CARDIAC OUTPUT IN CRITICALLY ILL PATIENTS CAN BE ESTIMATED EASILY AND ACCURATELY USING THE MINUTE DISTANCE OBTAINED BY PULSED-WAVE DOPPLER.

ABSTRACT: Background: Cardiac output (CO) assessment is essential for management of patients with circulatory failure. Among the different techniques used for their assessment, pulsed-wave Doppler cardiac output (PWD-CO) has proven to be an accurate and useful tool. Despite this, assessment of PWD-CO could have some technical difficulties, especially in the measurement of left ventricular outflow tract diameter (LVOTd). The use of a parameter such as minute distance (MD) which avoids LVOTd in the PWD-CO formula could be a simple and useful way to assess the CO in critically ill patients. Therefore, the aim of this study was to evaluate the correlation and agreement between PWD-CO and MD. Methods: A prospective and observational study was conducted over 2 years in a 30-bed intensive care unit (ICU). Adult patients who required CO monitoring were included. Clinical echocardiographic data were collected within the first 24 h and at least once more during the first week of ICU stay. PWD-CO was calculated using the average value of three LVOTd and left ventricular outflow tract velocity-time integral (LVOT-VTI) measurements, and heart rate. Minute distance was obtained from the product of LVOT-VTI × heart rate. Pulsed-wave Doppler cardiac output was correlated with MD using linear regression. Cardiac output was quantified from the MD using the equation defined by linear regression. Bland-Altman analysis was also used to evaluate the level of agreement between CO calculated from MD (MD-CO) and PWD-CO. The percentage error was calculated. Results: A total of 98 patients and 167 CO measurements were analyzed. Sixty-seven (68%) were male, the median age was 66 years (interquartile range [IQR], 53-75 years), and the median Acute Physiology and Chronic Health Evaluation II score was 22 (IQR, 16-26). The most common cause of admission was shock in 81 patients (82.7%). Sixty-nine patients (70.4%) were mechanically ventilated, and 68 (70%) required vasoactive drugs. The median CO was 5.5 L/min (IQR, 4.8-6.6 L/min), and the median MD was 1,850 cm/min (IQR, 1,520-2,160 cm/min). There was a significant correlation between PWD-CO and MD-CO in the general population ( R2 = 0.7; P < 0.05). This correlation improved when left ventricular ejection fraction (LVEF) was less than 60% ( R2 = 0.85, P < 0.05). Bland-Altman analysis showed good agreement between PWD-CO and MD-CO in the general population, the median bias was 0.02 L/min, the limits of agreement were -1.92 to +1.92 L/min. The agreement was better in patients with LVEF less than 60% with a median bias of 0.005 L/min and limits of agreement of -1.56 to 1.55 L/min. The percentage error was 17% in both cases. Conclusion: Measurement of MD in critically ill patients provides a simple and accurate estimate of CO, especially in patients with reduced or preserved LVEF. This would allow earlier cardiovascular assessment in patients with circulatory failure, which is of particular interest in difficult clinical or technical conditions.

[Prognostic implications of myocardial injury in patients with and without COVID-19 infection treated in a university hospital]. / Implicaciones pronósticas del daño miocárdico en pacientes con y sin diagnóstico confirmado de COVID-19 atendidos en un hospital universitario.

INTRODUCTION AND OBJECTIVES: Cardiac troponin, a marker of myocardial injury, is frequently observed in patients with COVID-19 infection. Our objective was to analyze myocardial injury and its prognostic implications in patients with and without COVID-19 infection treated in the same period of time. METHODS: The present study included patients treated in a university hospital with cardiac troponin I measurements and with suspected COVID-19 infection, confirmed or ruled out by polymerase chain reaction analysis. The impact was analyzed of cardiac troponin I positivity on 30-day mortality. RESULTS: In total, 433 patients were distributed among the following groups: confirmed COVID-19 (n = 186), 22% with myocardial injury (n = 41); and ruled out COVID-19 (n = 247), 21.5% with myocardial injury (n = 52). The confirmed and ruled out COVID-19 groups had a similar age, sex, and cardiovascular history. Mortality was significantly higher in the confirmed COVID-19 group than in the ruled out group (19.9% vs 5.3%, P < .001). In Cox multivariate regression analysis, cardiac troponin I was a predictor of mortality in both groups (confirmed COVID-19 group: HR, 3.54; 95%CI, 1.70-7.34; P = .001; ruled out COVID-19 group: HR, 5.57; 95%CI, 1.70-18.20; P = .004). The predictive model analyzed by ROC curves was similar in the 2 groups (P = .701), with AUCs of 0.808 in the confirmed COVID-19 group (0.750-0.865) and 0.812 in the ruled out COVID-19 group (0.760-0.864). CONCLUSIONS: Myocardial injury is detected in 1 in every 5 patients with confirmed or ruled out COVID-19 and predicts 30-day mortality to a similar extent in both circumstances.

Prognostic implications of myocardial injury in patients with and without COVID-19 infection treated in a university hospital.

