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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.
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?
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). In patients with narrow QRS ( not this patient), this pattern is highly suggestive of acute pulmonary embolism.
Bedside cardiac ultrasound showed moderately decreased LV function. CT of the chest showed no pulmonary embolism but bibasilar infiltrates. Even with tachycardia and a paced QRS duration of ~0.16 She was intubated. J Am Coll Cardiol.
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.
He was in acute distress from pulmonary edema, with a BP of 180/110, pulse 110. 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 hypertension alone is the likely etiology of the pulmonary edema.
She had acute pulmonary edema on exam. 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.
Ken (below) is appropriately worried about pulmonary embolism from the ECG. 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.
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.
Smith comment: before reading anything else, this case screamed pulmonary embolism to me. 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.
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.
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.
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.
Patients with pulmonary embolism or aortic dissection who have normal variant ST elevation are at high risk of being diagnosed with pericarditis when what they have is far more serious!! Beware a negative Bedside ultrasound. You diagnose pericarditis at your peril! Acute MI is frequently misdiagnosed as pericarditis. Pericarditis?
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 started on a heparin drip and CTA of the chest was ordered to rule out pulmonary embolism. This is a case like many others posted (see list below) and the EKG from the patient’s original presentation can be quickly recognized as diagnostic for pulmonary embolism. In fact, Kosuge et al. Accessed May 28, 2024.
The morphology of V2-V4 is very specific in my experience for acute right heart strain (which has many potential etiologies, but none more common and important in EM than acute pulmonary embolism). CT angiogram showed extensive saddle pulmonary embolism. He had multiple cardiac arrests with ROSC regained each time.
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.
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. and the patient was converted to veno-venous (V-V) ECMO due to persistent pulmonary insufficiency. Clinically — despite an initial 2-fold increased troponin, the normal bedside Echo was reassuring against OMI or pulmonary embolism. Here they are: Learning Points: 1.
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.
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). Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade. Good History and Physical exam, including a.
On arrival in the ED, a bedside ultrasound showed poor LV function (as predicted by the Queen of Hearts) with diffuse B-lines. Chest X-ray also showed pulmonary edema. Primary VF in this study refers to fibrillation occurring in the absence of shock or pulmonary edema. Initial BP was 120/96, HR 102, SpO2 98%. Potassium was 4.5
Smith : This is classic for pulmonary embolism (PE). Acute pulmonary embolism was confirmed on CT angiogram: The patient did well. See our other acute right heart strain / pulmonary embolism cases: A man in his 50s with shortness of breath Another deadly triage ECG missed, and the waiting patient leaves before being seen.
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