Systemic Hemodynamics Research Articles

THE ROLE OF BLOOD PRESSURE LEVEL IN THE DEVELOPMENT OF ATRIAL FIBRILLATION AFTER CORONAVIRUS INFECTION

Objective: It is known, that arterial hypertension (AH) is the main cause of atrial fibrillation (AF). The aim of our study was to assess the parameters of systemic hemodynamics as a predictor of AF development after coronavirus infection (CI). Design and method: We examined 118 patients with AF, at the age of 62.5 + 0.09 years with AF, who, on average, 6.2 + 0.5 months had undergone CI. Of these, 14 people (8.4%) also had atrial flutter. 72 people (61 %) had AF before CI (1st group of patients). The remaining 46 patients (39 %) had no history of this arrhythmia (2nd group of patients). Office blood pressure was measured according to the generally accepted method. Results: In the 1st group, the indicators of systolic blood pressure (SBP) were significantly lower than in the 2nd group (131.4 + 1.72 and 139.5 + 2.99 mm Hg, p < 0, 05), indicators of diastolic blood pressure (DBP) (81.5 + 0.74 and 87.9 + 2.41 Hg, p < 0.05), and heart rate (HR) (83, 0 + 1.86 and 98.0 + 2.4 bpm, p < 0.05). This difference in the groups was more significant between patients with hypertension: SBP, respectively (134.7 + 1.5 and 143.9 + 3.8 mm Hg, p < 0.05), DBP (83.3 + 1.1 and 90.5 + 2.6 Hg, p < 0.05), and heart rate HR (83.0 + 1.86 and 98.0 + 2.4 bpm, p < 0.001). In addition, in group 1, AH was found significantly less frequently (in 59 out of 72 patients, 81.9%) than in patients in group 2 (in 42 out of 46 patients, 91.3%), p < 0.05. Conclusions: An increase in SBP, DBP HR and AH, are predictors of the development of AF in patients after CI.

Microcirculation-guided treatment improves tissue perfusion and hemodynamic coherence in surgical patients with septic shock.

Severe sepsis and septic shock may impair microcirculatory perfusion and cause organ dysfunction. The aim of this pilot study was to assess a new microcirculation-guided resuscitation strategy in patients with septic shock undergoing emergency abdominal surgery. A microcirculation-guided treatment algorithm was developed and applied intraoperatively following restoration of systemic hemodynamics. Sublingual microcirculation was monitored with Sidestream DarkField (SDF +) imaging technique. The primary objective was to investigate the change in De Backer score, Consensus Proportion of Perfused Vessels (Consensus PPV), and Consensus PPV (small) and its association with venous-to-arterial carbon dioxide difference (v-aPCO2). Thirteen consecutive patients were included in the study. Microcirculation-guided resuscitation resulted in an increase of 0.49mm-1 in the De Backer score (p < 0.001), an increase of 2.28% in the Consensus PPV (p < 0.001), and an increase of 2.26% in the Consensus PPV (small) (p < 0.001) for every 30min of additional intraoperative time. All microcirculation variables were negativelycorrelated with v-aPCO2 (rho = -0.656, adj-p < 0.001; rho = -0.623; adj-p < 0.001; rho = -0.597, adj-p < 0.001, respectively) at each intraoperative time point. Lactate levels were negatively correlated with Consensus PPV (rho = -0.464; adj-p = 0.002) and Consensus PPV (small) (rho = -0.391, adj-p < 0.001). Survival at 30days, 90days, and 1year were 76.9%, 76.9%, and 61.5%, respectively. The intraoperative use of microcirculation-guided resuscitation strategy may improve tissue perfusion and hemodynamic coherence in patients with septic shock.

Contrast-Enhanced Ultrasonography Enables the Detection of a Cold Pressor Test-Induced Increase in Renal Microcirculation in Healthy Participants.

