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ACID-BASE IMBALANCE

byDr. Ali H. Sadiek

Prof. of Internal Veterinary Medicine and Clinical Laboratory Diagnosis

Faculty of Veterinary Medicine, Assiut UniversityE-mail: Sadiek59@yahoo.com

Course Objectives1. What are the Acid-base and Blood

Gases?

2. How its measured?3. Causes, signs, and Lab. diagnosis of

disorders in Acid-base imbalance:• Acidosis (Metabolic and Respiratory), • Alkalosis (Metabolic and Respiratory),

ACID-BASE BALANCEAcid-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 gainBase gainMineralH +

HCL

H2SO4

H2PO4

OH-

NH3-

SO4-

HPO4-

OrganicCO2

Lactic acid

B-OH butyric acid

HCO3-

Lactate-

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 H+ + HCO3-

Normal Values of Acid-Base

pH = 7.35-7.45pCO2= 40 mmHg

HCO3- = 25 mmol/l

BE =+ 4.0 mmol/lMost 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

H2CO3

Acid-Base Balance Control

1. Buffers sytem: 20 (NaHCO3 ) and 1 H2CO3)

• HCl + NaHCO3 ↔ H2CO3 + NaCl

• NaOH + H2CO3 ↔ NaHCO3 + H2O

• Buffers function almost immediately2. Respiratory control take several minutes to

hours

3. 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: 1. Blood pH2. PO23. PCO24. HCO35. BE 6. Electrolytes: Na, K, Cl, Ca

– Anion Gap = (Na+ K)- (Cl- - HCO3-)

Normal Blood pH and Blood Gases

Species Blood pH pCO2

mmHg

HCO3

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

•works with volatile acids

Most effective regulator of pH

•Eliminate acids, base, conserve and broduce 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 DisorderCompensatory Mechanism

Metabolic acidosisIncreased ventilation

Metabolic alkalosisDecreased ventilation

Respiratory acidosisIncreased renal reabsorption of HCO3-

in the proximal tubule

Increased renal excretion of H in the

distal tubule

Respiratory alkalosisDecreased renal reabsorption of HCO3-

in the proximal tubule

Decreased renal excretion of H+ in the

distal tubule

AcidosisAlkalosis

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 (↑ anion gap)– Lactic acid– Ketoacids– Renal failure– Intoxicants

• Salicylates

Lab. Findings: ↓ plasma Hco3 ↓ TCo2.

• Loss of HCO3-

(normal anion gap)– GIT loss in:

diarrhea, fistula, Saliva

– Renal Loss in tubular acidosis

• Hyperchloremia

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 of Alkalosis• 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• DysrhythmiasTreatment of Metabolic alkalosis:• Electrolytes to replace those lost• IV chloride containing solution• Treat underlying disorder

Respiratory Alkalosis: pCO2 < 361-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

imbalance

Compensating

response

Metabolic

acidosis

Decreased HCO3 pCO2

Metabolic

alkalosis

Increased HCO3 pCO2

Respiratory

acidosis

Increased pCO2 HCO3

Respiratory

alkalosis

Decreased pCO2 HCO3

Urine pHUrine 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

√ Na+ 128

√ K+ 2.5

√ Cl- 62

√ HCO3- 45

BUN 45

Cr 1.5

ABG: √ pH 7.65 √ pCO2 48

• It is a Metabolic Alkalosis

Summary of the Approach to ABGs

1. Check the pH

2. Check the pCO2

3. Select the appropriate compensation formula

4. Determine if compensation is appropriate

5. Check the anion gap

6. If the anion gap is elevated, check the delta-delta

7. If a metabolic acidosis is present, check urine pH

8. 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 osmolalitySerum 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