Peerbhai et al International Journal of Emergency Medicine (2017) 10: 3 DOI 10.1186 / s12245-017-0132-0 International Journal of Emergency Medicine BÁO CÁO TÌNH HUỐNG Truy cập mở Hyperkalemia được che giấu bởi mô hình nhồi máu giả cuống và ngừng tim Shareez Peerbhai1, Luke Masha2, Adrian DaSilva-DeAbreu1 và Abhijeet Dhoble1,2 * Cơ sở tóm tắt: Tăng kali máu là một bất thường điện giải phổ biến và có các biểu hiện điện tâm đồ sớm được nhận biết rõ ràng bao gồm kéo dài PR và đạt đỉnh sóng T đối xứng Với tăng kali huyết thanh nghiêm trọng, rối loạn nhịp tim và Các khối nhánh nhĩ thất và bó nhánh có thể được nhìn thấy trên điện tâm đồ Mặc dù ngừng tim là một hậu quả đáng lo ngại của tăng kali máu không được điều trị, nhưng hiếm khi tăng kali máu trên điện tâm đồ biểu hiện như thiếu máu cục bộ cấp tính. Trình bày trường hợp: Chúng tôi trình bày một trường hợp suy thận cấp phức tạp bởi tăng kali máu ác tính và cuối cùng là ngừng tim. Việc ghi nhận rối loạn này bị chậm trễ thứ phát do mẫu điện tâm đồ ban đầu gợi ý nhồi máu cơ tim cấp tính đoạn ST chênh lên (STEMI) liên quan đến tăng kali máu cấp tính và thường được mô tả nhất ở bệnh nhân không có triệu chứng tim cấp tính Đây là trường hợp đầu tiên như vậy biểu hiện đồng thời với ngừng tim Một đánh giá ngắn gọn về mô hình nhồi máu giả hiếm gặp này cũng được đưa ra Từ khóa: Ngừng tim, Tăng kali máu, Nhồi máu cơ tim, STEMI , Cơ sở điện tâm đồ Tăng kali huyết biểu hiện bằng điện tâm đồ phát hiện nhồi máu cơ tim đoạn ST chênh lên (STEMI) là rất hiếm Một số ít các trường hợp mô tả hiện tượng này đã được mô tả [1-5] Mặc dù cơ chế chưa được hiểu rõ, người ta cho rằng kali cao Đôi khi, có thể rút ngắn điện thế hoạt động trong giai đoạn tái cực ba và do đó dẫn đến đoạn ST chênh lên Những biểu hiện như vậy có thể làm trì hoãn liệu pháp điều trị cần thiết, đặc biệt nếu cũng có biến chứng tim nặng của tăng kali máu. và ngừng tim do điện tâm đồ che dấu mắc STEMI cấp tính phía trước * Thư từ: Shareez.Peerbhai@uth.tmc.edu Khoa Nội, Trường Y McGovern, Trung tâm Khoa học Y tế Đại học Texas tại Houston, 6431 Fannin, MSB 1.150, Houston 77030, TX, Hoa Kỳ Bộ Nội khoa, Khoa Tim mạch, Trung tâm Khoa học Y tế Đại học Texas tại Houston, Houston, Hoa Kỳ Trình bày trường hợp Một nam giới da trắng 27 tuổi có tiền sử bệnh tăng huyết áp đã được đưa đến phòng cấp cứu (ER) để đánh giá tim. bắt giữ Anh ta có tiền sử một tháng mệt mỏi tiến triển không giải thích được và giảm uống. Điện tâm đồ tại hiện trường phát hiện bệnh nhân bị rung thất cấp tính. Anh ta được khử rung tim khẩn cấp dẫn đến hô hấp nhân tạo không tâm thu ngay lập tức được thực hiện và tự phát trở lại. tuần hoàn não (ROSC) đã đạt được Dải nhịp tại thời điểm này cho thấy các đoạn ST chênh lên đáng kể ở V1 – V2, AVL, và AVR; Sóng Q ở V1 – V2; cũng như suy giảm ST lan tỏa ở II, III, AVF, và V3 – V6 (Hình 1) Những phát hiện này được chuyển tiếp đến ER phối hợp, và một phác đồ STEMI để cho phép thông tim khẩn cấp được bắt đầu trên đường đến bệnh viện, bệnh nhân Một lần nữa phát triển nhịp tim cấp tính CPR đã được bắt đầu và đang được xử lý khi đến phòng khám ER. Khi khám, bệnh nhân xanh xao, lạnh, suy nhược cơ thể rõ rệt và suy giảm thể tích nghiêm trọng Trung tâm © The Author 2017 Open Access Bài viết này được phân phối theo các điều khoản của Giấy phép Quốc tế Creative Commons Attribution 4.0 (http://creativecommons.org/licenses/by/4.0/), cho phép sử dụng, phân phối và sao chép không hạn chế trong bất kỳ phương tiện nào, miễn là bạn ghi công phù hợp cho (các) tác giả gốc và nguồn, cung cấp một liên kết đến giấy phép Creative Commons và cho biết nếu các thay đổi đã được thực hiện Peerbhai và cộng sự Tạp chí Y học Cấp cứu Quốc tế (2017) 10: 3 Trang của Hình Điện tâm đồ trước khi nhập viện cho thấy khả năng tiếp cận tĩnh mạch MI trước vách ngăn Q sóng Q không phải đạt được, và cho phép tiếp cận tĩnh mạch ngoại vi để truyền thuốc và dịch hồi sức nhưng không được rút máu để xét nghiệm do suy tĩnh mạch rõ rệt Hỗ trợ tim mạch nâng cao (ACLS) đã được tiếp tục trong khoảng 40 Trong thời gian này, người ta lưu ý rằng không tâm thu liên tục được chuyển đổi một cách tự nhiên thành nhịp nhanh / rung thất, và khử rung liên tục sẽ dẫn đến không tâm thu Bệnh nhân được dùng epinephrine, vasopressin, bicarbonate và nước muối bình thường trong giai đoạn này ROSC đã đạt được, và tất cả vasopressin, dopamine, và n
