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In Part 1 of our 2-part series on bradycardia and bradydysrhythmias we discussed a practical approach with electrophysiologist Paul Dorian and EM doc Tarlan Hedayati. How is the treatment of bradycardia different in the patient with hypothermia? Cardiac ischemia? In this, part 2, we discuss details of treatment. Myxedema coma?
Common explanations for unusual rhythms such as this one include: i ) Hyperkalemia ( or other severe electrolyte disorder ); ii ) Recent infarction/ischemia; iii ) Sleep apnea; iv ) Severe hypothyroidism; v ) Acute neurologic catastrophe (ie, stroke, bleed, trauma, tumor ); vi ) Some other toxicity.
No ischemia. Case continued Another ECG was recorded 3 hours later, still 1/10 pain: There is sinus bradycardia with RBBB. This is a conundrum, because it is clear that the patient is having an acute MI, the ECG is dynamic, but the pain is very mild and there is no ECG evidence of active transmural ischemia.
Her vital signs were within normal limits except for bradycardia at 55 bpm. It is probably sinus bradycardia with very small/depressed P-waves and prolonged PR interval. P EARL # 4 In my opinion, it is not worth wasting time trying to figure out the specific rhythm diagnosis of a bradycardia when there is hyperkalemia.
For instance, if there were inappropriate sinus bradycardia at less than 60 bpm, the atrial pacer would take over if it is programmed to wait 1 second before firing. The T-waves of both of these beats have, coincidentally , a superimposed P-wave Clinical course: The potassium was normal, there was no ischemia or drug toxicity.
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.
Altered Mental Status, Bradycardia == MY Comment , by K EN G RAUER, MD ( 2/2 /2024 ): == Dr. Meyers began today’s case with the clinical challenge of asking you to identify the underlying cause of ECG #2. -- Read this ECG -- Osborn Waves and Hypothermia (this is the "Figure" above) What does LBBB look like in severe hypothermia?
Even if we stopped here — We could conclude the following: There is marked bradycardia in today's rhythm ( ie, Heart rate in the low 30s ). Finally — If today's patient does not have significant underlying coronary disease — then her bradycardia with AV block may be the result of SSS ( S ick S inus S yndrome ).
I will leave more detailed rhythm discussion to the illustrious Dr. Ken Grauer below, but this use of calipers shows that the rhythm interpretation is: Sinus bradycardia with a competing (most likely junctional) rhythm. The fact that R waves 2 through 6 are junctional does make ischemia more difficult to interpret -- but not impossible.
The ECG does not show any definite signs of ischemia. IMPRESSION: The finding of sinus bradycardia with 1st-degree AV block + marked sinus arrhythmia + the change in PR interval from beat #5-to-beat #6 — suggests a form of vagotonic block ( See My Comment in the October 9, 2020 post in Dr.
There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( Some residual ischemia in the infarct border might still be present. Both episodes are initiated by an "R-on-T" phenomenon.
Below is the first ECG recorded by paramedics after 2 hours of chest pain, interpreted by the machine as “possible inferior ischemia”. There’s competing sinus bradycardia and junctional rhythm, with otherwise normal conduction, borderline right axis, normal R wave progression and voltages. What do you think?
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.
to 1828 msec. ) — which corresponds to a variation in the rate of sinus bradycardia from 36-to-33/minute. This makes sense given that the underlying rhythm in today's case appears to be marked sinus bradycardia and arrhythmia , with a ventricular escape rhythm appearing when the SA node rate drops below 33/minute.
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?
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?
During the night, while on telemetry, the patient became bradycardic, with periods of isorhythmic AV dissociation (nodal escape rhythm alternating with sinus bradycardia), and there were sporadic PVCs. Most such rhythms in the setting of ischemia are VF and will not convert without defibrillation. Acute ischemia?
The patient with no prior cardiac history presented in the middle of the night with acute chest pain, and had this ECG recorded during active pain: I did not see any ischemia on this electrocardiogram. Their apparently excessive length (QT interval) is due to bradycardia. This is a case I had quite a while back.
Description Sinus bradycardia. There is ST elevation in V2 and V3 There are inverted T-waves in V2 and V3 There are prominent U-waves in V2 and V3 Many responders were worried about ischemia or hypertrophic cardiomyopathy. This short QT at least makes ischemia all but impossible. There is high voltage. This is a normal variant.
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.
during which sinus bradycardia and arrhythmia are seen but not to a degree that produces symptoms. Thus, there is sinus bradycardia and arrhythmia sinus pauses ( which may be longlasting, ultimately leading to sinus arrest ) and SA nodal block. The indication for pacemaker placement with SSS is symptomatic bradycardia.
Monomorphic ventricular tachycardia in the setting of acute myocardial ischemia can also be treated by intravenous lignocaine bolus followed by infusion. Predisposing causes for ventricular tachycardia like ischemia and electrolyte imbalance has to be treated simultaneously to prevent recurrence.
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?
Discontinue all negative chronotropic agents, since the risk of torsade is much higher with bradycardia or pauses. 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.
