Jentzer, Jacob C.

Introduction Bumetanide can induce generalized musculoskeletal pain when administered as a continuous infusion, an effect that may be underrecognized. The purpose of this case series is to educate health care providers about the incidence and presentation of pain associated with bumetanide infusions, adding to the existing literature describing this adverse event. Clinical Findings Of 40 critically ill patients, 15 (38%) had increased pain scores after initiation of a continuous infusion of bumetanide, with symptoms commonly occurring 12 to 24 hours after initiation of the infusion. Reported descriptions of the pain included generalized aching, soreness, burning, allodynia, headaches, and exacerbation of underlying pain in localized areas. Increases in patient-reported pain correlated directly with initiation of the continuous infusion of bumetanide. Diagnosis Four of the 15 bumetanide-associated pain events (27%) were recognized as such by the health care team. Interventions Bumetanide was promptly discontinued in the 4 identified cases. The 11 patients (73%) whose pain was not recognized as related to bumetanide remained on a continuous infusion of bumetanide and received pain medications including opioids. Infusions were stopped when patients transitioned to dialysis (n = 8 [53%]), began receiving comfort care (n = 5 [33%]), or completed diuresis therapy (n = 2 [13%]). Outcomes For all patients, pain symptoms resolved within 24 to 48 hours after discontinuation of bumetanide infusion with no significant electrolyte abnormalities. Conclusion Bumetanide-induced pain is more common than previously described. Early recognition of this adverse event can prevent patient discomfort and escalation of treatment.

Background Impaired right ventricular (RV) pulmonary artery coupling has been associated with higher mortality in patients with chronic heart disease, but few studies have examined this metric in critically ill patients. We sought to evaluate the association between RV pulmonary artery coupling, defined by the ratio of tricuspid annular peak systolic tissue Doppler velocity (TASV)/estimated RV systolic pressure (RVSP), and mortality in cardiac intensive care unit patients. Methods and Results Using a database of unique cardiac intensive care unit admissions from 2007 to 2018, we included patients with TASV/RVSP ratio measured within 1 day of hospitalization. Hospital mortality was analyzed using multivariable logistic regression, and 1‐year mortality was analyzed using multivariable Cox proportional‐hazards analysis. We included 4259 patients with a mean age of 69±15 years (40.1% women). Admission diagnoses included acute coronary syndrome in 56%, heart failure in 52%, respiratory failure in 24%, and cardiogenic shock in 12%. The mean TASV/RVSP ratio was 0.31±0.14, and in‐hospital mortality occurred in 7% of patients. Higher TASV/RVSP ratio was associated with lower in‐hospital mortality (adjusted unit odds ratio, 0.68 per each 0.1‐unit higher ratio; 95% CI, 0.58–0.79; P <0.001) and lower 1‐year mortality among hospital survivors (adjusted unit hazard ratio, 0.83 per each 0.1‐unit higher ratio; 95% CI, 0.77–0.90; P <0.001). Stepwise decreases in hospital and 1‐year mortality were observed in each higher TASV/RVSP quintile. The TASV/RVSP ratio remained associated with mortality after adjusting for left ventricular systolic and diastolic function. Conclusions A low TASV/RVSP ratio is associated with increased short‐term and long‐term mortality among cardiac intensive care unit patients, emphasizing importance of impaired RV pulmonary artery coupling as a determinant of poor prognosis. Further study is required to determine whether interventions to optimize RV pulmonary artery coupling can improve outcomes.

Purpose: To describe the epidemiology, outcomes, and temporal trends of respiratory failure in the cardiac intensive care unit (CICU). Materials and Methods: Retrospective cohort analysis of 2,986 unique Mayo Clinic CICU patients from 2007 to 2018 with respiratory failure. Temporal trends were analyzed, along with hospital and 1-year mortality. Multivariable logistic regression was used to determine adjusted hospital mortality trends. Results: The prevalence of respiratory failure in the CICU increased from 15% to 38% during the study period ( P < 0.001 for trend). Among patients with respiratory failure, the utilization of invasive ventilation decreased and noninvasive ventilation modalities increased over time. Hospital mortality and 1-year mortality were 24% and 54%, respectively, with variation according to the type of respiratory support (highest among patients receiving invasive ventilation alone: 35% and 46%, respectively). Hospital mortality was highest among patients with concomitant cardiac arrest and/or shock (52% for patients with both). Hospital mortality decreased in the overall population from 35% to 25% ( P < 0.001 for trend), but was unchanged among patients receiving positive-pressure ventilation. Conclusions: The prevalence of respiratory failure in CICU more than doubled during the last decade. The use of noninvasive respiratory support increased, while overall mortality declined over time. Cardiac arrest and shock accounted for the majority of deaths. Further research is needed to optimize the outcomes of high-risk CICU patients with respiratory failure.

