This document discusses acid-base disorders and summarizes key points about acid-base balance, buffers, and the mechanisms that maintain homeostasis. It covers the respiratory, renal, and extracellular buffering systems and how they compensate for acid-base imbalances. Metabolic acidosis is discussed in depth, including causes like renal tubular acidosis and lactic acidosis. Treatment focuses on correcting the underlying disorder and using oral or intravenous sodium bicarbonate to gradually normalize pH.

1. Acid-Base disorders
Email:asterwakjira@gmail.com
By: Aster Wakjira
(B.Pharm ,MSc,clinical Pharmacist)

2. Acid-Base Balance
 Acidity of body fluids is quantified by hydrogen ion
concentration
🞑 pH…… degree of acidity
🞑 Inverse relationship between [H+] and pH
 Normal blood pH …..7.4
🞑 Used to analyze acid-base status
 Hydrogen ion concentration in blood may not be indicative of
concentration in other body compartments
2

3. Acid-Base Balance ….
 Three mechanisms collectively maintain acid–base balance:
🞑 Extracellular buffering
🞑 Ventilatory regulation of carbon dioxide elimination
🞑 Renal regulation of hydrogen ion and bicarbonate excretion
 Buffering
🞑 Ability of a weak acid and its corresponding anion (base) to
resist change in pH of a solution on addition of a strong acid or
base.
3

4. Extracellular Buffering
-
 Carbonic acid/bicarbonate system (H2CO3/ HCO3 )
🞑 the most important physiologic buffer system
-
 More HCO3 in ECF than any other buffer component
 CO2 supply is unlimited
-
 Acidity of ECF can be regulated by HCO3 concentration or PCO2
🞑 H2CO3 ….. respiratory component
 Changes in ventilation  changes in PCO2  regulates H2CO3level
🞑 HCO3
- …..metabolic component
-
 regulated by kidney: alters its reabsorption, generate new HCO3 , and
alters its elimination
4

5. Cont’d
 Phosphate buffer system
🞑 consists of serum inorganic phosphate, intracellular organic
phosphate, calcium phosphate in bone,
🞑 low extracellular concentration of phosphate and it is more
important as intracellular buffer
 Proteins as buffering systems
🞑 buffering provided by charged side chains of amino acids
🞑 more important as intracellular buffer because the concentration
of protein is much greater intracellularly than extracellularly
5

6. Respiratory Regulation
 Rate and depth of ventilation regulates excretion of CO2
generated by diet and tissue metabolism;
🞑 Increase respiratory rate →increase CO2 excretion →decrease
blood PCO2
🞑 Decrease respiratory rate →decrease CO2 excretion →increase
blood PCO2
 This system rapidly adjusts within minutes to changes in
acid–base balance.
6

7. Renal Regulation
 The kidney plays a central role in the regulation of acid–
base homeostasis through ….
🞑 excretion or reabsorption of filtered HCO3
-,
🞑 excretion of metabolic fixed acids
🞑 generation of new HCO3
-
 To maintain acid–base balance, the entire filtered HCO -
3
load must be reabsorbed, primarily in the proximal tubule.
7

8. Renal Regulation….
 In the tubular lumen, filtered HCO - combines with H+ secreted
3
by the Na+/H+-exchanger to form carbonic acid (H2CO3).
 H2CO3 is rapidly broken down to CO2 and water by carbonic
anhydrase located on the luminal surface of brush border
membrane.
 CO2 then diffuses into the proximal tubular cell, where it
reforms H2CO3 in the presence of intracellular carbonic
anhydrase.
 H2CO3 dissociates to form H+ that can again be secreted into
3
the tubular lumen, and HCO - that exits the cell and enters the
peritubular capillary.
8

9. 9
Renal Regulation….
Proximal tubular bicarbonate reabsorption

10. Renal Regulation….
 Excretion of metabolic fixed acids and generation of new
–
HCO3 is achieved via….
🞑 renal ammoniagenesis
🞑 distal tubular H+ secretion
 Ammoniagenesis plays a role in acid-base homeostasis,
🞑 ammonium (NH4
+) excretion comprise ~50% of renal acid
excretion
🞑 for each NH4
+ excreted in the urine, one HCO3
– is regenerated
and returned to the circulation.
10

