Chapter 4(1) Acid – Base Chapter 4(1) Acid – Base Disorders Disorders §1. Acid- Base balance 1.Concept of acid and base Acid: Acid is a proton donor. (HCl, NH 4 + ) HCl → H + + Cl - NH 4 + → H + + NH 3 Base: Base is a proton acceptor. (O H - , HCO 3 - , NH 3 ) OH - + H + → H 2 O
Chapter 4(1) Acid – Base Disorders. §1. Acid- Base balance 1.Concept of acid and base Acid: Acid is a proton donor. (HCl, NH 4 + ) HCl → H + + Cl - NH 4 + → H + + NH 3 Base : Base is a proton acceptor. (OH - , HCO 3 - , NH 3 ) - PowerPoint PPT Presentation
This document is posted to help you gain knowledge. Please leave a comment to let me know what you think about it! Share it to your friends and learn new things together.
Transcript
Chapter 4(1) Acid – Base DisordersChapter 4(1) Acid – Base Disorders
§1. Acid- Base balance 1.Concept of acid and base
Acid: Acid is a proton donor. (HCl, NH4+)
HCl → H+ + Cl-
NH4+ → H+ + NH3
Base: Base is a proton acceptor. (OH-, HCO3-, NH3)
OH- + H+ → H2O
HCO3- + H+ → H2CO3
NH3 + H+ → NH4+
2.Origins of acid and base in the body Source of acid: 1) origins of volatile acid
It results from an end-product of oxidative metabolism namely CO2. CO2+H2O = H2CO3
Normally produced CONormally produced CO2 2 300-400 L/d or H300-400 L/d or H++ 15 mol/ 15 mol/d.d.
2) origins of nonvolatile acid ( fixed acid )
It comes from metabolic processes or incomplete oxidation of glucose or fats and so on. as: H2SO4, H3PO4, lac
Incomplete oxidation of fatty acid.Incomplete oxidation of fatty acid.
Normally produced HNormally produced H++ 50-100 mmol/d . 50-100 mmol/d .
3) Exogenous acid intake
Salicin intoxication
Hydrochloric acid
Origin of bases:
1) NH3: It is formed by deamination of amines, amino acid, purines and so on. 2) Eatting salt of organic acid: Sodium citratc and sodium lactate come from vegetable and fruits.
3. Regulation of acid – base balance
1) Chemical buffers: Buffer system is composed by weak acid and weak acid salt. It may convert strong acid into weak acid or strong alkali into weak alkali.
NaHCO3+HCl → NaCl+H2CO3
H2CO3+NaOH → H2O+NaHCO3
Major buffer system in the bodyMajor buffer system in the bodyCarbonic acid/Bicarbonate(HCOCarbonic acid/Bicarbonate(HCO33
--/H/H22COCO33)) : :
The major extracellular bufferThe major extracellular buffer ,, regulated by lungregulated by lungs and kidneyss and kidneys ,, effectiveeffective ,, determining the pH of determining the pH of plasma. plasma.
Phosphate (HPOPhosphate (HPO442-2-/H/H22POPO44
-- )) : Intracellular : Intracellular
Protein (PrProtein (Pr--/HPr)/HPr) :: Plasma/Intracellular Plasma/Intracellular
Hemoglobin (HbHemoglobin (Hb--/HHb/HHb and and HbOHbO22--/HHbO/HHbO22 )) : : RBCRBC
*A buffer system cannot buffer itself.*A buffer system cannot buffer itself.
fast / no permanencefast / no permanence
2) Respiratory control:
Expelling more CO2 through respiration→to exclude volatile acid.
Fast / effectively / only excludFast / effectively / only excludes volatile acides volatile acid
PaCOPaCO22(40-80 mmHg)(40-80 mmHg)Blood-brain barrier permeBlood-brain barrier permeable to COable to CO22: CO: CO22+H+H22OOHH22COCO33 HH+++HCO+HCO33
--(in cerebr(in cerebrospinal fluid, CSF)ospinal fluid, CSF) [H[H++] ] Central chemoreceptorCentral chemoreceptor(beneath the ventral surface of the medulla oblong(beneath the ventral surface of the medulla oblongata)ata) Respiratory center Respiratory center VentilationVentilation (Main) (Main)
PCOPCO22 80 mmHg, inhibition of respiratory cente80 mmHg, inhibition of respiratory center.r.
