Decrease In Cardiac Output Research Articles

Hypoperfusion states could increase the risk of non-arteritic anterior ischemic optic neuropathy.

Non-arteritic anterior ischemic optic neuropathy (NAION) is a leading cause of acute optic nerve damage. While cardiovascular risk factors such as hypertension, diabetes mellitus, and obstructive sleep apnea are well-established, the association between NAION and states of hypoperfusion is underexplored. This study investigated this potential association. This retrospective case-control study analyzed all electronic medical records of Clalit Health Services' patients from 2001 to 2022. Patients diagnosed with NAION were matched in a 1:4 ratio by year of birth and sex, using propensity score analysis to adjust for various comorbidities. Events of hypoperfusion occurring in the month prior to the diagnosis of NAION were categorized into two physiological mechanisms: a decrease in SVR and a decrease in cardiac output due to cardiac dysfunction or diminished preload (attributed to hypovolemia). Conditional logistic regression was used to explore differences between the groups. A total of 1,374 patients diagnosed with NAION and 5,496 matched controls were included in the study. We found a nearly 6.5-fold increase in the likelihood of NAION in association with events of hypoperfusion that occurred in the month period preceding the diagnosis of NAION (odds ratio [OR] 6.48; 95% confidence interval [CI]: 5.05-8.32). In particular, the group of patients with cardiac dysfunction (OR 6.47; 95% CI: 4.63-9.04) and the group with hypovolemia (OR 6.1; 95% CI: 4.08-9.13) emerged as having the most substantial risk factors. The group with decreased Systemic Vascular Resistance (SVR) (OR 4.64; 95% CI: 2.84-7.59) was also strongly related with NAION. Cerebrovascular accident emerged as an independent significant risk factor for NAION (OR 16.1; 95% CI: 10.8-24). Hypoperfusion states are significant, independent risk factors for NAION.

Utilizing metagenomic next-generation sequencing and phylogenetic analysis to identify a rare pediatric case of Naegleria fowleri infection presenting with fulminant myocarditis.

Naegleria fowleri (N. fowleri), a rare and typically lethal amoeba, most commonly causes primary amoebic meningoencephalitis (PAM). This case report describes an exceptionally rare presentation of fulminant myocarditis as the primary manifestation in a 6-year-old child, diverging from the typical neurological pathogenesis associated with N. fowleri infection. Beyond neurological afflictions, the child developed arrhythmias and cardiac failure, necessitating treatment with extracorporeal membrane oxygenation (ECMO). Diagnosis was confirmed via metagenomic next-generation sequencing (mNGS) of both blood and cerebrospinal fluid (CSF). This analysis not only substantiated the infection but also revealed a potential new genotype of N. fowleri, designated k39_3, suggesting broader genetic diversity than previously recognized. Immediate treatment with Amphotericin B (Am B) and rifampin was initiated upon diagnosis. Despite aggressive management and supportive care, the patient failed to maintain hemodynamic stability, continued to show a decrease in cardiac output, and exhibited relentless progression of central nervous system failure, culminating in death within 72 h. Our report documents a rare pediatric case of N. fowleri infection presenting with fulminant myocarditis, revealing an unexpected clinical manifestation and broadening the known spectrum of its effects. This emphasizes the need for enhanced surveillance and targeted research to understand the pathogenic mechanisms and improve treatment strategies.

Abstract 4129440: Ventricular Stunning Following Direct Current Cardioversion: A Case Report

Background: Ventricular stunning refers to a transient mechanical dysfunction of the myocardium, typically manifesting in response to ischemic insults, reperfusion injury, inflammatory states, or neurohormonal overload. Here, we present an unusual case of ventricular stunning precipitated by direct current electrical cardioversion (DEC). Case Report: A 73-year-old man with a history of heart failure with reduced ejection fraction, paroxysmal atrial fibrillation (AF), coronary artery disease, and chronic kidney disease was admitted to a Veterans Affairs hospital for heart failure exacerbation. His hospitalization was complicated by recurrent episodes of symptomatic AF with ventricular rates in the 120-150’s. This was initially managed with intravenous amiodarone and eventually DEC. He continued to experience symptomatic episodes of AF. Later in the hospitalization a repeat DEC with a single 200 joule shock was performed with restoration of sinus rhythm. Several hours afterwards he was found to be unresponsive and hypotensive. Cool extremities and rising serum lactate raised suspicion for cardiogenic shock resulting in transfer to the intensive care unit where vasopressor and inotropic support were initiated. Echocardiogram revealed a precipitous decrease in left ventricular ejection fraction from 25% to 5%. Serum troponin concentrations were unchanged from prior and ECGs demonstrated rate-controlled AF. Clinical Decision Making: This case highlights an episode of unexpected decrease in cardiac output following an otherwise routine repeat DEC for recurrent AF requiring escalation to mechanical circulatory support. His decompensation worsened, necessitating transfer to the local university center for placement of catheter-based miniaturized ventricular assist device (Impella 5’5). Over the subsequent days, with supportive care, his left ventricular ejection fraction recovered to baseline, and mechanical and inotropic support were withdrawn. Conclusion: Ventricular stunning, leading to cardiogenic shock, is a rare and incompletely understood complication of DEC. It warrants consideration when monitoring patients after cardioversion. Implementing vigilant observation protocols post-DEC to detect ventricular stunning and predisposing risk factors could significantly enhance clinical management strategies.

