Acid Base disorders

1. ACID- BASE DISORDERS
Akram Fayed, MD
Fellow, Surgical ICU
Division of Critical Care Medicine
Department of Anesthesia
University of Iowa Hospitals and Clincs

2. Respiratory Metabolic
Acidosis
Respiratory Metabolic
Alkalosis
Acid- Base Disorders

3. Metabolic Acidosis
 Characterized by a primary decrease in bicarbonate
concentration and a compensatory decrease in CO2.
 Occurs from:
1. Loss of bicarbonate through the kidneys or the bowel.
2. Addition of H+:
A. Physiological ( normal metabolism).
B. Pathological ( Lactic acidosis and Diabetic ketoacidosis).
3. Reduced renal ability to excrete an acid load.

4. Metabolic Acidosis
 Has deleterious effects on:
1. Myocardium.
2. Blood vessels.
3. Central nervous system.
4. Diaphragmatic functions.
 Anion Gap:
The difference between measured cations and anions.
Normal: {Na}+ – { Cl}- + {HCO3}- = 8- 14 meq/ L

5. Metabolic Acidosis
Etiologies of Normal- Anion- Gap Metabolic Acidosis:
Gastrointestinal loss of bicarbonate
Diarrhea
Urinary diversion
Small bowel, Pancreatic, or bile drainage (fistulas, drains)
Cholestyramine
Renal loss of bicarbonate
Renal tubular acidosis
Recovery phase of DKA
Renal insufficiency
Posthypocapneic
Acidifying substances
HCl, NH4Cl, MgCl2

6. Metabolic Acidosis
Etiologies of Increased- Anion Gap Metabolic Acidosis:
Ketoacidoses
Diabetic
Alcoholic
Starvation
Lactic Acidosis
Uremia
Toxins
Ethylene Glycol
Methanol
Salicylate
Paraldehyde

7. Metabolic Acidosis
Management:
All medications and other substances contributing to the
acidosis should be withdrawn, if possible.
 In normal anion gap acidosis with an ongoing loss of HCO3,
bicarbonate therapy is indicated in amounts equal to losses.
 Bicarbonate is not effective in DKA ( rebound alkalemia).
 Alcoholic KA responds rapidly to glucose infusion.
 Starvation KA is easily controlled with nutritional support.

8. Metabolic Acidosis
Management:
 Salicylate overdose responds to alkaline diuresis and, if
severe, with hemodialysis
 Methanol and ethylene glycol poisoning, if severe and
associated with metabolic acidosis, should be treated with
Ethanol infusion
 Ethanol competitively inhibits metabolism to toxic products
via alcohol dehydrogenase
 If acidosis remains severe, hemodialysis should be done

9. Metabolic Alkalosis
 Primary increase in bicarbonate concentration and a
compensatory increase in carbon dioxide
 Results from:
1. Elevation of serum bicarbonate concentrations usually
due to acid loss from the stomach or the kidneys
2. Stimulus for bicarbonate reabsorption due to:
A. Hypovolemia with a chloride deficit
B. Hypokalemia
C. Increased mineralocorticoid activity

10. Metabolic Alkalosis
Etiologies of Metabolic Alkalosis:
Chloride- responsive
Renal H+ loss
Diuretic therapy
Posthypercapnia
Penicillin, Ampicillin, Carbenicillin therapy
Gastrointestinal H+ losses
Vomiting
Nasogastric suction
Villous adenoma
Alkali administration
Bicarbonate
Citrate in blood products
Acetate in Parenteral nutrition

11. Metabolic Alkalosis
Etiologies of Metabolic alkalosis:
Chloride Resistant
Increased mineralocorticoids activity
Primary aldosteronism
Cushing’s syndrome
Drugs with mineralocorticoid activity
Profound hypokalemia
Refeeding
Parathyroid disease
Hypercalcemia