11. Renal Regulation….
 Collecting duct acid excretion ….
🞑 Distal tubular H+ secretion accounts for 50% of net acid
excretion
🞑 In the distal tubular cell, CO2 combines with water in the
presence of intracellular carbonic anhydrase to form carbonic
acid, which dissociates to H+ and HCO3
−.
🞑 H+ is actively secreted into the tubular lumen.
🞑 HCO3
− exits the cell and enters the peritubular capillary.
11

12. Renal Regulation….
Collecting duct acid excretion
12

13. Arterial Blood Gas Analysis
 Blood gases (ABGs) are measured to determine the patient’s
acid–base status.
 Low pH values (<7.35) indicate an acidemia, whereas high pH
values (>7.45) indicate an alkalemia.
 In a metabolic acidosis, the pH is decreased in association with a
decreased serum bicarbonate concentration and a compensatory
decrease in PaCO2.
 In a respiratory acidosis, the pH is decreased; the PaCO2,
however, is elevated.
13

14. Arterial Blood Gas Analysis….
 In a metabolic alkalosis, the pH is elevated in association with
an increased bicarbonate concentration and a compensatory
increase in PaCO2.
 In a respiratory alkalosis, the pH is also elevated; the PaCO2,
however, is decreased.
 The normal values of each measurement;
🞑 pH = 7.4
🞑 PaCO2 = 40 mm Hg (5.3 kPa)
🞑 [HCO3
− ]= 24 mEq/L (24 mmol/L)
[PaCO : partial pressure of carbon dioxide]
14

15. Arterial Blood Gas Analysis….
15
pH
< 7.35
Acidemia
↑ PCO2
Respiratory
acidosis
↓ HCO3
Metabolic
acidosis
7.35 – 7.45
Normal or
compensated
disorder or mixed
disorder
> 7.45
Alkalemia
↓ PCO2
Respiratory
alkalosis
↑ HCO3
Metabolic
alkalosis

16. Interpretation of simple Acid–Base
Disorders
Acid or Base
Disorder
pH Primary
Disturbances
Compensation
ACIDOSIS
Respiratory   PaCO2
 HCO3-
Metabolic 
 HCO3- PaCO2
ALKALOSIS
Respiratory   PaCO2
 HCO3-
Metabolic 
 HCO3-  PaCO2
16

17. Acid-Base Disturbances
Physiologic Compensatory responses
 Metabolic acidosis: the respiratory response to metabolic
acidosis is hyperventilation, which results in an ↓d PaCO2.
🞑 ↑respiratory rate  ↑CO2 excretion  ↓PaCO2
 Metabolic alkalosis: hypoventilation results in an ↑d PaCO2.
🞑 Decrease respiratory rate  decrease CO2 excretion  increase
PaCO2
17

18. METABOLIC ACIDOSIS
 Decrease in serum bicarbonate concentration  ↓pH
 Pathophysiology
🞑 Buffering (consumption) of exogenous acid
🞑 Accumulation of organic acid due to metabolic disturbance
 e.g., lactic acid or ketoacids
🞑 Accumulation of endogenous acid due to impaired renal function
(e.g., phosphates and sulfates).
🞑 loss of bicarbonate-rich body fluids (e.g., diarrhea, biliary drainage)
🞑 Adm’n of non-alkali–containing IV fluids (dilutional acidosis)
18

19. Laboratory
 Serum anion gap (SAG)
🞑 SAG = [Na+] – [Cl-] – [HCO3
-]
🞑 SAG = [UAs] – [UCs]
🞑 Normal range 3 to 11 mEq/L (3 to 11 mmol/L)
🞑 High aniongap ---- accumulation of unmeasured anions in ECF.
 [UAs: unmeasured anions, UCs: Unmeasured cations]
19