Impact of arterial system alterations due to amputation on arterial stiffness and hemodynamics: a numerical study

Subjects with amputation of the lower limbs are at increased risk of cardiovascular mortality and morbidity. We hypothesize that amputation-induced alterations in the arterial tree negatively impact arterial biomechanics, blood pressure and flow behavior. These changes may interact with other biological factors, potentially increasing cardiovascular risk. To evaluate this hypothesis regarding the purely mechanical impact of amputation on the arterial tree, we used a simulation computer model including a detailed one-dimensional (1D) arterial network model (143 arterial segments) coupled with a zero-dimensional (0D) model of the left ventricle. Our simulations included five settings of the arterial network: (1) 4-limbs control, (2) unilateral amputee (right lower limb), (3) bilateral amputee (both lower limbs), (4) trilateral amputee (lower-limbs and right upper-limb), and (5) quadrilateral amputee (lower and upper limbs). Analysis of regional stiffness, as calculated by pulse wave velocity (PWV) for large-, medium- and small-sized arteries, showed that, while aortic stiffness did not change with increasing degree of amputation, stiffness of medium and smaller-sized arteries increased with greater amputation severity. Despite a staged decrease in cardiac output, the systolic and diastolic blood pressure values increased, resulting in an increase in both central and peripheral pulse pressures but with an attenuation of pulse pressure amplification. The most significant increase in peak systolic pressure and decrease in peak systolic blood flow was observed at the site of the abdominal aorta. Wave separation analysis indicated no changes in the shape of the forward and backward wave components. However, the results from wave intensity analysis showed that with extended amputation, there was an increase in peak forward wave intensity and a rise in the inverse peak of the backward wave intensity, suggesting potential alterations in cardiac hemodynamic load. In conclusion, this simulation study showed that biomechanical and hemodynamic changes in the arterial network geometry could interact with additional risk factors to increase the cardiovascular risk in patients with amputations.

Effect of a reduced arterial axial pre-stretch ratio during aging on the cardiac output and cerebral blood flow in the healthy elders

Background and objectiveIt is an indisputable physiological phenomenon that the arterial axial pre-stretch ratio (AAPSR) decreases with age, but little attention has been paid to the effect of this reduction on chronic diseases during aging. MethodsHere we reported an experimental method to simulate arteries aging, developed a fluid-structure interaction model with the effect of AAPSR changes, and compared it with the anatomy data and structural parameters of the human thoracic aorta. ResultsWe showed that with the process of aging, the decrease of AAPSR leads to a decline of arterial elasticity, a decrease of arterial elastic strain energy, which weakens the ability to promote blood circulation, the corresponding decrease in cardiac output (CO) and cerebral blood flow (CBF) causes distal organ and body tissue ischemia, which is one of the main causes of increased blood pressure and decreased cerebral perfusion in the elderly. ConclusionsThus, reduced AAPSR is the one of main manifestation of arteries aging and has an important impact on hypertension and hypoperfusion of the brain in the process of human aging. The research contributes to a better understanding of the physiological and pathological mechanisms of aging-related diseases.

