Download - Acid-Base Balance Final 2
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Acid-Base Disorders
S. Kadiri
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Introduction (cont)
H+
= 24 pCO2/HCO3-pCO2and HCO3change in line to stabilize H+
- pCO2by CNS and lungs
- HCO3by kidneys-response never returns H+to normal in pure ABDs
Base excess = 0.93 x [HCO3-24.4 + 14.8(pH-7.4)]normal = +/-2
1 ATM = 101.9 kPa
mmHg/7.5 = kPa
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pH
Normal
Acidaemia pH7.45
Acidaemia more common
Metabolic acidosis perhaps most important
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Definition
Buffer basethe sum of HCO3
-
and the nonvolatile weak acid buffers (A-
)
Base excess(BE)the amount of acid or base that must be added to asample of whole blood in vitro to restore the pH of the sample to 7.40 while
the PCO2is held at 40 mmHg-negative in acidaemia
-positive in alkalaemia
Standard base excess
-base excess at reference of Hb 5g/dL
- Hb buffers plasma and much larger extracellular fluid.
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Compensation
Kidneysslow: 1-2 days and full in 3-5 days
Lungscan be fast: within mins, full in 1-2 days Changes in C02, no change in H
+
With well functioning organs
pCO2changes not caused by overproduction
Metabolic acidosis or alkalosis features ofacute met disturbance or chronic lung disease
- not acute lung disease
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Steps to Interpretation
Note pH : normal, acid, alkaline
pCO2 serum HCO3 Compensation
Anion gapmay be the only abnormality
Mixed disorders
Acute or chronic
Severity of disorder
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Interpreting ABGs (Identifying
Imbalances)
1. Look at pH first. Is it normal, acidotic or alkalotic?
2. Look at pCO2next. Is it normal, high (acidotic) or low(alkalotic)?
***If pCO2is inverse with pH, its a respiratory problem.
3. Look at HCO3-next. Is it normal, low (acidotic) or high
(alkalotic).
***If HCO3-
is direct with pH, its a metabolic problem.
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pH CO2 HCO3 2ndary Responses
RAc < 7.4 > 40 > 24 increased renal acid excretion
(increased HCO3, rarely > 32 mEq/L)
R Alk > 7.4 < 40 < 24 Decreased renal acid excretion
(decreased HCO3, rarely 7.4 > 40 > 24 Hypoventilate
(pCO2 usually < 55 mmHg)
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Respiratory acidosis - compensation
Problem high pCO2
High H+, low pH
H+
stimulates kidney to retain HCO3 Complete in 2-4 days
Limit of compensation 45
Expected HCO3
= 0.44 x pCO2+ 7.6 +/- 2
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Respiratory alkalosis - compensation
Problem low pCO2
Low H+, high pH
Stimulates kidneys to excrete HCO3 Complete in 7-10 days
Limit is 12 mmol/L
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Metabolic acidosis - compensation
Problem low HCO3
High H+. Low pH
Stimulates respiration Complete in 12-24 hrs
Expected pCO2
= 1.5 x HCO3+ 8..+/-2 Limit 10 mmHg
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Metabolic alkalosis - compensation
Problem high HCO3
Low H+, high pH
Suppresses respiration which raises pCO2 Complete in 12-24 hrs
Expected CO2
= 0.9 x HCO3+ 9 ..+/- 2 Limit is 60
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Mixed acid-base disorders
Plasma HCO3and CO2change in differentdirections
Appropriate secondary responses not present
Secondary responses fully correct or overshootpH
Severity and worse outcomes with disorders thatenhance pH change
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pCO2respiratory component
pCO2inverse to pHrespiratory cause
If HCO3also lowcombined resp & metacidosis
If pCO2direct to pHnot resplow pCO2resp compensation for met acid
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HCO3/SBEmetabolic component
pH direct with HCO3/SBEmetabolic
If pCO2also highcombined met & resp acid
If SBE/HCO3inverse to pHnot metabolic
HCO3/SBE highcompensation
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In Metabolic acidosis
If there is a metabolic acidosis (pH
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In Metabolic Acidosis
Example: if the HCO3- is 12
pCO2exp = [12 x 1.5] +8 + 2 = 26 +2
Using this example, it is a simple disorder if the
pCO2is 24-28
If the pCO2 < 24, then it is too far: therefore, aprimary respiratory alkalosis
If the pCO2 > 28, not far enough, therefore, aprimary respiratory acidosis
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additional tips
Expected pCO2= last 2 digits of blood pH
If inadequate, additional respiratory acidosis
If excessive, additional respiratory alkalosis
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Acid-base rules
The compensating partner has five choices:
