WEBVTT 1 00:00:00.080 --> 00:00:02.759 So imagine you've got a fifty year old patient crashing 2 00:00:02.879 --> 00:00:05.639 right in front of you. I mean they are cold, 3 00:00:06.120 --> 00:00:11.640 they're clammy, and their blood pressure is well, it's completely unrecordable. 4 00:00:11.679 --> 00:00:13.240 Oh that's just a nightmare scenario. 5 00:00:13.279 --> 00:00:15.839 On the wards right, and the monitor is just flashing 6 00:00:15.880 --> 00:00:18.640 this insane heart rate of like three hundred beats per minute. 7 00:00:18.719 --> 00:00:22.399 You've got this little strip of paper with chaotic squiggles 8 00:00:22.399 --> 00:00:25.760 in your hand, and you have what maybe ten seconds 9 00:00:25.800 --> 00:00:28.519 to decide. Ten seconds on a good day, exactly, you 10 00:00:28.600 --> 00:00:30.600 have to choose whether to push a drug or just 11 00:00:30.640 --> 00:00:33.880 immediately reach for the defibrillator paddles. And if you make 12 00:00:33.920 --> 00:00:36.000 the wrong choice, I mean, it is. 13 00:00:36.000 --> 00:00:39.079 Fatal, it really is. And that right there, that's the 14 00:00:39.159 --> 00:00:43.479 absolute reality of clinical medicine. It's not the neat, linear 15 00:00:43.600 --> 00:00:45.960 chapter by chapter progression you get when you're sitting in 16 00:00:45.960 --> 00:00:47.359 a library reading a textbook. 17 00:00:47.520 --> 00:00:48.359 No, definitely not. 18 00:00:48.560 --> 00:00:53.719 It's just this landscape of total diagnostic unpredictability. Yeah, I mean, 19 00:00:53.759 --> 00:00:56.000 you don't get to choose the pathology that walks through 20 00:00:56.000 --> 00:00:57.000 the clinic door next. 21 00:00:57.280 --> 00:00:59.840 Yeah, they don't wear a sign saying what chapter they belong. 22 00:00:59.600 --> 00:01:03.200 To exactly, And that's why relying solely on like pattern 23 00:01:03.240 --> 00:01:06.519 recognition from some pristine reference manual, it just falls apart 24 00:01:06.560 --> 00:01:08.480 so quickly. In the emergency department. 25 00:01:08.159 --> 00:01:11.640 Which is actually the exact premise of our deep dive today, 26 00:01:11.719 --> 00:01:14.799 we are taking a really comprehensive look at the book 27 00:01:14.840 --> 00:01:18.760 one hundred and fifty ECG Problems by Emeritis Professor of 28 00:01:18.840 --> 00:01:20.319 Cardiology John R. Hampton. 29 00:01:20.560 --> 00:01:22.680 It's such a brilliant resource, it really is. 30 00:01:22.719 --> 00:01:25.040 And our mission today is to help you bridge that 31 00:01:25.159 --> 00:01:29.719 gap between basic theory and that super muddy high stakes 32 00:01:29.799 --> 00:01:33.040 clinical application. So just as a heads up, we aren't 33 00:01:33.120 --> 00:01:38.000 reviewing how to attach leads or you know, basic intervals today. 34 00:01:37.879 --> 00:01:39.319 Right, We're assuming you know the basics. 35 00:01:39.480 --> 00:01:42.519 Yeah, we are pulling the core clinical pearls directly from 36 00:01:42.560 --> 00:01:46.159 Hampton's work, and we're focusing intensely on the pathophysiology and 37 00:01:46.200 --> 00:01:46.760 the management. 38 00:01:46.799 --> 00:01:49.319 And honestly, the methodology of this text is what makes 39 00:01:49.319 --> 00:01:53.200 it so incredibly useful for your actual clinical practice. The 40 00:01:53.280 --> 00:01:55.560 scenarios are presented completely at random. 41 00:01:55.480 --> 00:01:57.359 Which feels super chaotic at first. 42 00:01:57.640 --> 00:02:01.519 It does, but it perfectly mirrors a real world shift, 43 00:02:02.480 --> 00:02:05.760 like you might face a totally benign physiological variant one 44 00:02:05.799 --> 00:02:08.680 minute and then boom, a cardiogenic shock. The next You 45 00:02:08.719 --> 00:02:11.199 don't know the difficulty ready of the case until you 46 00:02:11.240 --> 00:02:12.199 flip to the answer. 47 00:02:12.319 --> 00:02:14.719 But okay, let's unpack that for a second, isn't it, 48 00:02:14.840 --> 00:02:17.919 I don't know, a bit overwhelming to get hit with random, 49 00:02:18.280 --> 00:02:21.879 ungraded cases. It feels almost like getting a pop quiz 50 00:02:21.960 --> 00:02:23.879 every single time you open a clinic door. 51 00:02:24.199 --> 00:02:27.120 Well yeah, but that is the reality of medicine, right. 