INTRODUCTION AND OBJECTIVES: Cardiac troponin, a marker of myocardial injury, is frequently observed in patients with COVID-19 infection. Our objective was to analyze myocardial injury and its prognostic implications in patients with and without COVID-19 infection treated in the same period of time. METHODS: The present study included patients treated in a university hospital with cardiac troponin I measurements and with suspected COVID-19 infection, confirmed or ruled out by polymerase chain reaction analysis. The impact was analyzed of cardiac troponin I positivity on 30-day mortality. RESULTS: In total, 433 patients were distributed among the following groups: confirmed COVID-19 (n=186), 22% with myocardial injury (n=41); and ruled out COVID-19 (n=247), 21.5% with myocardial injury (n=52). The confirmed and ruled out COVID-19 groups had a similar age, sex, and cardiovascular history. Mortality was significantly higher in the confirmed COVID-19 group than in the ruled out group (19.9% vs 5.3%, P <.001). In Cox multivariate regression analysis, cardiac troponin I was a predictor of mortality in both groups (confirmed COVID-19 group: HR, 3.54; 95%CI, 1.70-7.34; P=.001; ruled out COVID-19 group: HR, 5.57; 95%CI, 1.70-18.20; P=.004). The predictive model analyzed by ROC curves was similar in the 2 groups (P=.701), with AUCs of 0.808 in the confirmed COVID-19 group (0.750-0.865) and 0.812 in the ruled out COVID-19 group (0.760-0.864). CONCLUSIONS: Myocardial injury is detected in 1 in every 5 patients with confirmed or ruled out COVID-19 and predicts 30-day mortality to a similar extent in both circumstances.

Basic critical care echocardiography training of intensivists allows reproducible and reliable measurements of cardiac output.

BACKGROUND: Although pulmonary artery catheters (PACs) have been the reference standard for calculating cardiac output, echocardiographic estimation of cardiac output (CO) by cardiologists has shown high accuracy compared to PAC measurements. A few studies have assessed the accuracy of echocardiographic estimation of CO in critically ill patients by intensivists with basic training. The aim of this study was to evaluate the accuracy of CO measurements by intensivists with basic training using pulsed-wave Doppler ultrasound vs. PACs in critically ill patients. METHODS: Critically ill patients who required hemodynamic monitoring with a PAC were eligible for the study. Three different intensivists with basic critical care echocardiography training obtained three measurements of CO on each patient. The maximum of three separate left-ventricular outflow tract diameter measurements and the mean of three LVOT velocity time integral measurements were used. The inter-observer reliability and correlation of CO measured by PACs vs. critical care echocardiography were assessed. RESULTS: A total of 20 patients were included. Data were analyzed comparing the measurements of CO by PAC vs. echocardiography. The inter-observer reliability for measuring CO by echocardiography was good based on a coefficient of intraclass correlation of 0.6 (95% CI 0.48-0.86, p < 0.001). Bias and limits of agreement between the two techniques were acceptable (0.64 ± 1.18 L/min, 95% limits of agreement of - 1.73 to 3.01 L/min). In patients with CO < 6.5 L/min, the agreement between CO measured by PAC vs. echocardiography improved (0.13 ± 0.89 L/min; 95% limits of agreement of - 1.64 to 2.22 L/min). The mean percentage of error between the two methods was 17%. CONCLUSIONS: Critical care echocardiography performed at the bedside by intensivists with basic critical care echocardiography training is an accurate and reproducible technique to measure cardiac output in critically ill patients.

[Early pleuropulmonary toxicity associated with cabergoline, an antiparkinsonian drug]. / Toxicidad pleuropulmonar precoz asociada al tratamiento con cabergolina, un fármaco antiparkinsoniano.

We report a case of pleural effusion, pericardial thickening, and pulmonary involvement in a patient with dry cough, dyspnea, edema, and changes in the skin of the lower limbs. Treatment with cabergoline (Sogilen) had been started 4 months earlier. Pleural effusion, pericardial thickening, and impaired pulmonary function (airflow obstruction, increased airway resistance, and reduced carbon monoxide diffusing capacity) were observed. The Naranjo scale pointed to a probable relationship between cabergoline and these adverse effects. We report on outcome after 2 months of follow-up, during which time there was a slow and incomplete improvement in respiratory function. This is the first case in our practice setting of early pleuropulmonary toxicity associated with cabergoline.

Community-acquired respiratory coinfection in critically ill patients with pandemic 2009 influenza A(H1N1) virus.

BACKGROUND: Little is known about the impact of community-acquired respiratory coinfection in patients with pandemic 2009 influenza A(H1N1) virus infection. METHODS: This was a prospective, observational, multicenter study conducted in 148 Spanish ICUs. RESULTS: Severe respiratory syndrome was present in 645 ICU patients. Coinfection occurred in 113 (17.5%) of patients. Streptococcus pneumoniae (in 62 patients [54.8%]) was identified as the most prevalent bacteria. Patients with coinfection at ICU admission were older (47.5±15.7 vs 43.8±14.2 years, P<.05) and presented a higher APACHE (Acute Physiology and Chronic Health Evaluation) II score (16.1±7.3 vs 13.3±7.1, P<.05) and Sequential Organ Failure Assessment (SOFA) score (7.0±3.8 vs 5.2±3.5, P<.05). No differences in comorbidities were observed. Patients who had coinfection required vasopressors (63.7% vs 39.3%, P<.05) and invasive mechanical ventilation (69% vs 58.5%, P<.05) more frequently. ICU length of stay was 3 days longer in patients who had coinfection than in patients who did not (11 [interquartile range, 5-23] vs 8 [interquartile range 4-17], P=.01). Coinfection was associated with increased ICU mortality (26.2% vs 15.5%; OR, 1.94; 95% CI, 1.21-3.09), but Cox regression analysis adjusted by potential confounders did not confirm a significant association between coinfection and ICU mortality. CONCLUSIONS: During the 2009 pandemics, the role played by bacterial coinfection in bringing patients to the ICU was not clear, S pneumoniae being the most common pathogen. This work provides clear evidence that bacterial coinfection is a contributor to increased consumption of health resources by critical patients infected with the virus and is the virus that causes critical illness in the vast majority of cases.