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With P waves labeled — Isn't it now much easier to appreciate that the atrial rhythm is quite regular ( with no more than a slight sinus arrhythmia )? P utting I t A ll T ogether : The precise mechanism of today's arrhythmia is complex and difficult to determine. For those with a special interest in cardiac arrhythmias — READ ON! —
Common explanations for unusual rhythms such as this one include: i ) Hyperkalemia ( or other severe electrolyte disorder ); ii ) Recent infarction/ischemia; iii ) Sleep apnea; iv ) Severe hypothyroidism; v ) Acute neurologic catastrophe (ie, stroke, bleed, trauma, tumor ); vi ) Some other toxicity.
The ECG does not show any definite signs of ischemia. Uncontrolled coronary spasm may be associated with serious arrhythmias , including cardiac arrest ( Looi et al — Postgrad Med, 2012 ; Tan et al — Eur Heart J Case Rep, 2018 ; Chevalier et al — JACC, 1998 ; Rodriguez-Manero — EP Europace, 2018 ).
Discontinue all negative chronotropic agents, since the risk of torsade is much higher with bradycardia or pauses. It should be kept in mind that on occasions, beta-one agonist can result in increased ventricular ectopy e.g., in severe myocardial ischemia (by increasing myocardial demand), or sometimes with congenital long-QT syndrome.
Altered Mental Status, Bradycardia == MY Comment , by K EN G RAUER, MD ( 2/2 /2024 ): == Dr. Meyers began today’s case with the clinical challenge of asking you to identify the underlying cause of ECG #2. -- Read this ECG -- Osborn Waves and Hypothermia (this is the "Figure" above) What does LBBB look like in severe hypothermia?
I will leave more detailed rhythm discussion to the illustrious Dr. Ken Grauer below, but this use of calipers shows that the rhythm interpretation is: Sinus bradycardia with a competing (most likely junctional) rhythm. The fact that R waves 2 through 6 are junctional does make ischemia more difficult to interpret -- but not impossible.
to 1828 msec. ) — which corresponds to a variation in the rate of sinus bradycardia from 36-to-33/minute. This makes sense given that the underlying rhythm in today's case appears to be marked sinus bradycardia and arrhythmia , with a ventricular escape rhythm appearing when the SA node rate drops below 33/minute.
The STD maximal in V1-V4 is diagnostic of acute transmural posterior wall ischemia, most likely due to posterior OMI. Subendocardial ischemia does not localize, and subendocardial ischemia presents with STD maximal in V5-6, II, and STE in aVR. Subendocardial ischemia does not localize.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Other Arrhythmias ( PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib ). Chest trauma was suspected on initial exam. Here is his initial ECG around 1330: What do you think?
during which sinus bradycardia and arrhythmia are seen but not to a degree that produces symptoms. The easy way to remember the arrhythmias most commonly associated with SSS is to think of what one might expect if the SA node became sick. The indication for pacemaker placement with SSS is symptomatic bradycardia.
Ventricular tachycardia is a potentially life threatening cardiac arrhythmia. Monomorphic ventricular tachycardia in the setting of acute myocardial ischemia can also be treated by intravenous lignocaine bolus followed by infusion. If the rate is very fast, hemodynamic deterioration can occur rapidly.
That said — obvious findings include: i ) Marked bradycardia! — This suggests ischemia of uncertain duration. L addergram I llustration : At this point — I needed to work out, and then draw a laddergram that I could then verify to ensure a plausible mechanism for today's arrhythmia. be regular! —
There are 3 etiologies I always think of with bradycardia and AV block: 1. There was no evidence of ischemia. In addition to ruling out rate-slowing medication serum electrolyte disorders and/or ischemia/infarction as potential causes of bradyarrhythmias one should also rule out hypothyroidism + sleep apnea. Hyperkalemia.
Baseline bradycardia in endurance athletes limits the use of ß-blockers. These include: i ) Use of rate-slowing medication ( ie, ß-blockers, digoxin, verapamil/diltiazem, etc. ) ; ii ) Acute or recent infarction or ischemia; iii ) Hypothyroidism; iv ) Neurologic injury; v ) Electrolyte disturbance; and , vi ) Sleep apnea. 25, 2022 ).
If you put the inferior and posterior findings together, it is diagnostic of OMI This was read as "inferior ischemia" without any other information by Dr. Richard Gray and as probable reperfused inferior-posterior OMI much later by both me and Pendell Meyers, also without any clinical information.
He has a family history concerning for arrhythmia. Given the circumstances of his car crash, we presume it was due to an underlying arrhythmia. He has a family history concerning for arrhythmia with his father requiring some sort of device (PPM, ICD, unclear) at a young age.
Additionally, his cardiac telemetry monitor showed runs of accelerated idioventricular rhythm, a benign arrhythmia often associated with coronary reperfusion. Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls.
2] Conduction through the accessory pathway can be intermittent (with different degrees of pre-excitation), and affected by ischemia. 3] So a patient with WPW can have the pattern induced by ischemia, and there is also a report of a patient with pre-existing WPW which was “ablated” by myocardial infarction after an LAD occlusion.[4]
Here was my answer: "Not ischemia. Instead — my thoughts were as follows: The rhythm is sinus , with marked bradycardia and a component of sinus arrhythmia. WPW Cardiac arrhythmias ( especially AFib ). This was texted to me in real time. The patient has acute chest pain. What do you think? I would not activate cath lab.