20. Metabolic
acidosis
SAG normal or
Hyperchloremic
states
GI HCO3
- loss
Drugs (magnesium sulfate,
calcium chloride)
Renal tubular acidosis (RTA)
SAG elevated
Renal failure
Lactic acidosis
Ketoacidosis
Salicylate overdose,
ingestion of methanol
or ethylene glycol
Starvation
20
-
SAG: serum anion gap; GI: gastrointestinal; HCO3 : bicarbonate

21. Hyperchloremic Metabolic Acidosis
 Causes
🞑 Increased GIT bicarbonate loss
 Diarrhea, biliary drainage
🞑 Renal bicarbonate wasting
 Proximal RTA, carbonic anhydrase inhibitors
🞑 Impaired renal acid excretion
 Distal RTA, moderate to severe renal insufficiency
🞑 Exogenous acid gain
 Hydrochloric acid, parenteral nutrition with unbuffered acid salts of
amino acids
21

22. Renal Tubular Acidosis (RTA)
 Type I (distal)
🞑Decreased distal acidification
 Urine pH during acidemia--- > 5.3
-
🞑Plasma [HCO3 ]---may be < 10 mEq/L
🞑Plasma [K+] ----usually reduced or normal
🞑Associated disease states
 Tubule defect, Multiple myeloma, Systemic lupus erythematosus,
Sjögren’s syndrome, Sickle cell disease, Renal transplant rejection
following amphotericin B, Nephrocalcinosis
22

23. Renal Tubular Acidosis….
 Type II (proximal)
-
🞑 Decreased proximal HCO3 reabsorption
-
🞑 Plasma [HCO3 ] ---- usually 14–20 mEq/L
🞑 Urine pH during acidemia--- variable: > 5.3 or < 5.3
🞑 Plasma [K+] --- normal or reduced
🞑Associated disease states
 Fanconi syndrome, Nephrotic syndrome, Paroxysmal nocturnal
hemoglobinuria, Carbonic anhydrase inhibitors, Impaired proximal
tubular glucose, phosphate, amino acid reabsorption
23

24. Renal Tubular Acidosis….
 Type IV (distal)
🞑Aldosterone deficiency or resistance
-
🞑 Plasma [HCO3 ] --- usually >15 mEq/L
🞑 Urine pH during acidemia---- <5.3
🞑 Plasma [K+] ----- Elevated
🞑Associated disease states
 Primary mineralocorticoid deficiency (Addison disease)
 Hyporeninemic hypoaldosteronism (diabetic nephropathy, mild
renal impairment)
 Impaired tubular potassium secretion and urinary obstruction
24

25. Elevated SAG Metabolic Acidosis
 Increased endogenous organic acid production
🞑 Anaerobic metabolism  lactic acid
🞑 Uncontrolled diabetes mellitus, alcohol intoxication, starvation
 ketoacids
🞑 Renal failure  accumulation of phosphate, sulfate, organic
anions
🞑 Likely present if SAG > 25 mEq/L
 Methanol/ethylene glycol ingestion
25

26. Lactic Acidosis
 Common cause of elevated SAG metabolic acidosis
 Glycolysis  lactic acid
🞑 In normal states, it is reoxidized and metabolized to CO2 and
H2O
 Present if lactate concentration > 4 to 5 mEq/L in acidemic
patients
26

27. Lactic Acidosis Causes
 Decrease in tissue oxygenation [tissue hypoxia] (type A)
🞑 Shock, Severe anemia, CHF, CO poisoning
 Deranged oxidative metabolism (type B)
🞑 Medications
 Catecholamines, metformin, NRTIs
 Overdose (iron, isoniazid, salicylates, theophylline)
 Propofol infusion syndrome, Propylene glycol toxicity, Na nitroprusside
🞑 Methanol, ethanol, ethylene glycol
🞑 Diabetes mellitus, Malignancy
🞑 Disorders associated with inborn errors of metabolism
27

