Burstein, Barry

Background Shock and preshock are defined on the basis of the presence of hypotension, hypoperfusion, or both. We sought to determine the hemodynamic underpinnings of shock and preshock noninvasively using transthoracic echocardiography (TTE). Methods and Results We included Mayo Clinic cardiac intensive care unit patients from 2007 to 2015 with TTE within 1 day of admission. Hypotension and hypoperfusion at the time of cardiac intensive care unit admission were used to define 4 groups. TTE findings were evaluated across these groups, and in‐hospital mortality was evaluated according to TTE findings in each group. We included 5375 patients with a median age of 69.2 years (36.8% women). The median left ventricular ejection fraction was 50%. Groups based on hypotension and hypoperfusion were assigned as follows: no hypotension or hypoperfusion, 59.7%; isolated hypotension, 15.3%; isolated hypoperfusion, 16.4%; and both hypotension and hypoperfusion, 8.7%. Most TTE variables of interest varied across these groups, with worse biventricular function, lower forward flow, and higher filling pressures as the degree of hemodynamic compromise increased. In‐hospital mortality occurred in 8.2%, and inpatient deaths had more TTE parameter abnormalities. In‐hospital mortality increased with the degree of hemodynamic compromise, and a marked gradient in in‐hospital mortality was observed when the clinical classification of shock and preshock was combined with TTE findings reflecting worse biventricular function, lower forward flow, or higher filling pressures. Conclusions Substantial differences in cardiac function are observed between cardiac intensive care unit patients with preshock and shock using TTE, and the combination of the clinical and TTE hemodynamic assessment provides robust mortality risk stratification.

AbstractAimsThe aims of the Critical Care Cardiology Trials Network (CCCTN) are to develop a registry to investigate the epidemiology of cardiac critical illness and to establish a multicentre research network to conduct randomised clinical trials (RCTs) in patients with cardiac critical illness.Methods and resultsThe CCCTN was founded in 2017 with 16 centres and has grown to a research network of over 40 academic and clinical centres in the United States and Canada. Each centre enters data for consecutive cardiac intensive care unit (CICU) admissions for at least 2 months of each calendar year. More than 20 000 unique CICU admissions are now included in the CCCTN Registry. To date, scientific observations from the CCCTN Registry include description of variations in care, the epidemiology and outcomes of all CICU patients, as well as subsets of patients with specific disease states, such as shock, heart failure, renal dysfunction, and respiratory failure. The CCCTN has also characterised utilization patterns, including use of mechanical circulatory support in response to changes in the heart transplantation allocation system, and the use and impact of multidisciplinary shock teams. Over years of multicentre collaboration, the CCCTN has established a robust research network to facilitate multicentre registry-based randomised trials in patients with cardiac critical illness.ConclusionThe CCCTN is a large, prospective registry dedicated to describing processes-of-care and expanding clinical knowledge in cardiac critical illness. The CCCTN will serve as an investigational platform from which to conduct randomised controlled trials in this important patient population.

Introduction: Ventricular dysfunction contributes to shock in cardiac intensive care unit (CICU) patients. We aimed to describe the associations between ventricular dysfunction with in-hospital mortality across the spectrum of shock severity. Hypothesis: Patients with biventricular dysfunction (BVD) have higher mortality at each Society for Cardiovascular Angiography and Intervention (SCAI) shock stage. Methods: We identified CICU patients from 2007 to 2015 with available echocardiography data within 1 day of admission. Left ventricular systolic dysfunction (LVSD) was defined as left ventricular ejection fraction <40% and right ventricular systolic dysfunction (RVSD) as moderate or greater systolic dysfunction by semi-quantitative assessment; BVD included the presence of both LVSD and RVSD. Predictors of in-hospital mortality were determined after adjustment using multivariable logistic regression. Results: We included 3,158 patients with a mean age of 68.2±14.6 years; 51.8% had acute coronary syndromes. LVSD was present in 22.3%, RVSD in 11.8%, and 16.4% had BVD. Hospital mortality increased with SCAI shock stage and was incrementally higher in patients with LVSD, RVSD and BVD across SCAI shock stages (Figure); patients with BVD had higher mortality in each SCAI shock stage. After adjustment, there was no difference in in-hospital mortality for patients with LVSD or RVSD versus those without ventricular dysfunction (p >0.05), but BVD was independently associated with higher in-hospital mortality (adjusted HR 1.815, 95% CI 1.237-2.663, p = 0.0023). Adding ventricular dysfunction to SCAI shock stage increased discrimination for hospital mortality (AUC 0.784 vs. 0.766, p <0.001). Conclusions: Among patients admitted to the CICU, BVD was independently associated with higher hospital mortality after adjustment for shock severity. Echocardiographic assessment may augment clinical risk stratification using the SCAI shock classification.

