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In this ECG Cases blog Dr. Jesse MacLaren guides us through 10 cases of patients who present with generalized weakness or acute neurologic symptoms and discusses how to look for ECG signs of dysrhythmias, electrolyte emergencies, acute coronary occlusion, and demand ischemia in patients with generalized weakness and in patients with neurologic symptoms, (..)
Clinical introduction A middle-aged patient with no prior comorbidities presented to the emergency department with a sudden onset of palpitations, dizziness and progressive dyspnoea. History was negative for any cardiac disorders in the past. On examination, the pulse rate was around 190 beats/min with a systolic blood pressure of 80 mm Hg.
In that sense, the term dysrhythmia is preferable because it does literally translate as a disturbance in normal rhythm which is exactly what it is meant to describe. Any unsolicited disturbance of the rate or rhythm can be termed a dysrhythmia and result in the heart beating less efficiently but only for the duration of the dysrhythmia.
Especially when present in the setting of bradycardia and syncopal episodes, this is very worrisome for high risk of lethal dysrhythmias including polymorphic ventricular fibrillation (termed Torsades when in the setting of long QT). This ECG shows sinus bradycardia with massively long QT (or QU?) interval, at over 600 msec.
Atrial fibrillation (AF) is the most common sustained cardiac dysrhythmia encountered in practice. It is currently estimated that AF affects approximately 2% of the general population; however, the true prevalence of AF is likely to be at least 3%–4% when asymptomatic AF is considered.
Because she has cardiomyopathy and ventricular dysrhythmias, the pacer included an Implanted Cardioverter-Defibrillator (ICD) Echo 6 days later after CRT: Normal estimated left ventricular ejection fraction. The septum is punctured with the active fixation screw of the lead - so essentially you bore the septum with the screw helix."
Relative contraindications to both include a known prolonged QT, especially if the dysrhythmia is believed to be caused by prolonged QT. Another benefit: Procainamide is very effective at terminating SVT. So if you are incorrect about your diagnosis, it might convert with procainamide anyway!
See these publications for more information Overall, management for cardiac contusion is mostly supportive unless surgical complications develop, involving appropriate treatment of dysrhythmias and hemodynamic instability.
The patient himself had never had syncope or dysrhythmias. He proceeded also with an implantable loop recorder to detect subclinical dysrhythmias, and this was negative. Without Brugada pattern on the baseline ECG, there is no Brugada syndrome. However, there is an uncertain history of sudden death as well as inducible Brugada pattern.
Imge courtesy of Won-Young Kim from Chung-Ang University milla1cf Thu, 01/11/2024 - 08:30 January 11, 2024 — Acute cardiovascular manifestations of COVID-19 , such as heart failure, thrombosis, and dysrhythmia, are associated with increased mortality.
No patient with a QRS of less than 160 ms had ventricular dysrhythmias. Blockade of cardiac fast sodium channels (leads to wide QRS, R-wave in aVR, R' wave in V1, Brugada pattern ECG, ventricular dysrhythmias.) Of 14 with initial QRS of 140 ms or longer, 8 (56%) had seizures. There are multiple mechanisms of toxicity of TCAs: a.
The patient was admitted to the cardiology service with a plan for EP study, however the cardiologist during that visit thought that the ECG showed only LBBB, and thought that the patient's dysrhythmia was atrial fibrillation with LBBB, instead of atrial fibrillation with WPW. So he was simply discharged without EP study.
Blunt cardiac injury my result in : 1) Acute myocardial rupture with tamponade 2) Valve rupture (tricuspid, aortic, mitral) 3) Coronary thrombosis or dissection (and thus Acute MI) from direct coronary blunt injury 4) Dysrhythmias of all kinds. Localized bleeding from contusion could cause hemopericardium even without rupture.
Is it sinus or is it a supraventricular dysrhythmia? If rapid, that means that the depolarization is rapidly advancing and that it must be using conducting fibers (Purkinje fibers), and is therefore supraventricular.
The second explanation (AIVR), whether as a reperfusion dysrhythmia or not, seems most likely. A repeat ECG had sinus rhythm at a rate of 54 and normal conduction (no LBBB), and was completely normal with no ischemia. The slow sinus rate supports the notion that this could be rate-related BBB.
There were no dysrhythmias on cardiac monitor during observation. This discussion comes from this previous post: Hyperthermia and ST Elevation Discussion Brugada Type 1 ECG changes are associated with sudden cardiac death (SCD) and the occurrence of ventricular dysrhythmias. He was found to be influenza positive. Is there fever again?
Flecainide : This is a potentially dangerous Na channel blocker which can cause ventricular dysrhythmias including ventricular fibrillation. It is possible that her disease has progressed to the point where she cannot be kept in sinus rhythm, but it is worth a try. She is already anti-coagulated, so that is not an issue.
If you don't know what the dysrhythmia is, then try procainamide. Pads were placed with ultrasound guidance, so they were in the correct position. What to do now? If you believe it is SVT, then try adenosine. Procainamide is proven better and safer than amiodarone for VT ( Procamio randomized trial ) AND it also works for SVT.
Accelerated idioventricular rhythm in newborns: a worrisome but benign entity with or without congenital heart disease Here are other examples of Accelerated Idioventricular Rhythm, Usually a Reperfusion "Dysrhythmia" I saw this on the computer. Most physicians, at first glance, get this wrong. What is it? What is the rhythm?
