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ACID-BASE
DISORDERS
By Dr. Raneem AlSayed
assistant professor of internal medicine and
nephrolgy
LEARNING OBJECTIVES:
By the end of this lecture, you should be able to:
 Recognize normal acid base regulation
 Recognize the clinical acid-base relationship.
 Outline the causes of respiratory acidosis
 Outline the causes of respiratory alkalosis
 Outline the causes of metabolic acidosis
 Outline the causes of metabolic alkalosis
 Discuss the role of the kidney in handling the HCO3.
Content of the lecture:
 Physiology of acid base balance.
 Case of respiratory acidosis (chest).
 Case of metabolic acidosis (Diabetic keto acidosis , renal tubular acidosis)
 Example of metabolic alkalosis
 Example of respiratory alkalosis
"POTENTIAL OF HYDROGEN" (PH)
 The acidity or alkalinity of a solution is measured as
pH.
 The more acidic a solution, the lower the pH.
 The more alkaline a solution , the higher the pH.
 Water has a pH of 7 and is neutral.
 The pH of arterial blood is normally between 7.35
and 7.45
BUFFER SYSTEMS
"Ability of weak acid and its corresponding base to
resist change in pH of a solution upon adding a strong acid
or base"
 Regulate pH by binding or releasing Hydrogen
 Most important buffer system:
 Bicarbonate-Carbonic Acid Buffer System
 (Blood Buffer systems act instantaneously and thus
constitute the body’s first line of defense against acid-base
imbalance)
CLINICALLY SIGNIFICANT ACID-BASE PAIRS
Acid
Carbonic acid (H2CO3)
Monobasic PO4 (H2PO4)
Ammonium (NH4+)
Lactic acid (H6C3O2)
Base
Bicarbonate (HCO3-)
Dibasic PO4 (HPO4-)
Ammonia (NH3)
Lactate (H5C3O2-)
RESPIRATORY REGULATION
 Lungs
 help regulated acid-base balance by eliminating or retaining carbon dioxide
 pH may be regulated by altering the rate and depth of respirations
 changes in pH are rapid,
 occurring within minutes
 normal CO2 level
 35 to 45 mm Hg
RENAL REGULATION
 Kidneys
 the long-term regulator of acid-base balance
 slower to respond
 may take hours or days to correct pH
 kidneys maintain balance by excreting or conserving bicarbonate and hydrogen ions
 normal bicarbonate level
 22 to 26 mEq/L.
IS IT RESPIRATORY OR METABOLIC?
1. Respiratory Acidosis
2. Respiratory Alkalosis
3. Metabolic Acidosis
4. Metabolic Alkalosis
 Increased pCO2 >50
 Decreased pCO2<30
 Decreased HCO3 <18
 Increased HCO3 >30
COMPENSATED OR UNCOMPENSATED—
WHAT DOES THIS MEAN?
1. Evaluate pH—is it normal? Yes
2. Next evaluate pCO2 & HCO3
• pH normal + increased pCO2 + increased HCO3 = compensated respiratory
acidosis
• pH normal + decreased HCO3 + decreased pCO2 = compensated metabolic
acidosis
COMPENSATED VS. UNCOMPENSATED
1. Is pH normal? No
2. Acidotic vs. Alkalotic
3. Respiratory vs. Metabolic
• pH<7.30 + pCO2>50 + normal HCO3 = uncompensated respiratory acidosis
• pH<7.30 + HCO3<18 + normal pCO2 = uncompensated metabolic acidosis
• pH>7.50 + pCO2<30 + normal HCO3 = uncompensated respiratory alkalosis
• pH>7.50 + HCO3>30 + normal pCO2 = uncompensated metabolic alkalosis
CAUSES OF ACIDOSIS
 Respiratory
 Hypoventilation
 Impaired gas exchange
 Metabolic
 Ketoacidosis
 Diabetes
 Lactic Acidosis
 Decreased perfusion
 Severe hypoxemia
 Renal Failure
 Renal Tubular Acidosis
 Severe Diarrheal illness
ACIDEMIA- PHYSIOLOGIC EFFECTS
 Cardiovascular
 Mild acidemia--Tachycardia
 Severe acidemia -- Bradycardia
 Decreased fibrillation threshold
 Decreased contractility
 Neuromuscular
 Increase in CBF -- Headaches/Confusion
 Due to hypercarbia or pH ??