BackgroundRenal microcirculation is essential for regulation of the glomerular filtration rate, the reabsorption of salt and water from the interstitium, and hence the blood pressure. Renal ultrasonography coupled to Doppler analysis and contrast-enhanced ultrasound enables the study of renal perfusion. So far, physiologic interventions have rarely been performed to assess the renal perfusion. The objective of our study was to measure the renal perfusion in response to a cold pressor test (CPT).MethodsHealthy adult participants were exposed to a 2 min CPT or a sham exposure (body temperature). Systemic hemodynamics, renal resistive index (RRI) and renal perfusion index (PI) were measured before and during the CPT or the sham exposure. Renal responses were compared using a paired Student's t-test or Wilcoxon signed rank test. Pearson correlation test was used to test association of variables of interest.ResultsForty-one normotensive participants (21 women) were included in the study. Mean blood pressure and heart rate both increased with the CPT. The RRI decreased from 0.60 ± 0.05 arbitrary units (AU) to 0.58 ± 0.05 AU (p < 0.05) and the PI increased from 2,074 AU (1,358–3,346) to 3,800 AU (2,118–6,399) (p < 0.05) (+66% (24–106%)). Compared to the sham exposure, the increase in PI with the CPT was more marked. There was a negative association between the increase in heart rate and mean blood pressure with the RRI (r: −0.550, p = 0.002 and r: −0.395, P = 0.016), respectively.ConclusionDoppler Ultrasound and CEUS enable the detection of physiological changes within the macro- and microvascular renal circulation. The CPT decreases the RRI and increases the PI. Whether these changes are present in pathological states such as diabetes or hypertension will need additional studies.

Neurovascular Dysregulation and Acute Exercise Intolerance in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Randomized, Placebo-Controlled Trial of Pyridostigmine

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is characterized by intractable fatigue, postexertional malaise, and orthostatic intolerance, but its pathophysiology is poorly understood. Pharmacologic cholinergic stimulation was used to test the hypothesis that neurovascular dysregulation underlies exercise intolerance in ME/CFS. Does neurovascular dysregulation contribute to exercise intolerance in ME/CFS, and can its treatment improve exercise capacity? Forty-five subjects with ME/CFS were enrolled in a single-center, randomized, double-blind, placebo-controlled trial. Subjects were assigned in a 1:1 ratio to receive a 60-mg dose of oral pyridostigmine or placebo after an invasive cardiopulmonary exercise test (iCPET). A second iCPET was performed 50min later. The primary end point was the difference in peak exercise oxygen uptake (Vo2). Secondary end points included exercise pulmonary and systemic hemodynamics and gas exchange. Twenty-three subjects were assigned to receive pyridostigmine and 22 to receive placebo. The peak Vo2 increased after pyridostigmine but decreased after placebo (13.3 ± 13.4mL/min vs-40.2 ± 21.3mL/min; P< .05). The treatment effect of pyridostigmine was 53.6mL/min (95%CI, -105.2 to -2.0). Peak vsrest Vo2 (25.9 ± 15.3mL/min vs-60.8 ± 25.6mL/min; P< .01), cardiac output (-0.2 ± 0.6 L/min vs-1.9 ± 0.6 L/min; P< .05), and right atrial pressure (1.0 ± 0.5mmHg vs-0.6 ± 0.5mmHg; P< .05) were greater in the pyridostigmine group compared with placebo. Pyridostigmine improves peak Vo2 in ME/CFS by increasing cardiac output and right ventricular filling pressures. Worsening peak exercise Vo2, cardiac output, and right atrial pressure following placebo may signal the onset of postexertional malaise. We suggest that treatable neurovascular dysregulation underlies acute exercise intolerance in ME/CFS. ClinicalTrials.gov; No.: NCT03674541; URL: www. gov.

Cardiomyocyte‐specific deletion of sarcoglycan‐δ leads to dilated cardiomyopathy, autonomic dysfunction, and exaggerated stress‐induced cardiovascular reactivity

