# Interpreting hypoxia on an ABG: PaO2 and SaO2

Let’s say you have a 57 year old patient breathing comfortably on room air, and when you walk in the next morning, he’s suddenly on 6 L O2 by nasal cannula. He doesn’t look like he’s in respiratory distress, but you decide to investigate by getting an ABG.

Result: 7.27/47/68

He is satting 93% on 6 L NC. Is that good? Is that bad? How does his O2 sat compare to the PaO2 on his ABG?

Normal PaO2=80-100 mm Hg. PaO2 is affected by age (tends to be lower) and altitude (tends to be lower).

PaO2 and O2 sat can be related through the oxygen-hemoglobin dissocation curve! See this table for PaO2 to O2 sat conversion. Remember that from first year of med school?

As you can see, under normal conditions, an O2 sat of 90% correlates with a PaO2 of 60 mm Hg  (bonus points if this makes you realize an O2 sat  of 90% is not totally normal, although for sick, hospitalized patients,  it is acceptable). This curve is useful because it shows that giving supplemental O2 is most useful when someone has an O2 sat <90%. The curve also shows that O2 sat falls slower than the PaO2–a change in PaO2 from 96 to 70 may only show up as a change in O2 sat from 97% to 92%.

FiO2 can also affect an ABG reading. The PaO2 on your ABG should equal FiO2 x 500. If it doesn’t, there’s probably an A-a gradient. The PaO2/FiO2 ratio (or P/F ratio) is useful for categorizing hypoxia as potentially severe (when applied to ARDS).

So what about the patient above? His PaO2 of 68 mm Hg correlated perfectly with an O2 sat of 93%. However, he was also on 6 L NC, and the FiO2 was 40%. This implied that there was a significant A-a gradient

Random notes below:

Why are air bubbles bad? The PO2 of room air is 150 mm Hg, which means any air bubbles trapped in the ABG sample will shift the oxygen value towards 150 mm Hg.

When does the ABG have to be put on ice? If it can’t be processed in 15 minutes. (Residual blood cells will continue to use oxygen and make the PaO2 seem lower than it really is.) An ABG on ice can still be analyzed for up to an hour after collection.

If I get a value like PaO2=213, what does that mean?! At least you know the patient’s not hypoxic? PO2 is measured directly via electrode. The electrode is calibrated for values between 0-140. Therefore values >150 are of unclear accuracy. Remember that FiO2 affects the value as well.

Sources:

UC Denver handout

Clinical Methods (E.P. Trulock III)

American Nurse Today

# What is a capping trial?

A capping trial is performed when you are considering decannulating (removing) a patient’s tracheostomy tube. It is often the final step before someone is able to breathe completely on their own again. It is a test of whether the patient can control secretions and feel comfortable breathing “normally.”

Who can undergo a capping trial?

• Anyone who has been successfully weaned from the vent for a good amount of time
• At most, they should be on 40% O2
• Secretions are not excessive
• Patients’ cuffs must be deflated (an inflated cuff will not allow ANY passage of air)

How does the capping trial work?
There is no standardized protocol. Like many aspects related to vent management, this varies by institution. This was a QI study at Hopkins on the creation and implementation of a capping trial protocol. There were two different options:

• Cap x24 hours and decannulate if successful (2 days)
• Cap x12 hours, rest, cap x24 hours, then decannulate if successful (3 days)

Patients should be monitored for signs of respiratory distress during the capping trial.

This trach weaning form created by St. George’s Hospitals gives you a sense of how to think about the final steps towards decannulating a trach:

# Can you run a pressor through a peripheral IV?

We’ve all heard horror stories of patients getting digital necrosis from peripheral pressors:

However, the data shows that you CAN run pressors safely through peripheral IVs with close monitoring and proper selection of an IV site. How?

The Journal of Critical Care from 2015 reviewed the available literature of the use of peripheral pressors in adults.This review concluded that there are very rare side effects in the first 6 hours of use, and that best practice is to place IVs in veins >4 mm in diameter (use an ultrasound to confirm!) and monitor at least every 2 hours for extravasation. There was poor quality data reporting adverse outcomes from site of administration of pressors–out of 85 studies included, there was only one randomized study. Furthermore, as this study notes, the rate of adverse effects is low when a good-sized vein in the forearm is used, and pressors can be restarted at another peripheral site when extravasation does occur.

# What’s the difference between dobutamine and dopamine?

These two medications SOUND similar, but are in different categories.

 Dobutamine Dopamine Class Inotrope Vasopressor Receptors affected B1 agonist A1 agonist (dose dependent) Effect Increased cardiac contractility Vasoconstriction, increased systemic vascular resistance Common uses “Tailored therapy” for heart failure, ?septic shock Septic shock (>8), cardiogenic shock (4-7), promoting urine flow (0.5-3) Side effects Tachycardia, may even cause hypotension (mild vasodilation), do not use in patients with HOCM Tachycardia/VT, tachyphylaxis, ischemic limb necrosis (do not give through a peripheral IV)

# How to manage chest tubes (5-minute version)

I am no expert in chest tubes, and will add the caveat that for this particular post I really hope everything is correct! If it’s not, let me know! See this post on the different kinds of chest tubes. This is a great but long nursing resource from RN.com.

