Acidosis

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Acidosis

• Dr. Elmukhtar Habas
• PhD
• Fachärzt Internal Medicine
• Fachärzt Nephrology
• Dr. med.

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Normal ABG
PaCO2 4.8-6.1 kPa (35-45 mmHg)
PaO2 10-13.3 kPa (75-100 mmHg)
pH 7.35-7.45 H 35-45 mol/L
Bicarbonate 22-26 mmol/L
BE Base Excess -2 to 2 
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Acid-Base disturbance
disturbance PH Pco2 HCO3
Metabolic Acidosis Low Low Low
Respiratory Acidosis Low High High
Metabolic Alkalosis High High High
Respiratory Alkalosis High Low Low
Normal ABG 7,36-7,44 35-45mmHg 22-26 mmol/l
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EC pH
NORMAL
LOW
HIGH
No disturbance Or Mixed disturbance Mixed if
PCO2HCO3 both low or both high or plasma anion
gap wide
Alkalemia
Acidemia
Respiratory Alkalosis
Metabolic Alkalosis
Metabolic Acidosis
Respiratory Acidosis
High PCO2
Low PCO2
High HCO3
Low HCO3
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Definition of Acidosis

• Is a process that tends to lower the
  extracellular fluid pH (which is equivalent to
  raising the hydrogen concentration) that can be
  either by
• A) a fall in the ECF (or plasma ) bicarbonate
  concentration.
• b) an elevation in the PCO2 in ECF.

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Types of Acidosis

• Metabolic acidosis.
• -Low bicarbonate, low PH, normal PCO2.
• -Usually associated with hyperK.
• Respiratory acidosis
• -Low PH, high PCO2 Normal or high Hco3
• -can be hyperk

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• Each day approximately 15,000 mmol of carbon
  dioxide (which can generate carbonic acid as it
  combines with water) and 50 to 100 meq of
  nonvolatile acid (mostly sulfuric acid derived
  from the metabolism of sulfur-containing amino
  acids) are produced.
• Acid-base balance is maintained by normal
  pulmonary and renal excretion of carbon dioxide
  and acid, respectively.
• Renal excretion of acid involves the combination
  of hydrogen ions with urinary titratable acids,
  particularly phosphate (HPO42- H gt H2PO4-) or
  with ammonia to form ammonium.
• since ammonia production from the metabolism of
  glutamine can be appropriately increased in the
  presence of an acid load.

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Henderson-Hasselbalch equation

• pH      6.10      log  (HCO3-    0.03  x  PC
  O2)
• -pH is equal to (-log H)
• -6.10 is the pKa (equal to -log Ka).
• -Ka is the dissociation constant for the reaction
• -0.03 is equal to the solubility constant for
  CO2 in the extracellular fluid.
• -PCO2 is equal to the partial pressure of carbon
  dioxide in the extracellular fluid .

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Metabolic acidosis diagnostic chart
diagnosis
Lab diagnostic
Metabolic acidosis Low Hco3-, low Ph
normal
HCO-3 loss, RF, RTA
AG Na - (Cl- HCO-3)
AG gt 12mmol/l
Lactat, Acetoacetic, ß-hydrxybutyric acid
high
Lactic or ketoacidosis
normal
High OGgt10mosm/Kg
Osmatic gape measured osmolality- (Na
K)glucose/18 urea/2.8
Methanol, ethylglycol or other intoxication
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Renal Tubular acidosis

• Four types
• Type 1. Distal renal tubular acidosis
  characterized by.
• Type II. Proximal renal tubular acidosis
  characterized by.
• Type III Mixed
• Type IV

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ANION GAP

•  AG Na - (Cl HCO3).
• The normal plasma AG had been considered to range
  between 7 and 13 meq/L.
• knowing the normal range in a particular
  laboratory is often essential.

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Calculation

• Anion gap AG Na - (Cl- HCO-3).
• 8-10mmol/l. hypoabulminaemia reduce AG.
• Osmotic gape (OG) measured osmolality-
  calculated osmolality.
• lt10mosm/Kg
• Calculated Osmolality (Na K)glucose/18
  urea/2.8.

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ANION GAP

• primarily determined by the negative charges on
  the plasma proteins, particularly albumin.
• patients with hypoalbuminemia. AG falling by
  about 2.5 meq/L for every 1 g/dL (10 g/L)
  reduction in the plasma albumin concentration.