Deficiency of sarcoglycan‐δ (Sgcd) induces disruption of the dystrophin glycoprotein complex, resulting in loss of membrane stability. We have reported that angiotensin II (AngII)‐mediated autonomic dysfunction precedes and predicts development of dilated cardiomyopathy (DCM) in the global Sgcd‐deficient mice [Exp Physiol 2015].The relative contribution of cardiomyocyte‐targeted Sgcd on DCM and autonomic dysfunction remains unknown. Our goal is to determine whether cardiac remodeling in the Sgcd mutations is an intrinsic process of the cardiomyocytes. We have also observed that global Sgcd‐deficient mice with DCM exhibit anxiety‐like behaviors. AngII via type 1 receptors (AT1R) is well‐known to mediate anxiety‐related behaviors, while Ang‐(1‐7) via Mas receptors is anxiolytic. Thus, we hypothesize that Sgcd in the ventricular myocytes is essential for the progression of DCM, and to elicit emotional stress responses. Cardiac‐specific Sgcd‐deficient (cSgcd‐KO) and littermate control (WT) mice were generated by breeding male αMHCcre+(αmyosin‐heavy chain Myh6 promoter drives expression of the cre‐recombinase) withfemaleglobal Sgcd‐deficientmice. Absence of Sgcdin the cardiomyocytes was confirmed by immunohistochemistry and qPCR in the cSgcd‐KO mice. WT (n=11) and cSgcd‐KO (n=14) mice were echoed every month, from 8 weeks of age, to monitor progression of DCM. At ~35 weeks of age, telemeters (DSI) were implanted to measure changes in blood pressure (BP), heart rate (HR) and locomotor activity during acute emotional stress challenge (20 min exposure to predator odor). Autonomic indices including baroreflex sensitivity (BRS, sequence technique), and resting cardiac vagal and sympathetic tone (HR responses to atropine and propranolol, respectively) were calculated. At 36±1 weeks of age, cSgcd‐KO mice exhibit 62% increase in left ventricular (LV) end‐diastolic volume, 58% decrease in LV ejection fraction, and increased cardiac fibrosis (p&lt;0.05 vs. 10 weeks of age). At baseline, cSgcd‐KO mice exhibit lower BP (100±6 vs.121±1 mmHg), reduced BRS (0.72±0.08 vs.2.01±0.05 ms/mmHg) and vagal tone (∆HR= +32±6 vs. +151±18 bpm), and increased sympathetic tone (∆HR= ‐212±12 vs. ‐123±10 bpm) (p&lt;0.05 vs.WT). Paradoxically, given increased basal sympathetic tone and decreased basal vagal tone, stress caused hypotension in the cSgcd‐KO mice with DCM, likely due to reduced cardiac output. This is accompanied by profound increase in AT1R, and reduced expression of Mas and MrgD receptors (ligand for newly identified heptapeptide alamandine) in LV and brainstem (p&lt;0.0001‐0.01 vs. baseline and WT). We conclude ‐ (i) Sgcddeleted exclusively from the cardiac myocytes creates a novel transgenic mouse strain that develops DCM at ~35 weeks of age. (ii) Stress‐evoked profound changes in CNS and systemic hemodynamics occur directly or indirectly, and cannot be ascribed to Sgcd loss in vascular smooth muscle, endothelium, neurons, or astrocytes. (iii) Contributions of the renin‐angiotensin system is pivotal in pathophysiology of Sgcd deficiencies.

Influence of Cognitive Challenges During Exercise on Post‐Exercise Cerebrovascular Function

Peripheral vascular function is acutely improved following a single session of aerobic exercise. This improvement is likely due to increased blood flow during aerobic exercise. Cognitive activity and aerobic exercise both acutely increase cerebral blood flow, and while previous studies have examined the influence of acute exercise on post‐exercise cerebrovascular function, the effects of increased cognitive activity during exercise on post‐exercise cerebrovascular function remains unclear. Therefore, the purpose of this study was to examine the influence of increased cognitive activity during aerobic exercise on post‐exercise cerebrovascular function. We hypothesized that performing cognitive challenges during exercise would result in greater post‐exercise cerebrovascular function. METHODS: Ten participants (age: 27 ± 5 y; VO2max = 53 ± 10 mL/kg/min; men = 5, women = 5) completed 2 study days, in a randomized order, in which they either walked at 30% VO2max for 30 min (WALK) or walked at 30% VO2max for 30 min while completing N‐back cognitive tasks (WALK+COG). Cerebrovascular reactivity to hypercapnia (CVR) was measured pre‐ and 90 min post‐exercise as a measure of cerebrovascular function. Middle cerebral artery velocity (MCAv), mean arterial pressure (MAP), and end‐tidal CO2 (ETCO2) were continuously monitored during the hypercapnia protocol. Cerebrovascular conductance index (CVCi) was calculated as MCAv/MAP. CVR was calculated as the slope between the changes in MCAv or CVCi and ETCO2. RESULTS: During WALK and WALK+COG, there was no difference in MCAv from pre‐ to post‐exercise (p ≥ 0.05 for both), despite a significant post‐exercise reduction in ETCO2 (WALK: pre = 43 ± 2 mmHg, post = 41 ± 3 mmHg; WALK+COG: pre = 41 ± 4 mmHg, post = 40 ± 3 mmHg; p &lt; 0.05 for both). While WALK had no significant change in MAP from pre‐ to post‐exercise (p = 0.10), WALK+COG had a significant increase in MAP (pre = 88 ± 18 mmHg, post = 98 ± 14 mmHg; p = 0.01). Both WALK and WALK+COG had a decrease in CVCi from pre‐ to post‐exercise (WALK: pre = 0.70 ± 0.15 cm/s/mmHg, post = 0.65 ± 0.17 cm/s/mmHg; WALK+COG: pre = 0.75 ± 0.15 cm/s/mmHg, post = 0.66 ± 0.14 cm/s/mmHg; p &lt; 0.05 for both). There was no significant change in CVR from pre‐ to post‐exercise during either study days (assessed as MCAv or CVCi; p ≥ 0.05 for both). Finally, there was no significant difference in the magnitude of change in CVR from pre‐ to post‐exercise between the study days (assessed as MCAv or CVCi; p ≥ 0.05 for both). CONCLUSION: Cognitive challenges during exercise did not influence post‐exercise cerebrovascular function. Despite this finding, cognitive challenges during walking may influence resting systemic hemodynamics, as it resulted in an increased post‐exercise MAP compared with walking alone.

