Items in AFP with MESH term: Electrocardiography
Diagnosing Pericarditis - Article
ABSTRACT: Pericarditis, or inflammation of the pericardium, is most often caused by viral infection. It can also develop as a result of bacterial or other infection, autoimmune disease, renal failure, injury to the mediastinal area, and the effects of certain drugs (notably hydralazine and procainamide). The clinical features of pericarditis depend on its cause, as well as the volume and type of effusion. Patients with uncomplicated pericarditis have pleuritic-type chest pain that radiates to the left shoulder and may be relieved by leaning forward. Chest radiographs, Doppler studies, and laboratory tests confirm the diagnosis and provide information about the degree of effusion. In most patients, pericarditis is mild and resolves spontaneously, although treatment with a nonsteroidal anti-inflammatory drug or a short course of a corticosteroid may be helpful. When a large pericardial effusion is produced, cardiac function may be compromised, and cardiac tamponade can occur. In patients with longstanding inflammation, the pericardium becomes fibrous or calcified, resulting in constriction of the heart. Drainage or surgical intervention may be necessary in patients with complicated pericarditis.
ABSTRACT: Sick sinus syndrome comprises a variety of conditions involving sinus node dysfunction and commonly affects elderly persons. While the syndrome can have many causes, it usually is idiopathic. Patients may experience syncope, pre-syncope, palpitations, or dizziness; however, they often are asymptomatic or have subtle or nonspecific symptoms. Sick sinus syndrome has multiple manifestations on electrocardiogram, including sinus bradycardia, sinus arrest, sinoatrial block, and alternating patterns of bradycardia and tachycardia (bradycardia-tachycardia syndrome). Diagnosis of sick sinus syndrome can be difficult because of its nonspecific symptoms and elusive findings on electrocardiogram or Holter monitor. The mainstay of treatment is atrial or dual-chamber pacemaker placement, which generally provides effective relief of symptoms and lowers the incidence of atrial fibrillation, thromboembolic events, heart failure, and mortality, compared with ventricular pacemakers.
ABSTRACT: In approximately 5 percent of sudden cardiac deaths, no demonstrable anatomic abnormality is found. Some cases are caused by sudden arrhythmia death syndrome. A prolonged QT interval is a common thread among the various entities associated with sudden arrhythmia death syndrome. A number of drugs are known to cause QT prolongation (e.g., terfenadine), as are hypokalemia, hypomagnesemia, myocarditis, and endocrine and nutritional disorders. Recently, attention has focused on a group of inherited gene mutations in cardiac ion channels that cause long QT syndrome and carry an increased risk for sudden death. Some of the highest rates of inherited long QT syndrome occur in Southeast Asian and Pacific Rim countries. The median age of persons who die of long QT syndrome is 32 years; men are predominately affected. In addition to a prolonged QT interval, which occurs in some but not all persons with long QT syndrome, another characteristic electrocardiographic abnormality is the so-called Brugada sign (an upward deflection of the terminal portion of the QRS complex). Most cardiac events are precipitated by vigorous exercise or emotional stress, but they also can occur during sleep. Torsades de pointes and ventricular fibrillation are the usual fatal arrhythmias. Long QT syndrome should be suspected in patients with recurrent syncope during exertion and those with family histories of sudden, unexpected death. Unfortunately, not all persons with long QT syndrome have premonitory symptoms or identifiable electrocardiographic abnormalities, and they may first present with sudden death. Beta blockers, potassium supplements, and implantable defibrillators have been used for treatment of long QT syndrome. Identifying the specific gene mutation in a given patient with long QT syndrome can help guide prophylactic therapy.
ABSTRACT: Family physicians frequently encounter patients with symptoms that could be related to cardiac arrhythmias, most commonly atrial fibrillation or supraventricular tachycardias. The initial management of atrial fibrillation includes ventricular rate control to provide adequate cardiac output. In patients with severely depressed cardiac output and recent-onset atrial fibrillation, immediate electrical cardioversion is the treatment of choice. Hemodynamically stable patients with atrial fibrillation for more than two days or for an unknown period should be assessed for the presence of atrial thrombi. If thrombi are detected on transesophageal echocardiography, anticoagulation with warfarin for a minimum of 21 days is recommended before electrical cardioversion is attempted. Patients with other supraventricular arrhythmias may be treated with adenosine, a calcium channel blocker, or a short-acting beta blocker to disrupt reentrant pathways. When initial medications are ineffective, radiofrequency ablation of ectopic sites is an increasingly popular treatment option.
ABSTRACT: Atrial fibrillation is the arrhythmia most commonly encountered in family practice. Serious complications can include congestive heart failure, myocardial infarction, and thromboembolism. Initial treatment is directed at controlling the ventricular rate, most often with a calcium channel blocker, a beta blocker, or digoxin. Medical or electrical cardioversion to restore sinus rhythm is the next step in patients who remain in atrial fibrillation. Heparin should be administered to hospitalized patients undergoing medical or electrical cardioversion. Anticoagulation with warfarin should be used for three weeks before elective cardioversion and continued for four weeks after cardioversion. The recommendations provided in this two-part article are consistent with guidelines published by the American Heart Association and the Agency for Healthcare Research and Quality.
