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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.
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.
He presented to the Emergency Department with a bloodpressure of 111/66 and a pulse of 117. 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. He had this ECG recorded.
The initial bloodpressure was 80/palp with a heart rate of 104, respirations 20, oxygen saturations of 94% and a finger stick blood glucose of 268. In addition, the patient received 750 mL of fluid resuscitation with transient improvement of bloodpressure.
This proves effective treatment of the recurrent ischemia. The patient had no further symptoms of ischemia. EKG 3 is diagnostic for developing re-occlusion, and EKG 4 proves that the nitrates relieved the ischemia. = This proves effective treatment of the recurrent ischemia." Here was her final EKG prior to discharge.
Bloodpressure was normal (109/83). 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.
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.
The ECG was incorrectly interpreted as no signs of ischemia. He is placed on heparin drip, he will have IV beta-blocker and oral beta blocker for heart rate control and bloodpressure management. There is sinus tachycardia at 100-105/minute. Admitted to the hospital service for further evaluation and management."
The flutter waves can conceal or mimic ischemic repolarization findings, but here I don't see any obvious findings of OMI or subendocardial ischemia. 2) Norepinephine to support BloodPressure. The rhythm in ECG #1 is not Sinus Tachycardia — because there is no upright P wave in lead II. The rhythm is 2:1 atrial flutter.
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?
Immediately after contrast injection into the LMCA, the patient had circulatory collapse, with a precipitous drop in bloodpressure. An Impella device was placed to maintain cardiac output and perfusion pressures. There is no definite evidence of acute ischemia. (ie, Epinephrine infusion was begun.
There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1] Although the bloodpressure resolved, his pain, however, did not.
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. RCA ischemia often results in sinus bradycardia from vagal reflex or ischemia of the sinus node. This is a perfect indication for atropine.
On arrival in the ED, he was hypotensive with a systolic bloodpressure in the 70s. After initiating treatment for hyperkalemia, repeat ECG showed resolution of Brugada pattern: The ECG shows sinus tachycardia. A Very Wide Complex Tachycardia. Fluid resuscitation was initiated. What is the Rhythm? Use Lewis Leads!!
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. Evidence of acute ischemia (may be subtle) vii. Any ED systolic bloodpressure less than 90 or greater than 180 mm Hg (+1) 4.
Her bloodpressure on arrival was 153/69. 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. An EKG was immediately recorded.
The bloodpressure was 170/100 in the critical care area. Cardiology wanted a CT of the aorta to rule out dissection, presumably partly due to the very high bloodpressure readings, but also because it is hard for people to believe that a 20-something woman could have acute thrombotic coronary artery.
This ECG was recorded: It is difficult to appreciate P-waves, but I believe this is sinus tachycardia. Time 7 hours lead reversal There is limb lead reversal (QRS in I and aVL are now inverted), but nevertheless one can see that the ischemia appears to have resolved. He was put on BiPAP. A Chest X-ray did not show pulmonary edema.
Be ready with prudent administration of IV fluids if bloodpressure drops ( See ECG Blog #190 for more on RV MI, and its different hemodynamics ). While its action improves AV conduction it may increase the sinus rate, producing a sinus tachycardia with adverse effect. Figure-2: The first leads to catch my "eye".
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