1. PhD ( physiology), IDRA , FICA , Certifícate in USGRA
Acid base balance 3
Dr. S. Parthasarathy
MD., DA., DNB, MD (Acu), Dip. Diabetes, Diploma in Software based statistics,
PhD ( physiology), IDRA , FICA , Certifícate in USGRA

2. Blood Normal pH is 7.36 – 7.44 < 7.35 - acidosis
> alkalosis
Actually the process is called acidosis
The result is called acidemia
DKA – process
Blood becomes acidemic

3. Basic types Acidosis and alkalosis Metabolic and respiratory
Acute and chronic

4. What is metabolic and what is respiratory acidosis
Acidosis that occurs when the lungs fail to remove excess carbon dioxide from our bloodstream during the process of respiration is respiratory acidosis. 
Acidosis that occurs when the digestive and urinary systems fail to breakdown and maintain the proper level of acids in the blood is known as metabolic acidosis.

5. Respiratory alkalosis is a disturbance in acid and base balance due to alveolar hyperventilation.
Alveolar hyperventilation leads to a decreased partial pressure of arterial carbon dioxide (PaCO2)
Metabolic alkalosis – non respiratory acid exit
Example if a patient vomits and throws acid out

8. Acute Respiratory acidosis
CNS lesions
Sedatives opioids
Pulmonary edema
Obstruction
FBs
Hemopneumothorax
Collapse
Compensations come last

9. Chronic Respiratory acidosis
Fibrosis
COPD
Asthma
Bronchiectasis
Kyphoscoliosis

10. Respiratory alkalosis
Head Injury, Stroke
Anxiety-hyperventilation syndrome (psychogenic)
Other 'supra-tentorial' causes (pain, fear, stress, voluntary)
Various drugs (eg analeptics, propanidid,)
Hypoxemia , hyperthyroidism
Pulmonary edema – sometimes
Compensatory

11. Acute Metabolic acidosis
MUD pilers
Methanol, Metformin
Uremia
Diabetic Ketoacidosis (DKA), Alcoholic Ketoacidosis or starvation ketosis
Paraldehyde, Phenformin (neither used in U.S. now)
, Isoniazid (due to Seizures)
Lactic Acidosis
Ethylene Glycol, Ethyl Alcohol
Rhabdomyolysis
Salicylates
Acute Metabolic acidosis

13. Metabolic alkalosis Vomiting Hypokalemia Diuretics Hyperaldosteronism
Nasogastric suction

14. Important clinical terms

15. Base excess !! Base deficit !!
Base excess as the amount of strong acid (in mmol/L) that needs to be added in vitro to 1 liter of fully oxygenated blood in order to return the sample to standard (normal) conditions (pH 7.40, pCO2 40 mmHg and temperature 37 °C.)
Base excess – alkalosis
Base deficit – acidosis

16. Of course, as the author ?? Sigaard anderson points out, if blood already has a pH of 7.40, a pCO2 of 40 mmHg and a temperature of 37 °C, then base excess is by definition 0 mmol/L. 

17. Base excess or deficit
A base deficit (i.e., a negative base excess) can be correspondingly defined in terms of the amount of strong base that must be added.
A further distinction can be made between actual and standard base excess:
actual base excess is that present in the blood, while standard base excess is the value when the hemoglobin is at 5 g/dl.
The latter gives a better view of the base excess of the entire extracellular fluid.

18. SBE = HCO3 (act )− 24.8 + [16.2 × (pH − 7.40)]
Base excess ( alkalosis ) or deficit ( acidosis)
Indicates a metabolic problem

19. Standard bicarbonate
Standard bicarbonate is the concentration of bicarbonate in the plasma from blood which is equilibrated with a normal PaCO2 (40 mmHg) and a normal pO2 (over 100 mmHg) at a normal temperature (37°C)
Bicarb is 18 and standard bicarb is also 18
Then - metabolic component

20. Previous Problems
Pitfalls of interpreting acid-base problems by use of standard bicarbonate and base excess can be:
1. Inaccurate identification of the severity of an underlying acid-base disturbance,
2. Inadequate estimation of the time course of adaptation to an acid-base disorder (acute versus chronic)
3. Failure to identify mixed acid-base disorders.

