Transcript 盛建中_Acid-base balance 2014

Acid-Base Balance
Jianzhong Sheng MD, PhD
Department of Pathophysiology
School of Medicine
Zhejiang University
Objectives
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Explain how the pH of the blood is stabilized by bicarb
buffer and define the terms acidosis and alkalosis.
Explain how the acid-base balance of the blood is affected
by CO2 and HCO3-, and describe the roles of the lungs and
kidneys in maintaining acid-base balance.
Explain how CO2 affects blood pH, and hypoventilation and
hyperventilation affect acid-base balance.
Explain how the interaction between plasma K+ and H+
concentrations affects the tubular secretion of these.
Normal Acid-Base Balance
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Normal pH 7.35-7.45
Narrow normal range
Compatible with life 6.8 - 8.0
pH
6.8
death
【H+】 160
7.35
7.45
acidosis
alkalosis
40
7.8
death
16 nmol/L
Structure of AQP1
Hg++ inhibitory site
What are acidosis and
alkalosis
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Normal pH: 7.40 (7.35-7.45)
Acidosis: pH<7.35; Alkalosis: pH>7.45
Simple types of acidosis: Metabolic
acidosis and Respiratory acidosis
Simple types of alkalosis: Metabolic
alkalosis and Respiratory alkalosis
Mixed types of acid-base disorders
pH
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pH of blood is 7.35 to 7.45
pH = 6.1 + log [HCO3-]
0.03 x Pco2
Types of Acids in the Body
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Volatile acids:
 Can leave solution and enter the
atmosphere.
 H2CO3 (carbonic acid).
 Pco2 is most important factor in
pH of body tissues.
Types of Acids in the Body
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Fixed Acids:
 Acids that do not leave solution.
 Sulfuric and phosphoric acid.
 Catabolism of amino acids,
nucleic acids, and phospholipids.
Types of Acids in the Body
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Organic Acids:
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Byproducts of aerobic metabolism,
during anaerobic metabolism and
during starvation, diabetes.
Lactic acid, ketones.
Types of Acids in the Body
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Organic Acids:
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Byproducts of aerobic metabolism,
during anaerobic metabolism and
during starvation, diabetes.
Lactic acid, ketones.
Chemical Buffers
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Act within fraction of a second.
Protein.
HCO3-.
Phosphate.
Proteins
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COOH or NH2.
Largest pool of buffers in the body.
pk. close to pH in plasma.
Albumin, globulins such as Hb.
HCO3
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pk. = 6.1.
Present in large quantities.
Open system.
Respiratory and renal systems act
on this buffer system.
Most important ECF buffer.
HCO3
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Limitations
Cannot protect ECF from
respiratory problems.
Cannot protect ECF from elevated
or decreased CO2.
Limited by availability of HCO3-.
Phosphates
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pk. = 6.8.
Low concentration in ECF, better
buffer in ICF, kidneys, and bone.
Respiratory System
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2nd line of defense.
Acts within min. -maximal in 12-24
hrs.
H2CO3 produced converted to CO2,
and excreted by the lungs.
Alveolar ventilation also increases as
pH decreases (rate and depth).
Coarse , CANNOT eliminate fixed acid.
Urinary Buffers
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Nephron cannot produce urine at
pH < 4.5.
IN order to excrete more H+, the
acid must be buffered.
H+ secreted into the urine tubule
and combines with HPO42- or NH3.
HPO42- + H+
H2PO4NH3 + H+
NH4+
Renal Acid-Base Regulation
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Kidneys help regulate blood pH by excreting
H+ and reabsorbing HC03-.
Most of the H+ secretion occurs across the
walls of the PCT in exchange for Na+.
 Antiport mechanism.
+ and H+ in opposite directions.
 Moves Na
Normal urine normally is slightly acidic
because the kidneys reabsorb almost all HC03and excrete H+.
 Returns blood pH back to normal range.
Reabsorption of
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HCO3
Apical membranes of tubule cells are
impermeable to HCO3-.
 Reabsorption is indirect.
When urine is acidic, HCO3- combines with H+ to
form H2CO3-, which is catalyzed by ca located in
the apical cell membrane of PCT (proximal convoluted tubule) .
 As [CO2] increases in the filtrate, CO2 diffuses
into tubule cell and forms H2CO3.
- and H+.
 H2CO3 dissociates to HCO3
HCO3- generated within tubule cell diffuses into
peritubular capillary.
Acidification of Urine
Na+ + HCO3-
H+
H+
H2CO3
H+ + HCO3-
CA
HPO42-
NH3
H2O + CO2
NH4 + H2PO4-