Pa OPa O2 2 30 mmHg, inhibition of respiratory cente30 mmHg, inhibition of respiratory centerr
3) Role of kidney (exclusion of acid with conservation of base)
hydrogen ion secreted ammonium excreted by renal tubular cell bicarbonate reabsorbed
Effectively ( fixed acid may be excludeEffectively ( fixed acid may be excluded ) / slowlyd ) / slowly
Role of the kidneysRole of the kidneys
powerfully, slowpowerfully, slowlyly## Proximal tubuleProximal tubule: : H H+ + secretion coupled with secretion coupled with HCHCOO33
-- reabsorption reabsorption
# # Collecting tubuleCollecting tubule H H+ + secretion and excretion cousecretion and excretion coupled with the addition of pled with the addition of newnew HCOHCO33
-- to the plasmato the plasma
Secreted ammonia once the noSecreted ammonia once the normal urinary phosphate buffermal urinary phosphate buffers are saturated.rs are saturated. NH NH3 3 + H+ H+ + NHNH44
++
4) Role of tissue and cell
cell: intra and extra ions exchange across the cellular membrane buffering in the cell or titrating base in ECF
• Effectively / but need timeEffectively / but need time
Acid-base balance: Acid and bases are continuously produced in the body, PH is maintained 7.35-7.45 by four regulation of the body, This condition is termed as acid-base balanceacid-base balance.
§2. Laboratory parameters of acid-base balance 1. PH : pH= pH= log [Hlog [H++]]=log1/ [H=log1/ [H++] (The logarithm to the ] (The logarithm to the base 10 of the reciprocal of the [Hbase 10 of the reciprocal of the [H++])])
Normal plasmaNormal plasma pH 7.35-7.45 ( average 7.pH 7.35-7.45 ( average 7.4 )4 )
2. PaCO2( respiratory parameter ):
Partial pressure of COPartial pressure of CO22dissolved in arterial plasma(dissolved in arterial plasma(The pressure is produced by CO2 dissolved in arterial plasma).
Normal range: 4.39~6.25kPa(33~46mmHg)Normal range: 4.39~6.25kPa(33~46mmHg) Average: 5.32kPa(40mmHg) Average: 5.32kPa(40mmHg)
PaCO2 > Normal (hypoventilation) a.primary change: RAC b.secondary change: MAL with respiratory compensation
PaCO2 < Normal (hyperventilation) a.primary change: RAL b.secondary change: MAC with respiratory compensation
3. SB AB BB BE (metabolic parameter): SB: HCO3
- in plasma under standard condition 22~27 mmol/L AB: HCO3
-] ↓ ; PH . AB↓ , SB↓ , BB↓ , BE ↓ ; PaCO2 ↓ ; AB < SB
2) clasification:
Normal AG MAC High AG MAC
3) pathogenesis and mechnisms: (1) lose of bases (2) gaining acids
Metabolic acidosisMetabolic acidosis CausesCauses:: (1) lose of bases (bicarbonate decreased)
Gastrointestinal lossesGastrointestinal losses: diarrhea, fistulae and so on. : diarrhea, fistulae and so on. Renal lossesRenal losses: proximal renal tubular acidosis and distal r: proximal renal tubular acidosis and distal renal tubular acidosisenal tubular acidosis
(2) gaining acids (bicarbonate consumed in buffering) Lactic acidosisLactic acidosis: tissue hypoxia, impaired oxygen utilizati: tissue hypoxia, impaired oxygen utilization, severe liver dysfunction, and shockon, severe liver dysfunction, and shock KetoacidosisKetoacidosis: diabetic,hepatic cirrhosis, alcoholic poison: diabetic,hepatic cirrhosis, alcoholic poisoning, or starvation ing, or starvation Renal failure: conservation of acids Renal failure: conservation of acids
Exogenous acid intakeExogenous acid intake: ammonium chloride, salicylate, e: ammonium chloride, salicylate, ethylene glycol(commonly used in antifreeze), or methanol ithylene glycol(commonly used in antifreeze), or methanol intoxication ntoxication
4) CompensationCompensation: all regulation system take part in5) Effects Effects: (1) Depression of central neural system a Elevated activities of glutamate decarboxylase →GABA ↑
b.ATP ↓ (2) Depression of heart and vessel(Ca2+ transport disorder; hyperkalemia;ATP↓): cardiac output ↓ ; cardiac arrhythmias; peripheral vasodilation.(3) Skin: warm and flashed(4) Alteration of skeleton: decacification, retarding growth and osteodystrophy6) TreatmentTreatment: administration of 5%NaHCO3, sodium lactate, THAM.
