by Dr. Lailmaah habibi 2nd year trainee of Rabia balkhee hospital Kabul Afghanistan 2016

1. ‫الرحیم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬
Acid base disturbances
BY DR.LAILMAAH Habibi 1st year trainee of KABUL RBH (AFG)
2015

2. • Normal values
• pa𝐶𝑜2= 40mm-Hg
• 𝐻𝑐𝑜3 =24mEq/L
• pH =7.4

3. Mixed acid base disturbances
• Two or three simultaneous disorders can be
present in a mixed acid-base disorder, but
there can never be two primary respiratory
disorders. Uncovering a mixed acid-base
disorder is clinically important
• Once the primary disturbance has been
determined, the clinician should assess
whether the compensatory response is
appropriate

4. • The anion gap should always be calculated for
two rea- sons. First, it is possible to have an
abnormal anion gap even if the sodium,
chloride, and bicarbonate levels are normal.
Second, a large anion gap (> 20 mEq/L)
suggests a primary metabolic acid-base
disturbance regardless of the pH or serum
bicarbonate level because a markedly
abnornmal anion gap is never a compensatory
response to a respiratory disorder

5. • Uncovering a mixed acid-base disorder is
clinically important, but requires a methodical
approach to acid-base analysis

6. Metabolic acidosis
• Metabolic acidosis can occur because of an
increase in endogenous acid production (such
as lactate and ketoacidosis ), loss of
bicarbonate (as in diarrhea), or accumulation
of endogenous acids (as in renal failure)

7. • The hallmark of metabolic acidosis is
decreased 𝐻𝐶𝑂3
• There are two major categories of clinical
metabolic acidosis: high-AG and non-AG， or
hyperchloremic acidosis
•

9. • Despite its usefulness, the anion gap can be
misleading. Non–acid- base disorders may
cause errors in anion gap interpretation

10. Increase anion gap
• Normochloremic metabolic acidosis generally
results from addition of organic acids such as
lactate, acetoacetate, beta- hydroxybutyrate,
and exogenous toxins.
• Uremia causes an increased anion gap
metabolic acidosis from unexcreted organic
acids and anions.

11. Lactic acidosis
• Lactic acid is formed from pyruvate in
anaerobic glycolysis, typically in tissues with
high rates of glycolysis, such as gut
(responsible for over 50% of lactate
production), skeletal muscle, brain, skin, and
erythrocytes.

12. Type A (hypoxic) lactic acidosis :is more
common, resulting from decreased tissue
perfusion; cardiogenic, septic, or hemorrhagic
shock; and carbon monoxide or cyanide
poisoning

13. • Type B lactic acidosis :may be due to
metabolic causes (eg, diabetes, ketoacidosis,
liver disease, kidney disease, malignancies,
nucleoside analogue reverse transcriptase
inhibitors in HIV, thiamine deficiency, severe
infections (cholera, malaria) ,seizures,
drugs/toxins (biguanides, ,ethanol, methanol,
propylene glycol, Isoniazid, fructose &
metformin ).

14. Diabetic Ketoacidosis (DKA)
• DKA is characterized by hyperglycemia and
metabolic acidosis with an increased anion gap
• beta-hydroxybutyrate or acetoacetate, the
ketones responsible for the increased anion gap
• correction of the serum sodium for the dilutional
effect of hyperglycemia will exaggerate the anion
gap.
• pts may have lactic acidosis from tissue
hypoperfusion and increased anaerobic
metabolism

15. • The kidney reabsorbs ketone anions poorly
but can compensate for the loss of anions by
increasing the reabsorption of Cl−.
• Patients with DKA and normal kidney function
may have marked ketonuria and severe
metabolic acidosis but only a mildly increased
anion gap.

16. • the urinary loss of Na+ or K+ salts of beta-
hydroxybutyrate will lower the anion gap
without altering the H+ excretion or the
severity of the acidosis
• Thus, the patient’s clinical status and pH are
better markers of improvement than the
anion gap or ketone levels.

17. Alcoholic acidosis
• Three types of metabolic acidosis are seen in
alcoholic ketoacidosis:
• (1) Ketoacidosis is due to beta
hydroxybutyrate and acetoacetate excess.
• (2) Lactic acidosis: Alcohol metabolism
increases the NADH:NAD ratio, causing
increased production and decreased
utilization
• (3) Hyperchloremic acidosis

18. Toxin and drugs
• Multiple toxins and drugs increase the anion
gap by increasing endogenous acid production

19. uremic
• GFR<15-30ml/min
• Unable to excrete hydrogen and organic acids

20. NORMAL ANION GAP ACIDOSIS
• The two major causes are gastrointestinal loss
and bicorbonate ,defect in renal acidification
(renal tubular acidosis).
• massive diarrhea or pancreatic drain- age can
result in HCO3− loss. Hyperchloremia occurs
because the ileum and colon secrete HCO3 in
exchange for Cl− by countertransport.

