Understanding the EKG changes in methemoglobinemia.

Methemoglobin is a form of hemoglobin that has been oxidized, changing its heme iron configuration from the ferrous to the ferric state. Unlike normal hemoglobin, methemoglobin does not bind oxygen and as a result, cannot deliver oxygen to the tissues. At the presentation in the emergency department, an electrocardiogram (EKG) is usually performed as a reflex for patients admitted for shortness of breath to rule out acute coronary syndrome. Very limited data is available on EKG abnormalities in patients with methemoglobinemia. In this study, we retrospectively analyzed the pattern of EKG changes in patients with methemoglobinemia.

Bradycardia, Renal Failure, Atrioventricular Nodal Block, Shock, and Hyperkalemia (BRASH) Syndrome-Induced Atrial Fibrillation: A Case Report.

BRASH syndrome is a syndrome that comprises bradycardia, renal failure, atrioventricular nodal block, shock, and hyperkalemia. This syndrome is usually associated with a junctional rhythm. Early recognition of this clinical entity is crucial for appropriate management. In this case report, we describe a 70-year-old female who presented with BRASH syndrome-induced atrial fibrillation with a slow ventricular response.

Dynamic Changes of EKG by Severe Hyperkalemia: Transient Left Bundle Branch Block.

Hyperkalemia is one of the most common electrolyte abnormalities seen in clinical practice and the most common life-threatening electrolyte abnormality seen in the emergency department. It is most often due to impaired renal potassium excretion due to acute on chronic kidney disease or the use of drugs that inhibit the renin-angiotensin-aldosterone axis. The most common clinical presentation is muscle weakness and cardiac conduction abnormalities. In the Emergency Department, ECG can come in handy as the first diagnosis of hyperkalemia before labs are drawn and reported. Early recognition of electrocardiographic (ECG) changes can prompt early correction and reduce mortality. We hereby, present a case of transient left bundle branch block in the setting of hyperkalemia secondary to statin-induced rhabdomyolysis.

Beyond Syncopal Episodes: A Complicated Hyperkalemic Emergency Manifesting As Complete Heart Block and Seizure Versus Convulsive Syncope Cascade.

We present a case involving an 87-year-old woman who had a hyperkalemic emergency. This condition was further complicated by complete heart block (CHB) and seizure-like activity. This case emphasizes the challenge of differentiating between seizures and convulsive syncope. Achieving an accurate diagnosis is essential for determining the appropriate medical treatment. This case report highlights the various symptoms and complications associated with hyperkalemia, emphasizing the importance of conducting a thorough examination to explore other potential causes. Additionally, it emphasizes the usefulness of the head-upright tilt test (HUTT) as a method to differentiate convulsive syncope from seizures, particularly in cases involving vagal stimulation.

Profound Hyperkalemia and Anemia in a Dialysis Patient With a Gastrointestinal Bleed.

An 80-year-old male receiving dialysis three times per week presented to the emergency room with general malaise after missing four consecutive dialysis appointments. During his workup, he was noted to have a potassium of 9.1 mmol/L, hemoglobin of 4.1 g/dL, and an electrocardiogram showing a first-degree atrioventricular (AV) block, a right bundle branch block, peaked T waves, and a wide QRS complex. During emergent dialysis and resuscitation, the patient suffered respiratory failure and was intubated. The next morning, he underwent an esophagogastroduodenoscopy (EGD), which found a healing duodenal ulcer. He was extubated the same day and was discharged in stable condition a few days later. This case appears to report the highest observed potassium coupled with significant anemia in a patient not affected by cardiac arrest.

Resolution of Left Bundle Branch Block After Calcium Administration in the Prehospital Setting.

Hyperkalemia is a medical emergency with potentially severe consequences that can be avoided by early recognition and effective treatment. Electrocardiogram (ECG) changes can help elucidate hyperkalemia prior to obtaining lab results and assist in early decisions on treatment, especially in the prehospital setting. ECG changes commonly associated with hyperkalemia are peaked T-waves, PR prolongation, P-wave flattening, QRS widening, or a sine-wave pattern at severely elevated potassium levels. Bundle branch blocks (BBBs) are associated with hyperkalemia but are less common and less well known in this setting. We report a case of a prehospital ECG showing a left bundle branch block (LBBB) in a patient who had end-stage renal disease, and the prehospital treatment with calcium chloride lead to resolution of the LBBB. The patient was eventually found to have a serum potassium level of 6.1 mEq/L.

A Case of Digoxin Toxicity Due to Acute Renal Failure.

