arterial blood gases
DESCRIPTION
TRANSCRIPT
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By
Dr Y.N MAURYA
M.B.B.S D.C.H Medical Officer
Deen Dayal Upadhyay Hospital Govt. of NCT New Delhi- 64
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ARTERIAL BLOOD GASES
Arterial blood gas sampling is a medical technique used to check gas levels in the blood. It typically involves using a thin needle and syringe to puncture an artery, This technique is commonly used on patients whose breathing is controlled by a mechanical respirator or who are having serious difficulties with breathing.
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A.B.G SAMPLE COLLECTION
ULNER,RADIAL BRACHIAL DORSALIS PEDIS FEMORAL ARTERIES CAN BE USED.
ARTERIAL LINE ---- FREQUENT SAMPLING INTERMITENT STAB---INFREQ. SAMPLING UNDER FULL ASEPTIC CONDITION IF ULNER/RADIAL ART IS USED ---
MODIFIED ALLEN’S TEST
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MODIFIED ALLEN’S TEST
1. INSTRUCT PATIENT TO CLENCH HIS FIST
2. USING YOUR FINGER APPLY OCCLUSIVE PRESSURE ON BOTH RADIAL & ULNER ARTERY
3. WHILE APPLYING OCCLUSIVE PRESSURE TO BOTH ARTERY,HAVE THE PATIENT RELAX HIS HAND.BLANCHING OF PALM &FINGER SHOULD OCCUR
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MODIFIED ALLEN’S TEST
4. RELEASE THE OCCLUSIVE PRESSURE ON ULNER ARTERY & NOTICE FLUSHING OF HAND WITHIN 7-10 SEC.THIS DENOTE THAT ULNER ARTERY SUPPLY IS ADEQUATE &IT’S SAFE TO PRICK RADIAL ARTERY. IF IT DOES’T OCCUR IT MAENS ULNER ARTERY SUPPLY IS NOT SUFFICIENT & RADIAL ARTERY IS NOT SAFE TO PRICK.
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SAMPLE SIZE & PRECAUTION
ABOUT 2 ml BLOOD IN AIR TIGHT HEPARINISED SYRINGE/ VIAL
GLASS CAPILLARY CAN ALSO BE USED
COTINUOUS AGITATION BY ROLLING
FIO2 SHOULD BE WRITTEN ON SAMPLE
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CONTRAINDICATION FOR ARTERIAL PUNCTURE
INFECTION AT SITE. ALLEN’S TEST NEGATIVE. ON ANTICOAGULANT THERAPY. SEVERE PERIPHERAL VASCULAR DISEASE. DISTAL TO SURGICAL SHUNT.
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SpO2 and SaO2
SpO2 and SaO2 are often used interchangeably, but they are not same
When O2 saturation is measured by pulse oximeter..... SpO2
When O2 saturation is measured by CO- oximeter..... SaO2
SpO2 is also called functional arterial O2 saturation and SaO2as fractional arterial O2 saturation
Only true CO-oximeter can determine an accurate value for SaO2
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SpO2 and SaO2
SpO2 == HbO2
HbO2 + Hb
SaO2 == HbO2
HbO2+ Hb+COHb+MetHb+SfHb+COSfHb
SaO2 == SpO2[1-SaCO]… (Nellcor equation)
Non functional Hb is 2-3%
In heavy smoaker it may be up to 15%
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O2 Saturation & Pulse oximetry
We can know arterial blood gases and arterial oxygen saturation from ABG machine with help of O2 DISSOCIATION CURVE .
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O2 DISSOCIATION CURVE
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O2 Saturation & Pulse oximetry
ABG machine calculates o2 saturation based on pH, PaCO2,temp,by using normal adult o2 dissociation curve
o2 dissociation curve in presence of
1) fetal Hb ,low 2,3 DPG……curve shifts Lt
2)sickle cell, chr. Hypoxia, cyanotic H D, chr. Asthama, high altitude…. curve shifts Rt. And ABG machine becomes inaccurate
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O2 Saturation & Pulse oximetry
If we can know arterial blood gases and arterial oxygen saturation with help of ABG machine, then what is need of pulse oximeter ?
