Cases reported "Hyperkalemia"

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1/18. syncope caused by nonsteroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors.

    A 85-year-old woman with diabetes mellitus and prior myocardial infarction was transferred to the emergency room with loss of consciousness due to marked bradycardia caused by hyperkalemia. The T wave during right ventricular pacing was tall and tent-shaped while the concentration of serum potassium was high, and its amplitude during pacing was decreased after correction of the serum potassium level. Simultaneously with the correction, normal sinus rhythm was restored. The cause of hyperkalemia was considered to be several doses of loxoprofen, a nonsteroidal anti-inflammatory drug (NSAID), prescribed for her lumbago by an orthopedic specialist, in addition to the long-term intake of imidapril, an angiotensin-converting enzyme inhibitor (ACEI), prescribed for her hypertension by a cardiologist. This case warns physicians that the combination of NSAID and ACEI can produce serious side effects in aged patients who frequently suffer from hypertension, diabetes mellitus, ischemic heart disease, and degenerative joint disease.
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2/18. Electrocardiographic manifestations of hyperkalemia.

    hyperkalemia is one of the more common acute life-threatening metabolic emergencies seen in the emergency department. early diagnosis and empiric treatment of hyperkalemia is dependent in many cases on the emergency physician's ability to recognize the electrocardiographic manifestations of hyperkalemia. The electrocardiographic manifestations commonly include peaked T-waves, widening of the QRS-complex, and other abnormalities of altered cardiac conduction. Peaked T-waves in the precordial leads are among the most common and the most frequently recognized findings on the electrocardiogram. Other "classic" electrocardiographic findings in patients with hyperkalemia include prolongation of the PR interval, flattening or absence of the P-wave, widening of the QRS complex, and a "sine-wave" appearance at severely elevated levels. A thorough knowledge of these findings is imperative for rapid diagnosis and treatment of hyperkalemia.
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3/18. Evidence for specialized atrioventricular conduction in hyperkalemia.

    A patient who had chronic coarse atrial fibrillation developed severe hyperkalemia accompanied by total loss of fibrillatory waves while an irregularly irregular ventricular rhythm persisted. Correction of hyperkalemia resulted in prompt return of coarse atrial fibrillation. This sequence of events renders strong support to direct atrioventricular conduction through the specialized internodal tracts.
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4/18. Patterns of acute inferior wall myocardial infarction caused by hyperkalemia.

    This is one of the first published articles dealing with two patients with hyperkalemia showing, not only a pattern of acute anteroseptal myocardial infarction, but of inferior myocardial infarction as well. This was attributed to uneven effects of high potassium in different regions of the heart. Marked reduction of resting potential of a large group of cells from the most affected regions could produce areas of inexcitability, capable of generating abnormal q waves. Likewise, ST-segment elevation could be attributed to a hyperkalemic diastolic current of injury (due to depolarization of resting potential) and to a combination of diastolic and systolic current of injury (due to a reduction of action potential amplitude). In addition, current flowing down voltage gradients on either side (epicardial and endocardial) of the M cell region could be responsible for the T wave, and even, to some extent, to the ST-segment changes. However, it cannot be excluded that the previously described changes may have resulted from coronary spasm without chest pain. In fact, an intriguing possibility, namely that hyperkalemia could trigger coronary spasm has to be considered also.
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5/18. hyperkalemia diagnosed by implantable cardioverter defibrillator T wave sensing.

    A patient with congestive heart failure and an ICD had undergone atrioventricular nodal ablation and optimization of heart failure medical therapy. Intracardiac T wave sensing by the ICD drew attention to the new development of asymptomatic hyperkalemia. Surface ECG features of hyperkalemia were not readily identified due to pacemaker dependence.
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6/18. The prominant T wave: electrocardiographic differential diagnosis.

    The prominent T wave is an abnormal T-wave morphology encountered in the earliest phase of ST-segment elevation acute myocardial infarction (AMI). Prominent T waves, however, are associated with other diagnoses, including hyperkalemia, early repolarization, and left ventricular hypertrophy (LVH). This article focuses on the electrocardiographic differential diagnosis of the prominent T wave with the presentation of 4 illustrative cases. We also recommend that the designation hyperacute should refer exclusively to the prominent T waves of ST-segment elevation AMI.
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7/18. Electrocardiographic manifestations of hypothermia.

    hypothermia is generally defined as a core body temperature less than 35 degrees C (95 degrees F). hypothermia is one of the most common environmental emergencies encountered by emergency physicians. Although the diagnosis will usually be evident after an initial check of vital signs, the diagnosis can sometimes be missed because of overreliance on normal or near-normal oral or tympanic thermometer readings. The classic and well-known electrocardiographic (ECG) manifestations of hypothermia include the presence of J (Osborn) waves, interval (PR, QRS, QT) prolongation, and atrial and ventricular dysrhythmias. There are also some less known (ECG) findings associated with hypothermia. For example, hypothermia can produce ECG signs that simulate those of acute myocardial ischemia or myocardial infarction. hypothermia can also blunt the expected ECG findings associated with hyperkalemia. A thorough knowledge of these findings is important for prompt diagnosis and treatment of hypothermia. Six cases are presented that show these important ECG manifestations of hypothermia.
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8/18. Transient Brugada-type electrocardiographic abnormalities in renal failure reversed by dialysis.

    The brugada syndrome (BRS) is a hereditary cardiac condition (characteristically with a gene mutation affecting sodium channel function) identified by an elevated terminal portion of the QRS complex (prominent J wave) followed by a descending ST-segment elevation ending in a negative T wave in the right precordial leads, and malignant tachyarrhythmias in patients without demonstrable structural heart disease. We report a patient with a previous history of epilepsy treated with psychotropic drugs (with a sodium channel blocking effect) and chronic renal failure on haemodialysis who developed hyperkalaemia (6.6 mmol/l) and ECG findings resembling BRS. This condition was manifested by the prominent J wave, the coved-type ST-segment elevation and the negative T wave in the right precordial leads. These ECG changes disappeared after haemodialysis when the potassium became normal. Subsequently, a flecainide test did not reproduce ST-segment elevation. We conclude that hyperkalaemia associated with cardiac membrane active drugs may cause ECG changes mimicking the brugada syndrome.
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9/18. "Serpentine heart". Direct observation of the human heart during profound hyperkalemia.

    We observed cardiac contractility in a patient who had inadvertently received a massive overdose of potassium chloride during open heart surgery. Slowly advancing waves of contraction were present while the surface electrocardiogram showed the sine wave configuration typical of severe hyperkalemia. This is the first report of such an observation and may serve to promote proper diagnosis and treatment of similar cases.
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10/18. hyperkalemia induced T wave oversensing leading to loss of biventricular pacing and inappropriate ICD shocks.

    Inappropriate ICD shocks remain a common problem. Double counting of single ventricular events can occur with biventricular ICDs implanted before univentricular sensing was available. Often this is due to a tachyarrhythmia or loss of left ventricular capture. This report describes a patient who developed hyperkalemia during hemodialysis, received inappropriate ICD shocks and experienced loss of biventricular pacing due to T wave rather than QRS double counting. Oversensing was abolished by reducing the potassium content of the dialysis bath. This underscores the need for careful interpretation of saved electrograms to determine the cause for, and appropriate treatment of, device related problems.
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