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Erschienen in: Critical Care 1/2020

Open Access 19.05.2020 | COVID-19 | Research Letter

Cardiovascular phenotypes in ventilated patients with COVID-19 acute respiratory distress syndrome

verfasst von: Bruno Evrard, Marine Goudelin, Noelie Montmagnon, Anne-Laure Fedou, Thomas Lafon, Philippe Vignon

Erschienen in: Critical Care | Ausgabe 1/2020

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Abkürzungen
ACP
Acute cor pulmonale
ARDS
Acute respiratory distress syndrome
COVID-19
Coronavirus disease 2019
ICU
Intensive care unit
LV
Left ventricle
RV
Right ventricle
SAPS II
Simplified acute physiology score II
SOFA
Sepsis-related organ failure assessment
Approximately two-thirds of patients admitted to the intensive care unit (ICU) for coronavirus disease-19 (COVID-19) pneumonia present with the acute respiratory distress syndrome (ARDS) [1]. COVID-19-associated acute cardiac injury is frequently reported based on troponin and electrocardiographic changes [2], but its impact on cardiac function is yet unknown [3]. Accordingly, we sought to describe cardiovascular phenotypes identified using transesophageal echocardiography (TEE) in ventilated COVID-19 patients with ARDS and to compare them to those of patients with flu-induced ARDS.
All patients with confirmed COVID-19 who were mechanically ventilated for ARDS in our medical-surgical ICU underwent prospectively a TEE assessment during the first 3 days and whenever required by clinical events during ICU stay, as a standard of care. Similarly, all patients ventilated for flu-associated ARDS who underwent a TEE assessment over the last 2 years were retrospectively analyzed for comparison. Cardiovascular phenotypes were identified using previously reported TEE criteria [4]. Same applied for acute cor pulmonale (ACP) [5]. TEE studies were read by two independent experts who had no access to the cause of ARDS and examination date. Results are expressed as medians and 25th–75th percentiles. Friedman ANOVA was used to compare quantitative parameters over time in COVID-19 patients, while Mann-Whitney U test and Fisher’s exact test were used for comparison of continuous and categorical variables, respectively, with flu patients. No use of previous value or interpolation rule was used in the presence of missing data.
Eighteen consecutive COVID-19 patients and 23 flu patients (21 A-H1N1) were studied. COVID-19 patients were significantly older (70 [57–75] vs. 58 [49–64] years, p = 0.006), less severe (SAPSII 34 [30–38] vs. 43 [32–54], p = 0.015; SOFA 4 [2–4] vs. 6 [4–9], p < 0.001), required less vasopressor support (2/18 [11%] vs. 10/23 [43%], p = 0.038), and had longer time lag between first symptoms and ICU admission, tracheal intubation, and TEE examination when compared to flu patients (Table 1). The prevalence of left ventricular (LV) failure (3/18 [17%] vs. 14/23 [61%], p = 0.009), ACP (3/18 [17%] vs. 11/23 [48%], p = 0.051), and severe ACP (1/18 [5.5%] vs. 8/23 [35%], p = 0.054) was significantly lower in COVID-19 patients. Hypovolemic and hyperkinetic phenotypes were similarly observed in both groups (Table 1). Despite similar tidal volume and PEEP level, COVID-19 patients had significantly higher P/F ratio and respiratory-system compliance, and lower driving pressure than flu patients (Table 1). Pulmonary embolism was identified in none of COVID-19 patients but in one flu patient with ACP. COVID-19 patients with ACP tended to exhibit lower respiratory-system compliance (34, 32, and 30 mL/cmH2O) when compared to others (40 [31–45] mL/cmH2O). Hemodynamic profile of COVID-19 patients remained stable during the first 3 days of ICU stay (Table 2).
Table 1
Characteristics, presentation and outcome of ventilated patients with COVID-19 and flu-related ARDS
 
