Showed Sinus Bradycardia Research Articles

Convulsion and cardiorespiratory collapse with first epidural test dose

To the Editor: Accidental intravascular injection of local anesthetic can cause central nervous system (CNS) toxicity, presenting as tremors, convulsions, dysrhythmias, and cardiorespiratory arrest. During epidural anesthesia, a test dose is used to diagnose inadvertent intravascular or intrathecal administration of drugs. We present a case where the test dose itself caused central neural toxicity. A 38-year-old woman, weighing 50 kg and 159 cm tall, with chondrosarcoma in the left femur, presented for tumor resection, irradiation, and reconstruction under a combined epidural and general anesthesia. She had no significant past or family medical history, with no associated comorbid illnesses or evidence of metastasis. She was positioned in the right lateral position for insertion of an epidural catheter under monitoring of heart rate (HR), blood pressure (BP), and oxygen saturation (SpO2). The baseline HR was 100 bpm, BP 124/75 mmHg, and room-air SpO2 98%. After inserting an epidural catheter in L2‐3 interspace and carefully confirming negative aspiration, a 3-ml test dose of 1.5% lidocaine with epinephrine 1:200,000 was injected slowly, with no change in HR. Approximately 1 min later, the patient had perioral paresthesia and twitching followed by loss of consciousness and generalized convulsions. She was immediately turned to the supine position and midazolam 2 mg was given intravenously, followed by thiopentone 250 mg to control the convulsions. After mask ventilation with 100% oxygen, the trachea was intubated and lungs were ventilated. The electrocardiograph (ECG) showed sinus bradycardia with HR 34 bpm during convulsion, (before institution of mask ventilation), which failed to respond to 0.6 mg atropine administered intravenously. A short period of hypoxia may have caused failure to respond to the atropine. As the radial pulse was not palpable, cardiopulmonary resuscitation was started, and 1 mg adrenaline was given intravenously. Radial pulse was noted immediately after resuscitation (ECG showing sinus rhythm), and the patient regained consciousness within 5 min. Aspiration of the epidural catheter revealed blood, and a diagnosis of probable intravascular injection was made. Subsequently, brain magnetic resonance imaging (MRI) was normal, and the patient underwent the planned operation the following week under combined epidural and general anaesthesia without any complication.

An unusual case of hypothermia associated with therapeutic doses of olanzapine: a case report

IntroductionWe report a case of a 42-year-old man who had symptomatic hypothermia as a result of taking olanzapine for paranoid schizophrenia. According to published data, only a few cases of hypothermia associated with olanzapine have been reported since its introduction into clinical use.Case presentationA 42-year-old Sri Lankan man with schizophrenia who was being treated with a therapeutic dose of olanzapine presented with reduced level of consciousness. He had a core temperature of 32°C and was bradycardic. At the time of admission, the electrocardiogram showed sinus bradycardia with J waves. He did not have any risk factors for developing hypothermia except the use of olanzapine. There was improvement in his clinical condition with reversal of electrocardiogram changes following gradual rewarming and the omission of olanzapine.ConclusionHypothermia induced by antipsychotic medications is not uncommon, but olanzapine-induced hypothermia is rare and occurrence has been reported during initiation or increasing the dose. But here the patient developed hypothermia without dose adjustment.

Ipotermia accidentale nell’anziano

An 88-year-old woman suffered a cerebrovascular accident and was found on the floor of her cold house. At the time of admission to our division, the patient was unresponsive with a rectal temperature of 28 °C, blood pressure of 120/80 mmHg, and a heart rate of 40 bpm. The cerebral CT revealed a hypodense lesion in the temporal region. The ECG showed sinus bradycardia, prolonged PR and QTc intervals, and a classic “J” (Osborn) wave that was most pronounced in the lateral and inferior leads. The patient presented a low respiratory rate, hypoventilation, severe acidosis (both respiratory and metabolic), hyperkalemia, elevated liver enzymes, mild anemia, hyporeflexia, and sluggish pupil responses. During rewarming with thermic blanket and heated intravenous fluids, the respiratory condition improved, and the ECG alterations disappeared. Twenty-four hours later, however, the patient died suddenly due to cardiac asystole. This report analyses the effects of hypothermia and its clinical manifestations and provides a brief discussion of the electrophysiologic mechanisms underlying Osborn waves and the other electrocardiographic changes associated with hypothermia.