Introduction: Lactate is a known prognostic marker in critically ill patients, including patients with shock and cardiac arrest (CA). We sought to describe the association between admission lactate and hospital mortality in cardiac intensive care unit (CICU) patients, particularly those with CA. Methods: We retrospectively evaluated adult patients admitted to a tertiary care CICU from January 1, 2007, to April 30, 2018, with measured lactate on admission. We examined hospital mortality as a function of admission lactate level in patients with and without CA. Multivariable logistic regression was used to determine predictors of hospital mortality in the overall cohort, after adjustment for clinical characteristics, therapies, and illness severity. Results: We included 3,042 patients with a median age of 70 years (IQR 60-80), including 40.5% (n=1,233) females. There were 789 patients (26.1%) with a diagnosis of CA. The median APACHE-4 predicted mortality was 24.2% (IQR 10.9-50.7), and 50.8% (n=1546) were treated with vasoactive infusions. The median lactate on admission was 1.8 mmol/L (IQR 1.1-3.0). CICU mortality occurred in 478 (15.7%) patients) and hospital mortality occurred in 706 (23.2%) patients. Hospital mortality rose progressively as a function of admission lactate ( Figure ). On univariable analysis, lactate was associated with increased hospital mortality among the overall cohort (OR 1.36, CI 1.31-1.42, P < .001; AUROC 0.71), patients with CA (OR 1.33 (95% CI 1.25-1.41, P < .01; AUROC 0.73), and patients without CA (OR 1.27, CI 1.21-1.34, P < .01; AUROC 0.64). On multivariable analysis, lactate was one of the most significant predictors of hospital mortality (adjusted OR 1.13 per mmol/L, 95% CI 1.08-1.18, P < .001). Conclusions: Admission lactate levels are strongly associated with increased hospital mortality among CICU patients, especially those with CA. The prognostic value of lactate levels may help inform clinicians caring for CICU patients.

Background: Post-arrest hypotension is common after out of hospital cardiac arrest (OHCA) and many patients resuscitated after OHCA will require vasopressors. We sought to determine the associations between echocardiographic parameters and vasopressor requirements in OHCA patients. Methods: We retrospectively analyzed adult patients with OHCA treated with targeted temperature management between December 2005 and September 2016 who underwent a transthoracic echocardiogram (TTE). Categorical variables were compared using 2-tailed Fisher’s exact and Pearson’s correlation coefficients and variance (r 2 ) values were used to assess relationships between continuous variables. Results: Among 217 included patients, the mean age was 62 ± 12 years, including 74% males. The arrest was witnessed in 90%, the initial rhythm was shockable in 88%, and 58% received bystander CPR. At the time of TTE, 41% of patients were receiving vasopressors; this group of patients was older, had greater severity of illness, higher inpatient mortality and left ventricular ejection fraction (LVEF) was modestly lower (36.8 ± 17.1% vs. 41.4 ± 16.4%, P = 0.04). Stroke volume, cardiac power output and left ventricular stroke work index correlated with number of vasopressors (Pearson r −0.24 to −0.34, all P < 0.002), but the correlation with LVEF was weak (Pearson r −0.13, P = 0.06). Conclusions: In patients after OHCA, left ventricular systolic dysfunction was associated with the need for vasopressors, and Doppler TTE hemodynamic parameters had higher correlation coefficients compared with vasopressor requirements than LVEF. This emphasizes the complex nature of shock after OHCA, including pathophysiologic processes not captured by TTE assessment alone.