Trang 1C A S E R E P O R T Open Access
Hyperkalemia masked by pseudo-stemi
infarct pattern and cardiac arrest
Shareez Peerbhai1 , Luke Masha2, Adrian DaSilva-DeAbreu1and Abhijeet Dhoble1,2*
Abstract
Background: Hyperkalemia is a common electrolyte abnormality and has well-recognized early electrocardiographic manifestations including PR prolongation and symmetric T wave peaking With severe increase in serum potassium, dysrhythmias and atrioventricular and bundle branch blocks can be seen on electrocardiogram Although cardiac arrest
is a worrisome consequence of untreated hyperkalemia, rarely does hyperkalemia electrocardiographically manifest as acute ischemia
Case presentation: We present a case of acute renal failure complicated by malignant hyperkalemia and eventual ventricular fibrillation cardiac arrest Recognition of this disorder was delayed secondary to an initial ECG pattern
suggesting an acute ST segment elevation myocardial infarction (STEMI) Emergent coronary angiography performed showed no evidence of coronary artery disease
Conclusions: Pseudo-STEMI patterns are rarely seen in association with acute hyperkalemia and are most commonly described with patient without acute cardiac symptomatology This is the first such case presenting concurrently with cardiac arrest A brief review of this rare pseudo-infarct pattern is also given
Keywords: Cardiac arrest, Hyperkalemia, Myocardial infarction, STEMI, ECG
Background
Hyperkalemia that manifests with electrocardiographic
findings of an ST segment elevation myocardial
infarc-tion (STEMI) is very rare A handful of cases describing
this phenomenon have been described [1–5] Although
the mechanism is poorly understood, it is proposed that
high potassium may, at times, shorten the action potential
in phase three repolarization and thus lead to ST segment
elevation Such presentations may delay necessary therapy
particularly if dramatic cardiac complications of
hyperka-lemia are also present We raise awareness of such
occur-rences by presenting a case of symptomatic acute
hyperkalemia and cardiac arrest masked by an ECG
sug-gesting an acute anterior STEMI
Case presentation
A 27-year-old Caucasian male with a past medical his-tory of hypertension presented to the emergency room (ER) for evaluation of a cardiac arrest He had a one-month history of unexplained progressive fatigue and de-creased oral intake He experienced a witnessed collapse
at home from a seated position, and emergency medical services (EMS) were called No bystander cardiopulmo-nary resuscitation (CPR) was given prior to EMS arrival, and ECG in the field found the patient to be in acute ven-tricular fibrillation He was defibrillated emergently which resulted in immediate asystole CPR was performed, and return of spontaneous circulation (ROSC) was achieved The rhythm strip at this time revealed significant ST seg-ment elevations in V1–V2, AVL, and AVR; Q waves in V1–V2; as well as diffuse ST depressions in II, III, AVF, and V3–V6 (Fig 1) These findings were relayed to the co-ordinating ER, and a STEMI protocol to allow for urgent cardiac catherization was initiated
On route to the hospital, the patient again developed acute asystole CPR was initiated and was in process at arrival to the ER On exam, the patient was pale, cold, markedly cachectic, and severely volume depleted Central
* Correspondence: Shareez.Peerbhai@uth.tmc.edu
1 Department of Internal Medicine, McGovern Medical School, The University
of Texas Health Science Center at Houston, 6431 Fannin, MSB 1.150, Houston
77030, TX, USA
2 Department of Internal Medicine, Section of Cardiology, The University of
Texas Health Science Center at Houston, Houston, USA