28. Metabolic Acidosis Clinical Presentation
 Acute
🞑 Severe acidemia: pH < 7.15 to 7.20
 Chronic:
🞑 usually not associated with severe acidemia
🞑 relatively asymptomatic
🞑 Bone demineralization- major manifestation
 Laboratory Tests
🞑 Low serum CO2
🞑 Hyperglycemia and hyperkalemia are common
🞑 pH < 7.2 = severe acidosis
28

29. Metabolic Acidosis Clinical Presentation
Signs/symptoms
 Cardiac
🞑 Initial: flushing, rapid HR, wide pulse pressure, ↑in cardiac output
🞑 Later: ↓in cardiac output, BP, liver & kidney blood flow
 Cerebral: coma
 Metabolic: insulin resistance, increased protein degradation
 GI: nausea, vomiting, loss of appetite
 Respiratory: dyspnea, hyperventilation with deep, &rapid respiration
PhysiologicCompensation
 ↑respiratory rate  ↑CO2 excretion  ↓PaCO2
29

30. Chronic Metabolic Acidosis Treatment
 Always treat underlying disease states
 Mild to moderate acidemia
🞑Gradual correction
🞑Oral alkali replacement
 GI disorders: replace other electrolytes as needed
 RTAwith hyporeninemic-hypoaldosteronemia (type IV)
 May be corrected by treating hyperkalemia
 Supplemental alkali
30

31. Oral Alkali Replacement
- - -
 LD = VDHCO3 x BW x (desired [HCO3 ] – current [HCO3 ])
-
 E.g., If 60 kg and HCO3 is 15 mEq/L
🞑 LD = (0.5 L/kg x 60 kg) x (24 mEq/L – 15 mEq/L)
= 30 L x 9 mEq/L
= 270 mEq/L
 Give doseoverseveral daysto avoidvolume overloadfrom the
accompanyingNa load.
31
LD: loading dose; VD: volume of distribution; BW: body weight

32. Acute Severe Metabolic Acidosis Treatment
 Focus treatment on correcting underlying cause,
cardiovascular status
 Emergent hemodialysis may be needed
 IV alkali (sodium bicarbonate)
🞑 Most widely used IV alkali
🞑 Often ineffective
🞑 May be deleterious in lactic acidosis
🞑 to increase arterial pH to ~7.20.
 No controlledstudies havedemonstratedit decreasesmorbidity/ mortality vs.
supportivecare
32

33. Pharmacologic Therapy
 Oral alkali replacement
🞑 Shohl’s solution (sodium citrate/citric acid)
🞑Sodium bicarbonate
🞑Potassium citrate
🞑 Potassium bicarbonate/potassium citrate
🞑Potassium citrate/citric acid
🞑 Sodium citrate/potassium citrate/citric acid
33

34. Sodium Bicarbonate
 Provides
🞑 Fluid and electrolyte replacement
🞑 Increases arterial pH
 Paradoxical effect with IV infusion
🞑 Can ↓ intracellular PH
 the CO2 generated diffuses morereadily than HCO3- across CM
 Excessive administration can result in
🞑 Impaired oxygenation of tissues
🞑 Sodium and water overload
🞑 Paradoxical tissue acidosis
34

35. Sodium Bicarbonate Dosing
 Prevent overshooting
🞑 Consider endogenous sources of bicarbonate
🞑 Goal: increase, not normalize, pH and plasma bicarbonate
🞑 Consider using VD of 50% of body weight─ to avoid
overtreatment
 Monitoring
🞑 ABGs 30 minutes after end of infusion to guide therapy
35

36. Investigational Therapies
 Carbicarb
🞑 Equimolar mixture of sodium carbonate and sodium
bicarbonate
🞑 Can correct intracellular acidosis if present
 Dichloroacetate (DCA)
🞑 Stimulates lactate dehydrogenase
🞑 Controlled studies comparing to conventional therapy show no
improved outcomes
36

