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He developed cardiacarrest shortly after the ECG in Figure-1 was recorded. IMPRESSION: Given the presence of a wide tachycardia — with 2 distinct QRS morphologies, and no sign of P waves — a presumed diagnosis of B i D irectional Ventricular Tachycardia has to be made. What is the most likely cause of this arrhythmia?
The ECG in Figure-1 — was obtained from a middle-aged man who presented to the ED ( E mergency D epartment ) in cardiacarrest. The rhythm is regular — at a rate just over 100/minute = sinus tachycardia ( ie, the R-R interval is just under 3 large boxes in duration ). Should you activate the cath lab?
The above ECGs show the initiation and continuation of a polymorphic ventricular tachycardia. Polymorphic ventricular tachycardia can be ischemic, catecholaminergic or related to QT prolongation. Cardiacarrest was called and advanced life support was undertaken for this patient. Without an MRI, it is impossible to know.
MY Approach to the Rhythm in Figure-1: As per ECG Blog #185 — I favor the P s, Q s, 3 R Approach for interpretation of the cardiac rhythm — beginning with whichever of these 5 KEY Parameters is easiest to assess for the tracing in front of me: At least in the single lead II rhythm strip seen in Figure-1 — The Q RS complex appears to be narrow.
Then I always look to see if the initial deflection of the QRS has a lot of voltage change per change in time (seen in tachycardias that are initiated from above the ventricle because the propagate through fast conducting purkinje fiber. Tachycardia exaggerates ST Elevation in LBBB and Paced rhythm 5. Pacemaker mediated tachycardia!
But cardiacarrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. After cardiacarrest, I ALWAYS wait 15 minutes after an ECG like this and record another. See these related cases: Cardiacarrest, defibrillated, diffuse ST depression and ST Elevation in aVR.
What is the cardiac rhythm shown in the long lead II rhythm strip? Figure-1: The initial ECG in today’s case — obtained from an elderly woman following successful resuscitation from cardiacarrest. ( These are reviewed in ECG Blog #343. To improve visualization — I've digitized the original ECG using PMcardio ).
See this post: How a pause can cause cardiacarrest 2. For more on Torsades de Pointes vs PMVT See My Comment in the October 18, 2023 post and the September 2, 2024 post in Dr. Smith's ECG Blog ). Even with tachycardia and a paced QRS duration of ~0.16 The plan: 1. Place temporary pacemaker 3. J Am Coll Cardiol.
Blood was drawn , and the patient was promptly placed in a room to be seen — but on entering, the ED physician found her unresponsive in cardiacarrest. Do you see any indication on this ECG of WHY this patient was about to arrest? Is there any indication on this ECG of WHY this patient shortly after had a cardiacarrest?
There was concern that the rhythm might represent ventricular tachycardia, so lidocaine was given and one attempt at cardioversion was performed. A woman in her 50s with dyspnea and bradycardia A patient with cardiacarrest, ROSC, and right bundle branch block (RBBB). HyperKalemia with CardiacArrest.
While on telemetry monitoring he suffered cardiacarrest and was resuscitated. What ECG finding may have contributed to (or precipitated) the cardiacarrest? Learning points : Takotsubo can lead to cardiacarrest from ventricular arrhythmia. There are no clear signs of OMI. There is a prolonged QTc.
This is obviously severe hyperkalemia and the patient is near cardiacarrest. There was no IV access, so we obtained intraosseous (IO) access, but she arrested before we could give her all the calcium. Hyperkalemia and CardiacArrest Could you have prevented this young man's cardiacarrest?
The Long Lead II Rhythm Strip: As always — I favor a systematic approach to rhythm interpretation, using the P s, Q s, 3 R memory aid ( See ECG Blog #185 ). As I have often emphasized — it takes a little time to get good at drawing laddergrams ( See ECG Blog #188 ). ECG Blog #108 — Reviews the concept of AIVR.
Edited by Bracey, Meyers, Grauer, and Smith A 50-something-year-old female with a history of an unknown personality disorder and alcohol use disorder arrived via EMS following cardiacarrest with return of spontaneous circulation. T wave alternans is a harbinger of cardiac instability and TdP. (3) No ischemic ST changes.
He had multiple cardiacarrests with ROSC regained each time. Then there is loss of pulses with continued narrow complex on the monitor ("PEA arrest") Learning Points: Sudden witnessed CardiacArrest due to ACS is almost always due to dysrhythmia. This patient arrested shortly after hospital arrival.
