Arterial Blood Gases

PATHOLOGY (3rd SHIFTING) | Dr. John Arnel H. Amata | 20 January 2020

OUTLINE → Reposition needle back inside arterial lumen

I. Arterial Blood Gases • Withdraw needle from skin
II. Procedure • Immediately apply pressure over entry site
III. Arterial Blood Gas Interpretation • Hold pressure at entry site for 5 minutes
IV. Summary
V. Sample Problems D. COMPLETING SAMPLE COLLECTION
1. Sample Preparation for lab
I. ARTERIAL BLOOD GASES
• Express any air bubbles from syringe
• Blood test that is performed using blood obtained from an artery • Cork needle or remove needle and cap syringe
• Involves puncturing an artery with a thin needle and syringe and → This is done so as to keep the blood sample in aerobic
drawing a small volume of blood condition thus preventing the entry of air from the
• Mainly used in pulmonology to determine gas exchange levels in environment and subsequent alteration of the test results
the blood related to lung function • If the sample is exposed to oxygen:
• Determines the: → pO2 is falsely increased
→ pH of the blood → pCO2 is falsely decreased
→ Partial pressure of carbon dioxide (PaCO2) → H2CO3 is falsely decreased
→ Partial pressure of oxygen (PaO2) → pH is falsely increased (basic)
→ Bicarbonate level • Roll syringe between fingers to mix Heparinized sample
• Immediately place sample on ice
II. PROCEDURE
2. Label Sample
A. ARTERIAL PUNCTURE SITE • Patient identification data
• Sample acquisition time
• Radial Artery • FIO2 at time of sample draw
→ preferred/common site • Patient’s body temperature
→ has least chance of hitting a nerve or another blood vessel
• Femoral Tap 3. Deliver Sample Quickly to the Lab
• Brachial Artery E. COMPLICATIONS
• For infants: • Nerve injury
→ Scalp • Ischemic changes hand and wrist
→ Umbilical cord → Always check Allen Test before radial artery puncture to check
B. PREPARATION FOR RADIAL ARTERY PUNCTURE the patency of the injured artery
• Perform Allen Test to confirm collateral circulation • Occult bleeding especially at the brachial and femoral
• Heparinize syringe (heparin is used because it is a naturally • Artery punctures
occurring anticoagulant of the body) F. REMINDERS
→ Start with a 3 cc syringe and 21-gauge needle • Label specimen
→ Draw up 0.5 ml of Heparin (1000 units/ml)
• Complete all the data in request (temp, HgB, etc)
→ Rotate syringe and work plunger to distribute heparin
• STAT (Short Turn-around Time): result should be out within 30
→ Minimal Heparin should remain (0.15ml)
minutes after collection since any delay in the processing the
• Clean radial entry site
sample may lead to erroneous results
→ Povidone-Iodine solution (betadine)
→ Alcohol swab → Glucose breakdown to pyruvate and lactic acid
• Consider local anesthetic at entry site → Glucose is consumed: falsely lowered because
• Small skin wheal of Lidocaine 1% ▪ 7% glycolysis occurs at room temperature per hour
▪ 2% per hour at refrigerator temperature
C. OBTAINING RADIAL ARTERY SAMPLE
▪ 0% in freezing temperature
Needle Entry → pO2 is falsely lowered
• Identify radial artery with gentle pressure → pCO2 is falsely elevated
• Patient dorsiflexes wrist → H2CO3 is falsely elevated
• Needle and syringe angled 45o towards arm
→ pH is falsely lowered
• Enter skin just distal to palpated artery site
• ABG specimen should be at least 1cc
• Slowly advance needle until spontaneous blood enters
→ Result of low sample volume specimen may not interpret true
Arterial Blood Collection patient’s condition
• Hold needle steady until 1-2 cc of blood is obtained • Submit specimen in ice (not in water only)
→ Specimen not in ice will affect the result (pH, pCO2, pO2)
III. ARTERIAL BLOOD GAS INTERPRETATION • Ideal ABG specimen: no clot, bubbles or airspace
• Allow syringe to fill itself (avoid aspirating) • Reflect oxygenation, gas exchange, and acid base balance
• If flow ceases slowly withdraw needle 1-2 mm
This study source was downloaded by 100000849895545 from CourseHero.com on 09-21-2022 18:44:41 GMT -05:00
S 03 / T 01 Adornado, Baliza, Camangon, Coja, Cuasay, De Belen, Ferrancol, Lunario, Moran, Tolentino 1 of 3