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: Recent data suggests improved outcomes among cardiac intensive care unit (CICU) patients treated with norepinephrine, especially patients with severe shock. We aimed to describe the association between norepinephrine and mortality in CICU patients with severe shock, defined as those requiring high-dose vasopressors (HDV). Materials and Results: We retrospectively evaluated Mayo Clinic CICU patients treated with vasopressors from 2007 to 2015. HDV was defined as a peak Cumulative Vasopressor Index of four for any vasopressor. Peak norepinephrine equivalent (NEE) dose was used to compare vasopressor doses. Multivariable logistic regression was used to determine predictors of hospital mortality. Results: We included 2,090 patients with a median age of 69 years (IQR 59–78), including 35% females; 44% of patients received HDV. Hospital mortality was higher among patients receiving HDV (42% vs. 16%, unadjusted OR 3.87, 95% CI 3.16–4.75, P < 0.01). On multivariable analysis in HDV patients, hospital mortality increased with rising peak NEE (adjusted OR 1.02 per 0.01 mcg/kg/min, 95% CI 1.01–1.02, P < 0.01) and the use of NE was associated with lower hospital mortality (adjusted OR 0.46, 95% CI 0.31–0.72, P < 0.01). After adjustment for illness severity, peak NEE and norepinephrine use were not associated with mortality among patients who did not require HDV. Conclusions: Mortality is high among CICU patients requiring HDV, and rises with increasing vasopressor requirements. Use of NE was associated with lower mortality among patients requiring HDV, but not among those without HDV, implying that patients with more severe shock may benefit from preferential use of NE.

Background: Previous studies have defined preshock as isolated hypotension or isolated hypoperfusion, whereas shock has been variably defined as hypoperfusion with or without hypotension. We aimed to evaluate the mortality risk associated with hypotension and hypoperfusion at the time of admission in a cardiac intensive care unit population. Methods: We analyzed Mayo Clinic cardiac intensive care unit patients admitted between 2007 and 2015. Hypotension was defined as systolic blood pressure <90 mm Hg or mean arterial pressure <60 mm Hg, and hypoperfusion as admission lactate >2 mmol/L, oliguria, or rising creatinine. Associations between hypotension and hypoperfusion with hospital mortality were estimated using multivariable logistic regression. Results: Among 10 004 patients with a median age of 69 years, 43.1% had acute coronary syndrome, and 46.1% had heart failure. Isolated hypotension was present in 16.7%, isolated hypoperfusion in 15.3%, and 8.7% had both hypotension and hypoperfusion. Stepwise increases in hospital mortality were observed with hypotension and hypoperfusion compared with neither hypotension nor hypoperfusion (3.3%; all P <0.001): isolated hypotension, 9.3% (adjusted odds ratio, 1.7 [95% CI, 1.4–2.2]); isolated hypoperfusion, 17.2% (adjusted odds ratio, 2.3 [95% CI, 1.9–3.0]); both hypotension and hypoperfusion, 33.8% (adjusted odds ratio, 2.8 [95% CI, 2.1–3.6]). Adjusted hospital mortality in patients with isolated hypoperfusion was higher than in patients with isolated hypotension ( P =0.02) and not significant different from patients with both hypotension and hypoperfusion ( P =0.18). Conclusions: Hypotension and hypoperfusion are both associated with increased mortality in cardiac intensive care unit patients. Hospital mortality is higher with isolated hypoperfusion or concomitant hypotension and hypoperfusion (classic shock). We contend that preshock should refer to isolated hypotension without hypoperfusion, while patients with hypoperfusion can be considered to have shock, irrespective of blood pressure.