Vital signs of severe COVID-19 patients during inter-hospital helicopter transfer

Background: During the COVID-19 pandemic in The Netherlands, critically ill ventilated COVID-19 patients were transferred not only between hospitals by ambulance but also by the Helicopter Emergency Medical Service (HEMS). To date, little is known about the impact of helicopter transport on critically ill patients and COVID-19 patients in particular. This study was conducted to explore the impact of inter-hospital helicopter transfer on vital signs of mechanically ventilated severe COVID-19 intensive care patients, with special focus on take-off, midflight, and landing.Methods: All ventilated critically ill COVID-19 patients who were transported between April 2020 and June 2021 by the Dutch ‘Lifeliner 5’ HEMS team and who were fully monitored, including noninvasive cardiac output, were included in this study. Three 10-minute timeframes (take-off, midflight and landing) were defined for analysis. Continuous data on the vital parameters heart rate, peripheral oxygen saturation, arterial blood pressure, end-tidal CO2 and noninvasive cardiac output using electrical cardiometry were collected and stored at 1-minute intervals. Data were analydzed for differences over time within the timeframes using 1-way analysis of variance. Significant differences were checked for clinical relevance.Results: Ninety-eight patients were included in the analysis. During take-off, an increase was noticed in cardiac output (from 6.7 to 8.1 Lmin-1; P<0.0001), which was determined by a decrease in systemic vascular resistance (from 1068 to 750 dyne·s·cm−5, P<0.0001) accompanied by an increase in stroke volume (from 92.0 to 110.2 ml, P<0.0001). Other parameters were unchanged during take-off and mid-flight. During landing, cardiac output and stroke volume slightly decreased (from 7.9 to 7.1 Lmin-1, P<0.0001 and from 108.3 to 100.6 ml, P<0.0001, respectively), and total systemic vascular resistance increased (P<0.0001). Though statistically significant, the found changes were small and not clinically relevant to the medical status of the patients as judged by the attending physicians.Conclusions: Interhospital helicopter transfer of ventilated intensive care patients with COVID-19 can be performed safely and does not result in clinically relevant changes in vital signs.This study was assessed by the medical ethical committee Arnhem-Nijmegen, the Netherlands (identifier 2021-7313). The committee waived the need for informed consent. The study was registered at www.trialregister.nl (identifier NL9307).

Vital signs of severe COVID-19 patients during inter-hospital helicopter transfer

Background: During the COVID-19 pandemic in The Netherlands, critically ill ventilated COVID-19 patients were not only transferred between hospitals by ambulance, but also by the Helicopter Emergency Medical Service (HEMS). To date, little is known about the impact of helicopter transport on critically ill patients, and COVID-19 patients in particular. This study was conducted to explore the impact of inter-hospital helicopter transfer on vital signs of mechanically ventilated severe COVID-19 intensive care patients, with special focus on take-off, midflight, and landing. Methods: All ventilated critically ill COVID-19 patients who were transported between April 2020 and June 2021 by the Dutch ‘Lifeliner 5’ HEMS team and who were fully monitored including non-invasive cardiac output, were included in this study. Three 10 minute timeframes (take-off, midflight and landing) were defined for analysis. Continuous data of vital parameters heartrate, peripheral oxygen saturation, arterial blood pressure, end-tidal CO2 and non-invasive cardiac output using electrical cardiometry were collected and stored at a 1 minute interval. Data were analysed for differences over time within the timeframes using 1-way analysis of variance. Significant differences were checked for clinical relevance. Results: Ninety-eight patients were included in the analysis. During take-off an increase was noticed in cardiac output (from 6.7 to 8.1 Lmin-1; P<0.0001) which was determined by a decrease in systemic vascular resistance (from 1068 to 750 dyne·s·cm−5, P<0.0001) accompanied by an increase in stroke volume (from 92.0 to 110.2 ml, P<0.0001). Other parameters were unchanged during take-off and mid-flight. During the landing cardiac output and stroke volume slightly decreased (from 7.9 to 7.1 Lmin-1, P<0.0001 and from 108.3 to 100.6 ml, P<0.0001 respectively) and total systemic vascular resistance increased (P<0.0001). Though statistically significant, the found changes were small and not clinically relevant to the medical status of the patients as judged by the attending physicians. Conclusions: Interhospital helicopter transfer of ventilated intensive care patients with COVID-19 can be performed safely and does not result in clinically relevant changes in vital signs. This study this has been assessed by the medical ethical committee Arnhem-Nijmegen, the Netherlands (identifier 2021-7313). The committee waived the need for informed consent. The study was registered at www.trialregister.nl (identifier NL9307).