Soon afterward, the patient’s symptoms return along with lightheadedness, bradycardia, and hypotension. The patient has also developed sinus bradycardia, which may result from right coronary artery ischemia to the SA node. The Queen of Hearts agrees: Around this time his initial high sensitivity troponin I resulted at 231 ng/L.
I see the following: The rhythm is sinus bradycardia at ~55-60/minute. ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL ( featured in Audio Pearl #2 in this blog post ). The PR and QRS intervals are both normal. ECG Blog #230 — How to compare serial ECGs.
There are 3 etiologies I always think of with bradycardia and AV block: 1. There was no evidence of ischemia. In addition to ruling out rate-slowing medication serum electrolyte disorders and/or ischemia/infarction as potential causes of bradyarrhythmias one should also rule out hypothyroidism + sleep apnea. Hyperkalemia.
That said — obvious findings include: i ) Marked bradycardia! — This suggests ischemia of uncertain duration. MY " Q uick T houghts" on Today's CASE: The ECG in Figure-1 is highly concerning — so it is indeed fortunate that this elderly woman came to the ED when she did! be regular! —
Here is his previous ECG: This was my interpretation of the first ECG: Sinus bradycardia with less than 1mm ST elevation in V4-V6, elevated compared to the previous ECG, suggestive of lateral MI. This is his first ECG in the department, which I saw as it was being printed: What do you think? Notice how useful serial ECGs are!
If you put the inferior and posterior findings together, it is diagnostic of OMI This was read as "inferior ischemia" without any other information by Dr. Richard Gray and as probable reperfused inferior-posterior OMI much later by both me and Pendell Meyers, also without any clinical information.
Sinus bradycardia, normal conduction, normal axis, normal R wave progression, no hypertrophy. 2] Here there is no posterior ST elevation, but the anterior ST depression is also less—so it is dynamic, confirming acute ischemia. What do you think? But it is still STEMI negative.
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.
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. Hypothermia can also produce bradycardia and J waves, with a pseudo-STEMI pattern. There is marked sinus bradycardia. What do you think? Pacing Clin Electrophysiol.
Followup ECG: No Change Absence of evolution is the best evidence against ischemia as the etiology. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chest pain for the ischemia and potential syncope for brugada. Ischemia/infarction. Bradycardia. Hypothermia.
Hyperkalemia causes peaked T waves and the "killer B's of hyperkalemia", including bradycardia, broad QRS complexes, blocks of the AV node and bundle branches, Brugada morphology, and otherwise bizarre morphology including sine wave. With a twist. Do you recognize this ECG yet? Right Bundle Branch Block with ST Elevation in V1?
2] Conduction through the accessory pathway can be intermittent (with different degrees of pre-excitation), and affected by ischemia. 3] So a patient with WPW can have the pattern induced by ischemia, and there is also a report of a patient with pre-existing WPW which was “ablated” by myocardial infarction after an LAD occlusion.[4]
In any case, there is bradycardia. There is ST depression beyond the end of the wide QRS in I, II, aVF, and V4-V6, diagnostic of with subendocardial ischemia. due to PE) may result in STEMI (and, if anterior, it can be from anterior LV or anterior RV ischemia, or both) from low coronary pressure and flow, simply due to the shock.
After the heart rate increased slightly, here was the repeat ECG: Sinus bradycardia, only slightly faster rate than prior. Learning Points: Ectopic atrial rhythm can produce atrial repolarization findings that can be confused for acute ischemia, STEMI, or OMI.
Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? Ischemia b. ST depression: is it ischemia? In my experience, Ive seen U waves not only with low K+/low Mg++ but also in patients with bradycardia, LVH, and sometimes in normal subjects.
Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls. He had multiple episodes of bradycardia and nonsustained ventricular tachycardia. The patient had none of these conditions. Patient 1 remained in the hospital overnight.
A fast heartbeat is called tachycardia, while a slow heartbeat is called bradycardia in medical terms. Poor blood supply Ischemia, or inadequate blood supply to the heart, is an abnormality that can be detected in an ECG test. Arrhythmia In simple words, arrhythmia refers to an irregular heartbeat.
There is a junctional bradycardia. Furthermore, there are T-wave changes in V2 and V3 which are highly suggestive of ischemia, but difficult to localize: anterior? Troponin was repeated and returned higher still. She was taken to the cath lab. What was the diagnosis? and right ventricular echo findings. right ventricular?
Such findings would normally suggest primary ischemia with concomitant surveillance of coronary occlusion, but these ST/T changes might very well be secondary to the Escape mechanism at hand. Lead V2 shows RR’ QRS configuration, and although ST depression is otherwise expected here, the discordance is a bit excessive.
lidocaine) can result in severe bradycardia or asystole (Weinberg, Sedowski and Alexander, below) The presence of accelerated idioventricular rhythm does not affect prognosis, and there is no definitive evidence that, if left untreated, the incidence of VF or death is increased. Do not treat AIVR. In fact, use of antidyrhythimcs (e.g.,
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