This document discusses acid-base disorders and their physiology, regulation, and treatment. It begins by introducing acid-base balance and pH in the body. It then covers the chemical buffer systems that help regulate pH, as well as the roles of respiration and the kidneys. It discusses different types of acid-base disorders like metabolic acidosis and alkalosis, respiratory acidosis and alkalosis, and mixed disorders. Interpretation of blood gas analysis and various approaches for analyzing acid-base status are also outlined. Throughout, compensation mechanisms and typical treatment approaches for each disorder are described.

1. ACID-BASE DISORDERS
By: Leonardo Paskah S, MD
Cardiology & Vascular Medicine of Universitas Padjadjaran
Bandung-Indonesia

2. INTRODUCTION
• Blood [H+] is only 0.00004 mEq/L & tightly
controlled
• [H+] is common represented in pH
pH = -log10 [H+]2

3. Acid
substances
Base
substances
solution
BUFFER
H+
H+
Balancing 
H+
Playing a key role in
regulation of acid-base in
the body
ACIDOSIS
ALKALOSIS

4. Normal pH in body fluid
Body fluid pH
ECF:
-Arterial blood
- venous blood
- interstitial
7.40
7.35
7.35
ICF 6.0-7.40
Urine 4.5-8.0
Gastric juice 0.8

5. PHYSIOLOGY
Carbohydrate & lipid
metabolism
-protein metabolism
- internal pathologic
process
- external pathologic
process
rapid
more gradual

6. REGULATION MECHANISMS
1. CHEMICAL BUFFER SYSTEM
 rapid action, but less effective in severe or chronic cases
 converting strong acid/ base to weak acid/base
 there are 3 kinds:
- bicarbonate systems  the strongest & most useful in ECF
- phosphate
- protein
2. VENTILATION (LUNGS)
 limited capability; only eliminates volatile acid
 by changing the depth or/and rate of respiration;
3. RENAL
 more gradual but can lead to total recovery in metabolic disorders
 by regulating excretion of H+ and excretion/ reabsorption HCO3-

7. Regulation of respiration
Central chemoreceptors
Peripheral chemoreceptors: carotid and aorta
 sensitive to Δ pO2, pCO2, pH

8. Acid (ammonium) excretion by
renal

9. Henderson-Hasselbalch equation
[H+] = (7.80-pH)x100 mEq/L
[H+] in normal pH 7.40 = 40 mEq/L
Respiration
Renal

10. ACIDOSIS or ALKALOSIS
pH correction
Respiratory system
 CO2 regulation
Kidney
 HCO3 regulation
Compensation
mechanisms

11. Acid-base nomogram and compensation
response
Lang F. Respiration, acid-base balance. In: Silbernagl S, Lang F, editors.
Color Atlas of Pathophysiology. NY: Thieme;2000.

12. Predicted compensation
response
Disorders For every.. Predicted response
Metabolic acidosis 1↓ HCO3 1↓ HCO3
Metabolic alkalosis 10↑ HCO3 7↑ p CO2
Acute respiratory
10↑ pCO2 1↑ HCO3
acidosis
Chronic respiratory
acidosis
10↑ pCO2 4↑ HCO3
Acute respiratory
alkalosis
10↓ pCO2 2↓ HCO3
Chronic respiratory
alkalosis
10↓ pCO2 5↓ HCO3
Note: Renal and respiration compensation are in the same direction

13. Blood Gases Analysis (BGA) test

14. Interpretation of BGA
Oxygenation status Acid-base status
pH correlated to [H+]  acid-base degree
pCO2 Oxygen partial pressure in blood; normal 80-100 mmHg
SaO2 Arterial oxygen saturation; normal 95-100%
pCO2 CO2 partial pressure in blood; normal 35-45 mmHg
HCO3- Bicarbonate in circulation (calculated); normal 22-26
mEq/L
Base Excess (BE) Deficit or excess of bicarbonate in blood; normal -2 to +2
mEq/L
Parameters in BGA test

