The argument against ABGs

The argument for venous blood gases instead of arterial blood gases

Something we've been discussing at Shoreline Medical recently is the possibility of doing fewer
arterial blood gases (ABG) and more venous blood gases.

Sure an ABG is necessary when monitoring a patient in respiratory distress, although for the most part, there really isn't any more information you can obtain in an ABG that you can't simply obtain from a venous blood gas, coupled with end tital CO2 monitoring (ETCO2) and oxygen saturation (SpO2) monitoring.

Consider you have a patient with diabetes. The doctor wants to determine pH. If a pH is all the doctor wants, then a venous blood gas will work just great, as venous and arterial pHs are basically the same.

A 1998 study (as noted in this article from Emergency Medicine) found that in patients with diabetic keto acidosis, the venous pH was remarkably similar to the arterial pH.

Our Sepsis protocol calls for any patient suspected of having Sepsis to have an ABG. The reason is to get a baseline pH. Since this is the only reason, a venous blood gas would suffice.

The same with overdose patients. Poison control wants an ABG to be drawn when certain medicines are overdosed on. The reason is to check for pH. This is another example when a venous poke would suffice.

Think about it though. A venous poke is much less invasive and risky as an arterial poke, and the lab is in the room of the patient anyway drawing all the other labs. So, then it would be much better on the patient just to have all labs, including ABG, on just one poke.

In fact, according to Emergency Medicine, "When Is Venous Blood Gas Analysis Enough?" (38(12):44-48, 2006), revealed that a study performed in 1996 determined that most patients said a venous poke was about half as painful as an arterial poke.

You have a patient on a ventilator. Currently our protocol calls for daily ABGs. Our medical director is presently trying to convince the medical staff where I work that serial ABGs are not needed. What is needed is a continuous pulse oximeter and an end tidal CO2 monitor.

Then, 30 minutes to an hour after intubation, an ABG should be drawn just to get your baseline pH and to make sure the ETCO2 monitor and SpO2 correlate with the actual PO2 and CO2. That's it. From then forth all you need is daily venous pH. To monitor PO2, all you have to do is monitor the SpO2 and ETCO2.

A normal SpO2 is 90 or better. According to the oxyhemoglobin association curve, the PO2 is 30 less than the SPO2, therefore an SPO2 of 90% is equivelent to an SpO2 of 60, and an SpO2 of 80 correlates to a PO2 of 50. So there you have it.

Thus, according to the oxyhemoglobin disassociation curve, the formula goes like this (SPO2 minus 30 = PO2):

SPO2 of 90 = a PO2 of 60
SPO2 of 80 = a PO2 of 50
SPO2 of 70 = a PO2 of 40

It's basically called the 4-5-6-7-8-9 rule.

As far as monitoring CO2, all you have to do is monitor ETCO2. As the ETCO2 rises and falls, so to does the PCO2. A normal ETCO2 would be 30 to 50. Unless the patient is a CO2 retainer, all ETCO2 results greater or less than that should be reported to the physician.

Basically, if you have a patient who is not in respiratory distress, an ABG is never needed.

The proof

The toughest argument I've had is convincing doctors that a venous pH is basically the same as arterial pH. I remember once being called to do a stat ABG on a patient, and the pH on the patient was 6.78 and the CO2 was 75. The doctor was convinced I got venous blood and wanted me to redraw.

I took the gas to a second doctor, and he too was convinced I had obtained venous blood. I knew I had arterial not just by how forcefully the blood entered the syringe, but because the bicarb was 33 which shows the patient was probably a CO2 retainer to start with. Yet the doctors made me redraw the ABG. Of course it came out exactly the same, and they once again were convinced I had venous blood.

So the debate is ongoing. Yet, as you can tell by the picture, venous and arterial pH are essentially the same in a healthy patient. Why doctors are so convinced there is a major difference between the two is beyond me. Likewise, the bicarb (HCO3) is essentially the same too.

The only major difference is PO2, which can be monitored by saturations, which is completely non-invasive. There is no reason to ever draw an ABG just to prove that the PO2 is low. Again, all you have to do is subtract 30 from the SpO2 and you have your PO2.

The Emergency Medicine article notes a study done way back in 1985 that basically proved that "a venous pH of 7.25 or higher predicted an arterial pH of 7.2 or higher in 98% of all cases, which makes VBG testing valuable as a screening procedure.If the results are normal, ABG analysis should not be necessary. Conversely, abnormal venous levels predicted abnormal arterial values, but again in a nonlinear fashion. A venous pH of 7 or lower, for example, predicted an arterial pH of 7.2 or lower in 98% of cases. "

Here's another catcher the Emergency Medicine article notes. I have tried to convince doctors for years that an ABG is not needed during a code because if a patient is not breathing you already know the pH is low. Likewise, regardless of what the ABG shows, it's not going to alter what you do to try to save the life of the patient. So there is no need to rush to do an ABG.

In other words, you do not need to do an ABG to diagnose hypoxemic respiratory failure when the patient is showing obvious signs of hypoxemic respiratory failure.  Attempts to draw blood only delay treatment, and this can only increase morbidity and mortality.

The article is the first I've found that attempts to prove my point. It notes the following:

In cardiac arrest victims, the disparity between arterial and venous values is even greater. During cardiac arrest, tissue hypoxia is all but a certainty and is reflected by the lower pH and higher PCO₂ on the venous side. A 1986 study by Weil demonstrated a significantly lower pH in venous samples (mean, 7.15 vs 7.41 in arterial samples) and a significantly elevated PCO₂ (mean, 74 mm Hg vs 32 mm Hg) in these patients. In clinical practice, however, knowledge of either the arterial or venous pH or PCO₂ during cardiac arrest does not alter management, making the debate less relevant.

What's most interesting is my point was proven way back in 1986. Why is this information not translated in medical school? Yet, regardless, the argument is simple, that ABGs are needed sometimes to help a physician manage the care of a patient, yet more often than not a VBG will suffice.