Acid Base Balance

D VHANDA

HBMLS, MDCB, MBL, HSME

 INTRODUCTION

 REGULATION OF ACID BASE BALANCE

 BLOOD BUFFERS

 RESPIRATORY MECHANISM

 RENAL MECHANISM

 ACID BASE DISORDERS

 Normal blood PH : 7.35-7.45

Maintenance of blood pH - important homeostatic mechanism of the

body.

pH affects all functional proteins and biochemical reactions, so closely regulated

PH <7.35 leads to Acidosis or acidemia pH >7.45 leads to Alkalosis

or alkalemia.
 Acids are proton
donors.
HA ↔ H+ + A- HCL ↔
H ++ CL -

 Bases are Acid Bas

proton acceptors. e
NH3+H+ ↔ NH4+
HCO3+H+ ↔ H2CO3

• Weak and strong

acids :
HCL → H ++ CL (COMPLETE) - Strong acid
- H+ + HCO3- ( PARTIAL) - Weak acid
H2CO3 →
pH = - log10[H+] ,

1. Enzyme activity
2. Action potential of myelinated nerve
3. Membrane permeability
4. Control of respiration
5. Heart activity
6. Plain muscle activity
7. Oxygen Haemoglobin dissociation curve
8. Nerve excitability
 Carbonic acid - Oxidation of c-compounds
 Sulphuric acid - Oxidation of sulphur containing amino acids.
 Phosphoric acid-metabolism of dietary phosphoproteins, nucleoproteins,
phosphatides .
 Organic acid- oxidation of carbohydrates, fats and proteins.
e.g. pyruvic acid, lactic acid, acetoacetic acid etc.

 Iatrogenic : - certain medicine like NH4Cl, mandelic acid etc.

NB :DIET RICH IN ANIMAL PROTEIN RESULTS IN MORE ACID PRODUCTION.
Acid Base Disturbances

What is it ?

changes in arterial PCO2, HCO3 & pH.

 Controlled by the Lungs, Kidneys and Buffers

 Disrupted by Vomiting, Diarrhea, Respiratory Failure, Kidney

Failure, Infections and Ingestions
 3 mechanisms

1. Blood (chemical) buffers : 1st line of defence

2. Respiratory regulation: 2nd line of defence (1-3 min)

3. Renal regulation: 3rd line of defence (hrs to days)- most

potent
Buffers - Buffers are able to limit changes in [H+]
Two types
Mixture of weak acids with their salt with a strong base.
Mixture of weak bases with their salt with a strong acid.
Examples
1.Bicarbonate buffer (H2CO3/ NaHCO3 )
2.Acetate buffer (CH3COOH / CH3COONa)
3.Phosphate buffer (Na2HPO4 /NaH2PO4 )
 Effects of Buffers on pH

 Bicarbonate is the major extracellular buffer. There are also intracellular buffers.

 The presence of buffers attenuates changes in pH in response to acid-base

disorders.

 Immediate onset

 Isohydric principle (all buffers change in the same direction)

If you go running you build up lactic acid in your muscles.
Therefore your pH will decrease.
Buffer will act to increase the pH.
And vice versa.
So how does it work using chemistry ?
H+ + A- → HA
OH- + HA → A- +
H2O
Eg;
H+ + HCO3- → H2CO3
OH- + H2CO3→HCO3- + H2O
Acid add [ H+ ] therefore ↑ [H-+]↓ pH
- +↑
Base bind [ H+ ] therefore ↓[H ] pH
.

Phosphate buffer
H2PO4↔HPO42-+H+
Protein buffer (amphoteric)
Amino acid
If pH ↓
In acidic medium amino acid (NH2) act as a base and absorbs
H+.
If pH↑
In alkaline medium amino acid (COOH) act as a acid and
release H+.
Sodium monohydrogen phosphate (Na2HPO4)

Sodium dihydrogen phosphate ( NaH2PO4)

Sodium bicarbonate ( NaHCO3)

Hydrogen carbonate (H2CO3)

Sodium proteinate

Hydrogen proteinate
 Erythrocytes Tissue cell

• Potassium proteinate
• Potassium bicarbonate
• Hydrogen proteinate
• Carbonic acid
• Potasium bicarbonate
• K2HPO4
• Hydrogen bicarbonate
• kH2PO4 • K2HPO4
• Potasium proteinate • kH2PO4
• Hydrogen proteinate
.
’ ..
 Chemical Buffer Systems

 Strong acids dissociate completely in water; can dramatically affect pH

 Weak acids dissociate partially in water; are efficient at preventing pH
changes
 Strong bases dissociate easily in water; quickly tie up H+
 Weak bases accept H+ more slowly
Chemical Buffer Systems

 Chemical buffer: system of one or more compounds that act to resist

pH changes when strong acid or base is added

 Bind H+ if pH drops; release H+ if pH rises

1. Bicarbonate buffer system

2. Phosphate buffer system (ICF & Urine)

3. Protein buffer system

•Third line of defense against change in hydrogen
ion concentration

•Permanent solution to the acid base

disturbances.