Veno-Venous Extracorporeal Membrane Oxygenation in Minipigs as a Robust Tool to Model Acute Kidney Injury: Technical Notes and Characteristics.

ObjectiveVeno-venous extracorporeal membrane oxygenation (vv-ECMO) can save lives in severe respiratory distress, but this innovative approach has serious side-effects and is accompanied by higher rates of iatrogenic morbidity. Our aims were, first, to establish a large animal model of vv-ECMO to study the pathomechanism of complications within a clinically relevant time frame and, second, to investigate renal reactions to increase the likelihood of identifying novel targets and to improve clinical outcomes of vv-ECMO-induced acute kidney injury (AKI).MethodsAnesthetized Vietnamese miniature pigs were used. After cannulation of the right jugular and femoral veins, vv-ECMO was started and maintained for 24 hrs. In Group 1 (n = 6) ECMO was followed by a further 6-hr post-ECMO period, while (n = 6) cannulation was performed without ECMO in the control group, with observation maintained for 30 h. Systemic hemodynamics, blood gas values and hour diuresis were monitored. Renal artery flow (RAF) was measured in the post-ECMO period with an ultrasonic flowmeter. At the end of the experiments, renal tissue samples were taken for histology to measure myeloperoxidase (MPO) and xanthine oxidoreductase (XOR) activity and to examine mitochondrial function with high-resolution respirometry (HRR, Oroboros, Austria). Plasma and urine samples were collected every 6 hrs to determine neutrophil gelatinase-associated lipocalin (NGAL) concentrations.ResultsDuring the post-ECMO period, RAF dropped (96.3 ± 21 vs. 223.6 ± 32 ml/min) and, similarly, hour diuresis was significantly lower as compared to the control group (3.25 ± 0.4 ml/h/kg vs. 4.83 ± 0.6 ml/h/kg). Renal histology demonstrated significant structural damage characteristic of ischemic injury in the tubular system. In the vv-ECMO group NGAL levels, rose significantly in both urine (4.24 ± 0.25 vs. 2.57 ± 0.26 ng/ml) and plasma samples (4.67 ± 0.1 vs. 3.22 ± 0.2 ng/ml), while tissue XOR (5.88 ± 0.8 vs. 2.57 ± 0.2 pmol/min/mg protein) and MPO (11.93 ± 2.5 vs. 4.34 ± 0.6 mU/mg protein) activity was elevated. HRR showed renal mitochondrial dysfunction, including a significant drop in complex-I-dependent oxidative capacity (174.93 ± 12.7 vs. 249 ± 30.07 pmol/s/ml).ConclusionSignificantly decreased renal function with signs of structural damage and impaired mitochondrial function developed in the vv-ECMO group. The vv-ECMO-induced acute renal impairment in this 30-hr research protocol provides a good basis to study the pathomechanism, biomarker combinations or possible therapeutic possibilities for AKI.

