Acid-base balance and acid-base disturbance

I.regulation of acid-base balance 1. origin of acid and base in the body volatile acid: H 2 CO 3 (15mol/day) sulfuric acid 1) acids phosphoric acid fixed acid: uric acid (90mmol/L) mesostate 2) base: salt of organic acid; NH 3

2. regulation of acid-base balance 1) role of buffer HCO - 3 /H 2 CO 3 53% Hb - /HHb buffer system HbO - 2 /HHbO 2 35% Pr - /HPr 7% Phosphate 5% Henderson-Hasselbalch pH = pKa + lg [HCO - 3 ]/[H 2 CO 3 ] = lg 20/1 = =7.4 buffer of fixed acid: HCO - 3 /H 2 CO 3 buffer of volatile acid: Hb - /HHb

血红蛋白缓冲对的缓冲作用 CO 2 Cl - CO 2 +H 2 O C.A. H 2 CO 3 HCO - 3 H + --Hb - RBC

2) respiratory regulation alteration of ventilation alteration of breathe out of CO 2 PaCO 2 central [H + ] peripheral respiration PaO 2 (receptor) PaCO 2 ( ＞ 80mmHg) inhibition of respiratory center 3) cellular action exchanges of H + and K +

4) renal regulation ① acidification of proximal renal tubule 血管 肾小管上皮 管腔 Na + Cl - HCO - 3 H 2 CO 3 H 2 0 泌 H + 与 Cl - 重吸收拮抗与泌 NH 3 协同 K+K+ NH 3 Na + H + H 2 CO 3 Na + C.A. HCO - 3 H 2 O+CO 2

② acidification of distal renal tubule H + -pump NH + 4 泌 H + 与泌 K + 拮抗，与泌 NH 3 协同， 与肾小管液流量正变 肾小管上皮细胞 H 2 CO 3 H + NH 3 HCO - 3 H 2 O+CO 2 K +

Ⅱ. parameters of acid-base 1. pH important and inexact parameter normal range: 7.35~ PaCO 2 partial pressure of CO 2 of dissolved in arterial plasma (respiratory parameter) normal range: 4.4~6.25kPa(33~46mmHg) primary change: respiratory acidosis PaCO 2 respiratory alkalosis PaCO 2 secondary change: metabolic acidosis PaCO 2 metabolic alkalosis PaCO 2

3. standard bicarbonate(SB) and actual bicarbonate(AB) SB: [HCO - 3 ] in plasma under standard condition (38 ℃ ; PO 2 =150mmHg; PCO 2 =40mmHg) AB: [HCO - 3 ] in plasma under actual condition Normal range: 22~27mmol/L ; AB=SB 4. buffer base(BB) sum of all buffer base in blood normal range: 45 ~ 55mmol/L 5. base excess(BE) normal range: ± 3mmol/L

6. anion gap (AG) + - Normal range: 12 ± 2 mmol/L Na + Cl - AG HCO - 3

Ⅲ. 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

diarrhea; GI: intestinal suction (loss of intestinal fistula HCO - 3 ) biliary fistula ② metabolic acidosis in early renal failure: normal AG NH 3 secretion H + secretion Renal tubular acidosis: H + secretion kidney: depressant of C.A. (loss of acetazolamide HCO - 3 ) intake of Cl - NaCl, NH 4 Cl Hyperkalemia

2) compensatory regulation ① buffer: ② respiratory compensation ③ cellular compensation ④ renal compensation [H + ] : C.A. H + secretion NH 3 secretion [HCO - 3 ] / [H 2 CO 3 ] = 20:1 compensation acidosis [HCO - 3 ] / [H 2 CO 3 ] < 20:1 decompensation acidosis (SB AB BB BE PaCO 2 AB < SB)

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

2. respiratory acidosis concept: The primary disturbance is an elevation in plasma [H 2 CO 3 ] 1) cause and pathogenesis Barbital depression of CNS head injury ① CO 2 breathe paralysis of respiratory muscles out disease of airway or lung chest injury ② inhalation of CO 2

2) compensation buffer: Hb - /HHb cells: exchange of H + and K + kidney: secretion of H + and NH 3 (PaCO 2 SB AB BB BE AB ＞ SB) 3) effect on body ① CNS CO 2 脑血管扩张、颅内压 头痛、谵妄 CO 2 narcosis respiration ② cardiovascular system

4) principles of treatment 改善通气，注意勿补 NaCO 3 3. metabolic alkalosis concept: the primary disturbance is an increase of [HCO - 3 ] in the arterial plasma 1) causes and pathogenesis

digestive tract vomiting; gastric suction(loss of HCl) ① loss diuretics distal flow rate of H + (furosemide) blood volume ADS kidney hyperaldosteronism H + -Na + exchange H + -K + exchange between Hypokalemia intra- and extra- cell renal secretion of H + hypochloremia renal secretion of H +

NaHCO 3 ② intake transfusion of banked blood of base (citrate) 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 PaCO 2 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 O 2 dissociation hypoxia Coma curve shifting to left ② neuromuscle pH free Ca 2+ tic ③ hypokalemia arrhythmia

4) principles of treatment loss of H + digestive tract diuretic ; hypokalemia 0.9%NaCl; KCl hyperaldosteronism antisterone; diamox( 乙酰唑胺 )

4. respiratory alkalosis concept: the primary disturbance is decrease of [H 2 CO 3 ] in plasma 1) cause and pathogenesis hypotonic hypoxia pneumonia hyperventilation hysteria( 癔病 ); fever; [NH 3 ] hyperthyroidism( 甲亢 ) misoperation of ventilator

respiration (slight inhibition) 2) compensation cells (exchange of H + -K + ) kidney secretion of H + (PaCO 2 ; SB AB BB BE ; AB ＜ SB) 3) effects on body It is as same as metabolic alkalosis. dizziness and convulsion are happened easily ( 头晕 ) ( 抽搐 ) 4) principles of treatment inhalation of 5%CO 2

IV. Mixed acid-base disturbance 1. dual acid-base disturbance 1) metabolic acidosis plus respiratory acidosis heart beat [HCO - 3 ] respiration stop character PaCO 2 pH 2) metabolic alkalosis plus respiratory alkalosis hepatic NH 3 PaCO 2 failure diuretic character [HCO - 3 ] pH 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)

discuss of case 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 PaCO 2 28mmHg CO 2.CP. 19.2ml% SB 13.6mmol/L BE -15.3mmol/L

The scope of compensatory responses of acid-base disorders acute respiratory acidosis : △ [HCO - 3 ]=0.1× △ PaCO 2 ±1.5 chronic respiratory acidosis: △ [HCO - 3 ]=0.4× △ PaCO 2 ±3.0 acute respiratory alkalosis : △ [HCO - 3 ]=0.2× △ PaCO 2 ±2.5 chronic respiratory alkalosis: △ [HCO - 3 ]=0.5× △ PaCO 2 ±2.5 metabolic acidosis: △ PaCO 2 =1.2× △ [HCO - 3 ] ±2.0 metabolic alkalosis: △ PaCO 2 =0.7 × △ [HCO - 3 ] ± 5.0

№2: patient, male, 45, chronic bronchitis pH 7.26 PaCO 2 60mmHg BB 46.2mmol/L SB 22mmol/L BE -7.5mmol/L after treatment pH 7.34 PaCO 2 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 7.56 PaCO 2 50mmHg CO 2.CP. 90ml% SB 34mmol/L BE 10mmol/L K + 3.2mmol/L Cl - 105mmol/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。