Since the publication of the Digitalis Investigation Group trial in 1997, digoxin use has declined significantly. Medications such as angiotensin-converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARBs) and beta-blockers that have been demonstrated to have a decrease in morbidity and mortality are prescribed in favor of digoxin. Despite the reduction in digoxin use and improved therapeutic monitoring, digoxin toxicity remains a significant cause of morbidity and mortality. When digoxin toxicity is suspected, patients should be managed with supportive care, including discontinuation of the medication, and consideration for administration of digoxin-specific antibody fragment. We present a case of digoxin toxicity precipitated by acute renal failure, with a discussion on the pathophysiology and diagnosis of digoxin toxicity, along with the indications for administration of digoxin-specific antibody fragments. While digoxin toxicity is prescribed less commonly, physicians need to maintain a high index of suspicion and be comfortable with administering digoxin-specific antibody fragment in these scenarios.

Transient Left Bundle Branch Block in the Setting of Hyperkalemia.

Hyperkalemia is a potentially life-threatening condition that can lead to sudden cardiac death. We report a case of transient left bundle branch block (LBBB) pattern on an electrocardiogram (EKG) secondary to hyperkalemia in a patient with a history of end-stage renal disease. A 48-year-old female presented to the emergency department (ED) with chief complaints of weakness and shortness of breath after a missed hemodialysis session. A 12-lead EKG in the ED showed the LBBB pattern with left axis deviation, prolonged PR interval, and peaked T-waves in the precordial leads. The initial serum potassium level was 8.5 mEq/L. EKG changes resolved after correcting the serum potassium level.

An Atypical Etiology of Acute Pericarditis: A Case Report.

Acute pericarditis is caused by inflammation of the pericardial sac and is characterized by sharp and pleuritic chest pain, which is accompanied by a pericardial friction rub and serial electrocardiogram (ECG) changes. Although there are many known etiologies of pericarditis, we present the first known case of a herbal supplement, the Tejocote root, causing acute pericarditis in a previously healthy 23-year-old female. Her ECG showed t-wave inversions that resolved with colchicine and non-steroidal anti-inflammatory drug therapy. Prior studies have demonstrated that it can cause adverse cardiovascular effects, but this is the first documented case of the Tejocote root causing acute pericarditis. This case report reinforces the importance of inquiring about supplements patients may be taking, especially when looking for the etiology of pericarditis.

Association of Non-alcoholic Fatty Liver Disease with Conduction Defects on Electrocardiogram.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a leading cause of liver disease in developed countries. The association of NAFLD with conduction defects is unknown. The aim of our study was to find whether an association exists between conduction defects and NAFLD. METHODS: This is a case-control retrospective study of 700 patients admitted to Orange Park Medical Center, Orange Park, Florida from 2009 to 2015. Patients with a history of alcohol use, congenital heart disease, infiltrative malignancy, and myocarditis were excluded from the study. NAFLD was diagnosed by detection of hepatic steatosis on abdominal ultrasound or computerized tomography (CT) scan. Electrocardiograms (EKGs) were performed on all 700 patients and were interpreted by a cardiologist. Univariate logistic regression was used to assess the association between NAFLD and the variables of demographics, clinical characteristics, medicine use, EKG changes, and conduction defects, while multivariate logistic regression with backward elimination method was performed to determine if NAFLD is one of the most important risk factors for conduction defects. RESULTS: The study population included 408 patients with NAFLD and 292 patients with No-NAFLD. A total of 155 conduction defects occurred in 140 patients; conduction defects included 25.7% (36) patients with first degree block, 2.1% (three) patients with Mobitz type 1 block, 41.4% (58) patients with right bundle branch block (RBBB), 17.9% (25) patients with left bundle branch block (LBBB), 11.4% (16) patients with bifascicular block, and 12.1% (17) patients with nonspecific intraventricular block. Multivariate logistic regression with backward elimination method identified six risk factors for conduction defects; these included NAFLD (odds ratio (OR) 2.38; 95% confidence interval (CI) 1.51-3.73, p<0.0001), hypertrophy (OR 2.52; 95% CI 1.57-4.05, p=0.0001), congestive heart failure (CHF) (OR 3.05; 95%CI 1.46-6.38, p=0.0031), male sex (OR 1.79; 95%CI 1.19-2.69, p=0.0051), diabetes mellitus (OR 1.63; 95% CI 1.08-2.47, p=0.02), and age (OR 1.04; 95% CI 1.02-1.06, p<0.0001). CONCLUSION: NAFLD is associated with conduction defects. Prospective randomized trials are needed to demonstrate that NAFLD causes conduction defects.