21. So came many more terms !!

22. Anion gap
The anion gap is the difference between primary measured cations (sodium Na+ and potassium K+) and the primary measured anions (chloride Cl- and bicarbonate HCO3-) in serum.
{Na+ + K+ } - {Cl- + HCO3- } = 8- 11
140 – 130 = 10
Normal is 8 – 11
We are electrically neutral !!

23. Minimal unmeasured cations also
Unmeasured anions
Minimal unmeasured cations also

24. Two types
Metabolic acidosis
Normal anion gap
Increased anion gap

25. Gold mark – increased anion gap
Glycols (ethylene glycol, propylene glycol)
Oxoproline (pyroglutamic acid, the toxic metabolite of excessive acetaminophen or paracetamol)
L-Lactate (standard lactic acid seen in lactic acidosis)
D-Lactate (exogenous lactic acid produced by gut bacteria)
Methanol (this is inclusive of alcohols in general)
Aspirin (salicylic acid)
Renal Failure (uremic acidosis)
Ketones (diabetic, alcoholic and starvation ketosis)

26. See the unmeasured anions

27. Increased anion gap Gap widens Usually above 22 meq
Anion gap = (Na K+ ) – ( HCO3- + Cl-)
There is no increase in Cl-
Gap widens
Usually above 22 meq

28. NAGMA – HARDUP
H = hyperalimentation (e.g., starting TPN). A = acetazolamide use. R = renal tubular acidosis (Type I = distal; Type II = proximal; Type IV = hyporeninemic hypoaldosteronism. D = diarrhea U = uretosigmoid fistula (because the colon will waste bicarbonate). P = pancreatic fistula (because of alkali loss–the pancreas secretes a bicarbonate-rich fluid).

29. Normal anion gap metabolic acidosis
NAGMA

30. HCO3 decreases but Cl increases i. e
HCO3 decreases but Cl increases i.e. the retention or excess of hydrochloric acid
Anion gap = (Na K+ ) – ( HCO3- + Cl-)

31. Ammonium chloride ingestion
NH4 → NH H+ ion
But chloride remains
Anion gap = (Na K+ ) – ( HCO3- + Cl-)
NAGMA

32. RTA
loss of bicarbonate, along with its counterbalancing cation sodium, produces volume contraction, thereby stimulating the renal tubule to retain sodium chloride.
The consequences of these events are the replacement of sodium bicarbonate by sodium chloride.
Anion gap = (Na K+ ) – ( HCO3- + Cl-)

33. Examples Nacl administration (150 + 150) ↓ NaHCO3 excreted
retention of Hydrogen ions and chloride ions
NAGMA

35. Gaps in anion gap
Serum chloride concentration was raised by approximately 3 mEq/L for every 1-mEq/L increase in the concentration of bromide
lithium is a cation, it can lower the serum anion gap when present in sufficient concentration
Hypercalcemia as a result of primary
hyperparathyroidism, the serum anion gap was reduced by approximately 2.4 mEq/L

36. Don’t worry – only two more terms !!

37. SID
The Strong Ion Difference (SID) is the difference between the positively- and negatively-charged strong ions in plasma.
Is it simply Na – Cl
Or adding ca, mg this side --- with lactate on the other side
35-40

38. What is delta gap ??

39. Delta gap Na = 145 K = 4 Cl = 101 HCO3 = 15 ?acidosis
Anion gap = ( ) – ( ) = 29
Delta gap = anion gap(29) – 12 = 17
( HCO3) = 32
Additional metabolic alkalosis

40. Winters' Formula for Metabolic Acidosis Compensation
expected PaCO2 = [1.5 x (serum HCO3)] + 8 [±2]
if PaCO2 lower, there is a concomitant primary respiratory alkalosis
if PaCO2 higher, there is a concomitant primary respiratory acidosis

41. Another metabolic acidosis situation
1.5 * 15 = = 30.5 ±2
PaCO2 = 32
No primary respiratory problem

43. Delta ratio AG – 12 / 25 – HCO3 < 0.4 due to a pure NAGMA
0.4 – 0.8 due to a mixed NAGMA + HAGMA
0.8 – 2.0 due to a pure HAGMA
>2.0 due to a mixed HAGMA + metabolic alkalosis

44. Summary Acidosis and acidemia Types
Causes of metabolic and respiratory acidosis
Causes of metabolic and respiratory alkalosis
Compensations
Anion gap, delta gap
Base excess
Standard bicarbonate