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BackgroundAcute myocardial ischemia (AMI)triggered ventricular arrhythmias are closely linked to maladaptive sympathetic hyperactivity mediated via the left stellate ganglion (LSG). Retigabine pretreatment significantly suppressed ischemiainduced LSG hyperactivity and reduced sympathetic activation markers compared with controls.
In some cases the ischemia can be seen "through" the flutter waves, whereas in other cases the arrhythmia must be terminated before the ischemia can be clearly distinguished. In this case, there is diffuse ischemic ST depression of subendocardial ischemia, of course with accompanying reciprocal STE in aVR.
The ECG shows severe ischemia, possibly posterior OMI. But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. It takes time for that ischemia to resolve. The patient was brought to the ED and had this ECG recorded: What do you think? And what do you want to do?
However, he suddenly developed a series of malignant ventricular arrhythmias. Below are printouts of some of the arrhythmias recorded. There is no definite evidence of acute ischemia. (ie, This time, the arrhythmia did not spontaneously terminate — but rather degenerated to VFib, requiring defibrillation.
Heart rate/rhythm: consider antidotes for brady/tachy-arrhythmias, and for sinus tachycardia consider fluids for vasodilation and benzodiazepines for agitation. Electrical conduction and axis: consider sodium bicarb for QRS > 100 especially if RBBB or terminal rightward shift, and magnesium for QTc> 500.
With P waves labeled — Isn't it now much easier to appreciate that the atrial rhythm is quite regular ( with no more than a slight sinus arrhythmia )? P utting I t A ll T ogether : The precise mechanism of today's arrhythmia is complex and difficult to determine. For those with a special interest in cardiac arrhythmias — READ ON! —
Ischemic cardiomyopathy, a severe cardiac condition resulting from prolonged myocardial ischemia, is characterized by ventricular dilation, dysfunction, and an increased risk of life-threatening arrhythmias. Arrhythmia, a common complication in ischemic cardiomyopathy, is associated with poor clinical outcomes.
The ECG does not show any definite signs of ischemia. Uncontrolled coronary spasm may be associated with serious arrhythmias , including cardiac arrest ( Looi et al — Postgrad Med, 2012 ; Tan et al — Eur Heart J Case Rep, 2018 ; Chevalier et al — JACC, 1998 ; Rodriguez-Manero — EP Europace, 2018 ).
Neural remodeling in the left stellate ganglion (LSG), as mediated by neuroimmune reactions, promotes cardiac sympathetic nerve activity (SNA) and thus increases incidence of VAs. Interleukin-6 is an important factor of the neuroimmune interaction.
The STD maximal in V1-V4 is diagnostic of acute transmural posterior wall ischemia, most likely due to posterior OMI. Subendocardial ischemia does not localize, and subendocardial ischemia presents with STD maximal in V5-6, II, and STE in aVR. Subendocardial ischemia does not localize. AI can do it too.
What is the most likely cause of this arrhythmia? Acute myocardial ischemia. He developed cardiac arrest shortly after the ECG in Figure-1 was recorded. QUESTIONS: How would YOU interpret the ECG in Figure-1 ? Figure-1: The initial ECG in today's case. ( To improve visualization — I've digitized the original ECG using PMcardio ).
DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR. The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.
My written interpretation on a tracing such as this one would read, "Marked LVH and 'strain' and/or ischemia — with need for clinical correlation." BOTTOM LINE: ECG changes of LV "strain" and/or ischemia that we see on today's initial ECG — were not present 9 years earlier. WPW Cardiac arrhythmias ( including AFib ).
This AI technology can detect 35 cardiac determinations (14 arrhythmias and 21 morphologies), including serious conditions like acute myocardial infarction ( MI ) and the most common types of cardiac ischemia, using a reduced leadset. KAI 12L employs multiple deep neural network algorithms, trained and validated on more than 1.75
A prior ECG was available for comparison: Normal One might be tempted to interpret the ST depression as ischemia, but as Smith says, "when the QT is impossibly long, think of hypokalemia and a U-wave rather than T-wave." QUESTION #2: If it were not for the markedly prolonged QTc — Wouldn't ECG #1 look like diffuse subendocardial ischemia?
