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ACID-BASE IMBALANCE

by
Dr. Ali H. Sadiek
Prof. of Internal Veterinary Medicine
and Clinical Laboratory Diagnosis
Faculty of Veterinary Medicine, Assiut University
E-mail:Sadiek59@yahoo.com
 Course Objectives
• What are the Acid-base and Blood
Gases?
• How its measured?
• Causes, signs, and Lab. diagnosis of
disorders in Acid-base imbalance:
• Acidosis (Metabolic and Respiratory),
• Alkalosis (Metabolic and Respiratory),
 ACID-BASE BALANCE
Acid-base balance means that the net quantity of acid or base ingested or
produced are quantitatively excreted by the lungs and kidney.
In this case, the systemic pH will be stable and in balance and the body
buffers preserved.
 Major physiologic acid/bases ingested or produced:

Acid gain Base gain

Mineral +H -OH
HCL -NH3
H2SO4 -SO4
H2PO4 -HPO4
Organic CO2 -HCO3
Lactic acid -Lactate
B-OH butyric acid -B-OH butyrate
The body produces more acids than bases
•Acids produced by foods, metabolism of lipids and proteins + Cellular
metabolism produces CO2.
 Acid-Base Homeostasis
Central Relationship
H2O + CO2 H2CO3
H2CO3 H+ + HCO3-

Normal Values of Acid-Base

pH = 7.35-7.45
pCO2= 40 mmHg
HCO3- = 25 mmol/l
BE =+ 4.0 mmol/l
Most enzymes function only with narrow pH ranges
Acid-base balance can also affect electrolytes (Na+, K+, Cl-)
Can also affect hormones
Small changes in pH can produce major disturbances
 Acid-Base Balance Control
• Buffers sytem: 20 (NaHCO3 ) and 1
H2CO3)
• HCl + NaHCO3 ↔ H2CO3 + NaCl
• NaOH + H2CO3 ↔ NaHCO3 + H2O
• Buffers function almost immediately
5. Respiratory control take several minutes to
hours
6. Renal control may take several hours to
days
 Measuring of Acid-Base Balance
• Sample required: Arterial /(Venous) blood
• Anticoagulant required: Lith. Heparin 1/1000
in a sealed syringe or capillary tube
• Injected directly in Blood Gas Analyzer
• Or refrigerated: Max 3 hours
• Measured Parameters:
 Blood pH
 PO2
 PCO2
 HCO3
 BE
 Electrolytes: Na, K, Cl, Ca
– Anion Gap = (Na+ K)- (Cl- - HCO3-)
Normal Blood pH and Blood Gases

Species Blood pH pCO2 HCO3

mmHg mmHg

Bovine 7.33-7.45 35-53 21-27

Ovine 7.32-7.45 37-46 20-25

Equine 7.32-7.44 38-46 24-34

Canine 7.31-7.42 38 18-24

Feline 7.24-7.40 36 17-21

 Most effective regulator of pH
•Eliminate acids, base,
conserve and broduce
•works with volatile acids bicarbonate
 Acid-Base Disorders
• Metabolic
– Acidosis: ↓ HCO3-
– Alkalosis: ↑ HCO3-
• Respiratory
– Acidosis: ↑ pCO2
– Alkalosis: ↓ pCO2
Compensatory Acid-Base Response
• When a primary acid-base disorder exists, the
body attempts to return the pH to normal via
the “other half” of acid base metabolism.
• Complete compensation if brought back within
normal limits
• Partial compensation if range is still outside
norms
• Metabolic acidosis: respiratory alkalosis
• Metabolic alkalosis: respiratory acidosis
• Respiratory acidosis: metabolic (Renal) alkalosis
• Respiratory alkalosis: metabolic (Renal) acidosis
 (Compensation (continued
Primary Disorder Compensatory Mechanism
Metabolic acidosis Increased ventilation
Metabolic alkalosis Decreased ventilation
Respiratory acidosis -
Increased renal reabsorption of HCO3
in the proximal tubule
Increased renal excretion of H in the
distal tubule
Respiratory alkalosis -
Decreased renal reabsorption of HCO3
in the proximal tubule
Decreased renal excretion of H+ in the
distal tubule
Alkalosis Acidosis
 Principal effects of Acidosis
• Depression of the CNS through ↓ in synaptic
transmission.
• Generalized weakness
• Deranged CNS function the greatest threat
• Severe acidosis causes
– Disorientation
– coma
– Death
• Treatment: IV lactate solution, NaHCO3
 Metabolic Acidosis: pH < 7.3, HCO3- < 22 meq/L

