Speaker 1: So imagine you've got a fifty year old patient crashing
Speaker 1: right in front of you. I mean they are cold,
Speaker 1: they're clammy, and their blood pressure is well, it's completely unrecordable.
Speaker 2: Oh that's just a nightmare scenario.
Speaker 1: On the wards right, and the monitor is just flashing
Speaker 1: this insane heart rate of like three hundred beats per minute.
Speaker 1: You've got this little strip of paper with chaotic squiggles
Speaker 1: in your hand, and you have what maybe ten seconds
Speaker 1: to decide. Ten seconds on a good day, exactly, you
Speaker 1: have to choose whether to push a drug or just
Speaker 1: immediately reach for the defibrillator paddles. And if you make
Speaker 1: the wrong choice, I mean, it is.
Speaker 2: Fatal, it really is. And that right there, that's the
Speaker 2: absolute reality of clinical medicine. It's not the neat, linear
Speaker 2: chapter by chapter progression you get when you're sitting in
Speaker 2: a library reading a textbook.
Speaker 1: No, definitely not.
Speaker 2: It's just this landscape of total diagnostic unpredictability. Yeah, I mean,
Speaker 2: you don't get to choose the pathology that walks through
Speaker 2: the clinic door next.
Speaker 1: Yeah, they don't wear a sign saying what chapter they belong.
Speaker 2: To exactly, And that's why relying solely on like pattern
Speaker 2: recognition from some pristine reference manual, it just falls apart
Speaker 2: so quickly. In the emergency department.
Speaker 1: Which is actually the exact premise of our deep dive today,
Speaker 1: we are taking a really comprehensive look at the book
Speaker 1: one hundred and fifty ECG Problems by Emeritis Professor of
Speaker 1: Cardiology John R. Hampton.
Speaker 2: It's such a brilliant resource, it really is.
Speaker 1: And our mission today is to help you bridge that
Speaker 1: gap between basic theory and that super muddy high stakes
Speaker 1: clinical application. So just as a heads up, we aren't
Speaker 1: reviewing how to attach leads or you know, basic intervals today.
Speaker 2: Right, We're assuming you know the basics.
Speaker 1: Yeah, we are pulling the core clinical pearls directly from
Speaker 1: Hampton's work, and we're focusing intensely on the pathophysiology and
Speaker 1: the management.
Speaker 2: And honestly, the methodology of this text is what makes
Speaker 2: it so incredibly useful for your actual clinical practice. The
Speaker 2: scenarios are presented completely at random.
Speaker 1: Which feels super chaotic at first.
Speaker 2: It does, but it perfectly mirrors a real world shift,
Speaker 2: like you might face a totally benign physiological variant one
Speaker 2: minute and then boom, a cardiogenic shock. The next You
Speaker 2: don't know the difficulty ready of the case until you
Speaker 2: flip to the answer.
Speaker 1: But okay, let's unpack that for a second, isn't it,
Speaker 1: I don't know, a bit overwhelming to get hit with random,
Speaker 1: ungraded cases. It feels almost like getting a pop quiz
Speaker 1: every single time you open a clinic door.
Speaker 2: Well yeah, but that is the reality of medicine, right.
Speaker 2: You are forced to interpret that electrical tracing strictly in
Speaker 2: the light of the patient's clinical presentation before you ever
Speaker 2: know the underlying diagnosis.
Speaker 1: Because an ECG and isolation is just a piece of
Speaker 1: paper exactly.
Speaker 2: It's totally meaningless without context. It requires synthesis. So let's
Speaker 2: actually look at how that synthesis works with some of
Speaker 2: the deceptively benign presentations you'll encounter.
Speaker 1: Okay, let's do it. Consider this. You've got a twenty
Speaker 1: five year old pregnant woman presenting to your clinic and
Speaker 1: she's complaining of palpitations, just this sort of irregular.
Speaker 2: Heartbeat, pretty common presentation, very.
Speaker 1: And on ouscultation. You note a soft systolic murmur, but
Speaker 1: the rest of her cardiovascular exam is, you know, otherwise
Speaker 1: totally unremarkable because you pull an ECG. It shows sinus rhythm,
Speaker 1: a normal access, normal intervals, but she has these frequent
Speaker 1: ventricular extra systiles. Now, I feel like your immediate instinct
Speaker 1: when you see those early wide complexes popping up might
Speaker 1: be to intervene.