CAUSES OF ALKALOSIS
 Respiratory
 Hyperventilation due
to:
 Hypoxemia
 Metabolic acidosis
 Neurologic
 CNS Lesions
 CNS Trauma
 Infection
 Metabolic
 Hypokalemia
 Gastric suction or
vomiting
 Hypochloremia
ALKALEMIA- PHYSIOLOGY
 CV
 Mild--Slight increase contractility
 Oxyhgb curve shift left ( decrease O2 delivery to tissue).
 Regional vasoconstriction
ASSESSING OXYGENATION
 Normal value for arterial blood gas 80-100mmHg
 Normal value for venous blood gas 40mmHg
 Normal SaO2
 Arterial: 97%
 Venous: 75%
IMPORTANT POINTS FOR ASSESSING
TISSUE OXYGENATION
 This is the O2 that’s really available at the tissue level.
 Is the Hb normal?
 Low Hb means the ability of the blood to carry the O2 to the tissues is decreased
 Is perfusion normal?
 Low perfusion means the blood isn’t even getting to the tissues
RESPIRATORY ALKALOSIS
 min. Vent. pCo2 & pH
 Most common causes
 Response to hypoxemia
 Response to acute metabolic acidosis
 CNS malfunction
 Correct underlying cause
 Rarely life-threatening
METABOLIC ACIDOSIS
 Causes
 High anion gap = Na - (Cl + HC03)(eg.LA)
 Normal-anion gap (Hyperchloremic)
 Treatment
 Correction of underlying cause
 Administer bicarbonate for life-threatening acidosis
METABOLIC ALKALOSIS
 Usually results from excess acid losses
 Causes
 Loss of gastric juices
 Diuretic therapy
 Adrenal cortical hormone excess
 Hepatic coma(hyper ammonemia )
 Administration of exogenous base
 Almost always accompanied by low K+
 Treatment
Highly acidic, pH =1.0
Secretes HCO3
-
pH varies from
4.0 to 8.0
Vomiting:
Loss of H+
leading to
alkalosis
Diarrhea:
Loss of HCO3
-
leading to
acidosis
Gastrointestinal losses can create acid-base disturbances
APPROACH TO ABG
 Check serum pH –
 Acidemia or Alkalemia ?
 Check PCO2
–
 Is disturbance respiratory or metabolic ?
 Is respiratory disturbance acute ?? Change in pH= -0.08 x (d Pco2/10)
 Is respiratory disturbance non acute ?? Bicarb change = 1-5 x (d Pco2/10)
APPROACH TO ABG
 Check PaO2 ?? -Good guide to patient course.. Not important with regard to Oxygen
Delivery..
 SaO2 - 90 % acceptable for Oxygen delivery.
Let’s Practice
 Case 1;
12 year old diabetic presents with Kussmaul breathing
 pH : 7.05
 pCO2: 12 mmHg
 pO2: 108 mmHg
 HCO3: 5 mEq/L
 BE: -30 mEq/L
 Severe partly compensated metabolic acidosis without hypoxemia due to ketoacidosis
 Case 2;
9 year old w/hx of asthma, audibly wheezing x 1 week, has not slept in 2 nights;
presents sitting up and Using acessory muscles to breath w/audible wheezes
 pH: 7.51
 pCO2: 25 mmHg
 pO2 55 mmHg
 HCO3: 22 mEq/L
 BE: -2 mEq/L
 Uncompensated respiratory alkalosis with severe hypoxia due to asthma exacerbation
 If the previous child was untreated or came later:
 pH: 7.28
 pCO2: 55 mmHg
 pO2 35 mmHg
 HCO3: 28 mEq/L
 BE: +6 mEq/L
 Partially compensated respiratory acidosis with severe hypoxia due to asthma exacerbation
 Case 3;
7 year old post op presenting with chills, fever and hypotension
 pH: 7.25
 pCO2: 32 mmHg
 pO2: 55 mmHg
 HCO3: 10 mEq/L
 BE: -15 mEq/L
 Uncompensated metabolic acidosis due to low perfusion state and hypoxia causing
increased lactic acid
Case 4
A 6 year old girl with severe gastroenteritis is admitted to the
hospital for fluid rehydration, and is noted to have a high [HCO3
-]
on hospital day #2. An ABG is ordered:
ABG: pH 7.47 Chem : Na+ 130
PCO2 46 K+ 3.2
HCO3
- 32 Cl- 86
PO2 96 HCO3
- 33
Urine pH: 5.8
Hypokalemic hypocholiremic metabolic alkalosis
 Thank you

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Acid Base Balance

  • 1. ACID-BASE DISORDERS By Dr. Raneem AlSayed assistant professor of internal medicine and nephrolgy
  • 2. LEARNING OBJECTIVES: By the end of this lecture, you should be able to:  Recognize normal acid base regulation  Recognize the clinical acid-base relationship.  Outline the causes of respiratory acidosis  Outline the causes of respiratory alkalosis  Outline the causes of metabolic acidosis  Outline the causes of metabolic alkalosis  Discuss the role of the kidney in handling the HCO3.