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O2 Saturation & Pulse oximetry
ADVANTAGE OF PULSE OXIMETRY Noninvasive Portability Continuous monitoring Ease of use (no calibration) Rapidity (warn decr. in saturation before sign and
symptom)
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Principle of Pulse oximetry It is based on different absorption coefficients of
oxyHb & deoxyHb for different wavelength of lights (BEER’S LAW)
For oxyHb & deoxyHb 805nm is isobestic point. Above 805 nm oxyHb absorbs more light than
deoxyHb & below it deoxyHb absorbs more light than oxyHb. Because of this fact by using two wavelength of lights actual o2saturatn level can be measured.
Pulse oximeter uses two wavelength of light red(660nm) and infrared (950nm).
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Principle of Pulse oximetry
Absorption Spectrum of Hemoglobin
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Pulse Oximetry1)Pulse oximeter emits two wavelength of lights (red
& infrared) from Xenon LED.These lights are sensed by photodiodes just opposite to LED or adjacent to LED.
2)It measures %saturation of deoxyHb with O2 (not PaO2) based on absorption spectrum of Hb in pulsatile arterial blood.
3) Sensitivity rapidly decreases at SpO2 >90%4) Normally in blood dysfunctional Hb is 2-3% hence
all oximeters are standardized against known standard CO-oximeter & adjusted, so that it can display SpO2close to SaO2.
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Pulse Oximetry
4)Accuracy depends on a) % of dysfunctional Hb. b) age of LED. (Aging of LEDcauses change in peak wavelength).
c) LED from same batch & same manufacturer may vary by 30nm in peak wavelength.
d) Good red & infrared waveform i.e signal strength (tissues are easily penetrated by infrared but not so easily by red. Thus red waveform is lost first, this is why false reading is given when signal is weak)
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Pulse Oximetry There are two types of probes 1) Transmission probe……Finger type 2) Reflectance probe…… Rectal type Do’t provide accurate reading in CO-
poisoning, methemoglobinemia, decreased cut. perfusion, strong vasoconstriction, deep pigmentation, nail polish, intravascular dye, movement, venous pulsation, infrared heating lamp & strong colored lights.
ECG synchronization technique can be used to remove movement artifact.
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Hypoxia & Pulse Oximetry
Hypoxic hypoxia…. Register low saturation Anaemic hypoxia…. Normal saturation Circulatory hypoxia… Low signal strength Histotoxic hypoxia… Normal saturation
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SaO2 and Pulse CO- Oximetry
Pulse oximeter do’t measure methemoglobin & carboxyHb.So becomes inaccurate in these cases.
IL-282 CO-oximeter is gold standard for o2 saturation measurement.
Pulse CO-oximeter emits at least four wavelength of light which measures oxyHb, deoxyHb, methemoglobin & carboxyHb
For infants pulse oximeter is more useful because CO-oximeter show false elevation of CO-Hb.(fetal Hb absorb more than two wavelength of lights)
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SaO2 and oxygen content
Tissues need a requisite amount of oxygen molecules for metabolism. Neither the PaO2 nor the SaO2 tells how much oxygen is in the blood. It is provided by the oxygen content, CaO2 (units = ml O2/dl). CaO2 is calculated as:
CaO2 = quantity O2 bound + quantity O2 dissolved to hemoglobin in plasma
CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)
Hb = hemoglobin in gm%; 1.34 = ml O2 that can be bound to each gm of Hb; SaO2 is percent saturation of hemoglobin with oxygen; .003 is solubility coefficient of oxygen in plasma: .003 ml dissolved O2/mm Hg PO2.
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Oxygen dissociation curve: SaO2 vs. PaO2
O2 content
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The Key to Blood Gas Interpretation:
Equation Physiologic Process
1) PaCO2 equation Alveolar ventilation
1) Alveolar gas equation Oxygenation2) Oxygen content equation Oxygenation3) Henderson-Hasselbalch equation Acid-base balance
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PaCO2 equation
PaCO2 =0.863VCO2/VA VCO2,ml of CO2 produced/ min; VA, alveolar ventilation
VA is increased……. PaCO2decreases
VA is decreased…. …PaCO2increases
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Alveolar Gas Equation
PAO2 = PIO2 - PaCO2/R , R= resp. quotient
PAO2 = PIO2 - PaCO2/ O.8 PAO2 = PIO2 - 1.2 (PaCO2),
PIO2 = FIO2 (PB – 47 mm Hg)
PAO2 = FIO2 (PB – 47 mm Hg) - 1.2 (PaCO2)
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Alveolar Gas Equation PAO2 = FIO2 (PB – 47 mm Hg) - 1.2
(PaCO2)
Except in a temporary unsteady state, alveolar PO2 (PAO2) is always higher than arterial PO2 (PaO2). Thus,
If FIO2 & PB are constant, as PaCO2 increases both PAO2 and PaO2 will decrease (hypercapnia causes hypoxemia).
