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The ECG in Figure-1 — was obtained from a middle-aged woman with positional tachycardia and diaphoresis with change of position from suprine to sitting. My THOUGHTS on the ECG in Figure-1: The rhythm is sinus tachycardia at ~105/minute ( ie, The R-R interval is regular — and just under 3 large boxes in duration ).
She had a single chamber ICD/Pacemaker implanted several years prior due to ventricular tachycardia. Are you confident there is no ischemia? Answer : The ECG above shows a regular wide complex tachycardia. Said differently, the ECG shows a rather slow ventricular tachycardia with a 2:1 VA conduction. Is this: 1.
An Initial ECG was performed: Initial ECG: Sinus tachycardia with prolonged QT interval (QTc of 534 ms by Bazett). She was admitted to the ICU where subsequent ECGs were performed: ECG at 12 hours QTc prolongation, resolution of T wave alternans ECG at 24 hours Sinus tachycardia with normalized QTc interval. No ischemic ST changes.
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. I said I think there is a fixed stenosis in the LAD and the tachycardia and stress caused a type 2 STEMI.
A 50-something male with unspecified history of cardiomyopathy presented in diabetic ketoacidosis (without significant hyperkalemia) with a wide complex tachycardia and hypotension. Analysis: there is a wide complex tachycardia. This was the interpretation I put into the system: WIDE COMPLEX TACHYCARDIA. It is regular.
Pediatric exercise testing may be used for evaluation of various disorders of cardiac rhythm rather than for inducible ischemia as in adults. Ventricular arrhythmias during exercise can be documented in congenital long QT syndromes as well as in catecholaminergic polymorphic ventricular tachycardia.
Stress echocardiogram ruled out myocardial ischemia. Repeat TTE and EKG then noted newly enlarged left atrium and atrial tachycardia. EKG, cardiac enzymes, and Initial echocardiogram(TTE) was unremarkable. CT scan noted mediastinal lymphadenopathy consistent with known sarcidosis.
ECG in a person with persistent anginal pain for the past several hours showing significant ST segment depression anterolateral leads along with sinus tachycardia. ST segment elevation in aVR in proximal LAD occlusion before first septal is thought to be due to transmural ischemia of the basal part of the septum.
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.
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.
In addition to sinus tachycardia, the only abnormalities listed by the computer were "low voltage, precordial leads" and "anteroseptal infarct, old.Q His HEAR score (before troponin resulted) was documented at 3, with documentation stating "low suspicion for ACS." Chest pain is documented as ongoing.
There is a run of polymorphic ventricular tachycardia — which given the QT prolongation, qualifies as Torsades de Points ( TdP ). This patient was having recurrent episodes of polymorphic ventricular tachycardia with an underlying long QT interval ( = Torsades des Pointes ). ECG #2 Interpretation of ECG #2: Underlying sinus rhythm.
This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). There is no definite evidence of acute ischemia. (ie, In both tracings — an exceedingly fast PMVT is documented. Below are printouts of some of the arrhythmias recorded.
He had no previously documented medical problems except polysubstance use. Automatic activity refers to enhanced pacemaking function (typically from a non sinus node source), for example atrial tachycardia. Possible mechanisms of ventricular arrhythmias elicited by ischemia followed by reperfusion. References: Ferrier, G.
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
They include myocardial ischemia, acute pericarditis, pulmonary embolism, external compression due to mass over the right ventricular outflow tract region, and metabolic disorders like hyper or hypokalemia and hypercalcemia. These are the conditions which have to be considered or excluded as they can sometimes manifest Brugada pattern on ECG.
Otherwise vitals after intubation were only notable for tachycardia. An initial EKG was obtained: Computer read: sinus tachycardia, early acute anterior infarct. Our patient had a Brugada Type 1 pattern elicited by an elevated core temperature, which is also a documented phenomenon.
If the patient has Abnormal Vital Signs (fever, hypotension, tachycardia, or tachypnea, or hypoxemia), then these are the primary issue to address, as there is ongoing pathology which must be identified. Evidence of acute ischemia (may be subtle) vii. Most physicians will automatically be worried about these symptoms. Left BBB vi.
The ECG shows sinus rhythm with normal QRS complex morphology and significant subendocardial ischemia (SEI) pattern (ST depression in many leads, worst in lateral areas including leads II, V5-6, with reciprocal STE in aVR). Here is her ECG within 30 minutes of PCI: Improved, but still with ischemia. Pre-intervention. Post-intervention.
Drug toxicity , especially diphenhydramine , which has sodium channel blocking effects, and also anticholinergic effects which may result in sinus tachycardia, hyperthermia, delirium, and dry skin. Unexplained cardiac arrest or documented VF/polymorphic VT: +3 3. Ischemia or infarction. Hyperkalemia 2. Clinical History 2.a.
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 ). If that limb gives out due to ischemia or another cause, the heart becomes reliant on a ventricular escape rhythm. PVCs and fusion beats can show signs of acute ischemia.
It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! Here is the final angiogram following placement of a stent in the ostial RCA. Galiuto, L., Yoshida, T., Manfredini, R., Deshmukh, A.,
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