ARTERIAL BLOOD GAS

 Definitions
 Indications And contraindications
 Procedure
 Technical Errors
 Stepwise approach in Acid- Base
interpretation
 Management

 Negative logarithm of the hydrogen ion [H+ ]
concentration in the blood, used as a positive
number.
 The negative logarithm of water 1×10-7.
 pH of water is 7
 (7) represents the midpoint of the pH scale.
 Normal range 7.35 to 7.45

 Pco2 is a measurement of the partial pressure
exerted by CO2 in solution in the blood.
 Normal range for PCo2 in arterial blood is 35
to 45 mmHg.

 Po2 measures the partial pressure exerted by
oxygen (O2) dissolved in the blood.
 Normal range for arterial Po2 is 70 to100
mmHg

 The pH of arterial blood is related to the
PaCo2 by the Henderson-Hasselbalch
equation:
o Correlates metabolic & respiratory regulations
HCO3
-
pH = pK + log ----------------
0.03 x [PaCO2]

 Determination of PaO2
PaO2 is dependant upon Age, FiO2, Patm
As Age the expected PaO2
• PaO2 = 109 - 0.4 (Age)
As FiO2 the expected PaO2
• Alveolar Gas Equation:
• PAO2= (PB-P h2o) x FiO2- pCO2/R
PAO2 = partial pressure of oxygen in alveolar gas, PB = barometric pressure
(760mmHg), Ph2o = water vapor pressure (47 mm Hg), FiO2 = fraction of
inspired oxygen, PCO2 = partial pressure of CO2 in the ABG, R = respiratory
quotient (0.8)

 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.
 Pre operative fitness.

 Site- (Ideally) Radial Artery
Brachial Artery
Femoral Artery
 Ideally - Pre-heparinised ABG syringes
- Syringe should be FLUSHED with 0.5ml of 1:1000
Heparin solution and emptied.
DO NOT LEAVE EXCESSIVE HEPARIN IN THE SYRINGE
HEPARIN DILUTIONAL HCO3
EFFECT PCO2
Only small 0.5ml Heparin for flushing and discard it
Syringes must have > 50% blood. Use only 2ml or less syringe.

 Ensure No Air Bubbles. Syringe must be sealed immediately
after withdrawing sample.
◦ Contact with AIR BUBBLES
Air bubble = PO2 150 mm Hg , PCO2 0 mm Hg
Air Bubble + Blood = PO2 PCO2
 ABG Syringe must be transported at the earliest to the
laboratory for EARLY analysis via COLD CHAIN

 Patients Body Temperature affects the values of PCO2
and HCO3.
ABG Analyser is controlled for Normal Body temperatures
Any change in body temp at the time of sampling leads to
alteration in values detected by the electrodes
 Cell count in PO2
 ABG Sample should always be sent with relevant
information regarding O2, FiO2 status and Temp .

A. pH (Sanz Electrode)
 Measures H+ ion concentration of sample against a known pH
in a reference electrode, hence potential difference. Calibration
with solutions of known pH (6.384 to 7.384)
B. P CO2 (Severinghaus Electrode)
 CO2 reacts with solution to produce H+
higher C02 more H+  higher P CO2 measured
C. P 02 (Clark Electrode)
 02 diffuses across membrane producing an electrical current
measured as P 02.

CONTRAINDICATIONS COMPLICATIONS
 Bleeding diathesis
 AV fistula
 Severe peripheral
vascular disease,
absence of an arterial
pulse
 Infection over site.
 Abnormal Allens test.
 Severe coagulopathy.
 Use of thrombolytic
agents.
 Pain and discomfort
 Hematoma
 Vasovagal response
 Thrombosis and
embolism
 Infection or
contamination
 Inadvertent needle
stick
 Vascular trauma or
occlusion
 Arterial spasm

 Wash your hands, introduce yourself to the
patient and clarify their identity.
 Explain what you would like to do and obtain
consent.
 This is a slightly uncomfortable procedure so
you should let the patient know this.
16

 Position the patient’s arm with the wrist
extended.
 Locate the radial artery with your index and
middle fingers.
17