21. Renal Tubular Acidosis (RTA
• Hyperchloremic acidosis with a normal anion
gap and normal (or near normal) GFR, and in
the absence of diar- rhea, defines RTA. The
defect is either inability to excrete H+
(inadequate generation of new HCO3–) or
inappropriate reabsorption of HCO3–.

22. • Three major types:
• 1. Classic distal RTA (type I)—
• 2. Proximal RTA (type II)—
• 3. Hyporeninemic hypoaldosteronemic RTA
(type IV)—

23. • Dilutional Acidosis :
Rapid dilution of plasma volume by 0.9% NaCl
may cause hyperchloremic acidosis.
• Recovery from DKA :
• Posthypocapnia
• Hyperalimentation

24. Assessment of Hyperchloremic Metabolic
Acidosis by Urinary Anion Gap
• Increased renal 𝑁𝐻4CL excretion to enhance
H+ removal is the normal physiologic response
to metabolic acidosis. The daily urinary
excretion of NH4Cl can be increased from 30
mEq to 200 mEq in response to acidosis. The
urinary anion gap (Na+ + K+ − Cl−) reflects the
ability of the kidney to excrete 𝑁𝐻4CL

25. Clinicle findings &lab exam:
• Symptoms of metabolic acidosis are mainly
those of the underlying disorder.
Compensatory hyperventilation is an
important clinical sign and may be
misinterpreted as a primary respiratory
disorder; Kussmaul breathing (deep, regular,
sighing respirations)

26. treatment
Increased Anion Gap Acidosis :
• Treatment is aimed at the underlying disorder, such as
insulin and fluid therapy for diabetes and appropriate
volume resuscitation to restore tissue perfusion
• Supplemental bicarbonate is indicated for treatment of
hyperkalemia
• In salicylate intoxication, alkali therapy must be started
to decrease central nervous system damage unless
blood pH is already alkalinized by respiratory alkalosis,
since an increased pH converts salicylate to more
impermeable salicylic acid.

28. Normal Anion Gap Acidosis
• Treatment of RTA ;administration of alkali (either as
bicarbonate or citrate) to correct metabolic abnormalities
and prevent nephrocalcinosis and CKD
• Large amounts of oral alkali (10–15 mEq/kg/d)) may be
required to treat proximal RTA
• mixture of sodium and potassium salts is preferred.
Thiazides may reduce the amount of alkali required.
• type 1 distal RTA requires less alkali (1–3 mEq/kg/d) than
proximal RTA. Potassium supplementation may be
necessary. type IV RTA, dietary potassium restriction may
be necessary and potassium-retaining drugs should be
with- drawn. Fludrocortisone may be effective in cases with
hypoaldosteronism

29. Metabolic alkalosis
• Caused by a loss of acid or by in increase in
serum bicarbonate level manifested by an
elevated arterial pH and an increase in p𝑎𝑐𝑜2
as a result of compensatory alveolar
hypoventilation
• The compensatory increase in Pco2 rarely
exceeds 55 mm Hg; higher Pco2 values imply a
superimposed primary respiratory acidosis

30. Etiology
• Abnormalities that generate HCO3– are called
“initiation factors,” whereas abnormalities
that promote renal conservation of HCO3– are
called “maintenance factors.”
• The causes of metabolic alkalosis are
classified into two groups based on “saline
responsiveness” using the urine Cl– as a
marker for volume status

32. Saline responsive MA
• characterized by normotensive extracellular
volume contraction and hypokalemia.
Hypotension and orthostasis may be seen
• (paradoxical aciduria)
• urine Cl– is low (< 10–20 mEq/L)
• urine Cl− is preferred to urine 𝑁𝑎+
as a measure
of extracellular volume
• Diuretics despite volume contraction
• Hypokalemia (RAAS)

33. SALINE responsive specific types
• 1. Contraction alkalosis
• 2. Posthypercapnia alkalosis
Saline unresponsive alkalosis
• 1. Hyperaldosteronism
• 2. Alkali administration with decreased GFR
Antacids, lactate, citrate, and gluconate
In milk-alkali syndrome (hypercalcemic injury)

34. features
• Orthostatic hypotension(volume depleted pt)
• weakness and hyporeflexia.(hypokalemia)
• Tetany and neuromuscular irritability occur
rarely

35. Laboratory findings
• pH and bicarbonate level ↑
• pa𝐶𝑜2 ↑ resultant of respiratory compensation
• If Serum potassium and chloride are
decreased. There maybe increased anion gap.
• The urine chloride can differentiate between
saline-responsive (< 25 mEq/L) and
unresponsive (> 40 mEq/L) causes.

