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<v Speaker 1>Usually when we talk about a medical diagnosis, there's this

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<v Speaker 1>expectation of total precision.

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<v Speaker 2>Oh, absolutely, like it's engineering or something.

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<v Speaker 1>Right, Like you break your arm, they take an X

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<v Speaker 1>ray and it shows that jagged white line and the

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<v Speaker 1>doctor just points and says, well, there it.

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<v Speaker 2>Is broken, clean and simple.

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<v Speaker 1>Yeah, it's binary. It gives everyone in the room this

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<v Speaker 1>massive sense of comfort because we like things to be

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<v Speaker 1>visible and easily categorized, you.

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<v Speaker 2>Know, we really do. But then you step into the

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<v Speaker 2>world of cardiac electrophysiology. Oh boy, yeah, you walk into

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<v Speaker 2>a chaotic emergency department and suddenly that pristine diagnostic clarity

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<v Speaker 2>it just vanishes.

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<v Speaker 1>It really does. We're looking at a landscape that is well, honestly,

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<v Speaker 1>it's murky.

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<v Speaker 2>It is the absolute definition of diagnostic muddy waters. I mean,

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<v Speaker 2>navigating those waters is exactly what we are going to

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<v Speaker 2>do today, and.

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<v Speaker 1>That unpredictable landscape is exactly why we're doing this deep

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<v Speaker 1>dive today. We are tearing into John R. Hampton's classic

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<v Speaker 1>text one hundred and fifty ECG Problems specific the fourth

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<v Speaker 1>edition from twenty thirteen.

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<v Speaker 2>A legendary book.

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<v Speaker 1>It really is. Yeah, and whether you're you know, a

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<v Speaker 1>medical studient, cramming for exams, or a junior doctor finding

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<v Speaker 1>your feet on the wards, or.

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<v Speaker 2>A paramedic making those split second calls in the back

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<v Speaker 2>of an ambulance.

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<v Speaker 1>Exactly, or even just a fiercely curious learner. You are

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<v Speaker 1>in the right place, because we're not just looking at

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<v Speaker 1>christine textbook squiggles today.

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<v Speaker 2>No, we're looking at the messy, chaotic, real world signals

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<v Speaker 2>that actually save lives.

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<v Speaker 1>Right. But before we even look at a single trace,

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<v Speaker 1>I think we need to establish the foundational premise of

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<v Speaker 1>Hampton's entire text.

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<v Speaker 2>Yeah, the golden rule, if you will, which is that

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<v Speaker 2>recording and reporting an ECG should never ever be an

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<v Speaker 2>end in itself.

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<v Speaker 1>Never.

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<v Speaker 2>I mean, it is a fundamental, cheap and totally harmless tool,

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<v Speaker 2>and it gives us this electrical information that we literally

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<v Speaker 2>cannot obpain in any other way. But it is absolutely

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<v Speaker 2>no substitute for taking a proper medical history and performing

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<v Speaker 2>a careful physical examination.

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<v Speaker 1>Yeah, and the structure of the book itself actually reinforces

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<v Speaker 1>that golden rule. It's designed to bridge the gap between

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<v Speaker 1>theoretical learning and clinical reality.

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<v Speaker 2>By presenting one hundred and fifty cases completely randomly.

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<v Speaker 1>Yes, you turn the page and you have no idea

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<v Speaker 1>what is coming next.

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<v Speaker 2>Which mimics the reality of A and E perfectly, because

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<v Speaker 2>patients don't walk through the hospital doors in order of

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<v Speaker 2>diagnostic difficulty right now.

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<v Speaker 1>No, they definitely do.

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<v Speaker 2>Not, and they don't arrive grouped by pathology. You don't

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<v Speaker 2>get a neat sequence of atrial fibrillation cases on a

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<v Speaker 2>Tuesday morning. That would be nice, but no, right, The

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<v Speaker 2>randomness maintains your clinical vigilance. You have to interpret the

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<v Speaker 2>data fresh every single time.

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<v Speaker 1>And Hampton also grades each case by difficulty to help

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<v Speaker 1>you gauge where you stand. So one star is for

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<v Speaker 1>the medical student.

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<v Speaker 2>Level, the classic presentations, right, this.

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<v Speaker 1>Stuff anyone who has read the basic theory should catch.

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<v Speaker 1>Then two stars step up the complexity for junior doctors,

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<v Speaker 1>specialist nurses or paramedics.

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<v Speaker 2>And the three star cases.

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<v Speaker 1>Yeah, those are the tough ones.

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<v Speaker 2>Those are designed to challenge MRCP candidates trying to gain

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<v Speaker 2>memptyship of the Royal Colleges of Physicians.

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<v Speaker 1>Exactly. So, you read the brief clinical scenario and you

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<v Speaker 1>have to interpret the ECG before you even know if

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<v Speaker 1>you're looking at a one star layup or a three

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<v Speaker 1>star nightmare.

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<v Speaker 2>And part of what makes those real world cases nightmarriage

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<v Speaker 2>is the physical state of the tracing itself.

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<v Speaker 1>Oh, the artifacts.

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<v Speaker 2>Yeah. In a textbook, an ECG trace is this beautiful,

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<v Speaker 2>smooth black line on a crisp pink grid, perfect baseline right.

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<v Speaker 2>But Hampton intentionally includes technically poor records, records filled with

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<v Speaker 2>artifact and baseline wander because.

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<v Speaker 1>In a clinical setting you were often dealing with patients

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<v Speaker 1>who are shivering or sweating, or moving in pain.

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<v Speaker 2>Or in extreme respiratory distress. You rarely get a perfect tracing,

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<v Speaker 2>and you just cannot afford to wait for one. You

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<v Speaker 2>have to interpret what is in front of you.

