Acid-base Banlance and Acid-base Disturbance

8/13/2019 Acid-base Banlance and Acid-base Disturbance

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Acid-base balance and

acid-base disturbance


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I. regulation of acid-base balance

1. origin of acid and base in the bodyvolatile acid: H2CO3 (15mol/day)

sulfuric acid1) acids phosphoric acid

fixed acid: uric acid(90mmol/L) mesostate

2)base: salt of organic acid; NH3


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2. regulation of acid-base balance1) 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/H2CO3buffer of volatile acid: Hb-/HHb


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CO2

Cl-

CO2+H2O

C.A.

H2CO3

HCO-3

H+--Hb-

RBC


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2)respiratory regulationalteration of ventilation

alteration of breathe out of CO2

PaCO2 central

[H+] peripheral respirationPaO2 (receptor)PaCO2 (80mmHg)

inhibition of respiratory center3) cellular action exchanges of H+and K+


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4) renal regulation acidification of proximal renal tubule

Na+ Cl-

HCO-3

H2CO3

H20

H+Cl-NH3

K+

NH3

Na+

H+H2CO3

Na+C.A.

HCO-3 H2O+CO2


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acidification of distal renal tubule

H+-pump

NH+4

H+K+NH3

H2CO3 H+NH3

HCO-3 H2O+CO2

K+


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parameters of acid-base1. pH important and inexact parameter

normal range: 7.35~7.452. PaCO2 partial pressure of CO2of 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 PaCO2metabolic alkalosis PaCO2


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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 conditionNormal range: 22~27mmol/L ; AB=SB

4. buffer base(BB)sum of all buffer base in bloodnormal range: 45 ~ 55mmol/L

5. base excess(BE)normal range:3mmol/L


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6. anion gap (AG)+ -

Normal range: 12 2 mmol/L

Na+

Cl-

AG

HCO-

3


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. simple acid-base disturbance1. metabolic acidosis

concept: the primary disturbance is a decreaseof [HCO-3] in the arterial plasma

1) cause and pathogenesislactic acidosis: hypoxia, diabetes

liver diseaseketoacidosis: diabetes, starvationmetabolic

acidosis in severe renal failure: fixed acidsincreased AG

salicylic acid acidpoisoning: intake food


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diarrhea;GI: intestinal suction(loss of intestinal fistulaHCO-3) biliary fistula metabolic

acidosis in early renal failure:

normal AG NH3

secretionH+secretion

Renal tubular acidosis:H+secretion

kidney: depressant of C.A.(loss of acetazolamide

HCO-3) intake of Cl-

NaCl, NH4ClHyperkalemia


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2) compensatory regulationbuffer:respiratory compensationcellular compensationrenal compensation

[H+

] : C.A. H+

secretionNH3 secretion

[HCO-3] / [H2CO3] = 20:1 compensation

acidosis

[HCO-3] / [H2CO3] < 20:1 decompensation

acidosis

(SB AB BB BE PaCO2 AB < SB)


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3) effect on bodycardiovascular system

hyperkalemia arrhythmia[H+] : contractility

peripheral resistance

central nervous system[H+] ATP , -amino butyric acid

(somnolence, coma)4) principles of treatment


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2. respiratory acidosisconcept: The primary disturbance is an

elevation in plasma [H2CO3]1) cause and pathogenesis

Barbitaldepression of CNS head injury CO2 breathe paralysis of respiratory muscles

out disease of airway or lungchest injury

inhalation of CO2


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2) compensationbuffer: Hb-/HHbcells: exchange of H

+

and K+kidney: secretion of H+and NH3

(PaCO2 SB AB BB BE ABSB)3) effect on bodyCNS

CO2 CO2 narcosis respirationcardiovascular system


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4) principles of treatmentNaCO3