52 00:02:27.599 --> 00:02:31.319 You are forced to interpret that electrical tracing strictly in 53 00:02:31.360 --> 00:02:34.680 the light of the patient's clinical presentation before you ever 54 00:02:34.759 --> 00:02:36.360 know the underlying diagnosis. 55 00:02:36.439 --> 00:02:39.199 Because an ECG and isolation is just a piece of 56 00:02:39.240 --> 00:02:40.319 paper exactly. 57 00:02:40.439 --> 00:02:44.159 It's totally meaningless without context. It requires synthesis. So let's 58 00:02:44.159 --> 00:02:47.280 actually look at how that synthesis works with some of 59 00:02:47.319 --> 00:02:49.800 the deceptively benign presentations you'll encounter. 60 00:02:49.840 --> 00:02:52.080 Okay, let's do it. Consider this. You've got a twenty 61 00:02:52.080 --> 00:02:54.479 five year old pregnant woman presenting to your clinic and 62 00:02:54.520 --> 00:02:57.960 she's complaining of palpitations, just this sort of irregular. 63 00:02:57.479 --> 00:03:00.560 Heartbeat, pretty common presentation, very. 64 00:03:00.400 --> 00:03:05.319 And on ouscultation. You note a soft systolic murmur, but 65 00:03:05.400 --> 00:03:08.280 the rest of her cardiovascular exam is, you know, otherwise 66 00:03:08.639 --> 00:03:12.960 totally unremarkable because you pull an ECG. It shows sinus rhythm, 67 00:03:13.080 --> 00:03:16.120 a normal access, normal intervals, but she has these frequent 68 00:03:16.280 --> 00:03:20.639 ventricular extra systiles. Now, I feel like your immediate instinct 69 00:03:20.680 --> 00:03:24.159 when you see those early wide complexes popping up might 70 00:03:24.199 --> 00:03:25.639 be to intervene. 71 00:03:25.360 --> 00:03:27.080 Right, because you see an earhythmia and you want to 72 00:03:27.080 --> 00:03:30.400 fix it. But if you synthesize that tracing with the 73 00:03:30.439 --> 00:03:33.159 actual physiological state of the patient sitting in front of you, 74 00:03:33.479 --> 00:03:35.360 the management pathway changes. 75 00:03:35.120 --> 00:03:36.520 Entirely because she's pregnant. 76 00:03:36.639 --> 00:03:41.240 Precisely, pregnancity induces this massive hyperdynamic state. I mean, maternal 77 00:03:41.280 --> 00:03:43.439 plasma volume increases by up to fifty percent. 78 00:03:43.560 --> 00:03:45.680 Wow, fifty percent is huge. 79 00:03:45.360 --> 00:03:48.840 It is, and that massively drives up cardiac output. In 80 00:03:48.960 --> 00:03:54.479 that specific physiological environment, ventricular extra systiles are incredibly common, 81 00:03:55.199 --> 00:03:57.919 and more importantly, they're usually entirely benign. 82 00:03:58.159 --> 00:04:00.719 And I guess that murmur plays right into that hyperdynamic 83 00:04:00.759 --> 00:04:05.199 state as well, absolutely, because with that significantly increased stroke 84 00:04:05.280 --> 00:04:08.759 volume just pushing through the same valve orifices, you're going 85 00:04:08.800 --> 00:04:12.800 to get turbulent flow. It's just a classic physiological flow murmur. 86 00:04:13.479 --> 00:04:15.599 Yeah, and you have to add in the dilutional anemia. 87 00:04:15.680 --> 00:04:19.439 That's well, it's almost universal in the second and third trimesters. 88 00:04:18.959 --> 00:04:22.439 Right, because the plasma volume outpaces the red blood cell 89 00:04:22.480 --> 00:04:24.040 production exactly. 90 00:04:23.600 --> 00:04:28.399 Which decreases blood viscosity, and that just amplifies that turbulence 91 00:04:28.399 --> 00:04:29.279 even more. So. 92 00:04:29.399 --> 00:04:32.600 Your management here is basically just conservative reassurance. 93 00:04:32.759 --> 00:04:35.879 Yep, you do not treat the extra systellies. In fact, 94 00:04:36.240 --> 00:04:41.279 the text explicitly warns against reflexively ordering an echo cardiogram 95 00:04:41.319 --> 00:04:44.160 for every pregnant patient with a systolic murmur. 96 00:04:44.000 --> 00:04:46.160 Because it's just a poor use of resources. 97 00:04:46.279 --> 00:04:49.040 Yeah, it's a terrible use of resources. Yeah, best practice 98 00:04:49.079 --> 00:04:52.639 dictates reserving the echo for murmurs that persist well into 99 00:04:52.639 --> 00:04:55.920 the postpartum period, once that plasma volume has actually had 100 00:04:55.920 --> 00:04:56.879 time to normalize. 