Arterial blood gas analysis assesment of oxygenation ventilation and acid base
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Transcript of Arterial blood gas analysis assesment of oxygenation ventilation and acid base
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Indications for Mechanical Ventilation&
Dr. T.R.ChandrashekarChief -Department of Critical Care
K.R.Hospital, BangaloreKarnataka, India
Arterial Blood Gas Analysis
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Blood Gas Interpretation-means analyzing the data to determine patient’s state of:
2
Ventilation
Oxygenation
Acid-Base
Discuss Indications for Mechanical Ventilation along with ABG interpretation and clinical examples
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Approach to ABG Interpretation
Assessment of Acid-Base Status
Assessment of Oxygenation & ventilatory Status
There is an interrelationship, but less confusing if considered separately…..
Volume –Osmolality Electrolytes
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Always mention and see… FiO2 / ct Hb
-----XXXX Diagnostics----Blood Gas Report
Measured 37.0 0CpH 7.452 pCO2 45.1 mm HgpO2 112.3 mm Hg
Calculated Data
HCO3 act 31.2 mmol / LO2 Sat 98.4 %O2 ct 15.8pO2 (A -a) 30.2 mm Hg pO2 (a/A) 0.78
Entered Data
FiO2 %Ct Hb gm/dl
-----XXXX Diagnostics-----
Blood Gas Report328 03:44 Feb 5 2006Pt ID 3245 / 00
Measured 37.0 0CpH 7.452 pCO2 45.1 mm HgpO2 112.3 mm Hg
Corrected 38.6 0CpH 7.436pCO2 47.6 mm HgpO2 122.4 mm Hg
Calculated Data
HCO3 act 31.2 mmol / LHCO3 std 30.5 mmol / LB E 6.6 mmol / LO2 ct 15.8 mL / dlO2 Sat 98.4 %ct CO2 32.5 mmol / LpO2 (A -a) 30.2 mm Hg pO2 (a/A) 0.78
Entered DataTemp 38.6 0CFiO2 30.0 %ct Hb 10.5 gm/dl
Calculated parameters
Measured parameters
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Why Order an ABG?
Aids in establishing a diagnosis Helps guide treatment plan Aids in ventilator management Improvement in acid/base management
allows for optimal function of medications Acid/base status may alter electrolyte
levels critical to patient status/care
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Matching delivery
= Requirement
Assessment of Oxygenation
O2 delivery is a Cardio-Respiratory function
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Oxygen Cascade
Atmospheric Air- 150 mmHg ( 21%)
PAO2-Alveolar Oxygen-100 mmHg ( CO2 / Water Vapour)
PaO2- 90mm Hg ( A-a difference)
SaO2 ( can be measured if Co-oximeter / calculated ODC)- Limitations
CaO2- Oxygen content (1.34 x Hb x Sao2)
DaO2-Oxygen delivery- CaO2 x Cardiac output
If A-a difference is more -does it tell us
anything ?
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OO22
COCO22
AlveoliPAO2
Atmospheric air /FIO2
Water vapour is added- Nose/ upper airway
Alveolar Oxygen
PaO2 (2% dissolved O2)
Measured in ABG
P(A-a)O2
SaO2
O.
D.
C.
Temp H+2,3-DPG
98% of O2 is Hb bound-1.34 x Hb% x Sao2CaO2-oxygen content +PaO2 x 0.003ml
Oxygen Delivery=CaO2 x Cardiac output
Cardiac output - SV x HR Preload / Afterload/ Contractility
Oxygen delivery DO2 is a Cardio- Respiratory Function
=
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DO2-Oxygen delivery- CaO2 x Cardiac output
Did oxygen delivery meet the demand?
Patient with sepsis on ventilator has fever 103F ,BP 80/60 mmHg, HR 140/mt, PaO2 100 mmHg, PcO2 42 mmHg, PH 7.23, HCO3 20, SaO2 98%Hb 12 gm%, Not responding to Fluids/ inotropesDelivery (DO2 )looks OKHow to assess the consumption?
