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CT of the chest showed no pulmonary embolism but bibasilar infiltrates. Discontinue all negative chronotropic agents, since the risk of torsade is much higher with bradycardia or pauses. She was intubated. Bedside cardiac ultrasound showed moderately decreased LV function. The plan: 1. Place temporary pacemaker 3.
The receiving staff suspects pulmonary embolism due to S1Q3T3 on the ECG and administers TPA. The patient did have massive pulmonary emboli, but he also had profound intraventricular and subarachnoid hemorrhages. Learning points: TCP is primarily recommended for bradycardia that does not respond to atropine, or other agents.
This middle-aged patient presented with SOB, weakness, and mild pulmonary edema. There are 3 etiologies I always think of with bradycardia and AV block: 1. She previously had Atrial fibrillation with LBBB. Here is her ED ECG: Does this reveal the etiology of her symptoms? This shows atrial fibrillation. Hyperkalemia.
KEY Point: Although true that patients with longstanding, severe pulmonary disease may manifest a QRST complex in standard lead I with marked overall reduction in QRST amplitude ( See ECG Blog #65 — regarding Schamroth’s Sign ) — you should never normally see a completely flat line in any of the standard limb leads.
The severe restriction causes elevation of pulmonary and systemic venous pressure which becomes equal to diastolic pressures in all cardiac chambers. Inspiratory fall in intrathoracic pressure is transmitted to the pulmonary veins, but not to the pericardial cavity. Relative change is more on the right sided chambers. Indian Heart J.
Q waves in association with RBBB are usually not seen in anterior leads unless there is pulmonary hypertension or anterior infarction. Other Arrhythmias ( PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib ). RBBB in blunt chest trauma seems to be indicative of several RV injury.
Some of the other useful parameters are mitral E velocity deceleration time, changes in mitral inflow with Valsalva maneuver, mitral L velocity, isovolumic relaxation time, left atrial maximum volume index, pulmonary vein systolic/diastolic velocity ratio, color M-mode Vp and E/Vp ratio. Stage IV is considered as advanced.
In any case, there is bradycardia. It makes pulmonary embolism (PE) very likely. The small LV implies very low LV filling pressures, which implies low pulmonary venous pressure. But it is bradyasystolic, so pulmonary embolism must be high on the differential. Possible, but huge pulmonary embolism is more likely.
Perhaps the patient has pulmonary hypertension and/or tricuspid regurgitation? There definitel are periods of bradycardia (so pacing may be needed for that). Hope this helps — :) ECG-3 — I see sinus bradycardia and arrhythmia. RED arrows show what looks to be sinus P waves that are HUGE !!!!
The D-dimer was elevated at 942, and the subsequent CT angiogram of the chest showed bilateral lower lobe subsegmental pulmonary emboli with a small right pleural effusion. Normal 0 false false false EN-US X-NONE X-NONE Normal 0 false false false EN-US X-NONE X-NONE The final diagnosis on his ED note: pulmonary embolism AND pericarditis.
Was there pulmonary edema? There is a junctional bradycardia. Then they were worried about sepsis as an etiology of hypotension. Then the notes mention "cardiogenic shock" but without any reference to a cardiac echo or to a chest x-ray. Not mentioned in physicians' notes. Troponin was repeated and returned higher still.
On his physical examination, cardiac and pulmonary auscultation was completely normal. His first electrocardiogram ( ECG) is given below: --Sinus bradycardia. Bi-phasic scan showed no dissection or pulmonary embolism. Peripheral pulses were all palpable. As he seemed very agitated, fentanyl and diazepam were given.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes.
There is sinus bradycardia with one PVC. pulmonary embolism, sepsis, etc.), Also notice that the arterial line mean arterial pressure is 63 mmHg, but there is no waveform (and SpO2 says "no pulse"), as the flow is continuous on ECMO and the LV function at this point was extremely poor, unable to add a pulse pressure. myocarditis).
The estimated pulmonary artery systolic pressure is 37 mmHg + RA pressure. He was admitted and serial troponins were measured: Because of elevated troponins, a next day echo was done: The estimated left ventricular ejection fraction is 50%. Normal estimated left ventricular ejection fraction lower limits of normal.
PVCs N ot generally considered abnormal ECG findings: Isolated PAC, First Degree AV Block, Sinus bradycardia at a rate of 35-45, and Nonspecific ST-T abnormalities (even if different from a previous ECG). 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.
she had severe pulmonary edema. This is the etiology of the blood from her nose and mouth (frothy bloody pulmonary edema) This is what frothy bloody pulmonary edema looks like. Subarachnoid hemorrhage causes extreme central catecholamine output, resulting in stress cardiomyopathy, just like takotsubo. From this site.
For many us, frying or freezing the atrial or pulmonary venous tissue would come to our mind first , overlooking systemic factors. Left atrial adiposity is a distinct entity, but rarely diagnosed (.Circ Circ Arrhythm Electrophysiol. 2010 Jun;3(3):230-6. Impact on AF therapeutics We are in aggressive space age & AI era.
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