• Addition of acid • Loss of HCO3-

(↑ anion gap) (normal anion gap)
– Lactic acid – GIT loss in:
– Ketoacids diarrhea, fistula,
Saliva
– Renal failure
– Renal Loss in
– Intoxicants
tubular acidosis
• Salicylates
• Hyperchloremia
 Lab. Findings:
↓ plasma Hco3
↓ TCo2.
 Respiratory Acidosis: pH < 7.3, pCO2 > 45
1-Common causes:
• Aspiration pneumonia.
• Laryngeal edema.
• Pneumonia and pleurisy
• Pneumothorax.
• Chronic obstructive pulmonary disease.
2-uncommon causes:
• Cardiac arrest.
• Tetanus, Botulism.
• Neonatal respiratory distress syndrome.
3- Lab. Finding:
- pH <7.3, increased pCO2,
 Respiratory Acidosis
• Carbonic acid excess caused by blood levels
of CO2 above 45 mm Hg.
• Hypercapnia – high levels of CO2 in blood
• Chronic conditions:
– Depression of respiratory center in brain that controls
breathing rate – drugs or head trauma
– Paralysis of respiratory or chest muscles
– Emphysema
• Acute conditons:
– Adult Respiratory Distress Syndrome
– Pulmonary edema
– Pneumothorax
 Signs and treatment 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 CO2
Treatment:
• Restore ventilation
• IV lactate solution
• Treat underlying dysfunction or disease
 Principal effects ofAlkalosis
• Alkalosis causes over excitability of the
central and peripheral nervous systems.
• Numbness
• Lightheadedness
• It can cause :
– Nervousness
– muscle spasms or tetany
– Convulsions
– Loss of consciousness
– Death
 Metabolic Alkalosis: pH >7.45, HCO3- > 27meq/L

1-Common causes:
• Gastric reflux in horses with ileus.
• Sequestration of fluid in abomasum and forestomach in
ruminants.
• Massive sweating in horses.
• Chloride depletion.
• Potassium depletion.
• Usage of diuretics.
2-Uncommon causes:
• Excessive bicarbonate supplementation for therapy.
• Mineralocorticoid excess.
• Vomiting.
3- Lab. Finding: Increased Bl. pH, increased HCO3,
Symptoms & treatment of Metabolic Alkalosis

• Respiration slow and shallow

• Hyperactive reflexes ; tetany
• Often related to depletion of electrolytes
• Atrial tachycardia
• Dysrhythmias
Treatment of Metabolic alkalosis:
• Electrolytes to replace those lost
• IV chloride containing solution
• Treat underlying disorder
 Respiratory Alkalosis: pCO2 < 36
1-Common causes:
• Hypoxemia.
• Pulmonary diseases.
• Congestive heart failure.
• Severe anemia.
• Gram negative septicemia.
2-Uncommon causes:
• Following correction of metabolic acidosis.
• Salicylate toxicity.
• Hyperventilation as a thermo regulatory
response to overheating
3- Lab: Increased Bl. pH, pCO2 < 36
 Respiratory Alkalosis

• Carbonic acid deficit

• pCO2 less than 35 mm Hg (hypocapnea)
• Most common acid-base imbalance
• Primary cause is hyperventilation
• Treated by IV Chloride containing
solution – Cl- ions replace lost
bicarbonate ions
 :Mixed acid-base imbalance
1-Primary respiratory acidosis & primary metabolic acidosis:
• Prolonged surgical anesthesia.
• Pneumonia with anorexia in newborn animals.
2-Primary respiratory alkalosis and primary metabolic
alkalosis:
• Following vomition.
• Following hyperventilation.
3-Primary respiratory acidosis & primary metabolic alkalosis:
• Vomition in dogs.
• Hyperventilation in dogs.
• Anesthesia in cattle.
• Nephritis-pneumonia complex.
4- Primary respiratory alkalosis & primary metabolic acidosis:
• Uremic nephritis in dogs.
 Acid-base imbalances
:and compensating responses