1. Change in the proper direction, but too far.
2. Change in the proper direction, just right.
3. Change in the proper direction but not far enough.4. Not changeat all.
5. Change in the other direction.
6. Only one of this is a simple disorderwith appropriate
compensation: #2.
7. All of the others have a second primary disorder
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Acute or chronic ?
Respiratory compensation fast
Renal compensation slow
Ac. R Ac - 10mmHg increase in CO2, HCO3up by 1 Ch. R Ac - 10mmHg increase in CO2, HCO3up by 4
Ac. R Aldecrease of 10, HCO3drop by 2
Ch. R Aldecrease of 10, HCO3drops by 5
PCO2 SBE
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severity
Adjective2
mmHg mEq/L
Alkalosis
Severe > 18 > 13
Marked 18 to 25 13 to 9
Moderate 25 to 30 9 to 6
Mild 30 to 34 6 to 4
Minimal 34 to 37 4 to 2
Normal Normal 37 to 43 2 to -2
Acidosis
Minimal 43 to 46 -2 to -4
Mild 46 to 50 -4 to -6
Moderate 50 to 55 -6 to -9
Marked 55 to 62 -9 to -13
Severe > 62 to < -13
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Acid-case patterns observed in humans
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Acid excretion
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Origin of acidosis
Addition of acid
endogenous
exogenous
Reduced excretion of acid
Loss of bicarbonate
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Renal excretion of acid
Secretion of ammonia
Titratable acidity
Reabsorption of bicarbonate
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Bicarbonate reabsorption
80-90% in PCT
Brush border carbonic anhydrase
10-20% in distal segments
Daily filtered about 4500 mEq
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Metabolic acidosis
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Classification
High and Normal anion gap MA
[Na][HCO3
-- Cl-}
Owing to serum albumin, unmeasured anions
Normal 4-12
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Limitations of AG
Potassium level (K+)ignored when 4 mEq/L
Normal values for AGin most laboratories
12 +/- 4if K+is considered
8 +/- 6if K+is not considered
Doubt of AGreliance on normal albumin and
phosphatewhich are changed by pH
At pH 7.4, 1 g/dL of albuminhas charge of 2.8 mEq/L
at pH 7.0, the charge is 2.3 mEq/L
at pH 7.6, the charge is 3.0 mEq/L
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Low anion gap - causes
Hypoalbuminaemia
Hyperlipidaemia
Hyperviscosity
Paraproteinaemia
Increased cations
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C f t b li id i
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Causes of metabolic acidosisNormal AG
Renal acidification defects Proximal renal tubular acidosis
Classic distal tubular acidosis
Hyperkalemic distal tubular acidosis
Early renal failure
Gastrointestinal loss of bicarbonate Diarrhea
Small bowel losses
Ureteral diversions
Anion exchange resins
Ingestion of CaCl2
Acid infusion
HCl
Arginine HCl
Lysine HCl
Increased AG
Endogenous acid load Ketoacidosis
-Diabetes mellitus
-Alcoholism
-Starvation
Uremia
Lactic acidosis
Exogenous toxins
Osmolar gap present
-Methanol
-Ethylene glycol
Osmolar gap absent
-Salicylates
-Paraldehyde
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Renal failure
Impaired secretion of NH3
-maybe NAG at this stage
Retention of PO4-and SO4
-
Bicarbonate wastage
-HAG at this stage
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Acid and Cl- administration
HCl from parenteral nutrition
NaCl infusion and expansion acidosis
Fall in blood pH
Cl-keeps anion gap
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Bicarbonate losses - kidneys
Proximal tubular disorder
Hypocapnia
Reduced bicarbonate reabsorption
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Reduced H+ excretion
