Lipps, Kirsten

Background There is limited evidence on the epidemiology and prognostic significance of acid-base disorders in the cardiovascular intensive care unit (CICU). This study examines the association of acid-base status at admission with in-hospital mortality among CICU patients. Methods We conducted a retrospective analysis of adults admitted to the Mayo Clinic CICU from 2007-2018 with available blood gas data, utilizing values obtained closest to CICU admission. Arterial pH, serum bicarbonate, base excess, and partial pressure of carbon dioxide (PaCO 2 ) were examined as predictors of in-hospital mortality. Multivariable logistic regression was used to assess associations, with adjustment for demographics, comorbidities, illness severity, and interventions. Results Among 3229 patients included for analysis, acidemia (pH < 7.35) emerged as the strongest predictor of in-hospital mortality (adjusted odds ratio [aOR] 1.60, 95% confidence interval [CI] 1.29-1.98, P < .003). Metabolic acidosis (HCO3 < 20 mEq/L, aOR 1.55, 95% CI 1.24-1.95, P < .001) and respiratory acidosis (PaCO2 > 45 mm Hg, aOR 1.44, 95% CI 1.14-1.81, P = .002) were associated with higher in-hospital mortality, whereas metabolic and respiratory alkalosis were not. After adjustment, lower pH and more negative base excess were associated with higher in-hospital mortality (both P < .001), whereas HCO3 and PaCO2 were not ( P = .053 and P = .051, respectively). Patients with combined metabolic and respiratory acidosis had the highest in-hospital mortality (56.3%). Conclusions Short-term survival in CICU patients decreases progressively with worse acidemia, especially in the context of combined metabolic and respiratory acidosis. Incorporating metabolic acid-base disorders as key therapeutic targets in randomized cardiogenic shock trials may improve outcomes in this complex population by addressing hemometabolic shock.

Background: Whether oral anticoagulation (OAC) can be discontinued after the resolution of left ventricular thrombus (LVT) remains controversial, particularly in patients without risk factors such as left ventricular aneurysms. This study aimed to identify patients who may safely discontinue OAC. Methods: We conducted a retrospective cohort study of patients with LVT resolution who completed their anticoagulation course and excluded patients with left ventricular (LV) aneurysm. Clinical and echocardiographic factors were compared between patients who experienced LVT recurrence (n = 22) and those without recurrence during follow-up (n = 94). Results: The cohort had a mean age of 64.5 ± 15.0 years, and half (50%) were male. Most had an ischemic cardiomyopathy (64.6%). LVT recurred in 19% (22/116) of patients following initial resolution. Patients with recurrence were older (mean age 71.3 ± 11.9 vs. 63.4 ± 15.7 years, p = 0.03) and were more likely to have prior ischemic stroke and arterial thromboembolism (18.2% vs. 4.3%, p = 0.02 for both). At the time of thrombus resolution, LVEF was significantly lower among patients who had recurrence (33.4 ± 13.6% vs. 42.5 ± 15.5%, p = 0.012). Stroke, systemic embolism, and mortality rates were similar regardless of recurrence status. Recurrence risk by presence or absence of stroke and LEVF >50% on the LVT resolution echocardiogram is shown in Figure 1. Notably, no recurrences were observed among patients with both LVEF > 50% and no history of stroke (0/32), which was statistically significant compared to each other category. Conclusion: Among patients without left ventricular aneurysm who discontinued oral anticoagulation after LVT resolution, those with preserved LVEF (>50%) and no prior history of stroke had a very low risk of recurrence, with no events observed in this subgroup. These findings suggest that some patients may safely discontinue anticoagulation after LVT resolution.

