Kidneys handles around 4000 mEq of HCO3 daily
 Almost all HCO3 are absorbed in renal tubules
 Regulate pH through excreting acidic or alkaline urine
by;
 Excreting excess H+ & regenerating or reabsorbing
HCO3 Excreting acidic urine decreases acid in the ECF &
excreting alkaline urine removes base
Respiratory & Renal response to acidosis
From Thibeodeau GA PattonKI, Anatomy & Physiology, 5th ed,2004
3. Intracellular and extracellular buffers
Bicarbonate/carbonic acid buffer
2. Protein buffers
1.
3. Phosphate Buffer
Blood Buffer system
1. Bicarbonate/carbonic acid buffer
Most abundant buffer in ECF
 Function almost instantaneously
 Cells utilizing O2 & produces CO2
 CO2 combines with water to form carbonic
acid(H2CO3), which dissociates to form H+ and HCO-3 :

H2O+CO2
H2CO3
H+ + HCO2-
 If acid added to the fluid, combines with HCO3 and
dissociate to H2O & CO2
Buffer system (Cont..)
2. Protein buffers:
 Extracellular proteins, mostly albumin
 Intracellular proteins, including hemoglobin.
 Protein buffers both hydrogen ions(H+ )and carbon
dioxide(CO2)
Buffer system (Cont..)
3. Phosphate Buffer System
 Phosphate is an intracellular buffer & important
buffer in the Urine
 Has a major role in the elimination of H+ via the
kidney
• Assists in the exchange of sodium for hydrogen
• It participates in the following reaction
HPO-24 + H+
H2PO – 4
 Essential within the erythrocytes
Disorder in acid base balance
Disorder in acid base balance
● ACIDOSIS (pH<7.35)
 Metabolic acidosis
 Respiratory acidosis
 Mixed acidosis(Combined )
● ALKALOSIS(pH>7.45)
 Metabolic alkalosis
 Respiratory alkalosis
DIAGNOSIS
 Clinical history & Examination
 Evaluation of an arterial blood gas sample
can usually explain the patient's acid-base
disturbance.
Terminology used

pH-Negative logarithm of hydrogen ion
concentration

PaCO2 -Partial pressure of carbon dioxide in arterial
blood.
PaO2- Partial pressure of oxygen in arterial blood
HCO3- Bicarbonate concentration in the serum in
mmol/l
BE- calculated the quantity of Acid or Alkali required to
return the plasma in-vitro to a normal pH under
standard conditions
Standard BE: is a calculation of the bicarbonate value if
the blood were to be equilibrated with a PaCO2 of 5.3
kPa (40 mmHg )
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How blood gas can be analyzed?
Blood gas can be analyzed by automated machine
using following types of blood samples:
 Arterial Blood Gas (ABG)
 Venous Blood Gas (VBG)
 Capillary Blood Gas (CBG)
Normal values
ABG
VBG
CBG
pH
7.35-7.45 7.25-7.35
7.35 – 7.45
PCO2 (mmHg)
35-45
41-51
35 – 48
PO2 (mmHg)
80-100
35-40
80-100
HCO3 (mmol/L)
22-26
22-26
22 – 27
±2
±2
BE (mmol/L)
±2
Stepwise interpretation of blood gas
 Step I: Acidosis or Alkalosis
1. Look for pH
 Normal pH 7.35-7.45
● pH < 7.35 Acidosis
● pH>7.45- Alkalosis
Stepwise interpretation of blood gas
Step 2: Respiratory or Metabolic
2. Look for pCO2
 paCO2 > 45mmHg Respiratory Acidosis
 paCO2 < 35mmHg Respiratory Alkalosis
3. Look for HCO3
 HCO3- < 22mEq/L Metabolic Acidosis
 HCO3- > 26mEq/L Metabolic Alkalosis
Stepwise interpretation of blood gas
Step 3: If respiratory acidosis
? Acute or Chronic
Look for bicarbonate
 Normal slightly raised HCO3 – Acute
 High HCO3 -chronic
Stepwise interpretation of blood gas
Step 4: For metabolic acidosis
Look for anion gap
 Nomal anion gap 12 ±4 mmol/l
 Anion gap > 16mmol/l- Anion gap metabolic acidosis
 Anion gap 12 ±4mmol/l =Normal or non-anion gap acidosis
Anion gap
Def: Calculated difference between anion & cation electrolytes
Anion gap = (Na+ +K+ ) - (Cl- + HCO3-), Normal: 12 mmol/l
• Nomal anion gap 12 ±4 mmol/l
 Anion gap metabolic acidosis (anion gap > 16):
Uremia
DKA(diabetic hyperglycemia)
Alcohol, methanol, ethylene glycol, paraldehyde, salicylates poisoning
Lactic acidosis (sepsis, left ventricular failure)
 Normal or non-anion gap acidosis (anion gap 12 ± 4)
GI loss of HCO3 (diarrhea)
Renal loss of HCO3
 Renal tubular acidosis
 Compensation for respiratory alkalosis
Ureteral diversion
Other causes: HCl or NH4Cl infusion, Cl gas inhalation,
Stepwise interpretation of blood gas
Step 5. Determine whether other metabolic disturbances
co-exist with an anion gap acidosis
Formula;
Corrected HCO3- = measured HCO3- + (anion gap - 12)
 If the corrected HCO3- is greater than 24, a metabolic
alkalosis co-exists.
