Transcript Metabolic acidosis

Acidosis
Dr. Elmukhtar Habas
PhD
Fachärzt Internal Medicine
Fachärzt Nephrology
Dr. med.
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
Acid-Base disturbance
disturbance
Metabolic
Acidosis
Respiratory
Acidosis
Metabolic
Alkalosis
Respiratory
Alkalosis
Normal ABG
PH
Low
Pco2
Low
HCO3
Low
Low
High
High
High
High
High
High
Low
Low
7,36-7,44
35-45mmHg 22-26 mmol/l
EC pH
NORMAL
LOW
No disturbance
Or
Mixed disturbance
Mixed if PCO2+HCO3
both low or both high or
plasma anion gap wide
Acidemia
Metabolic
Acidosis
Low HCO3
HIGH
Respiratory
Acidosis
High PCO2
Alkalemia
Metabolic
Alkalosis
High HCO3
Respiratory
Alkalosis
Low PCO2
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.
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+
 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+ —> 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.
Henderson-Hasselbalch equation:
 pH = 6.10 + log ([HCO3-] ÷ [0.03 x PCO2])
-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 .
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 > 12mmol/l
Lactat, Acetoacetic, β-hydrxybutyric
acid
normal
Osmatic gape= measured osmolality(Na+ + K+)+glucose/18+ urea/2.8
high
Lactic or ketoacidosis
High OG>10mosm/Kg
Methanol, ethylglycol or other
intoxication
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
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.
Calculation
 Anion gap AG = Na+ - (Cl- +HCO-3).
 8-10mmol/l. hypoabulminaemia reduce AG.
 Osmotic gape (OG) =measured osmolality- calculated
osmolality.
 <10mosm/Kg
 Calculated Osmolality = (Na+ + K+)+glucose/18+
urea/2.8.
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.
ANION GAP
A. an increase in the AG can be induced by a fall in
unmeasured cations (hypocalcemia or
hypomagnesemia)
B. 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).
C. Hypoalbuminemia (decreased unmeasured anions)
and hyperk+ (increased unmeasured cations) lower
the AG.
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).
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 .
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.
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.
HIGH-ANION-GAP ACIDOSES
The goal is to increase the [HCO3]to 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.
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
Metabolic acidosis with High AG
Cause
Main anion
Clinic/lab
Lactic acidosis.
Shock, hypoxia,
metformin, hepatitis.
lactate
Kussmaul breath
Ketoacidosis.
DM,alchol, hunger
Acetoacetic, βhydrxybutyric
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
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 typeI&IV.
 Reduced NH3+ formation, reduced distal Nh3+ excretion.
- ARF, hypoaldosternism & hyperkalaemia.
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
Clinical presentation
 Tachycardia.
 Breathlessness.
 Low BP.
 Headache.
 Electrolyte disorder.
 Dizziness.
 Coma.
General principles of treatment 1
A. varies markedly with the underlying disorder.
B. The aim Rx is restoration of a normal
extracellular pH.
C. exogenous alkali may not be required if the
acidemia is not severe (arterial pH >7.20), the
patient is asymptomatic, and the underlying
process, such as diarrhea that can be controlled
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.
HIGH-ANION-GAP ACIDOSES
The goal is to increase the [HCO3]to 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.
Treatment
 Treat the underlying cause.
 NaHCO3+. Indication of NaHCO3+ infusion.
- Significant hyperkalaemia with PH < 7.1.
- Bicarbonate < 8 & K+ <3mmol/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
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.
Treatment
 In server case when PH < 7.1
 NaHCo3 8,4 can be given: 1ml=Immol/.
 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
Advice
 In acidosis
 Do not be hurry for Bicarbonate infusion before you are sure
< 6.9 and you should
contact your superior.
that PH of blood
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.
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.
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?
1st Example
pH
7.24
PCO2
35 mmHg
PO2
90 mmHg
HCO3
12 mmol/L
BE
- 10 mmol/L
Na
145 mmol/L
K
4 mmol/L
Cl
100 mmol/L
2nd Example
pH
7.30
PCO2
40 mmHg
PO2
85 mmHg
HCO3
18 mmol/L
BE
- 5 mmol/L
Na
130 mmol/L
K
4 mmol/L
Cl
104 mmol/L
3rd Example
pH
7.25
PCO2
60 mmHg
PO2
70 mmHg
HCO3
22 mmol/L
BE
- 8 mmol/L
Na
139 mmol/L
K
4.3 mmol/L
Cl
105 mmol/L
4th Example
7.00
20 mmHg
88 mmHg
13 mmol/L
- 10 mmol/L
139 mmol/L
4.3 mmol/L
105 mmol/L
5.3 mg/dl
250 mg/dl
299mg%
pH
PCO2
PO2
HCO3
BE
Na
K
Cl
Crea.
Urea
FBS
Thanks and good luck