ACID-BASE BALANCE

ACIDOSIS & ALKALOSIS

SAVITHA R S
DEPT. PHARMACY PRACTICE
JSSCP, MYSORE
 INTRODUCTION
 Maintenance of normal pH required for normal organ
function
 Lungs, kidneys and a complex system of buffers allow body
to maintain acid-base homeostasis.
 pH of arterial blood maintained between 7.36-7.44
 pH values lower than 7.35 – acidemia
 pH values higher than 7.45 – alkalemia
 Acid-base disorders are categorized according to primary
abnormality, the underlying pathophysiologic event that
disturbs pH.
 Introduction
 CO2, excreted by lungs is the primary volatile acid in the
body.

 Respiratory acidosis – Lungs fail to adequately excrete

carbon dioxide and blood levels of CO2 rises

 Conversely when the lungs excessively excrete CO2 and

blood CO2 levels fall – Respiratory alkalosis is produced

 Kidneys regulate blood concentrations of bicarbonate

(HCO3-)

 Deficit of bicarbonate – metabolic acidosis

 Excess of bicarbonate – metabolic alkalosis
 Acid-base balance
 Metabolism of glucose, fats and protein result in daily
production of 15,000 mmol of CO2 & 50-100mEq of
nonvolatile acids (eg Sulfuric acid)
 This continual load of acidic substances must be
buffered to prevent acidosis; after buffering they must
be excreted
 CO2 excreted by lungs and nonvolatile acids excreted
by kidneys.
 Principal buffer in the body is carbonic acid/bicarbonate
system
 CO2 as acid and HCO3- as base are easily measured in
serum
 Carbonic acid/Bicarbonate
Buffer System
 HCO3- + H+ 
 H2CO3
 Any increase in hydrogen ions (cellular metabolism, etc)
there is a fall in pH
 But, large portion of hydrogen ions combine with
bicarbonate to form carbonic acid (acid is buffered) and pH
is near normal.
 HCO3- + H+ H2CO3  CO2 + H20 (Requires Carbonic

anhydrase enzyme)
 CO2 is the acid form of the carbonic acid-bicarbonate buffer
system. When excess of hydrogen ions present, bicarbonate
levels fall and concentration of CO2 gas rises as the acid is
buffered.
 Henderson – Hasselbach
equation

This equation describes mathematical relationship among pH,

bicarbonate concentration (mEq/L) and partial pressure of carbon dioxide
(PCO2) measure of concentration of carbon dioxide gas in fluid given in
mmHg.

erson Hasselbalch
The ratio formula
of the bicarbonate and carbon
absolute values determines pH.
provides
dioxide concentrations, NOT the ac
siology. It is the Mantra of Acid Base ph
 Role of Kidneys
 Bicarbonate readily filtered at glomerulus
 Kidneys reabsorb filtered bicarbonate to prevent depletion
 90% reabsorption takes place in PCT, catalyzed by carbonic
anhydrase

 Bicarbonate combines with hydrogen ions secreted by tubule cell to

form carbonic acid.

 Carbonic anhydrase present in brush border of tubule catalyzes

conversion of carbonic acid to CO2 gas

 CO2 readily crosses cell membrane and passively diffuses into renal
tubule cell where carbonic acid and bicarbonate are reformed
catalyzed by carbonic anhydrase

 Bicarbonate reabsorbed into capillary blood along with sodium

 50-100mEq of non-volatile acids excreted by kidney, primarily in DCT
requiring carbonic anhydrase

 Hydrogen ions secreted into tubules are buffered by phosphates,

ammonia – Urine pH is usually acidic (not less than 4.5)
 Role of Lungs
 After blood returns to right side of heart, pumped to lungs through PA.
 In capillaries, CO2 readily diffuses from blood into alveoli of lungs and
excreted in exhaled air

 Rate of CO2 excretion is directly proportional to rate of air passing

into and out of lungs.

 Normal individuals – 14-18 breaths/min, Tidal volume (amount of air

in each breath) – 500ml

 Ventilation can be increased by increasing either the rate of

respiration or tidal volume

 Chemoreceptors in arteries and the brain capable of increasing or

decreasing ventilation in response to changes in pH & PCO2

 Allows rapid response to changes in acid-base status.

 Elevated PCO2 – associated with hypoventilation
 Low PCO2 – associated with hyperventilation
 Acid-Base disorders
 Four major acid-base disorders
 Metabolic acidosis
 Respiratory acidosis
 Metabolic alkalosis
 Respiratory alkalosis

 For each disorder, the primary abnormality is

accompanied by compensatory change.

 For eg., in metabolic acidosis – fall in serum

bicarbonate; compensatory change – fall in PaCO2
 Metabolic Acidosis
 Arterial pH < 7.36 (acidemia)
 Low serum bicarbonate concentration (as determined
by arterial blood gases)

 In Most circumstances, the body compensates by

hyperventilating to increase carbon dioxide excretion –
resulting in low PaCO2 value.