Similarly, there have been case reports of patients who were taking beta blockers to control dangerous heart rhythm disturbances and when the beta blocker was abruptly stopped it led to precipitation of ventricular dysrhythmias and even in some cases death. This is termed as ‘Acute beta blocker withdrawal syndrome’.
Likewise, in some cases of ischemia concealed by flutter waves, the ischemia can be seen despite the flutter waves, whereas in other cases the dysrhythmia must be terminated before the ischemia can be clearly distinguished. Even when flutter waves conceal true ST segment deviations, the cause and effect relationship may be unclear.
So the real QT is shorter, but the computer does not mention the U-wave, and the U-wave is as important as the T-wave in predicting cardiac dysrhythmias. There is a very prominent U-wave and some of what may appear to be a QT interval is a QU interval. This is an extremely dangerous ECG. The K returned at 1.9 This is extremely low for DKA.
Opinions vary widely on the K level at which a patient must be admitted on a monitor because of the risk of ventricular dysrhythmias. My rationale is that if the K is affecting the ECG, then it is affecting the electrical milieu and can result in serious dysrhythmias. Until some real data is available, my opinion is this: 1.
But adenosine only lasts for seconds, and if the dysrhythmia recurs, then the adenosine is gone. Prevent the initiation of the dysrhythmia -- this can be done with a beta blocker by prenenting PACS 2. Smith: should we give adenosine again? Adenosine worked. It converted the rhythm. We need to do one or both of two things: 1.
Could the dysrhythmias have been prevented? Severe hypokalemia in the setting of STEMI or dysrhythmias is life-threatening and needs very rapid treatment. mmol/L (n = 11), and Measurements and Results: All patients tolerated the infusions without evidence of hemodynamic compromise, ECG change, or new dysrhythmia requiring treatment.
I also believe that we physicians and medics are eager to treat dysrhythmias, and we want to see them even when they are not there. Dilated pupils and hypertension are a strong clue to sympathetic overload, but don't forget anticholinergic syndromes, including tricyclics!
He was admitted for monitoring, as his risk of a ventricular dysrhythmia as cause of the syncope is high ( very high due to HFrEF and ischemic cardiomyopathy ). ECG 3 hours later was unchanged He was not started on heparin as type II MI was favored over NonSTEMI as the etiology of his troponin elevation.
The heart is an electrical organ and occasionally the electrics can choose to malfunction and the patient may develop a heart rhythm disturbance or a dysrhythmia such as AF or SVT or VT. Cardiac CT is now widely available and to my mind the easiest way to know about the blood vessels of the heart. You can only diagnose it in retrospect.
The limb lead abnormalities appear to be part of the Brugada pattern, as described in this article: Inferior and Lateral Electrocardiographic RepolarizationAbnormalities in Brugada Syndrome Discussion Brugada Type 1 ECG changes are associated with sudden cardiac death (SCD) and the occurrence of ventricular dysrhythmias.
A 30-something was in the ED for some minor trauma when he was noted to have a fast heart rate. He acknowledged that he had palpitations. but only when asked. He had a history heavy alcohol use. Blood pressure was normal (109/83).
I could find very little literature on the treatment of severe life-threatening hypokalemia. There is particularly little on how to treat when the K is less than 2, and/or in the presence of acute MI.
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.
Inferior MI results in scar tissue which is a likely source of a re-entrant ventricular dysrhythmia. Here is the post-cardioversion ECG: There is sinus with RBBB There are inferior Q-waves suggesting old inferior MI. This would be the likely source of the VT.
Atrial dysrhythmias, and atrial fi brillation in particular, are frequently misdiagnosed by computer algorithms and then by the physician who overreads them. Shah and Rubin studied the computer rhythm interpretation of 2160 12-lead ECGs, compared to 2 cardiologists [ 18 ].
Now you have ECG and troponin evidence of ischemia, AND ventricular dysrhythmia, which means this is NOT a stable ACS. (For those of you who are accustomed to the units of high sensitivity troponin (ng/L), this is equivalent to 20,956.00 Again, cath lab was not activated. What does this troponin level mean?
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 atrial fibrillation).
Introduction:Patients with atherosclerotic carotid artery disease are at high risk of mortality in the long-term follow-up after carotid endarterectomy (CEA), partly due to dysrhythmia. Atrial fibrillation (AF) is a common cardiac dysrhythmia linked to stroke and cardiovascular events.
Here is one full text article on the topic from Clinical Cardiology 2008: Diagnostic Approach and Treatment Strategy in Tachycardia-induced Cardiomyopathy Atrial Tachycardia (AT): another SVT in the ED Rapid dysrhythmia from non-sinus focus above AV node.
Sinus tach is often misinterpreted as a dysrhythmia. They often have good ejection fraction and tolerate the dysrhythmia quite well. There is no evidence that this elderly patient has suffered from VT or other primary dysrhythmias in the past. See this case, for example: A Relatively Narrow Complex Tachycardia at a Rate of 180.
He was admitted for monitoring and had no dysrhythmias. Amazingly, the Queen also recognizes it as "Not OMI". She is very good. The first troponin was < 3 ng/L. The 2 hour troponin was < 3 ng/L. He had a formal contrast echo that was completely normal: Normal estimated left ventricular ejection fraction; 69%.
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