The document outlines the fundamentals of acid-base balance, detailing blood pH, buffering systems, and types of acid-base disorders including acidosis and alkalosis. It explains the roles of blood components, the anion gap, arterial blood gases, and compensation mechanisms within the body. The document also describes common causes of metabolic and respiratory acid-base imbalances and methodical approaches to analyzing arterial blood gas results.

1. Dr. Saif Ababneh

2. outlines
 Blood pH and buffering systems
 Anion gap
 Normal ABG vs VBG
 Types of acid-base disorders

3.  Normal arterial blood pH range from 7.35-7.45.
 Blood pH inversely related to [H+], the more [H+] the lower the pH
 Blood pH is maintained by the balance between acid production in the
body and the function of the buffering systems, kidneys & lung.
 Buffering systems inculde: bicarbonate, phosphate, negative charged
proteins, ammonia  (any – charged molecule act as a buffering molecule
that bind’s H+)
 CO2 is considered acidic, we lose it by ventilation, (hyper ventilation =
more CO2 washout, hypoventilation = more CO2 retention in the body)
 The kidneys also control acid-base balance, through absorption or
secretion of HCO3- & H+.

4. Acidosis vs Alkalosis
 Acidosis : decrease pH of the blood (<7.4):
- Etiology of acidosis:
1- respiratory acidosis (due to CO2 retention “hypoventilation”)
2- metabolic acidosis due to increase acid production or bicarbonate loss
 Alkalosis: increase pH of blood (>7.4):
- Etiology of alkalosis:
1-respiratory alkalosis (due to hyperventilation)
2-metabolic alkalosis (due to increase bicarbonate absorption or increase
acid loss)

5. Normal ABG and MVBG

6. Anion gap (AG)
 Anion gap = [Na+] – ([HCO3-] + [Cl-])
 AG represents the anions “other than Cl- and HCO3
-” that are necessary to
counterbalance Na+ electrically
 Normal anion gap is 12 ± 2, any increase in AG > 14 is called wide anion
gap.
 AG is only important in metabolic acidosis.
Arterial blood gases ABG
• Arterial blood gases include the measurement of arterial PaCO2, PaO2,
blood pH, [HCO3-], O2 saturation “O sat”.
• Mixed venous blood gases include the measurement of PvCO2, PvO2,
venous blood pH, [HCO3-], O2 saturation

8. Metabolic acidosis
 Metaolic acidosis: decrease in blood PH due to increase acid production or increase bicarbonate loss
 Wide AG metabolic acidosis :
- Increased acid production:
1-Diabetic Ketoacidosis.
2-Alcoholic.
3-Starvation .
4-Lactic acidosis. (mesenteric ischemia, septic shock, hemorrhage)
5-Toxic ingestion (salicylates, ethylene glycol, methanol).
6- Renal failure.
 Aspirin (salisylic acid)  will cause mixed disorder (both respiratory alkalosis and metabolic acidosis)
 Normal AG metabolic acidosis :
- Renal tubular dysfunction:
1- Renal tubular acidosis
2- Hypoaldosteronism
3- Potassium-sparing diuretics, carbonic anhydrase inhibitors (acetazolamide).
- Loss of alkali
1- Diarrhea
2- GI fistula: pancreatic fistula, biliary fistula,
- Administration of acids that contain chloride (HCl, ammonium chloride, cationic amino acids)
- Excessive rehydration with normal saline (due to dissociation of H2CO3)

9. Metabolic alkalosis
- most commonly results from either diuretic use or gastrointestinal losses, such
as in vomiting or with Cushing syndrome, Primary aldosteronism, Bartter
syndrome.
- If the etiology of the alkalosis is unclear from the examination, a urinary
chloride concentration may be measured. Gastrointestinal losses are noted to
have low urinary chloride levels (< 20 mEq/L), while patients currently on
diuretic therapy present with high urinary chloride levels (>20 mEq/L).
- Associated with extracellular fluid volume (chloride) depletion
Vomiting or gastric drainage
Diuretic therapy (loop diuretics, thiazide diuretics).
Posthypercapnic alkalosis
- Associated with mineralocorticoid excess
Cushing syndrome
Primary aldosteronism
Bartter syndrome
- Severe K+ depletion
- Excessive alkali intake