Lactate-Anaerobic meatabolismLacti-timeScVo2- oxygen saturation in Superior vena Cava
ScVO2
DO2
Consumption O2
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CO2
O2
PaCO2=60 mmHg
PAO2 = FIO2 (BP-47) – 1.2 (PaCO2) =.21 (760-47) – 1.2 (60) = 150 – 72 = 78
An elevated PaCO2 will lower the PAO2
and as a result will lower the PaO2
FIO2
We always correlate PaO2 with FiO2
BUT…………………………. never forget to correlate with
PaCO2
PAO2=FIO2(Barometric Pressure-H2O)-1.2(PCO2)
PAO2 = FIO2 (760– 47 mm Hg)- 1.2 (PaCO2)
PAO2 = 0.21(713)-1.2(40)=100 mmHg
“1.2” is dropped when FIO2 is above 60%.
5 X FIO2=PaO2
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A-aDo2
A-aDo2 = PAO2-PaO2(from ABG)= 10-15 mmHg / Increases with age Increased P(A-a)O2 -lungs are not transferring oxygen
properly from alveoli into the pulmonary capillaries.
OO2 2
COCO22
PaO2
AlveoliPAO2
P(A-a)O2
Diffusion defect
V/Q Mismatch-Dead Space
Shunt
P(A-a)O2 signifies some sort of problem within the lungs
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Oxygenation Physiology
PAO2
Diffusion defect
Pao2
Shunt
Does not respond to FIO2
Responds to FIO2
Diffusion defect is a rare cause1µm
Oxygenation over within 1/3 timeIf HR >240 it affects
CO2 has over 20 times moreDiffusion coefficientSevere ARDS/ILD
CO2
Atmospheric air
Nitrogen
FIO2- O2
PaO2
V/Q Mismatch
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Alveolar-arterial Difference
OO22
COCO22
Alveolar – arterial G.
100 - 45 = 55 ……………….Wide A-a
Oxygenation Failure Wide Gap
PCO2 = 40PaO2 = 45
PAO2 = 150 – 1.2 (40)
= 150 - 50 = 100
Ventilation FailureNormal Gap
PCO2 = 80PaO2 = 45
PAO2 = 150-
1.2(80) = 150-100 = 50 Alveolar arterial G.
50 – 45 = 5…………….Normal A-a
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Interpretation of shunt fractions
<10%<10% NormalNormal
10-20%10-20% Mild shuntMild shunt
20-30%20-30% Significant shuntSignificant shunt
>30%>30% Critical shunt, even Critical shunt, even 100% O2 cannot 100% O2 cannot restore Pao2restore Pao2
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arterial-Alveolar O2 tension ratio
a/A ratio
>0.75 normal
0.40-0.75 acceptable
0.29-0.39 poor
<0.20 very poor
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a/A ratioNomogram
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Oxygen Dissociation Curve: SaO2 vs. PaO2
CaO2A B
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Which patient is more hypoxemic, and why?
Patient A: pH 7.48, PaCO2 34 mm Hg, PaO2 85 mm Hg, SaO2 95%, Hemoglobin 7 gm%-
Patient B: pH 7.32, PaCO2 74 mm Hg, PaO2 59 mm Hg, SaO2 85%, Hemoglobin 15 gm%-
Patient A: Arterial oxygen content = .95 x 7 x 1.34 = 8.9 ml O2/dl Patient B: Arterial oxygen content = .85 x 15 x 1.34 = 17.1 ml
O2/dl
Hypoxic/Hypercarbic
Anemic
98% of O2 is Hb bound-1.34 x Hb% x Sao2
+ ( 2% )PaO2 x 0.003mlCaO2 =
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The power of hemoglobin
Normal Hypoxemia Anemia
PaO2 90 mm Hg 45 mm Hg 90 mm Hg
SaO2 98% 80% 98%
Hb 15 g/dL 15 g/dL 7.5 g/dL
CaO2 200 ml/L 163 ml/L 101 ml/L
% change - 18.6% - 49.5%
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20 v
ol% 15 vol %
O2 Transport; Normal
= C.O X arterial O2 content5 L blood x150 /L blood x 1.39 ml O2/g Hb(= 20 ml O2/dl blood, or 20 vol %
= 1000 ml O2/min= 250 ml( oxygen consumption)
750 ml = Venous O2 return( = 15 vol%)
DO2
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ScVO2-60%-80% normal range
Is the central venous oxygen saturation measured from a CVP cannula
Reflects the global balance between oxygen Delivery and consumption
ScVO2 SVO2ScVO2 Range
60-80% Normal
60-50% More extraction warning sign
50-30% Lactic acidosis Demand > Supply
30-20% Severe lactic acidosisCell death
> 5-7
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Factors which alter ScVo2
Decreased DeliveryDO2
Increased Consumption VO2
Fever, ShiveringTraumaPain / anxiety
DysarhythmiaCCF/ MISepsis
Hypoxia/hypoxemiaSuctioning, ARDS/ COPD
HemorrhageOccult bleedingRBC disordersAnemia
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65 yr old male with DM IHD –in septic shock on ventilatorABG-PaO2-90 PH 7.42, PCO2 43Hb-12 gm%, Spo2 98%CaCo2-17 Vol%BP 90/40 mmHg ,Temp 103FWhat is the problem ?
