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Here is her ECG: Regular Wide Complex Tachycardia. Regular means it can't be atrialfibrillation --Most regular wide complex tachcardia are VT, especially if the patient has poor LV function, as in this case. Could it be atrialtachycardia with RBBB and LPFB aberrancy? What do you think? What do you want to do?
The ECGs show a wide complex, irregularly irregular tachycardia. The differential of wide complex irregularly irregular includes: polymorphic VT, atrialfibrillation with WPW, atrialfibrillation with other aberrancy. Thus, the patients rhythm is atrialfibrillation with WPW.
Here is the computer interpretation: ATRIALFIBRILLATION WITH RAPID VENTRICULAR RESPONSE WITH ABERRANT CONDUCTION OR VENTRICULAR PREMATURE COMPLEXES LEFT AXIS DEVIATION [QRS AXIS beyone -30] NONSPECIFIC ST and T-WAVE ABNORMALITY The over-reading physician confirmed this diagnosis, which is incorrect. It is not atrialfibrillation.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Atrialfibrillation is also a predictor of worse outcomes in this case (Alborzi). Between 81-95% of life-threatening ventricular dysrhythmias and acute cardiac failure occur within 24-48 hours of hospitalization.
Here is her ED ECG: Here is the ED physician's interpretation: IMPRESSION UNCERTAIN REGULAR RHYTHM, wide complex tachycardia, likely p-waves. LEFT BUNDLE BRANCH BLOCK [120+ ms QRS DURATION, 80+ ms Q/S IN V1/V2, 85+ ms R IN I/aVL/V5/V6] Comparison Summary: LBBB and tachycardia are new. This is clearly ventricular tachycardia.
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.
The rhythm is atrialfibrillation. Then there is loss of pulses with continued narrow complex on the monitor ("PEA arrest") Learning Points: Sudden witnessed Cardiac Arrest due to ACS is almost always due to dysrhythmia. Tachycardia is of course, quite common in patients following cardiac arrest.
There is atrialfibrillation. Comments: STEMI with hypokalemia, especially with a long QT, puts the patient at very high risk of Torsades or Ventricular fibrillation (see many references, with abstracts, below). See here for management of Polymorphic Ventricular Tachycardia , which includes Torsades. Learning Points: 1.
Smith comment: In a large randomized trial of dopamine vs. norepinephrine (11) for shock which was published after the above-mentioned recommendations, dopamine had more adverse events (especially severe dysrhythmias, and especially atrialfibrillation). Hypotension may of course be a result of a brady- or tachydysrhythmia.
Here was his ED ECG: There is sinus tachycardia (rate about 114) with nonspecific ST-T abnormalities. There is a large peaked P-wave in lead II (right atrial enlargement) There is left axis deviation consistent with left anterior fascicular block. See my quick review of atrialtachycardia below) The tachycardia spontaneously resolved.
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. Most physicians will automatically be worried about these symptoms. The tracings were considered abnormal in the following cases: 1.
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