 Take the cap off the needle, flush the heparin through the
syringe and again locate the radial artery using your
non-dominant hand.
 Insert the needle at 45 degrees to the skin at the point
of maximum pulsation of the radial artery
 Advance the needle until arterial blood flushes into the
syringe.
 The arterial pressure will cause the blood to fill the
syringe.
19

 Remove the needle/syringe placing the needle into the
bung. Press firmly over the puncture site with the gauze
to halt the bleeding. Remain pressed for 5 minutes.
20

Cap the syringe, push out any air within it, and
send immediately for analysis ensuring that the
sample is packed in ice. Remove your gloves
and dispose them in the clinical waste
bin. Wash your hands and thank the patient.
21

 Before attempting to interpret the
results you should know whether the
patient was on room air or on oxygen
when the sample was taken, and if on
oxygen, what concentration.
22

1. Was the blood gas specimen obtained
acceptably? Free of air bubbles and clots?
Analyzed promptly and/ or iced
appropriately?
2. Did the blood gas analyzer function
properly? Was there a recent acceptable
calibration of all electrodes or sensors? Was
analyzer function validated by appropriate
quality controls?

3. Is pH within the normal limits (7.35 to 7.45)?
If so, go to Step 4.
If below 7.35, acidosis is present;
If above 7.45, alkalosis is present.
Otherwise, look for compensatory changes or
combined disorders.
4. Calculate the anion gap. Is it within the
normal range?

Anion Gap
AG = [Na+
] - [Cl-
+HCO3
-
]
• Elevated anion gap represents
metabolic acidosis
• Normal value: 3 – 11 mEq/L
• Major unmeasured anions
– albumin
– phosphates
– sulfates
– organic anions

5. Is Pco2 within normal limits (35 to 45 mm
Hg)?
If so, go to Step 6.
If Pco2 > 45 and pH < 7.35, then respiratory
acidosis is present.
If Pco2 > 45 and pH > 7.35, then
compensated
respiratory acidosis is present.

If Pco2 < 35 and pH > 7.45, then respiratory
alkalosis is present.
If Pco2 < 35 and pH < 7.45, then compensated
respiratory alkalosis is present.

 EXCRETORY COMPONENT PROBLEMS:
1. Perfusion:
Massive PTE
Cardiac Arrest
2. Ventilation:
Severe pulmonary edema
Severe pneumonia
ARDS
Airway obstruction
3. Restriction of lung/thorax:
Flail chest
Pneumothorax
Hemothorax

4. Muscular defects:
Severe hypokalemia
Myasthenic crisis
5. Failure of Mechanical Ventilator
CONTROL COMPONENT PROBLEMS:
1. CNS:
Drugs (Anesthetics, Sedatives)
Trauma
Stroke
2. Spinal Cord & Peripheral Nerves:
Cervical Cord injury
Neurotoxins (Botulism, Tetanus, OPC)
Drugs causing Skeletal muscle paralysis
(SCh, Curare, Pancuronium, aminoglycosides)

 EXCRETORY COMPONENT PROBLEMS:
1. Ventilation:
COPD
Advanced ILD
 Restriction of thorax/chest wall:
Kyphoscoliosis, Arthritis
Fibrothorax
Hydrothorax
Muscular dystrophy
Polymyositis

 CONTROL COMPONENT PROBLEMS:
1. CNS: Obesity Hypoventilation Syndrome
Tumours
Brainstem infarcts
Myxedema
Ch sedative abuse
Bulbar Poliomyelitis
2. Spinal Cord & Peripheral Nerves:
Poliomyelitis
Multiple Sclerosis
ALS
Diaphragmatic paralysis

A) CARDIOVASCULAR:
Related to coronary vasodilation
1. Tachycardia
2. Ventricular arrythmias
B) BIOCHEMICAL ABNORMALITIES:
 CO2
 Cl-
 PO4
3-

C) NEUROMUSCULAR: Related to cerebral Artery
vasodilatation &  Cerebral BF
1. Anxiety
2. Asterixis
3. Lethargy, Stupor, Coma
4. Delirium
5. Seizures
6. Headache
7. Papilledema
8. Focal Paresis
9. Tremors, myoclonus