Speaker 2: Right, because you see an earhythmia and you want to
Speaker 2: fix it. But if you synthesize that tracing with the
Speaker 2: actual physiological state of the patient sitting in front of you,
Speaker 2: the management pathway changes.
Speaker 1: Entirely because she's pregnant.
Speaker 2: Precisely, pregnancity induces this massive hyperdynamic state. I mean, maternal
Speaker 2: plasma volume increases by up to fifty percent.
Speaker 1: Wow, fifty percent is huge.
Speaker 2: It is, and that massively drives up cardiac output. In
Speaker 2: that specific physiological environment, ventricular extra systiles are incredibly common,
Speaker 2: and more importantly, they're usually entirely benign.
Speaker 1: And I guess that murmur plays right into that hyperdynamic
Speaker 1: state as well, absolutely, because with that significantly increased stroke
Speaker 1: volume just pushing through the same valve orifices, you're going
Speaker 1: to get turbulent flow. It's just a classic physiological flow murmur.
Speaker 2: Yeah, and you have to add in the dilutional anemia.
Speaker 2: That's well, it's almost universal in the second and third trimesters.
Speaker 1: Right, because the plasma volume outpaces the red blood cell
Speaker 1: production exactly.
Speaker 2: Which decreases blood viscosity, and that just amplifies that turbulence
Speaker 2: even more. So.
Speaker 1: Your management here is basically just conservative reassurance.
Speaker 2: Yep, you do not treat the extra systellies. In fact,
Speaker 2: the text explicitly warns against reflexively ordering an echo cardiogram
Speaker 2: for every pregnant patient with a systolic murmur.
Speaker 1: Because it's just a poor use of resources.
Speaker 2: Yeah, it's a terrible use of resources. Yeah, best practice
Speaker 2: dictates reserving the echo for murmurs that persist well into
Speaker 2: the postpartum period, once that plasma volume has actually had
Speaker 2: time to normalize.
Speaker 1: Right. It's a perfect example of a normal abnormality. The
Speaker 1: tracing is technically abnormal, but physiologically it's totally expected. But
Speaker 1: what happens when we move away from those normal variants
Speaker 1: and look at an electrical system that is actively being
Speaker 1: poisoned from the outside Because external pharmacological agents leave these
Speaker 1: highly specific fingerprints on an ECG, don't they.
Speaker 2: Oh, they definitely do. And degoxin toxicity is a prime
Speaker 2: example of this. Oh yeah, when a patient is on
Speaker 2: a therapeutic dose of digoxin, you'll frequently see this characteristic
Speaker 2: downward sloping ST segment depression.
Speaker 1: It looks almost like a sagging scoop, right, or like
Speaker 1: a reverse tick mark.
Speaker 2: The reverse tick mark exactly. But here's the thing. Spotting
Speaker 2: the drug effect is one thing, the critical clinical pearl.
Speaker 2: Here is spotting the catalyst that's pushing that therapeutic dose
Speaker 2: over the edge into toxicity.
Speaker 1: Right. So, say you're looking at that same tracing, but
Speaker 1: you also happen to notice prominent U waves, particularly in
Speaker 1: the precordial leads like V two.
Speaker 2: Well, those U waves are the absolute hallmark of a
Speaker 2: hypocoleemia low potassium, and this is where the underlying mechanism
Speaker 2: completely dictates your management. How So, So, degoxin works by
Speaker 2: binding to and inhibiting the sodium potassium et PAS pump
Speaker 2: in the myocardial cell membrane. But the kicker is it
Speaker 2: binds to the exact same extracellular site that potassium does.
Speaker 1: Oh I see, so they are directly competing for real
Speaker 1: estate on that exact same pump.
Speaker 2: Precisely, So, if your patient is hypokolemic, say maybe they
Speaker 2: are on a loop diuretic like firosamine. That just washing
Speaker 2: potassium out of their system. There's less potassium round to
Speaker 2: compete for those binding sites.
Speaker 1: Which means more dioxin binds to the pump exactly.