  • 3. Content of the lecture:  Physiology of acid base balance.  Case of respiratory acidosis (chest).  Case of metabolic acidosis (Diabetic keto acidosis , renal tubular acidosis)  Example of metabolic alkalosis  Example of respiratory alkalosis
  • 4.
  • 5. "POTENTIAL OF HYDROGEN" (PH)  The acidity or alkalinity of a solution is measured as pH.  The more acidic a solution, the lower the pH.  The more alkaline a solution , the higher the pH.  Water has a pH of 7 and is neutral.  The pH of arterial blood is normally between 7.35 and 7.45
  • 6. BUFFER SYSTEMS "Ability of weak acid and its corresponding base to resist change in pH of a solution upon adding a strong acid or base"  Regulate pH by binding or releasing Hydrogen  Most important buffer system:  Bicarbonate-Carbonic Acid Buffer System  (Blood Buffer systems act instantaneously and thus constitute the body’s first line of defense against acid-base imbalance)
  • 7. CLINICALLY SIGNIFICANT ACID-BASE PAIRS Acid Carbonic acid (H2CO3) Monobasic PO4 (H2PO4) Ammonium (NH4+) Lactic acid (H6C3O2) Base Bicarbonate (HCO3-) Dibasic PO4 (HPO4-) Ammonia (NH3) Lactate (H5C3O2-)
  • 8. RESPIRATORY REGULATION  Lungs  help regulated acid-base balance by eliminating or retaining carbon dioxide  pH may be regulated by altering the rate and depth of respirations  changes in pH are rapid,  occurring within minutes  normal CO2 level  35 to 45 mm Hg
  • 9. RENAL REGULATION  Kidneys  the long-term regulator of acid-base balance  slower to respond  may take hours or days to correct pH  kidneys maintain balance by excreting or conserving bicarbonate and hydrogen ions  normal bicarbonate level  22 to 26 mEq/L.
  • 10. IS IT RESPIRATORY OR METABOLIC? 1. Respiratory Acidosis 2. Respiratory Alkalosis 3. Metabolic Acidosis 4. Metabolic Alkalosis  Increased pCO2 >50  Decreased pCO2<30  Decreased HCO3 <18  Increased HCO3 >30
  • 11. COMPENSATED OR UNCOMPENSATED— WHAT DOES THIS MEAN? 1. Evaluate pH—is it normal? Yes 2. Next evaluate pCO2 & HCO3 • pH normal + increased pCO2 + increased HCO3 = compensated respiratory acidosis • pH normal + decreased HCO3 + decreased pCO2 = compensated metabolic acidosis
  • 12. COMPENSATED VS. UNCOMPENSATED 1. Is pH normal? No 2. Acidotic vs. Alkalotic 3. Respiratory vs. Metabolic • pH<7.30 + pCO2>50 + normal HCO3 = uncompensated respiratory acidosis • pH<7.30 + HCO3<18 + normal pCO2 = uncompensated metabolic acidosis • pH>7.50 + pCO2<30 + normal HCO3 = uncompensated respiratory alkalosis • pH>7.50 + HCO3>30 + normal pCO2 = uncompensated metabolic alkalosis
  • 13. CAUSES OF ACIDOSIS  Respiratory  Hypoventilation  Impaired gas exchange  Metabolic  Ketoacidosis  Diabetes  Lactic Acidosis  Decreased perfusion  Severe hypoxemia  Renal Failure  Renal Tubular Acidosis  Severe Diarrheal illness
  • 14. ACIDEMIA- PHYSIOLOGIC EFFECTS  Cardiovascular  Mild acidemia--Tachycardia  Severe acidemia -- Bradycardia  Decreased fibrillation threshold  Decreased contractility  Neuromuscular  Increase in CBF -- Headaches/Confusion  Due to hypercarbia or pH ??
