Managing right ventricular dysfunction
Learn about the use of inotropic and vasopressor agents in the context of right ventricular dysfunction.
In this video, you'll learn about the use of inotropic and vasopressor agents in the context of right ventricular dysfunction.
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Although often less recognized right ventricular failure is just as important as left ventricular causes of heart failure. stroke volume and cardiac output through the right side of the heart must match that of the left side of the heart, except in cases of extreme shunting. However, there are several ways in which the right heart has a more fickle physiologic equilibrium.
The right side of the heart is much lower pressure system, thus the right ventricle is much more sensitive to increased afterload. Increased afterload may result from chronic conditions like left sided heart failure, or lung disease, and may be exacerbated acutely by volume overload hypoxemia hypercar via or positive pressure ventilation.
The muscle of the left ventricle is perfused during diastole II with a large pressure gradient but the muscle of the right ventricle as a Smaller pressure gradient and relies on perfusion throughout the cardiac cycle. Therefore, a small increase in the RV wall tension can have dramatic effects on RV perfusion.
Decreasing perfusion compromises the cardiac output further limiting perfusion and feeding into this vicious cycle. Increased right ventricular pressure also increases regurgitation through their tricuspid valve, further limiting forward flow. Normally, the left ventricle helps the right ventricle contract. increased pressure and the right ventricle will distort the normal architecture, decreasing the efficiency of right ventricular contraction and shifting the interventricular septum to the left, limiting left ventricular filling and stroke volume.
This is known as ventricular inter-dependence. If possible, underlying causes of pulmonary hypertension should be reversed. This may include the use of pulmonary vasodilators or pulmonary artery catheters in some patients, which should be done with expert consultation transferred to a specialized center or one capable of mechanical circulatory support should be considered early. positive pressure ventilation should be avoided if possible, although oxygenation and ventilation should be optimized, so this may be a tenuous balance.
Diary CES may help to decrease filling pressures, but hypovolemia may decrease cardiac output. If fluid boluses are necessary, they should be small, with frequent reassessment. ionotropic agents may be particularly useful with right ventricular dysfunction, but attention should be paid to their additional effects.
Dobutamine and milrinone may increase isotropy but usually decrease blood pressure which may compromise right ventricular perfusion vasopressors may help maintain perfusion pressure, especially vasopressin, which will not increase pulmonary vascular resistance and may in fact lower it. norepinephrine and epinephrine remain viable options depending on the degree of entropy and vasopressor activity needed.
Phenol Efrain should generally be avoided for right ventricular dysfunction because it increases right ventricular afterload and decreases cardiac output. Non sinus rhythms are not well tolerated in the setting of right ventricular dysfunction. Because the loss of atrial contraction decreases the cardiac output. Atrial Fibrillation should generally be cardiovert immediately, particularly if the patient is unstable.