Speaker 2: It heavily potentiates the drugs effect. So what was a
Speaker 2: perfectly safe therapeutic dose yesterday becomes highly toxic today simply
Speaker 2: because they're potassium dropped.
Speaker 1: That's fascinating. So the practical clinical application for you listening
Speaker 1: to this is all in the history taking. You see
Speaker 1: the sagging ST segments, you spot the U waves, You
Speaker 1: need to immediately ask the patient about their appetite.
Speaker 2: Yes, the text specifically notes that the very earliest symptom
Speaker 2: of digoxant toxicity is anorexia, just a total loss of appetite,
Speaker 2: followed pretty closely by nausea and vomiting.
Speaker 1: You obviously verify that with serum digoxin and potassium levels.
Speaker 1: But the ECG basically just handed you the entire physiological narrative.
Speaker 2: It really did. Now, let's contrast that external pharmacological poasoning
Speaker 2: with an internal, just catastrophic failure of the electrical wiring itself. Okay,
Speaker 2: consider a patient who presents after a sudden, completely unprovoked,
Speaker 2: sinkable episode and they sustain a fall. You run the
Speaker 2: ECG and you see complete atrioventricular dissociation.
Speaker 1: So complete heart block.
Speaker 2: Yeah, the P waves are firing at a normal intrinsic rate,
Speaker 2: let's say, seventy beats per minute, but the QRS complexes
Speaker 2: are completely divorced from them. They're firing at this slow,
Speaker 2: wide forty five beats permitted.
Speaker 1: Right, So the electrical signal from the essay node is
Speaker 1: basically hitting a brick wall at the AV node catal roadblock,
Speaker 1: and the ventricles realize they're getting no signal at all,
Speaker 1: so they trigger their own intrinsic escape rhythm just to
Speaker 1: keep the patient from diet exactly. And the reason those
Speaker 1: QRS complexes are wide is because that escape pace maker
Speaker 1: is located really low down in the ventricular myocardium, right
Speaker 1: below the Hysperkinji system.
Speaker 2: You nailed it. The depolarization wave has to spread slowly,
Speaker 2: literally muscle cell to muscle cell, rather than shooting down
Speaker 2: those fast.
Speaker 1: Electrical highways, and that slow ventricular rate just drastically drops
Speaker 1: the cardiac output, which leads to cerebral hypoperfusion and the syncope.
Speaker 2: Right, a classic Stokes atoms attack. And regardless of whether
Speaker 2: the patient remembers feeling dizzy before they fell, the management
Speaker 2: here is immediate.
Speaker 1: They need pacing.
Speaker 2: This patient requires a permanent pacemaker full stop. If there
Speaker 2: are any surgical delays, a temporary transvenous pacing wire has
Speaker 2: to be floated immediately. You physically have to bridge that
Speaker 2: broken electrical connection.
Speaker 1: Wow. Okay, so we've looked at what happens when the
Speaker 1: electrical wiring fails. Let's shift gears for a minute and
Speaker 1: look at what happens when the electrical system is perfectly
Speaker 1: intact but it is forced to drive a ructurally deformed pump.
Speaker 2: Oh, this is where it gets really interesting mechanically.
Speaker 1: Yeah, like, how does massive mechanical strain alter in electrical tracing.
Speaker 1: Let's picture a forty year old woman referred to your
Speaker 1: clinic with progressive severe dyspinea. Her ECG shows peaked P
Speaker 1: waves in laid two, marked right axis deviation and dominant
Speaker 1: tall R waves in lead V one, along with deep
Speaker 1: S waves in lead V six.
Speaker 2: And you'd probably see P wave inversions across the right
Speaker 2: sided and inferior leads too.
Speaker 1: Yep, So what's happening there.
Speaker 2: You really have to visualize the vector physics here. In
Speaker 2: a normal healthy heart, the left ventricle is massively thicker
Speaker 2: than the right, so the dominant electrical vector pulls leftward
Speaker 2: and posteriorly.
Speaker 1: Right away from lead V one, since V one sits
Speaker 1: right over the right ventricle.
Speaker 2: Exactly, and that a wave vector produces the normal deep
Speaker 2: negative S wave you expect to see in V one,
Speaker 2: But in this patient, V one shows a dominant positive
Speaker 2: R wave. The whole electrical vector has completely flipped, the
Speaker 2: electric literally surging towards the right.
