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From Artery to Analysis
1. Kristopher R. Maday, MS, PA-C
Program Director, Associate Professor
University of Tennessee Health Science Center
2. • Part I
– Discussing the arterial puncture procedure
• Part II
– Review of the components of an arterial blood
gas
• Part III
– Evaluate and analyze the acid/base
disturbances
3. • Acid-Base status determination
• O2/CO2 relationship
• Response to therapeutic interventions
• Detection and quantification of abnormal
hemoglobins
– Carboxyhemoglobin, methemoglobin
• Blood samples when venous samples not
feasible
• Acid-Base status determination
• O2/CO2 relationship
• Response to therapeutic interventions
• Detection and quantification of abnormal
hemoglobins
– Carboxyhemoglobin,methemoglobin
• Blood samples when venous samples not
feasible
4. • Not really any, but…..
– (-) Allen Test for radial artery
– Skin infection
– Coagulopathy (relative)
• Platelet < 50k
• INR > 3.0
– Active Raynaud’s
– Severe peripheral vascular disease
– Using the carotid artery
8. • Arterial puncture kit
• 1% lidocaine
• Skin prep cleaner
• Cup/bag of ice for transport
9.
10. • Position the hand for maximal exposure
• Prep skin
• Local anesthesia
11.
12.
13. • If left at room temperature, leukocytes in
blood consume oxygen and false lower
PaO2
• Heparin is acidic and can falsely lower pH
if less than 2 mL of blood is obtained
• Air bubbles in syringe > 2% of blood
volume can falsely elevate PaO2 and
falsely lower PaCO2
14.
15. • The body has a very narrow pH index in
order to carry on cellular function
– Deviation from this can have catastrophic
effects
• Delicate balance between lungs, kidneys,
and complex system of buffers
17. • Daily metabolism of energy sources
produces 15,000mmol of CO2 and 50-
100mEq of non-volatile acids
– CO2 excreted by lungs and metabolic acids
excreted by kidneys
• The principle buffering system in the human
body is the carbonic acid/bicarbonate
buffering system
18. • Kidneys = Bicarbonate
– HCO3
- is filtered (excreted) in the glomerulus
and reabsorbed (secreted) in the proximal
tubule
• 2 important things to remember
– It is the strongest buffer in the body
– It is slow to reach full effect
19.
20.
21. • Lungs = CO2
• The extent of CO2 excretion in the lungs is
dependant on one main variable
– Chemoreceptors in arteries and the medulla in
the brain regulate this
• Very rapid and often the first observable
change in a patient’s acid-base status
22.
23. • Normal - 7.35 – 7.45 (7.40)
• The first value to look at when interpreting
acid-base status
• A normal pH does not mean normal acid-
base status
– Mixed conditions
• pH < 6.8 is generally not compatible with
life
24. • Normal – 35 – 45 (40) mmHg
• Conditions related to CO2 use the suffix –
capnia
– PaCO2 > 45 is hypercapnia
– PaCO2 < 35 is hypocapnia
• CO2 has a very high diffusion coefficient
– Small changes in respiratory status have
immediate changes in PaCO2 levels
25. • Normal - 80 – 100 (100) mmHg
– PaO2 < 80 is termed hypoxemia
• Often used in conjunction with pulse
oximetry to determine oxygenation status
of a patient
26. • Normal – 22 – 26 (24)
• Conditions related to HCO3
- use the suffix
–carbia
– HCO3
- > 26 is hypercarbia
– HCO3
- < 22 is hypocarbia
• ***Calculated number***
• Must look at PaCO2 to interpret accurately
27. • Normal - +/-2 (0)
• The amount of base needed to raise/lower
1L of blood to a normal pH
• Common causes
– Deficit
• Increase in metabolic acid production
• Loss of HCO3
– Excess
• Increase in HCO3
28. • Body produces 15-20 mmol/kg/day
through the glycolytic pathway of glucose
metabolism
29.
30. • Normal - < 2 mEq/L
• Two types of lactic acidosis
– Type A (majority)
• Marked tissue hypoperfusion
– Type B
• Toxin-induced impairment of cellular metabolism
32. • Normal > 95%
• % saturation of hemoglobin in RBC
– Measures light refraction through tissue
• Placed on digits or ear lobe
• Non-invasive measurement of
“oxygenation”
• Causes of error
– Carbon monoxide, hypoperfusion, nail polish
33.
34.
35.
36. • Can be used if arterial access is difficult
• Ideally, a central venous sample should be
used
37. • Non-invasive estimation of end-tidal CO2
• Can be used in conjunction with pulse
oximetry
• Limitations
– Can’t distinguish between metabolic or
respiratory conditions
45. • -emia refers to pH
– Acidemia, alkalemia
• -osis refers to an abnormal condition or process
– Metabolic alkalosis, respiratory acidosis
Acidotic
Alkalotic
46. • Accurate assessment of a patient’s acid-
base status requires a measurement of
arterial pH, PCO2, and plasma HCO3
-
– Bedside analyzers directly measure pH and
PCO2
– HCO3
-
is calculated from Henderson-
Hasselbach equation
• A primary disturbance is usually
accompanied by a compensatory
response, but does not fully correct the
67. C arbon monoxide, cyanide
A minoglycosides
T heophyline, toluene
M ethanol
U remia
D iabetic ketoacidosis
P ropylene glycol
I nborn errors of metabolism
L actic acidosis
E thylene glycol, ethanol
S alicylates
70. U reteric diversion
S mall bowel fistulae
E xcessive saline
D iarrhea
C arbonic anhydrase inhibitors
R enal tubular acidosis
A drenal insufficiency
P ancreatic fistulae
71. Cause Renal Defect Urine
pH
Urinary
Anion Gap
Serum K
+
Dilutional None < 5.5 Negative Normal
GI Loss None < 5.5 Ne-GUT-ive ↓
Renal Tubular Acidosis
Type I (Distal) Distal H
+
secretion > 5.5 Positive ↓
Type II (Proximal) Proximal HCO3
-
reabsorption
< 5.5 Positive ↓
Type IV (adrenal
insufficiency)
Distal Na
+
reabsorption, K
+
and
H+
secretion
< 5.5 Positive ↑
UAG = (Na + K) - Cl