Implantation of a CRT-D in a Patient with Dextrocardia and Situs Inversus Totalis, Who Has Persistent Left Ventricular Dysfunction with VT/VF

Introduction: Dextrocardia is rare, with an incidence of 0.4 per 10,000 live birth. One-third of the cases are associated with situs inversus, where the major visceral organs, including the heart, are mirror image of their normal positions. Case Presentation. The patient was a 62-year-old woman with known dextrocardia and situs inversus totalis, who was diagnosed as hypertrophic cardiomyopathy in the 1990s. May 10, 2010, she visited our hospital with dyspnea and wheeze. After a while, she was founded to be in ventricular fibrillation, and she was successfully converted to sinus rhythm by multiple external defibrillations. Her transthoracic echocardiography was significant for persistent left ventricular dysfunction with an estimated ejection fraction of 28% and 12-lead electrocardiogram showed sinus bradycardia with left bundle branch block, QRS duration of 160 msec and QTc interval of 0.6. A cardiac catheterization revealed no significant coronary artery disease, non-ischemic cardiomyopathy. We concluded that it was necessary for the patient to receive implantation of a bi-ventricular implantable cardioverter defibrillator (CRT-D), and successfully performed on June 7, 2010. We report a rare case of a CRT-D implantation in a patient with dextrocardia and situs inversus totalis.

A case of asthma-complicated influenza myocarditis

A 36-year-old man with a history of asthma visited an outpatient clinic complaining of high fever and general fatigue, and was diagnosed as having influenza type A by influenza antigen test. Laboratory findings revealed mild inflammation, mild acidemia, and hypercapnea with radiologic infiltrations in the right lung, and remarkable wheezes in both lungs were heard on auscultation. He was diagnosed with asthma exacerbation and having influenza pneumonia, and was referred to us. Therapy was begun with oseltamivir for influenza infection and intravenous infusions of betamethasone and aminophylline with non-invasive pulmonary ventilation for asthma exacerbation and acute respiratory failure. Although he was weaned from mechanical ventilation and his general condition became good, electrocardiogram showed sinus bradycardia and negative T waves in V1-4 without any symptoms. Blood test and echocardiography showed almost normal findings except for slight elevation of LDH and AST. Influenza A antigen was already confirmed and he was diagnosed as having influenza myocarditis clinically. Although it is well known that influenza can cause asthma exacerbation and encephalopathy, influenza myocarditis is regarded as rare by physicians. In fact, the number of case reports about influenza myocarditis is few. Myocarditis may not appear to be serious, but could cause fatal arrhythmia and heart failure. All clinicians should be aware of the overall clinical picture and the possibility of severe complications of myocarditis caused by flu infection.

A Case of Excessive Yawning With Citalopram

A Case of Excessive Yawning With Citalopram

Fracture and Embolization of an Inferior Vena Cava Filter Strut Leading to Cardiac Tamponade

A 56-year-old woman presented to the Emergency Department of Parkland Memorial Hospital complaining of chest pain. She had a remote history of a hemorrhagic cerebrovascular accident complicated by pulmonary embolism, for which a Gunther-Tulip inferior vena cava (IVC) filter had been placed 6 years previously. In the triage area, the patient collapsed and was found to be hypotensive. An ECG showed sinus bradycardia with nonspecific ST and T-wave changes …