Speaker 1: It's almost as if the right ventricle is I don't
Speaker 1: know a bodybuilder who has been forced to push against
Speaker 1: a jam door for years.
Speaker 2: That's a really good way to picture it.
Speaker 1: The muscle mass of the right ventricular free wall has
Speaker 1: hypertrophied to such an extreme degree that it now electrically
Speaker 1: outweighs the left ventricle. So those electrical signals are literally
Speaker 1: traveling through a massive, heavy wall of muscle.
Speaker 2: And in this case that jam door you mentioned that
Speaker 2: is severe pulmonary vascular resistance. The text identifies these specific
Speaker 2: ECG findings as severe right ventricular hypertrophy.
Speaker 1: Or RVH and clinically the signs would align perfectly.
Speaker 2: Oh absolutely. When you lay hands on this patient, the
Speaker 2: physical exam will directly correlate with that tracing. You will
Speaker 2: feel a left peristernal heave because that massively hypertrophied right
Speaker 2: ventricle is literally lifting your hand off the chest wall
Speaker 2: with every single.
Speaker 1: System, and you're going to hear a super loud pulmonary
Speaker 1: second sound the P two as that high pressure pulmonary
Speaker 1: system forcefully slams the valve shut.
Speaker 2: Yep. And don't forget the jugular venus pressure. If you
Speaker 2: look at her neck, you'll see that characteristic flicking a wave.
Speaker 1: Because the right atrium is vigorously contracting against a really stiff,
Speaker 1: non compliant right ventricle. Right, it just sends a shockwave
Speaker 1: back up the jugular vein exactly.
Speaker 2: The clinical imperative for you here is uncovering the ideology
Speaker 2: of this massive right sided strain in a middle aged
Speaker 2: female presenting with this degree of pulmonary hypertension. You're primarily
Speaker 2: differentiating between recurrent microscopic pulmonary emboli that have been showering
Speaker 2: the lungs over time, or primary pulmonary hypertension.
Speaker 1: Where the pulmonary arterials themselves undergo pathological remodeling.
Speaker 2: Right, So she needs a VQ scan or a CT
Speaker 2: pulmonary angiogram immediately, and the management will undoubtedly involve long
Speaker 2: term anti coagulation. But honestly, the mechanical consequences are just severe.
Speaker 1: Yeah, the specific scenario detailed by Professor Hampton actually ultimately
Speaker 1: required a heart lung transplant.
Speaker 2: It's devastating. The mechanical destruction was absolute, but the very
Speaker 2: first clue to all of it was entirely electrical.
Speaker 1: That's incredible. Okay, Moving from chronic mechanical strain, we need
Speaker 1: to transition to acute immediate life threats. Let's talk about
Speaker 1: the tachycardia emergency.
Speaker 2: Oh, the adrenaline pumperson exactly.
Speaker 1: Let's return to the scenario we open the episode with.
Speaker 1: When a patient's heart rate suddenly jumps to two hundred
Speaker 1: and fifty or three hundred beats per minute, you must
Speaker 1: differentiate the rhythm instantly. Let's compare two patients in profound
Speaker 1: cardiogenic shock. They are both cold, clammy and hypertensive.
Speaker 2: Okay, late on me.
Speaker 1: Patient A is a fifty year old man with a
Speaker 1: narrow complex tachycardia at a blistering three hundred beats per minute.
Speaker 1: There are no discernible pa waves, just a continuous oscillation
Speaker 1: with some secondary st depression in the lateral leads.
Speaker 2: Got it.
Speaker 1: Patient B is a man with a known history of
Speaker 1: an anterior myocardial infarction. He is presenting with a broad
Speaker 1: complex tachycardia at two hundred and fifty beats per minute
Speaker 1: and the qr S duration is a massive two hundred milliseconds.
Speaker 1: With this ugly, just bizarre morphology, Okay.
Speaker 2: Let's attack Patient A first, A narrow complex at exactly
Speaker 2: three hundred beats per minute. That is the absolute hallmark
Speaker 2: of atrial flutter with one to one conduction.