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<v Speaker 1>So let's pull a specific piece of evidence from the

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<v Speaker 1>text to illustrate this. Let's look at ECG one th two.

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<v Speaker 1>The presentation is a thirty year old woman admitted to

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<v Speaker 1>the hospital with diabetic ketoacidosis.

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<v Speaker 2>pKa a profound acute metabolic crisis right, and.

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<v Speaker 1>Her ECG is described as not being a technically good record.

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<v Speaker 1>It exhibits considerable artifacts. The baseline is jumping all over

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<v Speaker 1>the place.

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<v Speaker 2>But you can't just throw your hands.

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<v Speaker 1>Up exactly looking through the noise. The rhythm is identified

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<v Speaker 1>as probably being sinus, but with coupled junctional extra systelase.

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<v Speaker 2>Which is a huge finding.

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<v Speaker 1>Yeah, and I don't want to just gloss over that.

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<v Speaker 1>We have a patient in DKA and her AV node

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<v Speaker 1>is getting irritable, firing off its own beats early. Why

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<v Speaker 1>is DKA causing junctional extra systelase.

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<v Speaker 2>Well, it really comes down to the cellular environment. Diabetic

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<v Speaker 2>ketoacidosis doesn't just mean high blood sugar.

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<v Speaker 1>Right, it's the acid.

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<v Speaker 2>Yeah, it means profound systemic acidosis and massive electrolyte shifts,

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<v Speaker 2>particularly potassium.

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<v Speaker 1>So what happens to the potassium.

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<v Speaker 2>The lack of insulin and the acidic environment forced potassium

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<v Speaker 2>out of the cells and into the bloodstream, even.

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<v Speaker 1>Though the total body potassium is actually being depleted through

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<v Speaker 1>the urine exactly.

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<v Speaker 2>And this constant shifting of potassium across the cardiac suum

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<v Speaker 2>membranes directly alters the resting membrane potential.

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<v Speaker 1>Okay, so they get twitchy, highly twitchy.

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<v Speaker 2>The myocardial cells, particularly in secondary pacemaker sites like the

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<v Speaker 2>AV junction, become hyper excitable. They reach their threshold potential

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<v Speaker 2>prematurely and fire off an impulse before the sinus node

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<v Speaker 2>gets a.

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<v Speaker 1>Chance and boom, that's your junctional extra system, got it?

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<v Speaker 1>And what about the P waves on this trace? The

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<v Speaker 1>text notes they are really difficult to identify here, appearing

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<v Speaker 1>almost completely flattened.

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<v Speaker 2>Well, the technical artifact makes it challenging, certainly, but that

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<v Speaker 2>flattening is also a direct physiological consequence of the metabolic.

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<v Speaker 1>State from the potassium. Again.

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<v Speaker 2>Yeah, as potassium levels fluctuate in DKA, the atrial myocardium's

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<v Speaker 2>ability to depolarize robustly is blunted, So the signal's just

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<v Speaker 2>weak exactly. The electrical vector generated by the atria is weakened,

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<v Speaker 2>which translates to a smaller, flatter P wave on the paper,

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<v Speaker 2>and it just hides underneath all that somatic tremor artifact

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<v Speaker 2>from the patient.

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<v Speaker 1>Which highlights another massive point the source emphasizes. Context is

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<v Speaker 1>everything normal and abnormal are highly relative to the specific

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<v Speaker 1>physiology of the person sitting right in front of.

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<v Speaker 2>You, because the ECG is not a standalone truth machine.

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<v Speaker 1>Right. For example, Hampton points out that widespread tea wave variations.

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<v Speaker 2>Which in many patients would immediately signal eschemia.

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<v Speaker 1>Right, but those can actually be considered a completely normal

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<v Speaker 1>variant in a healthy black woman exactly.

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<v Speaker 2>If you just looked at the trace without knowing the

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<v Speaker 2>demographics or the history, you might sound the alarm for

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<v Speaker 2>a heart attack.

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<v Speaker 1>You might initiate this whole cascade of stressful, expensive, and

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<v Speaker 1>potentially dangerous medical interventions.

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<v Speaker 2>With blood thinners are an angiogram, yeah.

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<v Speaker 1>All for a perfectly healthy heart.

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<v Speaker 2>That clinical history is the absolute lens through which the

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<v Speaker 2>ECG must be viewed.

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<v Speaker 1>It makes me think of an analogy. An ECG is

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<v Speaker 1>basically a single frame from a movie.

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<v Speaker 2>I like that.

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<v Speaker 1>Yeah, it tells you exactly what the electricity is doing

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<v Speaker 1>for what a ten second window, But without knowing the plot.

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<v Speaker 2>The patient's history, their symptoms.

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<v Speaker 1>Right, Without that, you're going to completely misinterpret the scene.

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<v Speaker 1>A character crying in a freeze frame could be experiencing

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<v Speaker 1>a profound tragedy, or it could be tears of joy.

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<v Speaker 1>You need the plot.

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<v Speaker 2>You definitely need the plot.

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<v Speaker 1>So if we need to synthesize the plot with the picture,

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<v Speaker 1>how does a clinician systematically train their eye to look

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<v Speaker 1>past the technical noise of artifacts without missing a subtle

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<v Speaker 1>life threatening signal.

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<v Speaker 2>The training requires rigid, unyielding discipline. I mean, you don't

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<v Speaker 2>just glance at the movie frame and try to guess

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<v Speaker 2>the emotion based on a general vibe.

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<v Speaker 1>Right, no vibes based medicine, No vibes.

