Tabi, Meir

Introduction: A low cardiac power output (CPO), measured invasively, identifies critically ill patients at increased risk of mortality. CPO can also be measured non-invasively with transthoracic echocardiography (TTE), although prognostic data in critically ill patients is not available. Hypothesis: Reduced CPO measured by TTE is associated with increased hospital mortality in cardiac intensive care unit (CICU) patients. Methods: Using a database of CICU patients admitted between 2007 and 2018, we identified patients with TTE within one day (before or after) of CICU admission who had data necessary for calculation of CPO. Multivariable logistic regression determined the relationship between CPO and adjusted hospital mortality. Results: We included 5,585 patients with a mean age of 68.3±14.8 years, including 36.7% females. Admission diagnoses included acute coronary syndrome (ACS) in 57%, heart failure (HF) in 50%, cardiac arrest (CA) in 12%, and cardiogenic shock (CS) in 13%. The mean left ventricular ejection fraction (LVEF) was 47±16%, and the mean CPO was 1.0±0.4 W. CPO was inversely associated with the risk of hospital mortality (Figure A), including among patients with ACS, HF, and CS (Figure B). On multivariable analysis, lower CPO was associated with higher hospital mortality (OR 0.96 per 0.1 W, 95% CI 0.0.93-0.99, p=0.03). Hospital mortality was highest in patients with low CPO coupled with reduced LVEF, increased vasopressor requirements, or higher admission lactate. Hospital mortality was higher among patients with a CPO <0.6 W (adjusted OR 1.57, 95% CI 1.13-2.19, p = 0.007), particularly in the presence of admission lactate level >4 mmol/L (50.9%). Conclusions: Echocardiographic CPO was inversely associated with hospital mortality in CICU patients, particularly among patients with increased lactate and vasopressor requirements. Routine measurement of CPO provides important information beyond LVEF and should be considered in CICU patients.

Purpose of review Cardiogenic shock continues to carry a high mortality, and recent randomized trials have not identified novel therapies that improve survival. Early optimization of patients with confirmed or suspected cardiogenic shock is crucial, as patients can quickly transition from a hemodynamic shock state to a treatment-resistant hemometabolic shock state, where accumulated metabolic derangements trigger a self-perpetuating cycle of worsening shock. Recent findings We describe a structured ABCDE approach involving stabilization of the airway, breathing and circulation, followed by damage control and etiologic assessment. Respiratory failure is common and many cardiogenic shock patients require invasive mechanical ventilation. Norepinephrine is titrated to restore mean arterial pressure and dobutamine is titrated to restore cardiac output and organ perfusion. Echocardiography is essential to identify potential causes and characterize the phenotype of cardiogenic shock. Coronary angiography is usually indicated, particularly when acute myocardial ischemia is suspected, followed by culprit-vessel revascularization if indicated. An invasive hemodynamic assessment can clarify whether temporary mechanical circulatory support is necessary. Summary Early stabilization of hemodynamics and end-organ function is necessary to achieve best outcomes in cardiogenic shock. Using a structured approach tailored to initial cardiogenic shock resuscitation may help to demonstrate benefit from novel therapies in the future.

ABSTRACT Background: Shock in patients resuscitated after out of hospital cardiac arrest (OHCA) is associated with an increased risk of mortality. We sought to determine the associations between lactate level, mean arterial pressure (MAP), and vasopressor/inotrope doses with mortality. Methods: Retrospective cohort study of adult patients with OHCA of presumed cardiac etiology treated with targeted temperature management (TTM) between December 2005 and September 2016. Multivariable logistic regression was performed to determine predictors of hospital death. Results: Among 268 included patients, the median age was 64 (55, 71.8) years, including 27% females. OHCA was witnessed in 89%, OHCA rhythm was shockable in 87%, and bystander CPR was provided in 64%. Vasopressors were required during the first 24 h in 60%. Hospital mortality occurred in 104 (38.8%) patients. Higher initial lactate, peak Vasoactive-Inotropic Score (VIS), and lower mean 24-h MAP were associated with higher hospital mortality (all P < 0.001). After multivariable regression, both higher initial lactate (adjusted OR 1.15 per 1 mmol/L higher, 95% CI 1.00–1.31, P = 0.03) and higher peak VIS (adjusted OR 1.20 per 10 units higher, 95% CI 1.10–1.54, P = 0.003) were associated with higher hospital mortality, but mMAP was not (P = 0.92). However, patients with a mMAP < 70 mm Hg remained at higher risk of hospital mortality after multivariable adjustment (adjusted OR 9.30, 95% CI 1.39–62.02, P = 0.02). Conclusions: In patients treated with TTM after OHCA, greater shock severity, as reflected by higher lactate levels, mMAP < 70 mmHg, and higher vasopressor requirements during the first 24 h was associated with an increased rate of hospital mortality.