Speaker 1: Because the flutter circuit in the right Ahroum circle is
Speaker 1: at exactly three hundred beats per.
Speaker 2: Minute precisely now. Usually the eighty note acts like a
Speaker 2: physiological gatekeeper. It blocks out every second or third impulse
Speaker 2: so the ventricles don't race too fast. But in one
Speaker 2: to one conduction that gate is just wide open. Every
Speaker 2: single flutter wave triggers a ventricular depolarization.
Speaker 1: It's kind of like thinking of the av note like
Speaker 1: a bouncer at a crowded nightclub.
Speaker 2: Oh I like that.
Speaker 1: Yeah. Normally he stopped in the line right, letting people
Speaker 1: in slowly one by one, But in one to one flutter,
Speaker 1: the bouncer just falls asleep. The doors fly open, and
Speaker 1: everyone rushes the floor all at once.
Speaker 2: It's a stampede, a total stampede. And the reason this
Speaker 2: patient is in shock is pure hemodynamics. At three hundred
Speaker 2: beats per minute, diastolic filling time essentially drops to zero. Wow.
Speaker 1: So they're just pumping empty air.
Speaker 2: Basically, the ventricles are vigorously squeezing, but there's literally no
Speaker 2: time for them to fill with blood between beats. Squeezing
Speaker 2: on empty means cardiac output plummets and the patient collapses.
Speaker 1: Right now, what about patient B?
Speaker 2: So patient B, the broad qres complex tells us that
Speaker 2: depolarization is not utilizing the his perkinga system at all.
Speaker 2: It's originating from within the ventricular muscle itself and spreading
Speaker 2: slowly cell by cell.
Speaker 1: So this is ventricular tachycardia.
Speaker 2: It is, and the absolute most critical clinical pearl here
Speaker 2: from the text is a fundamental rule of emergency medicine
Speaker 2: in the context of ischemic heart disease or a previous
Speaker 2: myocardial infarction. A broad complex tachycardia must always be treated
Speaker 2: as ventricular tachycardia, no exceptions, unless you have a prior
Speaker 2: tracing proving they had a pre existing bundle branch block.
Speaker 2: No exceptions. You assume VT.
Speaker 1: Because that post on my scar tissue forms the perfect
Speaker 1: re entry circuit for VT. It's the ultimate do not
Speaker 1: misdiagnosis exactly.
Speaker 2: But the fascinating convergence here is that, despite these being
Speaker 2: two completely distinct arrhythmias originating from totally different chambers, your
Speaker 2: acute management for both of these hypotensive crashing patients is identical.
Speaker 1: Because they're heemodynamically unstable.
Speaker 2: Right, there is zero time for pharmacological trials. I mean,
Speaker 2: anti rhythmics take time to circulate and work, and these
Speaker 2: patients have no effect to circulation, so you shock them.
Speaker 2: Immediate definitive treatment for both is synchronized DC cardioversion. You
Speaker 2: must electrically depolarize the entire myocardium simultaneously to reset the
Speaker 2: base makers.
Speaker 1: Okay, let's contrast that chaotic emergency with a hemodynamically stable presentation.
Speaker 1: Say you have a patient presenting with palpitations. Heart rate
Speaker 1: is a one eighty. The QRS is narrow and PA
Speaker 1: waves are either buried or retrograde. But they are sitting
Speaker 1: up chatting with you, and their blood pressure is a
Speaker 1: solid one twenty over eighty.
Speaker 2: Okay, so this is likely an av nodal re entry
Speaker 2: tactcardia or av NRT. And because they are stable, you
Speaker 2: have the luxury of an escalator management ladder.
Speaker 1: You don't have to jump straight to the paddles exactly.
Speaker 2: You start non invasively with vaguel maneuvers like the volsalva
Speaker 2: maneuver or carotid sinus.
Speaker 1: Massage, and those techniques increase parasmithetic tone via the vegus
Speaker 1: nerve rap They.
Speaker 2: Release acetocholine at the AV node to prolong the refractory period,
Speaker 2: which hopefully breaks that re entry circuit.
Speaker 1: But if the vagel maneuvers fail, then you move to
Speaker 1: your pharmacological options right starting with intravenous A dentisine.
