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ACID BASE DISORDERS
BY - YOGESH PANCHAL
GUIDED BY - DR.ANAND CHAUHAN
INTRODUCTION
• ACID - chemical substance that can donate H+ ions
• BASE – chemical substance that can accept H+ ions
• pH – refers to free H+ ion concentration
• ACIDOSIS – refers to any disorder that adds acid / removes base from
the body
• ALKALOSIS – refers to any disorder that adds alkali / removes acids
from the body
ANION GAP
• It denotes the concentration of unmeasured anions in the plasma
• Normal cations in plasma – Na+, K+, Ca+, Mg+
• Normal anions in plasma – Cl-, HCO3-, albumin, phosphate.
ANION GAP = {[Na]+[K]} – {[HCO3]+[Cl]}
ANION GAP = UNMEASURED ANIONS – UNMEASURED CATIONS
• Normal value 8 – 10 mEq/L
TYPES
1. SIMPLE ACID BASE DISORDER
• Metabolic acidosis
• Metabolic alkalosis
• Respiratory acidosis
• Respiratory alkalosis
2. MIXED ACID BASE DISORDER
• Metabolic acidosis-respiratory alkalosis
• Metabolic acidosis-respiratory acidosis
• Metabolic alkalosis-respiratory alkalosis
• Metabolic alkalosis-respiratory acidosis
• Metabolic acidosis-metabolic alkalosis
1. SIMPLE ACID BASE DISORDER
DISORDER pH H+ Pri. changes Sec. changes
Metabolic acidosis low high HCO3 low PaCO2 low
Metabolic alkalosis high low HCO3 high PaCO2 high
Respiratory acidosis low high PaCO2 high HCO3 high
Respiratory alkalosis high low PaCO2 low HCO3 low
METABOLIC ACIDISIS
• It is a primary acid base disorder with fall in pH and bicarbonate level
in plasma
• Occures when an endogenous acid starts to accumulate in the body
• MECHANISM
ETIOLOGY
NORMAL ANION GAP
1.gastrointestinal bicarbonate loss
2.renal acidosis
3.drug induced( with renal insuff
-iciency)
4.others
HIGH ANION GAP
1.Lactic acidosis
2.ketoacidosis – Diabetic/alcoholic/starvation
3.renal failure
4.Toxins - ethylene glycol
- methanol
. - salicylate
CLINICAL FEATURES
• Respiratory effects – hyperventilation/air hunger/kussmaul
breathing.
• CVS – decreased myocardial activity, sympathetic over activity
• CNS: Lethargy, disorientation, stupor, muscle twitching, coma, cranial
nerve palsies
• Others: Hyperkalemia
DISORDER MANAGEMENT
LACTIC ACIDOSIS A – poor tissue perfusion
B - impaired mitochondrial respiration
- Adequate tissue oxygenation
- Treat the underlying cause
- I.v.fluids to improve volume
- NaHCO3 in case of pH <7.15
- Dialysis
DKA It is due to overproduction of acetoacetic acid
and hydroxybutyric acid by liver due to relative
or absolute insulin deficiency
- i.v.fluids NS
- Insulin
- Bicarbonate if pH <7.1
Salicylate poisoning Accumulation of lactic acid and ketoacids largely
accounts for metabolic acidosis.