You’ve placed a chest tube: great! Now you hook it up to some weird box thing that is called a drainage system…now what? Knowing how chest tubes used to work helps you understand the box thing.

This picture is taken from a truly excellent little video on how chest tube drainage works:

There used to be 3 separate bottles hooked up to the chest tube itself: Bottle #1 is where the patient’s empyema fluid or blood leaked into. Bottle #2 is the waterseal: air is forced to travel through water and can only move in one direction (it cannot move back into the patient). Bottle #3 sets suction power based on how much water is in the bottle–more water=less suction, less water=more suction, and you need to make sure the suction power is just right. You can see how the drainage system has evolved over time on the right.

Should patients be “placed to waterseal” or “placed to -20 suction?”

“Place to waterseal”= don’t be too crazy with drainage, which is appropriate for most pleural effusions or a mild pneumothorax. If the lung is not fully expanded, you can “turn up the suction.”If you apply suction too aggressively, you put the patient at risk for re-expansion pulmonary edema.

How do I know if there is an “air leak” and what the heck does it mean?

An air leak is present if there is bubbling in the waterseal chamber when the suction is clamped/on waterseal–this indicates there is still air flowing from the chest to the tube. Positive pressure coming from the pleural space=air getting into the pleural space. Intermittent bubbling with expiration (when pleural pressure is highest in the non-ventilated patient) may be normal, but a continuous air leak is pathological and means the patient is not ready to have their chest tube pulled!

You can “clamp” the tubing, which should stop an air leak. If the air leak persists even with clamping, consider:

• ruptured bleb (severe emphysema)
• simple traumatic pneumothorax (from placing the chest tube)
• a leak in the actual tubing system
• mechanical ventilation (may see decreased tidal volumes, failure of PEEP increase)
• bronchopleural fistula (usually more severe or continuous)
• lung entrapment vs. trapped lung

NB: if your patient has a persistent air leak, think twice about pulling their chest tube because if you do, you may cause a recurrent pneumothorax.

What is “tidaling?”

You may see movement in the waterseal chamber with respiratory variation. It’s the water being sucked back towards the lung with inspiration due to negative inspiratory pressure. (In mechanically ventilated patients, it’s the opposite.)

How do I know when the tube can be taken out?

In a 2013 study out of Michigan State, the team found it is reasonable to remove chest tubes when drainage <200 ml/day, on waterseal, with no air leak. In stable patients on the floor, theoretically you don’t need a chest x-ray after removal, but given our litigious society, everyone gets one. In mechanically ventilated patients, you should get a chest x-ray 1-3 hours after removal. However there is no need for regular surveillance chest imaging while a patient has a chest tube in.

What do I do if the tube falls out?

Use common sense: cover the area and prepare to re-insert a chest tube. Maintain sterility. The patient is at risk of a tension pneumothorax, so someone should stay with them for close monitoring. More troubleshooting at this nursing website.

# What is vent dyssynchrony?

One of the problems that is not uncommon in patients on ventilators is correcting for “vent dyssynchrony.” Vent dyssynchrony is when the patient’s demand for oxygen is not being met by the ventilator.

Why? Consider three factors:

• LENGTH OF BREATH (how long is inspiration?)
• TIMING OF BREATH (when is the switch to expiration/inspiration?)
• ADEQUATE FLOW (how big are the volumes?)

If there are problems with any of those things, dyssynchrony can result. Dyssynchrony results in those annoying beeps you hear from the vent. This is called “triggering the vent.” This can happen if:

• ineffective triggering: PEEP is too high, musculoskeletal weakness
• inappropriate triggering: tidal volume is too low, inspiratory time is too short or flow is too low, coughing or hiccups
• autotriggering: coughing, hiccups, shivering, seizures

What should you do about it? The best thing would be to correct the underlying problem. You may have to change the vent setting, the flow rate or tidal volume, or the insp/exp times. Sometimes, all you need to do is change the trigger sensitivity threshold!

As with many of my posts, I turn to Life in the Fast Lane as a reference.

# When should the cooling protocol be used as part of ACLS?

“Cooling” is based on the theory that hypothermia can help stabilize patients in cardiopulmonary arrest and improve neurological outcomes.

Cooling should be started as soon as possible when applied (within 6 hours). It should be used in non-traumatic cases of cardiac arrest when ROSC is obtained within 30 minutes. There should be a low GCS and NO purposeful movement. Female patients should not be pregnant.

Parameters to use when titrating temperatures:

• MAP >65 or 90 when concerned about ICP
• PCO2 35-45
• FiO2 > 94%
• RASS -5
• EEG monitoring

You should be able to see a J-point on EKG:

Potential complications:

• Shivering and seizures (can use paralytics if there is concern this is causing respiratory complications. I’ve heard of surgeons using meperidine but haven’t done this myself)
• Hypo/hyperglycemia
• Skin injury from the pads
• Sepsis
• Rhabdomyolysis