中财网女主叫祸水 父亲叫霍泽:高钾血症深度学习(二)
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不同血钾水平时心电图的表现
高血钾致高大T波
高钾血症诊断程序，麻烦哪位战友合并在一起
高钾血症原因判断
高钾血症合并低血钙的表现
高钾血症致ST抬高而溶栓A 29-year-old diabetic man, while fishing in the West Indian summer sun, suddenly felt weak and nauseated, and started to vomit. He was helicoptered to an emergency department where he was diagnosed and treated with a thrombolytic agent. What diagnosis would you make based upon his ECG?
一名29岁的糖尿病人，夏日阳光下在西印度捕鱼，突然感到恶心软弱，并开始呕吐。他被用直升机送到急诊室，他被诊断并被进行溶栓治疗。依据他的心电图你会作出什么诊断后？
It is not widely appreciated that hyperkalemia can produce marked ST elevation and can do so selectively, with ST depression elsewhere, so that it looks like a localized infarct. This 29-year-old had no chest pain and should not have received thrombolytic therapy. When the serum potassium level was found to be 8.9 milliequivalents/L, therapy was promptly changed, and his ECG normalized over the next few hours. Two days later angiography revealed normal coronaries. His T waves are typically "tented" in several leads, which strongly suggest potassium intoxication.
一般不认为高血钾能够产生显着ST段抬高，而又选择性地在其他地方出现ST段压低，因此它看起来像一个部位的梗塞。这个29岁的患者无胸痛，不应该得到溶栓治疗。当发现血钾水平为8.9 milliequivalents / L时，及时改变了治疗措施，数小时后和他的心电图正常变为正常。两天后，冠状动脉造影显示正常。在几个导联，其T波是典型的“帐篷”样，，强烈提示钾中毒。
高血钾致假性心梗及其鉴别诊断心电图
1. LVH
2. LBBB
3. 心包炎. Only tracing with ST elevation also in lead II and significant PR-segment depression
4. 高血钾致假性心肌梗塞. Note tall, pointed, narrow T wave in V3
5. Acute AMI. Note smooth ST segment with no second “rabbit ear” sticking out
6. Acute AMI and RBBB. Note the second “rabbit ear” (R’) sticking out. Note also distinct transition between the downstroke of R’ and the beginning of the ST segment
7. Brugada syndrome. The elevated ST segment begins from the top of the R’ and is downsloping, ending with a negative T wave. Unlike in tracing 6, there is no distinct transition between the downstroke of R’ and the beginning of the ST segment
高钾血症导致的假性心肌梗塞及其分析Which of the following conditions is responsible for the ST elevation in leads V1-2? Choose from the list below.
A. Acute anteroseptal infarct
B. Pseudoinfarction pattern from hyperkalemia
Pseudoinfarction pattern from hyperkalemia
V1 - 2ST段抬高的原因是什么？？请从下表种选择。
A：急性前间隔心肌梗死
B：高钾血症导致的假性心肌梗塞
答案：高钾血症导致的假性心肌梗塞
Discussion
Sinus tachycardia at a rate of 130 beats per minute is present. The ST segment is elevated in V1 and V2, raising the possibility of acute anteroseptal myocardial infarction. However, the T wave is very tall, narrow, pointed, and tented; and the QRS is wide, measuring 140 msec.
These findings are characteristic of hyperkalemia. It is well known that hyperkalemia can cause ST-segment elevation (pseudoinfarction pattern or "dialyzable current of injury").
This tracing is from a patient with a serum potassium level of 7.5 mEq/L during diabetic ketoacidosis, who also is in renal failure and taking an angiotensin-converting enzyme inhibitor.
讨论
存在心率每分钟130次的窦性心动过速。V1和V2的ST段升高，，提高了前间隔急性心肌梗死的可能性。然而，T波非常高，窄，尖，和帐篷样； QRS波增宽，测量140毫秒。
这些发现是高血钾的特点。众所周知，高血钾可导致ST段抬高（假梗塞模式或“可透析的损伤电流” dialyzable current of injury究竟如何翻译？）。
这是一个有血钾7.5毫克当量/ L糖尿病酮症酸中毒病人的心电图，他有肾功能衰竭，并正在服用血管紧张素转换酶抑制剂
高血钾致Brugada型心电图
Answer: Hyperkalemia causing the Brugada electrocardiographic (ECG) pattern.
答：高血钾导致的Brugada样心电图（心电图）改变。
Discussion
In leads V1-2, the ST segment is elevated, which begins from the top of the R' wave and is downsloping, ending with an inverted T wave. These findings are characteristic of the Brugada ECG pattern. In the tracing, QRS complexes are widened, and T waves are tall, pointed, and tented. The P waves are flat and the PR interval is prolonged. All of these are characteristics of hyperkalemia. By inactivating the sodium channel, hyperkalemia can cause ST-segment elevation in V1-2, which is also a feature of Brugada syndrome.
