The 1St ASMIHA Digital Conference 23‐25 October 2020 Abstracts
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Indonesian Journal of Cardiology Indonesian J Cardiol 2020:41:suppl_A pISSN: 0126-3773 / eISSN: 2620-4762 doi: 10.30701/ijc.1075 The 1st ASMIHA Digital Conference 23‐25 October 2020 Abstracts: Case Reports Indonesian Journal of Cardiology Indonesian J Cardiol 2020:41:suppl_A pISSN: 0126-3773 / eISSN: 2620-4762 doi: 10.30701/ijc.1075 1. Challenging Case of Cardiac Arrest due to Pure Inferior STEMI with Bad Comorbidities: A Case Report I. Sabrina1, M. R. Felani2, I. A. Siregar3 1Faculty of Medicine, Trisakti University, Jakarta, Indonesia; 2Department of Cardiology and Vascular Medicine, University of Indonesia, Jakarta, Indonesia; 3Departement of Cardiology, Dr. Mintohardjo Naval Hospital, Jakarta, Indonesia Background: Cardiac arrest is the worst complication that can occur in ACS. Myocardial infarction causes conductivity disturbances of myocardial electric potential, thus often triggered malignant arrhythmias lead to cardiac arrest. However, malignant arrhythmias are not always present in all types of ACS, depends on the infarction areas, so that patient with pure STEMI inferior rarely presents with malignant arrhythmias caused by ACS itself. Case illustration:65‐Year‐Old patient presented into ER with worsening squeezing chest pain since 5 hours before admission. He had any similar complaint before and ever refused to get CAG previously. He had uncontrolled hypertension and Type‐2 DM. On physical examination, we obtained BP 125/70 mmHg, HR 72 bpm, RR 20 x/min, afebrile, and SpO2 98%, crackles (+), with normal in other general physical examination. 12‐lead ECG showed pure Inferior STEMI, no Posterior or RV involvement. Echocardiography showed LVEF 45% and diastolic dysfunction, RMWA (+), and moderate MR. He also had renal Insufficiency and mild hypokalemia. In ER, he suddenly got VF, so CPR and defibrillation were performed until he got ROSC then transferred to ICCU. Discussion: An acute anterior MI, acute RV Infarction, or a genetic predisposition can lead into cardiogenic shock or sudden cardiac arrest. In this case, the cardiac arrest maybe was triggered by pure Inferior STEMI (without anterior involvement) and other predisposition factors, such as uncontrolled diabetes, pneumonia, older age, metabolic impairment, and proven regional wall motion abnormality with LV dysfunction. Conclusion: Myocardial infarction can lead to any bad complications, which in this case showkdafied that acute pure Inferior STEMI with some bad uncontrolled comorbidites still can lead into sudden cardiac arrest. Keywords: Cardiac Arrest, Inferior STEMI Indonesian Journal of Cardiology Indonesian J Cardiol 2020:41:suppl_A pISSN: 0126-3773 / eISSN: 2620-4762 doi: 10.30701/ijc.1075 2. Are Furosemide and Nebulizer the Proper Treatment for Heart Failure and Community Acquired Pneumonia?: An Emergency Case‐Report Lourensia Brigita AP, M.D, RSUD Kraton, Pekalongan, Indonesia Background: Heart failure represents a major cause for increased mortality in community acquired pneumonia (CAP), contributing to more than 30% of deaths at long‐term follow‐up. CAP can exacerbate heart failure (85% cases), becomes a frequent triggering factor for decompensation of a chronic cardiac dysfunction. This case report exhibits everyday challenge found in patient with heart failure and CAP, as we know their incidence, timing, risk factors, and associations with mortality still remain unclear. Case Illustration: A 54 years old male with uncontrolled hypertension history brought to ER due to shortness of breath. On examination GCS 15 apathetic, BP 140/80, RR 28, HR 98, SpO2 85%, subfebrile. He had recurrent dyspnea on mild activities. Clinically, the patient showed diaphoresis, rhonchi found bilaterally (worse on the left) on auscultation. ECG showed sinus rhythm HR 88 LVH strain. Then thoracic imaging performed cardiomegaly with pneumonia representation and the blood test performed WCC: 10.20 103/uL, neutrophil 81.8 %. Furosemide and nebulizer was given to patient. Fourth days after the treatment he was found to have improvement of clinical condition. The patient was showed RR 20‐22, without adventitious lung sounds, and normal urine output. Discussion: This patient exhibits severe dyspnea that was caused by uncontrolled hypertension history, with CAP and history of active smoking. After given treatment showed recovery sign after day 4. We considered treating this patient intensively is needed based on timing and clinical consideration. Conclusion: We should considered careful monitoring dyspnea and urine output in all heart failure and CAP especially using furosemide combination with nebulizer, and proper treatment should be consider for good outcome. Keywords: Heart failure, CAP, uncontrolled hypertension