Hypothermia: an under-estimated risk

Prof. Bruno: A 80-year-old woman was found unconscious in the street from a passer-by. It was a cold January morning, and the patient had slept outdoor. She was a homeless known in the Emergency Department (ED) as an alcohol abuser. When she was admitted to the ED, she presented with stupor and apathy. She spoke very slowly, and her speech patterns were vague and slurred. Physical examination revealed that the skin was very cold, even on the torso; and there was marked pallor. The rectal body temperature was 29 C. She had an abnormally slow rate of breathing (8 breaths/ min), and the non-invasive SO2 was 86% on room air, and 96% after the administration of Oxygen by mask (6 L min). Blood pressure was 85/50 mmHg, and the pulse was 40 beats/min, and very weak. The 12-lead ECG showed sinus bradycardia at about 40 beats/min, and there were prominent J waves (Osborn Wave). Hemogasanalytic values were normal. A Glasgow Coma Scale (GCS) score was 10. The patient underwent oro-tracheal intubation to provide airway protection. The finger-stick glucose was normal (108 mg %). The laboratory tests were within normal ranges except for a hyponatremia (120 mmol/L). We hypothesize the hyponatremia was due to volume depletion. Our working diagnosis was accidental hypothermia. We immediately removed her wet cold clothing, and we covered the patient with an electric blanket. She was given warm saline fluids intravenously. Because she was classified as severe hypothermia with a high risk for cardiac arrest, she underwent extra-corporeal treatment by emergency haemodialysis to actively rewarm her blood rapidly outside the body. In this way it was possible to restore normal body temperature rapidly. This invasive method of rewarming permitted us to restore a normal core temperature providing safe treatment. The patient left the hospital after several; days in good health. We advised her to avoid sleeping outside, to adequately cover her body including extremities and particularly the head.

Calcium-Alkali Syndrome Due to Vitamin D Administration and Magnesium Oxide Administration

Calcium-Alkali Syndrome Due to Vitamin D Administration and Magnesium Oxide Administration

Suspicious stress induced cardiomyopathy following hemorrhoidectomy under spinal anesthesia: A case report.

A 48-year-old healthy woman was admitted in our hospital for elective hemorrhoidectomy. She developed sudden headache and chest pain, and showed sinus bradycardia, arrhythmia and hypotension forty minutes after spinal anesthesia with 0.5% hyperbaric bupivacaine. An EKG showed ST depression and an transthoracic echocardiogram performed in PACU demonstrated mild LV dysfunction with hypokinesia of LV inferolateral wall. An coronary angiography on postoperative day 1 revealed normal coronary vessel and akinesia of LV inferior wall. Levels of CK-MB and Troponin I were mildly elevated. With medical therapy, the patient's symptoms improved and recovered without any complication.

Prognosis and Natural History of Drug-Related Bradycardia

Background and ObjectivesThe prognosis and natural history of bradycardia related to drugs such as beta-blockers and non-dihydropyridine calcium channel blockers are not well known.Subjects and MethodsWe retrospectively analyzed 38 consecutive patients (age 69±11, 21 women) with drug-related bradycardia (DRB) between March 2005 and September 2007. A drug-associated etiology for the bradycardia was established based on the medical history and patient response to drug discontinuation. The mean follow-up duration was 18±8 months.ResultsThe initial electrocardiogram (ECG) showed sinus bradycardia (heart rate ≤40/min) in 13 patients, sinus bradycardia with junctional escape beats in 18 patients, and third-degree atrioventricular (AV) block in seven patients. Drug discontinuation was followed by resolution of bradycardia in 60% of patients (n=23). Among them, five (17.8%) patients resumed taking the culprit medication after discharge and none developed bradycardia again. Bradycardia persisted in 10 (26.3%) patients despite drug withdrawal, and a permanent pacemaker was implanted in seven of them. Third-degree AV block, QRS width, and bradycardia requiring temporary transvenous pacing were significantly associated with the bradycardia caused by drugs.ConclusionBeta-blockers were the most common drugs associated with DRB. However, in one quarter of the cases the DRB was not associated with drugs; in these patients permanent pacemaker implantation should be considered.

Hypothermia with Osborn Waves in Parkinson's Disease

Autonomic dysfunction in patients with Parkinson's disease has been recognized since the original description by James Parkinson in 1817. In the present case, an 80-year-old woman who had been diagnosed with Parkinson's disease 3 years earlier (Hoehn and Yahr stage III) was admitted with a few days history of lethargy and bradykinesia. She lived in a heated house and used an electric blanket at night. On examination, her core temperature was 29.7 degrees C. Her initial ECG showed sinus bradycardia, QT prolongation, and Osborn waves, which disappeared after rewarming. Successful rewarming was achieved with an external rewarming blanket over 12 hours. Follow-up ECG showed resolution of the Osborn waves. In Parkinson's disease, rapidly progressive hypothermia can occur in a well-heated house. Determining a rewarming strategy is a complex but not insurmountable task. In the elderly, the use of careful active external rewarming and a low stress strategy may be recommended.