Respiratory acidosis
1) ConceptConcept:
Primary change : retention of CO2; pH . PaCO2↑ ; AB↑ SB↑ BB ↑ BE ↑ ; AB > SB
3) CausesCauses : Disorder of external respiration - Overdosage of sedatives, narcotics,etc. Cerebrovascular accidents. Cardiopulmonary arrest Central nervous system trauma, infections Poliomyelitis Inhalation of foreign bodies Chronic obstructive pulmonary disease Asthma Pneumonia Increased CO2 inhalation – Misoperation of mechanical ventilator Inhalation CO2 of high concentration
4) CompensationCompensation:
In acute RAC:
ion exchange across the membrane and buffering in cell
HCO3-
+
H+ H++A- HA
K+ K+
体细胞( somatic cell )CO2+H2O
H2CO3
Red blood cell
CO2 CO2+H2O H2CO3
H++Hb - HHb
+
HCO3-
-
Cl-
In chronic RAC: excretion of more H+ and ammonia ion reabsorption of more HCO3
- in kindneys
5) Effects Effects: (1) Neurological effects: CO2 narcosis (2) Cardiovascular effects: arrhythmias; pulmonary artery hypertension; cardiac output decrease. (3) Mixed acid-base imbalance (RAC+MAC) (4) Inducting of hyerkalemia and hypochloremia
3) Causes and mechanismCauses and mechanism: MechanismMechanism: a. Excessive gain of alkali (bicarbonate)
b. Excessive loss of hydrogen ions, chloride or potassium ions
Causes:Causes:aa.Excessive gain of alkali (bicarbonate)Bicarbonate intake:treatment of MACcitrate-containing blood transfusionsParenteral solution containing lactate
bb.Excessive loss of hydrogen ions, chloride or potassium ionsGastrointestinal H+ loss:vomiting,gastric suctionRenal H+ loss:Aldosteronism,cushing’s syndromethiazide and loop diureticpotassium deficit
cc.Volume contraction DehydrationDiuretic therapy
4) CompensationCompensation: Blood buffer role limitation Respiratory regulation Ion exchange and H+ out cell to titrate bicarbonate Renal role: excluding bicarbonate and conserving H+
3) Causes and mechanismsCauses and mechanisms: Mechanisms: Mechanisms: Hyperventilation Causes:Causes:a. Psychogenic hyperventilation:Hysteria
b. Stimulation of respiratory center: High altitude hypooxia Salicylate toxication Blood ammonia↑(Hepatic encephalopathy) Encephalitis Brain injury Feverc. Inappropriately high ventilator settings
4) CompensationCompensation: In acute RAC: Ion exchange, H+ out of cell to titrate base in ECF In chronic RAC: Decreased excretion of H+ and NH4
+ Decreased reabeorption of HCO3
-
5) EffectsEffects: (1) Increased excitability of the nerve and muscle (2) Mental dysfunction (3) Hypokalemia,hypochloridemia
6) Principle of treatmentPrinciple of treatment: a. Decreased ventilation by administration of sedative. b. Application of a plastic bag to inspire more amount of CO2 gas
Parameter changes of simple typesParameter changes of simple types
Disorder Primary Change Second Response pHDisorder Primary Change Second Response pH
Compensated XCompensated X :: after compensation, pH still in normal. after compensation, pH still in normal. Uncompensated XUncompensated X : : after compensation, pH still abnormaafter compensation, pH still abnormal.l.
§4. Mixed acid –base disturbance
Definition : more than one primary acid-base disorder coexist in a patient.
Double disorders
1) MAC+RAC: diabetic ketosis with pulmonary disease 2) MAL+RAL: vomiting with hyperventilation 3) MAC+RAL: uremia with high fever 4) MAL+RAC: diuretics with respiratory failure 5) MAC+MAL: heart failure with hypokalemia
Triple disorders :
respiratory acidosis
+ MAC + MAL
respiratory alkalosis
§5. Diagnosis 1. According to pathogensis establishing primary change 2. Manifestation: excitation — alkalosis inhibition — acidosis 3. According to PH PH<7.35 —acidemia — acidosis PH>7.45 — alkalemia — alkalosis PH=7.35~7.45: normal condition complete compensation mixed acid-base disturbance 4. Condition of compensation:direction ; predicted compensative value ; compensative limit 5. Estabolilshed triple disorders: utilized AG
The patient was suffered from salicylate intoxication. His blood-gas parameters (lab. Value): PH = 7.45 PaCO2 = 2.6 kpa (20mmHg)
HCO3- =13mmol/L .what acid-base disorders presente
d in this patient ?
Causes: salicylate intoxication. Primary change is HCO3- decreased.
HCO3- =13mmol/L<24mmol/L MAC
pH: pH=7.45=N compensated MAC mixed acid-base imbalance (MAC+RAL) Compensatory condition: PaCO2 =2.6kpa(20mmHg)<5.32kpa(40mmHg) Calculate: 1.2×ΔHCO3±2=1.2 ×(24-13) ±2=13.2 ±2=11.2-15.2 Predicted PaCO2 value =40 - (11.2or15.2)=24.8-28.8mmHg Actual PaCO2=20mmHg < predicted PaCO2=24.8 –28.8mmHg