If PB & PaCO2 are constant, as FIO2 decreases both PAO2 and PaO2 will decrease (suffocation causes hypoxemia).
If PaCO2 & FIO2 are constant, as PB decreases (e.g., with altitude), both PAO2 and PaO2 will decrease (mountain climbing causes hypoxemia).
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P(A-a)O2
P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen. it actually results from gravity-related blood flow changes within the lungs (normal ventilation-perfusion imbalance).
PAO2 is always calculated, based on FIO2, PaCO2 and barometric pressure.
PaO2 is always measured, in a ‘blood gas machine’. Normal P(A-a)O2 ranges from @ 5 to 25 mm Hg at room air (it
increases with age). A higher P(A-a)O2 means the lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries. Except for right to left cardiac shunts, an elevated P(A-a)O2 signifies some sort of problem within the lungs.
If P(A-a)O2 is negative---there is error in calculation/measurement
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Ventilation-Perfusion imbalance
A normal amount of ventilation-perfusion (V-Q) imbalance accounts for the normal P(A-a)O2.
Most common cause of low PaO2 is an abnormal degree of ventilation-perfusion imbalance Virtually all lung disease lowers PaO2 via V-Q imbalance, e.g., asthma, pneumonia, atelectasis, pulmonary edema, COPD.
Diffusion barrier is seldom a major cause of low PaO2 (it can lead to a low PaO2 during exercise).
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Henderson - Hasselbalch equation
Weak acid ionizes as,
HA=H++ A-
pH = pK+ log[A-] / [HA]
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Causes of low PaO2
NON-RESPIRATORY P(A-a)O2Cardiac right to left shunt IncreasedDecreased PIO2 NormalLow mixed venous oxygen content* Increased
RESPIRATORYPulmonary right to left shuntIncreasedVentilation-perfusion imbalance IncreasedDiffusion barrier IncreasedHypoventilation (increased PaCO2) Normal
*Unlikely to be clinically significant unless there is right to left shunting or ventilation-perfusion imbalance
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NORMAL A.B.G VALUES
HB -- 12-15gm/dl HCT -- 35-55 FIO2 ----- PaO2 – 80(60)-
100mmHg PaCO2 – 35-45mmHg pH – 7.35-7.45 K+ -- 3.5-4.5 mmol/L Na+ -- 135-145 mmol/L HCO3ˉ -- 22-26 mmol/L BE -- ±2 mmol SaO2 -- >90%
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ABG Interpretation First, does the patient have an
acidosis or an alkalosis. Second, what is the primary
problem – metabolic or respiratory. Third, is there any compensation
by the patient – respiratory compensation is immediate while renal compensation takes time.
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ABG Interpretation It would be extremely unusual for
either the respiratory or renal system to overcompensate
The pH determines the primary problem
After determining the primary and compensatory acid/base balance, evaluate the effectiveness of oxygenation
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Abnormal ValuespH < 7.35 Acidosis (metabolic
and/or respiratory)pH > 7.45 Alkalosis (metabolic
and/or respiratory)paCO2 > 45 mm Hg Respiratory
acidosis (alveolar hypoventilation)
paCO2 < 35 mm Hg Respiratory alkalosis
(alveolar hyperventilation)
HCO3 < 22 meq/L Metabolic acidosis HCO3 > 26 meq/L Metabolic alkalosis
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Putting It Together - Respiratory
So,paCO2 > 45 with a pH < 7.35 represents a
respiratory acidosispaCO2 < 35 with a pH > 7.45 represents a
respiratory alkalosisFor a primary respiratory problem, pH and
paCO2 move in the opposite direction For each deviation in paCO2 of 10 mm Hg in
either direction, 0. 08 pH units change in the opposite direction
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Putting It Together - MetabolicAndHCO3 < 22 with a pH < 7.35 represents
a metabolic acidosis HCO3 > 26 with a pH > 7.45 represents
a metabolic alkalosisFor a primary metabolic problem, pH
and HCO3 are in the same direction, and paCO2 is also in the same direction
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Compensation The body’s attempt to return the acid/base
status to normal (i.e. pH closer to 7.4)Primary Problem Compensationrespiratory acidosis metabolic alkalosisrespiratory alkalosis metabolic acidosismetabolic acidosis respiratory alkalosismetabolic alkalosis respiratory acidosis
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CompensationDISORDER DECR.