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<v Speaker 2>You follow a strict analytical sequence every single time you

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<v Speaker 2>pick up the paper. You calculate the rate, You determine

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<v Speaker 2>the rhythm, check the axis, assess the cardiac axis. Yes,

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<v Speaker 2>then you analyze the more fall, the P waves, the

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<v Speaker 2>pr interval, the QRS complex, the st segment, and the

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<v Speaker 2>T waves as a checklist, a rigorous checklist. By forcing

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<v Speaker 2>your brain through that sequence, the somatic tremor and the

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<v Speaker 2>baseline wander kind of fade into the background, and the

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<v Speaker 2>true electrical narrative reveals itself.

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<v Speaker 1>Well, if we're relying on the plot, let's look at

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<v Speaker 1>what happens when the plot screams danger. Because when things

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<v Speaker 1>go wrong in the heart, they go wrong.

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<v Speaker 2>Fast, Oh incredibly fast.

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<v Speaker 1>Let's break down ECG twenty two. The presentation is a

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<v Speaker 1>forty eight year old man who comes in. He has

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<v Speaker 1>had severe central chest pain for one hour.

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<v Speaker 2>See that history alone dictates your response. One hour of

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<v Speaker 2>severe central chest pain in a middle aged man is

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<v Speaker 2>an acute coronary syndrome until proven otherwise.

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<v Speaker 1>Right, So we get the trace and the findings are

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<v Speaker 1>very specific sinus rhythm at seventy five beats per minute,

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<v Speaker 1>we have left axis deviations, specifically left anterior hemi block. Okay,

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<v Speaker 1>the qrs complexes are largely normal, but there's a small

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<v Speaker 1>probably septle q wave in lead VL. And then crucially

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<v Speaker 1>we see deeply inverted tea waves and leads V one

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<v Speaker 1>through V five.

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<v Speaker 2>That's the kicker right there.

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<v Speaker 1>Yeah, so looking the clues an hour of crushing pain

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<v Speaker 1>and those inverted tea waves and the anterior leads are

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<v Speaker 1>practically screaming.

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<v Speaker 2>A schemia loud and clear.

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<v Speaker 1>Even without the ST segment elevation. We have to be

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<v Speaker 1>looking at an acute anti non ST segment elevation myocardial infarction.

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<v Speaker 2>Right and then, Stemmy, You've diagnosed it perfectly. The electrical

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<v Speaker 2>repolarization of the anterior wall of the left ventricle is

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<v Speaker 2>deeply disturbed. But let's look at the mechanism at why

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<v Speaker 2>those two waves invert Exactly. The heart muscle is starving

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<v Speaker 2>for oxygen because a coronary artery is partially blocked, and

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<v Speaker 2>this lack of oxygen cripples the ATP dependent potassium channels

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<v Speaker 2>in the CARDIAXL membranes. Okay, Normally, repolarization spreads from the

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<v Speaker 2>outside of the heart inwards from the epicardium to the

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<v Speaker 2>endocardi Right.

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<v Speaker 1>That's the standard healthy pathway.

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<v Speaker 2>But is schemia changes the action potential duration. It actually

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<v Speaker 2>forces the repolarization wave to travel backward away from the

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<v Speaker 2>explore oring electrodes on the patient's chest.

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<v Speaker 1>In an electrical wave, moving away from a positive electrode

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<v Speaker 1>records as a negative.

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<v Speaker 2>Deflection, Hence the inverted teawave wow.

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<v Speaker 1>And the textbook demands immediate action for this and stemmy.

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<v Speaker 1>The medical management outline includes short and long acting nitrates,

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<v Speaker 1>beta blockers, and calcium.

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<v Speaker 2>Antagonists standard protocol.

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<v Speaker 1>But we shouldn't just list medications. Let's talk about how

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<v Speaker 1>they are actually saving this man's heart tissue in real time.

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<v Speaker 2>Well, the pharmacology is all about altering the supply and

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<v Speaker 2>demand mismatch. Nitrates are vasodilators. They open up the coronary

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<v Speaker 2>vessels to improve whatever blood flow can still get past.

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<v Speaker 2>The blockage is widening the pipes exactly. But beta blockers

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<v Speaker 2>are arguably the most fascinating intervention.

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<v Speaker 1>Here because they slow the heart down.

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<v Speaker 2>Yes, by blocking sympathetic nervous system stimulation. They force the

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<v Speaker 2>heart rate to drop, meaning the heart spends more time

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<v Speaker 2>in diastol the relaxation phase.

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<v Speaker 1>Okay, and why is that so.

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<v Speaker 2>Critical Because unlike every other organ in the body, the

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<v Speaker 2>heart muscle only he receives its own blood supply during diastyl.

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<v Speaker 1>Oh, wow, I didn't realize it was only during relaxation.

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<v Speaker 2>Yeah, when it squeozes, the vessels are clamped shut. So

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<v Speaker 2>by artificially prolonging diastol with a beta blocker, you are

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<v Speaker 2>maximizing the time the coronary arteries have to actually feed

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<v Speaker 2>that starving tissue.

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<v Speaker 1>That is brilliant, But the pills just stabilize him. Right.

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<v Speaker 1>The text states he also needs urgent coronary angiography.

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<v Speaker 2>Yes, to physically look inside those arteries with contrast dye.

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<v Speaker 1>With a view to performing a percutaneous coronary intervention, right,

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<v Speaker 1>putting in a stent to crush the plaque against the artery.

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<v Speaker 2>Wall or potentially a coronary artery bypass graft. Plus for

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<v Speaker 2>long term survival, he has to address the underlying plot

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<v Speaker 2>of his movie. His risk factor is like smoking, weight

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<v Speaker 2>and hypercholesterolemia.

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<v Speaker 1>Right, it is a massive coordinated systemic response entirely triggered

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<v Speaker 1>by combining inverted tea waves with his clinical story.

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<v Speaker 2>It's beautiful when it works.