15. Parameters for analysis of acid-base
disorders

16. Methods of interpretation

17. Nomogram of acid-base disorders

18. Stewart’s SID
• Dependent variables: [H+], [OH-], [HCO3-], [CO3 2-], [HA],
[A-]
• Independent variables: pCO2, [A-tot], [SID]
– [SID]= [Na]+[K]+[Ca]+[Mg] – [Cl] – [other strong anions]
 normal = 40 mEq/L  similar numerical value as BE
– [A-tot]= [Pi-tot] + [Pro-tot] + albumin
– [CO2] = pCO2 in blood
• Limitation:
– Complexity of the chemistry & mathematics
– Lack of clinical correlation
– SID neglects Hb as a buffer  less accurate than BE
www.acid-base.com/strongion.php

19. Interpretation of Handerson Hasselbalch approach
STEP 1 Re-check the data  [H+]=24 x pCO2 / [HCO3-]
[H+] mEq/L= (7.80-pH)x100
STEP 2 Acidemia (pH <7.37) or alkalemia (pH
>7.42) ?
STEP 3 Determining the primary disorder; metabolic or
respiratory ?  look any Δ pCO2 and HCO3-
STEP 4 Determining compensatory mechanisms  expected
or excessive deviation ?
STEP 5
(for metab acidosis)
Anion Gap= [Na]- ( [Cl] + [HCO3])…...... n<12
Hypoalbuminemia AGc= AG + (2.5x Δ albumin)
STEP 6
(for AG > 12)
Delta/delta = ΔAG/ΔHCO3 = (AG-12)/(24-HCO3)
Delta/delta > 1 = metab acidosis + alkalosis
Delta/delta < 1 = metab.acidosis gap + non-gap

20. 1. METABOLIC ACIDOSIS

21. Type of metabolic acidosis
GAP metab. acidosis
• Exogenous: salicylate
intoxication, methanol,
alcoholic ketoacidosis
• Endogenous: lactic
acidosis, diabetic
ketoacidosis, starvation,
uremia
NON-GAP metab.acidosis
• Renal loss: renal tubular
acidosis, carboanhydrase
inhibitor
• GI tract loss: diarrhea,
fistule,
ureterosigmoidostomy
Hyperchloremic acidosis

22. Alcoholic
intoxication

23. Therapy of metabolic
acidosis
• Correct underlying disease
• Correct hydration state and electrolyte imbalance
• Bicarbonate  controversial
- Indicated for severe acidosis (pH < 7.20), esp.
GAP metabolic acidosis
- total needed (mEq)= Base deficit x BW(kg)/4  ½ doses is given
within first 8 h
• Chronic non-severe acidosis: bicarbonate oral for
[HCO3-] <18 mmol/L + clinical symptoms

24. 2. METABOLIC ALKALOSIS

25. Type and therapy of metabolic
alkalosis
Chloride-sensitive Chloride-insensitive
* [Cl-] urine < 10 mEq/L
* prolonged Cl (and H+) loss
via urine/GI tract  Na and
HCO3 retention by renal
* GI tract loss: vomit, NGT
suction, diarrhrea
* renal loss: diuretic
* response to NaCl therapy
• [Cl-] > 10 mEq/L
• direct stimulation to renal
• causa: hyperaldosteronism,
steroid therapy, alkali intake
• not response to NaCl
therapy; therapy focused on
underlying cause (ex. stop
consuming steroid)
Therapy with strong acid (HCl, NH4Cl) is only for severe alkalosis and
resistant with standard therapy

26. 3. RESPIRATORY ACIDOSIS

27. 4. RESPIRATORY ALKALOSIS

28. 5. MIXED ACID-BASE DISORDERS
CLUE: - compensatory response exceeds expected value
- Δ pH is not suitable to known primary disorder
- pCO2 and HCO3 move not in same direction
- pH normal but with abN pCO2 and HCO3
Metab acidosis + resp
acidosis
Cardiac arrest, respiratory failure + renal failure
Metab acidosis + resp
alkalosis
Salicylate intox., sepsis, advanced liver disease + lactic acidosis
Metab alkalosis + resp
alkalosis
Hepatic cirrhosis + vomit/diuretic overuse, pregnancy +
hyperemesis, overventilation in COPD
Metab alkalosis + resp
acidosis
COPD with diuretic overuse/ vomit
Metab acidosis + metab
alkalosis
Uremia/ ketoacidosis + vomit
Triple disorders Ketoacidosis + muntah + liver disease + sepsis

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30. THANK YOU