101 00:04:56.959 --> 00:04:59.480 Right. It's a perfect example of a normal abnormality. The 102 00:04:59.519 --> 00:05:04.120 tracing is technically abnormal, but physiologically it's totally expected. But 103 00:05:04.279 --> 00:05:07.000 what happens when we move away from those normal variants 104 00:05:07.040 --> 00:05:09.600 and look at an electrical system that is actively being 105 00:05:09.639 --> 00:05:13.720 poisoned from the outside Because external pharmacological agents leave these 106 00:05:13.800 --> 00:05:16.480 highly specific fingerprints on an ECG, don't they. 107 00:05:16.560 --> 00:05:19.480 Oh, they definitely do. And degoxin toxicity is a prime 108 00:05:19.480 --> 00:05:21.800 example of this. Oh yeah, when a patient is on 109 00:05:21.839 --> 00:05:25.759 a therapeutic dose of digoxin, you'll frequently see this characteristic 110 00:05:25.879 --> 00:05:28.240 downward sloping ST segment depression. 111 00:05:28.480 --> 00:05:31.439 It looks almost like a sagging scoop, right, or like 112 00:05:31.480 --> 00:05:32.519 a reverse tick mark. 113 00:05:32.600 --> 00:05:35.480 The reverse tick mark exactly. But here's the thing. Spotting 114 00:05:35.480 --> 00:05:38.839 the drug effect is one thing, the critical clinical pearl. 115 00:05:38.879 --> 00:05:42.600 Here is spotting the catalyst that's pushing that therapeutic dose 116 00:05:42.879 --> 00:05:44.800 over the edge into toxicity. 117 00:05:44.920 --> 00:05:47.240 Right. So, say you're looking at that same tracing, but 118 00:05:47.319 --> 00:05:51.439 you also happen to notice prominent U waves, particularly in 119 00:05:51.480 --> 00:05:53.120 the precordial leads like V two. 120 00:05:53.439 --> 00:05:55.800 Well, those U waves are the absolute hallmark of a 121 00:05:55.879 --> 00:06:00.279 hypocoleemia low potassium, and this is where the underlying mechanism 122 00:06:00.360 --> 00:06:04.639 completely dictates your management. How So, So, degoxin works by 123 00:06:04.680 --> 00:06:09.279 binding to and inhibiting the sodium potassium et PAS pump 124 00:06:09.360 --> 00:06:12.759 in the myocardial cell membrane. But the kicker is it 125 00:06:12.839 --> 00:06:16.639 binds to the exact same extracellular site that potassium does. 126 00:06:16.800 --> 00:06:19.519 Oh I see, so they are directly competing for real 127 00:06:19.639 --> 00:06:21.399 estate on that exact same pump. 128 00:06:21.480 --> 00:06:25.240 Precisely, So, if your patient is hypokolemic, say maybe they 129 00:06:25.240 --> 00:06:28.000 are on a loop diuretic like firosamine. That just washing 130 00:06:28.040 --> 00:06:31.759 potassium out of their system. There's less potassium round to 131 00:06:31.800 --> 00:06:33.519 compete for those binding sites. 132 00:06:33.199 --> 00:06:35.959 Which means more dioxin binds to the pump exactly. 133 00:06:36.120 --> 00:06:38.839 It heavily potentiates the drugs effect. So what was a 134 00:06:38.879 --> 00:06:43.319 perfectly safe therapeutic dose yesterday becomes highly toxic today simply 135 00:06:43.360 --> 00:06:44.800 because they're potassium dropped. 136 00:06:45.000 --> 00:06:48.639 That's fascinating. So the practical clinical application for you listening 137 00:06:48.639 --> 00:06:50.839 to this is all in the history taking. You see 138 00:06:50.839 --> 00:06:53.600 the sagging ST segments, you spot the U waves, You 139 00:06:53.680 --> 00:06:56.360 need to immediately ask the patient about their appetite. 140 00:06:56.560 --> 00:06:59.879 Yes, the text specifically notes that the very earliest symptom 141 00:06:59.879 --> 00:07:03.879 of digoxant toxicity is anorexia, just a total loss of appetite, 142 00:07:03.920 --> 00:07:05.879 followed pretty closely by nausea and vomiting. 143 00:07:06.079 --> 00:07:09.439 You obviously verify that with serum digoxin and potassium levels. 144 00:07:09.800 --> 00:07:14.600 But the ECG basically just handed you the entire physiological narrative. 145 00:07:14.720 --> 00:07:18.519 It really did. Now, let's contrast that external pharmacological poasoning 146 00:07:18.560 --> 00:07:22.920 with an internal, just catastrophic failure of the electrical wiring itself. Okay, 147 00:07:23.360 --> 00:07:27.360 consider a patient who presents after a sudden, completely unprovoked, 148 00:07:27.439 --> 00:07:30.959 sinkable episode and they sustain a fall. You run the 149 00:07:31.000 --> 00:07:34.639 ECG and you see complete atrioventricular dissociation. 150 00:07:34.240 --> 00:07:35.319 So complete heart block. 