Postnatally overfed mice display cardiac function alteration following myocardial infarction

BackgroundCardiovascular (CV) pathologies remain a leading cause of death worldwide, often associated with common comorbidities such as overweight, obesity, type 2 diabetes or hypertension. An innovative mouse model of metabolic syndrome induced by postnatal overfeeding (PNOF) through litter size reduction after birth was developed experimentally. This study aimed to evaluate the impact of PNOF on cardiac remodelling and the development of heart failure following myocardial infarction. MethodsC57BL/6 male mice were raised in litter adjusted to 9 or 3 pups for normally-fed (NF) control and PNOF group respectively. After weaning, all mice had free access to standard diet and water. At 4 months, mice were subjected to myocardial infarction (MI). Echocardiographic follows-up were performed up to 6-months post-surgery and biomolecular analyses were carried-out after heart collection. FindingsAt 4 months, PNOF mice exhibited a significant increase in body weight, along with a basal reduction in left ventricular ejection fraction (LVEF) and an increase in left ventricular end-systolic area (LVESA), compared to NF mice. Following MI, PNOF mice demonstrated a significant decrease in stroke volume and an increased heart rate compared to their respective initial values, as well as a notable reduction in cardiac output 4-months after MI. After 6-months, left ventricle and lung masses, fibrosis staining, and mRNA expression were all similar in the NF-MI and PNOF-MI groups. InterpretationAfter MI, PNOF mice display signs of cardiac function worsening as evidenced by a decrease in cardiac output, which could indicate an early sign of heart failure decompensation.

Evaluation of Amiodarone Administration in Patients with New-Onset Atrial Fibrillation in Septic Shock.

Background and Objective: New-onset atrial fibrillation (NOAF) is a common cardiac condition often observed in intensive care units. When amiodarone is used to treat this condition, either to maintain sinus rhythm after electrical cardioversion or to control heart rate, complications can arise when a systemic pathology is present. Systemic pathology can result in a decrease in cardiac output and blood pressure, making the management of NOAF and septic shock challenging. Limited international research exists on the coexistence of NOAF and septic shock, making it difficult to determine the optimal course of treatment. While amiodarone is not the primary choice of antiarrhythmic drug for patients in septic shock, it may be considered for those with underlying cardiac issues. This paper aims to investigate the safety of administering amiodarone to patients with septic shock and explore whether another antiarrhythmic drug may be more effective, especially considering the cardiac conditions that patients may have. Materials and Methods: To write this article, we searched electronic databases for studies where authors used amiodarone and other medications for heart rate control or sinus rhythm restoration. Results: The studies reviewed in this work have shown that for the patients with septic shock and NOAF along with a pre-existing cardiac condition like a dilated left atrium, the use of amiodarone may provide greater benefits compared to other antiarrhythmic drugs. For patients with NOAF and septic shock without underlying heart disease, the initial use of propafenone has been found to be advantageous. However, a challenge arises when deciding between rhythm or heart rate control using various drug classes. Unfortunately, there is limited literature available on this specific scenario. Conclusions: NOAF is a frequent and potentially life-threatening complication occurring in one out of seven patients with sepsis, and its incidence is rising among patients with septic shock.

Non-invasive hemodynamic monitoring during initiation of positive airway pressure treatment in patients with obstructive sleep apnea: a feasibility study

BackgroundThe association of obstructive sleep apnea (OSA) with cardiovascular morbidity has been repeatedly reported in numerous studies and argues for treatment initiation even in the absence of significant day time sleepiness. While the long-term consequences of positive airway pressure (PAP) treatment on OSA related comorbidities like secondary hypertension are based on substantial clinical evidence, less is known about the immediate hemodynamic effects.MethodsThis study tried to investigate the impact of PAP treatment on different hemodynamic parameters in 48 patients with OSA by extending the standard polysomnographic assessment with non-invasive hemodynamic monitoring using impedance cardiography (ICG). On two consecutive nights under diagnostic and therapeutic conditions, polysomnographic and hemodynamic data were acquired. In addition, we subdivided the participants according to their treatment related change in stroke volume (SV) and assigned the hemodynamic measurements to the corresponding sleep stage.ResultsComparing both conditions, a non-statistically significant decrease in SV and cardiac output (CO) was observed for all participants. Treatment initiation was associated with a statistically significant prolongation of the pre-ejection period (PEP) for the entire study population (p = 0.001) and the subgroup with decreasing SV (p = 0.008). In addition, systolic blood pressure (SBP) (p = 0.026) and pulse pressure (PP) (p = 0.041) were lowered significantly for patients with a therapeutically reduced SV under treatment conditions. A higher BMI (p = 0.020) and a more pronounced reduction of the respiratory distress index (RDI) (p = 0.030) and the arousal-index (p = 0.021) were observed for patients with decreasing SV. Correlational analysis revealed a negative relationship between the diagnostic values for both SBP (r=-0.324, p = 0.025) and PP (r=-0.407, p = 0.004) with the change in SV and a positive correlation with the change of the SBP (r = 0.317, p = 0.028) for all participants.ConclusionsTo conclude, our results indicate that treatment with a PAP device in patients with OSA can lead to a decrease in SV which is associated with a lowering of the SBP. This may be caused by a reduced sympathetic tone due to less respiratory events and an improved sleep profile.