Arrhythmia was properly resolved after hematoma removal surgically. Ventricular tachyarrhythmias, including TdP, because of electrical inhomogeneity, would potentially be a lethal complication of CABG. Here, we report the occurrence of medically intractable TdP in the presence of an uncommon case of a post-CABG retrosternal hematoma.
There are three mechanisms of arrhythmia: automatic, re-entry, and triggered. The most common triggered arrhythmia is Torsades de Pointes. It is a benign arrhythmia which requires no specific treatment. Possible mechanisms of ventricular arrhythmias elicited by ischemia followed by reperfusion. What is the rhythm?
T-wave alternans and the susceptibility to ventricular arrhythmias. Chronic amiodarone evokes no torsade de pointes arrhythmias despite QT lengthening in an animal model of acquired long-QT syndrome. Alternation in ST segment appearance ( or in the amount of ST elevation or depression ) — is often linked to ischemia. 2017.3191.
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?
This includes sinus arrhythmia — in which there is often slight variation in the P-P interval. This slight variation in sinus P wave regularity tends to be greater when a 2nd- or 3rd-degree AV block is present ( called ventriculophasic sinus arrhythmia — as shown in ECG Blog #344 ). For clarity — I have done this in Figure-4.
This is especially problematic in the emergency department, where computer accuracy drops as clinical significance increases—with common errors for arrhythmias and ischemia. Computer interpretation of the ECG has been called a double-edged sword: when correct, it increases physician accuracy, but when incorrect it increases errors.
Osborn waves have been reported with hypercalcemia, brain injury, subarachnoid hemorrhage, Brugada syndrome, cardiac arrest from VFib — and — severe, acute ischemia resulting in acute MI ( See My Comment in the November 22, 2019 post on Dr. Smith’s Blog ). Rituparna et al — as well as Chauhan and Brahma ( Int.
The fact that R waves 2 through 6 are junctional does make ischemia more difficult to interpret -- but not impossible. Back to the assessment of ischemia: Returning to the ECG, the leads that catch my eye first are -- I, II, V4, V5, V6. Ischemia can be disguised by a wide escape rhythm, which decreases the sensitivity of ECG.
It should be kept in mind that on occasions, beta-one agonist can result in increased ventricular ectopy e.g., in severe myocardial ischemia (by increasing myocardial demand), or sometimes with congenital long-QT syndrome. Smith, this can be accomplished by either using beta-one agonists or temporary transvenous pacing.
This may result in ischemia (lack of oxygen to the heart muscle), causing parts of the heart to weaken and enlarge. Arrhythmias (Irregular Heartbeats) Persistent abnormal heart rhythms can disrupt the heart’s pumping efficiency, eventually causing it to enlarge to maintain blood flow.
Remember, in diffuse subendocardial ischemia with widespread ST-depression there may b e ST-E in lead s aVR and V1. There are well formed R-waves with good voltage/amplitude which is uncommon for ischemia. The ECG does not show any signs of ischemia. True Positive ECG#2 : Also sinus rhythm. There is ST depression in V1.
Implantable loop recorders (ILRs) are increasingly adopted in clinical practice but are constrained by their non-standard, single-lead format, limiting ECG analyses of arrhythmia localization, conduction abnormalities, QT measurement, and ischemia.
When I was shown this ECG, I said it looks like such widespread ischemia that is might be a left main occlusion, or LM ischemia plus circumflex occlusion (high lateral and posterior OMI). The "usual rules" of cardiac arrhythmias are simply not always followed in critically ill patients. There is STE in aVR.
The precordial STD persists in severity from V4-V6, rather than being maximal in V1-V4 (as in posterior OMI), and so the ECG overall best fits the subendocardial ischemia pattern (diffuse supply/demand mismatch). Meyers serves as a reminder of the important clinical entity known as diffuse subendocardial ischemia.
