Arterial Blood Gases are the gold standard in measuring pH, PaO2, PaCO2 and bicarbonate as indicators of overall respiratory and metabolic health. People seem to make a big deal out of getting an arterial blood gas. You find a pulse you put a needle in it. It’s not rocket science.
Tangent: Rocket science isn’t even really, idiomatically, rocket science. It’s simple trajectory and angles and trigonometry. It is firmly rooted in Newtonian physics. You want real “Rocket Science” in a metaphorical sense go for quantum physics. I now declare the phrase “It’s not rocket science” obsoleted and to be permanently replaced with the phrase “It’s not quantum physics”
Double Tangent: In rocket science if you go off on a tangent, you fall out of orbit and fly eternally into deep space. Which is the perfect metaphor for where this article has gone.
Anyhoo… back to ABGs. Different hospitals have different care protocols and cultures. In some places ABGs are as common as MRSA in others, they are a rare order. In places like the latter, VBGs are often used as proxy. But how exactly does VBG information correlate to ABG information?
First lets start with the basics of ABGs. They are easy to interpret. It’s not rocke…er… quantum physics.
Normal values are:
pH: 7.35 to 7.45
PaCO2: 35 to 45 mmHg
PaO2: 80 to 100 mmHg
SaO2: 93 to 100%
HCO3: 22 to 28 mEq/L
Fun Fact: Some people use mmHg and torr interchangeably as units. They are not exactly the same. However the margin of difference is so tiny, less than 0.000015%, that this indulgence can be forgiven with a simple haughty eyeroll.
Fun Fact 2: mEq, milliequivalents, are the atomic weight of each of the atoms in a compound divided by the valence. The valence is the combining power of the compound based on the absolute value of the number of extra or missing electrons in the molecules outermost valence shell which dictates acidity or alkalinity. Por ejemplo, HCO3– has a valence of 1. Negative and positive represent extra or missing electrons and anions and cations respectively. And that’s more than you ever need to actually know. It’s not exactly quantum physics, but easily as difficult as rocket science. But if you are curious, here’s a great tutorial:
Starting with oxygenation, if the PaO2 is low, you need to get more oxygen to the patient. Giant Duh. For a mechanically ventilated patient, this means two things: Increasing the PEEP or increasing the FiO2.
PaO2 can also be too high implying over-oxygenation. Breathing 100% O2 at sea level (760 mmHg), then your Alveolar partial pressure of O2, PAO2, is 760 mmHg. At 100% humidity water vapor has a partial pressure of 47. So subtract that out and we are left with the gas pressure of 713. The partial pressure of O2 in the blood is always lower than the partial pressure of O2 in the alveoli, otherwise it would flow in the wrong direction. The difference between these pressures is called the A-a gradient, and normal values depend on age. The equation to approximate this gradient is ((age/4) + 4)). Therefore an adult at age 40 has a gradient of 14. At 100% oxygen at sea level, his PaO2 would max out at 713-14, or 699 mmHg. My philosophy in life is “Math not Meth”.
If your patient has a PaO2 of 699, you are doing something very, very wrong. Oxygen toxicity. It’s a thing. Look it up. Actually I already looked it up for you. I’m nice that way. Horse to water. Here, take a drink:
Now onto ventilation which is slightly more complicated than oxygenation but still not quantum physics. Ventilation is about the removal of CO2 from the blood which affects the pH. An abnormal pH is either the result of a respiratory problem, meaning the patient is retaining or exhaling too much CO2, or it is a metabolic problem.
Differentiation between respiratory and metabolic derangements can be accomplished by simply comparing the PaCO2 with the pH. With respiratory issues, the pH and PaCO2 move in opposite directions. With metabolic issues, they move in the same direction. Easy as pie. Not irrational like pi.
If the problem is metabolic there is often respiratory compensation and, conversely, if the problem is respiratory, there is often metabolic compensation. Compensation can bring the pH back into the normal range. But generally the body does not overcompensate. So if your HCO3 and PaCO2 are both out of the normal range, whichever side of 7.40 the pH lands tells you if we are compensating from acidosis or alkalosis and whether or not the problem is primarily respiratory or metabolic. It CAN be both. But one will usually be dominant.
Here’s a nifty chart I made just for you. I’m a giver. I give and I give and I give.
|Respiratory Alkalosis with metabolic compensation||↑||↓||↓|
|Respiratory Acidosis with metabolic compensation||↓||↑||↑|
|Metabolic Alkalosis with respiratory compensation||↑||↑||↓|
|Metabolic Acidosis with respiratory compensation||↓||↓||↑|
So that’s the nitty-gritty, the lowdown, the brass tacks, the ABCs of ABGs. If you’re an RT none of this should have been new to you. However, if you’re education was like mine, a lot of time was dedicated to the interpretation of ABGs and VBGs were overlooked like an unwanted stepchild on Christmas morning. Santa loved ABG. VBG wept quietly in the corner, neglectedly nibbling on a shriveled fig that fell from the crowded plate of a drunken uncle.
VBG’s, not surprisingly, also have a set of normal values:
pH: 7.31 to 7.41
PaCO2: 41 to 51 mmHg
PaO2: 30 to 40 mmHg
HCO3: 23 to 29 mEq/L
When it comes to correlation between VBGs and ABGs there have been quite a few studies.
Studies show is that there is a strong reliable correlation between arterial and venous pH. That difference being ~.035, venous being obviously more acidotic due to the exchange of O2 for CO2 at the capillaries.
It gets more complicated when dealing with PaCO2. The correlation is good with normocapnia. PvCO2 is 100% specific in ruling out arterial hypercapnia with the cutoff being < 45 mmHg and 100% sensitive for detecting hypercapnia if > 45 mmHg. However, above 45 mmHg the correlation becomes less and less predictable so an actual measurement of PaCO2 cannot be calculated in a hypercapnic patient.
PaCO2 and PvCO2 are non-correlative in severe shock and in hypocapnic patients.
Good correlation. Arterial HCO3 can be reliably calculated by simply subtracting ~1.5 from the venous HCO3
Here’s where VBG’s fail us. These values have poor correlation. However, with SpO2’s handy everywhere we can still assess for adequate oxygenation. We cannot however, determine the PaCO2 which in many patients, is helpful to know. Notably, ARDS patients for who the PaO2/FiO2 ratio is both a diagnostic tool, and a helpful marker to trend for treatment success or failure.
In summary, we may need ABGs a lot less often than we tend to think. They are essential for patients in severe shock and patients with ARDS, both populations commonly already having an arterial line in place. And also to determine the specific PaCO2 in patients who are hypercapnic.
Maybe we’ve spent too long needling VBG’s when VBG’s can make a fine point. Stop groaning. That’s how I amuse myself.