About: BACKGROUND: In this observational study, the effects of norepinephrine‐induced changes in mean arterial pressure (MAP) on right ventricular (RV) systolic function, afterload and pulmonary haemodynamics were studied in septic shock patients. We hypothesised that RV systolic function improves at higher doses of norepinephrine/MAP levels. METHODS: Eleven patients with septic shock requiring norepinephrine after fluid resuscitation were included <24 hours after ICU arrival. Study enrolment and insertion of a pulmonary artery catheter was performed after written informed consent from the next of kin. Norepinephrine infusion was titrated to target mean arterial pressures (MAP) of 60, 75 and 90 mmHg in a random sequential order. At each target MAP, strain—and conventional echocardiographic—and pulmonary haemodynamic variables were measured. RV afterload was assessed as effective pulmonary arterial elastance, (E (pa)) and pulmonary vascular resistance index, (PVRI). RV free wall peak strain was the primary end‐point. RESULTS: At highest compared to lowest norepinephrine dose/MAP level, RV free wall peak strain increased from −19% to −25% (32%, P = .003), accompanied by increased tricuspid annular plane systolic excursion (22%, P = .01). At the highest norepinephrine dose/MAP, RV end‐diastolic area index (16%, P < .001), central venous pressure (38%, P < .001), stroke volume index (7%, P = .001), mean pulmonary artery pressure (19%, P < .001) and RV stroke work index (15%, P = .045) increased, with no effects on PVRI or E (pa). Cardiac index did not change, assessed by thermodilution (P = .079) and echocardiography (P = .054). CONCLUSIONS: Higher doses of norepinephrine to a target MAP of 90 mm Hg improved RV systolic function while RV afterload was not affected.   Goto Sponge  NotDistinct  Permalink

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  • BACKGROUND: In this observational study, the effects of norepinephrine‐induced changes in mean arterial pressure (MAP) on right ventricular (RV) systolic function, afterload and pulmonary haemodynamics were studied in septic shock patients. We hypothesised that RV systolic function improves at higher doses of norepinephrine/MAP levels. METHODS: Eleven patients with septic shock requiring norepinephrine after fluid resuscitation were included <24 hours after ICU arrival. Study enrolment and insertion of a pulmonary artery catheter was performed after written informed consent from the next of kin. Norepinephrine infusion was titrated to target mean arterial pressures (MAP) of 60, 75 and 90 mmHg in a random sequential order. At each target MAP, strain—and conventional echocardiographic—and pulmonary haemodynamic variables were measured. RV afterload was assessed as effective pulmonary arterial elastance, (E (pa)) and pulmonary vascular resistance index, (PVRI). RV free wall peak strain was the primary end‐point. RESULTS: At highest compared to lowest norepinephrine dose/MAP level, RV free wall peak strain increased from −19% to −25% (32%, P = .003), accompanied by increased tricuspid annular plane systolic excursion (22%, P = .01). At the highest norepinephrine dose/MAP, RV end‐diastolic area index (16%, P < .001), central venous pressure (38%, P < .001), stroke volume index (7%, P = .001), mean pulmonary artery pressure (19%, P < .001) and RV stroke work index (15%, P = .045) increased, with no effects on PVRI or E (pa). Cardiac index did not change, assessed by thermodilution (P = .079) and echocardiography (P = .054). CONCLUSIONS: Higher doses of norepinephrine to a target MAP of 90 mm Hg improved RV systolic function while RV afterload was not affected.
Subject
  • Sepsis
  • Intensive care medicine
  • Blood pressure
  • Cardiovascular physiology
  • Emergency medicine
  • Medical emergencies
  • Diagnostic intensive care medicine
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