37. METABOLIC ALKALOSIS
Pathophysiology
 It is an acid–base disorder that presents as alkalemia (↑d
arterial pH) with an increase in plasma bicarbonate.
 Evaluation of patients with metabolic alkalosis must consider
two separate issues:
🞑 the initial process that generates the metabolic alkalosis
🞑 alterations in renal function that maintain the alkalemic state
 Initial interpretation of labs
🞑 PaCO2 (mmHg) should increase by 0.4 to 0.6 times the rise in
plasma [HCO3
-]
37

38. Generation of metabolic alkalosis
 Excessive H+ loss from kidneys or stomach
 Ingestion of bicarbonate-rich fluids
 Diuretics that act on:
🞑 Thick ascending limb of the loop of Henle, e.g., furosemide
🞑 Distal convoluted tubule, e.g., thiazides
 Excessive mineralocorticoid activity
🞑 stimulate collecting duct H+ secretion→ ↑d renal acid excretion
 High dose penicillins….. act as nonreabsorbable anions,
🞑 in the distal renal tubule, ↑electronegativity
🞑 ↑secretion of potassium and H ions .
38

39. Maintenance of Metabolic Alkalosis
 Impaired renal bicarbonate excretion
🞑Sodium chloride-responsive
 Volume-mediated
 Intravascular volume depletion
 ↓GFR ---↓filtered bicarbonate ---↓bicarbonate excretion
 ↑ tubular Na reabsorption (with reabsorption of Cl- or HCO3-, or
exchange K or H) to maintain charge neutrality
🞑 Sodium chloride-resistant
 Volume-independent
 Excess mineralocorticoid activity … ↑H ion secretion
 Persistent hypokalemia─ ↑ HCO3 reabsorption and ↑ H secretion
- +
39

40. Metabolic Alkalosis Clinical Presentation
 Mild to moderate
🞑 No unique signs or symptoms, but related to underlying cause of
the disorder. e.g., muscleweaknesswith hypokalemia, posturaldizziness
with volume depletion
🞑 history of vomiting, gastric drainage, or diuretic use
 Severe alkalemia (blood pH >7.6)
🞑 Associated with arrhythmias, hyperventilation, hypoxemia
🞑 Neuromuscular irritability, with signs of tetany
🞑 Mental confusion, Muscle cramping
 The respiratory response to metabolicalkalosis is hypoventilation (decreaserespiratory
rate)  decreaseCO2 excretion increasePaCO2
40

41. Pharmacologic Therapy
Sodium chloride-responsive disorders
 resulted from volumedepletion& chlorideloss, which can accompany
severevomiting, diuretictherapy.
 Sodium & potassium chloride-containing solutions (e.g., NS)
🞑 for patients who can tolerate the volume load
 Carbonic anhydrase inhibitor,
 For patients who are volume overloaded or intolerant to volume
administration because of CHF
🞑 e.g., Acetazolamide---Inhibits renal bicarbonate reabsorption
 250 to 375 mg once or twice daily
41

42. Cont’d
 Acidifying agents (HCl, ammonium chloride)
🞑 for severe (initial pH >7.6) symptomatic metabolic alkalosis
 HCl dosing: Infuse IV over 12 to 24 hrs, with the rate of 100 to
125mL/h (10 to 25 mEq/h)
🞑 usually infused as a 0.1 to 0.25N HCl solution in either D5W or
NS, or sterile water, or parenteral nutrient solutions
🞑 Check ABGs and electrolytes every 4 to 8 hrs to guide therapy
🞑 too quick infusion ---- severe transient respiratory acidosis
🞑 Stop infusion when pH decreases to 7.5 to prevent overcorrection
 Ammonium chloride--- limited use
42

43. Cont’d
Sodium chloride-resistant disorders
 Treat the underlying cause: mineralocorticoidexcess
🞑In patients taking corticosteroid,
 Adjust corticosteroid therapy, or switch to a corticosteroid with
less mineralocorticoid activity e.g., methylprednisolone
🞑 For endogenous excess mineralocorticoid, eg. aldosterone
 Spironolactone--- antagonist of aldosterone-receptor thus inhibits
Na+ reabsorption and H+ secretion.
 Amiloride and triamterene---inhibit aldosterone-stimulated Na
reabsorption in the collecting duct
 May require surgery
43