Disorder pH Primary Compensating

imbalance response

Metabolic Decreased HCO3 pCO2

acidosis

Metabolic Increased HCO3 pCO2

alkalosis
Respiratory Increased pCO2 HCO3
acidosis
Respiratory Decreased pCO2 HCO3
alkalosis
 Urine pH
Urine pH is an important screening test for the diagnosis of renal disease,
respiratory disease, and certain metabolic disorders.
A highly acidic urine pH occurs in:
• Acidosis
• Diarrhea
• Starvation and dehydration
• Respiratory diseases in which carbon dioxide retention occurs and
acidosis develops
A highly alkaline urine occurs in:
• Urinary tract obstruction
• Pyloric obstruction
• Salicylate intoxication
• Renal tubular acidosis
• Chronic renal failure
• Respiratory diseases that involve hyperventilation (blowing off
carbon dioxide and the development of alkalosis)
 Examples of Acid-base imbalance
• A case of severe diarrhea in neonate
since 3 days.
• The arterial blood gas report:
– pH 7.3
– HCO3- = 20 mEq / L ( 22 - 26)
– pCO2 = 32 mm Hg (35 - 45)
• Diagnosis: Compensated Metabolic
acidosis
 Compensated metabolic Acidosis

ABG: pH 7.35 Chem : Na+ 135

PCO2 34 K+ 5.1
HCO3- 18 Cl- 110
PO2 92 HCO3- 16
Creat 1.4
Urine pH: 5.0
 A case of Respiratory Acidosis

ABG: pH 7.25 Chem : Na+ 137

PCO2 60 K+ 4.5
HCO3- 26 Cl- 100
PO2 55 HCO3- 25
Partially Compensated Respiratory alkalosis

ABG: pH 7.49 Chem 7: Na+ 133

PCO2 28 K+ 3.9
HCO3- 21 Cl- 102
PO2 52 HCO3- 22
 Part. compensated Metabolic alkalosis

ABG: pH 7.47 Chem : Na+ 130

PCO2 46 K+ 3.2
HCO3- 32 Cl- 86
PO2 96 HCO3- 33

Urine pH: 5.8

 What is your suggestion

ABG: √ pH 7.65 √ pCO2 48

√ Na+ 128 √ Cl- 62 BUN 45

√ K+ 2.5 √ HCO3- 45 Cr 1.5

• It is a Metabolic Alkalosis
 Summary of the Approach to ABGs
 Check the pH
 Check the pCO2
 Select the appropriate compensation formula
 Determine if compensation is appropriate
 Check the anion gap
 If the anion gap is elevated, check the delta-
delta
 If a metabolic acidosis is present, check urine
pH
 Generate a differential diagnosis
 Tissues and cellular osmolality
• Osmolality is a count of the number of particles
in a fluid sample intra and extracellular
• It is affected by the levels of electrolyte, fine
particles e.g glucose, urea, plasma proteins.
• In ECF it is about 300 mosmol (Isoosmolality)
• More than 300 mosmol ( Hyeprosmolality)
• Less than 300 mosmol ( Hypoosmolality)
• Water moves towerd hyperosmolalit
 Tissues and cellular osmolality
Serum Osmolality:
• It is measured via levels of NA, K, Urea,
sugar as follow:
• mOsm/kg= 2 (Na + K mmol/l) in normal
blood sugar and urea levels
• mOsm/kg= 2 {Na + K mmol/l)} +
{glucose (mg/dl) / 18} + BUN (mg/dl) /
28. in increased blood sugar and urea
levels
 Hyperosmolality
• It occurs when levels of Na, glucose,
urea, ketones increased in blood.
• Hyperosmolaity (the counted osmolitity
increased by more than 30 mosmol it
indicated the presence of fine toxic
molecules in blood (ethyl glycol, ethyle
propylene) that results in moving fluids
into extracellular fluids and shrinkage
of cells and hiding of dehydration