history, furosemide Indonesian Journal of Cardiology Indonesian J Cardiol 2020:41:suppl_A pISSN: 0126-3773 / eISSN: 2620-4762 doi: 10.30701/ijc.1075 3. Reversible Cause of Marked Symptomatic Bradycardia Associated with Hyperkalemia: A Case Report E Govardi1, H.A.P Lubis2 1. General Practitioner at Royal Prima General Hospital, Medan Indonesia 2. Cardiologist Consultant at Royal Prima General Hospital, Medan, Indonesia Background: Hyperkalemia is a common and potential life‐threatening with different types of presentation in the emergency department setting. Renal insufficiency can cause toxic effect of hyperkalemia on electrocardiography (ECG) abnormalities. The spectrum of ECG changes seen with hyperkalemia is known to process gradually with the increasing levels of potassium. Case Illustration:A 58 year old man presented to emergency department with generalized weakness and nausea since 4 days ago. He had no documented shortness of breath, fever and no other recent complaints. He had history of diabetic for 3 years and was taking metformin and glibenklamid. Clinical examination in ED revealed slight decrease blood pressure of 90/60 mmHg, severe bradycardia (<35 beats/minute) with cold extermities. Laboratory investigations obtained before treatment revelaled hemoglobin 13.5 g/dl, urea 52 mg/dl, creatinine 2.51 mg/dl, natrium 134 mEq/L, potassium 6.65 mEq/L, normal cardiac marker Metabolic acidosis (pH 7.24 and base excess (BE) of ‐15.8) was noted through arterial blood gases analysis. ECG showed absent of P waves and junctional bradycardia. Echocardiography revealed concentric hypertrophy with ejection fraction 58 %. The patient received intravenous fluid, dopamine, 10 ml of intravenous 10 % calcium gluconate, 10 unit intravenous insulin with 10 % of dextrose, 142,2 mEq/L sodium bicarbonate. The patient was admitted and monitored. A repeat ECG showed sinus rhytm, his vital sign was stable with blood pressure of 110/80 mmHg, and potassium level of 3.6 mEq/L. Metabolic acidosis was improved with PH of 7.46 and BE 0.7. The patient was discharged 5 days after hospitalized. Conclusion: Any patient with acute onset of bradycardia who presents to emergency department should be suspected of life‐threatening hyperkalemia. Renal insufficiency can cause hyperkalemia secondary to metabolic acidosis. Moderate hyperkalemia can be presented as severe bradycardia and the conversion to sinus rhytm was achieved after correcting potassium level as demonstrated by the finding in our case. Keywords : hyperkalemia, severe bradycardia, renal insufficiency Indonesian Journal of Cardiology Indonesian J Cardiol 2020:41:suppl_A pISSN: 0126-3773 / eISSN: 2620-4762 doi: 10.30701/ijc.1075 4. Conn Syndrome: Identifying And Managing The Rare Combination Of Hypertension And Hypokalemia T.S.R.S Sembiring1, M. Fahimi2 1Department of Cardiology and Vascular Medicine, Faculty of Medicine Universitas Indonesia 2Department of Internal Medicine, Dr. Mintohardjo Navy Hospital Background: Conn syndrome contributes to 5 – 15% of all hypertension cases. It has favorable prognosis through surgery making it necessary to identify and manage this disease to prevent the upcoming morbidity and mortality. Case Illustration and Discussion: A 37‐year‐old male came to ER due to worsening muscle weakness since 3 days prior to hospital admission with no history of trauma, seizure, slurred speech, headache, projectile vomiting, or decreased consciousness. He had been hypertensive for 9 years. His mother died due to hypertension and hemorrhagic stroke when she was 45 years old. On physical examination, BP was 200/100 mmHg, motor strength was 2 with no sensory deficit, changing physiological or existing pathological reflex. ECG showed flattening T wave, U wave, and prolonged QU interval suggesting hypokalemia confirmed by laboratory examination (1.68 mmol/liter). We found uncompensated metabolic alkalosis, increased sodium (296 mmol/day) and normal potassium urine level (14 mmol/day). We started continuous infusion of potassium 10 mEq/hour through CVC, captopril 50 mg t.i.d, spironolactone 100 mg o.d. The combination of hypertension and hypokalemia suggests mineralocorticoid excess of which Conn syndrome is the most prevalent. Hypokalemia was suspected through physical and ECG findings confirmed by the electrolyte examination. Uncompensated metabolic alkalosis occured due to hydrogen ion loss through urine causing blood pH to alkalinize. Unenhanced abdominal CT scan confirmed our suspicion of Conn syndrome as we found increase left adrenal size. Continuous potassium infusion corrected serum potassium level but spironolactone and captopril were ineffective to control BP because the main treatment for Conn syndrome is adrenalectomy especially if the patients are younger than 40 years old. We therefore planned for referral