Blood Gas Analisis,Acide Base

7/29/2019 Blood Gas Analisis,Acide Base

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Blood Gas Analysis


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Acids and bases

An acid is defined as any compound, which formshydrogen ions in solution ("proton donors).

An acid that entirely dissociated is said = strongacid i.e. : HCl

An acid that partially dissociated is said = weakacid i.e. : phosphoric acid A base is a compound that combines with

hydrogen ions in solution ("proton acceptors). A base that entirely dissociated is said = strong

base i.e. : NaOH An base that partially dissociated is said = weak

base i.e. : bicarbonate (conjugate base)


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pH : potenz (power) ofHydrogen Peter Sorensen (1909, Denmark) Negative Log Hydrogen ion concentration Wasserstoffionen exponent(Jerman)

pH = Log10[H+]


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[H+] (moles/liter) [H+] (moles/liter) pH

0.1 10-1 1

0.01 10

-2

20.001 10-3 3

0.0001 10-4 4

0.00001 10-5 5

0.000001 10-6 6

0.0000001 10-7 7

0.00000001 10-8 8

0.000000001 10-9 9

0.0000000001 10-10 10

0.00000000001 10-11 11

0.000000000001 10-12 12

0.0000000000001 10-13 13

0.00000000000001 10-14 14


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The regulation of the internal environmentincludes the regulation of the body fluidhydrogen ion concentration, [H+]Although [H+] is very small compared to mostsolutes, being around 107 equ/liter, it hasmarked effects on an important part of thebody machinery - enzymes.

An introduction to acid-base balance,Watson Philip D., 2004


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7.40 (7.35-7.45)

Extracellular fluid: 7.4 Intracellular: 7.0-7.2 Viable range: 6.80 - 7.80

Neutral pH


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Acid-base balance refers to the mechanisms thebody uses to keep its fluids close to neutral pHso that the body can function normally

Acid-base balance


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Production of Hydrogen Ions

Two groups of important acids : Carbonic acid(H2CO3) and Non carbonic acid Carbonic acid (volatile acids) from CHO and fat

metabolism; 15,000 mmol of CO2/day, mostlyhandled by respiration.

Non carbonic acid (non-volatile acids) fromprotein metabolism; 1.0-1.5 mmol H+/day/kg;captured in the form of H2SO4, H2PO4, etc., andexcreted by the kidneys.

Normal [H+] is ~40 nanomol/L (


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Control of [H+] Ion Concentration

Excretion of CO2 by the lungs

Blood and tissue buffering

Renal excretion of H+ and regeneration ofHCO3-


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Excretion of CO2 by the lungs

In plasma, there is very little CO2 in the formof carbonate (CO3 ) and carbonic acid Nearly all the CO2 is in the bicarbonate form The control of PCO2 level necessitates either

excretion or retention of CO2 by the lungs The respiratory system can produce rapid

compensation for changes in pH by altering thelevel of PaCO2

H+ + HCO3- H2CO3 CO2 + H2O

LUNGS


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The ability to reduce the magnitude

of changes in [H+] by binding orreleasing [H+]

Buffering


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a)BicarbonateThe most important buffer system; CO2 removedby the lungs and bicarbonate regenerated by thekidney

b)ProteinsContain weak acidic and basic groups within theirstructure; plasma proteins form importantbuffering systems; intracellular proteins limit pHchanges within cells; protein matrix of bone

buffer hydrogen ions in chronic acidosisc)Haemoglobin

Haemoglobin (Hb) carriage of O2 but alsotransport of CO2 and buffering hydrogen ions

Blood and tissue buffering


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H2CO3 HCO3-H+ + H+ + CO3=+ H2OCO2

If the H2CO3 is held constant1.2meq HCl causes the [HCO3- ] to diminish by 1.2meq

but the H2CO3 level remains constant at 1.2meq/l

Plasma has a [HCO3-] of approximately 24 meq/l and [H2CO3] of 1.2meq/l

pH =20

16.1 + log 7.4=

If 1.2meq HCl is added to 1 litre of a solution of 24meq NaHCO2 in water,

1.2meq HCO3- will be converted to H2CO3


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Renal [HCO3-] reabsorption and regeneration

Bicarbonate filtered/day = 4520 mmol Proximal tubule is major site of reabsorption

(75-90% of the filtered load); the remaining10-25% is reabsorbed in distal tubule;

generation of new HCO3- : 1.0 - 1.5mmol/kg/day Principle mechanism of HCO3- reabsorption is

with Na+; requires: Na+/K+ ATPase, Na+/Hantiport, carbonic anhydrase and glutamine

generation and luminal carbonic anhydrase Urine bicarbonate free (if pH is < 5.8, it is free

of HCO3-); urine pH is ~5.0 - 5.5 due to acidsecreted into urine


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Acidosis is a state of excess H+

