The document discusses acid-base balance and provides information on:
1. Normal acid-base balance is tightly controlled through chemical buffering, carbon dioxide levels, and bicarbonate concentration.
2. There are two types of acids - carbonic acids from carbon dioxide and non-carbonic acids from protein metabolism.
3. Diagnosis of acid-base imbalances involves obtaining a history, physical exam, and measuring pH, bicarbonate, carbon dioxide, and checking the adequacy of compensation.
4. Acid – Base Balance
Normal concentration of H + in
extracellular fluid is 40 nmol/L.
5. Acid – Base Balance
Roughly one millionth the concentration of
Na , K, Cl and Bicarb.
6. Acid – Base Balance
In normal conditions this concentration is
very well controlled
7. Acid – Base Balance
Three basic steps
1 – Chemical Buffering
2 - Control of PP of CO 2 ( alveolar
ventilation)
3 – Control of Bicarb concentration
( H excretion ).
8. Acid – Base Balance
Two kinds of acids
1- Carbonic
2- Non Carbonic
9. Acid – Base Balance
Metabolism results in the generation of
approximately 15000 mmol CO2
CO 2 + H2O = H2CO3
10. Acid – Base Balance
An acid is a substance that can donate H +
A base is a substance that can accept H +
H2CO3 , HCl, NH4, H2PO4 can act as
acids
11. Acid – Base Balance
Non Carbonic acids are derived from protein
metabolism .
50 to 100 meq/day of H + are produced daily
and excreted in the urine
12. Acid – Base Balance
If HCl is added
HCl + Na2HPO4 -----NaCl + NaH2PO4
13. Acid – Base Balance
H CO3 + H+ ------ H2O + CO2
15. Acid – Base Balance
Stop
Think
Get anamnesis
Physical examination
pH
Bicarbonate
pCO2
Adequacy of compensation
16. Diagnosis
The evaluation always starts with the anamnesis
Then determine the pH
See if compensation adequate
Remember, compensation is never complete
Metabolic acidosis, determine anion gap
Metabolic alkalosis, determine volume status
17. Metabolic Acidosis
Characterized by a fall in the plasma
bicarbonate and a low pH
Either by bicarbonate loss
Or addition of acid
This results in compensatory decrease of
pCO2
18. Metabolic Acidosis
Normal anion gap
Gastro- intestinal loss of bicarbonate
Renal loss:
a. Proximal RTA
b. Distal RTA
c. Type IV RTA (Hypoaldosteronism)
d. Ammonium chloride
e. Hyperalimentation
19.
20. Acid – base balance
If metabolic acidosis, determine anion gap
If metabolic alkalosis, determine volume status
21. Metabolic acidosis
High anion gap
Lactic acidosis
Ketoacidosis
Renal failure - Organic acids
Intoxications
a. Salicilate
b. Methanol
c. Ethylene glycol
d. Sulfur
Rhabdomyolysis
23. Metabolic Alkalosis
Results from elevation of plasma
bicarbonate associated with high pH
May be due to bicarbonate administration
May be due to H+ loss
Respiratory compensation consists of
hypoventilation and pCO2 elevation
24. Causes of Metabolic Alkalosis
Loss of H+: Gastrointestinal loss
Renal loss: Diuretics
Mineralocorticoid excess
Penicillins
Hypercalcemia
Hydrogen movement into the cells - Hypokalemia
Retention of bicarbonate: Blood transfusion
Bicarb administration
Contraction alkalosis: Diuretics
25.
26. Metabolic Alkalosis
Impaired HCO3 excretion with perpetuation of
metabolic alkalosis
Decreased GFR
Volume depletion
Increased tubular reabsorption
Volume depletion
Chloride depletion
Hypokalemia
Hyperaldosteronism
37. Example
20 y old vomiting, lethargy, tachypnea,
tachycardia BP 150/100. IDDM , no insulin
lately. Almost no food last few days, Na
142, K 3.6, Cl 106, Bic 16, Gluc 230, Urea
190 , Creatinine pending, pH 7.28, PCO2
34. Urine Ketones moderately positive-a
couple of hours ago. No urine since.
38. continuation
Diabetic ketoacidosis
Treated with insulin,2.5 Lt saline and Potassium
chloride
After 3 hours patient lethargic, Met Ac not
improved, Gluc 70, jugular ++ reflux++
Rales +++
Anuria
At last, Creatinine results………12…..
39. continuation
LESSONS
Consider all possibilities
Urine Ketones positive in starvation and
vomiting
Check urine output before giving IV
Control your patient often !!!
49. Continuation
Adequate compensation is ( - ) 5 mEq
Bicarbonate / 10 mm Hg
If acute, Bic should be 23
Since it is Chronic Respiratory Alkalosis ( more
than 48 hours) Bic should be ( 24- 5)= 19
Anion Gap is normal- there is no hidden Met Ac
Simple Chronic Respiratory Acidosis
51. CONTINUATION
For Met Alk pCO2 should be 40
= 0.6( 44-24)= 52
pCO2 is to high ( 65 ), so
Metabolic Alkalosis + Respiratory Acidosis
Why not respiratory acidosis +
compensation?