Type-1 renal tubular acidosis
Type-4 renal tubular acidosis
-hypoaldosteronism
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Type-1 RTA
Impaired H+extrusion from -intercalated
cells
Urine pH > 5.3
K+excretion for Na+reabsorption
Hypokalaemia
Hyperkalaemic form may occur withobstruction
Ca phosphate stones and nephrocalcinosis
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Calcium phosphate stones
Calcium citrate more soluble than calcium
phosphate
Increased PT reabsorption of citrate
Hypokalaemia promotes hypocitraturia
Hypocitraturia promotes phosphate stones
Ca phosphate stones less soluble than citratestones
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Type-4 RTA - causes
Diabetes mellitus
NSAID
Cyclosporin
ACEI, ARB
Heparin
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Type-4 RTA
Impaired Na+reabsorption
Impaired K+secretion
Hyperkalaemia inhibits NH3production
Acidosis, urine pH < 5.3
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Acidosisclinical features
Blood pH > 7.20
Counter regulatory hormones actives
Kussmauls respiration
Nausea, vomiting
Change in mental status
Bl d H < 7 20 C t l t
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Blood pH < 7.20 -- Counter regulatory
hormones ineffective
Hypotension
Depressed myocardial
contractility,vasodilatation
Reentrant arrhythmias
Ventricular fibrillation
reduced albumin
synthesis
Activation ofcomplement
Enhanced muscle
breakdown
Bone buffering and
resorption
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Investigations
pH
HCO3-
pCO2
H+
Anion gap
Serum K+
Increased anion gap
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Increased anion gap
Due to unmeasured anions
-Deplete bicarbonate
Corrected HCO3
= measured HCO3+ (anion gap12)
Normal = 22-26
If reduced, additional metabolic acidosis
If elevated, additional metabolic alkalosis
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Normal anion gap MAc
2 large groupsrenal/GI
Clinical differentiation
Urine anion gap
Positive UAG, renal cause
Negative UAG, GI cause
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Urine anion gap
UAG= [Na++ K+][Cl-]
0 in type-1 RTA
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Treatment
Of acidaemia
Of underlying disorder
Alkali
Dialysis
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Alkali therapy
Serum HCO3-< 12 mEq/L
Newer recommendations to keep level 20-25
0.5-1 mEq/Kg/day
0.3 x weight x BE
NaHCO3 K citrate in type-1 RTA
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Calculating BE
Van Slyke equation ~ Scan J Clin Lab Invest 977; 146:15-20
* Hb and HCO-3expressed in mmol/L
BE changes slightly with changes in PCO2 Modified hemoglobinon CO2titration
Still changes slightly as PCO2 and assume normal ATOT
BE = (HCO3-- 24.4 + [ 2.3 x Hb + 7.7 ] x [ pH7.4 ]) x (10.023 x Hb)
SBE = 0.9287 x (HCO3-- 24.4 + 14.83 x [ pH
7.4 ])
Six Classical Acid-Base Disturbances
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pH PCO2 SBE Interpretation Compensation
Acid
Acid
Alk Resp. Acid. CompSBE Half way - Normal
Met. Comp.
Norm Resp. Acid. PureSBE Normal - No Met.
Comp
Alk Acid Met. Acid. CompPCO
2
Half way -
Normal Resp. Comp.
Alk
Alk
Acid Resp. Alk. CompSBE Half way - Normal
Met. Comp.
Norm Resp. Alk. PureSBE Normal - No Met.
Comp
Acid Alk Met. Alk. CompPCO2Half way -
Normal Resp. Comp
Four Other Acid-Base Disturbances
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pH PCO2 SBE Interpretation Compensation
Acid
Acid Acid CombinedAcidosis
Not Applicable -Both Acid
Norm Acid Met. Acid. PurePCO2Normal -
No Resp. Comp
Alk
Alk AlkCombined
Alkalosis
Not Applicable -
Both
Components
Alkaline
Norm Alk Met. Alk. PurePCO2Normal -