A 60-something woman presented after a witnessed cardiacarrest. This is commonly found after epinephrine for cardiacarrest, but could have been pre-existing and a possible contributing factor to cardiacarrest. Final Diagnosis: CardiacArrest due to Torsades from long QT of unknown etiology.
We received 4 ECGs, including his baseline on file, and three from today, including triage, peri-arrest, and post-ROSC (sorry for the poor quality due to scanning). Prior ECG on file: Sinus tachycardia, imperfect baseline, otherwise unremarkable. Unfortunately, this was not recognized at this time.
Although one may have all kinds of ischemic findings as a result of cardiacarrest (rather than cause of cardiacarrest), this degree of ST elevation and HATW is all but diagnostic of acute proximal LAD occlusion. See Discussion in the June 29, 2024 post of Dr. Smith' ECG Blog ). This prompted cath lab activation.
NOTE: The ECGs in today's case are recorded in the Cabrera Format ( See Dr. Grauer Comment in the October 26, 2020 post of Dr. Smith's ECG Blog for review on the Cabrera Format ). The 2019 ESC Guidelines for the management of patients with supraventricular tachycardia indicated that IV Amiodarone should not be considered in these populations.
NOTE: For those interested — I review in detail determination of the artifact “culprit extremity” in My Comment in the September 27, 2019 post of Dr. Smith’s ECG Blog. This sinus tachycardia ( at ~130/minute ) — is consistent with the patient’s worsening clinical condition, with development of cardiogenic shock.
ECG is consistent with severe hypokalemia and/or hypomagnesemia causing prolonged QT (QU) at high risk of Torsades (which is polymorphic ventricular tachycardia in the setting of a long QT interval). Polymorphic Ventricular Tachycardia Long QT Syndrome with Continuously Recurrent Polymorphic VT: Management CardiacArrest.
This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). As we've often emphasized on Dr. Smith's ECG Blog — it is rare in practice to see LMCA occlusion, because most such patients die before reaching the hospital.
This patient is actively dying from a left main coronary artery OMI and cardiacarrest from VT/VF or PEA is imminent! Complete LMCA occlusion is associated with clinical shock and/or cardiacarrest. The arterial blood gas showed a lactic acidosis with a lactate level of 17mmol/L.
A man in his 30s with cardiacarrest and STE on the post-ROSC ECG == MY Comment , by K EN G RAUER, MD ( 12/31 /2023 ): == My only hope about today's tragic case — is that the involved providers learn from mistakes made. . == The 2 ECGs in Today's CASE: Figure-1: I've labeled the 2 ECGs shown in today's case. Junctional tachycardia? ).
Here was his initial ED ECG: There is sinus tachycardia at a rate of about 140 There is profound ST Elevation across all precordial leads, as well as I and aVL. If a patient presents with chest pain and a normal heart rate, or with shockable cardiacarrest, then ischemic appearing ST elevation is STEMI until proven otherwise.
We've presented numerous examples of hyperkalemia on Dr. Smith's ECG Blog. Descriptive analysis of the ECG in today's case reveals a regular, narrow tachycardia at ~130/minute , without clear sign of sinus P waves. But the rate is ~130/minute — which is a bit fast for sinus tachycardia. WHY Isn't the QRS Wide?
See here for management of Polymorphic Ventricular Tachycardia , which includes Torsades. If cardiacarrest from hypokalemia is imminent (i.e., As I indicated above, in our cardiacarrest case, after pushing 40 mEq, the K only went up to 4.2 Could the dysrhythmias have been prevented? mEq/L, from 1.9
Here is the ECG: Sinus tachycardia. If cardiacarrest from hypokalemia is imminent (i.e., CASE : Prehospital CardiacArrest due to Hypokalemia I recently had a case of prehospital cardiacarrest that turned out to be due to hypokalemia. This patient presented with severe DKA. What do you think?
Other than tachycardia, Other than slight tachycardia, vitals were within normal limits (including oxygen saturation). About two hours after admission, he suffered a cardiacarrest (whether it was VF/VT or PEA is not available) and expired. Apparently he denied chest pain. Here is his first ED ECG: What do you see?
There is sinus tachycardia (do not be fooled into thinking this is VT or another wide complex tachycardia!) Plus recommendations from a 5-member panel on cardiacarrest. This feature is invaluable for assessing QRS morphology with wide tachycardias in the differentiation between SVT vs VT rhythms.