 If the corrected HCO3- is less than 24 then a non-gap
acidosis co-exists.
Stepwise interpretation of blood gas
Step 6: Look for compensatory response
Compensatory responses: The body’s attempt to
return the acid/base status to normal
 Immediate buffering by ECF HCO3 Respiratory compensation: For each 1 mmol
decrease in HCO3-a 1 mmHg drop of PaC02
 Tissue phase: Entry of H+ into cells accounts for
~60% of rapid (~2 h) buffering of poorly
permeable acids (HCl or H2SO4).
 Renal compensation
Compensatory responses and their mechanisms.
Primary disorder
Primary
Chemical
change
Compensatory
response
Compensatory
Mechanism
Metabolic Acidosis
↓ HCO3-
↓ PCO2
Hyperventilation
Metabolic Alkalosis
↑ HCO3-
↑PCO2
Hypoventilation
Respiratory Acidosis
↑PCO2
↑HCO3-
Acute
Intracellular Buffering
Chronic
Renal Generation
HCO3-
Respiratory
Alkalosis
↓ PCO2
↓HCO3-
Acute
Intracellular Buffering
Chronic
Renal Generation
HCO3-
ABG Interpretation 1
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pH = 7.202
PaCO2 = 19.8
PaO2 = 86.6
HCO3- = 7.4
BE = -18.
Sat = 91.5
Hb = 12
Na+ = 153
K+ = 3.4
Cl- =123
•Metabolic acidosis
•? Anion gap
Anion gap=(153+3.4)-(123-7.4)= 26
∆ Anion gap metabolic acidosis
ABG Interpretation 2
ABG
 pH
7.31
 pCO2
33 mmHg
 HCO3
16 mmol/l
 PO2
93 mmHg
 Na+ 134, K+ 2.9, Cl- 108, BUN 31, Cr 1.5.
∆ Metabolic Acidosis
 ?Anion gap
 (134+2.9)-(108+16)=12.9
∆ Non anion gap metabolic acidosis
Metabolic acidosis
Def: pH<7.35 due ↑ H+ concentration
Cause:
● Exogenous source
● Endogenous ↑production; DKA, organic
acidemia, lactic acidosis
● Inadequate excretion; Renal failure
● Excessive loss of HCO3; GE
Metabolic acidosis
Consequence
Buffered by
● ECF - HCO3
● ICF – Hb, Po4, bone
● Respiratory compensation: ↑RR ↓ PCO2
● Renal compensation:
↑ Ammonia production + H+ excretion
↑HCO3 reabsorption
Metabolic acidosis
Clinical features
● Hyperventilation
● Decrease cardiac function
● Hypotension
● Pulmonary oedema
● Hypoxia
Metabolic acidosis -Diagnosis
 History & Physical examination
 Lab: BUN, serum creatinine, serum glucose, urinalysis,
and serum electrolytes
 Plasma anion gap:
 Those with normal anion gap e.g. GE, RTA
 Those with increased anion gap.
