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His medical history includes hypertension, a decade-long battle with diabetes, ischemic heart disease, a coronary bypass graft surgery ten years ago, a diagnosis of congestive heart failure for the last five years, and a prior ICD implantation five years ago. What is the rhythm? Smith : Are they P-waves?
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. The Initial ECG in Today's Case: As per Dr. Meyers — the initial ECG in today's case shows sinus tachycardia with bifascicular block ( = RBBB/LAHB ). Sinus Tachycardia ( common in any trauma patient. ).
Here is his ECG: Original image, suboptimal quality Quality improved with PM Cardio digitization The ECG is highly suggestive of acute right heart strain, with sinus tachycardia, S1Q3T3, and T wave inversions in anterior and inferior with morphology consistent with acute right heart strain. Moreover, there is tachycardia.
Sinus tachycardia has many potential causes. This is especially true for the elderly patient with sinus tachycardia. What is the cause of the sudden tachycardia? A VSR is more likely to occur in patients who are older, female, hypertensive, have chronic kidney disease, and have no prior history of smoking.
It was edited by Smith CASE : A 52-year-old male with a past medical history of hypertension and COPD summoned EMS with complaints of chest pain, weakness and nausea. DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR.
It should be known that each category can easily manifest the generic subendocardial ischemia pattern. In general, subendocardial ischemia is a consequence of global supply-demand mismatch that usually ameliorates upon addressing, and mitigating, the underlying cause. What’s interesting is that the ECG can only detect ischemia.
Case submitted and written by Mazen El-Baba MD, with edits from Jesse McLaren and edits/comments by Smith and Grauer A 90-year old with a past medical history of atrial fibrillation, type-2 diabetes, hypertension, dyslipidemia, presented with acute onset chest/epigastric pain, nausea, and vomiting. His response: “subendocardial ischemia.
A 56 year old male with a history of diabetes, dyslipidemia, hypertension, and coronary artery disease presented to the emergency department with sudden onset weakness, fatigue, lethargy, and confusion. The patient’s angiogram should have been expedited, but the EKG change was not recognized as recurrence of transmural ischemia.
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.
edits by Meyers A woman in her 60s with a history of chronic atrial fibrillation on Eliquis, ESRD on hemodialysis, type-II diabetes mellitus, prior CVA, hypertension, and hyperlipidemia presented to the emergency department with multiple complaints after missing dialysis. Tachycardia and ST Elevation. She was discharged home.
Although as a general rule, there should be no ST elevation in RBBB in the absence of ischemia, there sometimes is ST elevation that looks like this. If the ECG findings are truly new compared to a baseline (unavailable), this could suggest persistent ECG findings of ischemia, meaning poor downstream perfusion ("no reflow" phenomenon).
The flutter waves can conceal or mimic ischemic repolarization findings, but here I don't see any obvious findings of OMI or subendocardial ischemia. Chronic RVH is due to chronic pulmonary hypertension, and these patients are extremely difficult to manage when they are acutely ill. The rhythm is 2:1 atrial flutter.
Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? Ischemia b. ST depression: is it ischemia? Does this patient have hypertension and/or heart failure that has worsened? It was a baseline finding in 62% of patients, usually due to LVH.
In addition to sinus tachycardia, the only abnormalities listed by the computer were "low voltage, precordial leads" and "anteroseptal infarct, old.Q He was mildly tachycardic (105-110 bpm) and hypertensive (157/92 mm Hg) on arrival. Cardiologist interpretation: "Technically does not meet STEMI criteria but concerning for ischemia."
The patient stated he had a long history of well-controlled hypertension for which he was compliant with his ACE-inhibitor. These findings are concerning for inferior wall ischemia with possible posterior wall involvement. He was also treated for erectile dysfunction but had not taken any medications recently.
He was hypertensive and tachycardic, with mildly increased work of breathing. In some cases the ischemia can be seen "through" the flutter waves, whereas in other cases the arrhythmia must be terminated before the ischemia can be clearly distinguished. 2) Tachycardia to this degree can cause ST segment changes in several ways.
Written by Magnus Nossen The patient in today's case is a male in his 70s with hypertension and type II diabetes mellitus. The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. His wife contacted the ambulance service after the patient experienced an episode of loss of consciousness.
There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1] The patient was found to be hypertensive and treated accordingly.
In terms of ischemia, there is both a signal of subendocardial ischemia (STD max in V5-V6 with reciprocal STE in aVR) AND a signal of transmural infarction of the inferior wall with Q wave and STE in lead III with reciprocal STD in I and aVL. The rhythm is atrial fibrillation. The QRS complex is within normal limits.
If there is polymorphic VT with a long QT on the baseline ECG, then generally we call that Torsades, but Non-Torsades Polymorphic VT can result from ischemia alone. See here for management of Polymorphic Ventricular Tachycardia , which includes Torsades. If there is a pulse, you would call it Torsades. Serum potassium level (range 2.5
Higher troponin correlated with more history of heart failure, diabetes, and hypertension, as well as higher D-dimer, and nearly all inflammatory markers. Use of objective evidence of myocardial ischemia to facilitate the diagnostic and prognostic distinction between type 2 myocardial infarction and myocardial injury.
A 69 year old woman with a history of hypertension presented to the emergency department by EMS for evaluation of chest pain and shortness of breath. The status of the patients chest pain at this time is unknown : EKG 1, 1300: There is sinus tachycardia and artifact of low and high frequency. This was written by Hans Helseth.
But it also shows a massive area of total ischemia in the LAD territory: CT shows the infarct The CT is with contrast, which increases density (which looks more white). Most dissections which cause coronary ischemia are into the RCA ostium ("ostium" = locations of takeoff of the vessel). No ECG was recorded after pain resolution.
Written by Willy Frick A 52 year old man with hypertension, dyslipidemia, and seropositive rheumatoid arthritis (a risk factor for CAD) presented with acute substernal chest pressure with diaphoresis which woke him from sleep just after midnight. Ventricular tachycardia?) Severe ischemia can be present even when the chest pain is gone.
This ECG was recorded: It is difficult to appreciate P-waves, but I believe this is sinus tachycardia. Time 7 hours lead reversal There is limb lead reversal (QRS in I and aVL are now inverted), but nevertheless one can see that the ischemia appears to have resolved. He was put on BiPAP. A Chest X-ray did not show pulmonary edema.
A 30-something woman with chest pain and h/o pulmonary hypertension due to chronic pulmonary emboli A 30-something with 8 hours of chest pain and an elevated troponin Syncope, Shock, AV block, Large RV, "Anterior" ST Elevation.
Written by Hans Helseth, with edits and comments by Smith and Grauer An 84 year old man with chronic hypertension and CKD presented to a primary care clinic. There is sinus tachycardia with PVCs displaying various degrees of fusion ( See Ken Grauer's comment for below for a more detailed analysis of this rhythm ).
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