Acid Base Disorders For Vet. Students

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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:[email protected]

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 Mineral +H HCL H2SO4 H2PO4 Organic CO2 Lactic acid B-OH butyric acid

Base gain -OH -NH3 -SO4 -HPO4 -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 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

• • •

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-)

in a sealed syringe or capillary tube

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

•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 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 (↑ 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 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

Metabolic

pH

Primary

Compensating

imbalance

response

Decreased HCO3

pCO2

Increased HCO3

pCO2

Increased pCO2

HCO3

Decreased pCO2

HCO3

acidosis Metabolic alkalosis Respiratory acidosis Respiratory 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 PCO2

7.35 34

Na+ K+

135 5.1

HCO3- 18

Cl-

110

PO2

HCO3- 16

92

Chem :

Creat 1.4 Urine pH: 5.0

A case of Respiratory Acidosis ABG: pH PCO2

7.25 60

Na+ K+

137 4.5

HCO3- 26

Cl-

100

PO2

HCO3- 25

55

Chem :

Partially Compensated Respiratory alkalosis ABG: pH PCO2 HCO3PO2

7.49 28 21 52

Chem 7:

Na+ K+ ClHCO3-

133 3.9 102 22

Part. compensated Metabolic alkalosis

ABG: pH PCO2

Na+ K+

130 3.2

HCO3- 32

Cl-

86

PO2

HCO3- 33

Urine pH:

7.47 46 96 5.8

Chem :

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 deltadelta  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