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ARTERIAL BLOOD GAS
1.
2. Definitions
Indications And contraindications
Procedure
Technical Errors
Stepwise approach in Acid- Base
interpretation
Management
3. 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
4. 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.
5. Po2 measures the partial pressure exerted by
oxygen (O2) dissolved in the blood.
Normal range for arterial Po2 is 70 to100
mmHg
6. 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]
7. 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)
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.
9. 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.
10. 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
11. 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 .
12. 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.
13.
14. 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
15.
16. 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
17. Position the patient’s arm with the wrist
extended.
Locate the radial artery with your index and
middle fingers.
17
18.
19. 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
20. 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
21. 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
22. 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
23. 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?
24. 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?
25. 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
26. 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.
27. 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.
33. A) CARDIOVASCULAR:
Related to coronary vasodilation
1. Tachycardia
2. Ventricular arrythmias
B) BIOCHEMICAL ABNORMALITIES:
CO2
Cl-
PO4
3-
34. 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
35. 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
36. 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
37. 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
39. 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
40. 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
43. 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.
44. 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.
45. 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.
46. 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.
48. 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
49. 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.
50. 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)
52. 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
53. 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
54. 2) HCO3- Retention:
Massive Blood Transfusion
Ingestion (Milk-Alkali Syndrome)
Admn of large amounts of HCO3-
3) H+ movement into cells
Hypokalemia
55. 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.
56. 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.
57. 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
58.
59. 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
60. 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
For every 10 mmHg increase in PaCO2, the
HCO3
- will rise by 4 mmol/L
Expected HCO3 = 24 + (4 × (PaCO2-40) / 10)
61. 3)Acute Respiratory Alkalosis
For every 10 mmHg increase in PaCO2, the
HCO3
- will fall by 2 mmol/L
Expected HCO3 = 24 - (2 ×(PaCO2-40) / 10)
4)Chronic Respiratory Alkalosis
For every 10 mmHg increase in PaCO2, the
HCO3
- will fall by 5 mmol/L
Expected HCO3 = 24 - (5 ×(PaCO2-40) / 10)