ABG ANALYSIS. PART-1: PRIMARY GAS EXCHANGE FUNDAMENTALS & CLINICAL IMPLICATIONS.pdf

ABG Analysis :Basics

1. 1

2. 2

3. ABG Insights
Part 1: Pulmonary gas exchange: Fundamentals
and clinical implications
Part
-
3
: Unlocking the secrets: ABG Analysis and
interpretation
Part
-
2
: The
pH puzzle: Understanding Acid base disorders
Part
-
1
: Pulmonary gas exchange: Fundamentals and
clinical implications
Physio Shilpasree Saha,
MPT (Cardio-Thoracic disorders), MIAP
Certified BCLS Provider
YouTube Instagram & WhatsApp: Heal_th_talk
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Clinical scenario
A45yearsoldpatientisadmittedtoICUwithSevererespiratorydistress.Heisexperiencing
shortnessofbreath,chesttightnessandcough.TheemergencyroomphysicianordersanABG
toassessoxygenationandventilationstatus.
ABGShows:
pH:7.25
PaCO2:60mmHg
PaO2:50mmHg
HCO3
-
:24mmol/lt
Now what do these ABG result indicate and how do they relate to pulmonary gas exchange?
Let’s break the
result
Normal values
pH: 7.35-7.45
PaCO2: 35-45 mm Hg
PaO2: 75-100 mm Hg
HCO3
-
: 22-28 mmol/lt
Acidic
Respiratory
acidosis
Hypoxemia
No
compensation
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Arterial blood gases (ABGs)
•Help to assess the effectiveness of gas exchange by providing measurements of the
partial pressures of O2 and CO2 in arterial blood.
•Partial pressure describes the contribution of one individual gas within a gas mixture (such as
air) to the total pressure.
•When a gas dissolves in liquid (e.g. blood)
The amount dissolved
The partial pressure
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Arterial blood gases (ABGs)
•PO2 = partial pressure of O2
•PaO2 = partial pressure of O2 in arterial blood
•O2 molecules move from alveoli to blood and CO2 molecules move from blood to
alveoli until the partial pressures are equal.
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Pulmonary gas exchange
•TransferofO2fromthe
atmospheretothebloodstream
(oxygenation)andCO2fromthe
bloodstreamtotheatmosphere
(CO2elimination).
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O2 Transport
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CO2 Elimination
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•The Paco2is determined by
ALVEOLAR VENTILATION.
•VENTILATIONis regulated by
RESPIRATORY CENTER in the
BRAINSTEM.
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Hypoxic Drive
Stimulus:Low O2, high CO2
Response: Increase ventilation ( Increase rate and depth to compensate for
low O2)
Sensors: Chemoreceptors, carotid bodies and aortic bodies
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Detection of Hypoxia by chemoreceptors, located in:
Carotid bodies Aortic bodies
Located
in: Bifurcation of common carotid artery Near aortic arch
GlomuscellsinCB&ABreleaseneurotransmitters(Dopamine,Acetylcholine
inresponsetohypoxia
Carotidsinusnerve,whichinnervatescarotidbodiesisstimulatedandsend
signalstobrainstem
Brainstem processes and integrates signal with other sensory information to
regulate breathing
•Ventrolateralmedullareceivesinformationandsendoutputtorespiratory
centers
•Pre-brotzingercomplexgeneratesrespiratoryrhythmandpattern
Increaseventilationbyincreasingrateanddepthofrespirationand
recruitmentofaccessorymusclestoassistwithbreathing
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Hb concentration, SO2 & PO2
PO2only measures free, unbound O2 molecules –a tiny proportion
of the total.
Amount of O2 in blood depends on the following two factors:
1. Hb concentration:This factor determines how much O2 blood
has the capacity to carry.
2. Saturation of Hb with O2 (SO2): This factor is the percentage of
Hb binding sites that are filled with O2 molecule –i.e. how much of
the carrying capacity is being used.
SaO2is saturation of O2 in arterial blood.
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17. What is the importance of Po2?
Po2 can be thought to
regulate the So2, as it
works as the driving
force for O2 molecules to
bind to Hb.
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Oxyhaemoglobin Dissociation Curve
•So2 results from any given Po2.
•The higher the Po2, the higher
the So2, but the curve is not
linear.
•‘Steep part of the curve’: even
small changes in Po2 over this
range may have a major impact
on So2 (Inflection point).
•‘Flat part of the curve’:
changes in Po2 over this range
have relatively little effect on
the So2 (Plateau phase).
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1. Alveolar ventilation
2. Matching of ventilation with
perfusion (V/Q)
3. Concentration of O2 in inspired
air (FiO2)
Pao2
regulates
the Sao2.
But what
determines
Pao2?
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•Type 1 respiratory impairment: Low Pao2 with normal or low
Paco2.
*TheusualmechanismisV/Qmismatch
CAUSES
•Pneumonia
•Acute asthma
•Pulmonary embolism
•Acute respiratory distress syndrome
•Pneumothorax
•Fibrosing alveolitis
•Pulmonary oedema
•Chronic obstructive pulmonary disease
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Assessing severity of type 1 respiratory impairment
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Type 2 respiratory impairment:
•High Paco2 (hypercapnia) due to inadequate alveolar
ventilation
•Pao2 is usually low, but may be normal if the patient is on
supplemental O2.
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Hyperventilation leads to:
•A low Paco2 (hypocapnia)
•Corresponding rise in blood Ph,
•In chronic cases it is accompanied by a rise in HCO3, which
corrects blood pH.
Psychogenic hyperventilation
•Low Paco2 with a normal Pao2
Secondary hyperventilation
•Compensatory response to metabolic acidosis
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Common causes of hyperventilation
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Thank you
For any query, visit [email protected]
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