↑endogenous proudction of acid e.g. DKA, Organic
acidemia, Lactic acidosis
 Exogenous Acid e.g. Ethylene glycol, Methanol, Salicylate,
Paraldehyde

 Acid base status : pH <7.35, ↓ PCO2 ↓ HCO3
ABG Interpretation 3
 pH
 PCO2
 PO2
 HCO3
 BE
7.29
64.3 mmHg
84.6 mmHg
24.2 mmol/l
-2 mmol/l
Acute Respiratory acidosis
Respiratory acidosis
 Inadequate elimination of CO2 due to respiratory failure
 Causes:
 Obstruction
 Neuromuscular disease
 Sedative over dose
 Compensation mainly by renal reabsorption of HCO3
Acid base status:
pH <7.35, ↑PCO2, Normal or ↑HCO3
Respiratory acidosis -Management
 Treatment: with an acute respiratory acidosis are
hypoxic and need oxygen.
 Mechanical ventilation in some children
 Indication for mechanical ventilation
 Severe Respiratory acidosis PCO2 >75 mmHg &
pH<7.2
 Concomitant metabolic acidosis,
 slowly responsive underlying disease,
 Hypoxia that responds poorly to oxygen,
 If the patient is exhausted and respiratory arrest
seems likely
ABG Interpretation 4
pH
PCo2
PO2
SAT
HCo3
7.489
24.9 mmHg
72.4 mmHg
96.4%
21.6 mmol/l
 Respiratory alkalosis
Respiratory alkalosis
Excessive elimination of CO2
Cause
● Iatrogenic hyper ventilation
● Hyperventilation e.g early pneumonia, asthma
● Psychogenic
● Drugs like Salicylate poisoning
Acid base status:
pH >7.45, ↓ PCO2,
↓ HCO3
Respiratory alkalosis-Management
 Underlying cause should be treated
 If on mechanical ventilator, setting should be
adjusted
 Psychogenic hyperventilation may benefit from
 reassurance
 benzodiazepines.
 Rebreathing into a paper bag.
ABG Interpretation 5
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pH = 7.490
PaCO2 = 47.0
PaO2 = 58.0
HCO3- = 34.8
BE = 10.2
Sat = 88.9
Hb = 18.3
∆ Metabolic alkalosis
Metabolic alkalosis
Decrease acid below the normal range
Causes: divided into 2 categories on the basis of urinary
chloride level
1. Chloride responsive (Urinary chloride <15 mEq/l)
 Excessive loss of H+ e.g. vomiting, Nasogastric suction
● Diuretics (loop or thiazide)
● Decrease serum potassium, serum Cl-,
● Contraction of ECF
● Cystic fibrosis
● Chloride-losing diarrhea
● Post-hypercapnia
2. Chloride resistant Urinary chloride >20
● Hyperaldosteronism
● Cushing syndrome,
● Bartter’s synd
Metabolic alkalosis
 Clinical feature- muscle cramps, tetany,
● Respiratory compensation: ↓Respiratory rate, ↑
PCO2
● Renal compensation: loss of HCO3 in urine
 Acid base status:
pH >7.45 Normal or ↑ PCO2 ↑ HCO3
 Low S Potassium
 Calcium specially Ionized Ca++
Management
 Depends on the severity of the alkalosis and the underlying
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etiology.
In children with a mild metabolic alkalosis (HCO3− <32),
treatment is often unnecessary
Moderate or severe metabolic alkalosis need treatment
Treat underlying cause e.g, if receiving diuretic add
potassium sparing one
Supplement of sodium chloride and potassium chloride to
correct the volume deficit and the potassium deficit
ABG Interpretation 6
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pH
Pco2
PO2
BE
HCO3
SAT
Na
K
 Cloride
6.90
79.3 mmHg
25.2 mmHg
-15.8 mmol/l
12 mmol/l
31.5%
136 mmol/l
4.1 mmol/l
120 mmol/l
 Combined respiratory & metabolic acidosis
 REFERENCES
 Bishop, M., Fody, E., & Schoeff, l. (2010). Clinical
Chemistry: Techniques, principles, Correlations.
Baltimore: Wolters Kluwer Lippincott Williams &
Wilkins.
 Carreiro-Lewandowski, E. (2008). Blood Gas Analysis
and Interpretation. Denver, Colorado: Colorado
Association for Continuing Medical Laboratory
Education, Inc
 Acid-Base Balance;Larry A. Greenbaum; Nelson
textbook of Pediatrics, 19 ed