РЫБИЙ ЖИР ПРЕДУПРЕЖДАЕТ РАЗВИТИЕ АРТЕРИАЛЬНОЙ ГИПОТЕНЗИИ У КРЫС С ПОСТТРАВМАТИЧЕСКИМ СТРЕССОВЫМ РАССТРОЙСТВОМ

Objectives. To evaluate the nature and mechanisms of the protective effect of fish oil (FO) on systemic hemodynamics in rats with an experimental analogue of post-traumatic stress disorder (PTSD). Material and methods. The studies were carried out on 50 outbred white male rats weighing 210-240 g, divided into groups: «Control», «PTSD», «FO», «FO+PTSD». An analogue of PTSD was reproduced by rats contacting with cat feces for 10 days for 15 minutes daily. Fish oil was administered intragastrically in doses of 0.2 ml (100 mg/kg body weight of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, CJSC «Biosola», Lithuania) 3 days before modelling PTSD and during 10 days of stressor action. After 2 weeks, systolic, diastolic, mean arterial blood pressure (SBP, DBP, MAP) and heart rate (HR) were measured by a non-invasive method. The concentration of endothelial NO-synthase (eNOS), inducible NO-synthase (iNOS), corticosterone, C-reactive protein (C-RP), interleukin-1β (IL-1β) was determined in blood serum by enzyme-linked immunosorbent assay (ELISA); spectrophotometric method was used to determine the concentration of malondialdehyde (MDA), diene conjugates (DC), as well as the activity of catalase (CAT) and superoxide dismutase (SOD). Results. In animals with PTSD, there was a decrease in SBP, DBP and MAP by 18-23% and an increase in heart rate by 20%. The concentration of eNOS in the blood of rats with PTSD decreased by 28%, and iNOS increased 2.28 times, along with 3.3 and 3.6 times increase in the content of DC and MDA against the background of the decreased SOD activity by 27%, CAT by 59% and 1.6 and 3 times increase in the concentration of C-RP and IL-1β, respectively, compared with the control. The introduction of FO either prevented or significantly limited the severity of the detected changes. Conclusions. The introduction of fish oil to rats prevents the development of arterial hypotension, as well as the changes in the concentration of eNOS and iNOS, it also prevents the disruption of the prooxidant-antioxidant status of blood serum, and reduces the severity of systemic inflammation in animals with PTSD.

Adaptive Changes in the Indicators of Systemic Hemodynamics and Energy Consumption by Young Men during Passive Hyperthermia Procedures

Adaptive Changes in the Indicators of Systemic Hemodynamics and Energy Consumption by Young Men during Passive Hyperthermia Procedures

Extrarenal Effects of Aldosterone on Potassium Homeostasis.

The role of aldosterone in regulating K+ excretion in the distal nephron is well established in kidney physiology. In addition to effects on the kidney, aldosterone modulates K+ and Na+ transport in salivary fluid, sweat, airway epithelia, and colonic fluid. More controversial and less well defined is the role of aldosterone in determining the internal distribution of K+ across cell membranes in nontransporting epithelia. In vivo studies have been limited by the difficulty in accurately measuring overall K+ balance and factoring in both variability and secondary changes in acid-base balance, systemic hemodynamics, and other K+-regulatory factors such as hormones and adrenergic activity. Despite these limitations, the aggregate data support a contributory role of aldosterone along with insulin and catecholamines in the normal physiologic regulation of internal K+ distribution. The authors speculate differences in tissue sensitivity to aldosterone may also contribute to differential tissue response of cardiac and skeletal muscle to conditions of total body K+ depletion.

Lung ultrasound score parallels trends in systemic haemodynamics after PDA ligation: a case series.

A sustained fall in LUS after PDA ligation was identified, which most likely reflects reduction in pulmonary blood flow and interstitial edema. Changes in LUS paralleled changes in LVO, suggesting physiologic linkage. These data suggest that LU may be a useful tool to guide monitoring the biologic nature of pulmonary disease after PDA ligation. • Sustained exposure to a high-volume left-to-right patent ductus arteriosus (PDA) shunt is associated with interstitial pulmonary oedema. • In the most immature patients, cardiorespiratory deterioration, named post-ligation cardiac syndrome, presents 6-12 h post-operatively. • An early and sustained fall in lung ultrasound score (LUS) after PDA ligation most likely reflects reduction in pulmonary blood flow and interstitial oedema. LUS changes parallel changes in left ventricular output, suggesting linkage. • LU is a promising adjunctive tool in the post-operative management of PDA ligation.