151 00:07:35.519 --> 00:07:38.959 Yeah, the P waves are firing at a normal intrinsic rate, 152 00:07:39.040 --> 00:07:42.519 let's say, seventy beats per minute, but the QRS complexes 153 00:07:42.560 --> 00:07:45.560 are completely divorced from them. They're firing at this slow, 154 00:07:45.839 --> 00:07:47.800 wide forty five beats permitted. 155 00:07:47.639 --> 00:07:50.439 Right, So the electrical signal from the essay node is 156 00:07:50.480 --> 00:07:53.600 basically hitting a brick wall at the AV node catal roadblock, 157 00:07:53.800 --> 00:07:56.439 and the ventricles realize they're getting no signal at all, 158 00:07:56.480 --> 00:07:58.959 so they trigger their own intrinsic escape rhythm just to 159 00:07:59.040 --> 00:08:01.800 keep the patient from diet exactly. And the reason those 160 00:08:01.879 --> 00:08:05.120 QRS complexes are wide is because that escape pace maker 161 00:08:05.319 --> 00:08:08.439 is located really low down in the ventricular myocardium, right 162 00:08:08.759 --> 00:08:10.319 below the Hysperkinji system. 163 00:08:10.560 --> 00:08:14.399 You nailed it. The depolarization wave has to spread slowly, 164 00:08:14.879 --> 00:08:18.319 literally muscle cell to muscle cell, rather than shooting down 165 00:08:18.360 --> 00:08:19.160 those fast. 166 00:08:18.920 --> 00:08:24.000 Electrical highways, and that slow ventricular rate just drastically drops 167 00:08:24.120 --> 00:08:29.480 the cardiac output, which leads to cerebral hypoperfusion and the syncope. 168 00:08:28.959 --> 00:08:32.200 Right, a classic Stokes atoms attack. And regardless of whether 169 00:08:32.240 --> 00:08:35.679 the patient remembers feeling dizzy before they fell, the management 170 00:08:35.720 --> 00:08:36.559 here is immediate. 171 00:08:36.919 --> 00:08:37.759 They need pacing. 172 00:08:37.919 --> 00:08:41.399 This patient requires a permanent pacemaker full stop. If there 173 00:08:41.399 --> 00:08:45.559 are any surgical delays, a temporary transvenous pacing wire has 174 00:08:45.600 --> 00:08:48.320 to be floated immediately. You physically have to bridge that 175 00:08:48.399 --> 00:08:49.720 broken electrical connection. 176 00:08:50.279 --> 00:08:52.279 Wow. Okay, so we've looked at what happens when the 177 00:08:52.279 --> 00:08:55.320 electrical wiring fails. Let's shift gears for a minute and 178 00:08:55.320 --> 00:08:57.480 look at what happens when the electrical system is perfectly 179 00:08:57.480 --> 00:09:01.519 intact but it is forced to drive a ructurally deformed pump. 180 00:09:01.679 --> 00:09:03.799 Oh, this is where it gets really interesting mechanically. 181 00:09:04.080 --> 00:09:08.759 Yeah, like, how does massive mechanical strain alter in electrical tracing. 182 00:09:09.679 --> 00:09:12.120 Let's picture a forty year old woman referred to your 183 00:09:12.120 --> 00:09:16.879 clinic with progressive severe dyspinea. Her ECG shows peaked P 184 00:09:17.120 --> 00:09:21.679 waves in laid two, marked right axis deviation and dominant 185 00:09:21.720 --> 00:09:24.799 tall R waves in lead V one, along with deep 186 00:09:25.000 --> 00:09:26.440 S waves in lead V six. 187 00:09:26.600 --> 00:09:29.799 And you'd probably see P wave inversions across the right 188 00:09:29.840 --> 00:09:31.480 sided and inferior leads too. 189 00:09:31.679 --> 00:09:33.440 Yep, So what's happening there. 190 00:09:33.519 --> 00:09:36.480 You really have to visualize the vector physics here. In 191 00:09:36.519 --> 00:09:40.440 a normal healthy heart, the left ventricle is massively thicker 192 00:09:40.519 --> 00:09:43.399 than the right, so the dominant electrical vector pulls leftward 193 00:09:43.399 --> 00:09:44.919 and posteriorly. 194 00:09:44.320 --> 00:09:46.600 Right away from lead V one, since V one sits 195 00:09:46.720 --> 00:09:48.200 right over the right ventricle. 196 00:09:47.919 --> 00:09:51.000 Exactly, and that a wave vector produces the normal deep 197 00:09:51.159 --> 00:09:53.279 negative S wave you expect to see in V one, 198 00:09:53.720 --> 00:09:56.279 But in this patient, V one shows a dominant positive 199 00:09:56.399 --> 00:09:59.600 R wave. The whole electrical vector has completely flipped, the 200 00:09:59.600 --> 00:10:01.720 electric literally surging towards the right. 201 00:10:01.799 --> 00:10:03.600 It's almost as if the right ventricle is I don't 202 00:10:03.639 --> 00:10:06.120 know a bodybuilder who has been forced to push against 203 00:10:06.120 --> 00:10:07.320 a jam door for years. 