There was 100% proximal LAD occlusion with TIMI 0 flow, and cardiacarrest in the cath lab. Among others — See My Comment at the bottom of the page in the September 13, 2024 post of Dr. Smith's ECG Blog ). There is sinus tachycardia at ~100/minute. For clarity in Figure-1 — I've labeled the initial ECGs for both patients.
Here is his 12-lead: There is a wide complex tachycardia with a rate of 257, with RBBB and LPFB (right axis deviation) morphology. Read about Fascicular VT here: Idiopathic Ventricular Tachycardias for the EM Physician Case Continued He was completely stable, so adenosine was administered. See Learning point 1 below. Arch Intern Med.
Is it ventricular tachycardia (VT) due to hyperK or is it a supraventricular rhythm with hyperK? Here are other posts on hyperK, large calcium doses for hyperK, and ventricular tachycardia in hyperK Weakness, prolonged PR interval, wide complex, ventricular tachycardia Very Wide and Very Fast, What is it? How would you treat?
After initiating treatment for hyperkalemia, repeat ECG showed resolution of Brugada pattern: The ECG shows sinus tachycardia. Steve, what do you think of this ECG in this CardiacArrest Patient?" A woman in her 50s with dyspnea and bradycardia A patient with cardiacarrest, ROSC, and right bundle branch block (RBBB).
Thirty-six patients (36%) presented with cardiacarrest, and 78% (28/36) underwent emergent angiography. We’ve presented many variations on this theme on Dr. Smith’s Blog — with today’s case being distinguished by its discovery on abdominal exam ! Results Emergent angiography was performed in 80% (79/99) of patients.
Smith: This bizarre ECG looks like a post cardiacarrest ECG with probable acidosis or hyperkalemia in addition to OMI. The patient died of cardiogenic shock within 24 hours despite mechanical circulatory support. Below the J-point is marked out showing the ST pathologic deviations. What was the pH and K?
His prehospital ECG showed "inferior" ST depression and high voltage, with tachycardia. I suspected no OMI, that this could be due to LVH plus tachycardia. Conclusion: Type II MI probable due to hypoxia and tachycardia from resp arrest and amphetamine use. On arrival to the ED, the patient was diaphoretic, tachycardic.
This blog is full of cases in which OMI that did not meet STEMI millimeter criteria were dismissed. Series of Prehospital ECGs Showing Reperfusion == MY Comment by K EN G RAUER, MD ( 9/21/2020 ): == I wish those cardiologists who continue to strictly adhere to STEMI millimeter criteria would begin reading Dr. Smith’s ECG Blog.
The ECG shows sinus tachycardia, a narrow, low voltage QRS with alternating amplitudes, no peaked T waves, no QT prolongation, and some minimal ST elevation in II, III, and aVF (without significant reciprocal STD or T wave inversion in aVL). It is difficult to tell if there is collapse during diastole due to the patient’s tachycardia.
As we've discussed on numerous other posts in Dr. Smith's ECG Blog ( See My Comment at the bottom of the page in the May 5, 2022 post) — a growing number of conditions other than Brugada Syndrome have been found to temporarily produce a Brugada-1 ECG pattern. What are the ECG Findings of Cardiac Contusion?
Otherwise vitals after intubation were only notable for tachycardia. An initial EKG was obtained: Computer read: sinus tachycardia, early acute anterior infarct. She was ventilated by bag-valve-mask by EMS on arrival and was quickly intubated with etomidate and succinylcholine. A rectal temperature was obtained which read 107.9
Low body magnesium is often encountered in association with other electrolyte abnormalities ( ie, low sodium, potassium, calcium or phosphorus ) ; acute MI; cardiacarrest; digoxin/diuretic use; alcohol use and abuse; renal impairment. Figure-2: Sequential development of ST-T wave changes with hypokalemia. second ).
Written by Pendell Meyers, with edits by Steve Smith Thanks to my attending Nic Thompson who superbly led this resuscitation We received a call that a middle aged male in cardiacarrest was 5 minutes out. There is a regular, wide complex, (mostly) monomorphic tachycardia. He was estimated to be in his 50s, with no known PMHx.
Patients who present with chest pain or cardiacarrest and have an ECG diagnostic of STEMI could have myocardial rupture. In a report of 6 cases at our institution (Hennepin County Medical Center), 2 survived with cardiac surgery. In contrast to re-occlusion of the infarct-related artery, this reversal should be gradual.
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