Diagnosis of Acute Coronary Syndrome - Article
ABSTRACT: The term 'acute coronary syndrome' encompasses a range of thrombotic coronary artery diseases, including unstable angina and both ST-segment elevation and non-ST-segment elevation myocardial infarction. Diagnosis requires an electrocardiogram and a careful review for signs and symptoms of cardiac ischemia. In acute coronary syndrome, common electrocardiographic abnormalities include T-wave tenting or inversion, ST-segment elevation or depression (including J-point elevation in multiple leads), and pathologic Q waves. Risk stratification allows appropriate referral of patients to a chest pain center or emergency department, where cardiac enzyme levels can be assessed. Most high-risk patients should be hospitalized. Intermediate-risk patients should undergo a structured evaluation, often in a chest pain unit. Many low-risk patients can be discharged with appropriate follow-up. Troponin T or I generally is the most sensitive determinant of acute coronary syndrome, although the MB isoenzyme of creatine kinase also is used. Early markers of acute ischemia include myoglobin and creatine kinase-MB subforms (or isoforms), when available. In the future, advanced diagnostic modalities, such as myocardial perfusion imaging, may have a role in reducing unnecessary hospitalizations.
Diagnosis and Treatment of Hypothermia - Article
ABSTRACT: Although hypothermia is most common in patients who are exposed to a cold environment, it can develop secondary to toxin exposure, metabolic derangements, infections, and dysfunction of the central nervous and endocrine systems. The clinical presentation of hypothermia includes a spectrum of symptoms and is grouped into the following three categories: mild, moderate, and severe. Management depends on the degree of hypothermia present. Treatment modalities range from noninvasive, passive external warming techniques (e.g., removal of cold, wet clothing; movement to a warm environment) to active external rewarming (e.g., insulation with warm blankets) to active core rewarming (e.g., warmed intravenous fluid infusions, heated humidified oxygen, body cavity lavage, and extracorporeal blood warming). Mild to moderate hypothermia is treated easily with supportive care in most clinical settings and has good patient outcomes. The treatment of severe hypothermia is more complex, and outcomes depend heavily on clinical resources. Prevention and recognition of atypical presentations are essential to reducing the rates of morbidity and mortality associated with this condition.
Evaluation of Syncope - Article
ABSTRACT: Though relatively common, syncope is a complex presenting symptom defined by a transient loss of consciousness, usually accompanied by falling, and with spontaneous recovery. Syncope must be carefully differentiated from other conditions that may cause a loss of consciousness or falling. Syncope can be classified into four categories: reflex mediated, cardiac, orthostatic, and cerebrovascular. A cardiac cause of syncope is associated with significantly higher rates of morbidity and mortality than other causes. The evaluation of syncope begins with a careful history, physical examination, and electrocardiography. Additional testing should be based on the initial clinical evaluation. Older patients and those with underlying organic heart disease or abnormal electrocardiograms generally will need additional cardiac evaluation, which may include prolonged electrocardiographic monitoring, echocardiography, and exercise stress testing. When structural heart disease is excluded, tests for neurogenic reflex-mediated syncope, such as head-up tilt-table testing and carotid sinus massage, should be performed. The use of tests such as head computed tomography, magnetic resonance imaging, carotid and transcranial ultrasonography, and electroencephalography to detect cerebrovascular causes of syncope should be reserved for those few patients with syncope whose history suggests a neurologic event or who have focal neurologic signs or symptoms.
Diagnostic Approach to Palpitations - Article
ABSTRACT: Palpitations-sensations of a rapid or irregular heartbeat-are most often caused by cardiac arrhythmias or anxiety. Most patients with arrhythmias do not complain of palpitations. However, any arrhythmia, including sinus tachycardia, atrial fibrillation, premature ventricular contractions, or ventricular tachycardia, can cause palpitations. Palpitations should be considered as potentially more serious if they are associated with dizziness, near-syncope, or syncope. Nonarrhythmic cardiac problems, such as mitral valve prolapse, pericarditis, and congestive heart failure, and noncardiac problems, such as hyperthyroidism, vasovagal syncope, and hypoglycemia, can cause palpitations. Palpitations also can result from stimulant drugs, and over-the-counter and prescription medications. No cause for the palpitations can be found in up to 16 percent of patients. Ambulatory electrocardiographic (ECG) monitoring usually is indicated if the etiology of palpitations cannot be determined from the patient's history, physical examination, and resting ECG. When palpitations occur unpredictably or do not occur daily, an initial two-week course of continuous closed-loop event recording is indicated. Holter monitoring for 24 to 48 hours may be appropriate in patients with daily palpitations. Trans-telephonic event monitors are more effective and cost-effective than Holter monitors for most patients.
ABSTRACT: Each year, pacemaker therapy is prescribed to approximately 900,000 persons worldwide. Current pacemaker devices treat bradyarrhythmias and tachyarrhythmias and, in some cases, are combined with implantable defibrillators. In older patients, devices that maintain synchrony between atria and ventricles are preferred because they maintain the increased contribution of atrial contraction to ventricular filling necessary in this age group. In general, rate-responsive devices are preferred because they more closely simulate the physiologic function of the sinus node. Permanent pacemakers are implanted in adults primarily for the treatment of sinus node dysfunction, acquired atrioventricular block, and certain fascicular blocks. They also are effective in the prevention and treatment of certain tachyarrhythmias and forms of neurocardiogenic syncope. Biventricular pacing (resynchronization therapy) recently has been shown to be an effective treatment for advanced heart failure in patients with major intraventricular conduction effects, predominately left bundle branch block. Many studies have documented that pacemaker therapy can reduce symptoms, improve quality of life and, in certain patient populations, improve survival.