204 00:10:07.480 --> 00:10:08.799 That's a really good way to picture it. 205 00:10:08.960 --> 00:10:12.639 The muscle mass of the right ventricular free wall has 206 00:10:12.799 --> 00:10:16.799 hypertrophied to such an extreme degree that it now electrically 207 00:10:16.799 --> 00:10:20.639 outweighs the left ventricle. So those electrical signals are literally 208 00:10:20.679 --> 00:10:24.159 traveling through a massive, heavy wall of muscle. 209 00:10:24.039 --> 00:10:26.360 And in this case that jam door you mentioned that 210 00:10:26.440 --> 00:10:30.840 is severe pulmonary vascular resistance. The text identifies these specific 211 00:10:30.919 --> 00:10:35.200 ECG findings as severe right ventricular hypertrophy. 212 00:10:35.360 --> 00:10:38.639 Or RVH and clinically the signs would align perfectly. 213 00:10:38.679 --> 00:10:41.639 Oh absolutely. When you lay hands on this patient, the 214 00:10:41.639 --> 00:10:45.159 physical exam will directly correlate with that tracing. You will 215 00:10:45.159 --> 00:10:49.879 feel a left peristernal heave because that massively hypertrophied right 216 00:10:50.000 --> 00:10:52.960 ventricle is literally lifting your hand off the chest wall 217 00:10:53.000 --> 00:10:53.879 with every single. 218 00:10:53.639 --> 00:10:56.159 System, and you're going to hear a super loud pulmonary 219 00:10:56.159 --> 00:10:58.960 second sound the P two as that high pressure pulmonary 220 00:10:59.000 --> 00:11:00.960 system forcefully slams the valve shut. 221 00:11:01.039 --> 00:11:03.720 Yep. And don't forget the jugular venus pressure. If you 222 00:11:03.720 --> 00:11:06.879 look at her neck, you'll see that characteristic flicking a wave. 223 00:11:07.000 --> 00:11:10.720 Because the right atrium is vigorously contracting against a really stiff, 224 00:11:10.919 --> 00:11:14.159 non compliant right ventricle. Right, it just sends a shockwave 225 00:11:14.200 --> 00:11:16.159 back up the jugular vein exactly. 226 00:11:16.440 --> 00:11:20.240 The clinical imperative for you here is uncovering the ideology 227 00:11:20.320 --> 00:11:24.200 of this massive right sided strain in a middle aged 228 00:11:24.279 --> 00:11:29.240 female presenting with this degree of pulmonary hypertension. You're primarily 229 00:11:29.279 --> 00:11:34.399 differentiating between recurrent microscopic pulmonary emboli that have been showering 230 00:11:34.440 --> 00:11:38.639 the lungs over time, or primary pulmonary hypertension. 231 00:11:38.519 --> 00:11:42.559 Where the pulmonary arterials themselves undergo pathological remodeling. 232 00:11:42.679 --> 00:11:44.759 Right, So she needs a VQ scan or a CT 233 00:11:44.840 --> 00:11:49.440 pulmonary angiogram immediately, and the management will undoubtedly involve long 234 00:11:49.559 --> 00:11:53.919 term anti coagulation. But honestly, the mechanical consequences are just severe. 235 00:11:54.120 --> 00:11:57.440 Yeah, the specific scenario detailed by Professor Hampton actually ultimately 236 00:11:57.440 --> 00:11:59.159 required a heart lung transplant. 237 00:11:59.240 --> 00:12:02.200 It's devastating. The mechanical destruction was absolute, but the very 238 00:12:02.240 --> 00:12:04.720 first clue to all of it was entirely electrical. 239 00:12:04.840 --> 00:12:07.799 That's incredible. Okay, Moving from chronic mechanical strain, we need 240 00:12:07.840 --> 00:12:11.600 to transition to acute immediate life threats. Let's talk about 241 00:12:11.600 --> 00:12:12.879 the tachycardia emergency. 242 00:12:12.960 --> 00:12:14.919 Oh, the adrenaline pumperson exactly. 243 00:12:15.159 --> 00:12:17.320 Let's return to the scenario we open the episode with. 244 00:12:17.879 --> 00:12:20.440 When a patient's heart rate suddenly jumps to two hundred 245 00:12:20.440 --> 00:12:22.960 and fifty or three hundred beats per minute, you must 246 00:12:23.000 --> 00:12:27.799 differentiate the rhythm instantly. Let's compare two patients in profound 247 00:12:27.840 --> 00:12:32.120 cardiogenic shock. They are both cold, clammy and hypertensive. 248 00:12:32.399 --> 00:12:33.159 Okay, late on me. 249 00:12:33.559 --> 00:12:35.600 Patient A is a fifty year old man with a 250 00:12:35.679 --> 00:12:39.840 narrow complex tachycardia at a blistering three hundred beats per minute. 