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<v Speaker 1>But let's contrast that ischemic and stemic presentation with structural one.

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<v Speaker 1>ECG one nine carries a three star difficulty rating.

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<v Speaker 2>Oh this is a heavy one.

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<v Speaker 1>Yeah. A fifty year old man who has had attacks

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<v Speaker 1>of dizziness and palpitations for several years suddenly collapses at work.

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<v Speaker 1>He is brought into a and E cold and clammy.

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<v Speaker 1>His heart rate is rapid and his blood pressure is

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<v Speaker 1>completely unrecordable. Wow, there are clinical signs of left ventricular failure.

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<v Speaker 2>So he is in profound cardiogenic shock. His pump has

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<v Speaker 2>failed entirely.

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<v Speaker 1>Exactly, and the ECG shows gross massive tea wave inversion

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<v Speaker 1>in the intralateral leads. And according to the text, this

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<v Speaker 1>gross teawave inversion, coupled with the history of dizziness leading

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<v Speaker 1>to a sudden collapse suggests hypertrophic cardiomyopathy.

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<v Speaker 2>This is a phenomenal case because it perfectly illustrates how

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<v Speaker 2>structural muscle changes broadcasts themselves as electrical anomalies. How so

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<v Speaker 2>well in hypertrophic cardiomyopathy, the heart muscle of the left

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<v Speaker 2>ventricle grows abnormally thick.

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<v Speaker 1>But it's not just a big, strong muscle, is it.

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<v Speaker 1>To use an analogy, a healthy heart's electrical system is

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<v Speaker 1>like a high speed fiber optic network. The signal travels

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<v Speaker 1>fast and clean. But in hypertrophic cordiumyopathy, the muscle fibers

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<v Speaker 1>haven't just grown. They are disorganized and chaotic. It's like

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<v Speaker 1>trying to send that same high speed signal through a

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<v Speaker 1>tangled knot of copper wire.

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<v Speaker 2>That is an excellent way to conceptualize it. The cellular

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<v Speaker 2>architecture is literally called myocardial disarray.

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<v Speaker 1>Myocardial disarray that sounds bad.

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00:13:26.039 --> 00:13:29.399
<v Speaker 2>It is because the cells are disorganized. The electrical signal

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<v Speaker 2>slows down, distorts, and causes chaotic inverted repolarization waves on

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<v Speaker 2>the paper.

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00:13:34.480 --> 00:13:37.399
<v Speaker 1>Which explains the massive T wave inversions exactly.

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<v Speaker 2>Furthermore, that thick, disorganized muscle can physically obstruct the outflow

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<v Speaker 2>of blood from the heart during contraction.

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<v Speaker 1>So it's squeezing but nothing gets out right.

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<v Speaker 2>If the blood can't get out, the stroke volume drops

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<v Speaker 2>to near zero, the blood pressure becomes unrecordable, the brain

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00:13:53.679 --> 00:13:56.519
<v Speaker 2>loses perfusion, and the patient collapses.

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<v Speaker 1>Exactly as described in the case. Yes, but hold on,

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<v Speaker 1>if we are relying so heavily on the exact shape

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<v Speaker 1>of these squiggles and reading the plot of these tangled wires,

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00:14:05.720 --> 00:14:08.720
<v Speaker 1>isn't there a massive diagnostic blind spot here?

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00:14:09.000 --> 00:14:09.559
<v Speaker 2>What do you mean?

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<v Speaker 1>Well, what if a patient comes in clutching his chest,

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00:14:13.240 --> 00:14:18.279
<v Speaker 1>feeling absolutely terrible, but his resting ECG is pristine, not

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<v Speaker 1>a single te wave out of place? Do we just

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<v Speaker 1>send him home?

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00:14:21.279 --> 00:14:23.519
<v Speaker 2>Oh? That is a life or death question, and the

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<v Speaker 2>answer is an emphatic no. You absolutely do not send

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00:14:26.519 --> 00:14:26.840
<v Speaker 2>them home.

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00:14:26.919 --> 00:14:27.480
<v Speaker 1>Okay, good.

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00:14:27.639 --> 00:14:30.480
<v Speaker 2>A normal resting ECG does not guarantee a healthy heart.

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<v Speaker 2>And ECG is a static test. I mean it's a

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<v Speaker 2>ten second snapshot taken while the patient is lying quietly

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<v Speaker 2>in a hospital bed with minimal physical exertion.

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<v Speaker 1>Which brings us to the severe limitations of the resting ECG. Yeah,

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<v Speaker 1>and what happens when we force the heart to work harder?

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00:14:44.240 --> 00:14:47.840
<v Speaker 1>The stress test exactly? Yeah, let's look at ECG thirty eight.

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<v Speaker 1>We have a seventy year old man with long standing

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<v Speaker 1>high blood pressure who has been having attacks of dizziness

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00:14:53.679 --> 00:14:57.200
<v Speaker 1>over several weeks, and he has a known history's.

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00:14:56.840 --> 00:14:58.879
<v Speaker 2>Angina classic risk factors.

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00:14:59.039 --> 00:15:02.960
<v Speaker 1>But his resting EA is completely one hundred percent.

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<v Speaker 2>Normal because at rest, his coronary arteries, even if they

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00:15:06.919 --> 00:15:10.360
<v Speaker 2>are diseased and narrowed, are still capable of delivering enough

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00:15:10.440 --> 00:15:13.600
<v Speaker 2>blood to meet the low oxygen demands of a resting body.

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00:15:13.720 --> 00:15:17.399
<v Speaker 1>Ah, so there's no aeschemia happening at that exact moment.

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00:15:17.200 --> 00:15:20.080
<v Speaker 2>Right, So there is no electrical abnormality to record.