Relationship Between Left Ventricular Ejection Fraction Variation and Systemic Vascular Resistance: A Prospective Cardiovascular Magnetic Resonance Study

Introduction: This cardiovascular magnetic resonance (CMR) study aims to determine whether changes in systemic vascular resistance (SVR), obtained from CMR flow sequences, might explain the significant long-term changes in left ventricular (LV) ejection fraction (EF) observed in subjects with no cardiac disease history.Methods: Cohort subjects without any known cardiac disease but with high rates of hypertension and obesity, underwent CMR with phase-contrast sequences both at baseline and at a median follow-up of 5.2 years. Longitudinal changes in EF were analyzed for any concomitant changes in blood pressure and vascular function, notably the indexed SVR given by the formula: mean brachial blood pressure / cardiac output x body surface area.Results: A total of 118 subjects (53 ± 12 years, 52% women) were included, 26% had hypertension, and 52% were obese. Eighteen (15%) had significant EF variations between baseline and follow-up (7 increased EF and 11 decreased EF). Longitudinal changes in EF were inversely related to concomitant changes in mean and diastolic blood pressures (p = 0.030 and p = 0.027, respectively) and much more significantly to SVR (p &lt; 0.001). On average, these SVR changes were −8.08 ± 9.21 and +8.14 ± 8.28 mmHg.min.m2.L−1, respectively, in subjects with significant increases and decreases in EF, and 3.32 ± 7.53 mmHg.min.m2.L−1 in subjects with a stable EF (overall p &lt; 0.001).Conclusions: Significant EF variations are not uncommon during the long-term CMR follow-up of populations with no evident health issues except for uncomplicated hypertension and obesity. However, most of these variations are linked to SVR changes and may therefore be unrelated to any intrinsic change in LV contractility. This underscores the benefits of specifically assessing LV afterload when EF is monitored in populations at risk of vascular dysfunction.Clinical Trial Registration:ClinicalTrials.gov, identifier: NCT01716819 and NCT02430805.

342 Cardiorespiratory fitness and systemic vascular resistance: oxygen pressure as a novel marker of peripheral vascular response during cardiopulmonary exercise testing

Aims The key role of systemic vascular resistance (SVR) in cardiovascular performance during exercise has been invasively demonstrated, however no data have been non-invasively obtained by analysing SVR response using cardiopulmonary exercise testing (CPET). To investigate the relationship between SVR at peak, maximum oxygen uptake (VO2 peak), and its determinants using CPET. Methods and results 1130 consecutive subjects were enrolled; according to physiology, SVR was determined as the ratio between mean arterial pressure (MAP) and cardiac output (CO). A novel parameter, named oxygen pressure (MAP peak/VO2 peak) was also created. Mean age was 61 ± 12 years and male gender was prevalent (61%); 66% of patients had arterial hypertension, 74% dyslipidaemia, 19% diabetes, 20% had smoking habit, and 26% previous history of cardiovascular (CV) disease. Significant inverse correlations between SVR peak and VO2/kg peak (P &lt; 0.001), oxygen pulse (P &lt; 0.001), CV efficiency (P &lt; 0.001), chronotropic response (P &lt; 0.001), and oxygen uptake exaction slope (P &lt; 0.001) were found. Moreover, positive correlation between SVR peak and VE/VCO2 slope (P &lt; 0.001) was observed. After multivariate analysis, the inverse correlation between peak SVR and peak VO2 remained significant (P &lt; 0.001). Similar results were found considering oxygen pressure. Conclusions Low values of SVR at peak exercise, non-invasively evaluated with CPET, are associated with high levels of cardiorespiratory fitness. Oxygen pressure may represent a novel and simple CPET marker of peripheral vascular response to exercise, thereby representing a promising field of research in exercise medicine.

