2. Acid Base balance
Acid-base balance refers to the mechanisms the
body uses to keep its fluids close to neutral pH (that
is, neither basic nor acidic) so that the body can
function normally.
Arterial blood pH is normally closely regulated
to between 7.35 and 7.45.
3. acids ? Any ionic or molecular substance
that can act as a proton donor.
Strong acid : HCl, H2SO4, H3PO4.
Weak acid : H2CO3, CH3COOH.
bases ? Any ionic or molecular substance
that can act as a proton acceptor.
Strong alkali : NaOH, KOH.
Weak alkali : NaHCO3, NH3,
CH3COONa.
4. Origin of acids Much more
Intracellular metabolism
Volatile CO2+H2O=H2CO3 300~400L CO2 (15mol
acids H+)
Lactic acid
Fixed Ketone bodies 50~100 mmol H+
acids Sulfuric acid
Phosphoric acid
Origin of bases less NH3 , sodium citrate, sodium lactate
5. pH
- pH of ECF is between 7.35 and 7.45.
Deviations, outside this range affect
membrane function, alter protein function,
etc.
- You cannot survive with a pH <6.8 or >7.7
- Acidosis- below 7.35
Alkalosis- above 7.45
CNS function deteriorates, coma, cardiac
irregularities, heart failure, peripheral
vasodilation, drop in Bp.
6. Given that normal body pH is slightly alkaline and that
normal metabolism produces acidic waste products
such as carbonic acid (carbon dioxide reacted with
water) and lactic acid, body pH is constantly
threatened with shifts toward acidity.
In normal individuals, pH is controlled by two major
and related processes; pH regulation and pH
compensation. Regulation is a function of the buffer
systems of the body in combination with the
respiratory and renal systems, whereas compensation
requires further intervention of the respiratory and/or
renal systems to restore normalcy.
9. Major buffer system in the body
Carbonic acid/Bicarbonate(HCO3-/H2CO3) :
The major extracellular buffer , regulated by lungs
and kidneys , effective , determining the pH of
plasma.
Phosphate (HPO42-/H2PO4- ) : Intracellular
Protein (Pr-/HPr) : Plasma/Intracellular
Hemoglobin (Hb-/HHb and HbO2-/HHbO2 ) : RBC
*A buffer system cannot buffer itself.
fast / no permanence
10. 2) Respiratory control:
Expelling more CO2 through respiration→to
exclude volatile acid.
H+→chemoreceptor → excite respiratory
centre → hyperventilation → exclude volatile acid
Fast / effectively / only excludes
volatile acid
11. PaCO2↑ (40-80 mmHg)→ Blood-brain barrier
permeable to CO2: CO2+H2O↔ H2CO3 ↔ H++HCO3-(in
cerebrospinal fluid, CSF)→ [H+] ↑ → Central
chemoreceptor(beneath the ventral surface of the
medulla oblongata) → Respiratory center ↑ →
Ventilation↑ (Main)
12. 3) Role of kidney (exclusion of
acid with conservation of base)
hydrogen ion secreted
ammonium excreted by renal tubular
cell
bicarbonate reabsorbed
Effectively ( fixed acid may be
excluded ) / slowly
14. Definition of acid-base disorders
An acid base disorder is a change in the
normal value of extracellular pH that may result
when renal or respiratory function is abnormal
or when an acid or base load overwhelms
excretory capacity.
15. PLAY Animation: Relationship Between PCO2 and Plasma pH
Figure 27.6
16. Simple acid-base disorder
1. Metabolic acidosis
1) concept:
primary disturbance [HCO3-] ↓ ; PH .
PaCO2 ↓
2) clasification:
Normal AG
High AG
3) pathogenesis and mechnisms:
(1) lose of bases
(2) gaining acids
17. Metabolic acidosis
Causes:
(1) lose of bases (bicarbonate decreased)
Gastrointestinal losses: diarrhea
Renal losses: proximal renal tubular acidosis and distal
renal tubular acidosis
(2) gaining acids (bicarbonate consumed in buffering)
Lactic acidosis: tissue hypoxia, impaired oxygen utilization, severe liver
dysfunction, and shock
Ketoacidosis: diabetic,hepatic cirrhosis, alcoholic poisoning, or starvation
Renal failure: conservation of acids
Exogenous acid intake: ammonium chloride, salicylate, ethylene
glycol(commonly used in antifreeze), or methanol intoxication
18. 4) Compensation:all regulation system take part in
Compensation
5) Effects:
Effects
(1) Depression of central neural system
a Elevated activities of glutamate decarboxylase
→GABA ↑
b.ATP ↓
(2) Depression of heart and vessel(Ca2+ transport
disorder; hyperkalemia;ATP↓):
cardiac output ↓ ;
cardiac arrhythmias;
peripheral vasodilation.
(3) Skin: warm and flashed
(4) Alteration of skeleton:
decacification, retarding growth and
osteodystrophy
27. 3) Causes and mechanism:
mechanism
Mechanism:
Mechanism
a. Excessive gain of alkali (bicarbonate)
b. Excessive loss of hydrogen ions,
chloride or potassium ions
28. Causes:
a.Excessive gain of alkali (bicarbonate)
Bicarbonate intake:treatment of MAC
citrate-containing blood transfusions
Parenteral solution containing lactate
b.Excessive loss of hydrogen ions, chloride or
potassium ions
Gastrointestinal H+ loss:vomiting,gastric suction
Renal H+ loss:Aldosteronism,cushing’s syndrome
thiazide
c.Volume contraction
Dehydration
Diuretic therapy
29. 4) Compensation:
Compensation
Blood buffer role
limitation
Respiratory regulation
Ion exchange and H+ out cell to titrate bicarbonate
Renal role: excluding bicarbonate and conserving H +
5) Effects:
Effects
(1) Hypoventilation→ PaCO2 ↑, PaO2 ↓
(2) Agitation of central neural system: GABA↓ → seizures
(3) Increase excitability of the neuromuscle: free [Ca2+] decrease
→ muscle tremors
(4) Mental dysfunction: O2 dissociated curve leftshift → impairing
O2 release → ATP ↓. At 6-8 hs, 2,3-DPG↑ and curve shifts back
towards the right.
(5) Hypokalemia → reduced fibrillation threshold
30. 6) Principle of treatment:
treatment
a. Etiology treatment
b. Administration of KCl. or spironolactone if
K+ and Cl- deficits are present
c, Carbonic anhydrase inhibitor:
acetazolamide
31. Respiratory alkalosis
1) Concept:
Concept
Primary change : H2CO3 ↓ or PaCO2 ↓ ; pH
2) Classification:
Classification
a. Acute RAL
b. Chronic RAL
32. 3) Causes and mechanisms:
mechanisms
Mechanisms: Hyperventilation
Causes:
a. Psychogenic hyperventilation:Hysteria
b. Stimulation of respiratory center:
High altitude hypooxia
Salicylate toxication
Blood ammonia↑(Hepatic
encephalopathy)
Encephalitis
Brain injury
Fever
33. 4) Compensation:
Compensation
In acute RAC:
Ion exchange, H+ out of cell to titrate base in ECF
In chronic RAC:
Decreased excretion of H+ and NH4+
Decreased reabeorption of HCO3-
5) Effects:
Effects
(1) Increased excitability of the nerve and muscle
(2) Mental dysfunction
(3) Hypokalemia,hypochloridemia
6) Principle of treatment:
treatment
a. Decreased ventilation by administration of
sedative.
b. Application of a plastic bag to inspire more
34. The Central Role of the Carbonic Acid-Bicarbonate Buffer
System in the Regulation of Plasma pH
Figure 27.11b