Acidemia results when the blood pH7.45

Abnormal acid-base balance


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The Traditional Approach

A H+ + B-

[H+] [B-]

[A] = Q

[H+] [B-]

[A]= K [H+] = K

[A]

[B-]

log [H+] = log K + log[A]

[B-]

pX = - log X = log1

X

- pH = - pK - log [A]

[B-]

pH = pK + log[B-]

[A]

The Henderson-Hasselbalch equation


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pH =[HCO3-]

[H2CO3]pK + log

H2CO3 HCO3-H+ + H+ + CO3=+ H2OCO2

pH =[HCO3-]

[0.03 x PCO2]pK + log

pH =20

16.1 + log

pH = 7.4

Plasma has a [HCO3-] of approximately 24meq/l and [H2CO3] of 1.2meq/l

Control of HCO3- is assumed to be a primary parameter


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The difference between major plasma cations andmajor plasma anions : [Na+] - [Cl-] - [HCO3]

Anion Gap = 140-105-25 = 10 If chloride is reduced to 95 meq/l, bicarbonate

would be increased to 35.6; Anion gap = 140-95-

35.6 = 9.4 If lactic acid is increased from its normal 1 meq/l

to 10 meq/l, bicarbonate would fall to 18 meq/l;Anion gap = 140-105-18 = 17

Any strong acid will increase the anion gap byreducing the bicarbonate Some people include potassium in the anion gap

: [Na+] + [K+] - [ClG] - [HCO3]; the normalvalue = 14

The Anion Gap


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Acid-baseimbalance

PlasmapH

Primarydisturbance

Compensation

Respiratory

acidosis

LowincreasedpCO

2

increased renal net acidexcretion with resultingincrease in serumbicarbonate

Respiratoryalkalosis

HighdecreasedpCO2

decreased renal net acidexcretion with resultingdecrease in serumbicarbonate

Metabolicacidosis

LowdecreasedHCO3

-hyperventilation withresulting low pCO2

Metabolicalkalosis

HighincreasedHCO3

-

hypoventilation withresulting increase inpCO2

Classification of acid-base defect(Henderson-Hasselbalch)


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Techniques for measuringpH status

pH electrode, Blood sampling Astrup Method pH and PCO2 Electrode Systems


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Acid-Base Diagram

From Goldberg, M., Green, S.B., Moss, M.L., et al.: JAMA 223:269-275, 1973


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Arterial Blood Gas (ABG) Interpretation

Does the patient have an acidosis or analkalosis?

What is the primary problem metabolic

or respiratory? Is there any compensation? (respiratorycompensation is immediate while renalcompensation takes time)


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pHpaCO2

( mm Hg)

HCO3

(meq/L)

Interpretation

7.35 to 7.45 36 to 44 22 to 26

< 7.35

> 7.45

< 7.35 > 44 22 to 26

< 7.35 36 to 44 < 22

< 7.35 > 44 < 22

> 7.45 < 36 22 to 26

> 7.45 36 to 44 > 26

> 7.45 < 36 > 26closer to 7.35 > 44 > 26

closer to 7.35 < 36 < 22

closerto 7.45 < 36 < 22

closerto 7.45 > 44 > 26

Summary of ABG Interpretation

Normal

Acidosis

Alkalosis

Respiratory acidosis

Metabolic acidosis

Mixed acidosis

Respiratory alkalosis

Metabolic alkalosis

Mixed alkalosisCompensated respiratory acidosis

Compensated metabolic acidosis

Compensated respiratory alkalosis

Compensated metabolic alkalosis


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Clinical condition of AB disturbances

RespiratoryAcidosis

Acute: airway obstruction, severe pneumonia, chest trauma/pneumo-thorax; Drug intoxication (narcotics, sedatives);

NaHCO2 therapy; Neuromuscular blockade; head trauma.Chronic: BPD, COPD; Neuromuscular disease; Extremeobesity; Chest wall deformity; Increased production of CO2.

Respiratory

Alkalosis

Pain; Anxiety; Hysterical hyperventilation; Restrictive lungdisease; Severe CHF; Pulmonary emboli; Drugs; Sepsis;Fever; Thyrotoxicosis; Induced hyperventilation during

anaesthesia; Overaggressive mechanical ventilation; Hepaticfailure; Some types of CNS damage.

Metabolic

Acidosis

Elevated Anion Gap: Ketoacidosis-diabetic; Alcoholic;Starvation; Lactic acidosis-hypoxia; Shock; Sepsis; Seizures;Toxic ingestion (salicylates, methanol, ethylene glycol,ethanol, isopropyl alcohol, paraldehyde, toluene); Renal

failure

uremia.Normal Anion Gap: RTA; Hypoaldosteronism; Potassiumsparing diuretics; Pancreatic loss of bicarbonate; Diarrhea;Carbonic anhydrase inhibitors; Acid administration (HCl,NH4Cl, arginine HCl); Cholestyramine.