In acute anterior infarct with right bundle branch block, the downstroke of the R' wave and the beginning of the ST segment have a distinct transition, and the ST segment is horizontal or upsloping, not downsloping, as it is in this case. There is a P wave in front of every QRS complex indicating the rhythm is sinus rhythm, not accelerated
讨论
在V1 – 2导联，ST段升高，它从R'波开始然后下斜，以T波倒置结束。这些发现是Brugada样心电图改变的特点。图中，QRS波群的增宽，T波高大，锐利，和帐篷样。P波是平坦，PR间期延长。所有这些都是高血钾症的特点。通过失活钠离子通道，高钾血症可以导致V1- 2的ST段抬高，这也是Brugada综合征特点。
在伴急性右束支传导阻滞的前壁心梗， R'波的降枝和ST段的开始有一个明显的过渡，和ST段是水平或上斜，不是下斜，如同本图所示的那样。每个QRS前面有一个P波提示节律为窦性心律，而不是加速性心律。
高血钾正酷似房颤
http://www.medscape.com/viewarticle/458815
Which electrolyte problem does this tracing strongly suggest?
A.
View the correct answer.
Discussion
Hyperkalemia is correct!
A slow, irregular wide QRS rhythm is present and is most likely atrial fibrillation rather than an agonal rhythm. The QRSs are wide, which merge into T waves. The T wave is tall in V4.
These findings are highly suggestive of hyperkalemia, which is treatable. The serum K+ was 7.3 mEq/L from renal failure. Hyperkalemia causes more bradyarrhythmias than tachyarrhythmias. The second and third QRSs in V1 show ST elevation, which is the pseudo-infarction pattern of hyperkalemia.
高血钾致起搏QRS宽
Indian Pacing Electrophysiol. J. 2008;8(3):211-217
Case Report
Influence of Intrinsic Myocardial Conduction on Paced QRS Morphology During Cardiac Resynchronization Therapy Follow up
Download PDF 836 KB
Rajendra Deshmukh, MD, K Latchumanadhas, MD, DM, Ajit S Mullasari, MD, DM, Ulhas M Pandurangi, MD, DM.
Institute of Cardiovascular Diseases, Madras Medical Mission, 4A, Dr. J.J.Nagar, Mogappair, Chennai - 600 037. India.
Address for correspondence: Dr. Ulhas M.Pandurangi, Department of Cardiology, Institute of Cardiovascular Diseases, Madras Medical Mission, 4A, Dr. J.J.Nagar, Mogappair, Chennai - 600 037. E-mail: icvddoctors/at/mmm.org.in
Abstract
We report two cases of patients of cardiac resynchronization therapy (CRT) whose ECGs, during follow up, showed different paced QRS morphology as compared to those of immediate post-device implantation. Parameters of leads, including sensitivity and capture thresholds, were unchanged. There was no lead dislodgement confirmed on fluoroscopy. The ECGs obtained in device off mode showed different intrinsic QRS morphology as compared to those of pre-implant morphology. These changes were attributable to electrolyte imbalance in one patient and progressive intraventricular conduction defect in the other. These cases demonstrate that intrinsic myocardial conduction pattern influences paced QRS morphology. Irreversible change in paced QRS morphology may indicate poor prognosis.
Key Words: Cardiac resynchronization therapy; wide QRS; hyperkalemia; myocardial disease
Introduction
Change in the paced QRS morphology in patients with CRT devices can be due to loss of capture, dislodgement of ventricular pacing leads, change in the pacing timing of ventricular leads (V-V delay) as well as electrolyte and acid base imbalance without significant change in threshold1,2. Influence of change in intrinsic myocardial conduction pattern on paced QRS morphology has not been studied well so far.
Here we present two case reports in which change in paced QRS morphology was attributable exclusively to change in the intrinsic myocardial conduction pattern without change in lead parameters or position. In one case the change in intramyocardial conduction pattern was due to electrolyte imbalance and in another it was due to progression of myocardial disease.
Case 1
A 66 years old diabetic male with ischaemic cardiomyopathy had undergone CRT for symptomatic congestive heart failure despite optimal medical management. His baseline ECG (Figure 1a) showed sinus rhythm, complete RBBB with QRS duration of 130ms. The post-implant ECG (Figure 1b) showed sinus rhythm and paced QRS duration of 100 ms with North West QRS axis. Left ventricle was set to be paced 40 ms earlier than RV, to achieve optimal synchronization based on echocardiographic parameters.
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