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EKG with paced complexes shown below shows much narrower QRS complex and echocardiogram showed improved LV systolic function primarily due to improvement in LV dyssynchrony. (J Even with tachycardia and a paced QRS duration of ~0.16 J Am Coll Cardiol.
Corresponding echocardiogram demonstrated LV systolic dysfunction with an EF 30%. Readers of the Smith ECG Blog will probably recognize this a very subtle inferior OMI. Ultimately the patient went to Cath and was found to have multi-vessel obstructive coronary disease with an acute LCX culprit vessel, which was stented.
He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG: There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. ACS and STEMI generally do not cause tachycardia unless there is cardiogenic shock. He had this ECG recorded. Are the lungs clear?
This would have been fairly easy and much more expedient to diagnose with bedside echocardiogram. The constellation of dyspnea, tachycardia, and (relatively) low voltage on ECG should prompt immediate evaluation for pericardial effusion and tamponade.
Conventional algorithm interpretation: SINUS TACHYCARDIA ABNORMAL RHYTHM ECG Confirmed by over-reading physician Transformed ECG by PM Cardio: PM Cardio interpretation: OMI with Low Confidence Dr. Rob Reardon did a bedside echo using Speckle tracking. On arrival, lung ultrasound confirmed pulmonary edema (B lines).
Here is her ED ECG: Here is the ED physician's interpretation: IMPRESSION UNCERTAIN REGULAR RHYTHM, wide complex tachycardia, likely p-waves. LEFT BUNDLE BRANCH BLOCK [120+ ms QRS DURATION, 80+ ms Q/S IN V1/V2, 85+ ms R IN I/aVL/V5/V6] Comparison Summary: LBBB and tachycardia are new. This is clearly ventricular tachycardia.
It's a very "fun" ECG, with initial ectopic atrial tachycardia (negative P waves in inferior leads conducting 1:1 with the QRSs), followed by spontaneous resolution to sinus rhythm. The emergent echocardiogram showed normal EF, no WMA, and normal valve function. What About the Tachycardia? Triage ECG: What do you think?
This is ischemic ST depression, and could be due to increasing tachycardia, with a heart rate over 130, but that is unlikely given that the patient is now complaining of crushing chest pain and that there was tachycardia all along. See this post: What do you think the echocardiogram shows in this case?
This can initiate ventricular arrhythmias like polymorphic ventricular tachycardia (PMVT). Transthoracic echocardiogram showed normal biventricular systolic function. Background:R-on-T phenomenon occurs when an electrical stimulus is delivered at a critical point during ventricular repolarization.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Hopefully a repeat echocardiogram will be performed outpatient. 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 ).
A rapid echocardiogram was performed, revealing an ejection fraction of 20% with thinning of the anterior-apical walls. While the initial impression might not immediately suggest ventricular tachycardia (VT), a closer examination raises suspicion. The initial troponin T level was measured at 30 ng/L. What is the rhythm?
Patients with BrS can be asymptomatic or present with symptoms secondary to polymorphic ventricular tachycardia or ventricular fibrillation. The routine laboratory results, imaging study, coronary angiogram, and echocardiogram (ECG) were normal. The patient did not have underlying diseases.
This is the ECG of a 50 yo old woman who collapsed, was found to have a pulse, but then found to be in ventricular tachycardia. Echocardiogram showed an anteroapical wall motion abnormality. She was shocked into sinus rhythm. She presented to the ED comatose. The cath lab was activated for STEMI, but the patient had clean coronaries.
ECG at presentation was suggestive of ventricular tachycardia (VT) ( figure 1 A ). Resuscitation with urgent cardioversion in view of haemodynamic instability with wide complex tachycardia was done. The two-dimensional (2D) transthoracic echocardiogram revealed left ventricular ejection fraction of 40%.
EKG, cardiac enzymes, and Initial echocardiogram(TTE) was unremarkable. Stress echocardiogram ruled out myocardial ischemia. However, symptoms resolved spontaneously, cardiac workup paused and he was monitored conservatively with serial Echocardiogram(TTE) until onset of dyspnea 3 years later.
