Impact of norepinephrine on right ventricular afterload and function in septic shock—a strain echocardiography study

Abstract

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...

Effects of Collagen Antibacterial Functional Dressing plus Continuous Nursing on Lower Extremity Skin Injury Caused by Norepinephrine in Patients with Septic Shock

“…Mild injury symptoms include redness, pain, and local tissue necrosis, while severe cases may suffer dysfunction, seriously compromising the treatment effect and the nurse-patient relationship [ 6 , 7 ]. To this end, comprehensive nursing has been identified for complication prevention of the lower extremities to potentiate the efficacy of norepinephrine; nonetheless, the expected treatment outcome is somehow compromised [ 8 , 9 ]. Previous studies have found that in the treatment of the skin radiation injury of breast cancer patients during radiotherapy [ 10 , 11 ], the collagen antibacterial functional dressing accelerated cell metabolism, promoted wound healing, relieved skin pain, and regulated the level of local inflammatory factors, which is conducive to injured skin repair.…”

Effects of Levosimendan on cardiac function, size and strain in heart failure patients

“…Dalla et al described in his model with septic patients receiving norepinephrine that changes in afterload and preload i.e. an increase in systemic and pulmonary vascular resistance, impact LV EDV, but not ejection fraction or longitudinal strain [ 30 ]. The lack of changes in strain parameters in this cohort could also be explained by a lack of ability in the improvement of deformity based on longstanding LV dilatation, presence of valvular disease, and the presence of fibrosis.…”

Norepinephrine in Sepsis: Looking beyond Vasoconstriction!

“…Two recent studies have addressed this concern and assessed the cardiac effects of NE in a structured manner. 1,2 Hamzaoui et al demonstrated an inotropic effect of NE infusion in early phase of septic shock considering an improved echocardiographic profile of both the left ventricle and right ventricle (RV) function. 1 However, the understanding of the mechanisms behind an augmented ventricular performance, particularly RV, remained clouded in absence of data on preload and afterload parameters.…”

“…The subsequent study by Dalla et al formally evaluated RV preload, afterload, and function in background of a NE infusion in septic shock. 2 The study outlined an improvement of RV function without an increase in the PVR or the RV afterload. These findings are noteworthy considering the contradictory literature on effects of NE on the pulmonary vasculature in NE-dependent vasodilatory shock, with some studies depicting an elevated PVR 3 while the more recent studies do not suggest accentuated PVR with NE in a setting of septic shock.…”

“…It is noteworthy that the effects of NE on PVR are compounded by the combination of α-mediated increase and β-mediated decreased pulmonary vascular tone. 2–4 Considering the aforementioned points, a NE infusion is expected to improve the ventriculoarterial coupling, which is deleteriously affected in sepsis. However, the varying degree of the sepsis-induced β 1 -adrenoceptors downregulation, the extent of preload-responsiveness and the dynamic interplay of vascular resistances depending on the NE infusion dosages compound the cardiac effects of NE in septic patients.…”