44. 44
See next slide
Metabolic Alkalosis Treatment

45. 45
See previous slide

46. RESPIRATORY ALKALOSIS
 It is characterized by a primary ↓PaCO2 that leads to an ↑pH.
🞑 Respiratory excretion of CO2 exceeds its metabolic production.
 occur physiologically in normal pregnancy& at highaltitudes.
🞑 Low O2 content of air stimulate respiration--cause excess loss of CO2
 Stimulation of respiration
🞑 Anxiety, fever; brain tumors, vascular accidents, head trauma;
pregnancy; catecholamines, theophylline, nicotine, salicylates
🞑 Pulmonary emboli, Asthma
 Hypoxemia
🞑 High altitude, pneumonia, pulmonary edema, severe anemia
46

47. Respiratory Alkalosis— Clinical Presentation
 Mild and chronic
🞑 Most patients asymptomatic
 Severe:
🞑 ↓PaCO2 ----- ↓d cerebral blood flow
 Light-headedness, confusion, ↓d intellectual function, syncope, seizures
🞑 Nausea, Vomiting---- cerebral hypoxia
🞑 Cardiac arrhythmiasdue to sensitization of myocardium to circulating
catecholamines
🞑 Muscle cramps, tetany---due to reductions in the blood ionized Ca
 ↑ pH  ↑ binding of Ca to albumin
47

48. Respiratory Alkalosis— Clinical Presentation
 Laboratory Tests
🞑 Serum chloride concentration usually slightly ↑d
🞑 ↓d serum ionized Ca , potassium, phosphorus concentrations
 Acute alkalosis: Plasma [HCO -] should decrease by 0.2 times
3
the decrease in PaCO2 but usually not to <18 mEq/L
 Chronic alkalosis: Plasma [HCO -] should fall by 0.35 times
3
the decrease in PaCO2 but usually not to <14 mEq/L
48

49. Physiologic Compensation
 Compensation for acuterespiratory alkalosis
🞑 Occurs within minutes
🞑 Chemical buffering
 H+ release from physiologic buffers (such as intracellular proteins,
phosphates,) and titrate down the serum bicarbonate concentration.
 Metabolic compensation occurs when the alkalosis persists for
> 6 to 12 hrs
🞑 Renal compensation….within 1 to 2 days
 Inhibition of proximal tubule bicarbonate reabsorption
49

50. Respiratory Alkalosis Treatment
 Mild pH alteration (pH not exceeding 7.5)
🞑 Few or no symptoms,…..treatment often not required
 Acute respiratory alkalosis (pH >7.5)
🞑 Identify and correct underlying causes
🞑 Oxygenif severe hypoxemia
 Life threatening (pH >7.6)
🞑 May require mechanical ventilation with sedation to control
hyperventilation.
50

51. RESPIRATORY ACIDOSIS
 Occurs when the lungs fail to excrete CO2  decrease pH
 Causes;
🞑Respiratory center inhibition (CNS depression)
 Neurologic disorders, Drugs: anesthetics, opioids, sedatives
🞑 Neuromuscular abnormalities
 Myasthenia gravis
 Diaphragmatic paralysis
🞑Airway and pulmonary abnormalities
 Airway obstruction, Asthma, COPD,…
51

52. Respiratory acidosis—Clinical presentation
 Usually symptomatic
🞑 Confusion, difficulty thinking, headache
 Signs
🞑 Cardiovascular
 Moderate: increased cardiac output
 Severe: cardiac output declines and vascular resistance decreases leading
to refractory hypotension
🞑 CNS: neurologic symptoms (including altered mental status,
abnormal behavior, seizures, stupor, coma)
 Headache,Papilledema —due to the vasodilator effects of CO2 in the
brain that result in an increase in cerebral blood flow
52

