Blood Gas Analisis,Acide Base
Transcript of 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