Therefore, she underwent temporary pacemaker placement and overdrive pacing at a rate of 90 bpm to keep the heart rate up in order to prevent these PVCs triggering ventricular arrhythmia. Hypokalemia was unlikely because she continued to have ventricular arrhythmia despite of correcting electrolytes. Acute ischemia?
The patient later settled into sinus bradycardia. The above said — Dr. Smith's approach to today's arrhythmia highlights a number of important points! Just because a regular WCT is VT does not necessarily mandate immediate cardioversion — IF the patient is hemodynamically stable and tolerating the arrhythmia.
However, he suddenly developed a series of malignant ventricular arrhythmias. Below are printouts of some of the arrhythmias recorded. There is no definite evidence of acute ischemia. (ie, This time, the arrhythmia did not spontaneously terminate — but rather degenerated to VFib, requiring defibrillation.
Her vital signs were within normal limits except for bradycardia at 55 bpm. It is probably sinus bradycardia with very small/depressed P-waves and prolonged PR interval. P EARL # 4 In my opinion, it is not worth wasting time trying to figure out the specific rhythm diagnosis of a bradycardia when there is hyperkalemia.
There are three mechanisms of arrhythmia: automatic, re-entry, and triggered. The most common triggered arrhythmia is Torsades de Pointes. It is a benign arrhythmia which requires no specific treatment. Possible mechanisms of ventricular arrhythmias elicited by ischemia followed by reperfusion. Do not treat AIVR.
The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). What do you think?
A prior ECG was available for comparison: Normal One might be tempted to interpret the ST depression as ischemia, but as Smith says, "when the QT is impossibly long, think of hypokalemia and a U-wave rather than T-wave." QUESTION #2: If it were not for the markedly prolonged QTc — Wouldn't ECG #1 look like diffuse subendocardial ischemia?
Remember, in diffuse subendocardial ischemia with widespread ST-depression there may b e ST-E in lead s aVR and V1. There are well formed R-waves with good voltage/amplitude which is uncommon for ischemia. The ECG does not show any signs of ischemia. True Positive ECG#2 : Also sinus rhythm. There is ST depression in V1.
Extensive conduction system abnormalities can have various causes (ischemia, genetic, infectious, amyloid, etc). VT is the second most common presenting arrhythmia. Vaso or inotropic medications are not harmless, and can precipitate life threatening arrhythmias. Usually the medical history will provide clues to the cause.
There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Torsades in acquired long QT is much more likely in bradycardia because the QT interval following a long pause is longer still. malignant ventricular arrhythmias are present), rapid replacement of potassium is required.
Arrhythmia In simple words, arrhythmia refers to an irregular heartbeat. A fast heartbeat is called tachycardia, while a slow heartbeat is called bradycardia in medical terms. Poor blood supply Ischemia, or inadequate blood supply to the heart, is an abnormality that can be detected in an ECG test.
There’s sinus bradycardia, first degree AV block, normal axis, delayed R wave progression, and normal voltages. Hyperacute T waves are deflating, suggesting reperfusion but there is still reciprocal change in I/aVL and ST depression in V2, and the bradycardia is worse. Below is the ECG. What do you think? Take home 1.
Such findings would normally suggest primary ischemia with concomitant surveillance of coronary occlusion, but these ST/T changes might very well be secondary to the Escape mechanism at hand. Chapter 17: Ventricular Arrhythmias. 2] Although the clinical context in today’s case does not fit these descriptors for Type I OMI (e.g.
Osborn waves have been reported with hypercalcemia, brain injury, subarachnoid hemorrhage, Brugada syndrome, cardiac arrest from VFib — and — severe, acute ischemia resulting in acute MI ( See My Comment in the November 22, 2019 post on Dr. Smith’s Blog ). Rituparna et al — as well as Chauhan and Brahma ( Int.
Followup ECG: No Change Absence of evolution is the best evidence against ischemia as the etiology. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chest pain for the ischemia and potential syncope for brugada. Ischemia/infarction. Bradycardia. Hypothermia.
Prior to Mizusawa's study, it was thought that the incidence of syncope, arrhythmia, or SCD in this cohort was low [7]. In light of the risk of arrhythmia events observed in the Mizusawa trial, a formal EP study might be reasonable to obtain in those with fever induced asymptomatic Brugada ECG changes to help risk stratify these patients.
To improve visualization — I've digitized the original ECG using PMcardio ) MY Thoughts on the ECG in Figure-1: This is a challenging tracing to interpret — because there is marked bradycardia with an irregular rhythm and a change in QRS morphology. Was there a family history of sudden death or significant arrhythmia?
Evidence of acute ischemia (may be subtle) vii. PVCs N ot generally considered abnormal ECG findings: Isolated PAC, First Degree AV Block, Sinus bradycardia at a rate of 35-45, and Nonspecific ST-T abnormalities (even if different from a previous ECG). Left BBB vi. Pathologic Q-waves viii. LVH or RV d. Abnormal but less worrisome: i.
The possibility of an ischemic cause of the ventricular arrhythmia has to be considered! That said there were no clinical symptoms or ECG findings suggestive of ongoing ischemia. Below in Figure-5 is a 10-minute continuous lead II recording on oral Flecainide, now showing sinus bradycardia without a single PVC!
This ECG shows a sinus bradycardia with a normal conduction pattern (normal PR, normal QRS, and normal QTc), normal axis, normal R-wave progression, normal voltages. Hypothermia can also produce bradycardia and J waves, with a pseudo-STEMI pattern. ECG met STEMI criteria and was labeled STEMI by computer interpretation.
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