Metabolic

Alkalosis

Loss of gastric juice; Diuretic alkalosis; Ingestion or injectionof excess base; Steroid alkalosis.


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Effectiveness of Oxygenation Further evaluation of the arterial blood gas

requires assessment of the effectiveness ofoxygenation of the blood

Hypoxemia decreased oxygen content ofblood - paO2 less than 60 mm Hg and thesaturation is less than 90%

Hypoxia inadequate amount of oxygen

available to or used by tissues for metabolicneeds


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Mechanisms of Hypoxemia Inadequate inspiratory partial pressure

of oxygen

Hypoventilation Right to left shunt Ventilation-perfusion mismatch Incomplete diffusion equilibrium


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Assessment of Gas Exchange

*RQ=respiratory quotient= 0.8

Alveolar-arterial O2 tension difference A-a gradient PAO2-PaO2

PAO2 = FIO2(PB - PH2O) - PaCO2/RQ* Arterial-Alveolar O2 tension ratio PaO2/PAO2

Arterial-inspired O2 ratio

PaO2/FIO2 P/F ratio


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Assessment of Gas ExchangeABG A-a grad

PaO2 PaCO2 RA 100%

Low FIO2 N N

Alveolar hypoventilation N N

Altered gas exchange

Regional V/Q mismatch /N/ N/

Intrapulmonary R to L shunt N/

Impaired diffusion N/ N

Anatomical R to L shunt(intrapulmonary or intracardiac)

N/

N=normal


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Stewart ApproachHow to understand acid-baseA quantitative Acid-Base Primer for Biology and MedicinePeter A. Stewart, Edward Arnold, London 1981


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The independent and dependentfactors or variables

Strong Ion

Difference

PCO2

ProteinConcentration

pH[HCO3-]

Etc.

Chemistry

Law of Mass ActionCharge Balance etc.

Dependent

Variables

IndependentVariables


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Ions

Strong ions(entirely dissociated) Weak ions(partially dissociated)

Kation : Na+,K+,Mg+,Ca++

Anion : Cl-,SO4-,PO4=, laktat-,keto-

Albumin-, Posfat-, HCO3-


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Independent variables

Strong iondifference

(Na+ + K+ + Mg2+ + Ca2+) (Cl + lactate)

pCO2 H2O + CO2

H2CO3

H+ +HCO3

Weak acids/proteins

ATOT A + AH


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Ion Concentration

(meq/L)

Sodium 140

Potassium 4

Calcium 3Magnesium 1

Total strong

Cations 148

Chloride 104

Lactate 8

Total strong

anions 112Difference

(Cations - Anions) 36

Concentration

(meq/L)

SID 36

[H+] 6.6 x 10-10pH 12.2

[OH-] 36

Effects of strong ions

alone

Concentration

(meq/L)

SID 36

pCO2 (mmHg) 40

[HCO3

] 35.8[H+] 27 x 10-6

pH 7.6

[OH] microEq/L


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Computer program, Watson (AcidBasics II)


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Classification of Primary Acid-BaseDisturbances

Acidosis Alkalosis

I. Respiratory PCO2 PCO2

II. Nonrespiratory (metabolic)

1. Abnormal SID

a. Water excess/deficit* SID, [Na+] SID, [Na+]b. Imbalance of strong anions

i. Chloride excess/ deficit SID, [Cl-] SID, [Cl-]

ii. Unidentified anion excess SID, [XA-] -

2. Nonvolatile weak acids

a. Serum albumin [Alb] [Alb]

b. Inorganic phosphate [Pi] [Pi]

Fencl, Jabor, Kazda, et al.: Metabolic Acid-Base Disturbances, American Journal OfRespiratory and Critical Care Medicine Vol 162 2000


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Disturbances

Strong IonDifference

PCO2

ProteinConcentration

pH[HCO3-]

Etc.

Chemistry

Law of Mass ActionCharge Balance etc.

Lactic acidosis

Keto acidosisVomitingDiarrhea

Renal failure

Heart failure

Lung diseaseHyperventilationHypoventilation

MalnutritionDehydrationNephrotic syndrome


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Vomiting

Vomiting deplete Cl faster than the cations; SID

increases = metabolic alkalosis; Kidneycompensate by a decreased excretion of Cl,returns plasma SID towards normal

Diarrhea

The electrolytes lost and the subsequent acid-base disturbance depends upon the site and

nature of the disease, SID can move in eitherdirection

Lung disease andventilation rate

Direct effects on PCO2

Heart failure

Effects PCO2 and SID (poor tissue perfusion can

cause lactate production)

Dehydration Increases plasma protein concentration

Malnutrition andnephrotic syndrome

Cause significant decreases in serum albuminconcentration

Clinical condition and independent variables

Documents

Blood Gas Analisis,Acide Base