Acidosis

Dr. Elmukhtar HabasPhD

Fachärzt Internal MedicineFachärzt 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 PH Pco2 HCO3Metabolic 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

LOW

EC pH

HIGHNORMAL

No disturbanceOr

Mixed disturbanceMixed if PCO2+HCO3 both low or both high or plasma anion gap wide

AlkalemiaAcidemia

Low PCO2

Respiratory Alkalosis

High HCO3

Metabolic Alkalosis

Low HCO3 High PCO2

Metabolic Acidosis

Respiratory Acidosis

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 Low Hco3-, low Ph

Metabolic acidosis diagnostic chart

AG= Na+ - (Cl- +HCO-3)

HCO-3 loss, RF, RTA

Lactat, Acetoacetic, β-hydrxybutyric acid

Lactic or ketoacidosis

Osmatic gape= measured osmolality- (Na+ + K+)+glucose/18+ urea/2.8

Methanol, ethylglycol or other intoxication

Lab diagnosticdiagnosis

AG > 12mmol/l

normal

high

High OG>10mosm/Kgnormal

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/KgCalculated 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 increasedlevels 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 GITIf +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

CauseCause Main anionMain anion Clinic/labClinic/lab

Lactic acidosis.Lactic acidosis.

Shock, hypoxia, Shock, hypoxia, metformin, hepatitis.metformin, hepatitis.

lactatelactate Kussmaul breathKussmaul breath

Ketoacidosis.Ketoacidosis.

DM,alchol, hungerDM,alchol, hunger

Acetoacetic, Acetoacetic, ββ--hydrxybutyric hydrxybutyric acidacid

Kussmaul breath, Eventually Kussmaul breath, Eventually coma, ketonureacoma, ketonurea

Intoxications.Intoxications.

Aspirin. methanol, Aspirin. methanol, ethylachol, paraldehydeethylachol, paraldehyde

Salicylic, Salicylic, format,glycol/ format,glycol/ lactat, acetatlactat, acetat

High OG, ARFHigh OG, ARF

ARF &CRFARF &CRF Sulphate, Sulphate, phosphatephosphate

S Urea, Cr. Olig/anuriaS 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 that PH of blood < 6.9 and you should contact your superior.

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

pHpH 7.247.24

PCO2PCO2 35 35 mmHgmmHg

PO2PO2 9090 mmHgmmHg

HCO3HCO3 12 12 mmol/L mmol/L

BEBE - 10 mmol/L- 10 mmol/L

NaNa 145 mmol/L145 mmol/L

KK 4 mmol/L4 mmol/L

ClCl 100 mmol/L100 mmol/L

2nd ExamplepHpH 7.307.30

PCO2PCO2 40 40 mmHgmmHg

PO2PO2 85 85 mmHgmmHg

HCO3HCO3 18 mmol/L18 mmol/L

BEBE - 5 mmol/L- 5 mmol/L

NaNa 130 mmol/L130 mmol/L

KK 4 mmol/L4 mmol/L

ClCl 104 mmol/L104 mmol/L

3rd Example

pHpH 7.257.25

PCO2PCO2 60 60 mmHgmmHg

PO2PO2 70 70 mmHgmmHg

HCO3HCO3 22 mmol/L22 mmol/L

BEBE - 8 mmol/L- 8 mmol/L

NaNa 139 mmol/L139 mmol/L

KK 4.3 mmol/L4.3 mmol/L

ClCl 105 mmol/L105 mmol/L

4th Example

7.007.00 pHpH

20 20 mmHgmmHg PCO2PCO2

88 88 mmHgmmHg PO2PO2

13 mmol/L13 mmol/L HCO3HCO3

- 10 mmol/L- 10 mmol/L BEBE

139 mmol/L139 mmol/L NaNa

4.3 mmol/L4.3 mmol/L KK

105 mmol/L105 mmol/L ClCl

5.3 mg/dl5.3 mg/dl Crea.Crea.

250 mg/dl250 mg/dl UreaUrea

299mg%299mg% FBSFBS

Thanks and good luck