acid-base disturbance

What is acid ？ What is base ？

The concept of acid and base H2CO3 H++HCO3- NH4+ H++NH3 H2PO4 - H++HPO42- HPr H++Pr-

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/H2CO3 53% 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 Cl- CO2+H2O C.A. H2CO3 HCO-3 H+--Hb- RBC

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 regulation ① acidification of proximal renal tubule Blood vessel Renal tubule epithelium Tubule K+ Na+ H+ H2CO3 C.A. HCO-3 H2O+CO2 Na+ Cl- HCO-3 H2CO3 H20 泌H+ 与Cl- 重吸收拮抗与泌NH3协同 NH3

② acidification of distal renal tubule H+-pump NH+4 Renal tubular epithelial cells H2CO3 H+ NH3 HCO-3 H2O+CO2 K+

Acid Base parameter /Arterial Blood Gases (ABGs)

Arterial Blood Gas Sampling

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

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

acid-base disturbance Because of the pathological process of acid-base overload or regulation disorder lead to destruction of acid-basestability.

[HCO3－] pH=pKa+lg [H2CO3] 20 =pKa+lg 1 = 6.1 +1.3 = 7.4 Henderson-Hasselbalch方程 pH=pKa+lg [HCO3－] [H2CO3] =pKa+lg 20 1 = 6.1 +1.3 = 7.4

Simple Acid-Base Disorders Clinical disturbances of acid base metabolism classically are defined in terms of the HCO3¯  /CO2  buffer system. Acidosis – process that increases [H+] by increasing PCO2 or by reducing [HCO3-] Alkalosis – process that reduces [H+] by reducing PCO2 or by increasing [HCO3-] Henderson Hasselbalch equation:  pH = 6.1 + log [HCO3-]/ 0.03 PCO2 Since PCO2 is regulated by respiration, abnormalities that primarily alter the PCO2 are referred to as respiratory acidosis (high PCO2) and respiratory alkalosis (low PCO2). In contrast, [HCO3¯] is regulated primarily by renal processes. Abnormalities that primarily alter the [HCO3¯] are referred to as metabolic acidosis (low [HCO3¯]) and metabolic alkalosis (high [HCO3¯]).

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 NH3 secretion H+ secretion Renal tubular acidosis: 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 (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

cells: exchange of H+ and K+ kidney: secretion of H+ and NH3 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 Cerebral vascular dilatation,  intracranial pressure headache, delirium CO2 narcosis respiration ② cardiovascular system

concept: the primary disturbance is 4) principles of treatment improve ventilation 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

NaHCO3 ②intake 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 PaCO2 AB＞SB)

inhibition of glutamate decarboxylase 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+ tic ③ hypokalemia arrhythmia

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

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

Increased rate and depth of breathing ("Kussmaul breathing") Decreased heart rate (bradycardia)

Mixed acid-base disturbance 1. dual acid-base disturbance 1) metabolic acidosis plus respiratory acidosis heart beat [HCO-3] respiration stop character PaCO2 pH 2) metabolic alkalosis plus respiratory alkalosis hepatic NH3 PaCO2 failure diuretic character [HCO-3] pH 3) respiratory acidosis plus metabolic alkalosis pulmonary heart disease diuretic pH ±

5) metabolic acidosis plus metabolic alkalosis ketoacidosis(diabetes) 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 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. A 50 year old insulin dependent diabetic woman was brought to the ED by ambulance. She was semi-comatose and had been ill for several days. Current medication was digoxin and a thiazide diuretic for CHF. Lab results Serum chemistry: Na 132, K 2.7, Cl 79, Glu 815, Lactate 0.9 urine ketones 3+ ABG: pH 7.41 PCO2 32 HCO3¯ 19 pO2 82    What is the acid base disorder? Why?