This document discusses acid-base disorders and their management. It provides an overview of acid-base physiology, the approach to evaluating acid-base disorders, common causes and types of acid-base disorders, and guidelines for correcting acid-base imbalances. Key points include: evaluating the primary disturbance, compensatory responses, and anion gap; causes of high vs normal vs low anion gap acidosis; hazards of over-correcting alkalosis; and only treating with bicarbonate if pH is below 7.2.

1. Dr. Hamed Ezzat El-Eraky
Nephrology Specialist
Mansoura International Hospital
CME Director of Dakahlia Medical
Syndicate

2. PH
Is the –ve Log of H+ Concentration
Normal Plasma H+ Concentration is 40 nanomoles/litre
Thus, doubling or Halving H+ concentration Increases or
Decreases PH by Approximately 0.3
Acid An H+ Donor
Base An H+ Acceptor

3. Blood PH > 7.45Alkalaemia
Blood PH < 7.35Acidaemia
Acidosis
Is the Abnormal Process that Tends to
Lower the Blood PH
Alkalosis
Is the Abnormal Process that Tends to
Raise the Blood PH

4. PaO2 Is the Partial Pressure of O2 in arterial Blood Normal Value when Breathing Air: (Age Dependent)
95-100 mmHg or 12.5-13 Kpa at Age of 20 Years - 80 mmHg or 10.8 Kpa at Age of 65 Years
A Substance that Counteracts the Effect of Acid or Base on Blood PHBuffer
HCO3- Is the Blood Bicarbonate Concentration Normal Value is : 22-26 mmol/l
PaCO2 Is the Partial Pressure of CO2 in Arterial Blood Normal Value: 35-45 mmHg or 4.7-6 Kpa
Mixed Disorder Two or More Primary Acid-Base Disorder Coexist
Compensation The Normal Body Processes that Returns Blood PH Towards Normal

5.  Arterial blood
› pH 7.4 7.36-7.44
› PCO2 40mmHg 36-44
› HCO3 24 mm 22-26
 Venous Blood
› pH 7.38 7.34 -7.42
› PCO2 46mmHg 42-50
› HCO3 22 mm 20-24

6.  Acid-base balance is assessed in terms of CO2-HCO3
buffer system. It is expressed in pH:
pH = 6.10 + log ([HCO3-] ÷ [0.03 x PCO2])
 Large number of metabolic events are sensitive to pH
mainly brain and heart
 That is why a number of mechanisms are present in acid
base regulation holding blood pH in narrow limits
7.38-7.42

7.  An acidemia (low pH) can result from either a
low HCO3 or a high CO2 .
• An alkalemia (high pH) can result from either a
high HCO3 or a low CO2

9. 1. History taking and physical examination
2. Assess accuracy of data (validity).
3. Identify the primary disturbance
1. Check arterial pH-------- acidosis or alkalosis
2. HCO3
- & pCO2 analysis---primary disorder.
4. Compensatory responses
5. Calculate AG

10.  Step 1.
History taking and physical examination
Comprehensive history taking and physical
examination can often give clues as to the
underlying acid-base disorder

11. Respiratory alkalosisPulmonary embolus
Respiratory acidosisCOPD
Metabolic acidosis
Dehydration or shock
Hyperkalaemia
Metabolic alkalosisVomiting , Hypokalaemia
Metabolic acidosis
Severe diarrhea
salisylates or alcohol intoxication
Metabolic acidosisRenal failure
metabolic acidosisHyperglycaemia (DKA? if ketones present
Respiratory alkalosisCirrhosis

12. 1. History taking and physical examination
2. Assess accuracy of data (validity).
3. Identify the primary disturbance
1. Check arterial pH-------- acidosis or alkalosis
2. HCO3
- & pCO2 analysis---primary disorder.
4. Compensatory responses
5. Calculate AG

14. PH : 7.4 + 0.03
H : 40± 3 mmol/L
P CO2: 40 ± 5mmHg
HCO3: 24 ± 4 meq

15. 1. History taking and physical examination
2. Assess accuracy of data (validity).
3. Identify the primary disturbance
1. Check arterial pH-------- acidosis or alkalosis
2. HCO3
- & pCO2 analysis---primary disorder.
4. Compensatory responses
5. Calculate AG

16.  Continuous production of H+ from normal metabolism
Metabolic event Acid produced
Aerobic glycolysis CO2 (15,000 mmol/d)
Krebs Lactic acid
lipolysis Free FA
Hepatic metabolism ketones
Dietary protein amino acids

17.  Immediately buffers in blood (NaHCO3)
change strong acid to weak acid
 after several minutes this weak acid
decomposes to CO2 carried by Hb to be
expired by lungs
 After several hours the kidney smoothly
reabsorbs the HCO3 wasted

18.  Acidosis:
› hyperventilation to wash excess CO2 produced
› acidification of urine to remove H+
 Alkalosis
› only alkalization of urine
› respiration cannot stop!!!
 250 cases of acidosis for one case of alkalosis

19.  Respiratory Acidosis
› CO2 retention due to hypoventilation: type II respiratory failure e.g.COPD
› there is conservation of HCO3 by the kidney
› new steady state of h CO2 and h HCO3 occurs
 Metabolic Acidosis
› H+ buffered a H2CO3 a CO2 + H2O
› CO2 washed by hyperventilation a i CO2 falls
› HCO3 continuously consumed by H+ cannot raise and remains low i HCO3
 These compensatory mechanisms a keep pH constant
 When H+ production or CO2 retention > compensatory mechanisms a fall in pH a
acidosis