Brain oxygenation during multiple sets of isometric and dynamic resistance exercise of equivalent workloads: Association with systemic haemodynamics

ABSTRACT Brain function relies on sufficient blood flow and oxygen supply. Changes in cerebral oxygenation during exercise have been linked to brain activity and central command. Isometric- and dynamic-resistance exercise-(RE) may elicit differential responses in systemic circulation, neural function and metabolism; all important regulators of cerebral circulation. We examined whether (i) cerebral oxygenation differs between isometric- and dynamic-RE of similar exercise characteristics and (ii) cerebral oxygenation changes relate to cardiovascular adjustments occurring during RE. Fourteen men performed, randomly, an isometric-RE and a dynamic-RE of similar characteristics (bilateral-leg-press, 2-min×4-sets, 30% of maximal-voluntary-contraction, equivalent tension-time-index/workload). Cerebral-oxygenation (oxyhaemoglobin-O2Hb; total haemoglobin-tHb/blood-volume-index; deoxyhemoglobin-HHb) was assessed by NIRS and beat-by-beat haemodynamics via photoplethysmography. Cerebral-O2Hb and tHb progressively increased from the 1st to 4th set in both RE-protocols (p < 0.05); HHb slightly decreased (p < 0.05). Changes in NIRS-parameters were similar between RE-protocols within each exercise-set (p = 0.91–1.00) and during the entire protocol (including resting-phases) (p = 0.48–0.63). O2Hb and tHb changes were not correlated with changes in systemic haemodynamics. In conclusion, cerebral oxygenation/blood-volume steadily increased during multiple-set RE-protocols. Isometric- and dynamic-RE of matched exercise characteristics resulted in similar prefrontal oxygenation/blood volume changes, suggesting similar cerebral haemodynamic and possibly neuronal responses to maintain a predetermined force.

Blood Pressure Management After Intracerebral and Subarachnoid Hemorrhage: The Knowns and Known Unknowns.

Blood pressure (BP) elevations often complicate the management of intracerebral hemorrhage and aneurysmal subarachnoid hemorrhage, the most serious forms of acute stroke. Despite consensus on potential benefits of BP lowering in the acute phase of intracerebral hemorrhage, controversies persist over the timing, mechanisms, and approaches to treatment. BP control is even more complex for subarachnoid hemorrhage, where there are rationales for both BP lowering and elevation in reducing the risks of rebleeding and delayed cerebral ischemia, respectively. Efforts to disentangle the evidence has involved detailed exploration of individual patient data from clinical trials through meta-analysis to determine strength and direction of BP change in relation to key outcomes in intracerebral hemorrhage, and which likely also apply to subarachnoid hemorrhage. A wealth of hemodynamic data provides insights into pathophysiological interrelationships of BP and cerebral blood flow. This focused update provides an overview of current evidence, knowledge gaps, and emerging concepts on systemic hemodynamics, cerebral autoregulation and perfusion, to facilitate clinical practice recommendations and future research.

Ultraprotective versus apneic ventilation in acute respiratory distress syndrome patients with extracorporeal membrane oxygenation: a physiological study

BackgroundEven an ultraprotective ventilation strategy in severe acute respiratory distress syndrome (ARDS) patients treated with extracorporeal membrane oxygenation (ECMO) might induce ventilator-induced lung injury and apneic ventilation with the sole application of positive end-expiratory pressure may, therefore, be an alternative ventilation strategy. We, therefore, compared the effects of ultraprotective ventilation with apneic ventilation on oxygenation, oxygen delivery, respiratory system mechanics, hemodynamics, strain, air distribution and recruitment of the lung parenchyma in ARDS patients with ECMO.MethodsIn a prospective, monocentric physiological study, 24 patients with severe ARDS managed with ECMO were ventilated using ultraprotective ventilation (tidal volume 3 ml/kg of predicted body weight) with a fraction of inspired oxygen (FiO2) of 21%, 50% and 90%. Patients were then treated with apneic ventilation with analogous FiO2. The primary endpoint was the effect of the ventilation strategy on oxygenation and oxygen delivery. The secondary endpoints were mechanical power, stress, regional air distribution, lung recruitment and the resulting strain, evaluated by chest computed tomography, associated with the application of PEEP (apneic ventilation) and/or low VT (ultraprotective ventilation).ResultsProtective ventilation, compared to apneic ventilation, improved oxygenation (arterial partial pressure of oxygen, p < 0.001 with FiO2 of 50% and 90%) and reduced cardiac output. Both ventilation strategies preserved oxygen delivery independent of the FiO2. Protective ventilation increased driving pressure, stress, strain, mechanical power, as well as induced additional recruitment in the non-dependent lung compared to apneic ventilation.ConclusionsIn patients with severe ARDS managed with ECMO, ultraprotective ventilation compared to apneic ventilation improved oxygenation, but increased stress, strain, and mechanical power. Apneic ventilation might be considered as one of the options in the initial phase of ECMO treatment in severe ARDS patients to facilitate lung rest and prevent ventilator-induced lung injury.Trial registration: German Clinical Trials Register (DRKS00013967). Registered 02/09/2018. https://www.drks.de/drks_web/navigate.do?navigationId=trial.HTML&TRIAL_ID=DRKS00013967.