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.

We present an adolescent African American male admitted to the cardiac intensive care unit with cardiogenic shock and acute respiratory failure. Through an overview of his presentation, diagnostic workup, and treatment, we demonstrate the clinical utility of genetic testing in the evaluation of unexplained dilated cardiomyopathies.

AbstractDespite the widespread adoption of primary percutaneous intervention and modern antithrombotic therapy, ST-segment elevation myocardial infarction (STEMI) remains the leading cause of death in the United States and remains one of the most important causes of morbidity and mortality worldwide. Certain high-risk patients present a challenge for diagnosis and treatment. The widespread adoption of primary percutaneous intervention in addition to modern antithrombotic therapy has resulted in substantial improvement in the short- and long-term prognosis following STEMI. In this review, we aim to provide a brief analysis of the state-of-the-art treatment for patients presenting with STEMI, focusing on cardiogenic shock, current treatment and controversies, cardiac arrest, and diagnosis and treatment of mechanical complications, as well as multivessel and left main-related STEMI.

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.

AbstractAimsCardiogenic shock (CS) is associated with poor outcomes in older patients, but it remains unclear if this is due to higher shock severity. We sought to determine the associations between age and shock severity on mortality among patients with CS.Methods and resultsPatients with a diagnosis of CS from Mayo Clinic (2007–15) and University Clinic Hamburg (2009–17) were subdivided by age. Shock severity was graded using the Society for Cardiovascular Angiography and Intervention (SCAI) shock stages. Predictors of 30-day survival were determined using Cox proportional-hazards analysis. We included 1749 patients (934 from Mayo Clinic and 815 from University Clinic Hamburg), with a mean age of 67.6 ± 14.6 years, including 33.6% females. Acute coronary syndrome was the cause of CS in 54.0%. The distribution of SCAI shock stages was 24.1%; C, 28.0%; D, 33.2%; and E, 14.8%. Older patients had similar overall shock severity, more co-morbidities, worse kidney function, and decreased use of mechanical circulatory support compared to younger patients. Overall 30-day survival was 53.3% and progressively decreased as age or SCAI shock stage increased, with a clear gradient towards lower 30-day survival as a function of increasing age and SCAI shock stage. Progressively older age groups had incrementally lower adjusted 30-day survival than patients aged &lt;50 years.ConclusionOlder patients with CS have lower short-term survival, despite similar shock severity, with a high risk of death in older patients with more severe shock. Further research is needed to determine the optimal treatment strategies for older CS patients.

Abstract Aims An artificial intelligence-augmented electrocardiogram (AI-ECG) algorithm can identify left ventricular systolic dysfunction (LVSD). We sought to determine whether this AI-ECG algorithm could stratify mortality risk in cardiac intensive care unit (CICU) patients, independent of the presence of LVSD by transthoracic echocardiography (TTE). Methods and results We included 11 266 unique Mayo Clinic CICU patients admitted from 2007 to 2018 who underwent AI-ECG after CICU admission. Left ventricular ejection fraction (LVEF) data were extracted for patients with a TTE during hospitalization. Hospital mortality was analysed using multivariable logistic regression. Mean age was 68 ± 15 years, including 37% females. Higher AI-ECG probability of LVSD remained associated with higher hospital mortality [adjusted odds ratio (OR) 1.05 per 0.1 higher, 95% confidence interval (CI) 1.02–1.08, P = 0.003] after adjustment for LVEF, which itself was inversely related with the risk of hospital mortality (adjusted OR 0.96 per 5% higher, 95% CI 0.93–0.99, P = 0.02). Patients with available LVEF data (n = 8242) were divided based on the presence of predicted (by AI-ECG) vs. observed (by TTE) LVSD (defined as LVEF ≤ 35%), using TTE as the gold standard. A stepwise increase in hospital mortality was observed for patients with a true negative, false positive, false negative, and true positive AI-ECG. Conclusion The AI-ECG prediction of LVSD is associated with hospital mortality in CICU patients, affording risk stratification in addition to that provided by echocardiographic LVEF. Our results emphasize the prognostic value of electrocardiographic patterns reflecting underlying myocardial disease that are recognized by the AI-ECG.