251 00:12:39.879 --> 00:12:43.200 There are no discernible pa waves, just a continuous oscillation 252 00:12:43.679 --> 00:12:46.639 with some secondary st depression in the lateral leads. 253 00:12:46.720 --> 00:12:47.080 Got it. 254 00:12:47.360 --> 00:12:49.519 Patient B is a man with a known history of 255 00:12:49.559 --> 00:12:53.440 an anterior myocardial infarction. He is presenting with a broad 256 00:12:53.440 --> 00:12:56.240 complex tachycardia at two hundred and fifty beats per minute 257 00:12:56.320 --> 00:12:59.639 and the qr S duration is a massive two hundred milliseconds. 258 00:12:59.639 --> 00:13:02.480 With this ugly, just bizarre morphology, Okay. 259 00:13:02.279 --> 00:13:05.720 Let's attack Patient A first, A narrow complex at exactly 260 00:13:05.759 --> 00:13:08.879 three hundred beats per minute. That is the absolute hallmark 261 00:13:08.919 --> 00:13:11.399 of atrial flutter with one to one conduction. 262 00:13:11.120 --> 00:13:13.480 Because the flutter circuit in the right Ahroum circle is 263 00:13:13.519 --> 00:13:15.120 at exactly three hundred beats per. 264 00:13:15.000 --> 00:13:18.279 Minute precisely now. Usually the eighty note acts like a 265 00:13:18.279 --> 00:13:22.080 physiological gatekeeper. It blocks out every second or third impulse 266 00:13:22.120 --> 00:13:24.440 so the ventricles don't race too fast. But in one 267 00:13:24.440 --> 00:13:28.240 to one conduction that gate is just wide open. Every 268 00:13:28.279 --> 00:13:31.759 single flutter wave triggers a ventricular depolarization. 269 00:13:32.159 --> 00:13:33.960 It's kind of like thinking of the av note like 270 00:13:34.000 --> 00:13:35.679 a bouncer at a crowded nightclub. 271 00:13:35.879 --> 00:13:36.559 Oh I like that. 272 00:13:36.799 --> 00:13:39.480 Yeah. Normally he stopped in the line right, letting people 273 00:13:39.480 --> 00:13:42.799 in slowly one by one, But in one to one flutter, 274 00:13:43.039 --> 00:13:45.679 the bouncer just falls asleep. The doors fly open, and 275 00:13:45.759 --> 00:13:47.360 everyone rushes the floor all at once. 276 00:13:47.440 --> 00:13:50.360 It's a stampede, a total stampede. And the reason this 277 00:13:50.399 --> 00:13:53.799 patient is in shock is pure hemodynamics. At three hundred 278 00:13:53.840 --> 00:13:57.960 beats per minute, diastolic filling time essentially drops to zero. Wow. 279 00:13:58.039 --> 00:13:59.320 So they're just pumping empty air. 280 00:13:59.440 --> 00:14:04.000 Basically, the ventricles are vigorously squeezing, but there's literally no 281 00:14:04.039 --> 00:14:07.120 time for them to fill with blood between beats. Squeezing 282 00:14:07.159 --> 00:14:10.679 on empty means cardiac output plummets and the patient collapses. 283 00:14:10.799 --> 00:14:11.879 Right now, what about patient B? 284 00:14:12.200 --> 00:14:16.279 So patient B, the broad qres complex tells us that 285 00:14:16.399 --> 00:14:19.759 depolarization is not utilizing the his perkinga system at all. 286 00:14:20.039 --> 00:14:23.519 It's originating from within the ventricular muscle itself and spreading 287 00:14:23.519 --> 00:14:24.679 slowly cell by cell. 288 00:14:24.879 --> 00:14:26.559 So this is ventricular tachycardia. 289 00:14:26.720 --> 00:14:29.679 It is, and the absolute most critical clinical pearl here 290 00:14:29.840 --> 00:14:33.720 from the text is a fundamental rule of emergency medicine 291 00:14:33.799 --> 00:14:37.279 in the context of ischemic heart disease or a previous 292 00:14:37.279 --> 00:14:41.759 myocardial infarction. A broad complex tachycardia must always be treated 293 00:14:41.799 --> 00:14:45.080 as ventricular tachycardia, no exceptions, unless you have a prior 294 00:14:45.159 --> 00:14:47.799 tracing proving they had a pre existing bundle branch block. 295 00:14:47.919 --> 00:14:50.200 No exceptions. You assume VT. 296 00:14:50.240 --> 00:14:52.759 Because that post on my scar tissue forms the perfect 297 00:14:52.759 --> 00:14:55.399 re entry circuit for VT. It's the ultimate do not 298 00:14:55.480 --> 00:14:56.960 misdiagnosis exactly. 299 00:14:57.279 --> 00:15:00.480 But the fascinating convergence here is that, despite these being 300 00:15:00.519 --> 00:15:04.879 two completely distinct arrhythmias originating from totally different chambers, your 301 00:15:04.879 --> 00:15:09.159 acute management for both of these hypotensive crashing patients is identical. 