IN pHCHANGE IN HCO3
Ac. Resp. Acid. (10 Incr. in PaCO2) 0.08 Increase 1 mmol/L
Chr. Resp. Acid. (10 Incr. in PaCO2) 0.03 Increase 3.5 mmol/L
Ac. Resp. Alk. (10 Decr. in PaCO2) 0.08 Decrease 2 mmol/L
Chr. Resp. Alk. (10 Decr. in PaCO2) 0.17 Decrease 4mmol/L
DISORDER
PaCO2 Change inPaCO2/ Change in HCO3
Met.Acidosis
PaCO2=1.5(HCO3ˉ)+8±2 Dec. 1-1.5/1Dec in HCO3ˉ
Met.Alkalosis
PaCO2=0.7(HCO3ˉ)+20±1.5
Inc. 0.5-1/ 1 Inc in HCO3
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HOW KNOW THE DISORDER
pH PaCO2 HCO3ˉ
Respiratory Acidosis
Acute < 7.35 > 45 Normal
Partly Compensated < 7.35 > 45 > 26
Compensated ~ Normal > 45 > 26
Respiratory Alkalosis
Acute > 7.45 < 35 Normal
Partly Compensated > 7.45 < 35 < 22
Compensated ~ Normal < 35 < 22
Metabolic Acidosis
Acute < 7.35 Normal < 22
Partly Compensated < 7.35 < 35 < 22
Compensated ~ Normal < 35 < 22
Metabolic Alkalosis
Acute > 7.45 Normal > 26
Partly Compensated > 7.45 > 45 > 26
Compensated ~ Normal > 45 > 26
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pH < 7.35Acidosis
pH > 7.45Alkalosis
pCO2 > 45Respiratory
HCO3 < 22Metabolic
pCO2 < 35Respiratory
HCO3 > 26
Metabolic
PaCO2 ↑10→HCO3 ↑3.5
PaCO2 ↑10→HCO3 ↑1
PaCO2 ↓10→HCO3 ↓4
PaCO2 ↓10→HCO3 ↓2
PaCO2 ↑7
→HCO3 ↑10
Urine Cl < 10 Cl ResponsiveAnion Gap < 12
Non-Anion GapAnion Gap > 12
Anion Gap
Urine Cl > 10 Cl Unresponsive
Interpreting ABGs
Osm Gap > 10Methanol
Ethylene Glycol
Osmolar Gap < 10Ketoacidosis
Lactic acidosis Uremia
Aspirin/salicylate tox
DiarrheaRenal tubular acidosis
AcetazolamideTotal parenteral nutrition
Ureteral diversionPancreas transplant
CNS depressantsNeuromuscular disorder
Thoracic cage abnormalitiesObstructive lung disease
Obesity/hypoventilation syndromeMyxedema coma
Anxiety/painSepsis
CNS (stroke)Aspirin OD
Chronic liver diseasePulmonary embolism
PregnancyHyperthyroidism
Loss of body fluids:Vomiting
Nasogastric suctioningDiuretic use
Excess body fluids:Exogenous steroidsCushing’s syndromeHyperaldosteronismBartter’s syndrome
=Na - (Cl+HCO3)
Acute
Chronic
PaCO2 ↓15→HCO3 ↓10
Compensation:If: ΔPCO2/ΔHCO3
=CO2/HCO3ratioThen it IS comp.
Acute
Chronic
(2xNa) + (Glu/18) + (BUN/2.8) = calculated serum osmoles
HCO3 loss Extra H+
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Effectiveness of Oxygenation Further evaluation of the arterial blood
gas requires assessment of the effectiveness of oxygenation of the blood
Hypoxemia – decreased oxygen content of blood - paO2 less than 60 mm Hg and the saturation is less than 90%
Hypoxia – inadequate amount of oxygen available to or used by tissues for metabolic needs
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Causes 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 Alveolar-arterial O2 tension difference
A-a gradient PAO2-PaO2
PAO2 = FIO2(PB - PH2O) - PaCO2/RQ*
arterial-inspired O2 ratio PaO2/FIO2
P/F ratio*RQ=respiratory quotient= 0.8
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