https://www.coursehero.com/file/111268045/CLINPATH-S03-T01-Arterial-Blood-Gasespdf/
 • PaO2 – partial pressure of oxygen dissolved in arterial blood • Lungs compensate faster but only partially while kidneys
• SaO2 – amount of oxygen bound to hemoglobin compensate slower but may fully compensate. (see sample
• Oxygen is transported from alveoli into the plasma problem 6)
• Ex. pH – 7.30, PCO2 -28, HCO3 – 15
NORMAL VALUES → Interpretation: pH ↓ -acidosis; PCO2 ↓ - respiratory alkalosis;
PaO2 80 – 100 mmHg at sea level HCO3 ↓ - metabolic acidosis
→ pH same result w/ HCO3 = metabolic acidosis -> lungs tried to
SaO2 93 – 100%
return the pH into homeostasis -> decrease PCO2 -> partial
pH 7.35 – 7.45 respiratory compensation
PaCO2 35 – 45 mmHg → For values, dapat same kung inc or dec to say na may
compensation since baliktaran sila. (↓PCO2 alka ↓HCO3 acid)
HCO3 22 – 26 mEq/L
→ For interpretation, dapat baliktad sila, if one is acidotic, the
BE -2 to +2 mEq/L other is alkalotic to cancel. (see sample problem 4)
→ If normal pH, but with metabolic imbalance, renal
A. ABG RANGES
compensation since siya lang kaya full compensation (see sp6)
O2
• PaO2 80 – 100 mmHg at sea level IV. SUMMARY
→ < 80 mmHg = hypoxemia
• Determine if pH is acidotic (↓), alkalotic (↑), or within normal.
→ < 60 mmHg may be seen in COPD patients
• Evaluate pCO2 if ↓ (respiratory alkalosis), ↑ (respiratory acidosis)
→ < 40 mmHg is life threatening
or within normal range.
• SaO2 93 – 100% = normal saturation
• Evaluate HCO3 if ↓ (metabolic alkalosis), ↑ (metabolic acidosis) or
• Hypoxia is decreased oxygen at the tissue level within normal range.
pH • Determine if with compensation (renal or respiratory
• Negative log of H+ concentration compensation) and to what extent (partial or full compensation)
• In blood, normal range is 7.35 – 7.45
→ pH < 7.35 = acidosis V. SAMPLE QUESTION
→ pH > 7.45 = alkalosis
• Check the pH, acidic or basic?
• pH < 7.0 or > 7.8 can cause death
• Which is abnormal, PaCO2 or HCO3?
CO2 → If pCO2 is abnormal
• PaCO2 – partial pressure of CO2 dissolved in arterial plasma ▪ RESPIRATORY
• Normal: 35 – 45 mmHg ▪ the kidney will try to compensate
• Regulated in the lungs → If HCO3 is abnormal
• A primary respiratory problem is when PaCO 2 is: ▪ METABOLIC
→ > 45 mmHg = respiratory acidosis ▪ the lungs will try to compensate
→ < 35 mmHg = respiratory alkalosis
→ HCO3 will be normal
HCO3 (Bicarbonate)
• Normal: 22 – 26 mEq/L • SMOR
• Regulated by the kidneys → Same: Metabolic
• A primary metabolic or renal disorder is when the HCO3 is when: → Opposite: Respiratory
→ < 22 mEq/L = metabolic acidosis *Only true if without compensation
→ > 26 mEq/L = metabolic alkalosis
→ PaCO2 is normal VI. REFERENCES

**Abnormalities will be discussed at the end of the trans • Dr. Amata’s Lecture
B. BASE EXCESS (BE) • Henry’s Clinical Diagnosis and Management by Laboratory
Methods 22ed
• Another metabolic component reported
• Calculation of circulating buffer / base
• Normal range: -2 to +2 mEq/L
→ e.g BE value = -8 = metabolic acidosis
→ BE value = +10 = metabolic alkalosis
• Determines presence of metabolic imbalance
C. COMPENSATION
• Body attempts to recover from primary problem and return to
homeostasis
• Bicarbonate (HCO3 by kidneys) – carbonic acid (H2C03 by lungs)
buffer system
*Recall Respi and renal physio. CO2 + H2O -> H2CO3 -> HCO3 + H
• If respiratory acidosis/alkalosis, kidneys may compensate; if
metabolic acidosis/alkalosis, lungs may compensate.

