酸碱平衡及紊乱 acid – base balance and disturbances
DESCRIPTION
酸碱平衡及紊乱 Acid – Base Balance and Disturbances. Acid-Base Balance Maintenance of the H + concentration in body fluid in a normal range. H + mol/L pH Extracellular fluid Arterial blood 4.0 x 10 -8 7.40 ± 0.05 Venous blood 4.5 x 10 -8 7.35 - PowerPoint PPT PresentationTRANSCRIPT
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酸碱平衡及紊乱Acid – Base Balance
and Disturbances
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Acid-Base BalanceMaintenance of the H+ concentration
in body fluid in a normal range H+ mol/L pH
Extracellular fluid Arterial blood 4.0 x 10-8 7.40 ± 0.05Venous blood 4.5 x 10-8 7.35 Interstitial fluid 4.5 x 10-8 7.35Intracellular fluid 1.0 x 10-6 6.0 to 4.0 x 10-8 7.4pH = - lg H+
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Why is the acid - base balance important for life ?
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Acid generation
•Volatile acid
CO2 + H2O H2CO3 H+ + HCO3-
H+ 15 –20 mol /d
• Fixed acids
phosphoric, sulfuric, lactic, ketone bodies etc.
H+ < 0.05 –0.10 mol /d
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Regulation of acid – base balance
•Buffering Buffer system can bind and release H+
Dissociated buffer + H+ H undissociated buffer
Principal buffers in blood:
in Plasma in RBC
H2CO3 / HCO3- 35% 18%
HHb / Hb- 35%
HProt / Prot- 7%
H2PO4- / HPO4
2- 5%
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Bicarbonate buffer system determines the pH of blood plasmaCO2 + H2O H2CO3 H+ + HCO3
-
Handerson-Hasselbalch Equation +
pH = pK + lg HCO3- / H2CO3 Na+
= 6.1 + lg HCO3- / 0.03 x PCO2
= 6.1 + lg 24 / 1.2 = 7.4
• Bicarbonate-carbonic acid system is the major extracellular buffer 53%
• H2CO3 can be regulated by lung• HCO3
- can be regulated by kidney
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•Respiratory regulation
PaCO2, pH Chemorecertor Pulmonary ventilation PaCO2
pH 7.0 VA increases by 4-5 times pH VA decreases less
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•Renal regulation Plasma pH
HCO3- H+
Reabsorption & Excretion Regeneration
Plasma pH
Renal H+ excretion = fixed acid production = 1mmol/kg/d
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Reabsorption of HCO3- in different segments
of renal tubule
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Reabsorption of HCO3- coupled with
H+ excretion in proximal tubules
CANa+
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Regeneration
Regeneration of HCO3- coupled with the buffering
of secreted H+ by filtered Na2HPO4 in distal tubules
Cl-
ATP
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Regeneration of HCO3- coupled with
buffering of H+ by NH3 in proximal tubular cells
Glutamine Tubular
lumen
glutaminase
NH3 NH3
-keto glutaric acid
NH4+ NH4
+
H2CO3 Na+
Na+
HCO3- H+ H+
ATP
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Regeneration of HCO3- coupled with buffering
of H+ by NH3 in collecting tubular cells
Cl-
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Net acid excretion by kidney
= NH4+ excretion + urinary titratable acid
– bicarbonate excretion
= nonvolatile acid production
In acidosis, a net addition of HCO3- back to blo
od as more NH4+ and urinary titratable acid are
excreted
In alkalosis, titratable acid and NH4+ excretion d
rop to 0, whereas HCO3- excretion increases
(No new bicarbonate is generated)
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Parameters of acid – base balance
1.pH = 6.1 + lg HCO3-/ H2CO3
Normal value of pH in arterial blood 7.4±0.05
pH normal, may be
1) acid-base balance
2) compensatory acid-base disorder
3) mixed acid-base disorder
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2. PaCO2 x 0.03 = H2CO3
Normal PaCO2 40 ± 6 mmHg
determined by the rate of CO2 elimination (alveolar ventilation), not by its production.
--- Respiratory parameter
3. Bicarbonate ( HCO3- )
Normal value of HCO3- in plasma under actual
condition is 24 ± 2 mmol/L
HA + NaHCO3 NaA + H2CO3
determined by the amount of nonvolatile acid produced in metabolism
--- Metabolic parameter
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4. Anion gap (AG) = UA - UC
Na+
(140)
HCO3-
(24)
Cl-
(104)
UC(11)
UA(23)
mEq/L
= Na+ - ( HCO3-+Cl- )
= 140 - ( 24+104 )
= 12±2mEq/L
dAG =dUA = dHCO3-
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Summary•The maintenance of H+ concentration of body fluid in a normal range is very important for life.
•Normal value of arterial pH is 7.35 – 7.45,
which is determined by the HCO3-/H2CO3 ratio, a
nd regulated by buffering, lung and renal regulation.
•Buffers act to minimize changes in pH induced by acid or base load; PaCO2 is controlled by alteration of pulmonary ventilation; HCO3
- in plasma is regulated by renal reabsorption and regeneration of HCO3
- coupled with equivalent H+ excretion.
