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A prehospital 12-lead was recorded: There is a regular wide complex tachycardia. The computer diagnosed this as Ventricular Tachycardia. There is a wide complex regular tachycardia at a rate of 226. Toothache, incidental Wide Complex Tachycardia Could it be fascicular VT or Bundle Branch VT ( i.e., idiopathic VT )?
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.
The ECG shows severe ischemia, possibly posterior OMI. But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. It takes time for that ischemia to resolve. The patient was brought to the ED and had this ECG recorded: What do you think? And what do you want to do?
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. Again, not an expected outcome with diltiazem).
Ventricular tachycardia is a potentially life threatening cardiac arrhythmia. On the ECG, ventricular tachycardia can be defined as three or more ventricular ectopic beats occurring in a sequence at a rate more than 100 per minute. Another rare form of ventricular tachycardia is bidirectional ventricular tachycardia.
What is the most likely cause of this arrhythmia? IMPRESSION: Given the presence of a wide tachycardia — with 2 distinct QRS morphologies, and no sign of P waves — a presumed diagnosis of B i D irectional Ventricular Tachycardia has to be made. Acute myocardial ischemia. Figure-1: The initial ECG in today's case. (
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. Even with tachycardia and a paced QRS duration of ~0.16 J Am Coll Cardiol.
Shortly after isoprenalin infusion was initiated, there were short runs of ventricular tachycardia. Extensive conduction system abnormalities can have various causes (ischemia, genetic, infectious, amyloid, etc). VT is the second most common presenting arrhythmia. She was started on isoprenalin (isoproterenol).
Heart rate/rhythm: consider antidotes for brady/tachy-arrhythmias, and for sinus tachycardia consider fluids for vasodilation and benzodiazepines for agitation. Electrical conduction and axis: consider sodium bicarb for QRS > 100 especially if RBBB or terminal rightward shift, and magnesium for QTc> 500.
However, he suddenly developed a series of malignant ventricular arrhythmias. This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). Below are printouts of some of the arrhythmias recorded. What do you think?
A series of cardiac arrhythmias were seen during the course of her resuscitation — including the interesting arrhythmia shown in the long lead II of Figure-1. At about this point in the process — I like to take a closer LOOK at the 12-lead tracing, to ensure there is no acute ischemia or infarction that might need immediate attention.
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.
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. ).
ECG is consistent with severe hypokalemia and/or hypomagnesemia causing prolonged QT (QU) at high risk of Torsades (which is polymorphic ventricular tachycardia in the setting of a long QT interval). Polymorphic Ventricular Tachycardia Long QT Syndrome with Continuously Recurrent Polymorphic VT: Management Cardiac Arrest.
Pediatric exercise testing may be used for evaluation of various disorders of cardiac rhythm rather than for inducible ischemia as in adults. QT prolongation and the occurrence of ventricular arrhythmias with exercise are another important aspect of exercise testing in children. Discussion on pediatric exercise testing.
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?
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. The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.
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.
There are three mechanisms of arrhythmia: automatic, re-entry, and triggered. The most common triggered arrhythmia is Torsades de Pointes. Automatic activity refers to enhanced pacemaking function (typically from a non sinus node source), for example atrial tachycardia. This has been discussed many times before on this blog.
Arrhythmia? Today’s case recalled that scenario for me, in that it features recognition of an arrhythmia that fooled ED staff into thinking the ECG was showing an acute infarction. The ED staff failed to do this — and as a result, they completely overlooked the arrhythmia. Would you give lytics? Yes, but not because of the ECG!
There are a number of things to look for in an ECG that can hint at arrhythmia as the cause of an apparent seizure. There is a run of polymorphic ventricular tachycardia — which given the QT prolongation, qualifies as Torsades de Points ( TdP ). Below are some of the conditions to be aware of: Preexcitation Brugada syndrome.
During active chest pain an ECG was recorded: Meyers ECG interpretation: Sinus tachycardia, normal QRS complex, STD in V2-V6, I, II, III and aVF. Learning Points: You must learn and recognize the ECG patterns of OMI and subendocardial ischemia to best understand the ECG in acute care medicine.
