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These result in diagnoses such as postural orthostatic tachycardia syndrome and orthostatic hypotension. Because CBF is not easy to measure, rises in heart rate or drops in blood pressure are used as proxies for abnormal CBF.
Bedside ED ultrasound showed exceedingly poor global LV function, and no B lines. Then I always look to see if the initial deflection of the QRS has a lot of voltage change per change in time (seen in tachycardias that are initiated from above the ventricle because the propagate through fast conducting purkinje fiber.
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.
male with pertinent past medical history including Atrial fibrillation, atrial flutter, cardiomyopathy, Pulmonary Embolism, and hypertension presented to the Emergency Department via ambulance for respiratory distress and tachycardia. Bedside ultrasound showed volume depletion and no pulmonary edema. SVT with aberrancy?
I find AV dissociation in VT to be very difficult to differentiate from artifact, as there are always random blips on tachycardia tracings. Pads were placed with ultrasound guidance, so they were in the correct position. Read this post: Idiopathic Ventricular Tachycardias for the EM Physician 2. Ken notes AV dissociation.
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.
It shows sinus tachycardia with right bundle branch block. Taking a step back , remember that sinus tachycardia is less commonly seen in OMI (except in cases of impending cardiogenic shock). Answer : Bedside ultrasound! Smith : RV infarct may also have this appearance on ultrasound. Both were wrong.
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?
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?
Intracardiac echocardiography (ICE) represents a valuable image integration technique, with the unique advantage of dynamic real-time scar characterization.
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. An older patient with no previous medical history arrived at triage complaining of SOB. If it is VT, there will be no effect.
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.
Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis Answer: pulmonary embolism. Now another, with ultrasound. and tachycardia, 1.8. Finally , they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. What is the Diagnosis? This is a quiz.
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.
What I had not told him before he made that judgement is that the patient also had ultrasound B-lines of pulmonary edema. A Closer LOOK at the ECG in Figure-1: The ECG in Figure-1 shows sinus tachycardia — with QRS widening due to complete RBBB. What do you think? Here is my interpretation: There is sinus rhythm with RBBB.
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.
This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). Another approach is sympathetic chain (stellate ganglion) blockade if you have the skills to do it: it requires some expertise and ultrasound guidance.
Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis Answer: pulmonary embolism. Now another, with ultrasound. Tachycardia , especially in association with rapid AFib — is notorious for producing transient ST elevation not due to acute infarction ( that often resolves once heart rate slows ).
Interpretation: There is sinus tachycardia, with right bundle branch block (RBBB). Hemodynamic instability in trauma is usually due to bleeding, but if ultrasound shows poor contractility, then this may be due to cardiac contusion. She was pulseless, with a narrow complex tachycardia on the monitor. She was intubated.
On arrival, lung ultrasound confirmed pulmonary edema (B lines). 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. This is proximal LAD Occlusion until proven otherwise.
I would do bedside ultrasound to look at the RV, look for B lines as a cause of hypoxia (which would support OMI, and argue against PE), and if any doubt persists, a rapid CT pulmonary angiogram. There is sinus tachycardia at ~100/minute. As for the ECG, it could represent OMI, but RBBB is also a clue that it may be PE. As per Dr.
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?
He had diffuse crackles on exam and B-lines on chest ultrasound, and chest x-ray also confirmed pulmonary edema. 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.
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.
Automatic activity refers to enhanced pacemaking function (typically from a non sinus node source), for example atrial tachycardia. However the patient continued to have chest pain and bedside ultrasound showed hypokinesis of the septum with significantly reduced LVEF. The most common triggered arrhythmia is Torsades de Pointes.
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.
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.
Further ultrasound showed no B-lines (no pulmonary edema). 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. These patients are often on beta blockers to prevent such a scenario.
So I immediately left the room to get an ultrasound machine. While calling for some help and arranging to have her transported to our critical care zone, I got this quick ultrasound which confirmed my suspicion: This quick view was all I was able to obtain in the circumstances.
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.
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. In multivariate analysis, serum potassium level was negatively and age positively related to ventricular tachycardia.
A bedside cardiac ultrasound was normal, with no effusion. This sinus tachycardia ( at ~130/minute ) — is consistent with the patient’s worsening clinical condition, with development of cardiogenic shock. He had the following EKG recorded: Low voltage, suggests effusion. There is minimal, probably normal STE in V2-V6.
Beware a negative Bedside ultrasound. That said — the heart rate is significantly faster than it was for the prior 2 tracings ( ECGs #1 and #3 ) — so there is really no way to distinguish what might represent ST-T wave changes due to tachycardia vs evolution of the patient’s underlying disorder. Pericarditis?
Although the shock is no doubt partly a result of poor pump function, with low stroke volume, especially of the RV, it should be compensated for by tachycardia. They did not have an ultrasound on the ambulance (some local crews are starting to utilize POC limited US in our service areas). This is a perfect indication for atropine.
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
5 of 6 presented with chest pain and an ECG indicating reperfusion therapy, but were detected by bedside ultrasound. In a report of 6 cases at our institution (Hennepin County Medical Center), 2 survived with cardiac surgery. Plummer D et al. Annals of EM 23(6):1333-1342; June 1994.
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). Most physicians will automatically be worried about these symptoms. Good History and Physical exam, including a.
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.
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. However, there is also significant tachycardia , with heart rate of 116, and known hypoxia. She arrived to the ED with a nonrebreather mask. Her blood pressure on arrival was 153/69.
And almost all of them could be detected by bedside ultrasound. Conclusion: you may take a few moments to look for dissection with your bedside ultrasound, but when it is a clear STEMI, do NOT waste time with a CT scan. It is not a waste of time to use bedside ultrasound to look for dissection 3. Ultrasound Med.
Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis Answer: pulmonary embolism. Now another, with ultrasound. Submitted by a Med Student, with Great Commentary on Bias! Chest pain, SOB, Precordial T-wave inversions, and positive troponin. What is the Diagnosis? This is a quiz. The ECG is nearly pathognomonic.
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