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00:15:20.279 --> 00:15:23.240
<v Speaker 1>But the clinician didn't stop there because the resting ECG

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00:15:23.480 --> 00:15:26.519
<v Speaker 1>didn't match the clinical suspicion of the plot. They put

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00:15:26.600 --> 00:15:29.039
<v Speaker 1>him on a treadmill for a low level exercise.

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00:15:28.639 --> 00:15:30.840
<v Speaker 2>Stress test, and that is when the truth came out.

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00:15:31.000 --> 00:15:35.279
<v Speaker 1>YEP, during exercise st segment, elevation suddenly appeared on the tracing.

328
00:15:35.440 --> 00:15:38.519
<v Speaker 2>The action in the movie started and the pathology.

329
00:15:37.919 --> 00:15:40.120
<v Speaker 1>Was unmasked because he needed more oxygen.

330
00:15:40.240 --> 00:15:43.559
<v Speaker 2>Exactly when the patient exercises, the heart rate increases, the

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<v Speaker 2>blood pressure increases, and the heart muscle demands vastly more oxygen.

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<v Speaker 1>But his narrow, diseased coronary arteries physically cannot dilate to

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00:15:52.000 --> 00:15:53.399
<v Speaker 1>provide that extra blood flow.

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00:15:53.679 --> 00:15:58.639
<v Speaker 2>Right, A supplying demand mismatch occurs instantly the subndocardial tissue

335
00:15:58.639 --> 00:16:02.919
<v Speaker 2>becomes a schemic, the cellular metabolism shifts to anaerobic.

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00:16:02.440 --> 00:16:04.279
<v Speaker 1>Pathways, lactic acid builds up.

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00:16:04.399 --> 00:16:08.159
<v Speaker 2>Yes, lactic acid builds up, and the electrical baseline shifts,

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00:16:08.519 --> 00:16:11.320
<v Speaker 2>presenting as st elevation on the monitor.

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00:16:11.399 --> 00:16:15.559
<v Speaker 1>So the falsely reassuring resting test hit a severe underlying

340
00:16:15.600 --> 00:16:18.919
<v Speaker 1>coronary artery disease. Good, And the text dictates that a

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00:16:19.000 --> 00:16:22.639
<v Speaker 1>positive exercise test at a low level of exertion urgently

342
00:16:22.639 --> 00:16:26.240
<v Speaker 1>indicates a coronary angiogram along with strict long term medical

343
00:16:26.279 --> 00:16:29.799
<v Speaker 1>management aspirin statins and an ACE inhibitor.

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00:16:29.960 --> 00:16:32.639
<v Speaker 2>And we should note the mechanism of that acee inhibitor

345
00:16:32.679 --> 00:16:36.279
<v Speaker 2>because it's important for it blocks the angutensin converting enzyme,

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00:16:36.360 --> 00:16:38.879
<v Speaker 2>preventing the formation of angi tensin the second which is

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00:16:38.879 --> 00:16:40.360
<v Speaker 2>a potent vasoconstrictor.

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00:16:40.440 --> 00:16:43.159
<v Speaker 1>Okay, So it stops the vessels from clamping down right.

349
00:16:43.399 --> 00:16:46.799
<v Speaker 2>By relaxing the blood vessels body wide, the ACE inhibitor

350
00:16:46.840 --> 00:16:49.919
<v Speaker 2>lowers the overall pressure the failing heart has to pump against,

351
00:16:50.320 --> 00:16:52.679
<v Speaker 2>reducing its workload and its oxygen demand.

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00:16:53.039 --> 00:16:56.000
<v Speaker 1>So the ECG is an incredible tool, but you have

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00:16:56.080 --> 00:16:57.919
<v Speaker 1>to know its blind spots, and sometimes you have to

354
00:16:57.919 --> 00:17:00.759
<v Speaker 1>put the system under stress to see the cracks. Absolutely,

355
00:17:00.919 --> 00:17:03.879
<v Speaker 1>but it's not just about the coronary arteries supplying the

356
00:17:03.919 --> 00:17:08.839
<v Speaker 1>heart itself. Hampton's text beautifully illustrates how the ECG acts

357
00:17:08.839 --> 00:17:11.319
<v Speaker 1>as a window to systemic issues happening throughout the rest

358
00:17:11.319 --> 00:17:11.839
<v Speaker 1>of the body.

359
00:17:12.039 --> 00:17:14.440
<v Speaker 2>Yeah, the heart doesn't exist in a vacuum. It is

360
00:17:14.599 --> 00:17:17.359
<v Speaker 2>deeply sensitive to the systemic environment.

361
00:17:17.559 --> 00:17:19.759
<v Speaker 1>If you look at the index references in the book,

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00:17:19.799 --> 00:17:23.640
<v Speaker 1>the ECG frequently acts as a systemic alarm bell. Take

363
00:17:23.680 --> 00:17:28.720
<v Speaker 1>atrial fibrillation APHIB. Yeah, the atriar quivering chaotically instead of

364
00:17:28.759 --> 00:17:33.119
<v Speaker 1>contracting smoothly, firing hundreds of erratic electrical impulses down into

365
00:17:33.119 --> 00:17:33.759
<v Speaker 1>the ventricles.

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00:17:34.039 --> 00:17:38.079
<v Speaker 2>Most people associate APHIB purely with structural heart disease, but

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00:17:38.119 --> 00:17:42.519
<v Speaker 2>the text explicitly links it to systemic external triggers like

368
00:17:42.559 --> 00:17:47.559
<v Speaker 2>what well. Hypothermia can trigger atrial fibrillation. Didoxin toxicity can

369
00:17:47.559 --> 00:17:51.000
<v Speaker 2>present with APHIB, sometimes with a controlled ventricular rate because

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00:17:51.000 --> 00:17:54.759
<v Speaker 2>the drug increases intercellular calcium and enhances vagal tone at

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00:17:54.759 --> 00:17:59.279
<v Speaker 2>the AV node. And the text also highlights hypokalemia, which

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00:17:59.319 --> 00:18:01.680
<v Speaker 2>is low blood potassium, as the trigger.