H2CO3
CA
CO2 + H2O
Urinary Buffers
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Nephron cannot produce urine at
pH< 4.5.
In order to excrete more H+, the
acid must be buffered.
H+ secreted into the urine tubule
and combines with HPO42- or NH3.
HPO42- + H+
H2PO4NH3 + H+
NH4+
Anion Gap
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The difference between [Na+] and
the sum of [HC03-] and [Cl-].
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[Na+] – ([HC03-] + [Cl-]) =
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140 - (24 + 105) = 11
 Normal = 12 ± 2
Clinicians use the anion gap to
identify the cause of metabolic
acidosis.
Anion Gap
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Law of electroneutrality:
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Blood plasma contains an =
number of + and – charges.
The major cation is Na+.
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Minor cations are K+, Ca2+ ,
Mg2+.
The major anions are HC03- and
Cl-.
 (Routinely measured.)
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Minor anions include albumin,
phosphate, sulfate (called
unmeasured anions).
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Organic acid anions include
lactate and acetoacetate,.
Anion Gap
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In metabolic acidosis, the strong
acid releases protons that are
buffered primarily by [HC03-].
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This causes plasma [HC03-] to
decrease, shrinking the [HC03-]
on the ionogram.
Anions that remain from the
strong acid, are added to the
plasma.
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If lactic acid is added, the
[lactate] rises.
 Increasing the total
[unmeasured anions].
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If HCl is added, the [Cl-] rises.
 Decreasing the [HC03 ].
Anion Gap in Metabolic
Acidosis
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Salicylates raise the gap to 20.
Renal failure raises gap to 25.
Diabetic ketoacidosis raises the gap
to 35-40.
Lactic acidosis raises the gap to >
35 (>50).
Largest gaps are caused by
ketoacidosis and lactic acidosis.
Simple Acid-Base
Disturbance
1. Metabolic acidosis
Concept: the primary disturbance is a decrease
of [HCO-3] in the arterial plasma
1) Cause and pathogenesis
lactic acidosis: hypoxia, diabetes
liver disease
ketoacidosis: diabetes, starvation
① Metabolic
acidosis in
severe renal failure: fixed acids
increased AG
salicylic acid
acid
poisoning:
intake food
GI:
(loss of
HCO-3)
② Metabolic
acidosis in
normal AG
Kidney:
(loss of
HCO-3)
diarrhea;
intestinal suction
intestinal fistula
biliary fistula
early renal failure:
NH3 secretion
H+ secretion
Renal tubular acidosis:
H+ secretion
depressant of C.A.
acetazolamide
intake of ClNaCl, NH4Cl
Hyperkalemia
2) Compensatory regulation
① Buffer:
② Respiratory compensation
③ Cellular compensation
④ Renal compensation
[H+]
: C.A.
H+ secretion
NH3 secretion
[HCO-3] / [H2CO3] = 20:1 compensation
acidosis
[HCO-3] / [H2CO3] < 20:1 decompensation
acidosis
(SB AB BB BE PaCO2 AB < SB)
Discussion of case 1
Method:
1. pH
2. primary factor and parameter
3. secondary factor and compensation
4. expected range of compensation
№1:
patient, female, 46, chronic pyelitis
pH
7.32 (Normal: 7.35-7.45)
PaCO2
28mmHg (Normal: 35-45mmHg)
SB
13.6mmol/L (Normal: 22-27mmol/L)
BE
-15.3mmol/L (Normal: -3.0-+3.0mmol/L)
3) Effect on body
① Cardiovascular system
hyperkalemia
arrhythmia
[H+]
contractility
peripheral resistance
② Central nervous system
[H+]
ATP , γ-amino butyric acid
(somnolence, coma)
4) Principles of treatment
① Correction of underlying disorders;
② Administration of NaHCO3;
③ Correction of water-electrolyte disturbances.
Summary of Metabolic
Acidosis
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Gain of fixed acid or loss of
HCO3-.
 Plasma HCO3 decreases.
 PCO2 decreases.
 pH decreases.
2. Respiratory acidosis
Concept: The primary disturbance is an
elevation in plasma [H2CO3]
1) Cause and pathogenesis
Barbital
depression of CNS head injury
①CO2 breathe paralysis of respiratory muscles
out
disease of airway or lung
chest injury
② Inhalation of CO2
2) Compensation
Buffer: Hb-/HHb
Cells:
exchange of H+ and K+
Kidney: secretion of H+ and NH3
(PaCO2 SB AB BB BE AB＞SB)
3) Effect on body
① CNS
CO2
celebral vascular dilation, intracranial
pressure
headache、fatigue
CO2 narcosis
respiration
② Cardiovascular system
4) Principles of treatment
improve ventilation. Do not add NaHCO3
№2:
Patient, male, 45, chronic bronchitis
pH
7.26 (Normal: 7.35-7.45)
PaCO2 60mmHg (Normal: 35-45mmHg)
BB
46.2mmol/L (Normal: 45-55mmol/L)
SB
22mmol/L (Normal: 22-27mmol/L)
BE
-7.5mmol/L (Normal: -3.0-+3.0mmol/L)
after treatment
pH
7.34
PaCO2 70mmHg
BB
58mmol/L
BE
5.5mmol/L
Respiratory Acidosis