•Kidneys require hours to days to compensate

for changes in body-fluid pH
1. Excretion of H+.

2. Reabsorption of bicarbonate

3. Excretion of titratable acid

4. Excretion of ammonium
(NH4+)
 ACIDOSIS: PH <7.35

a ) METABOLIC ACIDOSIS
b ) RESPIRATORY ACIDOSIS

 ALKALOSIS : PH >7.45

a ) METABOLIC ALKALOSIS
b ) RESPIRATORY ALKALOSIS
Metabolic Disorders

 Processes that directly alter bicarbonate

concentration
 Metabolic acidosis: decreased bicarbonate
 Metabolic alkalosis: increased bicarbonate
 Respiratory Disorders

 Processes that directly alter CO2

 Respiratory acidosis: increased CO2

 Respiratory alkalosis: decreased CO2

 Buffer effect: slightly increased HCO3 with respiratory acidosis. Slightly

decreased HCO3 with respiratory alkalosis.

Terms and Definitions

Variable Primary Normal Range, Primary

Disorder arterial Gas Disorder
pH Acidemia 7.35 - 7.45 Alkalemia
pCO2 Respiratory 35 - 45 Respiratory
alkalosis acidosis
HCO3 Metabolic 22 – 26 Metabolic
acidosis Alkalosis
 Respiratory compensation for metabolic disorders is rapid
 Full metabolic compensation for respiratory disturbances
requires renal adjustment and takes 3-5 days
Purpose of Acid-Base Balance

•Maintain normal pH by buffer systems

Buffer Pair H+ Acceptor H+ Donor

Bicarbonate HCO3- H2CO3

(ECFV)
Phosphate HPO42- H2PO4
(urine)
Ammonia (urine) NH3 NH4+

Protein Protein Protein

 Secondary(Compensatory) Mechanisms

 In addition to buffering mechanisms, additional secondary (compensatory)

physiologic responses occur in response to changes in pH.

 Invariably present in simple acid-base disorders (if not present, it is a mixed

disorder)
 The respiratory system compensates for metabolic disorders by altering CO2
(via the lungs, rapid onset, minutes)
 Compensation for respiratory disorders occurs by alterations in bicarbonate
concentration (via the kidney, slower onset 1-2 days)
 Respiratory Mechanisms

• Arterial PCO2 stimulates chemoreceptors in the medulla oblongata

• An elevated arterial blood PCO2 is a stimulus to increase ventilation leading

to increased expiration of CO2 hence increase blood pH
• Conversely, a drop in blood PCO2 inhibits ventilation; the consequent rise in

blood [H2CO3] reduces the alkaline shift in blood pH

 Renal Mechanisms

• 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

 Mechanisms that Buffer an Acid Load

Buffer systems Extracellular fluid Immediate

(primarily bicarbonate) (HCO3- + H+ ↔ H2CO3 ↔ CO2 + H20)

Increased rate and depth of Lungs Minutes to hours

breathing to decrease CO2

Buffer systems (phosphate, Intracellular fluid 2-4 hours

bicarbonate, protein)

Hydrogen ion excretion, bicarb Kidneys Hours to days

reabsorption, & bicarb generation
 Summary

Disorder pH HCO3- pCO2 Comment

Metabolic ↓ ↓ (primary) ↓(compensatory) All 3 markers go

acidosis in same direction

Metabolic (primary) (compensatory) All 3 markers go

alkalosis in same direction

Resp. acidosis ↓ (compensatory) (primary) pH goes opp.

other 2 markers

Resp. alkalosis ↓ (compensatory) ↓ (primary) pH goes opp.

other 2 markers
 Diagnosis of acid Base Disorder

1. Determine the primary disturbance:

– Acidemia or Alkalemia: look at the pH

< 7.35 = acidemia

> 7.45 = alkalemia

Respiratory or Metabolic: look at HCO3 and CO2 HCO3 = primary
metabolic acidosis pCO2 = primary respiratory acidosis

and vice versa for alkalosis

 Normal values

pH 7.35 – 7.45
PCO2 35 – 45mmHg
PO2 80 -100mmHg
K+ 3.5 – 5.0meq/l
Na+ 135 -145meq/l
Cl- 98 – 108mmol/l
HCO3- 22 – 26meq/l
Anion gap 9 - 16
Simple Acid-Base Disorders