Early- to mid-gestational testosterone excess leads to adverse cardiac outcomes in postpartum sheep.

Cardiovascular dysfunctions complicate 10-20% of pregnancies, increasing the risk for postpartum mortality. Various gestational insults, including preeclampsia are reported to be associated with adverse maternal cardiovascular outcomes. One such insult, gestational hyperandrogenism increases the risk for preeclampsia and other gestational morbidities but its impact on postpartum maternal health is not well known. We hypothesize that gestational hyperandrogenism such as testosterone (T) excess will adversely impact the maternal heart in the postpartum period. Pregnant ewes were injected with T propionate from day 30 to day 90 of gestation (term 147 days). Three months postpartum, echocardiograms, plasma cytokine profiles, cardiac morphometric, and molecular analysis were conducted [control (C) n = 6, T-treated (T) n = 7 number of animals]. Data were analyzed by two-tailed Student's t test and Cohen's effect size (d) analysis. There was a nonsignificant large magnitude decrease in cardiac output (7.64 ± 1.27 L/min vs. 10.19 ± 1.40, P = 0.22, d = 0.81) and fractional shortening in the T ewes compared with C (35.83 ± 2.33% vs. 41.50 ± 2.84, P = 0.15, d = 0.89). T treatment significantly increased 1) left ventricle (LV) weight-to-body weight ratio (2.82 ± 0.14 g/kg vs. 2.46 ± 0.08) and LV thickness (14.56 ± 0.52 mm vs. 12.50 ± 0.75), 2) proinflammatory marker [tumor necrosis factor-alpha (TNF-α)] in LV (1.66 ± 0.35 vs. 1.06 ± 0.18), 3) LV collagen (Masson's Trichrome stain: 3.38 ± 0.35 vs. 1.49 ± 0.15 and Picrosirius red stain: 5.50 ± 0.32 vs. 3.01 ± 0.23), 4) markers of LV apoptosis, including TUNEL (8.3 ± 1.1 vs. 0.9 ± 0.18), bcl-2-associated X protein (Bax)+-to-b-cell lymphoma 2 (Bcl2)+ ratio (0.68 ± 0.30 vs. 0.13 ± 0.02), and cleaved caspase 3 (15.4 ± 1.7 vs. 4.4 ± 0.38). These findings suggest that gestational testosterone excess adversely programs the maternal LV, leading to adverse structural and functional consequences in the postpartum period.NEW & NOTEWORTHY Using a sheep model of human translational relevance, this study provides evidence that excess gestational testosterone exposure such as that seen in hyperandrogenic disorders adversely impacts postpartum maternal hearts.

Characteristics of Akinetic and Dyskinetic Left Ventricular Aneurysms in the Context of Echocardiographic Diagnosis and Treatment Selection.

Background and Objectives. Distinct pressure curve differences exist between akinetic (A-LVA) and dyskinetic (D-LVA) aneurysms. In D-LVA, left ventricular (LV) ejection pressure decreases relative to the aneurysm size, whereas A-LVA does not impact pressure curves, indicating that the decrease in stroke volume (SV) and cardiac output is proportional to the size of dyskinesia. This study aimed to assess the frequency of A-LVA and D-LVA, determine aneurysm size parameters (volume and surface area), and evaluate predictive parameters using echocardiography in A-LVA and D-LVA. Furthermore, it aimed to compare individual echocardiographic parameters, according to ejection fraction (EF) and SV, with hemodynamic events shown in experimental models of A-LVA and D-LVA and their significance in everyday clinical practice. Materials and Methods. This clinical study included patients with post-infarction left ventricular aneurysm (LVA) admitted to the cardiovascular institute ''Dedinje", Serbia. Echocardiographic volume and surface area of LV and LVA were determined (by the area-length method) along with EF (by Simpson's method). Results. A-LVA was present in 62.9% of patients, while D-LVA was present in 37.1%. Patients with D-LVA had significantly higher systolic aneurysm volume (LVAVs) (94.07 ± 74.66 vs. 51.54 ± 53.09, p = 0.009), systolic aneurysm surface area (LVAAs) (23.22 ± 11.73 vs. 16.41 ± 8.58, p = 0.018), and end-systolic left ventricular surface areas (LVESA) (50.79 ± 13.33 vs. 42.76 ± 14.11, p = 0.045) compared to patients with A-LVA. The ratio of LVA volume to LV volume was higher in the D-LVA in systole (LVAVs/LVESV). The end-diastolic volume of LV (LVEDV) and end-systolic volume of LV (LVESV) did not significantly differ between D-LVA and A-LVA. EF (21.25 ± 11.92 vs. 28.18 ± 11.91, p = 0.044) was significantly lower among patients with D-LVA. Conclusions. Differentiating between A-LVA and D-LVA using echocardiography is crucial since D-LVA causes greater hemodynamic disturbances in LV function, and thus surgical resection of the aneurysm or LV reconstruction must have a positive effect regardless of myocardial revascularization surgery.