Temporary Cardiac Pacing for Fatal Arrhythmia in Living-Donor Liver Transplantation: Three Case Reports

Cardiac pacing often turns out to be the only effective treatment of severe, life-threatening arrhythmias. We performed 77 living-donor liver transplantations (LDLT) from 1999 to 2007. In these cases, three recipients experienced fatal arrhythmia and required temporary cardiac pacing during the perioperative period. The first case was a 68-year-old woman diagnosed with liver cirrhosis and hepatocellular carcinoma (HCC). Her Model for End-Stage Liver Disease (MELD) score was 34. We performed LDLT using a right lobe graft. She showed complete atrioventricular block with cardiac arrest at postoperative day (POD) 42 after a bacterial infection. We performed a resuscitation and instituted temporary cardiac pacing. However, she was dead at POD 43. Pathologic findings at autopsy showed a diffuse myocardial abscess, which caused the fatal arrhythmia. The second case was a 58-year-old man diagnosed with HCC and liver cirrhosis; his MELD score was 9. We performed LDLT using a right lobe graft. He showed atrial fibrillation after septic shock. He also showed sinus bradycardia with a cardiac arrest at POD 10. We performed resuscitation and emergent temporary pacing. He recovered and was alive without recurrence of arrhythmia or infection. The third case was a 58-year-old woman diagnosed with multiple HCC. During preoperative regular check-up, she was diagnosed to have cardiac hypertrophy and was started on beta-blockers as treatment for cardiac hypertrophy. However, severe bradycardia necessitated temporary cardiac pacing. LDLT was performed safely after implantation of a pacemaker. Early use of temporary cardiac pacing for severe arrhythmias may be effective to maintain the hemodynamic state in LDLT.

Premature Ventricular Contractions Causing Sinus Arrhythmia and Alternating P‐R Prolongation

A 68-year-old male patient was referred because of an irregular heart rhythm. The electrocardiogram (Fig. 1) showed sinus bradycardia with interpolated premature ventricular complexes (PVCs) occurring in a trigeminal pattern. There are two interesting observations in Figure 1. First, there is an alternating pattern of P-P intervals, with intervals of 1,320–1,340 ms whenever there is a PVC between two conducted sinus beats and longer P-P intervals of 1,420–1,470 ms when there is not. Secondly, there is also an alternating pattern of P-R intervals, with a P-R interval of 280 ms fol-

Sinus bradycardia during exercise: Unusual manifestation of ischemia in the territory of the left anterior descending artery

Autonomic disturbances in heart rate regulation during myocardial ischemia are well known. 1 Inferior wall ischemia is usually associated with bradyarrhythmia and anterior wall involvement with tachyarrhythmia. 2 Furthermore, severe sinus bradycardia has been described in inferior wall ischemia both in humans and in experimental animal models. We present a case of sinus node deceleration during exercise-induced anterior wall ischemia in a 79year-old white woman. The patient underwent exercise myocardial perfusion imaging. The baseline electrocardiogram showed T-wave changes ( Figure 1A ). She exercised for almost 6 minutes and stopped because of fatigue. Blood pressure increased from 124/65 to 142/80 mm Hg. Immediately after cessation of exercise, she became pale and light-headed and complained of angina. The electrocardiogram showed sinus bradycardia with ST elevation in leads V 2 and V3 and ST depression in 2, 3, and aVF ( Figure 1B ); the heart rate was 45 beats/min, and systolic blood pressure was 70 mm Hg. She remained bradycardiac for 5 minutes and gradually returned to a baseline heart rate of 68 beats/min. Single photon emission computed tomography images showed a large area of anteroseptal ischemia involving almost 30% of the left ventricle and an increased stress-rest left ventricular cavity ratio (transient ischFrom the Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Ala. Reprint requests: Rajesh Venkataraman, MD, MPH, Division of Cardiovascular Disease, University of Alabama at Birmingham, LHR 314, 1530 Third Ave S, Birmingham, AL 35294-0007; rajeshv@uab.edu. J Nucl Cardiol 2008;15:e24-e25. 1071-3581/$34.00 Copyright © 2008 by the American Society of Nuclear Cardiology. doi:10.1016/j.nuclcard.2008.02.030

Is this heart broken?

