Akademik Veri Yönetim Sistemi
Przegla̧d lekarski, cilt.61, sa.6, ss.705-711, 2004 (Scopus)
Acute right ventricular infarction (RVI) is usually caused by proximal occlusion of the right coronary artery. RVI is frequent, as it occurs in as many as one out of every two left ventricular interior and/or posterior wall infarctions. The involvement of the right ventricle in acute myocardial infarction has been shown to be associated with an increased risk of life-threatening arrhythmias and sudden cardiac death. Clinical course of RVI can vary from being completely silent to cardiogenic shock (seen in 10-15% patients with inferior wall infarction). RVI diagnosis is based on clinical signs (hypotension and increased jugular venous pressure while pulmonary fields are clear), ECG (ST elevation by > or = 1 mm in V4R), echocardiography (right ventricular wall regional motion abnormalities and/or right ventricle distension, paradoxical motion of the interventricular septum, tissue Doppler), technetium pyrophosphate scanning with ventriculography, and invasive patient monitoring. In addition to its important diagnostic part, the invasive patient monitoring plays a key role in risk stratification and can dynamically guide the treatment (such as fluid loading). In most cases, successful reperfusion in the infarct-related artery territory can be achieved by interventional management (i.e. angioplasty) or--if the latter is not available--by thrombolytic therapy. Patients with arterial hypotension require volume expansion which is best guided by the central venous pressure (CVP; a measure of the right atrial pressure, RAP) and the pulmonary capillary wedge pressure (PCWP). If the hemodynamics does not improve despite optimal fluid loading, pharmacological (catecholamine infusion) or mechanical (intra-aortic balloon pump) circulatory assistance needs to be implemented. Patients with significant sinus bradycardia or 3rd degree AV block may require temporary cardiac pacing. In addition, inhalatory nitric oxide (iNO) has been shown to reduce right ventricular afterload in a selective manner and its potential clinical role is currently being evaluated. Within several months after RVI, the right ventricular performance improves in most patients, including those without successful reperfusion of IRA. Such patients, however, have an increased risk of complications (including sudden death) while the recovery of right ventricular function is slow.