373
00:18:01.839 --> 00:18:04.640
<v Speaker 1>Let's connect that back to what we discussed earlier with DKA.

374
00:18:05.480 --> 00:18:09.279
<v Speaker 1>Low potassium in the bloodstream means a larger concentration ingredient

375
00:18:09.319 --> 00:18:10.839
<v Speaker 1>across the cell membrane.

376
00:18:10.480 --> 00:18:15.039
<v Speaker 2>Right exactly, which prolongs phase three of the cardiac action potential,

377
00:18:15.079 --> 00:18:16.880
<v Speaker 2>the repolarization phase.

378
00:18:16.519 --> 00:18:17.880
<v Speaker 1>So it takes longer to reset.

379
00:18:18.079 --> 00:18:22.759
<v Speaker 2>Yes, and this extended vulnerable period gives ectopic pacemakers in

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00:18:22.799 --> 00:18:27.680
<v Speaker 2>the atria the perfect opportunity to fire spontaneously, triggering the

381
00:18:27.759 --> 00:18:29.960
<v Speaker 2>chaotic cascade of atrial fibrillation.

382
00:18:30.559 --> 00:18:33.279
<v Speaker 1>So the electrical trace is demanding that you investigate the

383
00:18:33.319 --> 00:18:36.359
<v Speaker 1>whole patient. Check their temperature, check their electrolytes, check their

384
00:18:36.440 --> 00:18:37.000
<v Speaker 1>drug levels.

385
00:18:37.039 --> 00:18:38.400
<v Speaker 2>You have to look at the whole picture.

386
00:18:38.720 --> 00:18:41.599
<v Speaker 1>We see the heart responding to systemic mechanical problems too

387
00:18:42.240 --> 00:18:45.400
<v Speaker 1>severe aortic stenosis the physical narrowing of the main valve

388
00:18:45.480 --> 00:18:48.519
<v Speaker 1>leaving the heart. It forces the left ventricle to pump

389
00:18:48.519 --> 00:18:50.759
<v Speaker 1>against immense pressure just to get blood.

390
00:18:50.480 --> 00:18:53.240
<v Speaker 2>To the body right, and over time, the physical toll

391
00:18:53.279 --> 00:18:56.440
<v Speaker 2>of pushing against the stenotic valve forces the heart muscle

392
00:18:56.440 --> 00:18:56.920
<v Speaker 2>to adapt.

393
00:18:56.960 --> 00:18:57.640
<v Speaker 1>It gets bigger.

394
00:18:57.759 --> 00:19:01.960
<v Speaker 2>The muscle fibers undergo hypertrophy, They thicken and grow to generate.

395
00:19:01.640 --> 00:19:05.279
<v Speaker 1>More force and on the ECG, this presents as left

396
00:19:05.319 --> 00:19:09.279
<v Speaker 1>atrial and left ventricular hypertrophy. Because there is literally more

397
00:19:09.359 --> 00:19:13.759
<v Speaker 1>muscle mass generating electricity, the amplitude of the QRS complexes

398
00:19:13.920 --> 00:19:15.160
<v Speaker 1>dramatically increases.

399
00:19:15.319 --> 00:19:19.359
<v Speaker 2>Yes, the electrical squiggles get much taller, reflecting the increased

400
00:19:19.440 --> 00:19:22.759
<v Speaker 2>voltage required to depolarize that massive wall of muscle.

401
00:19:23.000 --> 00:19:26.160
<v Speaker 1>But here is a wild caveat from the text. Huge

402
00:19:26.240 --> 00:19:29.680
<v Speaker 1>voltages or strained rhythms are not always assigned to disease.

403
00:19:30.519 --> 00:19:34.640
<v Speaker 1>Sometimes the heart adapts to extreme healthy stress. The text

404
00:19:34.680 --> 00:19:37.880
<v Speaker 1>points out that elite athletes can present with some incredibly

405
00:19:37.880 --> 00:19:38.960
<v Speaker 1>strange ECGs.

406
00:19:39.039 --> 00:19:42.200
<v Speaker 2>Oh, they absolutely can. The text specifically notes that athletes

407
00:19:42.240 --> 00:19:45.880
<v Speaker 2>can present with accelerated idiotodal rhythms and bifed PE waves.

408
00:19:45.880 --> 00:19:48.400
<v Speaker 1>A bifed P wave meaning the P wave that first

409
00:19:48.400 --> 00:19:51.799
<v Speaker 1>little bump on the trays showing atrial depolarization is notched

410
00:19:51.880 --> 00:19:54.720
<v Speaker 1>or split into two distinct peaks. In a normal person,

411
00:19:54.759 --> 00:19:57.359
<v Speaker 1>you look at that and immediately suspect left atrial enlargement,

412
00:19:57.440 --> 00:20:00.799
<v Speaker 1>perhaps from mitroveil disease, but in a highly condition athlete

413
00:20:00.839 --> 00:20:02.279
<v Speaker 1>it might just be their baseline.

414
00:20:02.359 --> 00:20:05.839
<v Speaker 2>It all comes down to the physiology of intense athletic training.

415
00:20:06.559 --> 00:20:11.200
<v Speaker 2>Chronic heavy aerobic exercise forces the cardiovascular system to become

416
00:20:11.319 --> 00:20:12.440
<v Speaker 2>incredibly efficient.

417
00:20:12.680 --> 00:20:13.519
<v Speaker 1>Okay, how so.