Echocardiogram showed severe RV dilation with McConnell’s sign and an elevated RVSP. and tachycardia, 1.8. Finally , they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. The patient was upgraded to the ICU for closer monitoring. inverted T-waves in V1 and V2, 1.8;
EMS reports intermittent sinus tachycardia and bradycardia secondary to some type of heart block during transport. It is hard to make out P waves but you can see them best in V2, and notches in the T waves in other leads - this is a sinus tachycardia with a very long PR interval indicating first degree block.
There is sinus tachycardia. Sinus tachycardia, which exaggerates ST segments and implies that there is another pathology. I have always said that tachycardia should argue against acute MI unless there is cardiogenic shock or 2 simultaneous pathologies. Here is that ECG: What do you think? No wall motion abnormality.
Twenty-one (41%) had normal echocardiogram, 13 (25%) a hypokinetic non-dilated cardiomyopathy (HNDC) and 17 (33%) a dilated cardiomyopathy (DCM). Significant right ventricular involvement was an exclusion criterion. Results Fifty-two patients (63% males, age 45 years (31–53)) composed the study cohort.
Results Initially, 526 440 echocardiograms representing 266 601 unique patients were identified. vs 83.7%, p<0.046) and more often had a history of ventricular tachycardia (74.5% vs 83.7%, p<0.046) and more often had a history of ventricular tachycardia (74.5% A secondary analysis was performed for LVEF 36%–40%.
An external monitor revealed one episode of non-sustained supraventricular tachycardia, otherwise was unremarkable. Pre-stress echocardiogram revealed a sigmoid septum with septal wall thickness of 1.6 Post-stress echocardiogram revealed severe SAM with septal contact, LVOT gradient of 70 mmHg, as well as hypotension.
Elevated troponins prompted an echocardiogram — which revealed an apical wall motion abnormality (WMA). NOTE #1: Sinus tachycardia is not usually seen in an uncomplicated acute MI. Patient #1 in today's post did not get expert ECG interpretation. As a result — the heart rate of ~115/minute in ECG #1 is a worrisome finding.
Additionally, a bedside echocardiogram showed no wall motion abnormality and normal LV function. He had multiple episodes of bradycardia and nonsustained ventricular tachycardia. A formal echocardiogram for patient 2 showed normal LV size, wall thickness, and global systolic function. It was stented.
She underwent exercise echocardiogram in mid October where she exercised for nearly 7 minutes on the standard Bruce protocol and had typical anginal pain and shortness of breath. Baseline echocardiogram showed moderate LV systolic dysfunction with no wall motion abnormalities. There is inferoseptal hypokinesis. link] Shvilkin et al.
EKG initially negative but repeat shows a few T wave abnormalities… There is a chance this could be non-cardiac pain” At 1518, an echocardiogram showed normal LV size and systolic function with hypokinesis of the mid and distal anterior wall and the mid and distal septum. Smith: The Queen of Hearts diagnosed Not OMI with high confidence.
We see a regular tachycardia with a narrow QRS complex and no evidence of OMI or subendocardial ischemia. The differential of a regular narrow QRS tachycardia is sinus tachycardia, SVT, and atrial flutter with regular conduction. Now the patient is in sinus tachycardia. She had an echocardiogram which was normal.
Echocardiogram was unchanged from baseline. He was counseled to abstain from cannabis use.Conclusion:At low to moderate doses, cannabis can lead to a surge in sympathetic activity causing tachycardia and hypertension, while parasympathetic activity is predominant at higher doses, causing bradycardia and hypotension.
Interpretation: There is sinus tachycardia, with right bundle branch block (RBBB). No further ECG, troponin, or echocardiogram was done because she was asymptomatic, and had a normal rhythm and rate. She was pulseless, with a narrow complex tachycardia on the monitor. She was intubated.
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. Learning points 1.