Introduction: Pressure-adjusted heart rate (PAHR) provides an integrated assessment of hemodynamic decompensation in critically ill patients. Research Question: How does PAHR perform in critically ill patients with cardiovascular disease? Aims: We sought to evaluate the prognostic value of PAHR on mortality in patients admitted to the cardiovascular intensive care unit (CICU). Methods: A retrospective cohort of patients admitted to the CICU at a tertiary-care academic institution, between 2007 and 2018, who had a transthoracic echocardiogram (TTE) within one day of admission were evaluated. Heart rate (HR), right atrial pressure (RAP), and mean arterial pressure (MAP), obtained from TTE, were used to calculate PAHR as RAP * HR / MAP. Results: Among 5411 patients included for analysis (median age 70.1 years, 38.6% female, 92.4% White), higher PAHR was associated with greater severity of acute illness, burden of comorbidities, and use of critical care therapies. Median values (25 th percentile, 75 th percentile) for HR were 73.0 (63.0, 87.0) beats per minute (bpm), RAP 10.0 (5.0, 14.0) mm Hg, and MAP 81.3 (72.3, 91.7) mm Hg. Median PAHR was significantly higher among patients who died during hospitalization (14.3 bpm vs 6.8 bpm, p <0.001). In addition, TTE measurements of biventricular function, intracardiac filling pressures, and cardiac output were worse among those with higher PAHR (Table). Adjusted in-hospital mortality increased incrementally with higher PAHR, regardless of admission diagnosis, biventricular function, and critical care therapies (adjusted odds ratio [OR] 1.03 per 1 bpm higher, 95% confidence interval [CI] 1.01-1.05, p = 0.001; adjusted OR per quartile 1.37, 95% CI 1.19-1.59, p <0.001, Figure 1). Similarly, one-year mortality increased incrementally with higher PAHR (adjusted hazard ratio 1.03 per 1 bpm higher, 95% CI 1.02-1.04, p <0.001, Figure 2). When compared to component values, including the modified shock index, which is defined by HR / MAP, PAHR had the highest area under the curve (C-statistic 0.75). Conclusions: PAHR is a readily determinable composite measure of filling pressures and vascular resistance that enhances clinical risk stratification of critically ill patients by TTE. Among a diverse cohort of CICU patients, higher PAHR was associated with greater in-hospital and one-year mortality, regardless of admission diagnosis, biventricular function, or illness severity.

Background: Little is known about the epidemiology and prognostic significance of acid-base disturbances in the cardiovascular intensive care unit (CICU). This study examines the association of acid-base status at admission with in-hospital mortality among CICU patients. Methods: We conducted a retrospective analysis of adults admitted to the Mayo Clinic CICU from 2007-2018 who had available blood gas data, utilizing laboratory values obtained closest to the time of CICU admission. Arterial pH, serum bicarbonate, base excess, and partial pressure of carbon dioxide (PaCO 2 ) were examined as predictors of in-hospital mortality. Logistic regression models were used to assess associations, with adjustment for demographics, comorbidities, illness severity, and interventions. A composite acidosis score (CAS, range 0–5), incorporating predefined cut-offs for arterial pH, base excess, and anion gap was calculated to quantify acid-base disturbance severity. Results: A total of 3,229 patients were included for analysis. Of all acid-base variables, acidemia (pH<7.35) emerged as the strongest predictor of in-hospital mortality (adjusted odds ratio [aOR] 1.60, 95% confidence interval [CI] 1.29-1.98, p <0.003). Metabolic acidosis (HCO 3 <20 mEq/L) aOR 1.55, 95% CI 1.24-1.95, p <0.001) and respiratory acidosis (PaCO 2 >45 mmHg, aOR 1.44, 95% CI 1.14-1.81, p =0.002) were associated with worse adjusted in-hospital mortality, whereas alkalemia, metabolic alkalosis, and respiratory alkalosis were not (Fig. 1A-C). After adjustment, lower pH and more negative base excess were associated with higher in-hospital mortality (both p <0.001), whereas HCO 3 and PaCO 2 were not ( p =0.053&p=0.051, respectively; Fig. 2). Patients with combined metabolic and respiratory acidosis had the highest in-hospital mortality (56.3%), followed by patients with isolated or compensated metabolic acidosis (Fig.1D). Patients with severe acidosis (CAS>1) had higher mortality (aOR 2.34, 95% CI 1.88–2.90; p<0.001, Fig. 3AB). In-hospital mortality rose with increasing CAS (aOR 1.36 per point higher, 95% CI 1.26–1.47; p<0.001), with consistent effects across admission diagnoses (Fig. 3C). Conclusions: Acidemia, especially in the context of combined metabolic and respiratory acidosis, strongly predicts in-hospital mortality in the CICU. Incorporating combined acid-base disorders into risk stratification scores may facilitate earlier recognition and prevent progression of hemometabolic shock, thereby improving prognosis.