Acid-Base Balance Final 2

8/12/2019 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 -

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Acid-Base Balance Final 2