There is a narrow complex tachycardia at a rate of 130. ECGs: there is a regular narrow complex tachycardia still at a rate of exactly 130, with no P-waves and also no change since the prehospital ECG. During tachycardia, in this case, the baseline continuously undulates especially in leads II, aVR and V1; very good for atrial flutter.
Instead, antiarrhythmic drugs such as amiodarone or ß-blockers may be needed — and/or treatment targeted to correcting ischemia. This may explain the poorer response of pleomorphic VT to antiarrhythmic therapy — and the higher morbidity and mortality that seems to be associated with this arrhythmia.
Is there ischemia? Idioventricular rhythm is a common "reperfusion arrhythmia." ECG Diagnosis is either : 1) junctional rhythm with new LBBB, and possibly ischemia 2) accelerated idoventricular rhythm with possible ischemia, and possibly related to restoration of normal perfusion. But it is not conclusive.
Precordial ST depression may be subendocardial ischemia or posterior STEMI. Notice there is tachycardia. I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia. V4-V6, is much more likely to be posterior than subendocardial ischemia. There is no ST elevation.
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.
Mechanism is thought to be due to sustained sympathetic stimulation, probably caused by dysfunction of insular cortex resulting in reversible neurogenic damage to the myocardium which could include contraction bands and subendocardial ischemia [2]. But the number of persons with lobar hemorrhage in that study was only 17%.
First, we have a narrow-complex, regular tachycardia, with a rate of about 135-140. This narrows our differential for the rhythm down to sinus tachycardia, paroxysmal supraventricular tachycardia (PSVT, or SVT), and atrial flutter. Tachycardia and ST Elevation. She was discharged home. Christmas Eve Special Gift!!
His response: “subendocardial ischemia. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. With the history of Afib, CTA abdomen was ordered to r/o mesenteric ischemia vs ischemic colitis vs small bowel obstruction. Anything more on history?
Initial vital signs include: NIBP 99/58 HR 150-160 (trend) RR 10 (spontaneous, but shallow) SpO2 86 (RA) BBS CTA The initial rhythm strip is attached: Figure 1 There is a wide complex tachycardia of varying morphology, amplitude, and R-R cycle length. The rS configuration in Lead I displays a persistent rightward axis.
Here is the only prehospital 12-lead: Sinus tachycardia, somewhat wide QRS, Ischemia Here is the first ED ECG: What is the rhythm here? Medics found patient in PEA arrest. He was resuscitated into a perfusing rhythm. He went in and out of arrest until arrival at the ED.
In the days before I learned to look for OMI, back when I was counting ST elevation boxes, I used to save ischemia for last.) This is sinus tachycardia (rhythm) with complete heart block (AV node function) with ventricular escape rate just below 30. Never forget that sinus tachycardia is the scariest arrhythmia.
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. Her initial EKG is below. Adenosine worked.
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. Arch Intern Med.
The ECG there reportedly showed an irregular tachycardia, and the patient was immediately referred to the emergency room. Here is her ECG on arrival: There is a wide complex tachycardia that is irregularly irregular (this is difficult to determine at these very high rates). Vitals were within normal limits other than heart rate.
This is the proposed mechanism of precipitation of arrhythmias in Brugada syndrome during febrile episodes. There is a potential risk for drug challenge in that life threatening ventricular arrhythmias could be precipitated. This leads to shortening of action potential duration. With proper precautions, risk can be reduced.
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. AFib ( Atrial Fibrillation ) is the most common sustained cardiac arrhythmia.
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. since sleep apnea is a readily treatable cause of nighttime bradycardia, as well as of other arrhythmias ). No pause beyond 2.0
The finding of all negative QRS complexes in leads V3-thru- V6 therefore strongly suggests that the arrhythmia-associated impulse is not traveling over an AP ( Steurer et al — Clin. Given the rapid rate of the tachycardia and the amorphous shape of the QRS — the decision was made to sedate the patient and cardiovert.
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. Mean baseline [K] p was 2.9
NOTE: As discussed in detail in ECG Blog #108 — " A IVR" is an "enhanced" ventricular ectopic rhythm that occurs faster than the intrinsic ventricular escape rate ( which is typically between 20-40/minute ) — but slower than hemodynamically significant Ventricular Tachycardia ( ie, VT at rates >130-140/minute ).
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.
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.
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