PCO2 increases.
 Plasma HCO3 increases.
 pH decreases.
3. Metabolic alkalosis
Concept: the primary disturbance is
an increase of [HCO-3] in the
arterial plasma
1) Causes and pathogenesis
① loss
of H+
digestive tract
vomiting; gastric suction(loss of HCl)
diuretics
distal flow rate
(furosemide) blood volume Ald
hyperaldosteronism H+-Na+exchange
kidney
H+-K+exchange between
hypokalemia intra- and extra-cell
renal secretion of H+
hypochloremia
renal secretion of H+
②intake
of base
NaHCO3
transfusion of banked blood (citrate)
Gastric fluid loss and AB balance
Esophagus
Blood vessel
Stomach
Cl
-
H+
HCO3-
H+
HCO3-
H2CO3
Pancreas
-
HCO3-
HCO3-
Na+
Duodenum
Cl
Cl H2CO3
H+
Na+
H+
Na+
2) Compensation of the body
① respiration
compensation are limited
(hypoxia)
② cells
compensation
hypokalemia
③ kidney pH
inhibition of carbonic
anhydrase (C.A.)
secretion of H+
(SB AB BB BE PaCO2 AB＞SB)
3) Effects on body
inhibition of glutamate decarboxylase
① CNS
γ-amino butyric acid
dysphoria
insanity
pH
brain-vessel
dizziness
contraction
brain
delirium
O2 dissociation
hypoxia Coma
curve shifting to left
② neuromuscle pH
free Ca2+
③ hypokalemia
arrhythmia
tic
4) Principles of treatment
loss of H+ digestive tract
diuretic ; hypokalemia
0.9%NaCl; KCl
hyperaldosteronism
antisterone; diamox(乙酰唑胺)
Metabolic Alkalosis
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Loss of fixed acid or gain of
HCO3-.
 Plasma HCO3 increases.
 PCO2 increases.
 pH increases.
4. Respiratory alkalosis
Concept: the primary disturbance is
decrease of [H2CO3] in plasma
1) cause and pathogenesis
hypotonic hypoxia
pneumonia
hyperventilation hysteria, fever, [NH3]
hyperthyroidism
misoperation of ventilator
respiration (slight inhibition)
2) Compensation cells (exchange of H+-K+)
kidney secretion of H+
(PaCO2 ; SB AB BB BE ; AB＜SB)
3) Effects on body
It is as same as metabolic alkalosis.
dizziness and convulsion are happened easily
4) Principles of treatment
inhalation of 5%CO2
Mixed acid-base disturbance
1. Dual acid-base disturbance
1) metabolic acidosis plus respiratory acidosis
heart beat
[HCO-3]
stop
character
pH
respiration
PaCO2
2) metabolic alkalosis plus respiratory alkalosis
hepatic NH3
PaCO2
character [HCO- ]
pH
failure diuretic
3
3) respiratory acidosis plus metabolic alkalosis
pulmonary heart disease
diuretic
pH ±
4) respiratory alkalosis plus metabolic acidosis
infective shock
fever
pH ±
5) metabolic acidosis plus metabolic alkalosis
ketoacidosis(diabetes)
vomiting
pH ±
2. triple acid-base disturbance
1) respiratory acidosis; metabolic acidosis
and alkalosis
pulmonary heart disease; vomiting
2) respiratory alkalosis; metabolic acidosis
and metabolic alkalosis
fever; vomiting; diarrhea (food poisoning)
№3.
Patient, male, 47, purulent appendicitis. He
was treated with abdominal suction and
persistent gastrointestinal decompression
after operation.
pH
PaCO2
SB
BE
K+
Cl-
7.56 (Normal: 35-45mmHg)
50mmHg (Normal: 35-45mmol/L)
34mmol/L (Normal: 22-27mmol/L)
10mmol/L (Normal: -3.0-+3.0mmol/L)
3.2mmol/L (Normal: 3.5-5.5mmol/L)
105mmol/L (Normal: 103mmol/L)
Respiratory Alkalosis