ScVO2 48%, Lactate 8 mMoles/L
Fluids Nor adrenaline / Dobutamine
Fever control
Case ….
65 yr old male with DM IHD –in septic shock on ventilatorABG-PaO2-90 PH 7.42, PCO2 43Hb-12 gm%, Spo2 98%CaCo2-17 Vol%BP 90/40 mmHg ,Temp 103FWhat is the problem ? ScVO2 68%, Lactate 2 mMoles/L
Microcirculatory Mitochondrial Dysfunction (MMDS)
ScVo2
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Lactate metabolism
Glucose
Pyruvate Lactate
Oxidative phosphorylation
2 ATP
36 ATP NAD+CO2+H2O
O2 + NADH
GlycolysisADP
Cell Cytoplasm
Mitochondria
Oxygen
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cc
Energy Failure and Lacti-Time
Aerobic
metabolism
36 ATP
Lack of O
2 delivery
Anaerobic
metabolism
2 ATP +
Lactic a
cid
The time before lactate becomes less than 2 is important prognostic indicator-LACTI- TIME
Septic patient admitted to ICU BP 90/50, HR 150/mtScVO2-45%, Lactate 6 mmoles/L ,PH 7.16, PaO2/PCO2- 68/39 mmHg
After 2hrs- fluid resuscitation/Noradrenaline
BP140/80 mmHgScVo2-65% Lactate
3 mmoles/L
After 2hrs- fluid resuscitation/Noradrenaline
BP 70/40 mmHgScVo2-45% Lactate
7mmoles/L Microcirculatory mitochondrial
dysfunction (MMDS)
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Summary –Oxygenation assessment
CaO2 x CO =Delivery ScVO2=consumption Lactate=Delivery not meeting demand
Anaerobic metabolism- decreased ATP production -cell death
Lacti-Time- prognostic indicator
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Assessment of Ventilatory Status….
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Oxygenation Acid-Base
HCO3
PAO2 = FIO2 (BP-47) – 1.2 (PCO2) pH ~ ------------
PaCO2
PaO2
» VCO2 x .863» PaCO2 = --------------------» VA » VA=Minute ventilation-Dead space volume » f(VT) – f(VD)
PaCO2 is key to the blood gas universe; without understanding PaCO2 you can’t understand oxygenation or acid-base.
The ONLY clinical parameter in PaCO2 equation is RR
VCO2=CO2 production
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Breathing pattern’s effect on PaCO2
Patient Vt f Ve Description A (400)(20) = 8.0L/min (slow/deep) B (200)(40) = 8.0L/min (fast/shallow) Patient Vt-Vd f Va A (400-150)(20) =5.0L/min (slow/deep) B (200-150)(40) =2.0L/min (fast/shallow)
PaCO2 = alveolar ventilation
Not on Minute ventilation which is measured Dead space quantification at bed side not possible
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Condition State of
PaCO2 in blood alveolar ventilation
> 45 mm Hg Hypercapnia Hypoventilation
35 - 45 mm Hg Eucapnia Normal ventilation
< 35 mm Hg Hypocapnia Hyperventilation
PaCO2 abnormalities…
PCO2-65 mmHg with rate 7/mt in Drug overdosage 65/7-true hypoventilation
PCO2-65 mmHg with rate 37/mt in bilateral consolidation 65/37- Reduced alveolar ventilation/ dead space ventilation
PCO2-22 mmHg with rate of 37/mt in post operative patient with pain and fever-Increased alveolar ventilation
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Quantification of Dead space
VD
VVTT=
25-40% NORMAL (2ml/Kg)
In MV pts till 55% is normal
More than 60% is abnormal
dead space
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Quantification of Dead spaceQuantification of Dead space
VD/VT=(PaCO2-PETCO2)/PaCO2
Minute volume in liters Ҳ PaCO2(mmHg)
Body weight in kg
Normal index<5
More than 8 indicates an increase dead space
Limitation-need to measure minute volume accurately
Difficulties in sampling and accurate measurement limits the usefulnessOf dead space in clinical practice
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Case Scenarios ….