© The Author(s) 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
Trang 2venous access could not be achieved, and peripheral
ven-ous access allowed for the infusion of medications and
re-suscitation fluids but not for withdrawal of blood for
laboratory testing due to marked venous collapse
Advanced cardiovascular life support (ACLS) was
con-tinued for approximately 40 min During this time, it was
noted that asystole consistently converted spontaneously
to ventricular tachycardia/fibrillation, and defibrillation
would consistently result in asystole The patient received
epinephrine, vasopressin, bicarbonate, and normal saline
during this period ROSC was achieved, and all
vasopres-sin, dopamine, and norepinephrine were required to
maintain a perfusing blood pressure At this time, an
initial in-hospital ECG was acquired (Fig 2)
Given the findings and presentation, the patient was
then taken emergently to the cardiac catheterization lab
for coronary angiography Blood samples for laboratory
testing were then drawn from femoral access catheters,
and coronary angiography was performed The coronary
arteries were found to be fully patent Echocardiography
revealed normal cardiac systolic function without wall
motion abnormalities or pericardial effusion
A right femoral angiogram revealed an extremely small
right common femoral artery, which was nearly
com-pletely occluded by the utilized 6-french catheter Distal
pulses were absent, and the patient’s foot was cold to
touch The catheter was removed promptly, and the
patient was transferred to the coronary care unit (CCU) for initiation of therapeutic hypothermia and further care Upon arrival to the CCU, laboratory testing began to re-veal several marked laboratory abnormalities (Table 1) in-cluding profound hyperkalemia with a serum potassium of 9.8 mEq/L and disseminated intravascular coagulation (INR of >5, D-dimer >20μg/mL, and fibrinogen <60 mg/ dL) Emergent hemodialysis to correct his metabolic abnor-malities was performed, and fresh frozen plasma was ad-ministered to correct his coagulopathy After hemodialysis, his ECG normalized (Fig 3)
The remainder of his hospitalization was complicated
by aspiration pneumonia, shock liver, acute kidney in-jury, and mild anoxic brain injury all due to prolonged resuscitation However, he slowly recovered with sup-portive care The etiology of his severe volume depletion and profound renal failure was never identified He was transferred from the hospital to a rehabilitation facility with a need for intermittent scheduled hemodialysis and eventually discharged home
Conclusions Hyperkalemia is a common electrolyte abnormality with protean manifestations It may present as almost any dys-rhythmia including sinus bradycardia, atrioventricular blockade of various degrees, intermittent bundle branch blocks, ventricular tachycardia, and ventricular fibrillation
Fig 1 Pre-hospital ECG showing antero-septal Q wave MI
Fig 2 Post ROSC ECG showing marked peaked T waves
Trang 3[6] PR prolongation and symmetric T wave peaking are well-recognized early manifestations of mild to moderate hyperkalemia QRS widening is a harbinger of impending cardiac arrest
It is poorly recognized however that acute hyperkale-mia on ECG may resemble an acute STEMI as descrip-tions of this in the literature are rare The mechanism is unclear but may be related to shortening of phase three repolarization where potassium efflux is the predomin-ant ionic shift A potassium current channel (Ikr) located
on myocyte cell membranes is responsible for most po-tassium efflux during phase two and phase three of the cardiac action potential and increases potassium efflux when extracellular potassium is elevated [7] This leads
to the shortening of phases two and three of the action potential in the setting of hyperkalemia and therefore shortening of repolarization Similar ST segment eleva-tions may be seen in other condieleva-tions of shortened phases two and three repolarization including genetic benign early repolarization and acute hypercalcemia [8] Approximately 28 case descriptions of acute hyperka-lemia mimicking acute STEMI have been described in the literature at this time One review [9] notes that 80%