12. Metabolic Alkalosis
Management:
 Replacement of diuretic- induced potassium losses with
KCl
 Minimization of Nasogastric suction and use of H2 blockers
with prolonged Nasogastric suction
 Avoid rapid decreases in PaCO2 patients with COPD
 Adequate Chloride must be provided in those cases
associated with volume and chloride deficit

13. Metabolic Alkalosis
Management:
 In volume overload with metabolic alkalosis:
1. Acetazolamide ( reduces bicarbonate)
2. Continuous arteriovenous hemodialysis, which removes
bicarbonate in proportion to its concentration in plasma,
and fluid replacement with a lesser volume of
bicarbonate- free NaCl
Rapid correction:
Indicated at a pH of 7.6 with arginine hydrochloride,
ammonium chloride, and hydrochloric acid

14. Respiratory Acidosis
 Primary increase in PaCO2 and a compensatory increase
in the bicarbonate concentration
 Respiratory acidosis occurs when alveolar ventilation is
decreased relative to CO2 production
 Decrease in alveolar ventilation results from a decrease in
minute ventilation, or from an increase in dead space
without a compensatory rise in minute ventilation
 A rise in CO2 production will not produce hypercapnia unless
ventilation does not increase appropriately

15. Respiratory Acidosis
 This develops in patients with near maximal ventilation
or with fixed mechanical ventilation
 In acute respiratory acidosis, tissue buffers can increase
HCO3 level only by 4 to 5 meq/L so, acidemia is usually
severe
 In chronic respiratory acidosis, increase renal reabsorption
of bicarbonate buffers the acidosis, so acidosis is less
severe even with marked hypercapnia

16. Respiratory Acidosis
 Etiologies of Respiratory Acidosis:
Inhibition of repsiratory control
Drugs ( narcotics, sedatives, anesthetics)
Sleep apnea
CNS lesions
Myxedema
Cerebral Edema
Status asthmaticus
Compensation for metabolic acidosis
Disorders of the chest wall
Kyphoscoliosis
Morbid obesity
Burns

17. Respiratory Acidosis
 Etiologies of Respiratory Acidosis:
Neuromuscular disease
Myasthenia gravis
Guillian- Barre syndrome
Poliomyelitis
Botulism
Severe hypophosphatemia
Severe hypokalemia
Myopathy
Multiple sclerosis
Periodic paralysis
Spinal cord injury

18. Respiratory Acidosis
 Etiologies of Respiratory Acidosis:
Upper airway obstruction
Obstructive sleep apnea
Laryngospasm
Foreign body
Tracheal stenosis
Disorders of the lung
COPD
Asthma
Severe Pneumonia
Pulmonary Edema
Pneumothorax
ARDS

19. Respiratory Acidosis
Management:
 Aimed at reversing the disorders that led to decreased
alveolar ventilation
 All factors leading to respiratory acidosis should be
corrected:
Increasing minute ventilation
Decreasing dead space
Decreasing CO2 production

20. Respiratory Acidosis
Management:
 Narcotic overdose can be reversed with Naloxon
 Aggressive correction is needed in neurologic injuries, as
acidemia can increase cerebral blood flow and intracranial
pressure with a deleterious effects
 Permissive hypercapnia is allowed in ARDS to avoid the
risk of barotrauma

21. Respiratory Alkalosis
 Primary reduction in PaCO2 when alveolar ventilation is
increased relative to CO2 production
A secondary, compensatory, two- phase reduction in
bicarbonate level occurs with:
1. Small acute decrease owing to tissue buffers
2. A large chronic decrease due to renal acid excretion
and an increase in renal bicarbonate excretion

22. Respiratory Alkalosis
Etiologies of respiratory alkalosis:
Hypoxia
High altitude
Pulmonary disease
Decreased Fio2
Profound anemia
Pulmonary disorders
Pneumonia
Pulmonary embolism
Restrictive lung disease
Pulmonary edema
Pneumothorax
Pleural effusion

