This document outlines a lecture on acid-base disorders given by Dr. Raneem AlSayed. The learning objectives are to recognize normal acid-base regulation and relationships, outline causes of respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. The content will cover physiology of acid-base balance, case studies of different disorders, and the roles of lungs, kidneys, and buffer systems in regulation. Key concepts to be discussed are the pH scale, clinically significant acid-base pairs, respiratory versus renal regulation, and approaches to analyzing arterial blood gases.

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

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.

25. Let’s Practice

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

31.  Thank you