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Ventricular tachycardia is a potentially life threatening cardiac arrhythmia. On the ECG, ventricular tachycardia can be defined as three or more ventricular ectopic beats occurring in a sequence at a rate more than 100 per minute. Another rare form of ventricular tachycardia is bidirectional ventricular tachycardia.
Sinus tachycardia – sinus rhythm above 100 bpm is a sinus tachycardia. Sinus bradycardia – sinus rhythm below 60 bpm is a sinus bradycardia. Ventricular tachycardia – more than 7 consecutive complexes originating from ventricles at a rate of > 100 bpm. Usually does not exceed 160 bpm.
He denied any known medical history, specifically: coronary artery disease, hypertension, dyslipidemia, diabetes, heart failure, myocardialinfarction, or any prior PCI/stent. Breath sounds were clear in all lung fields. No appreciable skin pallor. He reported to be a social drinker, but used tobacco products daily.
Both of these features make inferior + RV MI by far the most likely ( Pseudoanteroseptal MI is another name for this ) There is also sinus bradycardia and t he patient is in shock with hypotension. A narrow complex bradycardia without any P-waves is also likely to respond to atropine, as it may be a junctional rhythm.
Then, why is it mentioned that, implanting a defibrillator soon after an acute myocardialinfarction, in those with left ventricular dysfunction and prone for ventricular arrhythmias and sudden cardiac death, is not useful? Then, why is it mentioned that, an implantable defibrillator, is not useful, soon after myocardialinfarction?
There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Torsades in acquired long QT is much more likely in bradycardia because the QT interval following a long pause is longer still. See here for management of Polymorphic Ventricular Tachycardia , which includes Torsades.
Automatic activity refers to enhanced pacemaking function (typically from a non sinus node source), for example atrial tachycardia. AIVR is not always the result of significant pathology, but is classically associated with the reperfusion phase of acute myocardialinfarction. Do not treat AIVR. Am Heart J 1999;137:799–805.
Troponin T peaked at 38,398 ng/L ( = a very large myocardialinfarction, but not massive-- thanks to the pre-PCI spontaneous reperfusion, and rapid internvention!! ). This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ).
The mean cost per hospital discharge was the highest for peripheral vascular disease ($33 700 [95% CI, $33 300–$34 000]) and ventricular tachycardia/ventricular fibrillation ($32 500 [95% CI, $32 100–$32 900]).
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. Thus, if there is documented sinus bradycardia, and no suspicion of high grade AV block, at the time of the syncope, this is very useful.
Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. If this were OMI, I would favor proximal RCA culprit (since that commonly produces inferolateral changes and occasionally produces anterior HATW from RV infarct ), but LAD is also possible. Bradycardia and heart block are very common in RCA OMI.
This ECG shows a sinus bradycardia with a normal conduction pattern (normal PR, normal QRS, and normal QTc), normal axis, normal R-wave progression, normal voltages. Clinical questions : Is this an occlusion myocardialinfarction and does the patient need the cath lab? There is marked sinus bradycardia. What do you think?
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