20 year old male with OP poisoning with fasciculation's, neck muscle weakness with RR 35/mt, increased WOB, SPO2 on 4l/mt on RBM
84%, pooling secretions, HR 150/mt on atropine drip, BP 140/60
ABG PH 7.37 Pao2-52 Pco2-32 Do we intubate this guy?
YES
Intubated minimal settings ABG stabilisedHas Pulse oximeter/ ETCO2Do we require to repeat ABG’s NO
If pt develops hypotensionOn inotrope /not synchronising Yes
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Treat the Patient not the ABG
ABG-PCO2-60mmHg, PO2-58mmHg
with HR-80/min, BP- 130/80mmHg, RR-14/min,
A 45 yr old patient with chronic neurological weakness conscious, comfortable
ABG-PCO2-60mmHg, PO2-58mmHg
and with HR-120/min,BP-100/70 mmHg,RR-40/min,
A 24yr old asthmatic severe respiratory
distress, drowsy
Intubate
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Case Scenario….
40 yr old diabetic male pt with urinary sepsis Has BP 90/60 mmHg after fluid resuscitation,
high dose noradrenaline,has tready pulse, is tachypenic 35/mt with increased WOB-is restless. On 6L of O2 RBM
ABG PH-7.38
PaCO2-36 mmHg
PCO2-100 mmHg
Sao2-98%, ScVo2-50%, Lactate 6 mmoles/L
Do we intubate this patient
Normal respiratory effort-5% CONearly 20-30% CORest respiratory muscle and so CO is utilised by essential organs
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55 year old chronic smoker, Diabetic male admitted with Lower limb cellulitis has Sepsis and Rt mid and lower zone pneumonia on 6L of O2 on RBM
HR 140/mt BP 100/60 mmHg RR- 35 with increased WOB ABG PH-7.28
PaCO2-56 mmHg
PCO2 - 58 mmHg
FIO2 70%Pao2-58 hypoxemicPco2-56/35- decreased Alveolar ventilationIntubation
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IF the same guy is already on 5L/O2 / on noradrenaline fluid resuscitation- we probably intubate
40 yr old male Diabetic in ketosis with pylonephritis
Drowsy received in casualty- BP 70/50 mmHg, RR 28/mt,
Fever-103F, HR 150/mt, WOB normal
SC-1.6 WBC 20,000, LFT normal
ABG done on room air PH-7.28
PCO2-36 mmHg
PaO2 - 58 mmHg
HCO3 18 mmoles/L
O2 4L RBM Fluids 2l Noradrenaline Imipenem +cilastin 1g IV,
Paracetamol BP 140/80, HR 100/mt, UO 100ml/hr
ABG PH-7.38
PaCO2-36 mmHg
PCO2 - 78 mmHg
HCO3 20 mmoles/L Mentation better
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A 29-year-old woman has excessive bleeding normal delivery has Hb of 5 g%, fluids-3L/mt given
Bp 100/60mmHg HR 114/mt PH-7.38
PaCO2-33 mmHg
PCO2 - 78 mmHg
HCO3 22 mmoles/L
Cao2- 7 vol % ScVO2 55 % Lactate 5 mMoles/L What do we do? Packed cells FFP Platelet 1:1:1 (FFP to PRBC
to platelets)
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Causes of Respiratory failure
Respiratory Center in Brain
Neuromuscular Connections
Thoracic Bellows
Airways (upper & lower)
Lung parenchyma (alveoli)
Head injuryDrug overdose
Spinal cord injury
MyopathiesMyasthenia
C
COPD
ARDS
Brain
Nerves
Bellows
Airways
Alveoli
It only requires one disrupted “link” to cause respiratory failure !
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Some points which help us to decide when to ventilate patients?
Primary cause for Respiratory failure-time for the disease to resolve
Hypoxemia on high FIO2 Increased PCO2 Increased WOB Airway protection ?
