Septic shock is defined as a subset of sepsis, characterised by, after adequate volume resuscitation, the need of vasopressors in order to maintain a normal mean arterial pressure (MAP) ≥65 mmHg. 1Myocardial dysfunction is commonly seen in sepsis also involving the right ventricle (RV). The number of studies on RV function in sepsis by conventional echocardiography is limited. Using American Society of Echocardiography criteria, 2 an RV dysfunction has been described in septic shock. 3,4 Furthermore, it was recently shown that the incidence of isolated right and combined right and left ventricular dysfunction in sepsis/septic shock were 47% and 53%, respectively. 5Norepinephrine administration increases arterial pressure due to its vasoconstrictor effect and is recommended as the first-choice vasopressor in this group of patients. 6 Concerns have been raised regarding a potentially negative effect of norepinephrine on myocardial function due to a norepinephrine-induced increase in left ventricular (LV) afterload. 7 The RV afterload is frequently elevated 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.
S U PP O RTI N G I N FO R M ATI O NAdditional supporting information may be found online in the Supporting Information section at the end of the article.
How to cite this article: Dalla K, Bech-Hanssen O, RickstenS-E...