3. metabolic alkalosisconcept: the primary disturbance is

an increase of [HCO-3] in the

arterial plasma

1) causes and pathogenesis


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digestive tractvomiting; gastric suction(loss of HCl)

loss diuretics distal flow rateof H+ (furosemide) blood volume ADS

kidney hyperaldosteronism H+-Na+exchange

H+-K+exchange betweenHypokalemia

intra- and extra-

cell

renal secretion of H+hypochloremia

renal secretion of H+


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NaHCO3intake transfusion of banked bloodof base (citrate)

2) compensation of the bodyrespiration compensation are limited

(hypoxia)cells compensation hypokalemiakidney pH inhibition of carbonic

anhydrase (C.A.)secretion of H+

(SB AB BB BE PaCO2

ABSB)


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3) effects on bodyinhibition of glutamate decarboxylase

CNS -amino butyric acid dysphoriainsanity

pH brain-vessel dizzinesscontraction brain delirium

O2dissociation hypoxia Comacurve shifting to left

neuromuscle pH free Ca2+ tichypokalemia arrhythmia


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4) principles of treatmentloss of H+digestive tractdiuretic ; hypokalemia 0.9%NaCl; KCl

hyperaldosteronism

antisterone; diamox()


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4. respiratory alkalosis

concept: the primary disturbance is decrease

of [H2CO3] in plasma1) cause and pathogenesis

hypotonic hypoxia

pneumoniahyperventilation hysteria(); fever; [NH3]

hyperthyroidism()misoperation of ventilator


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respiration (slight inhibition)2) compensation cells (exchange of H+-K+)

kidney secretion of H+

(PaCO2 ; SB AB BB BE ; ABSB)3) effects on body

It is as same as metabolic alkalosis.dizziness and convulsion are happened easily() ()

4) principles of treatmentinhalation of 5%CO2


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IV. Mixed acid-base disturbance1. dual acid-base disturbance1)metabolic acidosisplusrespiratory acidosis

heart beat [HCO-3]respiration

stop character PaCO2pH

2) metabolic alkalosis plus respiratory alkalosishepatic NH3 PaCO2

failure diuretic character [HCO-3]pH

3)respiratory acidosis

plusmetabolic alkalosis

pulmonary heart diseasediuretic pH


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4) respiratory alkalosis plus metabolic acidosisinfective shockfever

pH5) metabolic acidosis plus metabolic alkalosis

ketoacidosis(diabetes)vomiting pH

2. triple acid-base disturbance1) respiratory acidosis; metabolic acidosis

and alkalosispulmonary heart disease; vomiting2) respiratory alkalosis; metabolic acidosisand metabolic alkalosis

fever; vomiting; diarrhea (food poisoning)


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discuss of casemethod:

1. pH2. primary factor and parameter3. secondary factor and compensation4. expected range of compensation

1:

patient, female, 46, chronic pyelitispH 7.32PaCO2 28mmHgCO2.CP. 19.2ml%SB 13.6mmol/LBE -15.3mmol/L


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The scope of compensatory

responses of acid-base disordersacute respiratory acidosis : [HCO-3]=0.1 PaCO2 1.5chronic respiratory acidosis: [HCO-

3

]=0.4 PaCO2

3.0

acute respiratory alkalosis : [HCO-3]=0.2 PaCO2 2.5chronic respiratory alkalosis:[HCO-3]=0.5 PaCO22.5

metabolic acidosis: PaCO2=1.2 [HCO-3] 2.0metabolic alkalosis: PaCO2=0.7[HCO-3]5.0


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2:patient, male, 45, chronic bronchitispH 7.26PaCO2 60mmHgBB 46.2mmol/LSB 22mmol/L

BE -7.5mmol/L

after treatmentpH 7.34PaCO2 70mmHgBB 58mmol/LBE 5.5mmol/L


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3.

patient, male, 47, purulent appendicitis, he

was treated with abdominal suction andpersistent gastrointestinal decompressionafter operation.

pH 7.56PaCO2 50mmHgCO2.CP. 90ml%SB 34mmol/LBE 10mmol/LK+ 3.2mmol/LCl- 105mmol/L


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4.

, 3, 20 / T 39.81200ml.

Acid-base Banlance and Acid-base Disturbance

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