418
00:20:13.799 --> 00:20:17.720
<v Speaker 2>The body increases its resting vagual tone. That's the parasympathetic

419
00:20:17.799 --> 00:20:19.960
<v Speaker 2>nervous system's breaking mechanism on the heart.

420
00:20:19.960 --> 00:20:22.640
<v Speaker 1>Ah, the rest and digest system exactly.

421
00:20:23.079 --> 00:20:27.319
<v Speaker 2>This vagual dominance drastically suppresses the sinus node, dropping the

422
00:20:27.359 --> 00:20:30.480
<v Speaker 2>resting heart rates significantly, sometimes into the thirties.

423
00:20:30.599 --> 00:20:34.319
<v Speaker 1>Wow. And when the primary pacemaker slows down that much,

424
00:20:34.720 --> 00:20:36.799
<v Speaker 1>the safety mechanisms kick in right precisely.

425
00:20:37.079 --> 00:20:40.119
<v Speaker 2>Other latent pacemakers in the heart, like the AV node,

426
00:20:40.480 --> 00:20:43.319
<v Speaker 2>naturally step up to prevent the heart from stopping entirely.

427
00:20:43.759 --> 00:20:46.480
<v Speaker 2>The AV node escapes the suppression and fires off its

428
00:20:46.480 --> 00:20:50.039
<v Speaker 2>own beats, causing those accelerated idioonodal rhythms.

429
00:20:49.839 --> 00:20:51.759
<v Speaker 1>And the bified pea waves, while.

430
00:20:51.559 --> 00:20:55.160
<v Speaker 2>In athlete's heart chambers naturally stretch and dilate to accommodate

431
00:20:55.160 --> 00:20:58.440
<v Speaker 2>a larger stroke volume of blood per beat. Okay, that

432
00:20:58.559 --> 00:21:02.119
<v Speaker 2>physiological atrial streke which alters the electrical vector of the atria,

433
00:21:02.200 --> 00:21:05.319
<v Speaker 2>causing the notched bifed pee waves. It is an adaptation

434
00:21:05.440 --> 00:21:08.440
<v Speaker 2>to extreme physical demand, not a pathological failure.

435
00:21:08.640 --> 00:21:10.720
<v Speaker 1>It brings us right back to the golden rule. You

436
00:21:10.799 --> 00:21:13.440
<v Speaker 1>have to know whose chest those electrodes are attached to.

437
00:21:14.079 --> 00:21:16.880
<v Speaker 1>Is it an Olympic marathon runner with high vagual tone

438
00:21:17.440 --> 00:21:20.680
<v Speaker 1>or a sedentary seventy year old with long standing hypertension?

439
00:21:21.079 --> 00:21:24.759
<v Speaker 2>Because the context fundamentally changes the interpretation of the exact

440
00:21:24.799 --> 00:21:26.480
<v Speaker 2>same electrical signal.

441
00:21:26.359 --> 00:21:28.880
<v Speaker 1>Which is why John Hampton's text remains so vital for

442
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<v Speaker 1>medical education. It forces you to practice that synthesis, to

443
00:21:33.599 --> 00:21:36.480
<v Speaker 1>combine the raw data with the human being in front

444
00:21:36.519 --> 00:21:36.720
<v Speaker 1>of you.

445
00:21:36.839 --> 00:21:37.759
<v Speaker 2>It's essential learning.

446
00:21:38.039 --> 00:21:41.640
<v Speaker 1>So let's summarize the educational journey we've taken today. The

447
00:21:41.720 --> 00:21:45.839
<v Speaker 1>ECG is the ultimate first line investigation. It is cheap,

448
00:21:46.079 --> 00:21:48.960
<v Speaker 1>it is harmless, and it is irreplaceable, giving us a

449
00:21:49.000 --> 00:21:52.839
<v Speaker 1>window into cellular ion channels and electrical vectors that we

450
00:21:52.839 --> 00:21:55.559
<v Speaker 1>can obtain in no other way. But it is strictly

451
00:21:55.599 --> 00:21:58.160
<v Speaker 1>a tool. It is a way to differentiate between the

452
00:21:58.200 --> 00:22:00.680
<v Speaker 1>diagnoses that you should have already started for formulating by

453
00:22:00.680 --> 00:22:03.039
<v Speaker 1>talking to your patient and taking their history. You have

454
00:22:03.079 --> 00:22:05.720
<v Speaker 1>to talk to the patient from the potassium shifts of

455
00:22:05.759 --> 00:22:11.200
<v Speaker 1>diabetic ketoacidosis causing junctional extra systiles to the hidden sebendocardial

456
00:22:11.319 --> 00:22:15.480
<v Speaker 1>ischemia masked by a normal resting ECG. The pink paper

457
00:22:15.519 --> 00:22:16.720
<v Speaker 1>only tells half the story.

458
00:22:17.000 --> 00:22:19.200
<v Speaker 2>The clinician's mind has to do the heavy lifting to

459
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<v Speaker 2>find the other half.

460
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<v Speaker 1>Absolutely Now, as promise for our medical learners out there,

461
00:22:23.720 --> 00:22:26.559
<v Speaker 1>the students, the paramedics, the junior docs trying to earn

462
00:22:26.599 --> 00:22:30.039
<v Speaker 1>their three stars, here is a quick review question to

463
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<v Speaker 1>test your retention of today's deep dive.

464
00:22:32.519 --> 00:22:34.319
<v Speaker 2>Ooh, a pop quiz.