23. Respiratory Alkalosis
Etiologies of respiratory alkalosis:
Mechanical Ventilation
Increased CNS respiratory dirve
Anxiety and pain
Voluntary hyperventilation
CNS disease ( CVA, Tumors, Infection, Trauma)
Fever
Sepsis and endotoxin
Drugs ( Salicylate, Catecholeamines, progesterone)
Hyperthyroidism
Liver disease
Pregnancy
Exercise
Epinephrine

24. Respiratory Alkalosis
Management:
 Treatment of the underlying cause of hyperventilation
 Alkalemia from respiratory alkalosis does not require
therapy unless superimposed on a metabolic alkalosis,
sedation is then indicated
 In sepsis, a significant portion of cardiac output can go to
the respiratory muscles, intubation and muscle relaxation
can be used to control hyperventilation and redirect blood
flow to more important organs

25. Acid- Base Interpretation
 Any measurement that falls outside the following ranges
is considered to be abnormal:
pH= 7.36 to 7.44
PaCO2 = 36 to 44 mmHg
HCO3 = 22 to 26 mmHg
Rule 1:
A primary metabolic acid- base disorder is present if the
pH is abnormal and the pH and PaCO2 change in the same
direction

26. Acid- Base Interpretation
 Rule 2:
A superimposed respiratory acid- base disorder is present
if any of the following conditions are satisfied
1. The measured PaCO2 is normal.
2. The measured PaCO2 is higher than the expected PaCO2
( denotes superimposed respiratory acidosis)
3. The measured PaCO2 is less than the expected PaCO2
( denotes a superimposed respiratory alkalosis)

27. Acid- Base Interpretation
 Rule 3:
A primary respiratory acid- base disorder is present if the
PaCO2 is abnormal and the PaCO2 and pH change in opposite
Directions
 Rule 4:
A mixed (acidosis and alkalosis) acid- base disorder is
present if the PaCO2 is abnormal and the pH is unchanged
or normal, or if the pH is abnormal and the PaCO2 is
unchanged or normal

28. Acidemia
 If the pH is below 7.36, check the PaCO2 and
proceed as follows:
 A low or normal PaCO2 indicates a primary
metabolic acidosis.
 The difference between the measured and
expected PaCO2 is then used to identify a
superimposed respiratory disorder.
 A high PaCO2 indicates a primary respiratory
acidosis.
 The change in pH is then used to determine
whether the disorder is acute or chronic.

29. Alkalemia
 If the pH is above 7.44, check the PaCO2 and
proceed as follows:
 A normal or high PaCO2 indicates a primary
metabolic alkalosis.
 A comparison of the measured and expected
PaCO2 is then used to identify an associated
respiratory disorder.
 A low PaCO2 indicates a primary respiratory
alkalosis.
 The change in pH is then used to determine
whether the disorder is acute or chronic, or
whether a superimposed metabolic disorder is
present.

30. Normal pH
 If the arterial pH is unchanged or normal, the
PaCO2 should be checked:
 A high PaCO2 indicates a mixed respiratory
acidosis- metabolic alkalosis.
 A low PaCO2 indicates a mixed respiratory
alkalosis- metabolic acidosis.
 A normal pH combined with a normal PaCO2 is not
absolute evidence against an acid- base disorder
because a metabolic acidosis coexisting with a
metabolic alkalosis can be accompanied by a
normal pH and PaCO2.

31. Expected Changes In Acid- Base Disorders
Primary Disorder Expected Changes
Metabolic Acidosis PaCO2= 1.5* HCO3+(8±2)
Metabolic Alkalosis PaCO2= 0.7* HCO3+(21±2)
Acute Respiratory Acidosis ΔpH= 0.008 * (PaCO2-40)
Chronic Respiratory Acidosis ΔpH= 0.003 * (PaCO2-40)
Acute Respiratory Alkalosis ΔpH= 0.008 * (40- PaCO2)
Chronic Respiratory Alkalosis ΔpH= 0.017 * (40- PaCO2)

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36. Respiratory Metabolic
Acidosis
Respiratory Metabolic
Alkalosis
Acid Base Disorders