PCO2 decreases.
 Plasma HCO3 decreases.
 pH increases.
The scope of compensatory
responses of acid-base disorders
Acute respiratory acidosis: △[HCO-3]=0.1×△PaCO2 ±1.5
Chronic respiratory acidosis: △[HCO-3]=0.4×△PaCO2
±3.0
Acute respiratory alkalosis: △[HCO-3]=0.2×△PaCO2 ±2.5
Chronic respiratory alkalosis: △[HCO-3]=0.5×△PaCO2
±2.5
Metabolic acidosis: △PaCO2 =1.2×△[HCO-3] ±2.0
Metabolic alkalosis: △PaCO2 =0.7×△[HCO-3] ±5.0
Summary of Simple ABD
1. 概念：
根据原发变化因素及方向命名
2. 代偿变化规律：
代偿变化与原发变化方向一致
代偿变化规律
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代酸
[HCO-3]
[H2CO3]↓

代碱
[HCO-3]
[H2CO3]↑

呼酸
[HCO-3]↑
[H2CO3]

呼碱
[HCO-3]↓
[H2CO3]
3. 基本特征：
 呼吸性ABD，血液pH与其它指标变化方
向相反
 代谢性ABD，血液pH与其它指标变化方
向相同
4. 原因和机制
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代酸：
固定酸生成↑及HCO3-丢失↑→HCO3-降低
呼酸：
CO2排出减少吸入过多，使血浆[H2CO3]升高
代碱：
H＋丢失, HCO3-过量负荷，血HCO3-增多
呼碱：
通气过度CO2呼出过多，使血中[H2CO3]降低
对机体的影响
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CNS
离子改变
酸中毒 抑制性紊乱 血钾增高
其它
血管麻痹
心律失常
收缩力降低
碱中毒 兴奋性紊乱 血钾降低 肌肉痉挛
或麻痹
6. 代偿调节
1. 代谢性ABD：各调节机制都起作用，尤
其是肺和肾
2. 呼吸性ABD：肺一般不起作用；
急性紊乱细胞内外二对离子交换；
慢性紊乱肾调节
酸碱平衡紊乱类型的判断
一划五看简易判断法