465
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<v Speaker 1>Just a quick one. I'm going to ask the question

466
00:22:36.160 --> 00:22:37.839
<v Speaker 1>and I want you to mentally answer it before we

467
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<v Speaker 1>give it away. Ready. Ready, If a forty eight year

468
00:22:40.599 --> 00:22:44.119
<v Speaker 1>old man presents with severe central chest pain for one

469
00:22:44.200 --> 00:22:48.519
<v Speaker 1>hour and his ECG shows left axis deviation with inverted

470
00:22:48.559 --> 00:22:51.640
<v Speaker 1>tea waves and leads V one through V five, what

471
00:22:51.759 --> 00:22:55.960
<v Speaker 1>is the classic clinical diagnosis according to Hampton's text, and

472
00:22:56.000 --> 00:22:58.880
<v Speaker 1>what are the immediate pharmacological and procedural steps should take.

473
00:22:59.000 --> 00:23:00.480
<v Speaker 2>That's a good one second.

474
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<v Speaker 1>Think about those anterior leads, think about the ATP dependent

475
00:23:04.079 --> 00:23:07.319
<v Speaker 1>potassium channels and the cascade of treatments required to fix

476
00:23:07.359 --> 00:23:08.640
<v Speaker 1>that supply and demand mismatch.

477
00:23:08.680 --> 00:23:09.359
<v Speaker 2>Give them a moment.

478
00:23:09.519 --> 00:23:10.599
<v Speaker 1>Okay, what is the answer.

479
00:23:10.799 --> 00:23:15.440
<v Speaker 2>Well, the diagnosis is an acute anterior non st segment elevation,

480
00:23:15.559 --> 00:23:17.640
<v Speaker 2>myocardial infection, and then.

481
00:23:17.640 --> 00:23:19.359
<v Speaker 1>Stemmy right and the treatments.

482
00:23:19.559 --> 00:23:23.279
<v Speaker 2>Pharmacologically, you administer short and long acting nitrates to dilate

483
00:23:23.279 --> 00:23:27.319
<v Speaker 2>the vessels, beta blockers to prolonged diastol and improve perfusion time,

484
00:23:27.759 --> 00:23:32.119
<v Speaker 2>and calcium antagonists. And procedurally, procedurally you must prepare the

485
00:23:32.160 --> 00:23:36.279
<v Speaker 2>patient for urgent coronary angiography with a view toward a

486
00:23:36.319 --> 00:23:39.599
<v Speaker 2>percutaneous coronary intervention or bypass surgery.

487
00:23:39.759 --> 00:23:42.160
<v Speaker 1>Perfect. If you got that, you are well on your

488
00:23:42.160 --> 00:23:45.680
<v Speaker 1>way to mastering the diagnostic muddy waters. We've covered a

489
00:23:45.720 --> 00:23:47.960
<v Speaker 1>tremendous amount of ground today, but I want to leave

490
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<v Speaker 1>you with a final provocative thought to explore on.

491
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<v Speaker 2>Your own, okay, late on me.

492
00:23:51.799 --> 00:23:54.559
<v Speaker 1>Hampton's text mentions that an ECG is often just the

493
00:23:54.599 --> 00:23:58.000
<v Speaker 1>beginning of the diagnostic pathway. It's usually followed by advanced

494
00:23:58.000 --> 00:24:03.599
<v Speaker 1>imaging echocardiogram CT scans, MRIs and radio nuclient studies. Oh

495
00:24:03.640 --> 00:24:06.640
<v Speaker 1>for sure, Today we can literally watch the heart muscle

496
00:24:06.680 --> 00:24:10.119
<v Speaker 1>pump in real time in high definition three D, observing

497
00:24:10.119 --> 00:24:13.240
<v Speaker 1>the mechanical flow of blood with incredible precision.

498
00:24:13.279 --> 00:24:14.759
<v Speaker 2>The technology is mind blowing.

499
00:24:15.000 --> 00:24:18.839
<v Speaker 1>It is so as these high tech imaging modalities become cheaper, faster,

500
00:24:18.960 --> 00:24:22.720
<v Speaker 1>and vastly more detailed, it begs the question, will there

501
00:24:22.720 --> 00:24:24.680
<v Speaker 1>ever come a day when the one hundred year old

502
00:24:24.720 --> 00:24:29.440
<v Speaker 1>electrical squiggles of the traditional ECG are finally rendered completely

503
00:24:29.480 --> 00:24:31.079
<v Speaker 1>obsolete by advanced imaging?

504
00:24:31.240 --> 00:24:31.799
<v Speaker 2>Wow?

505
00:24:31.920 --> 00:24:35.279
<v Speaker 1>Or is there something so fundamental, so irreplaceable about the raw,

506
00:24:35.680 --> 00:24:40.160
<v Speaker 1>instantaneous speed of capturing a cellular electrical action potential that

507
00:24:40.240 --> 00:24:43.240
<v Speaker 1>the twelve lead ECG will always secure its place in

508
00:24:43.279 --> 00:24:44.079
<v Speaker 1>the emergency room.

509
00:24:44.119 --> 00:24:47.160
<v Speaker 2>It's a fascinating question about the future of medical technology

510
00:24:47.240 --> 00:24:48.960
<v Speaker 2>versus foundational physiology.

511
00:24:49.119 --> 00:24:51.599
<v Speaker 1>Definitely something to mull over on your commute or before

512
00:24:51.640 --> 00:24:54.000
<v Speaker 1>your next shift on the warts. Yeah, because until that

513
00:24:54.079 --> 00:24:56.880
<v Speaker 1>day of three D holograms arrives, we are all still

514
00:24:56.880 --> 00:24:59.240
<v Speaker 1>staring at the pink grid paper, trying to make sense

515
00:24:59.279 --> 00:24:59.720
<v Speaker 1>of the noise.

516
00:25:00.000 --> 00:25:02.680
<v Speaker 2>It's navigating the messy reality of clinical medicine

517
00:25:02.759 --> 00:25:04.680
<v Speaker 1>Exactly one ten second frame at a time.