10. Respiratory acidosis
 Ventilation depends on two factors: respiratory rate and tidal volume.
 Respiratory acidosis is an acid-base balance disturbance due to alveolar
hypoventilation (decrease CO2 exchange) or increase CO2 production.
 The hallmark of respiratory acidosis is increase in PCO2.
1- decrease CO2 exchange :
- COPD (emphysema), obesity, pleuritic chest pain, morphine, hypnotics,
disease affectinig NMJ or motor neurons of the diaphragm ( botulism,
GBS), Chest wall disorders Severe kyphoscoliosis, flail chest, and, less
commonly, ankylosing spondylitis, pectus excavatum, or pectus carinatum.
 Steroids  will cause mixed disorder (both respiratory acidosis and
metabolic alkalosis)
2- increase in CO2 production: in case of malignant hyperthermia

11. Respiratory alkalosis
 is the result of acute or chronic hyperventilation.
 The causes of respiratory alkalosis include:
1- acute hypoxia (e.g., pneumonia, pneumothorax, pulmonary embolism,
pulmonary edema, bronchospasm),
2- chronic hypoxia (e.g., cyanotic heart disease, anemia),
3- respiratory center stimulation (e.g., anxiety, pain, fever, Gram-negative
sepsis, salicylate intoxication, central nervous system disease, cirrhosis,
pregnancy).
4- Excessive ventilation may also cause respiratory alkalosis in the
mechanically ventilated patient.
 Clinical findings are noanspecific  Carpopedal spasm maight occur??
 the only effective treatment is correction of the underlying disorder.

12. compensation
 When the blood pH decrease due to hypoventilation  the kidney will try
to normalize the pH so it will start to absorb HCO3-
 When the pH degrease due to increase acid production or decrease
excretion from the kidney  the respiratory system will try to normalize
that pH by hyperventilation (CO2 washout).
 The same principles applied to any increase in pH, so the kidney or the
lung will try to compensate each other.
 Compensation will try to normalize the blood pH, but it can’t return it to
the normal value (7.4)

13. Respiratory compensation
 Respiratory compensation: occur in case of metabolic imbalance (M. alkalosis or
M.acidosis).
 Respiratory compensation: based on winter’s formula:
 Winters' formula:is a formula used to evaluate respiratory compensation when
analyzing acid–base disorders and a metabolic acidosis is present. It can be given
as:
 PCO2 = ( 1.5 × HCO3− ) + 8 ± 2
 where HCO3− is given in units of mEq/L and pCO2 will be in units of mmHg.
 Winters' formula gives an expected value for the patient's PCO2; the patient's actual
(measured) PCO2 is then compared to this:
- If the two values correspond, respiratory compensation is considered to be
adequate.
- If the measured PCO2 is higher than the calculated value, there is also a secondary
respiratory acidosis or mixed acid base disorder.
- If the measured PCO2 is lower than the calculated value, there is also a secondary
respiratory alkalosis or mixed acid base disorder.

14. Metabolic compensation
 Occur in case of respiratory imbalance (R.acidosis or R.alkalosis).

15. How to read ABG
 Check the pH  7.4 normal, (>7.4 alkalosis), (<7.4 acidosis)
 Check [HCO3-]: is it directly related to pH or not?
- yes  metabolic
no  respiratory
normal  check pCO2  if normal then normal ABG
 is there appropriate compensation or not?
- yes  pure metabolic or respiratory cause
no  mixed condition (both respiratory and metabolic problem together)
 if there is metabolic acidosis  check the AG (wide or normal)

16. Case 1
 PCO2 = ( 1.5 × HCO3− ) + 8 ± 2
 1.5 X 11.5 +8 ± 2 = 23 – 27 mmHg
 AG = 128 – (82 +11.5) = 34 wide anion gap

17. Case 2
 PCO2 = ( 1.5 × HCO3− ) + 8 ± 2
 1.5 x 37 + 8 ± 2 = 61 - 66

18. Case 3
 PCO2 = ( 1.5 × HCO3− ) + 8 ± 2
 1.5 x 9 + 8 ± 2 = 19.5 – 23.5
 AG= 101 – 73 -9 = 19

19. Case 4
 Lactate elevated

20. Answers:
 Case 1: mixed wide anion gap metabolic acidosis and respiratory acidosis
.
 Case2: metabolic alkalosis wit respiratory compensation (NG suction).
 Case 3: mixed wide anion gap metabolic acidosis and respiratory
alkalosis: aspirin toxicity.
 Case 4: mixed wide AG m.acidosis and respiratory acidosis (seizure)