一划：将多种指标简化成三
项，并用箭头表示其升降
SB  AB  BB↓，BE(-)↑
pH 
[HCO3-]
[H2CO3]
[H+]
PaCO2↓
五看：
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
一看pH定酸碱
1 pH升高：失偿型碱中毒
pH降低：失偿型酸中毒
2 pH正常可能是
（1） 酸碱平衡
（2） 代偿性单纯性ＡＢＤ
（3）混合性相消型ＡＢＤ

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二看原发因素定代呼
１．病史中有＂获酸＂，＂失碱＂或
相反情况，为代谢性ABD
２．病史中有肺过度通气或相反情况，
为呼吸性 ABD
例1
病史？
[HCO-3]↓
[H2CO3]↓
pH N
三看“继发性变化”定单混
1 ＂继发性变化＂的方向
(1) 与原发性变化方向一致：

单纯型ABD or 混合型ABD
(2)与原发性变化方向相反：

混合型
例2

PaCO2↑,HCO-3↓，

pH ↓↓↓
例3


PaCO2↑
HCO-3↑
pH 接近正常
２．“继发性变化”的数值

(代偿预计值）
（1）数值在代偿预计值范围内，为单
纯型ABD
（2）数值明显超过或低于代偿预计值，
为混合型ABD
四看ＡＧ定单混，定两三
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1．AG升高＞14mmol/L，提示有代酸，
＞ 30 mmol/L肯定有代酸
2 在AG增高型代酸，AG增高数＝[HCO3-]
降低数．即ΔAG＝Δ[HCO3-]
潜在[HCO3-]=[HCO3-]实测值+ΔAG
例7
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
一位肺心病合并腹泻病人，
pH = 7.12, PaCO2 = 84.6 mmHg,
HCO-3 = 26.6mmol/L,
Na+= 137 mmol/L,Cl-=85 mmol/L。该病
人发生何种酸碱平衡紊乱？
AG = Na+- (HCO-3 + Cl- )= 137-(26.6+85)
= 25.4 mmol/L
五看临床表现做参考
Discussion of cases
Method:
1. pH
2. primary factor and parameter
3. secondary factor and compensation
4. expected range of compensation
№1:
patient, female, 46, chronic pyelitis
pH
7.32 (Normal: 7.35-7.45)
PaCO2
28mmHg (Normal: 35-45mmHg)
SB
13.6mmol/L (Normal: 22-27mmol/L)
BE
-15.3mmol/L (Normal: -3.0-+3.0mmol/L)
№2:
Patient, male, 45, chronic bronchitis
pH
7.26 (Normal: 7.35-7.45)
PaCO2 60mmHg (Normal: 35-45mmHg)
BB
46.2mmol/L (Normal: 45-55mmol/L)
SB
22mmol/L (Normal: 22-27mmol/L)
BE
-7.5mmol/L (Normal: -3.0-+3.0mmol/L)
after treatment
pH
7.34
PaCO2 70mmHg
BB
58mmol/L
BE
5.5mmol/L
№3.
Patient, male, 47, purulent appendicitis. He
was treated with abdominal suction and
persistent gastrointestinal decompression
after operation.
pH
PaCO2
SB
BE
K+
Cl-
7.56 (Normal: 35-45mmHg)
50mmHg (Normal: 35-45mmol/L)
34mmol/L (Normal: 22-27mmol/L)
10mmol/L (Normal: -3.0-+3.0mmol/L)
3.2mmol/L (Normal: 3.5-5.5mmol/L)
105mmol/L (Normal: 103mmol/L)
№4.
患儿, 3个月, 入院前一天开始发热、呕
吐、水样便20+次/日，伴烦躁、烦渴。
查体：T 39.8℃，嗜睡，醒后烦躁，皮肤
弹性差，明显腹胀。
处理：庆大霉素抗感染，静脉点滴生理盐水
1200ml.
次日病情加重，极烦渴，呼吸深，惊厥，
昏迷，并发肠麻痹死亡。
Thank you