52. EXERCISE
21 y old IDDM presents with vomiting
pH 7.75
pCO2 24
BIC 32
Anion Gap 30
53. CONTINUATION
Adequate Compensation : pCO2 should be
40+ 0.6 ( 32-24 )= 44.8, so
Respiratory Alkalosis.
Anion Gap is 30 , so
Hidden Metabolic Acidosis.
Delta Anion Gap 16, Bic should have fallen to
+ - 6-8, but is 32
1. check pt\n2. check blood gases\na. pH (compensation is never complete)\n\n\n
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pH goes down- resp center works more bc of receptors that sense pH\n\n- always have same amount of - and + charges all over\n- anion gap: other things we dont measure in the blood that contribute \n- Na: 140 (positive)\n- Cl: 100 (negative)\n- bicarb: 22/23 (negative)\n- cl and bicarb should equal na, but it doesnt bc of other things affecting it\n- normal anion gap: 14-16\n- created when pt loses bicarbonate\n- met acidosis, w normal anion gap: means pt lost bicarb\n- lose bicarb: GIT or renal losses\n
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high anion gap: \n- when add acid\n\nadd acid:\n1. severe prolonged exercise: lactic acidosis\n2. diabetes: great amount of ketones in the body\n3. renal failure: kidneys cant eliminate the end product of metabolism: acids\n4. Intoxications\n- methanol dx: have severe optic nerve neuritis- disc is very fuzzy\n- salicilate: combo of metabolic acidosis and resp alkalosis: aspirate\ncreatinine- component of the muscle\n- have about 1\n- useful to measure kidney fnxn in steady state\n- takes time to rise\n- of take out 2 kidneys: and measure:\n- cr = normal (takes time to accum)\n- GFR = 0\n\n
add acid- get met acidosis\nadd base- no problem\nwhay?\nbc bicarb: peed out\n- this is how all bicarb, w normal kidneys, gets out\nmost common acid/base problem in the hospital = metabolic alkalosis\nmet alkalosis:\n-get bicarb\n- impede bicarb excretion\n\n1) excess of suprarenal homones\n2) dehydration\n- GFR go down, bicarb reabsorbed, bicarb of blood increases\n
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- can lose H whenever H goes into the cells\n\n
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- pH low = acidosis\n- bicarb low = met acidosis\n- high anion gap\n- high creatinine \n- you almost ALWAYS get traces of ketones (so prob not ketonuria)\n- is compensation adequate? compensation (low pco2)... next slide\n\n\n\n\n\n\n
approximation: level of pco2 should be equal to the last 2 digits of the pH\n(doesnt alway work- bc there is a level of pco2 that you cant reach- cant go below 20)\n... so it IS ADEQUATE\n
resp compensation in metabolic problems is immediate\n- metabolic compensations to resp problems is SLOW\n\namount of coompensation by the kidneys- depends on how long the resp problem has been present\n\nacute: less than 24 hours: 1\nchronic: 3.5-5\n\n
normal pH - can be due to fact that have 2 alterationds in 2 diff directions\nwhen have high cl- anion gap is prob normal\n- lways check the anion gap! \n\n- when have normal pH- and other problems- must have at least 2 problems- bc compensation is never complete\n\nASPIRIN DOES THAT\n
pH low - acidosis\nbicarb low: met acidosis\nanion gap is high\npco2- normal\n- should be low! no compensation\n
only calculate anion gap in metabolic acidosis\n\nph high: alkalosis\nbicarb high: met alkalosis\ncompensation: pco2 should be higher- not enough compensation\n\nmet acidosis and resp alkalosis\n
ph: lower border of what expect: acidosis\nbicarb: low (by ~ 12) - met acidosis\npco2: low (by 20)\nanion gap: high\ncompensation: not adequate\n\nthere is no such thing as OVER-COMPENSATION\n\n
ph: acidosis\nbicarb: low (by 7) - met acidosis\nanion gap: 20: high\ncompensation: about 28, with pco2 of 34 (bc also have vomiting)\nhigh anion gap metabolic acidosis\n\n\nurinary ketones in a person who is not eating- makes sense\n- its enough for a person to get ketones in urine after dont eat for 16 hours\n\n\n\n\n
also has renal failure\n\n\nnormal cr = 0.9!- acute renal failure\n\n\ncheck all possibilities- bc certain tx can be problematic\n
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ph: high- alkalosis\nbicarb: high- met alkalosis\ncompensation: adequate\n\n\n\n
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ph: high= alkalosis\nbicarb: high = met alkalosis\ncompensation: not adequate\n\n(can start by assuming that the pt has two problems in the same direction- bc the ph is so high)\n\n
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resp acidosis\npco2: high\n\nacute: bc kidneys havent started to compensate yet-\n- bicarb only changed 2, and pco2 is 20 over the normal \n
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ph: high\nbicarb- low: resp alkalosis\npco2- low: \n\nresp alkalosis\n\n\nevery 10 change in pco2: should have:\n- 1 change in bicarb = acute; \n- up to 5= chronic\n
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alkalosis\nmetabolic\n\n
why not resp acidosis and compensation?\n- bc cant have too much compensation- no such thing- this cant happen- ph is too high\n