We present the case of a woman presenting with chest pain that illustrates the importance of recognizing an atypical presentation of coronary artery disease in women, as well as the role of myocardial perfusion imaging in the differential diagnosis. Case presentation. A 54-year-old black woman presented to the emergency department with atypical chest pain and left shoulder and arm pain of 8 hours’ duration. She was known to have fibromyalgia and an anxiety disorder, with a recent exacerbation related to domestic unrest. Her risk factors for coronary artery disease consisted of hypertension, hyperlipidemia, tobacco use, and a family history of myocardial infarction. The 12-lead electrocardiogram at presentation showed sinus bradycardia and T-wave inversion in the inferior and lateral leads. The cardiac troponin I level was elevated, at 0.5 g/L. Aspirin, -blocker, heparin, and intravenous nitrate therapy was initiated. Several hours later, the patient had worsening chest discomfort associated with diaphoresis, bradycardia, and nonsustained ventricular tachycardia. An electrocardiogram showed more pronounced and extensive T-wave inversion (Figure 1), and the second troponin I level was 9.8 g/L. Emergent cardiac catheterization was performed and revealed a left anterior descending coronary artery that tapered distally, with luminal irregularity ( 50% diameter stenosis) in its midportion. The left circumflex and right coronary arteries were normal (Figure 2). Contrast left ventriculography was remarkable for severe regional dysfunction localized to the left ventricular (LV) apex and the adjacent anterior and inferior walls, with hypercontractility of the basal portions of the ventricle (Figure 3). A clinical diagnosis of takotsubo cardiomyopathy, also referred to as transient LV apical ballooning or “broken heart” syndrome, was entertained. The cardiac troponin I level peaked at 32 g/L on serial testing. A resting technetium 99m sestamibi myocardial single photon emission computed tomography (SPECT) scan was performed the next day. It revealed a severe perfusion abnormality involving the apex and the adjacent anterior and inferior walls, with a complete absence of Tc-99m sestamibi uptake (Figure 4). A rest thallium 201/exercise Tc-99m sestamibi myocardial gated SPECT study was performed 2 months later and showed a large fixed defect associated with regional dysfunction, essentially unchanged from the initial scan (Figure 5). An echocardiogram obtained shortly thereafter showed persistent LV apical dyskinesis (Figure 6). Discussion. Several features of this patient’s initial presentation were typical of takotsubo cardiomyopathy. These include her gender, age, recent emotional distress, and severe regional LV dysfunction in the absence of epicardial coronary obstruction. Takotsubo cardiomyopathy, originally described in Japanese patients, is being increasingly recognized in the Western world, including the United States, and is characterized by acute, reversible LV apical dysfunction in the absence of obstructive epicardial coronary disease. The prevalence of this syndrome is reported to be 1% to 2% in patients presenting with clinical features suggestive of an acute coronary syndrome. The majority of patients are postmenopausal women, with the following features common to most accounts: (1) chest symptoms, electrocardiographic changes, and mild elevation in cardiac biomarkers consistent with acute myocardial ischemia; (2) a temporal relationship to a recent stressful event, giving this condition its alternate name of “broken heart” syndrome (some form of either emotional or physical stress preceded onset in about 65% of cases); (3) regional dysfunction localized to the LV apex, associated with hyperkinesis of the basal portions of the left ventricle with normal epicardial coronary arteries (Takotsubo is Japanese for octopus trap or pot and refers to the characteristic shape of the dysmorphic left ventricle seen on the ventriculogram of patients with this syndrome); and (4) complete resolution of the regional dysfunction in days to weeks after the acute event. The pathogenesis of myocardial perfusion and functional abnormalities in takotsubo cardiomyopathy remains speculative. Proposed mechanisms include (1) coronary spasm, (2) LV dysfunction induced by From the Department of Internal Medicine and Division of Cardiology, University of Pittsburgh Medical Center, Pittsburgh, Pa. Reprint requests: Prem Soman, MD, PhD, MRCP(UK), Division of Cardiology, University of Pittsburgh Medical Center, Room A 429, Scaife Hall, 200 Lothrop St, Pittsburgh, PA 15213; somanp@ upmc.edu. J Nucl Cardiol 2008;15:142-5. 1071-3581/$34.00 Copyright © 2008 by the American Society of Nuclear Cardiology. doi:10.1016/j.nuclcard.2007.11.011