302 00:15:09.159 --> 00:15:11.080 Because they're heemodynamically unstable. 303 00:15:11.320 --> 00:15:14.960 Right, there is zero time for pharmacological trials. I mean, 304 00:15:15.000 --> 00:15:17.600 anti rhythmics take time to circulate and work, and these 305 00:15:17.600 --> 00:15:20.279 patients have no effect to circulation, so you shock them. 306 00:15:20.840 --> 00:15:26.279 Immediate definitive treatment for both is synchronized DC cardioversion. You 307 00:15:26.360 --> 00:15:31.159 must electrically depolarize the entire myocardium simultaneously to reset the 308 00:15:31.200 --> 00:15:31.840 base makers. 309 00:15:32.000 --> 00:15:37.000 Okay, let's contrast that chaotic emergency with a hemodynamically stable presentation. 310 00:15:37.759 --> 00:15:40.960 Say you have a patient presenting with palpitations. Heart rate 311 00:15:41.039 --> 00:15:43.960 is a one eighty. The QRS is narrow and PA 312 00:15:44.000 --> 00:15:47.120 waves are either buried or retrograde. But they are sitting 313 00:15:47.240 --> 00:15:50.120 up chatting with you, and their blood pressure is a 314 00:15:50.159 --> 00:15:51.879 solid one twenty over eighty. 315 00:15:52.120 --> 00:15:54.559 Okay, so this is likely an av nodal re entry 316 00:15:54.559 --> 00:15:58.360 tactcardia or av NRT. And because they are stable, you 317 00:15:58.399 --> 00:16:00.919 have the luxury of an escalator management ladder. 318 00:16:00.960 --> 00:16:03.120 You don't have to jump straight to the paddles exactly. 319 00:16:03.200 --> 00:16:06.200 You start non invasively with vaguel maneuvers like the volsalva 320 00:16:06.279 --> 00:16:08.080 maneuver or carotid sinus. 321 00:16:07.759 --> 00:16:11.159 Massage, and those techniques increase parasmithetic tone via the vegus 322 00:16:11.200 --> 00:16:12.200 nerve rap They. 323 00:16:12.120 --> 00:16:15.440 Release acetocholine at the AV node to prolong the refractory period, 324 00:16:15.440 --> 00:16:17.600 which hopefully breaks that re entry circuit. 325 00:16:17.799 --> 00:16:19.960 But if the vagel maneuvers fail, then you move to 326 00:16:20.000 --> 00:16:23.879 your pharmacological options right starting with intravenous A dentisine. 327 00:16:23.399 --> 00:16:26.200 A dnasceine is such a fascinating drug, it really is. 328 00:16:26.600 --> 00:16:30.440 You give it as this rapid large bore IV bollus. 329 00:16:30.840 --> 00:16:34.720 It binds to the A one pure innergic receptors on 330 00:16:34.799 --> 00:16:38.399 the AV node, which causes potassium channels to open and. 331 00:16:38.320 --> 00:16:40.000 Then potassium just rushes out of the. 332 00:16:39.960 --> 00:16:44.080 Cell exactly, deeply, hyperpolarizing the AV node and inducing a 333 00:16:44.159 --> 00:16:48.200 transient total AV block for about what five to ten seconds? 334 00:16:48.279 --> 00:16:51.360 Yeah? About that, and the patient will likely experience a 335 00:16:51.440 --> 00:16:55.200 profound sense of impending doom and severe flushing during those 336 00:16:55.240 --> 00:16:57.120 few seconds before the half life clears. 337 00:16:57.320 --> 00:16:58.840 It's verifying for them, it. 338 00:16:58.799 --> 00:17:02.320 Is, But the text includes a super vital contraindication you 339 00:17:02.360 --> 00:17:05.599 have to check for first. A dentisine can activate purenergic 340 00:17:05.640 --> 00:17:08.160 receptors in the bronchial smooth muscle. 341 00:17:07.960 --> 00:17:10.160 OH, triggering severe bronchospasm. 342 00:17:10.319 --> 00:17:13.880 Right, it is strictly contraindicated in asthmatics. If they have asthma, 343 00:17:13.920 --> 00:17:16.720 you pivot entirely and use intravenous vrap mil, which is 344 00:17:16.759 --> 00:17:19.680 a calcium channel blocker, just to slow that AV node down. 345 00:17:19.880 --> 00:17:22.880 And you only move to DC cardioversion for a stable 346 00:17:22.920 --> 00:17:27.119 patient if literally every pharmacological option on that ladder completely fails. 347 00:17:27.359 --> 00:17:27.839 Exactly. 348 00:17:28.240 --> 00:17:31.079 All right, Let's shift our focus for our final analysis 349 00:17:31.119 --> 00:17:33.319 to the most common presentation you will face in the 350 00:17:33.599 --> 00:17:37.319 er chess pain. We really need to distinguish actual aeschemia 351 00:17:37.359 --> 00:17:40.160 from a pathology that mimics. It almost perfectly. 