Association between intraoperative hypotension and postoperative nausea and vomiting: a retrospective cohort study

Objective Postoperative nausea and vomiting (PONV) occurs in up to 30% of patients and its pathophysiology and mechanisms have not been completely described. Hypotension and a decrease in cardiac output are suspected to induce nausea. The hypothesis that intraoperative hypotension might influence the incidence of PONV was investigated. Material and methods The study was conducted as a retrospective large single center cohort study. The incidence of PONV was investigated until discharge from post anesthesia care unit (PACU). Surgical patients with general anesthesia during a 2-year period between 2018 and 2019 at a university hospital in Germany were included. Groups were defined based on the lowest documented mean arterial pressure (MAP) with group H50: MAP <50mmHg; group H60: MAP <60mmHg; group H70: MAP <70mmHg, and group H0: no MAP <70mmHg. Decreases of MAP in the different groups were related to PONV. Propensity-score matching was carried out to control for overlapping risk factors. Results In the 2-year period 18.674 patients fit the inclusion criteria. The overall incidence of PONV was 11%. Patients with hypotension had a significantly increased incidence of PONV (H0 vs. H50: 11.0% vs.17.4%, Risk Ratio (RR): 1.285 (99%CI: 1.102–1.498), p < 0.001; H0 vs. H60: 10.4% vs. 13.5%, RR: 1.1852 (99%CI: 1.0665–1.3172), p < 0.001; H0 vs. H70: 9.4% vs. 11.2%, RR: 1.1236 (99%CI: 1.013 − 1.2454); p = 0.0027). Conclusion The study demonstrates an association between intraoperative hypotension and early PONV. A more severe decrease of MAP had a pronounced effect.

Relationship between changes in the electrical axis of the heart during inspiration and the structural and functional state of the heart according to echocardiography in patients with precapillary pulmonary hypertension

Introduction. A deep breath causes a whole range of physiological effects that are reflected in the electrocardiogram. The purpose of the study is to assess the position of the electrical axis of the heart during deep inspiration compared to quiet breathing in patients with precapillary pulmonary hypertension and compare these data with echocardiographic characteristics of the structural and functional state of the heart. Materials and methods. The study included 40 patients with idiopathic pulmonary hypertension and 40 patients with chronic thromboembolic pulmonary hypertension. Echocardiography assessed the size of the heart chambers, systolic and diastolic function of the right and left ventricles, pulmonary artery pressure, pulmonary vascular resistance and indicators of cardiovascular coupling. Results. The values of the electrical axis of the heart during free breathing were 106° [84°; 123°], on inspiration – 89° [87°; 120°] (p = 0.68). In 50 (62.5 %) patients, during a deep inspiration, the electrical axis of the heart shifted to the left from the original one, and in 30 (37.5 %) patients – to the right. In patients with a displacement of the electrical axis of the heart to the left from the original, compared with the others, the end-diastolic size of the left ventricle, end-diastolic and end-systolic volumes of the left ventricle, stroke volume, cardiac output were statistically significantly lower, and the eccentricity index, pulmonary vascular resistance and effective aortic stiffness – significantly larger. Conclusion. In patients with precapillary pulmonary hypertension, two variants of changes of the heart electrical axis during deep inspiration were identified: a shift to the right from the original and to the left from the original. Patients with a displacement of the electrical axis to the left from the original were characterized by a significantly greater increase in pulmonary vascular resistance, a decrease in left ventricular volumes, stroke volume and cardiac output.

Mechanical ventilation in a conscious male during exercise: a case report.