- Gastric Lawage
- Activated charcoal through RT
- Fluids to correct hypovolemia
- diuresis
Renal failure Result in an increased anion gap acidosis due to
retention of sulphate, phosphate and organic
anions
- In children, bicarbonate suppliment
- Dialysis
- Alkali therapy (risk of volume
overload)
METABOLIC ALKALOSIS
• it is characterized by rise in both plasma bicarbonate and plasma PH
• Types 1) hypovolemic. 2) normovolemic
• MECHANISM
ETIOLOGY
CLINICAL FEATURES
• Decreased myocardial activity / arrhythmias
• Hypoventilation/confusion/neuromuscular excitability
• Reduced cerebral blood flow
• Pulmonary microatelectasis
RESPIRATORY ACIDOSIS
• Characterized by increased PaCO2 and decreased pH
• It may be 1.ACUTE <24 hrs 2.CHRONIC >24 hrs
ETIOLOGY
A. Central 1.Drugs (anesthetics, morphine, sedatives) 2.Stroke 3.infection
• B. Airway 1.Obstruction 2.Asthma
• C. Parenchyma 1.Emphysema 2.Pneumoconiosis 3.Bronchitis 4.Adult respiratory
distress syndrome 5.Barotrauma
• D. Neuromuscular 1.Poliomyelitis 2.Kyphoscoliosis3.Myasthenia4. Muscular
dystrophies
• E. Miscellaneous 1.Obesity 2.Hypoventilation 3.Permissive hypercapnia
Clinical features
• RS - tachypnea and dyspnea
• CNS – increased cerebral blood flow amd and ICT, papilledema
• CO2 narcosis – disorientation, confusion, headache, lethargy
• COMA
• CVS – Tachycardia,
• OTHERS – Peripheral vasodilation ( warm, flushed, sweaty)
RESPIRATORY ALKALOSIS
• Characterized by reduced plasma PaCO2 and low pH with
compensatory fall in plasma HCO3 ions
• It is the most frequently encountered acid base disorder, since it
occurs in normal pregnancy and high altitude residence.
• Clinical features
• CNS tingling,numbness,tetany,reduced ICT, Headache, confusion
• CVS increased CO and SBP
• Others hypokalemia, hyponatremia,hypochloremia
ETIOLOGY
• 1. Hypoxemia
• A Pulmonary disease : Pneumonia,emboli and oedema
• B. CHF, hypotension or severe anaemia
• c. High altitude residence
• 2. Pulmonary diseases
• 3. Direct stimulation of the medullary respiratory center
• a Psychogenic or voluntary hyperventilation, pain, pregnancy
• b. Hepatic failure, gram-negative septicemia
• c. Salicylate intoxication
• d. Rapid correction of metabolic acidosis
• e. Neurological disorders, accidents, pontine tumour
APPROACH TO ABD
• Step 1 – look of pH (7.35 – 7.45)
• pH <7.35 => acidosis.
• pH >7.45 => alkalosis
• Step 2 – look of PaCO2 ( 35 – 45 mmHg) and HCO3( 22 – 26 mEq/L)
• PaCO2 increased => respiratory acidosis
• PaCO2 decreased => respiratory Alkalosis
• HCO3 increased => metabolic alkalosis
• HCO3 decreased => metabolic acidosis
• Step 3 – look for compensation (pH/PaCO2/HCO3)
• PaCO2/ HCO3 same direction => compensated
• PaCO2/ HCO3 opposite direction => mixed disorder
MANAGEMENT
• METABOLIC ACIDOSIS
• Correct the underlying disorder
• Sodium bicarbonate in sever acidosis (alkali therapy)
• NaHCO3 bolus infusion over 30 min 50 – 100 mEq if pH<7.1,HCO3 < 10
Infusion 3-4 hrs
• THAM – tris hydroxymethyl aminomethane alternative
• Dialysis for renal failure
•
• METABOLIC ALKALOSIS
• NS to correct hypovolemia
• Dilute 0.1 N HCl infusion if non responsive
• Correct hypokalemia
• Acetazolamide 600 mg BD/TID for aldosterone excess
• Avoid exogenous source of alkali
• Use H2 blockers which reduces H+ secretion
RESPIRATORY ACIDISIS
Treat underlying cause
Oxygen Therapy
