From Artery to Analysis

Kristopher R. Maday, MS, PA-C
Program Director, Associate Professor
University of Tennessee Health Science Center

• 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

• 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

• 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

• Hemorrhage/hematoma
– May form pseudoaneurysm
• Arterial spasm
• Radial nerve damage

• Arterial puncture kit
• 1% lidocaine
• Skin prep cleaner
• Cup/bag of ice for transport

• Position the hand for maximal exposure
• Prep skin
• Local anesthesia

• 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

• 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

pH / PaCO2 / PaO2 / HCO3 / Base
7.40 / 40 / 100 / 24 / 0
Normal Range
pH 7.40 7.35 - 7.45
PaCO2 (mmHg) 40 35 – 45
PaO2 (mmHg) 100 80 – 100
HCO3
- (mEq/L) 24 22 – 26
Base Excess/Deficit (mEq/L) 0 ± 2

• 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

• 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

• 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

• 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

• 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

• Normal - 80 – 100 (100) mmHg
– PaO2 < 80 is termed hypoxemia
• Often used in conjunction with pulse
oximetry to determine oxygenation status
of a patient

• 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

• 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

• Body produces 15-20 mmol/kg/day
through the glycolytic pathway of glucose
metabolism

• Normal - < 2 mEq/L
• Two types of lactic acidosis
– Type A (majority)
• Marked tissue hypoperfusion
– Type B
• Toxin-induced impairment of cellular metabolism

• Increased pyruvate production
– Catacholamine stimulation of glycolysis
• Beta-agonists, sepsis, pheochromocytoma
– Salicylate intoxication
• Decreased pyruvate utilization
– Congenital
• Increased metabolic rate
– Seizures, exercise
• Decreased oxygen delivery
– Shock, cardiac arrest, hypoxemia
• Decreased lactate utilization
– Liver disease
• Unknown
– Diabetes, biguanides, malignancy,

• 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

• Can be used if arterial access is difficult
• Ideally, a central venous sample should be
used

• Non-invasive estimation of end-tidal CO2
• Can be used in conjunction with pulse
oximetry
• Limitations
– Can’t distinguish between metabolic or
respiratory conditions

7.31 35 94 16 -4
Metabolic Acidosis with
Respiratory
Compensation

• -emia refers to pH
– Acidemia, alkalemia
• -osis refers to an abnormal condition or process
– Metabolic alkalosis, respiratory acidosis
Acidotic
Alkalotic

• 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

7.40 / 40 / 100 / 24 / 0
“Normal” Range
pH 7.40 7.35 - 7.45
PaCO2 (mmHg) 40 35 – 45
PaO2 (mmHg) 100 80 – 100
HCO3
- (mEq/L) 24 22 – 26
Base Excess/Deficit (mEq/L) 0 ± 2

Step #1
Look at the pH
7.35 – 7.45

Metabolic Alkalosis
Increase in HCO3, increases
pH

Metabolic Alkalosis
Increase in HCO3, increases pH
Metabolic Acidosis
Decrease in HCO3,
decreases pH

Metabolic Alkalosis
Increase in HCO3, increases pH.
Metabolic Acidosis
Decrease in HCO3, decreases pH.
Respiratory Acidosis
Increase in pCO2, decreases
pH

Metabolic Alkalosis
Increase in HCO3, increases pH.
Metabolic Acidosis
Decrease in HCO3, decreases pH.
Respiratory Acidosis
Increase in pCO2, decreases pH.
Respiratory Alkalosis
Decrease in pCO2, increases
pH

Step #2
Respiratory or Metabolic?
35 - 45 22-26

Step #3
Is there
compensation
and is it
adequate?
Acute
Chronic

Primary Compensation
pCO2HCO3Metabolic acidosis
pCO2HCO3Metabolic alkalosis
HCO3pCO2Respiratory acidosis
HCO3pCO2Respiratory alkalosis
pH

Minute Ventilation
Tidal volume Respiratory Ratex

CNS Depression
Neuromuscular Impairment
Thoracic restriction
Obstruction (late)
Alveoli dysfunction
Perfusion defect
Normal Abnormal

Metabolic Compensation
10:1 10:3
For every 10 mmHg increase of PaCO2,
serum HCO3
- increase by 1 (acute) or 3 (chronic) mEq/L

C ardiac
H ypoxemia
A nemia
M edications
P regnancy
I atrogenic
O bstruction (early)
N eurologic
S tress

Metabolic Compensation
10:2 10:4
For every 10 mmHg decrease of PaCO2,
serum HCO3
- decreases by 2 (acute) or 4 (chronic) mEq/L

pH will change 0.08 for every
10 mmHg change in PaCO2

Step #4
If metabolic acidosis,
calculate anion gap

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

Step #5
If HAGMA,
calculate delta gap

Delta Gap =
AG - 12
24 - HCO3
-
Δ Gap Interpretation
< 0.4 Hyperchloremic NAGMA
0.4-1.0 HAGMA + NAGMA
1.0-2.0 Uncomplicated/Pure HAGMA
> 2.0 HAGMA + metabolic alkalosis/compensation

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

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

Respiratory Compensation
Expected PaCO2
8 + (1.5 x HCO3
-)  2

C ontraction
L icorice
E ndocrine
V omiting
E xcessive NG suction
R inger’s solution
P ost-hypercapnia
D iuretics

Respiratory Compensation
Expected PaCO2
20 + (0.7 x HCO3
-)  5

7.24 / 60 / 74 / 26 / -3
Step 1
Step 2
Acidosis
Respiratory

7.24 / 60 / 74 / 26 / -3
Expected HCO3
- (if acute) =
Expected HCO3
- (if chronic) =
26
30
Expected pH (if acute) = 7.24

7.54 / 25 / 94 / 22 / +3
Step 1
Step 2
Alkalosis
Respiratory

7.54 / 25 / 94 / 22 / +3
Expected HCO3
- (if acute) =
Expected HCO3
- (if chronic) =
21
18
Expected pH (if acute) = 7.52

7.51 / 46 / 102 / 31 / +4
Step 1
Step 2
Alkalosis
Metabolic

37-47 mmHg
7.51 / 46 / 102 / 31 / +4

7.22 / 35 / 87 / 18 / -2
Step 1
Step 2
Acidosis
Metabolic

7.22 / 35 / 87 / 18 / -2 144
5.3
104
18
13
1.1
162
Anion Gap = Na – (Cl- + HCO3
-) 22
1.67
33-39 mmHg

w w w . p a i n e p o d c a s t . c o m

From Artery to Analysis

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