We recently explored the cardiopulmonary interactions during partial unloading of the respiratory muscles during exercise. Expanding upon this work, we present a noteworthy case study whereby we eliminated the influence of respiration on cardiac function in a conscious but mechanically ventilated human during exercise. This human was a young healthy endurance-trained male who was mechanically ventilated during semi-recumbent cycle exercise at 75 Watts (W) (∼30% Wmax). During mechanically ventilated exercise, esophageal pressure was reduced to levels indistinguishable from the cardiac artefact which led to a 94% reduction in the power of breathing. The reduction in respiratory pressures and respiratory muscle work led to a decrease in cardiac output (-6%), which was due to a reduction in stroke volume (-13%), left ventricular end-diastolic volume (-15%), and left-ventricular end-systolic volume (-17%) that was not compensated for by heart rate. Our case highlights the influence of extreme mechanical ventilation on cardiac function while noting the possible presence of a maximal physiological limit to which respiration (and its associated pressures) impacts cardiac function when the power of breathing is maximally reduced.

Norepinephrine or phenylephrine for the prevention of post-spinal hypotension after caesarean section: A double-blinded, randomized, controlled study of fetal heart rate and fetal cardiac output

Study objectiveSpinal anesthesia often causes hypotension, with consequent risk to the fetus. The use of vasopressor agents has been highly recommended for the prevention of spinal anesthesia-induced hypotension during caesarean delivery. Many studies have shown that norepinephrine can provide more stable maternal hemodynamics than phenylephrine. We therefore tested the hypothesis that norepinephrine preserves fetal circulation better than phenylephrine when used to treat maternal hypotension consequent to spinal anesthesia. DesignProspective, randomized, double-blinded study. SettingOperating room. PatientsWe recruited 223 parturients with uncomplicated singleton pregnancies who were scheduled for elective caesarean section under combined spinal-epidural anesthesia. InterventionsThe patients received prophylactic intravenous infusion of either 0.08 μg/kg/min norepinephrine or 0.5 μg/kg/min phenylephrine for prevention of spinal anesthesia-induced hypotension. MeasurementsChanges in fetal heart rate and fetal cardiac output before and after spinal anesthesia were measured using noninvasive Doppler ultrasound. Main results90 subjects who received norepinephrine infusion and 93 subjects who received phenylephrine infusion were ultimately analyzed in the present study. The effects of norepinephrine and phenylephrine on the change of fetal heart rate and fetal cardiac output at 3 and 6 min after spinal block were similar. Although there was a statistically significant decrease in fetal cardiac output at 6 min after subarachnoid block initiation in both the norepinephrine group (mean difference 0.02 L/min; 95% CI, 0–0.04 L/min; P = 0.03) and the phenylephrine group (mean difference 0.02 L/min; 95% CI, 0–0.04 L/min; P = 0.02), it remained within the normal range. ConclusionsProphylactic infusion of comparable doses of phenylephrine or norepinephrine has similar effects on fetal heart rate and cardiac output changes after spinal anesthesia. Neither phenylephrine nor norepinephrine has meaningful detrimental effects on fetal circulation or neonatal outcomes.

PDGFRALPHA ACTIVATION LEADS TO BLOOD PRESSURE INCREASE AND SMALL ARTERIES MEDIAL HYPERTROPHY IN MALE MICE

Objective: Arterial remodeling is associated with vascular function alteration and with hypertension development. This remodeling is due to cells reorganization within the vascular wall and in some cases to smooth muscle cells proliferation. PDGF (Platelet-derived Growth Factor) is a major regulator of arterial remodeling and some studies suggest that PDGFRα, one of its receptors, could be activated during hypertension. Our aim is to determine the role of PDGFRα and of PDGFRα-expressing progenitor cells in vascular remodeling. Design and method: We used a tamoxifen-inducible genetic mouse model of PDGFRα constitutive activation. Blood pressure was measured by the tail-cuff method and by carotid catheter. Small mesenteric arteries reactivity was studied using ex vivo arteriography. Vascular remodeling was analyzed by immunofluorescence. Results: PDGFRα constitutive activation for 6 weeks led to a 25% increase in blood pressure (p&lt;0.05) and a 25% decrease in cardiac output in male mice (p&lt;0.05), without changes in other cardiac parameters. In these mice, small mesenteric arteries showed no alteration in contractility or endothelium-dependent and independent relaxation but an increase of media thickness, whereas larger vessels did not show structure or function alteration. Echo-doppler analyses showed an increased resistivity index of the renal artery (+13% p&lt;0.05) but not of the aorta suggesting an increased resistance of small renal arteries. The remodeling of small mesenteric arteries was characterized by an early proliferation of perivascular cells at 4 days but not of medial cells followed by the production of new smooth muscle cells after 2 weeks. Female mice did not show blood pressure increase following induction of PDGFRα constitutive activation for 6 weeks. Small mesenteric arteries showed a reduced contractility with alteration of endothelium-dependent and independent relaxation. Conclusions: These results suggest that PDGFRα activation could participate in arterial hypertension development by leading to increased media thickness and stiffness in small arteries in males. Our results suggest that in females the increased resistance of small vessels is compensated by a decreased contractility.