  • 15. CAUSES OF ALKALOSIS  Respiratory  Hyperventilation due to:  Hypoxemia  Metabolic acidosis  Neurologic  CNS Lesions  CNS Trauma  Infection  Metabolic  Hypokalemia  Gastric suction or vomiting  Hypochloremia
  • 16. ALKALEMIA- PHYSIOLOGY  CV  Mild--Slight increase contractility  Oxyhgb curve shift left ( decrease O2 delivery to tissue).  Regional vasoconstriction
  • 17. ASSESSING OXYGENATION  Normal value for arterial blood gas 80-100mmHg  Normal value for venous blood gas 40mmHg  Normal SaO2  Arterial: 97%  Venous: 75%
  • 18. IMPORTANT POINTS FOR ASSESSING TISSUE OXYGENATION  This is the O2 that’s really available at the tissue level.  Is the Hb normal?  Low Hb means the ability of the blood to carry the O2 to the tissues is decreased  Is perfusion normal?  Low perfusion means the blood isn’t even getting to the tissues
  • 19. RESPIRATORY ALKALOSIS  min. Vent. pCo2 & pH  Most common causes  Response to hypoxemia  Response to acute metabolic acidosis  CNS malfunction  Correct underlying cause  Rarely life-threatening
  • 20. METABOLIC ACIDOSIS  Causes  High anion gap = Na - (Cl + HC03)(eg.LA)  Normal-anion gap (Hyperchloremic)  Treatment  Correction of underlying cause  Administer bicarbonate for life-threatening acidosis
  • 21. METABOLIC ALKALOSIS  Usually results from excess acid losses  Causes  Loss of gastric juices  Diuretic therapy  Adrenal cortical hormone excess  Hepatic coma(hyper ammonemia )  Administration of exogenous base  Almost always accompanied by low K+  Treatment
  • 22. Highly acidic, pH =1.0 Secretes HCO3 - pH varies from 4.0 to 8.0 Vomiting: Loss of H+ leading to alkalosis Diarrhea: Loss of HCO3 - leading to acidosis Gastrointestinal losses can create acid-base disturbances
  • 23. APPROACH TO ABG  Check serum pH –  Acidemia or Alkalemia ?  Check PCO2 –  Is disturbance respiratory or metabolic ?  Is respiratory disturbance acute ?? Change in pH= -0.08 x (d Pco2/10)  Is respiratory disturbance non acute ?? Bicarb change = 1-5 x (d Pco2/10)
  • 24. APPROACH TO ABG  Check PaO2 ?? -Good guide to patient course.. Not important with regard to Oxygen Delivery..  SaO2 - 90 % acceptable for Oxygen delivery.
  • 26.  Case 1; 12 year old diabetic presents with Kussmaul breathing  pH : 7.05  pCO2: 12 mmHg  pO2: 108 mmHg  HCO3: 5 mEq/L  BE: -30 mEq/L  Severe partly compensated metabolic acidosis without hypoxemia due to ketoacidosis
  • 27.  Case 2; 9 year old w/hx of asthma, audibly wheezing x 1 week, has not slept in 2 nights; presents sitting up and Using acessory muscles to breath w/audible wheezes  pH: 7.51  pCO2: 25 mmHg  pO2 55 mmHg  HCO3: 22 mEq/L  BE: -2 mEq/L  Uncompensated respiratory alkalosis with severe hypoxia due to asthma exacerbation
  • 28.  If the previous child was untreated or came later:  pH: 7.28  pCO2: 55 mmHg  pO2 35 mmHg  HCO3: 28 mEq/L  BE: +6 mEq/L  Partially compensated respiratory acidosis with severe hypoxia due to asthma exacerbation
  • 29.  Case 3; 7 year old post op presenting with chills, fever and hypotension  pH: 7.25  pCO2: 32 mmHg  pO2: 55 mmHg  HCO3: 10 mEq/L  BE: -15 mEq/L  Uncompensated metabolic acidosis due to low perfusion state and hypoxia causing increased lactic acid
  • 30. Case 4 A 6 year old girl with severe gastroenteritis is admitted to the hospital for fluid rehydration, and is noted to have a high [HCO3 -] on hospital day #2. An ABG is ordered: ABG: pH 7.47 Chem : Na+ 130 PCO2 46 K+ 3.2 HCO3 - 32 Cl- 86 PO2 96 HCO3 - 33 Urine pH: 5.8 Hypokalemic hypocholiremic metabolic alkalosis