53. Cont’d
 Laboratory tests
🞑 Moderate increase in serum potassium
🞑 Moderate to severe hypercapnia
 PaCO2 = 50 to 55 mm Hg (moderate), PaCO2 >80mm Hg (severe)
🞑 Hypoxia often present (PaO2 <70 mm Hg)
🞑 Acute acidosis: plasma [HCO3-] should increase by 0.1 times the
increase in PaCO2
🞑 Chronic acidosis: plasma [HCO3-] should increase by 0.35 times the
increase in PaCO2
53

54. Physiologic Compensation
 Acute respiratoryacidosis
🞑 Chemical buffering
 Increase PaCO2  increase H2CO3 dissociation  H+ release
 H+ buffered by bicarbonate and nonbicarbonate buffers
  Serum bicarbonate is increased
 Respiratory acidosis >12 to 24 hours
🞑 Metabolic compensation
 Increase tubular bicarbonate reabsorption, and hydrogen secretion
Increase serum bicarbonate
54

55. Respiratory Acidosis Treatment
 Acute respiratoryacidosis
🞑 Restore adequate oxygenation
🞑 Treat underlying causes
🞑 Bicarbonate rarely needed and rapid correction of acidosis with
bicarbonate may precipitate metabolic alkalosis.
 Monitor ABGs every 2 to 4 hours then every 12 to 24 hours
as acidemia improves
55

56. Respiratory Acidosis Treatment
 Chronicrespiratoryacidosis
🞑 Goals of therapy---adequate oxygenation.
🞑 Adequate oxygenation
 PaO2 = 50 mmHg: oxygen not necessary
 PaO2 <50 mmHg: initiate oxygen slowly using controlled flow
🞑 Treat underlying causes
🞑 Check ABGs periodically
 If PaCO2 increases during oxygen therapy---indicate syndrome of carbon
dioxide narcosis-----thus, need to discontinue O2 therapy
56

57. MIXED ACID-BASE DISORDERS
Diagnosis
 Blood gases do not decreasewithin range of expected
responses for a simple acid-base disturbance.
🞑 Suspect a mixed disorder
🞑 Perform a thorough history and physical exam for common
causes
57

58. Mixed Respiratory Acidosis and Metabolic Acidosis
 Develop in cardiopulmonary arrest, chronic lung disease, shock,
and in metabolic acidosis pts who develop respiratory failure
 Compensatory mechanisms inhibited
🞑 Respiratory decrease in PaCO2
🞑 Buffering and renal mechanisms that increase bicarbonate
🞑 Thus, the pH decreases markedly.
 Treatment
🞑 Oxygenation [to improve hypercarbia and hypoxia]
🞑 Alkali to reverse the metabolic acidosis
58

59. Mixed Respiratory Alkalosis and Metabolic
Alkalosis
 Most common mixed acid-base disorder
🞑 Critically ill surgical patients, hepatic cirrhosis
 Compensatory mechanisms inhibited
🞑 Renal bicarbonate excretion
🞑 Retention of PaCO2
🞑 Results in severe alkalemia
 Treatment
🞑 Metabolic: NaCl and KCl solutions
🞑 Respiratory: treat underlying cause of hyperventilation
59

60. Mixed Metabolic Acidosis and Respiratory
Alkalosis
 Advanced liver disease, salicylate intoxication, pulmonary-renal
syndromes
 Laboratory
🞑 Decrease in PaCO2
🞑 Decrease in bicarbonate
🞑 Normal or near normal pH ----because of the enhanced
compensation
 Treat underlying cause
60

61. Mixed Metabolic Alkalosis and Respiratory
Acidosis
 Occurs in patients with COPD and chronic respiratory acidosis
treated with salt restriction, diuretics, glucocorticoids
 Diuretics increase plasma bicarbonate
🞑 pH increases but may be near normal
 Treatment is to maintain PaO2 and PaCO2 at acceptable levels
🞑 Sodium chloride and potassium chloride ---to decrease plasma
bicarbonate by increasing its renal excretion
 Caution not to exacerbate CHF
61