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Acid-base balance and acid-base disturbance. 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
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Acid-base balance and acid-base disturbance
regulation of acid-base balance 1.origin of acid and base in the body volatile acid: H2CO3 (15mol/day) sulfuric acid 1) acids phosphoric acid fixed acid: uric acid (90mmol/L) mesostate 2)base: salt of organic acid; NH3
2.regulation of acid-base balance 1) role of buffer HCO-3/H2CO353% Hb-/HHb buffer system HbO-2/HHbO2 35% Pr-/HPr 7% Phosphate 5% Henderson-Hasselbalch pH = pKa + lg [HCO-3]/[H2CO3] = 6.1 + lg 20/1 = 6.1 + 1.3 =7.4 buffer of fixed acid: HCO-3/H2CO3 buffer of volatile acid: Hb-/HHb
CO2+H2O C.A. H2CO3 HCO-3 H+--Hb- RBC 血红蛋白缓冲对的缓冲作用 CO2 Cl-
2)respiratory regulation alteration of ventilation alteration of breathe out of CO2 PaCO2 central [H+] peripheral respiration PaO2 (receptor) PaCO2 (>80mmHg) inhibition of respiratory center 3) cellular action exchanges of H+ and K+
4) renal regulation①acidification of proximal renal tubule血管 肾小管上皮 管腔 Na+ Cl- HCO-3 H2CO3 H20 泌H+与Cl-重吸收拮抗与泌NH3协同 K+ Na+ H+ H2CO3 Na+ C.A. HCO-3 H2O+CO2 NH3
②acidification of distal renal tubule H+-pump NH+4 泌H+与泌K+拮抗,与泌NH3协同, 与肾小管液流量正变 肾小管上皮细胞 H2CO3 H+ NH3 HCO-3 H2O+CO2 K+
Ⅱ.parameters of acid-base 1. pH important and inexact parameter normal range: 7.35~7.45 2. PaCO2 partial pressure of CO2 of dissolved in arterial plasma (respiratory parameter) normal range: 4.4~6.25kPa(33~46mmHg) primary change: respiratory acidosis PaCO2 respiratory alkalosis PaCO2 secondary change: metabolic acidosis PaCO2 metabolic alkalosis PaCO2
3.standard bicarbonate(SB) and actual bicarbonate(AB) SB: [HCO-3] in plasma under standard condition (38℃; PO2=150mmHg; PCO2=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
Na+ Cl- 6.anion gap (AG) + - Normal range: 12 ± 2 mmol/L HCO-3 AG
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 ①metabolic 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 NH3 secretion H+ secretion Renal tubular acidosis: H+ secretion kidney: depressant of C.A. (loss of acetazolamide HCO-3) intake of Cl- NaCl, 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)
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 [H2CO3] 1) cause and pathogenesis Barbital depression of CNS head injury ① CO2 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脑血管扩张、颅内压 头痛、谵妄 CO2 narcosis respiration ② cardiovascular system
4) principles of treatment 改善通气,注意勿补NaCO3 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) ①loss 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+
NaHCO3 ②intake transfusion of banked blood of base (citrate) 2)compensation of the body ①respiration compensation are limited (hypoxia) ②cells compensation hypokalemia ③kidney 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 ①CNS γ-amino butyric acid dysphoria insanity pH brain-vessel dizziness contractionbrain delirium O2dissociation hypoxia Coma curve shifting to left ②neuromuscle pH free Ca2+ 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 [H2CO3] in plasma 1)cause and pathogenesis hypotonic hypoxia pneumonia hyperventilation hysteria(癔病); fever; [NH3] hyperthyroidism(甲亢) 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 (头晕) (抽搐) 4) principles of treatment inhalation of 5%CO2
IV. Mixed acid-base disturbance 1.dual acid-base disturbance 1)metabolic acidosisplusrespiratory acidosis heart beat [HCO-3] respiration stop character PaCO2pH 2) metabolic alkalosisplusrespiratory alkalosis hepatic NH3PaCO2 failure diuretic character [HCO-3] pH 3) respiratory acidosisplusmetabolic alkalosis pulmonary heart disease diuretic pH ±
4) respiratory alkalosisplusmetabolic acidosis infective shock fever pH ± 5) metabolic acidosisplusmetabolic 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 PaCO2 28mmHg CO2 .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×△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
№2: patient, male, 45, chronic bronchitis pH 7.26 PaCO2 60mmHg BB 46.2mmol/L SB 22mmol/L BE -7.5mmol/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 7.56 PaCO2 50mmHg CO2 .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。