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