Breathing 5% carbon dioxide for 1 minute increases cerebral blood flow during lower body negative pressure

Objective: Lower body negative pressure (LBNP) is an established surrogate of hypergravity to investigate responses to central hypovolemia, including the reduction in cerebral blood flow. Increased inspired carbon dioxide (CO2) causes cerebrovascular dilation and increases cerebral blood flow. We aimed to determine whether breathing 5% CO2 for 1 minute increased cerebral blood flow during LBNP. We hypothesized 5% inspired CO2 would increase cerebral blood flow during LBNP. Methods: We collected data from 15 (9 M/6 F, 31±8 yr, 25.6±3.2 kg/m2) healthy individuals. Subjects breathed room air or a mix of 5% CO2, 21% oxygen, balance nitrogen gas for 1 minute prior to initiation of 2 minutes of -60 mmHg LBNP and throughout the duration of LBNP. We allowed a 2-minute wash-out between trials. We measured middle cerebral artery velocity (MCAv) with transcranial Doppler ultrasound and continuous, non-invasive blood pressure (MAP) with a finger plethysmograph. We corrected MCAv for MAP and present it as cerebrovascular conductance index (CVCi). We also measure ventilation and gas exchange with a pneumotachometer and gas analyzer. Results: All measured variables were similar prior to the initiation of room air and 5% CO2 prebreathe ( p &gt; 0.05). Inspired (1±1 vs. 36±1 mmHg) and end-tidal (38±4 vs. 47±3 mmHg) CO2 were greater during the 5% inspired CO2 trial ( p &lt; 0.05, main effect of gas). LBNP caused an increase in heart rate, decrease in stroke volume, decrease in cardiac output, and an increase in total peripheral resistance ( p &lt; 0.05, main effect of LBNP). These variables were similar regardless of inspiratory gas. MCAv (40±16 vs. 53±19 cm/s), MAP (94±10 vs. 99±11 mmHg), and CVCi (0.46±0.22 vs 0.56±0.24 cm/s/mmHg) were all greater during the 5% inspired CO2 trials ( p &lt; 0.05, main effect of gas). Discussion: Breathing a mixture of 5% CO2 for 1 minute increased cerebral blood flow and blood pressure during a mimic of hypergravity stress. Despite technical challenges of integration into high-performance aircraft, increasing inspired CO2 could contribute to better tolerance to hypergravity stress. Funding was provided by the Air Force Offce of Scientific Research and King’s College London. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Incidence of hypotension in lower segment Caesarean section - a comparison of intrathecal Fentanyl- Bupivacaine combination with Bupivacaine alone

Introduction: After subarachnoid block with conventional heavy Bupivacaine, hypotension is the most common complication and is caused by decrease in systemic vascular resistance and/or cardiac output. Even with standard doses of the drug for parturient, there are evidences of severe hypotension and other complications despite adequate analgesia and anaesthesia. Adjuvants are used to enhance the quality of blocks with less complications. Objectives: It was to evaluate the effectiveness of combining bupivacaine and fentanyl for spinal anesthesia during lower segment Caesarean section (LSCS) as opposed to using bupivacaine alone for the incidence of hypotension. Methodology: This is a prospective study of 210 patients aged 18-35 years of American society of Anesthesiologists Physical Status II undergoing elective lower segment Caesarean section, randomly assigned to two groups: Group A, received a mixture of intrathecal 2ml of 0.5% Bupivacaine and 10 mcg Fentanyl(2.2ml) and Group B, received only 2.2 ml of Bupivacaine. Noninvasive blood pressure was checked at 1,2,4,6,10,20,40 and 60 min after subarachnoid block and then post-surgery. Results: The occurrence of hypotension was higher in Group B (26.6%) compared to Group A (8.6%). Conclusion: Our study suggests that the intrathecal Fentanyl-Bupivacaine combination is effective in reducing the incidence of hypotension after SAB for elective LSCS. Additional research is needed to determine this combination’s optimal dosage and timing.