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Simple acid-base disorders
Metabolic acidosis
Primary decrease in plasma HCO3-
Causes of metabolic acidosis:
• High AG type ---- Fixed acid HCO3-
1. Production of fixed acids
2. Retention of fixed acids --- GFR
3. Acid intake – salicylate etc.
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• Normal AG type ---- hyperchloremic
1. HCO3- reabsorption or regeneratio
n in renal tubules: Renal tubular acidosis ( RTA ) Renal failure Carbonic anhydrase inhibitor
2. HCO3- losses in alimentary tract:
Diarrhea
3. HCl, NH4Cl intake 4. Hyperkalemia
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§ Hyperchloremia in normal AG type due to reabsorption of Cl-
RTA HCO3- reabsorption
Cl-reabsorption Diarrhea Ald NaCl reabsorption
§ Paradoxical alkaluria in acidosis Renal tubular acidosis ---
HCO3- reabsorption or H+ excretion
Hyperkalemia renal H+ excretion
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Compensation of metabolic acidosis:
1) Extracellular buffering --- immediately
HA + NaHCO3 NaA + H2CO3
2) Respiratory compensation
Ventilation in few min, maximal in 12-24 h
d PaCO2 = 1.2 d HCO3- ± 2
3) Intracellular buffering --- in 2-4h
4) Renal compensation
begin in several h, maximal in 3-5d
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Respiratory acidosis Primary increase of PaCO2
Causes:
1) External respiratory dysfunction
2) PCO2 in inspired air
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Compensation of respiratory acidosis
1. Buffering ---- immediately
CO2 H2O
H2CO3
HCO3-
HHb
KHb
K+ K+
H+
H2CO3
HCO3-HCO3
-
Cl-
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2. Renal compensation
Acute --- d [ HCO3-] = 0.1 d PaCO2 ± 1.5
Chronic ---d [HCO3-] = 0.4 d PaCO2 ± 3
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Pathophysiological changes caused by acidosis
• Cardiovascular system
1) Decrease of myocardial contractility – pH<7.2 Responsiveness of -adrenoceptor
Contraction
Ca2+influx
SR [Ca2+]i↑
Binding to Troponin
H+
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2) Cardiac arrhythmia
Acidosis hyperkalemia arrhythmia
3) Vasodilation
Responsiveness of -adrenoreceptor
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•Central nervous system depression, coma ( pH < 6.9 ) 1) GABA ---- glutamate decarboxylase activity
2) Oxidase activity ATP 3) Cerebral vasodilation intracranial pressure
What kind of acidosis has more effect on CNS, metabolic or respiratory?
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H+ (-)
Na+ Na+ AldAld ATPase [K+]e K+channel K+ K+ [K+]e H+ (-)
Mg2+(-)
Urine flow K+
• Hyperkalemia --- 1) [H+]e exchange for [K+]i
2) Decreased excretion of K+ by distal renal tubules
Tubular l Principal cell Interstitial fluid
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Metabolic alkalosis Primary increase of HCO3
-
Causes:
1) Excess bicarbonate load ---- intake
2) Gastric H+ loss ---- vomiting
Why HCO3- in plasma is increased?
3) Renal H+ loss
Diuretics --- distal urine flow
Hyperaldosteronism ---
activation of H+ pump and Na+-K+ pump
4) Hypokalemia
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Compensation of metabolic alkalosis
1) Buffering --- in cells
2) Respiratory compensation ---incomplete
3) Renal compensation --- tremendous
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•The causes of paradoxical aciduria?
•What kind of metabolic alkalosis is saline responsive? or saline resistant?
vomiting? diuretics?
primary hyperaldosteronism?
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Respiratory alkalosis
Primary decrease of PaCO2
• Cause ---- alveolar hyperventilation
Hypoxia, psychoneurosis, fever etc.
• Compensation
Buffering
Renal compensation
Acute -----dHCO3 = 0.2 d PaCO2 2.5
Chronic ---dHCO3 = 0.5 d PaCO2 2.5
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Functional and Metabolic Changes caused by alkalosis
•Central nervous system Dysphoria, confusion, seizure, coma etc.
1) GABA
2) Hypoxia from:
hypoventilation, cerebral vasoconstriction
left-shift of oxyhemoglobin dissociation curve
• Neuromuscular excitability ---- cramping
ionic calcium in plasma
• Hypokalemia --- paresis, arryhthmia
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Analysis of simple acid-base disorder
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Mixed acid-base disorders
•Double acid base disorders
Metabolic Metabolic
acidosis alkalosis
Respiratory Respiratory
acidosis alkalosis
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•COPDO2HCO3- PaCO2 pH
CO2PaCO2 HCO3- pH
HCO3-/ PaCO2 pH
• COPD + O2 PaCO2 HCO3- pH
+ Diuretics HCO3- PaCO2 pH
HCO3- / PaCO2 pH normal
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•Renal failure HCO3- PaCO2 pH
Vomiting HCO3- PaCO2 pH
N HCO3- / N PaCO2 pH normal
All these parameters are normal,
how to find out the acid-base disorder?
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•Triple acid-base disorders
Metabolic Metabolic
acidosis alkalosis
Respiratory Respiratory
acidosis alkalosis
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Exp:
COPD O2 HCO3- PaCO2 pH
CO2 PaCO2 HCO3 pH
Diuretics HCO3- PaCO2 pH
HCO3- PaCO2 pH
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Summery
•Metabolic acidosis is induced by primary decrease of HCO-
3 owing to increased production or retention of fixed acides or HCO-
3 loss.
•Metabolic alkalosis is induced by primary increase of HCO-
3 due to H+ loss.
•Respiratory acidosis or alkalosis is induced by primary increase or decrease of CO2 caused by hypoventilation or hyperventilation.
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•Acidosis depresses activity of CNS and myocardial contractility, and induces cardiac arrhythmia and vasodilation.
•Alkalosis results in dysfunction of CNS and cramping.
•Different kinds of acid-base disorders may coexist in patients.