This study source was downloaded by 100000849895545 from CourseHero.com on 09-21-2022 18:44:41 GMT -05:00
S 03 / T 01 Arterial Blood Gases 2 of 3

https://www.coursehero.com/file/111268045/CLINPATH-S03-T01-Arterial-Blood-Gasespdf/
 Table 1. Metabolic Acidosis vs. Alkalosis
METABOLIC
ACIDOSIS
RISK • Ketogenic diet
FACTORS • Patients with diabetes, sepsis
and renal failure
• Dialysis patients
ETIOLOGY • Organic acid prdcn or when
ingestion exceeds excretion rate
• Decreased HCO3- prdcn
• Disorders:
→ Diabetic ketoacidosis – 
prdcn of acetoacetic acid and
B-hydroxybutyric acid
→ Lactic acidosis
→ Uremic acidosis
→ Poisoning from salicylate,
ethylene glycol and methyl
alcohol
→ Reduced acid excretion due
to renal failure or tubular
acidosis
→ Loss HCO3- due to diarrhea or
excessive renal excretion
PATHOLOGY • Compensatory hyperventilation
• Hyperkalemia – shift of acid
from plasma to ICF
CLINICAL • Lab finding in metab acidosis:
→  pH, HCO3-, Normal PCO2
• Lab after respi compensation
→ Normal pH,  pCO2
SIGNS AND • Cardiac dysrhythmias
SYMPTOMS • CNS dysfunction
• Headache, Diarrhea, Tremors
This study source was downloaded by 100000849895545 from CourseHero.com on 09-21-2022 18:44:41 GMT -05:00
S 03 / T 01 Arterial Blood Gases
https://www.coursehero.com/file/111268045/CLINPATH-S03-T01-Arterial-Blood-Gasespdf/
Powered by TCPDF (www.tcpdf.org)
ALKALOSIS
• Hypovolemia
• Excess aldosterone
• Iatrogenic base administration
• Ingestion of excess base,
decreased elimination of base,
or loss of acidic fluids
• Disorders:
→ Excessive intake of antacids
→ IV administration of
bicarbonate
→ Renal bicarbonate retention
→ Prolonged use of diuretics
→ Vomiting – loss of HCl from
stomach
→ Intestinal obstruction
→ Gastric suction
→ Cushing’s syndrome –
glucocorticoid excess
→ Hyperaldosteronism –
mineralocorticoid excess
• Limited respi compensation
→ pH increase slows breathing
(hypoventilation), therefore
increasing CO2 retention
→  CO2 causes an increase in
carbonic acid which then
lowers the blood pH
• Hypokalemia: K from ECF shifts
to ICF due to H+ moving out of
the cell; depleted K stores from
use of loop diuretics, NGT
• Lab finding in metab alkalosis
→  pH, HCO3-, Normal PCO2
• Lab after respi compensation
→ Normal pH,  PCO2
• Cardiac dysrhythmias
• Seizures
• Confusion, Agitation
• Muscle twitching
RESPIRATORY
ACIDOSIS
• Excess acid in body fluids
• Hypoventilation
• Lung diseases: COPD; Cystic
Fibrosis; airway obstruction;
spinal cord injury; CVA;
depressant drugs;
inadequate mechanical
ventilation
• Paralysis of respiratory
muscles (ie. Myasthenia
gravis,hypokalemia, Guillain-
barre syndrome)
• Thoracic deformity or airway
obstruction
• Hypercapnia; CO2 diffuses
easily across biological
membranes
• ↓pH, ↑PaCO2
• HCO3- normal or  in renal
compensation
• achieved by  net acid
excretion, in the form of NH4
• Cardiac arrhythmias
• Vasodilatation, Tachycardia
• Somnolence
• Decreased ventilation
ALKALOSIS
• Relative excess of base in
body fluids secondary to:
→ ventilatory release of CO2
→ pneumonia, shock, severe
anemia
• Hypoxemia (<PaO2) causing
hyperventilation in an
attempt to raise CO2
• Can be caused by
anxiety/acute pain
• The two most common causes
(Henry’s)
→ hypoxic stimulation of the
peripheral respiratory
center
→ stimulation through
pulmonary receptors
caused by various
disorders of the lung
(pneumonia, pulmonary
congestion, and
pulmonary embolism)
• Compensation is through
renal and tissue buffering
• Buffer response is to shift acid
from ICF to the blood by
moving HCO3 into the cells in
exchange of chloride
• ↑pH, ↓PaCO2
• HCO3 is normal or low due to
compensation
• Nausea
• Vomiting
• Tingling of fingers
3 of 3