+ABG values
Do not treat the ABG, treat the patient If you’re not sure whether or not the patient needs a
ventilator, the patient needs a ventilator
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Shibu lijack
Acid Base Acid Base analysisanalysis
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Basics •[H+]= 40 nEq/L at pH-7.4•For every 0.3 pH change = [H+] double
160nEq/L40 nEq/L
16nEq/L
[ H+] in nEq/L = 10 (9-pH)
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Acid-Base Physiology
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CO2 + H2O H2CO3 H+ + HCO3-
CO2H+
HCO3-
Acid-Base physiology
Respiratory
Metabolic
Ventilation controls PCO2
Kidney losses H+ and reabsorbs bicarbonate (HCO3-)
Bicarbonate is the transport from of CO2 hence should move in the same direction
PCO2-Respiratory acidosis (Hypoventilation)
PCO2-Respiratory alkalosis(Hyperventilation)
HCO3- Metabolic acidosis
HCO3- Metabolic Alkalosis
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Very fast 80% in ECF
Starts within minutes good response by 2hrs, complete by 12-24 hrs
Starts after few hrs complete by 5-7 days
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Acid-base Balance Henderson-Hasselbalch Equation
[HCO3-]
pH = pK + log ------------- .03 [PaCO2]
For teaching purposes, the H-H equation can be shortened to its basic relationships:
HCO3- ( KIDNEY)
pH ~ --------------------
PaCO2 (LUNG)
Maximum compensationHCO3-= 40/10
CO2=60/10
24/4036/60
24/4018/30
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Characteristics of acid-base disorders
DISORDER PRIMARY RESPONSES
COMPENSATORY RESPONSE
Metabolic acidosis
PH HCO3- pCO2
Metabolic alkalosis
PH HCO3- pCO2
Respiratory acidosis
PH pCO2 HCO3-
Respiratory alkalosis
PH pCO2 HCO3-
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pH HCO3 CO2
7.20 15 40
7.25 15 30
7.37 15 20
Un Compensated
Partially Compensated
Fully Compensated
(pH abnormal)
(pH in normal range)
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Body’s physiologic response to Primary disorder in order to bring pH towards NORMAL limit
Full compensationPartial compensationNo compensation…. (uncompensated)
BUT never overshoots, If a overshoot pH is there, Take it granted it is a MIXED disorder
Normal functioning
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RESPIRATORY disorders…Expected HCO3 for a Change in CO2 ......... 1 2 3 4
Acidosis…. (expected) HCO3 = 0.1 x ∆ CO2
Alkalosis…. (expected) HCO3 = 0.2 x ∆ CO2
Acidosis…. (expected) HCO3 = 0.35 x ∆ CO2
Alkaosis…. (expected) HCO3 = 0.4 x ∆ CO2
Acute respiratory
Chronic respiratory
HCO3- ( KIDNEY)
pCO2 (LUNG)pH=
what has changed ? CO2
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Compensation
Metabolic Acidosis: Compensation
Winters’ formula
pCO2 = 1.5 x [HCO3-] + 8 ± 2
Metabolic Alkalosis: Compensation pCO2 = 0.7x [HCO3-] + 20 ± 5
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Na+
Unmeasured cations Unmeasure
d anions
Cl-
HCO3-
‘Mind the gap’
cations = Anions
Anion gap = metabolic acidosis
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Anion Gap
AG = [Na+] - [Cl- +HCO3-]• Elevated anion gap represents
metabolic acidosis• Normal value: 12 ± 4mmol/L• Major unmeasured anions
– albumin– phosphates– sulfates– organic anions
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-- Clinical history
-- pH normal, abnormal PCO2 and HCO3
-- PCO2 and HCO3 moving opposite directions
-- Degree of compensation for primary - disorder is inappropriate
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2. Look at pH?
3. Look up HcO3-// PCo2
4. Match either pCO2ot the HCO3with pH
5. Fix the level of compensation.
6.If metabolic acidosis, calculate-Anion gap
7.Correlate clinically
1. Consider the clinical settings! Anticipate the disorder
7 steps to analyze ABG
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First Step-Clinical History
COPD- Chronic Respiratory Acidosis-Met alkalosis
Asthma-Acute Respiratory Acidosis not well compensated
Cardiac arrest-Acute Metabolic/Respiratory acidosis
Septic shock-Acute Metabolic acidosis
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The second step
Look at the pH - Label it.
pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L. Na+ 143, CL-104
ACIDOSIS
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Look at -pCO2. Label it. pH of 7.30, PaCO2 of 80 mm Hg, and
HCO3- of 27 mEq/L. Increased
Normal pCO2 levels Normal pCO2 levels are 35-45mmHg. are 35-45mmHg. Below 35 is Below 35 is alkalotic, above 45 alkalotic, above 45 is acidic.is acidic.