Mechanical ventilation support
Alkali administration only in prolonged cardiopulmonary arrest
Rapid correction of PaCO2 should be avoided
RESPIRATORY ALKALOSIS
Treat the underlying cause
Reassurance,closed bag breathing
correct hypokalemia
In acute cases sedation
THANK YOU

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Understanding Acid-Base Disorders

  • 1. ACID BASE DISORDERS BY - YOGESH PANCHAL GUIDED BY - DR.ANAND CHAUHAN
  • 2. INTRODUCTION • ACID - chemical substance that can donate H+ ions • BASE – chemical substance that can accept H+ ions • pH – refers to free H+ ion concentration • ACIDOSIS – refers to any disorder that adds acid / removes base from the body • ALKALOSIS – refers to any disorder that adds alkali / removes acids from the body
  • 3. ANION GAP • It denotes the concentration of unmeasured anions in the plasma • Normal cations in plasma – Na+, K+, Ca+, Mg+ • Normal anions in plasma – Cl-, HCO3-, albumin, phosphate. ANION GAP = {[Na]+[K]} – {[HCO3]+[Cl]} ANION GAP = UNMEASURED ANIONS – UNMEASURED CATIONS • Normal value 8 – 10 mEq/L
  • 4. TYPES 1. SIMPLE ACID BASE DISORDER • Metabolic acidosis • Metabolic alkalosis • Respiratory acidosis • Respiratory alkalosis 2. MIXED ACID BASE DISORDER • Metabolic acidosis-respiratory alkalosis • Metabolic acidosis-respiratory acidosis • Metabolic alkalosis-respiratory alkalosis • Metabolic alkalosis-respiratory acidosis • Metabolic acidosis-metabolic alkalosis
  • 5. 1. SIMPLE ACID BASE DISORDER DISORDER pH H+ Pri. changes Sec. changes Metabolic acidosis low high HCO3 low PaCO2 low Metabolic alkalosis high low HCO3 high PaCO2 high Respiratory acidosis low high PaCO2 high HCO3 high Respiratory alkalosis high low PaCO2 low HCO3 low
  • 6. METABOLIC ACIDISIS • It is a primary acid base disorder with fall in pH and bicarbonate level in plasma • Occures when an endogenous acid starts to accumulate in the body • MECHANISM
  • 7. ETIOLOGY NORMAL ANION GAP 1.gastrointestinal bicarbonate loss 2.renal acidosis 3.drug induced( with renal insuff -iciency) 4.others HIGH ANION GAP 1.Lactic acidosis 2.ketoacidosis – Diabetic/alcoholic/starvation 3.renal failure 4.Toxins - ethylene glycol - methanol . - salicylate
  • 8. CLINICAL FEATURES • Respiratory effects – hyperventilation/air hunger/kussmaul breathing. • CVS – decreased myocardial activity, sympathetic over activity • CNS: Lethargy, disorientation, stupor, muscle twitching, coma, cranial nerve palsies • Others: Hyperkalemia
  • 9. DISORDER MANAGEMENT LACTIC ACIDOSIS A – poor tissue perfusion B - impaired mitochondrial respiration - Adequate tissue oxygenation - Treat the underlying cause - I.v.fluids to improve volume - NaHCO3 in case of pH <7.15 - Dialysis DKA It is due to overproduction of acetoacetic acid and hydroxybutyric acid by liver due to relative or absolute insulin deficiency - i.v.fluids NS - Insulin - Bicarbonate if pH <7.1 Salicylate poisoning Accumulation of lactic acid and ketoacids largely accounts for metabolic acidosis. - Gastric Lawage - Activated charcoal through RT - Fluids to correct hypovolemia - diuresis Renal failure Result in an increased anion gap acidosis due to retention of sulphate, phosphate and organic anions - In children, bicarbonate suppliment - Dialysis - Alkali therapy (risk of volume overload)