20.  Fixed acids: which produces H+ cannot be excreted except
by kidneys e.g. lactic
 Volatile acids can be changed into CO2 e.g. H2CO3 and
aerobic glycolysis
 fixed : volatile = 100 : 15000 meq/day!!
 Severe acidosis develops rapidly in respiratory
embarrassment
 Acidosis develops slower in renal failure

21. HCl + NaHCO3 H2CO3 + Na Cl
CO2H2O
HCO3
Kidney's
CO2 + H2O H2CO3
H+ Na+
CA

22.  Normally blood is neutral
› amount of anions = amount of cations
 Most abundant cations are
› Na+ 140 meq/L (135-145)
› K+ 4 meq/L (3.5-5.0)
 Most abundant anions are
› HCO3 25 meq/L (22-26)
› Cl 104 meq/L (100-108)

23. Actually there is no gap
CATIONSANIONS
Calcium 5Organic acids 5
Magnesium 1.5Sulfates 1
Potassium 4.5Phosphates 2
Sodium 140Proteins 15
Bicarbonates 24
Chlorides 104
Total 151Total 151

24.  If you measure all the anions they should be equal to all the
cations
› cations - anions = zero
 it is difficult to measure them all.
 An easy way is measure the most abundant
 [Na + K] - [HCO3 + Cl] = [144] - [129] = 16
 Why is this difference? Are the cations more?
 Of course not

25.  It is due to presence of unmeasured anions (and cations) and if you
measure them all definitely your sum will be zero
[Na + K + UC] - [HCO3 + Cl + UA] = 0
 Unmeasured anions are mainly albumin and proteins
 Unmeasured cations are mainly Ca and Mg
 under normal conditions:
[Na + K] - [HCO3 + Cl] = 15 +/- 2
This is called normal anion gap

26.  High anion gap acidosis
 Normal anion gap acidosis

27. › There is a load of non chloride containing acid e.g. lactic
acid
› lactic acid + NaHCO3 Na lactate + H2CO3
› There is a fall in HCO3 conc and rise in lactate
› calc: [Na + K] - [HCO3 + Cl] = > 17
› The fall in HCO3 is compensated by the unmeasured
lactate

28.  There is addition of a Cl acid e.g. HCl or Loss of
HCO3 (with renal absorption of chloride)
› HCl + NaHCO3 n NaCl + H2CO3
› There is fall in HCO3 concentration and rise in chloride
› calc: [Na + K] - [HCO3 + Cl] = 15 +/- 2
 since chloride is increased it is easier to name it
hyperchloremic acidosis

29.  Three main causes (DAD)
1. Diversion of ureters (uretero-colic)
2. Diarrhea
3. Aldosterone deficiency (1ry or 2ry)
– Other less common causes (mainly drugs)
› RTA
› Diamox - ammonium chloride -arginine -Lysine

30.  Renal failure (many organic acids)
 Ketoacidosis (ketone bodies)
 Lactic acidosis (lactic acid)
 Toxins (many for example)
› salcylates overdose (salcylic acid)
› methanol poisoning (formic acid)
 A higher anion gap>25 may implicate lactic acidosis

31.  Sometimes you can get a mixed type
› renal failure due to obstructive uropathy
› Addison with pre-renal failure
› In such cases chloride is not that high and AG is just above normal
 If there is hypoalbuminemia
› less unmeasured negative charges available
› body has to get rid of Na to reach isoelectric
› anion gap will seem less than it should be

32.  Kusmull’s respiration
› deep and rapid , shallow and rapid
 Heart
› -ve inotrope , low AF threshold
 Mental confusion
 extracellular K shift
› Hyperkalemia
 Effect on ODC
› Shift of ODC to the
right opposing 2-DPG

33. urine for ketones
+VE -VE
RBS
LOW OR N
STARVATION
high
DIABETES
Anion gap
high
renal failure
lactic acidosis
toxins
hyperchloremic
hypoaldosteronism
for workup
if renal function
and lactate
do not explain
send to toxicology

34.  ECLS Approach
 Emergency
 Cause
 Losses
 Specific

35. › history
 diarrhea
 drugs
 diabetes
 surgery
 food intake
› general exam
› Urine
› electrolytes
› ABG
› urea
› RBS
You have to identify the cause and treat it

36.  Hazards of giving
› hypertonic solution
 volume overload (ESP IN RENAL FAILURE)
› Overshoot alkalosis :ketones and lactate could further be
metabolized to bicarbonates
› Rapid correction of acidosis may shift ODC to left and 2DPG will
dominate to cause hypoxia
› Bicarb will decompose to CO2 which passes easily to BBB and
cause CSF paradoxical acidification (the use of carbicarb)

37.  Hazards of not giving
› effects on heart brain and muscle
 At a certain stage with acidosis (pH7.15) all the
compensatory mechanisms are at their maximum power
› No more compensatory mechanisms available:
› any mild change in concentrations of CO2 or HCO3 will greatly affect
the pH

38.  Judge your decision by the pH and never by the HCO3
or CO2 levels
 Do not give HCO3 unless pH is lower than 7.2 (7.1 by
some authors)
 Calculate the deficit by the formula
[24-HCO3] x 50% of body weight
 Correction should be slowly over 3 hours guided by
hourly blood gases and HCO3