443 Arterial hypertension in aortic valve stenosis: a critical update

Aims Aortic stenosis (AS) is a very common valve disease and is associated with high mortality once it becomes symptomatic. Arterial hypertension (HT) has a high prevalence among patients with AS leading to worst left ventricle remodelling and faster degeneration of the valve. HT also seems to interfere with the assessment of the severity of AS leading to an underestimation of the real degree of stenosis. Treatment of HT in AS has historically been associated with reluctance due to both the lack of clear guidelines and the fear of adverse effects, but the most recent evidence shows as several drugs that can be used. Methods The pathophysiology of the combination of AS and HT is the association of a first fixed mechanical obstruction of the aortic root and a second obstruction due to systemic vascular resistance. Consequently, a decrease in systemic vascular resistance through, for example, the administration of vasodilators could theoretically cause a drop in systemic pressure due to the fixed mechanical obstruction given by the stenosis which prevents an increase in cardiac output. This theory was the basis for avoiding vasodilators in patients with AS. Results There is a unanimous opinion on maintaining blood pressure values of 130–139 mmHg of systolic and 70–90 mmHg of diastolic, but there is not the same agreement on which drugs to adopt to achieve the aforementioned values. Renin-Angiotensin-Aldosterone system inhibitors are certainly the first-line treatment thanks to their cardioprotective, plaque stabilizing, and antiarrhythmic effect since they are also associated with increased survival rates and greater left ventricular mass reduction in patients after surgical or transcatheter aortic valve replacement for severe AS. If blood pressure is not yet controlled, the addition of a beta-blocker should be considered: metoprolol has the greatest literature, showing not only an improvement in haemodynamic and metabolic performance but also a reduction in mortality in patients who already presented with coronary artery disease. Mineralocorticoid receptor antagonist can be used, among them eplerenone has been studied and can be useful to relieve symptoms of patients with a flare-up of heart failure by reducing the preload, provided that a close fluid and echocardiographic monitoring is implemented. Conclusions The use of phosphodiesterase 5 inhibitors can improve the haemodynamic status of patients with aortic stenosis and reduce the level of left ventricular hypertrophy, as well as improve pulmonary circulation and exercise tolerability of patients with AS, however it should be considered that in other studies sildenafil was associated with a worse clinical outcome. Calcium channel blocker are one the most used medications in patients with HT, but their use was associated with a 7-fold relative risk of all-cause mortality independent of known confounders and was also associated with an adverse effect on treadmill exercise and higher risk of all-cause mortality in patients with AS.

Is measurement of central venous pressure required to estimate systemic vascular resistance? A retrospective cohort study

Background The clinical range of central venous pressure (CVP) (typically 5 to 15 mmHg) is much less than the range of mean arterial blood pressure (60 to 120 mmHg), suggesting that CVP may have little impact on estimation of systemic vascular resistance (SVR). The accuracy and feasibility of using an arbitrary CVP rather than actual CVP for the estimation of SVR during intraoperative period is not known. Methods Using vital records obtained from patients who underwent neurological and cardiac surgery, the present study retrospectively calculated SVR using fixed values of CVP (0, 5, 10, 15, and 20 mmHg) and randomly changing values of CVP (5 to 15 mmHg) and compared these calculated SVRs with actual SVR, calculated using actual CVP. Differences between actual SVR and SVRs based on fixed and random CVPs were quantified as root mean square error (RMSE) and mean absolute percentage error (MAPE). Bland-Altman analysis and four-quadrant plot analysis were performed. Results A total of 34 patients are included, including 18 who underwent neurosurgery and 16 who underwent cardiac surgery; 501,380 s (139.3 h) of data was analyzed. The SVR derived from a fixed CVP of 10 mmHg (SVRf10) showed the highest accuracy (RMSE: 115 and 104 [dynes/sec/cm− 5] and MAPE: 6.3 and 5.7% in neurological and cardiac surgery, respectively). The 95% limits of agreement between SVRf10 and actual SVR were − 208.5 (95% confidence interval [CI], − 306.3 to − 148.1) and 242.2 (95% CI, 181.8 to 340.0) dynes/sec/cm− 5 in neurosurgery and − 268.1 (95% CI, − 367.5 to − 207.7) and 163.2 (95% CI, 102.9 to 262.6) dynes/sec/cm− 5 in cardiac surgery. All the SVRs derived from the fixed CVPs (regardless of its absolute value) showed excellent trending ability (concordance rate > 0.99). Conclusions SVR can be estimated from a fixed value of CVP without causing significant deviation or a loss of trending ability. However, caution is needed when using point estimates of SVR when the actual CVP is expected to be out of the typical clinical range. Trial registration This study was registered Clinical Research Information Service, a clinical trial registry in South Korea (KCT0006187).

