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Right-sided electrocardiogram (ECG) in inferior myocardial infarction (MI) has no value.
Cardiogenic shock is not possible with preserved left ventricular (LV) function.
Intravenous nitroglycerin or morphine should be given to all patients with acute MI and ongoing chest pain.
Infarction of the right ventricle (RV) is a common clinical event, occurring in one-third of patients with inferior MI.
Right ventricular MI confers a worse prognosis in patients with inferior wall MI.
Because of the requirement for different treatment strategies in RVMI, prompt recognition and appropriate treatment require a thorough understanding of the unique anatomy and pathophysiology of the RV.
In the 85% of patients with right dominant coronary circulation, the RV receives its blood supply almost exclusively from the right coronary artery (RCA), with the septum and part of the posterior wall supplied by the posterior descending artery and the anterior and lateral RV walls supplied by acute marginal branches of the RCA.
The left anterior descending artery supplies a small portion of the anterior wall of the right ventricle.
In left dominant circulation, the left circumflex coronary artery supplies the posterior descending artery, and a nondominant RCA supplies the acute marginal branches.
Isolated RV infarct without any LV involvement can occur with occlusion of a nondominant RCA.
The angiographic hallmark of RVMI is thrombotic occlusion of the RCA proximal to the origin of the acute marginal branches.
Not every case of proximal RCA occlusion results in RVMI.
This relative protection of the right ventricle from infarction is thought to be a consequence of its lower oxygen demand, its continued perfusion during systole, and the potential presence of collaterals from the left anterior descending coronary artery, which, because of the lower systolic pressure on the right side, are more capable of supplying blood in the direction of the right ventricle than in the reverse direction.
The concept of ventricular interdependence in RVMI is central to understanding the pathogenesis of the resultant low cardiac output state.
Ventricular interdependence is mediated through the common pericardium and shared septum.
In RVMI, acute RV dilation occurs, and because the RV shares a relatively fixed space with the LV, the pericardial pressure abruptly increases, leading to impaired LV filling.
Except in rare cases of isolated RVMI, some degree of LVMI accompanies RVMI.
The pericardial constraint and alterations in septal geometry lead to reduced LV filling; cardiac output is diminished further by the decrease in LV systolic function.
Development of shock syndrome with isolated RVMI proves that LV systolic dysfunction is not necessary for the development of shock.
The Hemodynamic Hallmarks of right ventricular myocardial inraction ( Table 4.1 ) ( Fig. 4.1 )
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