Inotropic agents
Medical > Therapy > Basic treatments
Inotropic agents
Right heart failure may complicate severe pulmonary hypertension. Increased right ventricular afterload causes right ventricular end-diastolic volume to increase and, hence, reduces left ventricular end-diastolic volume by diastolic interaction. Consequently, stroke volume, cardiac output and systemic blood pressure decrease. Decreased systemic blood pressure causes right ventricular coronary blood flow to decrease, which results in right ventricular ischemia, which impairs right ventricular contraction. After preaload has been optimized by volume filling, inotropic support of right ventricular function in pulmonary hypertension aims to increase systemic blood pressure and to improve right ventricular contraction (Wiedermann and Matthay, 1989). Improvement of right ventricular function may be achieved by using norepinephrine 0,1 to 1 µg.kg.min-1 to increase systemic blood pressure, hence, right coronary perfusion, and dobutamine at the dose of 2 to 10 µg.kg.min-1 to enhance myocardial contractility. In very severe cases a short course of adrenaline infusion up to 1 µg.kg.min-1 may be considered. Accurate hemodynamic monitoring is mandatory, when catecholamines are used in decompensated pulmonary hypertension. Animal data suggest that limited doses of catecholamines do not increase pulmonary vascular resistance (Delcroix et al., 1995). As an interventional option for the management of right heart failure following chronic pulmonary hypertension, balloon atrial septostomy may be considered (Barst, 2000).
Cardiac glycosides can improve cardiac function in chronic pulmonary hypertension. There is evidence that short-term digoxin therapy improves cardiac function and decreases plasma norepinephrine and atrial natriuretic peptide levels in patients with right ventricular dysfunction due to pulmonary hypertension (Rich et al., 1998). Treatment with digoxin may be useful in counteracting the negative inotropic effect of nifedipine in these patients, but there are no data to support this. However, calcium channel blockers such as diltiazem may interact with the metabolism of digoxin causing harmful effects (Clarke et al., 1993). Digoxin does not improve right ventricular dysfunction or exercise capacity in patients with severe chronic airflow obstruction without left ventricular dysfunction. Right ventricular ejection fraction improved only in patients, in whom the left ventricular ejection fraction normalized during treatment (Mathur et al., 1981, Brown et al., 1984). In conclusion, in patients with right heart failure due to pulmonary hypertension digoxin is not recommended for routine use, especially if left ventricular function is normal.
References
Back to > Medical > Therapy > Basic treatments
Inotropic agents
Right heart failure may complicate severe pulmonary hypertension. Increased right ventricular afterload causes right ventricular end-diastolic volume to increase and, hence, reduces left ventricular end-diastolic volume by diastolic interaction. Consequently, stroke volume, cardiac output and systemic blood pressure decrease. Decreased systemic blood pressure causes right ventricular coronary blood flow to decrease, which results in right ventricular ischemia, which impairs right ventricular contraction. After preaload has been optimized by volume filling, inotropic support of right ventricular function in pulmonary hypertension aims to increase systemic blood pressure and to improve right ventricular contraction (Wiedermann and Matthay, 1989). Improvement of right ventricular function may be achieved by using norepinephrine 0,1 to 1 µg.kg.min-1 to increase systemic blood pressure, hence, right coronary perfusion, and dobutamine at the dose of 2 to 10 µg.kg.min-1 to enhance myocardial contractility. In very severe cases a short course of adrenaline infusion up to 1 µg.kg.min-1 may be considered. Accurate hemodynamic monitoring is mandatory, when catecholamines are used in decompensated pulmonary hypertension. Animal data suggest that limited doses of catecholamines do not increase pulmonary vascular resistance (Delcroix et al., 1995). As an interventional option for the management of right heart failure following chronic pulmonary hypertension, balloon atrial septostomy may be considered (Barst, 2000).
Cardiac glycosides can improve cardiac function in chronic pulmonary hypertension. There is evidence that short-term digoxin therapy improves cardiac function and decreases plasma norepinephrine and atrial natriuretic peptide levels in patients with right ventricular dysfunction due to pulmonary hypertension (Rich et al., 1998). Treatment with digoxin may be useful in counteracting the negative inotropic effect of nifedipine in these patients, but there are no data to support this. However, calcium channel blockers such as diltiazem may interact with the metabolism of digoxin causing harmful effects (Clarke et al., 1993). Digoxin does not improve right ventricular dysfunction or exercise capacity in patients with severe chronic airflow obstruction without left ventricular dysfunction. Right ventricular ejection fraction improved only in patients, in whom the left ventricular ejection fraction normalized during treatment (Mathur et al., 1981, Brown et al., 1984). In conclusion, in patients with right heart failure due to pulmonary hypertension digoxin is not recommended for routine use, especially if left ventricular function is normal.
References
Back to > Medical > Therapy > Basic treatments
Druckversion
Suche
SSPH Research Prize 2012
Deadline for submission: April 30, 2012
Further information
Symposium "pulmonal-arterielle Hypertension im Kindesalter"
Donnerstag, 10. Mai 2012, 16.00-18.00, Bern
Further information:
5th International Congress of the Swiss Society of Pulmonary Hypertension (SSPH)
28.-29. September 2012, Thun, Congress Hotel Seepark Thun
Informationen: www.imk.ch/sgph2012
mehr