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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.
Even if we stopped here — We could conclude the following: There is marked bradycardia in today's rhythm ( ie, Heart rate in the low 30s ). Finally — If today's patient does not have significant underlying coronary disease — then her bradycardia with AV block may be the result of SSS ( S ick S inus S yndrome ).
There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( Some residual ischemia in the infarct border might still be present. Both episodes are initiated by an "R-on-T" phenomenon.
Sinus bradycardia, normal conduction, normal axis, normal R wave progression, no hypertrophy. 2] Here there is no posterior ST elevation, but the anterior ST depression is also less—so it is dynamic, confirming acute ischemia. What do you think? But it is still STEMI negative.
That said — obvious findings include: i ) Marked bradycardia! — This suggests ischemia of uncertain duration. The October 25, 2021 post in Dr. Smith's ECG Blog — My Comment ( at the bottom of the page ) reviews my approach to another case of a Dual-Level Wenckebach block. be regular! —
Extensive conduction system abnormalities can have various causes (ischemia, genetic, infectious, amyloid, etc). For example — bradycardia and AV conduction disturbances are not uncommon with Hyperkalemia , with these conduction disturbances most often resolving once serum K+ is corrected.
Hyperkalemia causes peaked T waves and the "killer B's of hyperkalemia", including bradycardia, broad QRS complexes, blocks of the AV node and bundle branches, Brugada morphology, and otherwise bizarre morphology including sine wave. With a twist. Do you recognize this ECG yet? Right Bundle Branch Block with ST Elevation in V1?
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. Lead V2 shows RR’ QRS configuration, and although ST depression is otherwise expected here, the discordance is a bit excessive. 6] Tabrizi, F.,
Triage physician interpretation: -sinus bradycardia -lateral ST depressions While there are lateral ST depressions (V5, V6) the deepest ST depressions are in V4. Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). 121.022866.
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. Figure-1: The initial ECG in today's case. ( The QRS complex is wide ( ie, >0.10
There is ST elevation in 9/12 leads with ST depression only seen in lead aVR>V1 ( ie, virtually the opposite of what is seen with diffuse subendocardial ischemia in which there is diffuse ST depression except for ST elevation in aVR>V1 ).
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! You have given IV MgSO4 a fast acting -blocker and IV amiodarone bolus and infusion. No PVCs are seen.
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