Is there ischemia? Idioventricular rhythm is a common "reperfusion arrhythmia." ECG Diagnosis is either : 1) junctional rhythm with new LBBB, and possibly ischemia 2) accelerated idoventricular rhythm with possible ischemia, and possibly related to restoration of normal perfusion. But it is not conclusive.
Are you confident there is no ischemia? Primary VT , and the VT with tachycardia is causing ischemia with chest discomfort (supply-demand mismatch/type 2 MI)? Ischemia from ACS causing the chest discomfort, with VT another consequence (or coincidence)? Do you agree with this strategy? How can you better assess the ST segments?
Ventricular tachycardia is a potentially life threatening cardiac arrhythmia. Monomorphic ventricular tachycardia in the setting of acute myocardial ischemia can also be treated by intravenous lignocaine bolus followed by infusion. If the rate is very fast, hemodynamic deterioration can occur rapidly.
Precordial ST depression may be subendocardial ischemia or posterior STEMI. I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia. Whether it is subendocardial ischemia or posterior STEMI, if you cannot get it to resolve, you must activate the cath lab. There is no ST elevation.
Pediatric exercise testing may be used for evaluation of various disorders of cardiac rhythm rather than for inducible ischemia as in adults. QT prolongation and the occurrence of ventricular arrhythmias with exercise are another important aspect of exercise testing in children. Discussion on pediatric exercise testing.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Other Arrhythmias ( PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib ). Chest trauma was suspected on initial exam. Here is his initial ECG around 1330: What do you think? QTc prolongation.
Mechanism is thought to be due to sustained sympathetic stimulation, probably caused by dysfunction of insular cortex resulting in reversible neurogenic damage to the myocardium which could include contraction bands and subendocardial ischemia [2]. Risk is thought to be higher with damage to right hemisphere than left hemisphere.
Arrhythmia? Today’s case recalled that scenario for me, in that it features recognition of an arrhythmia that fooled ED staff into thinking the ECG was showing an acute infarction. The ED staff failed to do this — and as a result, they completely overlooked the arrhythmia. Would you give lytics? Yes, but not because of the ECG!
ECG is recorded periodically during the test in addition to documenting any specific events like arrhythmias. The recording in early phase of recovery at 1 minute, shows very little ST segment depression, making us suspect further whether the earlier recording was really due to myocardial ischemia.
These complications include new-onset arrhythmias, which are also common in stroke patients who have not experienced heart disease before. For post-stroke patients, arrhythmias represent a key risk factor for complications and a worse prognosis. The authors of the study stated that rhythm disturbances may also lead to brain ischemia.
Extensive conduction system abnormalities can have various causes (ischemia, genetic, infectious, amyloid, etc). VT is the second most common presenting arrhythmia. Vaso or inotropic medications are not harmless, and can precipitate life threatening arrhythmias. Usually the medical history will provide clues to the cause.
His response: “subendocardial ischemia. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. With the history of Afib, CTA abdomen was ordered to r/o mesenteric ischemia vs ischemic colitis vs small bowel obstruction. Anything more on history?
There are a number of things to look for in an ECG that can hint at arrhythmia as the cause of an apparent seizure. In my experience, the pathologic finding in the above ECG is the easiest one to overlook — especially if you are in a rush and do not do a systematic review. Learning Points: LQTS can have normal QTc. mEq/L for K+ and 1.76
The computer called it a normal ECG Algorithm unknown Aside : [There is some "sinus arrhythmia", which is indeed a normal finding. Sinus arrhythmia is sinus rhythm whose rate varies with respiration. If the longest P-P interval is 120 ms greater than the shortest, it is sinus arrhythmia. Burning pain subxiphoid and into throat."
This was interpreted by the treating clinicians as not showing any evidence of ischemia. This is a critically important determination because of the 2017 AHA/ACC/HRS Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. Here is his presenting ECG: ECG 1, t = 0 What do you think?
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