 Review of patient’s medication list to rule out potential

drug causes
Common causes of Metabolic
Acidosis
 Renal failure  Diarrhea
 Ketoacidosis  Drugs/Toxins
 Diabetes Mellitus  Carbonic anhydrase inhibitors
 Starvation (acetazolamide)
 Ethanol  Amphotericin B
 Ammonium Chloride
 Lactic acidosis
 Shock – septic, cardiogenic,
hypovolemic
 CO poisoning
 Tonoc-clonic seizures
 Drugs
 Metformin, Propofol, NRTIs,
IV Lorazepam
 Metabolic Alkalosis
 Elevated pH with elevated serum bicarbonate concentration
 Respiratory compensation by hypoventilation and CO2
retention- compensation is very minor
 Most common causes
 Loss of gastric acid due to persistent vomiting
 Loss of intravascular volume and chloride ion due to diuretic
use

 Other causes – improper anion balance in parenteral

nutrition solutions (acetate & chloride), overtreatment of
metabolic acidosis with NaHCO3
Common causes of Metabolic
Alkalosis
 Loss of gastric acid
 Vomiting
 Nasogastric suction
 Excess of mineralocorticoids
 Hyperaldosteronism
 Hypokalemia
 Alkali administration
 Parenteral nutrition with excessive acetate
 Excessive administration of bicarbonate in metabolic acidosis
 Diuretic therapy – loop diuretics and thiazide diuretics
 Respiratory Acidosis
 Usually synonymous with hypoventilation
 Low pH with elevated PaCO2 (indicating inadequate
excretion of CO2)
 Condition results from three usual categories
 Impaired CNS respiratory drive
 Impaired gas exchange in lungs
 Impaired neuromuscular function affecting diaphragm and chest
wall

 Kidneys require 3-5 days for complete compensation by

raising serum bicarbonate levels
 Acute respiratory acidosis is associated with hypoxemia may
be life-threatening; chronic compensated respiratory
acidosis often requires no therapeutic intervention
 Common causes of
Respiratory Acidosis
 CNS disorders
 CVA
 Tumour
 Sleep apnea
 Drugs (opioids, sedative hypnotics)
 Lung disorders
 Airway obstruction
 Asthma
 COPD
 Neuromuscular disorders
 Myasthenia gravis
 Guillian-Barre syndrome
 Hypokalemia
 Hypophosphatemia
 Respiratory Alkalosis
 Increased ventilation results in increased CO2 excretion
(low PaCO2), elevated pH, and respiratory alkalosis.

 Acute respiratory alkalosis usually reverses

spontaneously or as a result of rebreathing expired air.

 CO2 more readily diffuses from capillary blood to alveoli

than does oxygen; some conditions (pulmonary
embolism) may produce hypoxemia and resulting
hyperventilation may over compensate for CO2
excretion resulting in respiratory alkalosis
 Common causes of
Respiratory Alkalosis
 Hypoxemia
 Lung disease
 Pneumonia
 Pulmonary embolism
 CNS- respiratory stimulation
 CVA
 Fever
 Lung disease
 Anxiety-hyperventilation syndrome
 Normal Serum Range
 Arterial pH
 7.36-7.44
 Arterial partial pressure of carbon dioxide
 36-44mm Hg or 4.8-5.9 kPa
 Arterial serum bicarbonate
 21-27mEq or mmol/L
 Laboratory results in Acid-Base disorders
Disorder pH Primary alteration Compensatory Normal level
alteration of
compensation

Metabolic 
acidosis

Metabolic 
alkalosis

Respiratory 
acidosis

Respiratory 
alkalosis
 Laboratory results in Acid-Base disorders
Disorder pH Primary alteration Compensatory Normal level
alteration of
compensation

Metabolic  HCO3−
acidosis

Metabolic  HCO3−
alkalosis

Respiratory  PaCO2
acidosis

Respiratory  PaCO2
alkalosis
 Laboratory results in Acid-Base disorders

Disorder pH Primary alteration Compensator Normal level of

y alteration compensation

Metabolic  HCO3− PaCO2

acidosis

Metabolic  HCO3− PaCO2

alkalosis

Respiratory  PaCO2 HCO3−

acidosis

Respiratory  PaCO2 HCO3−

alkalosis
 Laboratory results in Acid-Base disorders

Disorder pH Primary Compensatory Normal level of

alteration alteration compensation

Metabolic  HCO3− PaCO2 PaCO2 = 1.2 X HCO3−

acidosis

Metabolic  HCO3− PaCO2 PaCO2 = 0.6 X HCO3−

alkalosis

Respiratory  PaCO2 HCO3− HCO3− = 0.1 X PaCO2

acidosis

Respiratory  PaCO2 HCO3− HCO3− = 0.2 X PaCO2

alkalosis
 Tests to assess acid-base
balance and oxygenation
 Venous Total Carbon Dioxide (Serum Bicarbonate)
 Serum Lactate
 Venous partial pressure of oxygen (70mm Hg)
 Oxygen saturation by pulse oximetry (> 95%)
 Learning Points
 What is key buffer system in body
 How are components of that system used to assess
acid-base status?
 Learning Points
 Carbonic acid/Bicarbonate buffer system
 Carbonic acid hydrolyzed to carbon dioxide
 Arterial partial pressure of carbon dioxide
 Bicarbonate ion
 pH
 Problem
 A patient with an acute rise in PaCO2 to 60mm Hg has
a pH of 7.26 with serum bicarbonate of 26mEq/L. If
PaCO2 remains at 60mm Hg for 3-5 full days when
renal compensation occurs, serum bicarbonate will rise
to?
Henderson-Hasselbach
Thank You
 Problem
 A patient with an acute rise in PaCO2 to 60mm Hg has
a pH of 7.26 with serum bicarbonate of 26mEq/L. If
PaCO2 remains at 60mm Hg for 3-5 full days when
renal compensation occurs, serum bicarbonate will rise
to?

 Ans: 32mEq/L