of case descriptions involve an antero-septal pseudo-infarct pattern with Q waves present in V1–V2 and ST segment elevation in AVR The mean serum potassium
in this series was 8.1 meq/L [9] Patterns of isolated in-ferior and antero-lateral infarcts have also been reported
As a rule, with therapy for acute hyperkalemia, these in-jury patterns resolve There is a strong association with concomitant diabetic ketoacidosis and renal failure with these presentations, and overwhelmingly, these patients have no serious active cardiac symptomatology In our review, we found no prior descriptions of hyperkalemic pseudo-STEMI patterns occurring concurrently with an acute cardiac arrest
Based on his age and the absence of significant risk factors, our patient’s presentation was unlikely to be
Table 1 Laboratory studies upon admission
White blood cell count 27.1 K/mm3
Alanine transaminase (ALT) 85 U/L
Aspartate aminotransferase (AST) 63 U/L
Fig 3 ECG after 24 h of admission
Trang 4secondary to an acute STEMI However, due to the
grav-ity of his presentation, this possibilgrav-ity could not have
been ignored Performing a cardiac catheterization for
this patient was not truly harmless as it resulted in a
minor vascular complication, delays for initiation of
appropriate therapy, and unnecessary ionic contrast
ex-posure to a patient in significant acute renal failure In
hindsight, there were several subtle clinical cues present
suggesting acute hyperkalemia as the etiology of his
arrest prior to the retrieval of laboratory results With
initial ROSC in the field, the typical antero-septal
pseudo-infarct pattern associated with hyperkalemia was
seen [9] Post resuscitation in the ER, a second ECG
showed diffuse T wave peaking and an incomplete right
bundle branch block These findings were also attributed
as representative of an acute myocardial infarction as
they were similar in nature to the hyper-acute T waves
sometimes seen preceding STEMIs [10] However, with
resolution of ST segment elevation associated with an
acute MI, the T wave in general normalizes or inverts
[11]; acute peaking would only be representative of
an-other factor such as hyperkalemia or acute pericarditis
Finally, the refractory ventricular tachycardia/ventricular
fibrillation is highly suggestive of an electrolyte disturbance
especially when defibrillation of these ventricular rhythms
or initiation of an anti-arrythmic drug is repeatedly
followed by asystole These phenomena are well described
clinically [12–14] and in vitro [15] Steady escalation in
serum potassium levels reliably leads to profound
suppres-sion of myocardial conduction, with atrial tissue and AV
nodal tissue being particularly sensitive to hyperkalemia’s
inhibition of phase one depolarization Defibrillation of a
ventricular rhythm in the setting of untreated severe
hyper-kalemia often exposes asystole secondary to atrial arrest
(or exposes other severe bradyarrhythmias) and is a useful
clue to determine the underlying etiology
In summary, we describe the presentation of a young
Caucasian gentleman who experienced a cardiac arrest
sec-ondary to acute ventricular fibrillation due to malignant
hyperkalemia On presentation, he had
electrocardio-graphic evidence of an acute STEMI, which clouded
recog-nition of hyperkalemia and delayed necessary treatment
This hyperkalemic pseudo-infarct pattern is rare overall
Furthermore, this is the first reported case of this ECG
oc-curring in the setting of an acute cardiac arrest Awareness
of this unusual ECG presentation of a relatively common
electrolyte abnormality may help expedite recognition and
treatment of a potentially life-threatening disorder
Authors ’ contribution
SP, LM, ADS-D, and AD conceived of the study SP, LM, and ADS-D drafted
the article LM, ADS-D, and AD carried out the critical revision of the article.
