1 / 30

Acid-base balance and acid-base disturbance

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

lore
Download Presentation

Acid-base balance and acid-base disturbance

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Acid-base balance and acid-base disturbance

  2. 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

  3. 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

  4. CO2+H2O C.A. H2CO3 HCO-3 H+--Hb- RBC 血红蛋白缓冲对的缓冲作用 CO2 Cl-

  5. 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+

  6. 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

  7. 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+

  8. 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

  9. 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

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

  11. 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

  12. 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

  13. 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)

  14. 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

  15. 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

  16. 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

  17. 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

  18. 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+

  19. 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)

  20. 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

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

  22. 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

  23. 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

  24. 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 ±

  25. 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)

  26. 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

  27. 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

  28. №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

  29. №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

  30. №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。

More Related