Correlations between heart sound components and hemodynamic variables

Although the esophageal stethoscope is used for continuous auscultation during general anesthesia, few studies have investigated phonocardiographic data as a continuous hemodynamic index. In this study, we aimed to induce hemodynamic variations and clarify the relationship between the heart sounds and hemodynamic variables through an experimental animal study. Changes in the cardiac contractility and vascular resistance were induced in anesthetized pigs by administering dobutamine, esmolol, phenylephrine, and nicardipine. In addition, a decrease in cardiac output was induced by restricting the venous return by clamping the inferior vena cava (IVC). The relationship between the hemodynamic changes and changes in the heart sound indices was analyzed. Experimental data from eight pigs were analyzed. The mean values of the correlation coefficients of changes in S1 amplitude (ΔS1amp) with systolic blood pressure (ΔSBP), pulse pressure (ΔPP), and ΔdP/dt during dobutamine administration were 0.94, 0.96, and 0.96, respectively. The mean values of the correlation coefficients of ΔS1amp with ΔSBP, ΔPP, and ΔdP/dt during esmolol administration were 0.80, 0.82, and 0.86, respectively. The hemodynamic changes caused by the administration of phenylephrine and nicardipine did not correlate significantly with changes in the heart rate. The S1 amplitude of the heart sound was significantly correlated with the hemodynamic changes caused by the changes in cardiac contractility but not with the variations in the vascular resistance. Heart sounds can potentially provide a non-invasive monitoring method to differentiate the cause of hemodynamic variations.

Positive Vasoreactivity Testing in Pulmonary Arterial Hypertension: Therapeutic Consequences, Treatment Patterns, and Outcomes in the Modern Management Era.

Among patients with pulmonary arterial hypertension (PAH), acute vasoreactivity testing during right heart catheterization may identify acute vasoresponders, for whom treatment with high-dose calcium channel blockers (CCBs) is recommended. However, long-term outcomes in the current era remain largely unknown. We sought to evaluate the implications of acute vasoreactivity response for long-term response to CCBs and other outcomes. Patients diagnosed with PAH between January 1999 and December 2018 at 15 pulmonary hypertension centers were included and analyzed retrospectively. In accordance with current guidelines, acute vasoreactivity response was defined by a decrease of mean pulmonary artery pressure by ≥10 mm Hg to reach <40 mm Hg, without a decrease in cardiac output. Long-term response to CCBs was defined as alive with unchanged initial CCB therapy with or without other initial PAH therapy and World Health Organization functional class I/II and/or low European Society of Cardiology/European Respiratory Society risk status at 12 months after initiation of CCBs. Patients were followed for up to 5 years; clinical measures, outcome, and subsequent treatment patterns were captured. Of 3702 patients undergoing right heart catheterization for PAH diagnosis, 2051 had idiopathic, heritable, or drug-induced PAH, of whom 1904 (92.8%) underwent acute vasoreactivity testing. A total of 162 patients fulfilled acute vasoreactivity response criteria and received an initial CCB alone (n=123) or in combination with another PAH therapy (n=39). The median follow-up time was 60.0 months (interquartile range, 30.8-60.0), during which overall survival was 86.7%. At 12 months, 53.2% remained on CCB monotherapy, 14.7% on initial CCB plus another initial PAH therapy, and the remaining patients had the CCB withdrawn and/or PAH therapy added. CCB long-term response was found in 54.3% of patients. Five-year survival was 98.5% in long-term responders versus 73.0% in nonresponders. In addition to established vasodilator responder criteria, pulmonary artery compliance at acute vasoreactivity testing, low risk status and NT-proBNP (N-terminal pro-B-type natriuretic peptide) levels at early follow-up correlated with long-term response and predicted survival. Our data display heterogeneity within the group of vasoresponders, with a large subset failing to show a sustained satisfactory clinical response to CCBs. This highlights the necessity for comprehensive reassessment during early follow-up. The use of pulmonary artery compliance in addition to current measures may better identify those likely to have a good long-term response.

Implementation Of Relaxation Therapy Listening To Music In Hypertensive Patients

Background : Hypertension causes the aorta and large arteries to reduce their ability to accommodate the volume of blood pumped by the heart, resulting in a decrease in heart rate. To overcome a decrease in cardiac output, this is by providing classical music therapy. Objective: This study aims to find out the description of nursing care for patients with reduced cardiovascular function and hypertension with the implementation of music listening therapy. Methods: This research was conducted using a case study. Results: The results of the assessment showed that the client said he had a history of hypertension, felt headache, shoulder and leg pain, was worried about his illness, and tired quickly. A nursing diagnosis of acute pain, ineffective health care and obesity was obtained. The intervention is by providing music therapy and health education. Conclusion: After carrying out these actions, the results showed that the problem of pain and health maintenance, while the problem of obesity was partially resolved. The evaluation results showed blood pressure in the range of 130/90 mmHg.