All authors read and approved the final manuscript.
Competing interests
Consent for publication Informed consent was obtained from the patient for the publication of this report and any accompanying images.
Received: 21 September 2016 Accepted: 18 January 2017
References
1 Ziakas A, Basagiannis C, Stiliadis I Pseudoinfarction pattern in a patient with hyperkalemia, diabetic ketoacidosis and normal coronary vessels: a case report J Med Case Rep 2010;4:115.
2 Simon BC Pseudomyocardial infarction and hyperkalemia: a case report and subject review J Emerg Med 1988;6:511 –5.
3 Lim YH, Anantharaman V Pseudo myocardial infarct —electrocardiographic pattern in a patient with diabetic ketoacidosis Singapore Med J 1998;39:504 –6.
4 Chawla KK, Cruz J, Kramer NE, Towne WD Electrocardiographic changes simulating acute myocardial infarction caused by hyperkalemia: report of a patient with normal coronary arteriograms Am Heart J 1978;95(5):637 –40.
5 Gelzayd EA, Holzman D Electrocardiographic changes of hyperkalemia simulating acute myocardial infarction Report of a case Dis Chest 1967; 51(2):211 –2.
6 Alfonzo AV, Isles C, Geddes C, Deighan C Potassium disorders —clinical spectrum and emergency management Resuscitation 2006;70(1):10 –25.
7 Roden DM, Lazzara R, Rosen M, Schwartz PJ, Towbin J, Vincent GM Multiple mechanisms in the long-QT syndrome Current knowledge, gaps, and future directions The SADS Foundation Task Force on LQTS Circulation 1996;94:
1996 –2012.
8 Littmann L, Taylor L, Brearly WD ST-segment elevation: a common finding
in severe hypercalcemia J Electrocardiol 2006;40:60 –2.
9 Bellazzini MA, Meyer T Pseudo-myocardial infarction in diabetic ketoacidosis with hyperkalemia J Emerg Med 2010;39(4):e139 –41.
10 Sovari AA, Assadi R, Lakshminarayanan B, Kocheril AG Hyperacute T wave, the early sign of myocardial infarction Am J Emerg Med 2007;25(7):859.e1 –7.
11 Tamura A, Nagase K, Mikuriya Y, Nasu M Significance of spontaneous normalization of negative T waves in infarct-related leads during healing of anterior wall acute myocardial infarction Am J Cardiol 1999;84(11):1341 –4 A7.
12 Quick G, Bastani B Prolonged asystolic hyperkalemic cardiac arrest with no neurologic sequelae Ann Emerg Med 1994;24(2):305 –11.
13 Lehmann F, Shively B, Tzamaloukas A Asystole associated with lidocaine use in a hyperkalemic patient during advanced cardiac life support J Intensive Care Med January 1993;8:47 –50.
14 Turner P Repetitive atrial standstill with idioventricular rhythm from hyperkalaemia: case report Br Heart J 1962;24:389 –92.
15 Hariman RJ, Chen CM Effects of hyperkalaemia on sinus nodal function in dogs: sino-ventricular conduction Cardiovasc Res 1983;17(9):509 –17.
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