basics in arterial blood gas interpretation.ppt

7/27/2019 basics in arterial blood gas interpretation.ppt

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Basics in Arterial

Blood Gas

InterpretationCrisbert I. Cualteros, M.D.


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Obtaining Blood Gas

Samples

Radial artery- best site

located superficially, easy to palpate

& stabilize excellent collateral circulation via

ulnar artery

not adjacent to large veins probing needle relatively pain-free if

periosteum is avoided


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Techniquefor Radial Artery Puncture

Explain process to patient. Examine skin,

palpate radial & ulnar arteries. Performmodified Allen Test.


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The Allen Test

have the patientclench his/her fist

press on both

radial and ulnararteries

have the patientunclench fist

test for goodcollateral flow.


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Technique for Radial Artery Puncture

Position patient- hyperextend wrist. Clean

site with 70% isopropyl alcohol. Use latex gloves while doing procedure. Local anesthesia may be used. Use G20 or G21 needle. Flush syringe with

sodium heparin (10 mg/ml or 1,000units/ml) & empty. 0.15-0.25 ml of heparin willanticoagulate 2-4 ml of blood.


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Technique for Radial Artery Puncture

Palpate artery with one hand while holdingproperly prepared syringe & needle with other hand. Hold syringe like a pencil & enter skinat 45

o. Advance needle slowly.

Never redirect needle without first withdrawing tosubcutaneous tissue.

Obtain 2-4 ml blood. If possible dont aspirate.

Remove air bubbles from syringe. Immediately

seal syringe with cap. Place sample in ice slush. Analyze blood sample

within 10 minutes.

Apply pressure to site until bleeding has stopped.


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Potential Complications

Pain

Hematoma, hemorrhage

Trauma to vessel

Arteriospasm

Air or clotted-blood

emboli

Vasovagal response Arterial occlusion

Infection


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Indications for ABG

Assess ventilation & acid-basebalance

Assess oxygenation status


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Ventilatory/

Acid-Base Status

H d H lb h P t & th i


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Henderson-Hasselbach Parameters & theirnormal laboratory ranges

pH= [HCO3]p

PC02

pH PCO2

(mmHg)

[HCO3]p

(mmol/L)Normal 7.35-7.45 35-45 22-26

Acidotic < 7.35 > 45 < 22

Alkalotic > 7.45 < 35 > 26

T di i l M b li A id B N l


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Traditional Metabolic Acid-Base Nomenclature

Nomenclature pH PCO2

[HCO3]p

BE

Metabolic acidosisUncompensated (acute) q N q q(-)Partly compensated(subacute)

q q q q(-)

Compensated (chronic) N q q q(-)Metabolic alkalosisUncompensated (acute) p N p p(+

)Partly compensated(subacute)

p p p p(+)

Compensated (chronic) N p p p(+)


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Traditional Respiratory Acid-Base Nomenclature

Nomenclature pH PCO2

[HCO3]p

BE

RespiratoryacidosisUncompensated (acute) q p N NPartly compensated(subacute) q p p p

Compensated (chronic) N p p p

Respiratory

alkalosisUncompensated (acute) p q N NPartly compensated(subacute)

p q q q

Compensated (chronic) N q q q


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Base Excess/ Deficit

Blood with large buffering capacity:significant changes in acid content with little change in freeH+concentrations (pH)

Acidemia or alkalemia: i buffering capacity, > potential forpH change from any given change in H+content

Buffering capacity depends on:[HCO3-]

RBC massother factors

Base excess/deficit= (measured pH predicted pH) x 100 x2/3

Normal metabolic acid-base status: + 3 mmol/LRelatively balanced metabolic acid-base status: + 5

mmol/LClinically significant imbalance: + 10

mmol/L


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Nomenclature & Criteria for Clinical Interpretation

Clinical Terminology Criteria

Ventilatory failure(respiratory acidosis) PaCO2> 45mm Hg

Acute ventilatory failure(respiratory acidosis) PaCO2> 45mmHg pH < 7.35

Chronic ventilatory failure(respiratory acidosis) PaCO2 > 45mmHg

pH 7.36- 7.44

Alveolar hyperventilation(respiratory alkalosis) PaCO2< 35mmHg

Acute alveolar hyperventilation(respiratory PaCO2< 35mmHg

alkalosis) pH > 7.45

Chronic alveolar hyperventilation(respiratory PaCO2 < 35mmHg alkalosis) pH 7.36-

7.44


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Nomenclature & Criteria for Clinical Interpretation

