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A prehospital 12-lead was recorded: There is a regular wide complex tachycardia. The computer diagnosed this as Ventricular Tachycardia. He arrived in the ED and had an immediate bedside cardiac ultrasound while this ECG was being recorded. There is a wide complex regular tachycardia at a rate of 226. Pulse is 169.
Bedside cardiac ultrasound showed moderately decreased LV function. Even with tachycardia and a paced QRS duration of ~0.16 (And of course Ken's comments at the bottom) An elderly obese woman with cardiomyopathy, Left bundle branch block, and chronic hypercapnea presented hypoxic with altered mental status. She was intubated.
There is a regular wide complex tachycardia. Remember : Adenosine is safe in Regular Wide Complex Tachycardia. Rather, from this one: Very Fast Very Wide Complex Tachycardia Ideally, one would cardiovert. PEARL #1: The most commonly overlooked arrhythmia is AFlutter ( A trial F lutter ).
Here was his prehospital ECG, which I viewed immediately while the resident performed cardiac ultrasound: What do you think? There is a narrow complex tachycardia at a rate of 130. Here is the cardiac ultrasound which the resident performed as I viewed the ECG: This shows a huge pericardial effusion. Is is sinus? Comment from K.
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? See Table for diagnostic utility.
Is it ventricular tachycardia (VT) due to hyperK or is it a supraventricular rhythm with hyperK? On arrival, the patient was in shock, was intubated, and had an immediate cardiac ultrasound. What does a heart look like on ultrasound when the EKG looks like that? They transported to the ED. How would you treat?
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.
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 emergent cardiology consult can be helpful for equivocal cases. A normal PR interval.
Smith comment: This patient did not have a bedside ultrasound. Had one been done, it would have shown a feature that is apparent on this ultrasound (however, this patient's LV function would not be as good as in this clip): This is recorded with the LV on the right. In fact, bedside ultrasound might even find severe aortic stenosis.
She was awake, alert, well perfused, with normal mental status and overall unremarkable physical exam except for a regular tachycardia, possible rales at both bases, some mild RUQ abdominal tenderness. Thus, I believe it is a regular, monomorphic, wide complex tachycardia. Or it could simply still be classic VT. What is the Diagnosis?
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.
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?
Here was his ED ECG: There is sinus tachycardia (rate about 114) with nonspecific ST-T abnormalities. A bedside POC cardiac ultrasound was done: Findings: Decreased left ventricular systolic function. An ECG was recorded: This shows a regular narrow complex tachycardia at a rate of about 160. BP:143/99, Pulse 109, Temp 37.2 °C
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. See here for management of Polymorphic Ventricular Tachycardia , which includes Torsades. IV administration of potassium is indicated when arrhythmias are present or hypokalemia is severe (potassium level of less than 2.5
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.
Further ultrasound showed no B-lines (no pulmonary edema). WPW Cardiac arrhythmias ( especially AFib ). There is very little filling, and thus very poor stroke volume. The heart rate is too fast for this poor filling. Preload must be increased and the heart rate slowed in order to allow more LV filling.
Check : [vitals, SOB, Chest Pain, Ultrasound] If the patient has Abdominal Pain, Chest Pain, Dyspnea or Hypoxemia, Headache, Hypotension , then these should be considered the primary chief complaint (not syncope). The most recent and probably best study is this: Canadian Syncope Arrhythmia Risk Score. orthostatic vitals b. Mukarram, M.,
There is sinus tachycardia and also a large R-wave in aVR. 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. Her temperature was 106 degrees. As part of the workup, she underwent an ECG.
On arrival in the ED, a bedside ultrasound showed poor LV function (as predicted by the Queen of Hearts) with diffuse B-lines. If breakthrough ventricular arrhythmias occurred, additional 50-mg boluses were given every 5 minutes, as needed to a maximum of 325 mg. I don't know what the device algorithm interpretation stated.
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