36. treatment
• If primary aldosteronism, renal artery stenosis
， or Cushing's syndrome is present
• [H+] loss by the stomach or can be mitigated
by the use of proton pump inhibitors
• discontinuation of diuretics
• The second aspect is, treatment of ECFV
contraction or K deficiency
• Acetazolamide, a carbonic anhydrase inhibitor

37. • if associated conditions preclude infusion of
saline, renal HC03 loss can be accelerated by
administration of acetazolamide， a carbonic
anhydrase inhibitor , which is usually effective
in patients with adequate renal function but
can worsen K+ losses. Dilute hydro chloric acid
(0.1 N HCI) is also effective but can cause
hemolysis , and must be delivered slowly in a
central vein

38. Respiratory acidosis
• Caused by decrease in alveolar ventilation
relative to total body production of
𝑐𝑜2(hypoventilation), the result is:
 Increase in p𝑐𝑜2 causes to ↑𝐻+(decrease pH).
 And slight ↑in 𝐻𝑐𝑜3
• For every 10mm-Hg ↑in p𝑐𝑜2 the 𝐻𝑐𝑜3 ↑to
1mmol/L and pH should fall into 0.08 pH units
• For every one 𝐻+is produced one 𝐻𝑐𝑜3 is produced
• Some rise in 𝐻𝑐𝑜3 always occur in uncompensated
respiratory acidosis

39. • In chronic respiratory acidosis (>24 h)， renal
adaptation increases the [HC03] by 4 mmol/L
for every 10-mmHg increase in Pa𝑐𝑜2. The
serum 𝐻𝑐𝑜3 usual does not increase above
38 mmol/L

40. features
• A rapid increase in Pa𝑐𝑜2 may cause anxiety ,
dyspnea ,confusion , psychosis and
hallucinations may progress to coma
• chronic hypercapnia include sleep
disturbances; loss of memory; daytime
somnolence; personality changes; impairment
of coordination; and motor disturbances such
as tremor, myoclonic jerks, and asterixis

41. • . Severe hypercapnia increases cerebral blood
flow, cerebrospinal fluid pressure, and
intracranial pressure; papilledema and
pseudotumor cerebri may be seen.

43. • Acute hypercapnia follows sudden occlusion
of the upper air way or generalized
bronchospasm as in severe asthma，
anaphylaxis ,inhalational burn or toxin injury

44. Laboratory Findings
• Arterial pH is low and Pco2 is increased.
Serum HCO3– is elevated but does not fully
correct the pH. If the disorder is chronic,
hypochloremia is seen.

45. treatment
• treatment is directed at the underlying
disorder to improve ventilation
• If there is no other cause for hypoventilation,
the clinician should consider a diagnostic and
therapeutic trial of intra- venous naloxone

46. Respiratory alkalosis
• Increase in alveolar ventilation relative to body
production of 𝑐𝑜2(hyperventilation).
• ↓ 𝑝𝑎𝑐𝑜2 causes ↓ in 𝐻+
(increased pH) and ↓ 𝐻𝐶𝑂3
• For every one 𝐻+consumed one 𝐻𝐶𝑂3 is also
consumed
• Quantitatively for every 10mm-Hg ↓in pa𝑐𝑜2 the
𝐻𝐶𝑂3 will ↓1mmol/L and the (pH) ↑0.08 pH unit.
• Chronic hypocapnia reduces the serum [HC03-] by 4.0
mmol/L for each 10-mmHg decrease in Pa𝑐𝑜2.

47. • Determination of appropriate metabolic
compensation may reveal an associated
metabolic disorder .
• As in respiratory acidosis, the metabolic
compensation is greater if the respiratory
alkalosis is chronic . Although serum HCO3− is
frequently < 15 mEq/L in metabolic acidosis, such
low level in respiratory alkalosis is unusual and
may represent a concomitant primary metabolic
acidosis.

49. Symptoms and Signs
• In acute cases (hyperventilation), there is
light-headedness, anxiety, perioral numbness,
and paresthesia.

50. Laboratory findings
• Arterial blood pH is elevated, and Pco2 is low.
Serum bicarbonate is decreased in chronic
respiratory alkalosis (slightly)

51. treatment
• Underlying cause
• Paper bag breathing
• Anxious pts
• Treatment of hyperventilation
• Treatment of alkalosis

52. References
• 19th edition HARRISON’s principle of internal
medicine
• Current treatment and medical diagnosis of
internal medicine latest updated 2015
• USLME 2014 book of physiology
• USLME 2014 book of internal medicine