The third step
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• look at the HCO3- Label it. pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L
• INCREASEDA normal HCO3 level is 22-26 A normal HCO3 level is 22-26 mEq/L. If the HCO3 is below mEq/L. If the HCO3 is below 22, the patient is acidotic. If 22, the patient is acidotic. If the HCO3 is above 26, the the HCO3 is above 26, the patient is alkaloticpatient is alkalotic
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Next match either the pCO2 or the HCO3 with the pH to determine the acid-base disorder.
• pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L• pH is on acidotic side & PCO2 is
increased. So it is respiratory acidosis
The Fourth Step
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• Does either the CO2 or HCO3 go in the opposite direction of the pH?
• pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L
• To find the primary and what is compensatory
• HCO3 is going in opposite direction of pH. So it is metabolic compensation
Fifth Step
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RESPIRATORY disorders…Expected HCO3 for a Change in CO2 ......... 1 2 3 4
Acidosis…. (expected) HCO3 = 0.1 x ∆ CO2
Alkalosis…. (expected) HCO3 = 0.2 x ∆ CO2
Acidosis…. (expected) HCO3 = 0.35 x ∆ CO2
Alkaosis…. (expected) HCO3 = 0.4 x ∆ CO2
Acute respiratory
Chronic respiratory
HCO3- ( KIDNEY)
pCO2 (LUNG)pH=
what has changed ? CO2
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Is the compensation full or partial??
Do the calculations…. pH of 7.30, PaCO2 of 80 mm Hg, and HCO3-
of 27 mEq/L
PCO2 is increased by =40 HCO3-=should be increased by 4 i.e. 24+4=28( for full compensation)
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• Calculate the anion gap if it is more there is Metabolic acidosis
AG = [Na+] - [Cl- +HCO3-AG = [Na+] - [Cl- +HCO3-]]
Sixth Step
pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L. Na+ 143, CL-104
AG+143- (104+27)=140-131=12
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Pathogenesis of Metabolic Acidosiswith AG
Fixed acid accumulation and low serum bicarbonate
Renal failure Renal,GI Lactic Salicylate
Ketones Methanol
Phosphate Ethylene glycol
HCl
AG = [Na+] - [Cl- +HCO3-]
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Equivalent rise of AG and Fall of HCO3……
….Pure Anion Gap Metabolic Acidosis
Discrepancy…….. in rise & fall
+ Non AG M acidosis, + M Alkalosis
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Delta gap = HCO3 + ∆ AG
Delta Gap = 24….Pure AG acidosis
< 24 = non AG acidosis
> 24 = metabolic alkalosis
∆ AG =Measured Anion gap-12
Delta Gap = 24 …… AG Met Acidosis < 24 ….. Non AG Met acidosis > 24 ….. Non AG Met acidosis + Meta. Alkalosis
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Finally
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RESPIRATORY disorders…Expected HCO3 for a Change in CO2 ......... 1 2 3 4
Acidosis…. (expected) HCO3 = 0.1 x ∆ CO2
Alkalosis…. (expected) HCO3 = 0.2 x ∆ CO2
Acidosis…. (expected) HCO3 = 0.35 x ∆ CO2
Alkaosis…. (expected) HCO3 = 0.4 x ∆ CO2
Acute respiratory
Chronic respiratory
HCO3- ( KIDNEY)
pCO2 (LUNG)pH=
what has changed ? CO2
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Compensation
Metabolic Acidosis: Compensation
Winters’ formula
pCO2 = 1.5 x [HCO3-] + 8 ± 2
Metabolic Alkalosis: Compensation pCO2 = 0.7x [HCO3-] + 20 ± 5
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Uncompensated Respiratory Acidosis
pH = 7.4PaCO2 = 40 HCO3 = 24
Post op pt –drowsy
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Uncompensated Respiratory Alkalosis
pH = 7.4PaCO2 = 40 HCO3 = 24
Pt on vent pressure support has pain
Acute asthmatic
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Normal A.B.G.Normal A.B.G.
pH = 7.4PaCO2 = 40 HCO3 = 24
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Partially compensated Metabolic Acidosis
pH = 7.4PaCO2 = 40 HCO3 = 24 20 yr old male with Acute Gastroenteritis…..