 Look at the pH in order to determine the primary

abnormality

 Pathophysiologic principle: body does not fully

compensate even for chronic acid-base disorders
Example #1

Acute Respiratory
pH 7.50 Alkalosis
Variable Primary Normal Primary
pCO2 29 Disorder Range, Disorder
arterial Gas

HCO3 22 pH Acidemia 7.35-7.45 Alkalemia

pCO2 Respiratory 35 - 45 Respiratory

alkalosis acidosis

HCO3 Metabolic 22 – 26 Metabolic

acidosis Alkalosis
Respiratory alkalosis

 Reduced carbon dioxide due to increased alveolar ventilation

 Buffering processes lower plasma bicarbonate concentration (rapid but

limited response, ~1-2 meq/l)

 Kidney response is to reduce net acid excretion (eliminate bicarbonate

into the urine or decrease ammonium excretion). Delayed response, 1-
2 days)
Respiratory Alkalosis Compensation

 Acute

 Plasma [HCO3-] is lowered by 2mEq/L for every 10-mm

Hg decrease in PaCO2

 Chronic

 Plasma [HCO3-] is lowered by 5mEq/L for every 10-mm

Hg decrease in PaCO2
 Causes of Acute Respiratory Alkalosis
 Anxiety
 Hypoxia
 Lung disease with or without hypoxia
 CNS disease
 Drug use—salicylates, catecholamines, progesterone
 Pregnancy
 Sepsis
 Hepatic Encephalopathy
 Mechanical Ventilation
Example #2

pH 7.25 Acute Respiratory

Acidosis
pCO2 60 Variable Primary Normal Primary
Disorder Range, Disorder
HCO3 26 arterial Gas

pH Acidemia 7.35-7.45 Alkalemia

pCO2 Respiratory 35 - 45 Respiratory

alkalosis acidosis

HCO3 Metabolic 22 – 26 Metabolic

acidosis Alkalosis
Respiratory acidosis

 Induced by hypercapnia (decreased alveolar ventilation)

 Buffering mechanisms raise plasma bicarbonate concentration (rapid

but limited response, ~1-2 meq/l)

 Kidney minimizes the change in extracellular pH by increasing acid

excretion (NH4+) generating new bicarbonate ions (delayed
response, 2-3 days).
Respiratory disorders

 Acute respiratory acid base disorders always have a greater

change in pH than chronic disorders

 Plasma Cl changes equally and inversely with plasma HCO3.

 Plasma anion gap does not change with respiratory

disorders

 Plasma sodium is not directly altered by acid base disorders

Example #3

pH 7.34 Chronic Respiratory Acidosis

with Metabolic Compensation
pCO2 60
Variable Primary Normal Primary
Disorder Range, arterial Disorder
HCO3 31 Gas

pH Acidemia 7.35-7.45 Alkalemia

pCO2 Respiratory 35 - 45 Respiratory

alkalosis acidosis

HCO3 Metabolic 22 – 26 Metabolic

acidosis Alkalosis
Example #4
pH 7.50
pCO2 48 Metabolic Alkalosis
Variabl Primary Normal Primary
HCO3 36 e Disorder Range, arterial Disorder
Gas

pH Acidemia 7.35-7.45 Alkalemia

pCO2 Respiratory 35 - 45 Respiratory

alkalosis acidosis

HCO3 Metabolic 22 – 26 Metabolic

acidosis Alkalosis
 Causes of Metabolic Alkalosis

Processes that raise plasma bicarbonate concentration

 Vomiting (loss of H+ from GIT)

 Diuretics (loss of H+ in urine)

 Excess mineralocorticoid activity—Cushing’s syndrome, Conn’s syndrome,

exogenous steroids, licorice ingestion, increased renin states, Bartter’s
syndrome [Excessive urinary net acid excretion (primary hyperaldosteronism)]

 Excess alkali administration


Example #5
pH 7.20
Metabolic Acidosis with
pCO2 21
Respiratory Compensation
HCO3 8 Variable Primary Normal Range, Primary
Disorder arterial Gas Disorder

pH Acidemia 7.35-7.45 Alkalemia

pCO2 Respiratory 35 - 45 Respiratory

alkalosis acidosis

HCO3 Metabolic 22 – 26 Metabolic

acidosis Alkalosis
 Causes of Metabolic Acidosis

Acidemia created by increase in [H+] or decrease in [HCO3-]

Compensated for by hyperventilation to reduce PaCO2
 Non-Gap
 GI HCO3 loss: diarrhea, intestinal fistulas, ureteral diversions
 Renal HCO3 loss: RTA, aldosterone inhibitors, carbonic anhydrase inhibitors
 Iatrogenic: normal saline
 Anion Gap
 Ketoacidosis: diabetic, alcoholic
 Renal failure
 Lactic Acidosis
 Rhabdomyolysis
 Toxins: methanol, ethylene glycol, paraldehyde, salicylates

Thank you

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