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KEY POINTS

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  • Right heart syndromes (RHS) as a cause of hemodynamic instability and shock are less common than left heart dysfunction, but recognizing them requires a high level of vigilance.

  • RHS result from a combination of pressure or volume overload and impaired RV contractility. Progression to acute cor pulmonale (the combination of acute pulmonary hypertension with profound RV systolic and diastolic dysfunction) results in spiraling end-organ dysfunction.

  • Clues to recognizing RHS as a cause of shock include a history of a condition that is associated with pulmonary hypertension, elevated neck veins, peripheral edema greater than pulmonary edema, or a right-sided third heart sound, in addition to electrocardiographic, radiographic, and echocardiographic findings.

  • Plasma biomarkers are nonspecific but echocardiography is extremely valuable, not only for demonstrating the presence of RHS, but also for guiding hemodynamic management.

  • Progressive right heart shock can be worsened by excessive fluid infusion, concomitant left ventricular failure, inappropriate application of extrinsic positive end-expiratory pressure (PEEP) and hypoxia.

  • The drug of choice for resuscitation to reduce systemic oxygen demand while improving oxygen delivery is dobutamine, initially infused at 5 μg/kg per minute. Systemically active vasoconstrictors may provide additional benefit.

  • Inhaled nitric oxide or prostacyclin and oral PDE-inhibitors (eg, sildenafil) or extracorporeal mechanical assist devices may be beneficial in improving pulmonary hemodynamics and oxygenation, but may not improve survival.

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In the majority of patients with shock due to “pump failure,” assessment is focused appropriately on the left ventricle. However, in a substantial minority of patients, right heart dysfunction is the cause of shock. Examples include acute pulmonary embolism (PE), other causes of acute right heart pressure overload (eg, acute respiratory distress syndrome [ARDS] treated with positive pressure ventilation), acute deterioration in patients with chronic pulmonary hypertension, and right ventricular infarction. Although right ventricular infarction differs from the other right heart syndromes (RHS) in that the pulmonary artery pressure is not high, in many other regards right ventricular infarction resembles the other syndromes, so we will consider them together. Failure to consider the right heart in the differential diagnosis of shock risks incomplete or inappropriate treatment of the shock. It would be hard to overemphasize the importance of echocardiography, both in aiding the recognition of the right heart syndromes and in guiding management. In this chapter, we review the notable features that distinguish the right heart from the left, describe the themes that unify the acute RHS and allow their recognition, discuss the pathophysiology and differential diagnosis of RHS, and review their management.

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RIGHT VENTRICULAR PHYSIOLOGY

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The right ventricle (RV) has long been considered the “forgotten ventricle,” because under normal pressure and volume loading conditions the RV is thought to function as a passive conduit for systemic venous return. When the pulmonary vasculature is normal, right ventricular performance has little impact on the maintenance of cardiac output. In animal models, complete ablation of the right ventricular free wall has little effect on venous pressures.

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