Effect of Levosimendan on Acute Decompensated Right Heart Failure in Patients With Connective Tissue Disease-Associated Pulmonary Arterial Hypertension.

AimsAcute decompensated right heart failure (RHF) in chronic precapillary pulmonary hypertension is often typified by a swiftly progressive syndrome involving systemic congestion. This results from the impairment of the right ventricular filling and/or a reduction in the flow output of the right ventricle, which has been linked to a dismal prognosis of short duration. Despite this, there are limited therapeutic data regarding these acute incidents. This study examined the effect of levosimendan on acute decompensated RHF in patients with connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH).MethodsThis retrospective study included 87 patients with confirmed CTD-PAH complicated acute decompensated RHF between November 2015 and April 2021. We collected biological, clinical, and demographic data, as well as therapy data, from patients with acute decompensated RHF who required levosimendan treatment in the cardiac care unit (CCU) for CTD-PAH. The patients were divided into two groups according to the levosimendan treatment. Patient information between the two groups was systematically compared in hospital and at follow-up.ResultsOxygen saturation of mixed venose blood (SvO2), estimated glomerular filtration rate (eGFR), 24-h urine output, and tricuspid annular plane systolic excursion (TAPSE) were found to be considerably elevated in the levosimendan cohort compared with the control cohort. Patients in the levosimendan cohort exhibited considerably reduced levels of C-reactive protein (CRP), white blood cell (WBC), troponin I, creatinine, NT-proBNP, and RV diameter compared with those in the control cohort. A higher survival rate was observed in the levosimendan cohort.ConclusionsLevosimendan treatment could effectively improve acute decompensated RHF and systemic hemodynamics in CTD-PAH patients, with positive effects on survival in hospital and can, therefore, be considered as an alternative treatment option for improving clinical short-term outcomes.

СОВРЕМЕННЫЕ ВОЗМОЖНОСТИ МЕДИКАМЕНТОЗНОЙ КОРРЕКЦИИ ЭНДОТЕЛИАЛЬНОЙ ДИСФУНКЦИИ У ПАЦИЕНТОВ С ИШЕМИЧЕСКОЙ БОЛЕЗНЬЮ СЕРДЦА В ИНТРАОПЕРАЦИОННОМ И РАННЕМ ПОСЛЕОПЕРАЦИОННОМ ПЕРИОДЕ ПОСЛЕ РЕВАСКУЛЯРИЗАЦИИ МИОКАРДА

Background: Endothelial dysfunction is the main link in the development of cardiovascular diseases, which leads to ischemic heart disease (coronary artery disease) and its complications. There are many medicines available for the treatment of coronary artery disease. However, not all groups of drugs are able to positively affect endothelial function. Purpose. Based on the literature data, to study the effect of the main groups of drugs for the treatment of coronary artery disease on endothelial function and systemic hemodynamics in cardiac surgery patients after myocardial revascularization. Material and methods: The review and analysis of literature data from 46 sources are presented. Results: Angiotensin converting enzyme receptor inhibitors, calcium sensitizers, phosphodiesterase type III inhibitors as well as beta blockers have a positive effect on endothelial function. Nitrates have a negative effect on its function in conditions of critical circulation and should be used with caution in endothelial dysfunction. Conclusion: The data obtained indicate a positive effect of angiotensin converting enzyme receptor inhibitors, calcium sensitizers, type III phosphodiesterase inhibitors and beta blockers on endothelial function. However, these groups of drugs can negatively affect systemic hemodynamics in the perioperative period, which requires a deliberate approach when prescribing them.

Contrast-Enhanced Ultrasound of Brain Perfusion in Cardiopulmonary Resuscitation.