Speaker 2: A dnasceine is such a fascinating drug, it really is.
Speaker 1: You give it as this rapid large bore IV bollus.
Speaker 1: It binds to the A one pure innergic receptors on
Speaker 1: the AV node, which causes potassium channels to open and.
Speaker 2: Then potassium just rushes out of the.
Speaker 1: Cell exactly, deeply, hyperpolarizing the AV node and inducing a
Speaker 1: transient total AV block for about what five to ten seconds?
Speaker 2: Yeah? About that, and the patient will likely experience a
Speaker 2: profound sense of impending doom and severe flushing during those
Speaker 2: few seconds before the half life clears.
Speaker 1: It's verifying for them, it.
Speaker 2: Is, But the text includes a super vital contraindication you
Speaker 2: have to check for first. A dentisine can activate purenergic
Speaker 2: receptors in the bronchial smooth muscle.
Speaker 1: OH, triggering severe bronchospasm.
Speaker 2: Right, it is strictly contraindicated in asthmatics. If they have asthma,
Speaker 2: you pivot entirely and use intravenous vrap mil, which is
Speaker 2: a calcium channel blocker, just to slow that AV node down.
Speaker 1: And you only move to DC cardioversion for a stable
Speaker 1: patient if literally every pharmacological option on that ladder completely fails.
Speaker 2: Exactly.
Speaker 1: All right, Let's shift our focus for our final analysis
Speaker 1: to the most common presentation you will face in the
Speaker 1: er chess pain. We really need to distinguish actual aeschemia
Speaker 1: from a pathology that mimics. It almost perfectly.
Speaker 2: This is such a critical distinction. Let's start with a
Speaker 2: really challenging ischemic presentation. Say a patient arrives with crushing
Speaker 2: chest pain and an ECG showing acute anterior st elevation. However,
Speaker 2: they report the ping started over eighteen hours ago.
Speaker 1: Okay, so conventionally strict textbook protocols might suggest they are
Speaker 1: well outside the window for thrombolytic therapy because you'd assume
Speaker 1: the myocardium is already fully infarcted.
Speaker 2: But those rigid textbook rules completely break down here. The
Speaker 2: clinical reality is that if the patient is still experiencing
Speaker 2: severe pain and appears acutely unwell, the eschemic cascade is
Speaker 2: still active.
Speaker 1: Meaning there is still dying salvageble myocardium.
Speaker 2: Yes, the text insists that theromolysis should absolutely still be
Speaker 2: considered regardless of that eighteen hour mark. Right alongside your
Speaker 2: standard aspirin, heparin and analgesia. You treat the ongoing aeschemia,
Speaker 2: not just the clock on the wall.
Speaker 1: That makes total sense. And if you happen to note
Speaker 1: an incidental finding of an old inferior infarction indicated by
Speaker 1: pathological Q waves and inverted T waves and leads two
Speaker 1: three in AVF. Your clinical responsibility extends beyond just the
Speaker 1: acute event.
Speaker 2: Right, because that patient requires really aggressive secondary prevention strip
Speaker 2: lipid control with statins, anti platelet therapy, and likely a
Speaker 2: functional stress test to evaluate the need.
Speaker 1: For geography, which brings us perfectly to the great mimic.
Speaker 1: You are evaluating a thirty five year old man who
Speaker 1: complains of exertional chest pain and occasional exertional syncope.
Speaker 2: Okay, you pull the.
Speaker 1: ECG and see massive gross symmetrical T wave inversions across
Speaker 1: the antirelateral leads, so I AVL and V four through
Speaker 1: V six. Now, those massive inversions usually scream one thing,
Speaker 1: a massive acute non st elevation myocardial infection. You assume
Speaker 1: a critical laed lesion.
Speaker 2: Right, But you have to look at the patient profile.
Speaker 2: This is a young man with exertional syncope.
Speaker 1: Right.
Speaker 2: While extreme keywave inversion can represent severe ischemia in a
Speaker 2: young patient who lacks other voltage criteria for profound hypertensive
Speaker 2: left ventricular hypertrophy, this specific gross antilateral repolarization abnormality is
Speaker 2: a classic hallmark of hypertrophic cardiomyopathy or ehgm Wow.