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Case
A 46-year-old man has been in the hospital for two days with pneumonia. He was recovering but has just become diaphoretic, dyspneic, and hypotensive. He is breathing oxygen through a nasal cannula at 3 l/min.
pH 7.41
PaCO2 20 mm Hg HCO3- 12 mEq/LCaO2 17.2 ml O2/dl
PaO2 80 mm Hg
SaO2 95%
Hb 13.3 gm%
How would you characterize his state of oxygenation,ventilation, and acid-base balance?
Normal pH Respiratory alkalosis and Metabolic acidosis.
Winters formulapCo2=1.5 x 12 +8=26
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Case
Mrs. H is found pulseless and not breathing this morning. After a couple minutes of CPR she responds with a pulse and starts breathing on her own. A blood gas is obtained:pH----------- 6.89 pCO2 -------70 pO2 ---------42 HCO3------- 13 SaO2-------- 50%
What is your interpretation? What interventions would be appropriate for
Mrs. H?
Mrs. H has a severe metabolic and respiratory acidosis with hypoxemia
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Case …..
A 44 year old moderately dehydrated man was admitted with a two day history of acute severe diarrhea. Electrolyte results: BP 90/60 mmHg
Na+ 134, K+ 2.9, Cl- 108, BUN 31, Cr 1.5.
ABG: pH 7.31 PCO2 33 mmHg
HCO3 16 PaO2 93 mmHg What is the acid base disorder?
HistoryAcidosis from diarrhea or lactic acidosis as a result of hypovolemia and poor perfusion.
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Normal anion gap acidosis with adequate compensation
Look at the pH- acidemic. What is the process? Look at the PCO2, HCO3- .
PCO2 and HCO3- are abnormal in the same direction, therefore less likely a mixed acid base disorder.
Calculate the anion gap
The anion gap is Na - (Cl + HCO3-) = 134 -(108 + 16) = 10
Is compensation adequate? Calculate the estimated PCO2.
Winter's formula;
PCO2 = 1.5 × [HCO3-]) + 8 ± 2 = 1.5 ×16 + 8 ± 2 = 30-34.
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Case....
A 50 year old insulin dependent diabetic woman was brought to the ED by ambulance. She was semi-comatose and had been ill for several days. Current medication was digoxin and a thiazide diuretic for CHF.Lab results Serum chemistry:
Na 132, K 2.7, Cl 79, Glu 815, Lactate 0.9 urine ketones 3+ ABG: pH 7.41 PCO2 32
HCO3- 19 pO2 82
History:Elevated anion gap acidosis secondary to DKA Metabolic alkalosis in the setting of thiazide diuretics use.
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Case...... 2. Look at the pH. - Note that the pH is normal which would suggest no
acid base disorder. But remember, pH may be normal in the presence of a mixed acid base disorder.
3. What is the process? Look at the PCO2, HCO3- . PCO2 is low indicating a possible respiratory alkalosis. The HCO3- is also low indicating a possible metabolic acidosis. Because the pH is normal, we are unable to distinguish the initial, primary change from the compensatory response.
We suspect however that the patient has DKA, and therefore should have a metabolic acidosis with an anion gap that should be elevated. We can confirm this by calculating the anion gap.
4. Calculate the anion gap The anion gap is Na - (Cl + HCO3-) = 132 -(79 + 19) = 34 Since gap is greater than 16, it is therefore abnormal and confirms the presence of metabolic acidosis.
Why is the pH normal? If the patient has metabolic acidosis, we suspect a low ph unless there is another process acting to counteract the acidosis, i.e alkalosis.
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Delta Gap 34-12=22 + 19=41 Met alk Since the delta ratio is greater than 2, we can deduce
that there is a concurrent metabolic alkalosis. This is likely due to to the use of thiazide diuretic. Note that DKA is often associated with vomiting, but in this case;vomiting was not mentioned.
Another possibility is a pre-existent high HCO3- level due to compensated chonic respiratory acidosis. But we have no reason to suspect chronic respiratory acidosis based on the history.
Assessment: Mixed elevated anion gap metabolic acidosis and metabolic alkalosis likely due to DKA and thiazide diuretics.
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• I shall practice gentle mechanical ventilation and not try to bring ABG to perfect normal.
• I shall treat the patient not the ABG report
• I shall always correlate ABG report clinically
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PaO2
O2 CASCADE
AIR
ALVEOLAR
POST PULMONARY
ARTERIAL
Hb
MICRO-
CIRCULATION
MIXED VENOUS