Abstract 11340: Increasing Mean Arterial Pressure or Cardiac Output in Comatose Out-of-Hospital Cardiac Arrest Patients Undergoing Targeted Temperature Management: Effects on Cerebral Tissue Oxygenation

Introduction: There are few data regarding the effects of norepinephrine-uptitration on global and regional hemodynamics in cardiac intensive care patients. Methods: We prospectively studied 10 OHCA patients at our cardiac intensive care unit. The trial consisted of 5 phases. The first 4 phases were achieved by titrating norepinephrine to reach targets of mean arterial pressure (MAP). First a MAP of 65 mmHg, second 75 mmHg, third 85 mmHg, fourth 65 mmHg again. The fifth phase was with a constant MAP of 65 mmHg but aiming at an increased PaCO2 from 6.5-7.3 kPa to increase cardiac output. During each phase, 20 minutes steady state was achieved before measurements. We measured hemodynamic variables with a Swan-Ganz catheter, arterial and mixed venous blood gases, and near-infrared spectroscopy at the forehead (cerebral oxygen saturation). Results: To obtain a MAP at 85 mmHg, norepinephrine was increased from 0.11±0.02 to 0.18±0.02 μg · kg–1 · min–1 (P < 0.001). Norepinephrine uptitration significantly increased MAP, systemic vascular resistance and pulmonary artery pressure, without affecting cardiac output or heart rate. After phase 3, norepinephrine was decreased to basal values, and all variables returned to baseline. Increasing pCO2, resulted in a significant increase in cardiac output and cerebral oxygen saturation, while decreasing systemic vascular resistance. MAP (and NE dose) was unaffected by increasing pCO2. Conclusions: A short-term increase in MAP with norepinephrine in resuscitated OHCA-patients is associated with increased SVR and PVR without affecting cardiac output or NIRS of the brain. An increase in CO caused by an increase in pCO2 and thereby a decreased SVR increased NIRS potentially improving brain oxygenation.

Acute hyperoxia reveals tonic influence of peripheral chemoreceptors on systemic vascular resistance in heart failure patients

Peripheral chemoreceptors’ (PCh) hyperactivity increases sympathetic tone. An augmented acute ventilatory response to hypoxia, being a marker of PCh oversensitivity, was also identified as a marker of poor prognosis in HF. However, not much is known about the tonic (chronic) influence of PCh on cardio-respiratory parameters. In our study 30 HF patients and 30 healthy individuals were exposed to 100% oxygen for 1 min during which minute ventilation and hemodynamic parameters were non-invasively recorded. Systemic vascular resistance (SVR) and mean arterial pressure (MAP) responses to acute hyperoxia differed substantially between HF and control. In HF hyperoxia caused a significant drop in SVR in early stages with subsequent normalization, while increase in SVR was observed in controls. MAP increased in controls, but remained unchanged in HF. Bilateral carotid bodies excision performed in two HF subjects changed the response to hyperoxia towards the course seen in healthy individuals. These differences may be explained by the domination of early vascular reaction to hyperoxia in HF by vasodilation due to the inhibition of augmented tonic activity of PCh. Otherwise, in healthy subjects the vasoconstrictive action of oxygen remains unopposed. The magnitude of SVR change during acute hyperoxia may be used as a novel method for tonic PCh activity assessment.