To evaluate the feasibility and potential utility of contrast-enhanced ultrasound for real-time imaging of whole-brain perfusion during cardiopulmonary resuscitation (CPR), cardiac arrest was induced in 8- to 7-week-old 10-kg piglets ( Sus scrofa domesticus ). Contrast-enhanced ultrasound was performed through a parietal cranial window in the coronal plane visualizing the thalami during hemodynamic-directed CPR. Whole-brain mean and maximum pixel intensities in each slice during resuscitation were calculated. Piglets were monitored for 24 hours postarrest. Seven piglets achieved return of spontaneous circulation and 6 survived to 24 hours. Of the 6 surviving piglets, 2 piglets demonstrated greater intra-CPR brain enhancement at maximum 73.2% and 42.1% and mean 36.7% and 31.9% enhancement above background, respectively, compared with maximum 5.8%, 22.9%, 6.0%, and 26.6% and mean 5.1%, 8.9%, 2.9%, and 6.6% above background, respectively, in the other 4. Intra-CPR average mean arterial pressures were similar between all 6 surviving piglets. One piglet achieved return of spontaneous circulation but expired 10 minutes later with enhancement maximum 45.2% and mean 18.9% enhancement above background. The final piglet did not achieve return of spontaneous circulation and exhibited minimal enhancement at maximum 2.8% and mean 0.9% enhancement above background. Contrast-enhanced ultrasound can detect brain perfusion during CPR, identifying a spectrum of cerebral blood flow responses in the brain despite similar systemic hemodynamics. This novel application can form the basis for future large animal model studies and eventually human clinical studies to further explore the neurologic implications of cerebral blood flow responses during resuscitation and stimulate novel strategies for optimizing brain perfusion restoration.

Characterization of Systemic and Regional Hemodynamics and Vascular Dysfunction in Mice with Fecal Induced Peritonitis.

Sepsis is associated with circulatory dysfunction contributing to disturbed blood flow and organ injury. Decreased organ perfusion in sepsis is attributed, in part, to the loss of vasoregulatory mechanisms. Identifying which vascular beds are most susceptible to dysfunction is important for monitoring the recovery of organ function and guiding interventions. This study aimed to investigate the development of vascular dysfunction as sepsis progressed to septic shock. Anesthetized C57Bl/6 mice were instrumented with a fiberoptic pressure sensor in the carotid artery for blood pressure measurements. In subgroups of mice, regional blood flow measurements were taken by positioning a perivascular flow probe around either the left carotid, left renal, or superior mesenteric arteries. Hemodynamic parameters and their responsiveness to bolus doses of vasoactive drugs were recorded prior to and continuously after injection of fecal slurry (1.3 mg/g body weight) for 4 h. Fecal slurry-induced peritonitis reduced mean arterial pressure (62.7 ± 2.4 mmHg vs. 37.5 ± 3.2 mmHg in vehicle and septic mice, respectively), impaired cardiac function, and eventually reduced organ blood flow (71.9%, 66.8%, and 65.1% in the superior mesenteric, renal, and carotid arteries, respectively). The mesenteric vasculature exhibited dysregulation before the renal and carotid arteries, and this underlying dysfunction preceded the blood pressure decline and impaired organ blood flow.

Особенности коррекции системной и церебральной гемодинамики при токсико-гипоксических энцефалопатиях

Представлены данные об эффективности двух вариантов коррекции системной и церебральной гемодинамики у 40 пациентов с токсико-гипоксической энцефалопатией в ранней стадии острых тяжелых отравлений нейротропными психолептиками. Наиболее эффективным оказалось использование в комплексе интенсивной терапии реосорбилакта, допамина, дексазона, пентоксифиллина в сочетании с ноотропилом. Их применение способствует более раннему восстановлению системной и церебральной гемодинамики, сосудистого тонуса артериального и венозного русла, сознания и снижению летальности.

Легенева гіпертензія при сепсисі в дітей та її корекція за допомогою донатора оксиду азоту L-аргініну

У статті обговорюється проблема гемодинамічних розладів у малому колі кровообігу при сепсисі, тяжкому сепсисі та септичному шоку в дітей. Продемонстровано наявність легеневої гіпертензії, що виявляється при дослідженні середнього артеріального тиску в легеневій артерії методом допплерометрії за Kitabatake. Також показано, що легенева гіпертензія поєднується з розладами системної гемодинаміки та тканинною гіпоксією, які існують, незважаючи на збільшення рівня NO у крові. Наведено результати впливу внутрішньовенної інфузії аргініну гідрохлориду на показники вмісту оксиду азоту в сироватці та показники центральної та легеневої гемодинаміки при легеневій гіпертензії на тлі септичних станів у дітей. Продемонстровано здатність внутрішньовенної інфузії аргініну гідрохлориду в дозі 5 мл/кг/добу протягом 24–48 годин вірогідно збільшувати вміст NO у крові та знижувати тиск у легеневій артерії й легеневий судинний опір при септичних станах у дітей.