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ANION GAP

1. an increase in the AG can be induced by a fall in
   unmeasured cations (hypocalcemia or
   hypomagnesemia)
2. more commonly and more markedly, by a rise in
   unmeasured anions (as with hyperalbuminemia due
   to volume contraction or the accumulation of an
   organic anion in metabolic acidosis).
3. Hypoalbuminemia (decreased unmeasured anions) and
   hyperk (increased unmeasured cations) lower the
   AG.

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Initial screening to differentiate the
high-AG acidose

• (1) history for evidence of drug and toxin
  ingestion and measurement of arterial blood gas
  to detect coexistent respiratory alkalosis
  (salicylates).
• (2) determination of whether diabetes mellitus is
  present (diabetic Ketoacidosis)
• (3) a search for evidence of alcoholism or
  increased
• levels of -hydroxybutyrate (alcoholic
  ketoacidosis)
• (4)observation for clinical signs of uremia and
  determination of the blood urea nitrogen (BUN)
  and creatinine (uremic acidosis)
• (5) Inspection of the urine for oxalate crystals
  (ethylene glycol).
• (6) Recognition of the numerous clinical settings
  in which lactate levels may be increased
  (hypotension, shock, cardiac failure, leukemia,
  cancer, and drug or toxin ingestion).

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Elevated anion gap

• The diagnostic utility of a high AG is greatest
  when the AG is above 25 meq/L.
• Lactic acidosis, usually due to marked systemic
  hypoperfusion or to malignancy.
• Ketoacidosis due to diabetes mellitus, alcohol,
  or fasting, in which ß-hydroxybutyrate is the
  primary unmeasured anion.
• Is modestly in nonketotic hyperglycemia even
  though there is little or no metabolic acidosis.
  In this setting, due to the phosphate other
  anions release from the cells .

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Elevated anion gap

• Most of renal failure, in whom there is retention
  of both hydrogen and anions, such as sulfate,
  phosphate, and urate.
• Ingestion of methanol, glycolate and oxalate with
  ethylene glycol aspirin.
• metabolic acidosis may be absent and the anion
  gap may be normal in methanol or ethylene glycol
  intoxication if there is concurrent alcohol
  ingestion.

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Urinary anion gap

• To evaluate metabolic acidosis in normal anion
  gap.
• As to distinguish the cause is from renal or GIT
  ( Diarrhoea )
• URINARY ANION GAP
• ( Urinary Na Urinary K ) Urinary Cl
• If ve the cause is diarrhea GIT
• If ve the cause is distal renal tubular acidois.

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HIGH-ANION-GAP ACIDOSES

• The goal is to increase the HCO3to 10 meq/L and
  the pH to 7.15, not to increase these values to
  normal.
• There are four principal causes of a high-HIGH AG
  acidosis
• (1) lactic acidosis.
• (2) ketoacidosis.
• (3) ingested toxins.
• (4) acute and chronic renal failure.

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normal anion gap metabolic acidosis
U ureterosignoidostomy S saline in presence of
CRI E endocrine - hypoaldosteronism D
diarrhoea C carbonic anhydrase inhibitor A
ammonia or alimentation eg TPN R renal tubular
acidosis
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Metabolic acidosis with High AG
Cause Main anion Clinic/lab
Lactic acidosis. Shock, hypoxia, metformin, hepatitis. lactate Kussmaul breath
Ketoacidosis. DM,alchol, hunger Acetoacetic, ß-hydrxybutyric acid Kussmaul breath, Eventually coma, ketonurea
Intoxications. Aspirin. methanol, ethylachol, paraldehyde Salicylic, format,glycol/ lactat, acetat High OG, ARF
ARF CRF Sulphate, phosphate S Urea, Cr. Olig/anuria
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Metbolic acidosis with normal AG

• Acid infusion.
• - Arginin chloride.
• HCO3- loss
• - Urtersigmoidostoy, ileum conduct to ureter or
  bladder.
• - Diarrhoea.
• - Carbonic anhydrase inhibitor. Timolol.
• - RTA type II.
• Reduced H-secretion, NHr-excretion.
• - RTA typeIIV.
• Reduced NH3 formation, reduced distal Nh3
  excretion.
• - ARF, hypoaldosternism hyperkalaemia.

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Metabolic acidosis and anion gap
High Anion gape M. A. Increased production of acid or acid equivalant substances
Ketoacidosis DM, Hunger, Alchol.
Lactatic acidosis Tissue hypoxia by cardiac shock, respiratory insufficiency, malignacy, liver cell failure.
High A.G with normochloremic M.A. Intoxication with Methanol, Ethyle glycole,Biguanides.
Decrease in acid excretion by kidney as in CRF, ARF
Normal A.G metabolic acidosis Renaltubular dysfunction as in RTA
Hypercholeraemic M.A. Loss of HCO3 Diarrhea, carbonic anhydrase inhibitor (dimox
Ingestion of acid with chloriode
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Clinical presentation

• Tachycardia.
• Breathlessness.
• Low BP.
• Headache.
• Electrolyte disorder.
• Dizziness.
• Coma.