COVID-19 (n = 18)
Flu (n = 23)
p value
Patients’ characteristics
 Age, years
70 (57–75)
58 (49–64)
0.006
 Male (%)
12 (67)
12 (52)
0.524
 BMI, kg/m2
29 (26–32)
29 (25–34)
0.519
 Hypertension (%)
11 (61)
10 (43)
0.350
 Diabetes mellitus (%)
4 (22)
3 (13)
0.679
 Time from illness onset to ICU admission, days
11 (7–13)
5 (4–10)
0.017
 Time from illness onset to intubation, days
12 (8–15)
6 (4–10)
0.002
 Time from illness onset to echocardiography, days
14 (9–17)
13 (6–17)
0.001
 SAPS II
34 (30–38)
43 (32–54)
0.015
 SOFA score
4 (2–4)
6 (4–9)
< 0.001
Clinical presentation and treatment
 ECG changes* (%)
1 (5%)
3 (13%)
0.618
 Documented coinfection (%)
3 (17)
9 (39)
0.171
 Septic shock (%)
0 (%)
10 (43)
 Vasopressor support (%)
2 (11)
10 (43)
0.038
 Prone position (%)
10 (56)
14 (61)
1.000
 Neuromuscular blockers (%)
17 (94%)
12 (52%)
0.005
Biology on admission
 Troponin I (ng/L)
73 (51–94)
53 (37–66)
0.020
 Lactate, mmol/L
1.17 (0.89–1.57)
1.51 (1.02–2.54)
0.143
 Creatinine, μmol/L
58 (42–87)
88 (59–160)
0.021
 Prothombine time, %
87 (78–96)
87 (71–101)
0.979
 AST, U/L
55 (27–71)
107 (46–203)
0.020
 ALT, U/L
37 (27–65)
45 (27–115)
0.527
 CPK, U/L
72 (34–103)
419 (180–2456)
< 0.001
 White blood cell count, G/L
7.98 (6.61–11.25)
5.96 (4.02–8.05)
0.003
 Lymphocyte count, G/L
0,78 (0.55–1.05)
0.75 (0.47–1.13)
0.770
 Eosinophils count, G/L
0.02 (0.02–0.09)
0.01 (0.00–0.01)
0.094
 Platelet count, G/L
318 (218–425)
172 (153–225)
< 0.001
 Hemoglobin, g/dl
11.2 (10.2–12.3)
13.1 (11.6–14.2)
0.007
Respiratory parameters
 PaO2/FiO2
130 (81–217)
70 (62–100)
< 0.001
 Arterial pH
7.35 (7.29–7.45)
7.32 (7.23–7.41)
0.121
 PaCO2, mmHg
44 (33–51)
47 (36–60)
0.430
 RR, breaths/min
24 (22–27)
25 (24–28)
0.139
 Tidal volume, mL/kg
5.2 (4.5–6.2)
5.3 (4.0–6.1)
0.885
 PEEP, cmH2O
10 (8–12)
10 (8–12)
0.476
 Plateau pressure, cmH2O
23 (20–26)
28 (20–28)
0.144
 Driving pressure, cmH2O
12 (10–15)
18 (17–18)
0.001
 Respiratory-system compliance**, mL/cmH2O
38 (31–45)
23 (22–27)
0.001
Hemodynamic parameters
 Heart rate, bpm
90 (72–109)
105 (69–118)
0.494
 Mean arterial blood pressure, mmHg
102 (85–110)
78 (71–94)
< 0.001
 CVP, mmHg
9 (7–10)
11 (9–14)
0.058
Cardiovascular phenotypes
 ACP (%)
3 (17)
11 (48)
0.051
 Severe ACP (%)
1 (5)
8 (35)
0.054
 LV failure
3*** (17)
14 (61)
0.009
 Hypovolemia
2 (11)
1 (4)
0.573
 Hyperkinesia
6 (33)
7 (30)
1.00
 Normal hemodynamic profile
8 (44)
5 (22)
0.179
Echocardiographic indices
 Cardiac index**** (L/min/m2)
3.1 (2.5–4.2)
2.5 (2.0–3.0)
0.034
 RVEDA/LVEDA
0.55 (0.37–0.60)
0.70 (0.54–0.80)
0.021
 RVFAC, %
46 (35–50)
33 (24–39)
0.002
 TAPSE, mm
25 (23–29)
18 (16–22)
< 0.001
 Tricuspid S′, cm/s
16.0 (15.0–20.5)
12.2 (11.0–13.4)
0.005
 TR peak velocity, m/s
3.2 (2.9–3.6)
2.9 (2.4–3.2)
0.113
 IVC diameter, mm
22 (19–26)
22 (21–24)
0.762
 LVEF (%)
52 (44–61)
44 (28–59)
0.265
 LVOT VTI, cm
22 (18–25)
18 (13–24)
0.106
 Mitral E/E′ ratio
7.3 (6.5–10.9)
7.8 (6.1–10.6)
0.730
Outcome
 ICU mortality***** (%)
1 (6)
9 (39)
0.025
Abbreviations: BMI body mass index, SAPSII Simplified Acute Physiology Score, SOFA Sepsis Organ Failure Assessment, AST aspartate aminotransferase, ALT alanine aminotransferase, CPK creatinine phosphokinase, RR respiratory rate, PEEP positive end-expiratory pressure, CVP central venous pressure, ACP acute cor pulmonale, LV left ventricle, RVEDA right ventricular end-diastolic area, LVEDA left ventricular end-diastolic area, RVFAC right ventricular fractional area change, TAPSE tricuspid annular plane systolic excursion, TR tricuspid regurgitation, IVC inferior vena cava, LVEF left ventricular ejection fraction, LVOT left ventricular outflow tract, VTI velocity-time integral, ICU intensive care unit
*One patient had anterior negative T-wave in the COVID-19 group; 2 patients had inferior negative T-wave, and 1 patient had anterior negative T-wave in the flu group [2]
**Calculated as the tidal volume divided by the driving pressure (difference between the inspiratory plateau pressure and positive end-expiratory pressure)
***One patient was diagnosed with a Tako-tsubo syndrome during transesophageal echocardiography examination performed shortly after tracheal intubation, after 6 days of high-flow nasal cannula; full recovery of left ventricular systolic function was documented under mechanical ventilation 10 days later
****Measured using the Doppler method applied at the left ventricular outflow tract
*****As per April 24, with still 6 patients hospitalized in the intensive care unit, 5 of them being invasively ventilated
Table 2
Evolution of hemodynamic profile during daily transesophageal echocardiography assessments of COVID-19 patients ventilated for ARDS
 