  • 10. METABOLIC ALKALOSIS • it is characterized by rise in both plasma bicarbonate and plasma PH • Types 1) hypovolemic. 2) normovolemic • MECHANISM
  • 12. CLINICAL FEATURES • Decreased myocardial activity / arrhythmias • Hypoventilation/confusion/neuromuscular excitability • Reduced cerebral blood flow • Pulmonary microatelectasis
  • 13. RESPIRATORY ACIDOSIS • Characterized by increased PaCO2 and decreased pH • It may be 1.ACUTE <24 hrs 2.CHRONIC >24 hrs ETIOLOGY A. Central 1.Drugs (anesthetics, morphine, sedatives) 2.Stroke 3.infection • B. Airway 1.Obstruction 2.Asthma • C. Parenchyma 1.Emphysema 2.Pneumoconiosis 3.Bronchitis 4.Adult respiratory distress syndrome 5.Barotrauma • D. Neuromuscular 1.Poliomyelitis 2.Kyphoscoliosis3.Myasthenia4. Muscular dystrophies • E. Miscellaneous 1.Obesity 2.Hypoventilation 3.Permissive hypercapnia
  • 14. Clinical features • RS - tachypnea and dyspnea • CNS – increased cerebral blood flow amd and ICT, papilledema • CO2 narcosis – disorientation, confusion, headache, lethargy • COMA • CVS – Tachycardia, • OTHERS – Peripheral vasodilation ( warm, flushed, sweaty)
  • 15. RESPIRATORY ALKALOSIS • Characterized by reduced plasma PaCO2 and low pH with compensatory fall in plasma HCO3 ions • It is the most frequently encountered acid base disorder, since it occurs in normal pregnancy and high altitude residence. • Clinical features • CNS tingling,numbness,tetany,reduced ICT, Headache, confusion • CVS increased CO and SBP • Others hypokalemia, hyponatremia,hypochloremia
  • 16. ETIOLOGY • 1. Hypoxemia • A Pulmonary disease : Pneumonia,emboli and oedema • B. CHF, hypotension or severe anaemia • c. High altitude residence • 2. Pulmonary diseases • 3. Direct stimulation of the medullary respiratory center • a Psychogenic or voluntary hyperventilation, pain, pregnancy • b. Hepatic failure, gram-negative septicemia • c. Salicylate intoxication • d. Rapid correction of metabolic acidosis • e. Neurological disorders, accidents, pontine tumour
  • 17. APPROACH TO ABD • Step 1 – look of pH (7.35 – 7.45) • pH <7.35 => acidosis. • pH >7.45 => alkalosis • Step 2 – look of PaCO2 ( 35 – 45 mmHg) and HCO3( 22 – 26 mEq/L) • PaCO2 increased => respiratory acidosis • PaCO2 decreased => respiratory Alkalosis • HCO3 increased => metabolic alkalosis • HCO3 decreased => metabolic acidosis
  • 18. • Step 3 – look for compensation (pH/PaCO2/HCO3) • PaCO2/ HCO3 same direction => compensated • PaCO2/ HCO3 opposite direction => mixed disorder
  • 19. MANAGEMENT • METABOLIC ACIDOSIS • Correct the underlying disorder • Sodium bicarbonate in sever acidosis (alkali therapy) • NaHCO3 bolus infusion over 30 min 50 – 100 mEq if pH<7.1,HCO3 < 10 Infusion 3-4 hrs • THAM – tris hydroxymethyl aminomethane alternative • Dialysis for renal failure • • METABOLIC ALKALOSIS • NS to correct hypovolemia • Dilute 0.1 N HCl infusion if non responsive • Correct hypokalemia • Acetazolamide 600 mg BD/TID for aldosterone excess • Avoid exogenous source of alkali • Use H2 blockers which reduces H+ secretion
  • 20. RESPIRATORY ACIDISIS Treat underlying cause Oxygen Therapy Mechanical ventilation support Alkali administration only in prolonged cardiopulmonary arrest Rapid correction of PaCO2 should be avoided RESPIRATORY ALKALOSIS Treat the underlying cause Reassurance,closed bag breathing correct hypokalemia In acute cases sedation