Clinical Terminology Criteria

Acidemia pH < 7.35Alkalemia pH > 7.45Acidosis HCO3

- < 22 mmol/L

BD > 5 mmol/LAlkalosis HCO3

-> 26 mmol/LBE > 5 mmol/L

Combined Respiratory Acidosis & Metabolic AcidosisRespiratory Alkalosis & Metabolic Alkalosis

Mixed Respiratory Acidosis & Metabolic AlkalosisRespiratory Alkalosis & Metabolic Acidosis


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Respiratory Acidosis

Acute

r pH = 0.08 x (PCO240)

10

ex. PCO2 = 60

rpH = 0.08 x (60 - 40) = 0.16

10

expected pH = 7.40 0.16 = 7.24

HCO3-increases 0.1 1 meq/L per 10 mmHg PCO2increase

Compensation: cellular buffering: HCO3

renal adaptation: H+secretion, Cl- reabsorption,

net acid excretion


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Respiratory acidosis

Chronic

r pH = 0.03 x (PCO240)

10

ex. PCO2= 60r pH = 0.03 x (60 40) = 0.06

10

expected pH = 7.40 0.06 = 7.34

HCO3-increases 1-3.5 meq/L per 10 mmHg PCO2

increase


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COPD O2excess in COPD

Drugs Barbiturates

Anesthetics Narcotics

Sedatives

Extreme ventilation-perfusion mismatch

Exhaustion

Inadequate MV

Neurologic disorders

Neuromusculardisease Poliomyelitis

ALL

G-B syndrome

Electrolyte deficiencies(K+, PO4

-)

Myasthenia gravis

Excessive CO2

production TPN Sepsis

Severe burns

NaHCO3administration


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Respiratory Alkalosis

Acute

r pH = 0.08 x (40 PCO2)

10

ex. PCO2= 20

rpH = 0.08 x (40 20) = 0.16

10

expected pH = 7.40 + 0.16 = 7.56

HCO3-decreases 0-2 meq/L per 10 mmHg PCO2decrease

Compensation: cellular buffering

renal response: retention of endogenous acids,

excretion of HCO3


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Chronic

r pH = 0.03 x (40 PCO2)

10

ex. PCO2= 20r pH = 0.03 x (40 20) = 0.06

10

expected pH = 7.40 + 0.06 = 7.46

HCO3-decreases 2-5 meq/L per 10 mmHg PCO2

decrease


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Primary centraldisorders

Hyperventilationsyndrome, anxiety

Cerebrovascular disease Meningitis, encephalitis

Pulmonary disease

Interstitial fibrosis

Pneumonia Pulmonary embolism

Pulmonary edema(some patients)

HypoxiaSepticemia,

hypotension

Hepatic failure

Drugs Salicylates

Nicotine

Xanthines

Progestationalhormones

High altitude

Mechanical ventilators


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Metabolic Acidosis

Anion Gap

artificial disparity between major plasma cations& anions that are routinely measured

major plasma cationsmajor plasma anions [Na+]([Cl-] + [HCO3-])

12 + 2 (normal)

Minor cations: K+, Ca++

Minor anions: phosphates, sulfates, organicanions


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Metabolic Acidosis

Anion gap acidosis

~ process increases minor anions

~ ex. lactatemia, ketonemia, renal failure,excessive

organic salt treatment, dehydration,

ingestion

(salicylates, methanol, ethylene glycol,paraldehyde)

~ process which decreases minor cations rare!