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General principles of treatment 1

• varies markedly with the underlying disorder.
• The aim Rx is restoration of a normal
  extracellular pH.
• exogenous alkali may not be required if the
  acidemia is not severe (arterial pH gt7.20), the
  patient is asymptomatic, and the underlying
  process, such as diarrhea that can be controlled

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General principles of treatment 2

• In other settings, correction of the acidemia can
  be achieved more rapidly by the administration of
  sodium bicarbonate IV.
• The initial aim of therapy is to raise the
  systemic pH to above 7.20 this is a level at
  which the major consequences of severe acidemia
  should not be observed.

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HIGH-ANION-GAP ACIDOSES

• The goal is to increase the HCO3to 10 meq/L and
  the pH to 7.15, not to increase these values to
  normal.
• There are four principal causes of a high-HIGH AG
  acidosis
• (1) lactic acidosis.
• (2) ketoacidosis.
• (3) ingested toxins.
• (4) acute and chronic renal failure.

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Treatment

• Treat the underlying cause.
• NaHCO3. Indication of NaHCO3 infusion.
• - Significant hyperkalaemia with PH lt 7.1.
• - Bicarbonate lt 8 K lt3mmol/l substitution is
  given.
• Calculation of bicar mmol/l . Substitution
  KG(kg)x0,7x(desired NaHCO3 NaHCO3).
• Haemodialysis. In severe RF or sever acidosis
  with hyperkalaemia

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Calculation of bicarbonate deficit

• If the respiratory function is normal, pH of
  7.20 usually requires raising the plasma
  bicarbonate to 10 to 12 meq/L .
•     HCO3 deficit  HCO3 space xHCO3 deficit /L.
•  Bicarbonate space 0.4  (2.6 HCO3)
    x  body weight ( kg).
• If more alkali is given, oral Nahco3 or citrate
  (metabolised to Hco3can replace IV therapy.

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Treatment

• In server case when PH lt 7.1
• NaHCo3 8,4 can be given 1mlImmol/.
• Needed NaCO3 neg. Bace excess x 0,3. Kg(KG).
• -divided to halfs the last half according to
  ABG
• Be careful about Hypokalemia and over correction.
• In chronic metabolic acidosis
• slow correction with oral calcium or sodium
  bicarbonate up to 10g/day

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Advice

• In acidosis
• Do not be hurry for Bicarbonate infusion before
  you are sure that PH of blood lt 6.9 and you
  should contact your superior.

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Respiratory acidosis (RA)

• High CO 2 and low PH.
• Acute RA
• Respiratory passage obstruction
• cardiopulmary arrest
• neuromuscular defect
• restrictive LD
• mechanical defect of respiration
• respiratory centre defect.
• Chronic RA.
• COAD
• lesion of respiratory centres defect
• obesity
• COAD
• restrictive LD.

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Treatment

• Acute RA.
• Treat the underlying diseases.
• O2 inhalation.
• Chronic RA.
• Therapy of the underlying disease.
• Controlled O2 inhalation and slow correction.
• Slow correction of PCO2.

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Case 1

• A patient with diarrhea has an arterial pH of
  7.23, bicarbonate concentration of 10 meq/L, and
  PCO2 of 23 mmHg. The low pH indicates acidemia,
  and the low plasma bicarbonate concentration
  indicates What?

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1st Example
7.24 pH
35 mmHg PCO2
90 mmHg PO2
12 mmol/L HCO3
- 10 mmol/L BE
145 mmol/L Na
4 mmol/L K
100 mmol/L Cl
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2nd Example
7.30 pH
40 mmHg PCO2
85 mmHg PO2
18 mmol/L HCO3
- 5 mmol/L BE
130 mmol/L Na
4 mmol/L K
104 mmol/L Cl
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3rd Example
7.25 pH
60 mmHg PCO2
70 mmHg PO2
22 mmol/L HCO3
- 8 mmol/L BE
139 mmol/L Na
4.3 mmol/L K
105 mmol/L Cl
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4th Example
7.00 pH
20 mmHg PCO2
88 mmHg PO2
13 mmol/L HCO3
- 10 mmol/L BE
139 mmol/L Na
4.3 mmol/L K
105 mmol/L Cl
5.3 mg/dl Crea.
250 mg/dl Urea
299mg FBS
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• Thanks and good luck