Speaker 1: So it is not an atherrosclerotic plumbing problem at all,
Speaker 1: Not at all.
Speaker 2: It is a genetic mutation causing a massive, disorganized hypertrophy
Speaker 2: of my cardium, specifically the interventricular septum.
Speaker 1: And the physical exam signs for this are just a
Speaker 1: master class in hemo dynamics. Because that thickened septum bulges
Speaker 1: into the left ventricular outflow tract, it creates a dynamic obstruction.
Speaker 1: So when you palpate the carotid pulse, you feel what's
Speaker 1: called a jerky pulse, a rapid initial upstroke as the
Speaker 1: ventricle starts to empty, followed immediately by a sharp decline
Speaker 1: as that hypergropeed septum literally gets sucked across the outflow tract,
Speaker 1: obstructing the rest of the stroke volume.
Speaker 2: It's wild, but honestly, the most brilliant physiological pearl in
Speaker 2: the text involves the ouscultation of the harsh systolic injection murmur.
Speaker 1: Oh, this is fascinating.
Speaker 2: If you listen really closely, this murmur gets characteristically louder
Speaker 2: following a premature of ventricular contraction or PVC.
Speaker 1: Wait, why would a PVC make it louder?
Speaker 2: Well, if you map the mechanics, the PBC causes a
Speaker 2: compensatory pause the heart rests for an extra second, which
Speaker 2: massively increases a diastolic filling time.
Speaker 1: And increase filling time means increased preload exactly.
Speaker 2: And according to the Frank Starling mechanism, the extra stretch
Speaker 2: on those myocardial fibers causes the left ventricle to contract
Speaker 2: significantly harder on the very next beat.
Speaker 1: Oh so that hypercontractile squeeze forcefully narrows the outflow tract
Speaker 1: even further against that bulky septum.
Speaker 2: Yes, worsening the obstruction and driving up the volume of
Speaker 2: the murmur.
Speaker 1: It's an incredibly elegant physical sign for just a terrifying pathology.
Speaker 1: I mean, an echocardiogram will confirm the asymmetric septal hypertrophy
Speaker 1: and demonstrates systolic anterior movement or SAM of the mitral
Speaker 1: valve apparatus where the valve leaflets are literally pulled into
Speaker 1: the outflow track by the Venturi effect.
Speaker 2: It really is a structural nightmare presenting as an electrical.
Speaker 1: Mystery, which honestly brings us full circle. The primary lesson
Speaker 1: from Professor Hampton is that your interpretation of the electrical
Speaker 1: tracing can never ever be decoupled from the physiology of
Speaker 1: the patient in the bed.
Speaker 2: Never the ECG provides the vectors and the intervals, but
Speaker 2: the patient provides the hemodynamics, the history, and the context.
Speaker 1: You cannot treat the paper. You have to treat the
Speaker 1: patient exactly.
Speaker 2: And to ensure we're really cementing that philosophy, I want
Speaker 2: to leave you with a clinical exercise to review before
Speaker 2: you clock into your next shift. Consider this scenario. You
Speaker 2: have a patient presenting with a broad complex tachycardia very
Speaker 2: similar to the postmi ventricular tacic cardia we just discussed,
Speaker 2: but unlike that crashing patient who required immediate cardio version,
Speaker 2: this patient is sitting comfortably. They're fully conscious with a
Speaker 2: blood pressure of one hundred and thirty over eighty.
Speaker 1: So they are hemodynamically stable, but they are.
Speaker 2: In VT exactly. Knowing what we discussed about the escalating
Speaker 2: ladder of interventions for stable narrow complex tachycardias, how does
Speaker 2: your management pathway adapt for a stable broad complex tachycardia.
Speaker 2: Think critically about the pharmacology.
Speaker 1: What specific anti rhythmic agents would you prepare.
Speaker 2: Right and what physiological parameters are you constantly monitoring before
Speaker 2: you ever even consider the defibrillator.
Speaker 1: It's a great question. Rely on your synthesis of the mechanics,
Speaker 1: trust your clinical exam, and whatever you do, don't let
Speaker 1: the squiggles on the page panic you. Take that question
Speaker 1: with you onto the wards and we'll catch you on
Speaker 1: the next deep dive.