You bet.

A lot has changed with lipid management since Frankly Speaking began podcasting back in 2017.

You know, back then we were just starting to use the pool cohort equations for assessing cardiovascular risk.

Prior to that, the main tools had been models derived from data from the Framingham Heart Study.

And so there was the Framingham 10-year risk score.

And none of the data that those models were based on came from randomized controlled trials.

It was all cohort data.

What are some of the main differences between those two?

You bet.

A lot has changed with lipid management since Frankly Speaking began podcasting back in 2017.

You know, back then we were just starting to use the pool cohort equations for assessing cardiovascular risk.

Prior to that, the main tools had been models derived from data from the Framingham Heart Study.

And so there was the Framingham 10-year risk score.

And none of the data that those models were based on came from randomized controlled trials.

It was all cohort data.

What are some of the main differences between those two?

You

bet.

A lot has changed with lipid management since Frankly Speaking began podcasting back in 2017.

You know, back then we were just starting to use the pool cohort equations for assessing cardiovascular risk.

Prior to that, the main tools had been models derived from data from the Framingham Heart Study.

And so there was the Framingham 10-year risk score.

And none of the data that those models were based on came from randomized controlled trials.

What are some of the main differences between those two?

You

bet.

A lot has changed with lipid management since Frankly Speaking began podcasting back in 2017.

You know, back then we were just starting to use the pool cohort equations for assessing cardiovascular risk.

Prior to that, the main tools had been models derived from data from the Framingham Heart Study.

And so there was the Framingham 10-year risk score.

And none of the data that those models were based on came from randomized controlled trials.

What are some of the main differences between those two?

What was recommended with regards to testing and what's new about that?

So I'll cover a couple of things.

There's a lot, again, there's so much in this guideline, we're going to be obviously somewhat selective in what we cover, but they do recommend a single lipid profile before adolescence to look for familial hypercholesterolemia.

The rate of familial hypercholesterolemia is somewhere between 1 in 250 and 1 in 300.

So we're talking about something relatively rare.

However, the logic is that atherosclerosis is is something that takes decades to develop, and the duration of exposure to high LDL is correlated with atherosclerotic cardiovascular disease.

So picking this up early and intervening at the very least with lifestyle interventions seems appropriate, and I think that seems reasonable.

How are we going to incorporate them into our clinical decision making?

How exactly does a pulse ox work, and what are some of the factors that can cause it to be inaccurate?

The pulse oximeter projects light at two different frequencies into the vascular bed.

Oxygenated blood has higher absorption of infrared light, so by projecting one frequency in the visual spectrum, and one in the infrared spectrum, a calculation can be done that can determine the percent of oxygenated hemoglobin.

Now, there are a variety of things that can cause a false reading, including abnormal hemoglobins, such as in patients with thalassemia or sickle cell disease.

Cigarette smoking tends to elevate the pulse ox reading from what it otherwise would be.

If the patient's moving, so a patient who's got tremors or a patient having rigors, that can also affect the reading.

That tends to cause a low reading, as does severe anemia, hyperbilirubinemia, or even fingernail polish.

How clinically significant is this?

How exactly does a pulse ox work, and what are some of the factors that can cause it to be inaccurate?

The pulse oximeter projects light at two different frequencies into the vascular bed.

Oxygenated blood has higher absorption of infrared light, so by projecting one frequency in the visual spectrum, and one in the infrared spectrum, a calculation can be done that can determine the percent of oxygenated hemoglobin.

Now, there are a variety of things that can cause a false reading, including abnormal hemoglobins, such as in patients with thalassemia or sickle cell disease.

Cigarette smoking tends to elevate the pulse ox reading from what it otherwise would be.

If the patient's moving, so a patient who's got tremors or a patient having rigors, that can also affect the reading.

That tends to cause a low reading, as does severe anemia, hyperbilirubinemia, or even fingernail polish.

How clinically significant is this?