 In response to rise in CO2 (& H2CO3)  blood
and tissue buffers take up H+ ions, H2CO3
dissociates and HCO3- increases with rise in pH.
 Steady state reached in 10 min & lasts for 8
hours.
 PCO2 of CSF changes rapidly to match PaCO2.
 Hypercapnia that persists > few hours induces
an increase in CSF HCO3- that reaches max by
24 hr and partly restores the CSF pH.
 After 8 hrs, kidneys generate HCO3-
 Steady state reached in 3-5 d

 Ensure adequate oxygenation - care to avoid
inadequate oxygenation while preventing
worsening of hypercapnia due to supression
of hypoxemic respiratory drive
 Correct underlying disorder if possible

 Alkali (HCO3) therapy rarely in acute and
never in chronic respiratory acidosis  only if
acidemia directly inhibiting cardiac functions
 Problems with alkali therapy:
1)Decreased alveolar ventilation by decrease in
pH mediated ventilatory drive
2)Enhanced carbon dioxide production from
bicarbonate decomposition

 NEUROMUSCULAR: Related to cerebral artery
vasoconstriction &  Cerebral BF
1. Lightheadedness
2. Confusion
3. Decreased intellectual function
4. Syncope
5. Seizures
6. Paraesthesias (circumoral, extremities)
7. Muscle twitching, cramps, tetany
8. Hyperreflexia
9. Strokes in pts with sickle cell disease

CENTRAL RESPIRATORY STIMULATION
(Direct Stimulation of Respiratory Center):
Structural Causes Non Structural
Causes
• Head trauma Pain
• Brain tumor Anxiety
• CVA Fever
• Voluntary
PERIPHERAL RESPIRATORY STIMULATION
(Hypoxemia  Reflex Stimulation of Respiratory
Center via Peripheral Chemoreceptors)
• Pul V/Q imbalance
• Pul Diffusion Defects Hypotension
• Pul Shunts High Altitude

 INTRATHORACIC STRUCTURAL CAUSES:
1. Reduced movement of chest wall & diaphragm
2. Reduced compliance of lungs
3. Irritative lesions of conducting airways.
 MIXED/UNKNOWN MECHANISMS:
1. Drugs – Salicylates Nicotine
Progesterone Thyroid hormone
Catecholamines
Xanthines (Aminophylline & related compounds)
2. Cirrhosis
3. Gram –ve Sepsis
4. Pregnancy
5. Heat exposure
6. Mechanical Ventilation

 CARDIOVASCULAR: Related to coronary
vasoconstriction
1. Tachycardia
2. Angina
3. ECG changes (ST depression)
4. Ventricular arrythmias
 GASTROINTESTINAL: Nausea & Vomitting
 BIOCHEMICAL ABNORMALITIES:
 CO2 PO4
3-
Cl-  Ca2+

 In response to fall in CO2 (& H2CO3)  release of
H+ by blood and tissue buffers  react with
HCO3-  fall in HCO3- (usually not less than 18)
and fall in pH
 Cellular uptake of HCO3- in exchange for Cl-
 Steady state in 15 min - persists for 6 hrs
 After 6 hrs kidneys increase excretion of HCO3-
(usually not less than 12-14)
 Steady state reached in 11/2 to 3 days.

 Respiratory alkalosis by itself not a cause of
respiratory failure unless work of increased
breathing not sustained by respiratory muscles.
 Rx underlying cause
 Usually extent of alkalemia produced not
dangerous.
 Admn of O2 if hypoxaemia
 If pH>7.55 pt may be sedated/anesthetised/
paralysed and/or put on Mechanical Ventilation.

6. Is calculated HCO3
 - within the normal limits
 (22 to 27 mEq/L)? If so, the acid-base status is
 probably normal; go to Step 7.
 If HCO3 < 22 and pH < 7.35, then metabolic*
 acidosis is present.
 If HCO3 < 22 and pH > 7.35, then compensated
 metabolic* acidosis is present.

 If HCO3 >27 and pH > 7.45, then metabolic
 alkalosis is present.
 If HCO3 >27 and pH < 7.45, then
compensated
 metabolic alkalosis is present.

