Question about Desaturation

So here we go. Fever will affect SV02, which is your venous O2 sat. Tachypnea shouldn't affect it. Tachycardia shouldn't either, less the tachycardia is sufficient to cause decompensation and hypotension (which is going to be profound tachycardia...170+?).

The reason hypotension is the answer has to do with the lungs. Basically the lungs are divided into 3 zones of oxygenation. In the apex of the lungs, the pressure inside the lungs is higher than capillary pressure, so the lungs tamponade the capillaries off. Almost zero oxygenation goes on there. In the middle zone of the lungs, lung pressure is roughly equal to capillary pressure, and some oxygenation occurs throughout. The majority of oxygenation occurs in the lung bases, where the pressure inside the lungs is lower than capillary pressure, allowing for consistant O2 exchange. Now, the location of these lung "zones" is relative and can shift based on blood pressure. A person with higher blood pressure can oxygenate closer to the apex (because of capillary pressure being increased). A person who is hypotensive will not utilize as much lung for oxygenation, thus decreasing SpO2.

The patient is vented, so the breaths are adequate. Taking deep breaths might put more air in the lungs, but a hypotensive patient can't move the air across the capillary membranes so it's a problem of exchange.

Edit: I think swirlything is right. Haha, long explanation which answers a sort of different question.

I think the question is asking what would give you a reading that is not accurate. Yes, breathing more will increase SaO2... but the reading will be accurate. However if there is less blood at the extremeties for the sensor to read, you may get a falsely low reading.

So here we go. Fever will affect SV02, which is your venous O2 sat. Tachypnea shouldn't affect it. Tachycardia shouldn't either, less the tachycardia is sufficient to cause decompensation and hypotension (which is going to be profound tachycardia...170+?).

The reason hypotension is the answer has to do with the lungs. Basically the lungs are divided into 3 zones of oxygenation. In the apex of the lungs, the pressure inside the lungs is higher than capillary pressure, so the lungs tamponade the capillaries off. Almost zero oxygenation goes on there. In the middle zone of the lungs, lung pressure is roughly equal to capillary pressure, and some oxygenation occurs throughout. The majority of oxygenation occurs in the lung bases, where the pressure inside the lungs is lower than capillary pressure, allowing for consistant O2 exchange. Now, the location of these lung "zones" is relative and can shift based on blood pressure. A person with higher blood pressure can oxygenate closer to the apex (because of capillary pressure being increased). A person who is hypotensive will not utilize as much lung for oxygenation, thus decreasing SpO2.

The patient is vented, so the breaths are adequate. Taking deep breaths might put more air in the lungs, but a hypotensive patient can't move the air across the capillary membranes so it's a problem of exchange.

Edit: I think swirlything is right. Haha, long explanation which answers a sort of different question.

Yes finally an answer with a scientific rationale. They never taught us these things in nursing school..

Be_Moore, so SaO2 is directly affected by how much O2 you are breathing in correct? But if O2 sats drop when perfusion and diffusion at the lungs is not a problem then we have to look at other causes?

When someone desats when I turn and position them what is the most probable cause of this phenomenon?

Rationale: Hypotension, hypothermia, and vasoconstriction may alter pulse ox values by reducing arterial blood flow. Likewise movement of the finger to which the oximeter is applied may interfere with interpretation of SaO2.

Taking deep breaths will not change the reading the Pulse Ox gives you because in hypotension, hypothermia ( think vasocontriction) and vasocontriction the problem is with circulation to the area where the pulse ox is, not necesarily with oxygenation. This is meant to be a vary basic question...arteries are the pipes and the pulse ox tells you how much O2 is attched to the Hgb in the RBCs going through that pipe. If the pipe is blocked the reading is going to be inaccurate due to the decreased circulation. You can take deep breath and even mechanically ventilate this patient and the reading in that extremity that is "blocked" or hypoperfused will not improve significantly. An ABG can give you a much more accurate O2 level for that patient.

I think the question was worded poorly. Many things will alter the pulse ox value, but only one of those answers will alter it in a way that may make the reading inaccurate.

Let's complicate this a bit more, LOL. Technically, all of the above will at least indirectly effect the pulse oximetry values. As stated pulse oximetry is a non invasive method of monitoring the amount of hemoglobin that is bound with oxygen. However, we may be able to assume a few things from the clinical findings and labs.

There exists a concept known as the oxyhemoglobin dissociation curve. It describes the relationship of PO2 and SaO2, and hemoglobin's affinity for oxygen. Why is this important? Well if hemoglobin has a low affinity for oxygen, it is safe to assume we may have a difficult time loading oxygen onto hemoglobin. If the affinity is high, we may have a difficult time unloading oxygen. Obviously, the best case scenario is hemoglobin with a high affinity in the lungs (wants to on-load), and lower affinity in the body tissues (wants to offload). Typically, a molecule known as 2-3-DPG and acid base changes of blood keep this process in check. You can research the Bohr effect and reverse Borh effect for additional information.

So let's talk about low versus high affinity conditions

Low affinity conditions are known as a RIGHT SHIFT. You can see this shift on a graphical representation of the curve.

Right shift = Hemoglobin wants to RELEASE oxygen (Low affinity)

-Raised Temp

-Raised Acids (Acidosis)

-Reduced Oxygen

-Raised 2-3-DPG

Left shift = Hemoglobin wants to LOCK onto oxygen (High affinity)

-Low Temp

-Low Acids (aLkalosis)

-Low 2-3-DPG

So, an example of this in action might be a head injury. Lets say we intubate and ventilate the heck out of our head injury patient. So much we induce a respiratory alkalosis. This will shift the curve left and potentially create a situation where hemoglobin will not want to release oxygen to the ischemic brain tissue. The pulse oximeter may be reading 100%; however, that oxygen is not being effectively offloaded to the tissue.

Let's look at your examples:

Fever----> Right Shift

Tachypnea---> Possible Left Shift in the absence of an underlying metabolic derangement

Tachycardia---> Variable depending on the underlying problem

Hypotension---> Possible Right Shift with anaerobic metabolism and profound lactic acidosis

NOTE OF CAUTION!

This is supplemental material and using these advanced concepts will most likely cause you to fail the NCLEX. The NCLEX tests fairly basic concepts, therefore go with what you study for your NCLEX answers. In addition the rational regarding hypotension is correct.