352 00:17:40.720 --> 00:17:43.240 This is such a critical distinction. Let's start with a 353 00:17:43.240 --> 00:17:48.599 really challenging ischemic presentation. Say a patient arrives with crushing 354 00:17:48.680 --> 00:17:54.039 chest pain and an ECG showing acute anterior st elevation. However, 355 00:17:54.079 --> 00:17:56.400 they report the ping started over eighteen hours ago. 356 00:17:56.599 --> 00:17:59.799 Okay, so conventionally strict textbook protocols might suggest they are 357 00:17:59.799 --> 00:18:02.960 well outside the window for thrombolytic therapy because you'd assume 358 00:18:02.960 --> 00:18:05.039 the myocardium is already fully infarcted. 359 00:18:05.200 --> 00:18:08.440 But those rigid textbook rules completely break down here. The 360 00:18:08.480 --> 00:18:11.000 clinical reality is that if the patient is still experiencing 361 00:18:11.039 --> 00:18:15.640 severe pain and appears acutely unwell, the eschemic cascade is 362 00:18:15.640 --> 00:18:16.640 still active. 363 00:18:16.559 --> 00:18:19.880 Meaning there is still dying salvageble myocardium. 364 00:18:20.200 --> 00:18:24.599 Yes, the text insists that theromolysis should absolutely still be 365 00:18:24.640 --> 00:18:28.599 considered regardless of that eighteen hour mark. Right alongside your 366 00:18:28.640 --> 00:18:33.599 standard aspirin, heparin and analgesia. You treat the ongoing aeschemia, 367 00:18:33.680 --> 00:18:34.880 not just the clock on the wall. 368 00:18:34.960 --> 00:18:37.000 That makes total sense. And if you happen to note 369 00:18:37.079 --> 00:18:41.519 an incidental finding of an old inferior infarction indicated by 370 00:18:41.559 --> 00:18:44.720 pathological Q waves and inverted T waves and leads two 371 00:18:44.920 --> 00:18:48.519 three in AVF. Your clinical responsibility extends beyond just the 372 00:18:48.519 --> 00:18:49.480 acute event. 373 00:18:49.480 --> 00:18:53.839 Right, because that patient requires really aggressive secondary prevention strip 374 00:18:53.880 --> 00:18:57.599 lipid control with statins, anti platelet therapy, and likely a 375 00:18:57.640 --> 00:18:59.720 functional stress test to evaluate the need. 376 00:18:59.599 --> 00:19:02.960 For geography, which brings us perfectly to the great mimic. 377 00:19:03.160 --> 00:19:05.119 You are evaluating a thirty five year old man who 378 00:19:05.119 --> 00:19:08.279 complains of exertional chest pain and occasional exertional syncope. 379 00:19:08.319 --> 00:19:09.319 Okay, you pull the. 380 00:19:09.279 --> 00:19:13.640 ECG and see massive gross symmetrical T wave inversions across 381 00:19:13.640 --> 00:19:17.359 the antirelateral leads, so I AVL and V four through 382 00:19:17.400 --> 00:19:19.839 V six. Now, those massive inversions usually scream one thing, 383 00:19:20.200 --> 00:19:24.559 a massive acute non st elevation myocardial infection. You assume 384 00:19:24.599 --> 00:19:26.359 a critical laed lesion. 385 00:19:26.240 --> 00:19:27.839 Right, But you have to look at the patient profile. 386 00:19:28.119 --> 00:19:30.720 This is a young man with exertional syncope. 387 00:19:30.799 --> 00:19:31.000 Right. 388 00:19:31.200 --> 00:19:35.359 While extreme keywave inversion can represent severe ischemia in a 389 00:19:35.400 --> 00:19:39.559 young patient who lacks other voltage criteria for profound hypertensive 390 00:19:39.880 --> 00:19:47.039 left ventricular hypertrophy, this specific gross antilateral repolarization abnormality is 391 00:19:47.079 --> 00:19:51.640 a classic hallmark of hypertrophic cardiomyopathy or ehgm Wow. 392 00:19:51.799 --> 00:19:54.759 So it is not an atherrosclerotic plumbing problem at all, 393 00:19:54.799 --> 00:19:55.359 Not at all. 394 00:19:55.480 --> 00:19:59.400 It is a genetic mutation causing a massive, disorganized hypertrophy 395 00:19:59.599 --> 00:20:03.160 of my cardium, specifically the interventricular septum. 396 00:20:02.920 --> 00:20:05.279 And the physical exam signs for this are just a 397 00:20:05.359 --> 00:20:09.599 master class in hemo dynamics. Because that thickened septum bulges 398 00:20:09.640 --> 00:20:13.240 into the left ventricular outflow tract, it creates a dynamic obstruction. 399 00:20:13.839 --> 00:20:16.640 So when you palpate the carotid pulse, you feel what's 400 00:20:16.680 --> 00:20:19.480 called a jerky pulse, a rapid initial upstroke as the 401 00:20:19.519 --> 00:20:22.519