Flavivirus-like particles in the cardiac myocyte of a patient with arrhythmogenic right ventricular cardiomyopathy

Flavivirus-like particles in the cardiac myocyte of a patient with arrhythmogenic right ventricular cardiomyopathy

Outcome of infants from mothers with anti-SSA/Ro antibodies

To evaluate the incidence of electrocardiographic and laboratory abnormalities in neonates born from mothers with connective tissue disease and positive for anti-SSA/Ro antibodies. Electrocardiogram, blood cell counts, liver and renal function tests prospectively obtained from 51 infants born from anti-SSA/Ro-positive mothers with connective tissue disease were compared with those obtained from 50 control infants born from mothers with anti-extractable nuclear antigen (ENA)-negative connective tissue disease. One infant with congenital complete heart block was excluded from analysis. No infant showed sinus bradycardia. A first-degree atrioventricular block at birth was observed in five study group and no control group infants, P=0.023. Atrioventricular blocks spontaneously reverted or remained stable during the first year of life. Mean corrected QT value of infants born from anti-SSA/Ro-positive mothers was slightly prolonged as compared with the control group (0.404+/-0.03 s vs 0.395+/-0.02 s; P=0.060). Infants exposed to anti-SSA/Ro antibodies had a significantly higher prevalence of first-degree atrioventricular block. At variance with previous studies, we observed a low frequency of hematologic abnormalities and no cases of hepatobiliary disease.

Anomalous origin of the right coronary artery diagnosed by cardiac computed tomography

Case Presentation A 34 year old female with no significant past medical history presented with intermittent left shoulder and chest pain. The pain was burning in nature over her left chest and radiated to her left arm. There were no alleviating or exacerbating factors. Initial electrocardiogram showed sinus bradycardia. Cardiac computed tomography angiography revealed anomalous origin of the right coronary artery, which arises from the left sinus of Valsalva (Figure 1) and then travels towards the right side between the pulmonary outflow tract and the aortic root, where it shows mild narrowing of about 50%, (Figure 2) for a length of approximately 1 cm. The woman performed 9 mets during her exercise stress nuclear test which demonstrated electrocardiographic evidence of ischemia with normal myocardial perfusion.

Asympomatic intramyocardial mass: Tissue characterization by cardiovascular magnetic resonance

A 44-year-old female with no past medical history was evaluated for hypertension. High blood pressure was recorded (160/100 mm Hg) and EKG showed sinus bradycardia and left anterior fascicular block. Physical examination was unremarkable. Transthoracic echocardiography showed normal systolic function and concentric left ventricular (LV) hypertrophy (14 mm); an incidental intramyocardial hyperechogenic mass (1×2 cm in diameter) located in the mid-inferior wall of the left ventricle was described (Fig. 1). The patient was referred for a cardiovascular magnetic resonance (CMR) for appropriate noninvasive evaluation and tissue characterization of the mass. CMR was performed with a 1.5-T scanner (Siemens Medical System). Fast-gradient-echo steady-state-free-precession (SSFP) sequence confirmed the echo findings of LV hypertrophy and normal global and regional LV function; an intramyocardial hypointense focal area in themid-inferior wall was identified in the cine sequences. The area appeared hypointense in T1-weighted images (Fig. 2, A and B) with a significant signal reduction on fat saturation T1-weighted sequence (Fig. 2, C andD). In the inversion-recovery sequence the lesion appeared hyperintense pre-contrast with no enhancement after contrast administration (Fig. 2, E and F). Based on CMR findings, intramyocardial cardiac lipoma was diagnosed. In fact, fat can be easily characterized with CMR due to the typical T1 relaxation time and suppression