 Metabolic Anion Gap
Acidosis
◦ M - Methanol
◦ U - Uremia
◦ D - DKA
◦ P - Paraldehyde
◦ L - Lactic Acidosis
◦ E - Ehylene Glycol
◦ S - Salicylate
Non Gap Metabolic
Acidosis
Hyperalimentation
Acetazolamide
RTA (Calculate
urine anion gap)
Diarrhea
Pancreatic Fistula

 When to treat?
Severe acidemia  Effect on Cardiac function most
important factor for pt survival since rarely lethal in
absence of cardiac dysfunction.
Contractile force of LV  as pH  from 7.4 to 7.2
However when pH < 7.2, profound reduction in cardiac
function occurs and LV pressure falls by 15-30%
Most recommendations favour use of base when pH
< 7.15-7.20 or HCO3 < 8-10 meq/L.

Rx Undelying Cause
HCO3- Therapy
 Aim to bring up pH to 7.2 & HCO3-  10 meq/L
 Qty of HCO3 admn calculated:
0.5 x LBW (kg) x HCO3 Deficity (meq/L)

 Met alkalosis common (upto 50% of all
disorders)
 pH, HCO3
 PCO2 by 0.7 for every 1mEq/L  in HCO3
 Severe met alkalosis assoc with significant
mortality
1)Arterial Blood pH of 7.55  Mortality rate of 45%
2)Arterial Blood pH of 7.65  Mortality rate of 80%
 Metabolic alkalosis has been classified by the
response to therapy or underlying
pathophysiology

1) H+ loss:
GIT Chloride Losing Diarrhoeal
Diseases
Removal of Gastric Secretions
(Vomitting, NG suction)
Renal Diuretics (Loop/Thiazide)
Mineralocorticoid excess
Hypercalcemia
High dose i/v penicillin

2) HCO3- Retention:
Massive Blood Transfusion
Ingestion (Milk-Alkali Syndrome)
Admn of large amounts of HCO3-
3) H+ movement into cells
Hypokalemia

 Rx underlying cause
 While replacing Cl- deficit, selection of
accompanying cation (Na/K/H) dependent
on:Assessment of ECF vol status
 Presence & degree of associated K
depletion,
 Pts with vol depletion usually require
replacement of both NaCl & KCl.

Dialysis
 In presence of renal failure or severe fluid
overload state in CHF, dialysis +/- UF may
be reqd to exchange HCO3 for Cl & correct
metabolic alkalosis.
Adjunct Therapy
 PPI can be admn to  gastric acid
production in cases of Cl-depletion met
alkalosis resulting from loss of gastric
H+/Cl- (e.g. pernicious vomiting, req for
continual removal of gastric secretions.

MILK-ALKALI SYNDROME & OTHER
HYPERCALCEMIC STATES
 Cessation of alkali ingestion & Ca sources
(often milk and calcium carbonate)
 Treatment of underlying cause of hypercalcemia
 Cl- and Vol repletion for commonly associated
vomiting

 In the presence of acidosis or alkalosis, regulatory mechanisms occur
which attempt to maintain the arterial pH in the physiologic range.
 Disturbances in HCO3- (metabolic acidosis or alkalosis) result in
respiratory compensation while changes in CO2 (respiratory
acidosis/alkalosis) are counteracted by renal compensation
a. Renal compensation – kidneys adapt to alterations in pH by
changing the amount of HCO3- generated/excreted. Full renal
compensation takes 2-5 days
b. Respiratory compensation – alteration in ventilation allow
immediate compensation for metabolic acid-base disorders
59

1)Acute Respiratory Acidosis
 For every 10 mmHg increase in PaCO2, the
HCO3
- will rise by 1 mmol/L
 Expected HCO3 = 24 + (PaCO2-40) / 10)
2) Chronic Respiratory Acidosis
HCO3
- will rise by 4 mmol/L
 Expected HCO3 = 24 + (4 × (PaCO2-40) / 10)

3)Acute Respiratory Alkalosis
HCO3
- will fall by 2 mmol/L
 Expected HCO3 = 24 - (2 ×(PaCO2-40) / 10)
4)Chronic Respiratory Alkalosis
HCO3
- will fall by 5 mmol/L
 Expected HCO3 = 24 - (5 ×(PaCO2-40) / 10)

5)Metabolic Acidosis
 For complete compensation,
 expected PaCO2 = (1.5 × HCO3
-) + 8
6)Metabolic Alkalosis
 For complete compensation,
 expected PaCO2 = (0.7 × HCO3
-) + 20

ARTERIAL BLOOD GAS

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ARTERIAL BLOOD GAS