From afar, there is gross tachycardia, cadence irregularities, and narrow QRS complexes that may, or may not, be Sinus in origin; and finally – a cacophony of wide complexes that might very well be ventricular in origin. McLaren : We’ve answered the first question – Sinus Tachycardia with episodic runs of wide QRS (RBBB morphology) and PVC’s.
Notice there is tachycardia. I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia. In this case, the patient had failed to take his atenolol in the AM and was having reflex tachycardia in addition to ACS. Seventh , an immediate echocardiogram can make the distinction.
We believe they are likely a normal variant in this context, and the study above failed to identify any clinically significant finding after exam and echocardiogram in 110 children with bifid T waves. sec and voltage greater than or equal to 0.05
However, an echocardiogram is a different test, also conducted for heart activity. A fast heartbeat is called tachycardia, while a slow heartbeat is called bradycardia in medical terms. Electrocardiogram, echocardiogram, and some other tests are done for patients with cardiac arrest. ECG and EKG refer to the same thing.
Here is his ED ECG: There is sinus tachycardia. The amount of ST elevation and depression is slightly less than on the ECG above, but there is also no tachycardia, which tends to exaggerate ST deviation. He had diffuse crackles on exam and B-lines on chest ultrasound, and chest x-ray also confirmed pulmonary edema.
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.
Category 2 : An increase in myocardial oxygen demand due to tachycardia, elevated ventricular afterload (BP or aortic stenosis), or increased wall stretch (admittedly this latter is more complicated) or a decrease in oxygen supply due to hypotension, anemia, hypoxia, or a combination of all of the above. This results in Type I MI.
We can see enough to make out that the rhythm is sinus tachycardia. Tachycardia is unusual for OMI, unless the patient is in cardiogenic shock (or getting close). A bedside ultrasound should be done to assess volume and other etiologies of tachycardia, but if no cause of type 2 MI is found, the cath lab should be activated NOW.
See this case: what do you think the echocardiogram shows in this case? Systematic Assessment of the ECG in Figure-1: My Descriptive Analysis of ECG findings in Figure-1 is as follows: Sinus tachycardia at ~110/minute. A slightly prolonged QTc ( although this is difficult to assess given the tachycardia ). A normal PR interval.
Otherwise vitals after intubation were only notable for tachycardia. An initial EKG was obtained: Computer read: sinus tachycardia, early acute anterior infarct. A formal echocardiogram was completed the next day and again showed a normal ejection fraction without any focal wall motion abnormalities to suggest CAD.
Prior ECG available on file from 2 months before: We do not know the clinical events happening during this ECG, but there is borderline tachycardia, PVCs, and likely some evidence of subendocardial ischemia with small STDs maximal in V5-6/II, slight reciprocal STE in aVR. QS waves from V2-V5 consistent with LV aneurysm morphology.
Get an emergent contrast echocardiogram. I learned more about the history: 30-something African American with 5-7days of sharp R-sided shoulder/scapula/chest discomfort, presented with sinus tachycardia. QTc's were 330 ms and 373 ms This is what I texted back: These look like they are a very pronounced case of Benign T-wave Inversion.
Unfortunately there is no echocardiogram accessible because the patient checked himself out of the hospital in order to get back to his home state before it could be completed. C linically — the rhythm we see in the long lead II of ECG #3 behaves similar to MAT, even though there is no tachycardia.
An echocardiogram was done. Sinus Tachycardia ( common in any trauma patient. ). The pneumothorax was expanded with a chest tube At 17 hours, another ECG was recorded: It is now much less dramatic and has the morphology of Type 2 Brugada The hs troponin I peaked at 6500 ng/L -- this strongly suggests myocardial contusion.
The next morning the patient went for his routine echocardiogram, where the operator noticed a dilated aortic root at 5.47 Here is a quote from his initial cardiology admission note (after cath was done showing no acute culprit): ".chest Troponins gradually trended down from 0.19 cm with severe aortic insufficiency.
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