Non-anion gap acidosis

~ associated with increased plasma Cl-that hasreplaced

HCO3-


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Metabolic Acidosis

Abnormalities:

Overproduction of acids

Loss of buffer stores

Underexcretion of acids


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Metabolic Acidosis

Expected PCO2= ( [HCO3-] x 1.5) + 8 + 2

ex. [HCO3-

] = 11expected PCO2= (11 x 1.5) + 8 + 2 = 22.5-

26.5

PCO2decreases 1- 1.5 mmHg per 1 meq/L HCO3-decrease


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Metabolic Acidosis

Compensation

pCO2(hyperventilation)

Pathway:

pCO2

HCO3ratio H

+conc

Acidification of ECF ECF pH

Stimulation of brainstem RR pCO2

Normalization of pH

HCO3


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Metabolic Acidosis

Compensation

Ionic shift

K+moves extracellularly for H+

HCO3-generation, H+excretion


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Corrected [HCO3-] for Anion Gap

Metabolic Acidosis

Measured serum [HCO3-] + (anion gap12)


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Metabolic Alkalosis

Expected PCO2= ( [HCO3-] x 0.75 ) + 20 + 5

ex. [HCO3-

] = 34expected PCO2 = (34 x 0.75) + 20 + 5 = 40.5-

50.5

PCO2increases 0.5- 1 mmHg per 1 meq/L HCO3-increase


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Metabolic Alkalosis

Pathway

HCO3 PaCO2HCO3

ratio H+conc

Alkalinization of ECF PaCO2with mild hypoxemia

Normalization of pH


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Causes of Metabolic lkalosisHypokalemia*

Ingestion of large amounts of alkali or licoriceGastric fluid loss: Vomiting, NG suctioning*

Hyperaldosteronism 20to nonadrenal factors

Bartters syndrome

Inadequate renal perfusion

diuretics (inhibiting NaCl reabsorption)*

Bicarbonate administration

Sodium bicarbonate overcorrection

Blood transfusion

Adrenocortical hypersecretion (e.g tumor)Steroids*

Eucapnic ventilation posthypercapnia

* Common in the ICU

Limits of Compensation


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Limits of Compensation

Imbalance [HCO3-] meq/L PCO2mmHg


Acute h0.1- 1/ 10 mmHg

PCO2h

Chronic h1- 3.5/ 10 mmHg

PCO2

h


Acute i0- 2/ 10 mmHg PCO2i

Chronic i2- 5/ 10 mmHg PCO2i

Metabolic Acidosis i1- 1.5/ 1 meq/L

[HCO3-] i

Metabolic Alkalosis h0.5- 1/ 1 meq/L

[HCO3-] h


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Steps for Analyzing Acid- Base Disturbances

Is patient acidemic or alkalotic? pH

Is disturbance primarily respiratory or metabolic?

PCO2, [HCO3-]

If disturbance respiratory, is it acute or chronic?

If disturbance metabolic, is anion gap normal orabnormal?

If disturbance metabolic, is the respiratorysystem compensating adequately?

If disturbance is anion gap metabolic acidosis,are there any other metabolic disturbancespresent?


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Oxygenation Status


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Normal Values

Seated PO2 = 104.2 0.27 (age in years)

Supine PO2 = 103.5 0.42 (age in years)

Patients < 60 y. o.

PO2 = 100 + 20

Patients > 60 y. o.PO2 = 80 (# years > 60)


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Steps for Analyzing

Oxygenation Status


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1. Is the patient hypoxemic or normoxemic?

Indices of Oxygenation:

a. AaDO2= PAO2PaO2PAO2= FiO2(713) PaCO2

0.8PaO2= obtained from blood gas determination

b. aAO2= PaO2PAO2c. P/F ratio = PO2

FiO2Normal Value: patients < 60 y. o. > 400

patients > 60 y. o. expected P/F =400

[(age in years 60) x 5]Actual P/F Ratio < expected =hypoxemic

Actual P/F Ratio > expected = normoxemic


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2. If hypoxemic, is it uncorrected,

corrected, or overcorrected?

With O2 supplementationPaO2 (mmHg)

Uncorrected hypoxemia < 80Corrected hypoxemia 80 120

Overcorrected > 120

FiO2to PaO2Relationship in Normal LungsFiO2 PaO2(mmHg)0.30 > 1500.40 > 2000.50 > 2500.80 > 4001.00 > 500


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Room Air (patient < 60 y. o.)

PaO2(mmHg)

Mild hypoxemia 60 to < 80

Moderate hypoxemia 40 to < 60

Severe hypoxemia < 40

For each year > 60 subtract 1 mmHg for limits ofmild &

moderate hypoxemia.At any age, PaO2 < 40 mmHg indicates severe

hypoxemia.


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3. If normoxemic, is oxygenation

adequate or more than

adequate?


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Thank you !

basics in arterial blood gas interpretation.ppt

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