Day 1 (n = 18)
Day 2 (n = 10)
Day 3 (n = 12)
p value
Respiratory parameters
 PaO2/FiO2
130 (81–217)
128 (100–210)
137 (98–187)
0.066
 PaCO2, mmHg
44 (33–51)
50 (32–56)
47 (37–57)
0.964
 RR, breaths/min
24 (22–27)
27 (20–28)
24 (24–30)
0.651
 PEEP, cmH2O
10 (8–12)
10 (8–13)
10 (10–12)
0.444
 Plateau pressure, cmH2O
23 (20–26)
22 (18–27)
24 (21–27)
0.127
 Driving pressure, cmH2O
12 (10–15)
11 (9–12)
13 (11–17)
0.368
 Tidal volume, mL/kg
5.2 (4.5–6.2)
5.3 (4.6–6.6)
5.5 (4.3–6.7)
0.210
 Respiratory-system compliance*, mL/cmH2O
38 (31–45)
33 (33–53)
37 (28–45)
0.692
Hemodynamic parameters
 Heart rate, bpm
90 (72–109)
93 (78–107)
98 (89–104)
0.368
 CVP, mmHg
9 (7–10)
7 (6–10)
9 (5–13)
0.678
 Mean blood pressure, mmHg
102 (85–110)
105 (87–110)
95 (84–109)
0.102
 Lactate, mmol/L
1.17 (0.89–1.57)
1.85 (1.24–3.01)
1.62 (1.49–1.95)
0.264
Echocardiography indices
 Cardiac index (L/min/m2)**
3.1 (2.5–4.2)
2.8 (2.6–3.9)
4.1 (3.2–4.8)
0.115
 RVEDA/LVEDA
0.55 (0.37–0.60)
0.53 (0.35–0.66)
0.55 (0.48–0.58)
0.549
 RVFAC, %
46 (35–50)
40 (33–46)
40 (32–58)
0.821
 TAPSE, mm
25 (23–29)
24 (20–28)
25 (23–28)
0.368
 Tricuspid S′, cm/s
16.0 (15.0–20.5)
16.1 (14.0–18.1)
16.8 (14.9–19.9)
0.867
 TR peak velocity, m/s
3.2 (2.9–3.6)
3.0 (2.7–3.7)
3.6 (2.4–3.9)
0.060
 IVC diameter, mm
22 (19–26)
24 (14–30)
22 (17–24)
1.000
 LVEF, %
52 (44–61)
46 (41–64)
55 (49–60)
0.549
Abbreviations: RR respiratory rate, PEEP positive end-expiratory pressure, CVP central venous pressure, RVEDA right ventricular end-diastolic area, LVEDA left ventricular end-diastolic area, RVFAC right ventricular fractional area change, TAPSE tricuspid annular plane systolic excursion, TR tricuspid regurgitation, IVC inferior vena cava, LVEF left ventricular ejection fraction
*Calculated as the tidal volume divided by the driving pressure (difference between the inspiratory plateau pressure and positive end-expiratory pressure)
**Measured using the Doppler method applied at the left ventricular outflow tract
The higher prevalence of LV failure and lower cardiac index in patients with flu-related ARDS is presumably related to septic cardiomyopathy since they sustained associated septic shock more frequently than COVID-19 patients. Depressed indices of RV systolic function and elevated central venous pressure reflecting systemic venous congestion reflect the higher prevalence of RV failure in flu ARDS patients (Table 1). This presumably results from the lower P/F, higher driving pressure, and lower respiratory-system compliance observed in this group. COVID-19 patients with ACP tended to have lower respiratory-system compliance than their counterparts, presumably due to distinct ARDS phenotypes [6]. This pilot study is limited by its small sample size and the retrospective comparison with historical flu-related ARDS patients.
This first study assessing hemodynamically ventilated COVID-19 patients with TEE shows a lower prevalence of LV and RV failure than in flu-related ARDS patients. Whether herein reported cardiovascular phenotypes are influenced by the type of COVID-19 ARDS remains to be determined [6]. These preliminary data warrant confirmation in large-scale multicenter cohorts.

Acknowledgements

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Local Ethical Committee approval #368-2020-24, which waived the need for informed consent. All patients agreed on the use of anonymized information as per the French law on the General Data Protection Regulation (GDPR).
N/A

Competing interests

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Metadaten
Titel
Cardiovascular phenotypes in ventilated patients with COVID-19 acute respiratory distress syndrome
verfasst von
Bruno Evrard
Marine Goudelin
Noelie Montmagnon
Anne-Laure Fedou
Thomas Lafon
Philippe Vignon
Publikationsdatum
19.05.2020
Verlag
BioMed Central
Schlagwort
COVID-19
Erschienen in
Critical Care / Ausgabe 1/2020
Elektronische ISSN: 1364-8535
DOI
https://doi.org/10.1186/s13054-020-02958-8

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