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Introduction: Currently phenylephrine is a preferred 1 line vasopressor for maintenance of blood pressure during spinal anaesthesia, may be associated with reflex bradycardia and decreased cardiac output, posing risk to mother or foetus. Norepinephrine may be an useful alternative as being potent alpha with weak beta adrenergic agonist activity. Aims: This study compared the effectiveness of prophylactic and treatment boluses of norepinephrine and phenylephrine to maintain systolic blood pressure at or above 80% of baseline value during spinal anesthesia for cesarean delivery with the primary aim to compare cardiac output. Secondary aims were total doses of study drug required, neonatal outcome and perioperative complications. Materials and Methods: Total 100, term pregnant women with ASA status II undergoing caesarean delivery under spinal anaesthesia were enrolled in this prospective, double blind controlled study. Patients were randomized to receive prophylactic bolus dose of norepinephrine (6 µg) or phenylephrine (100 µg) immediately after spinal anaesthesia. Systolic blood pressure, cardiac output and heart rate were monitored. Intermittent bolus doses were repeated whenever required. Student ‘t’ test and chi square test were used for analysing the data. Results: Both the drugs were able to maintain the systolic blood pressure ? 80% of baseline (p=0.356). Significant difference observed in cardiac output while comparing both the groups from 3 to 15 minutes after spinal anesthesia (p=0.014). The incidence of bradycardia was lower in norepinephrine group as compared to phenylephrine group (P=0.018). Conclusion: Norepinephrine is as effective as phenylephrine for maintenance of blood pressure after spinal anaesthesia for caesarean delivery with stable heart rate and cardiac output. Keywords: Caesarean delivery, Norepinephrine, Phenylephrine, Spinal anaesthesia, Vasopressor.

Background. Brain edema is excessive accumulation of fluid in the intracranial or extracellular space of the brain. It can be caused by head trauma, brain tumors, hypoxia, metabolic disorders, or acute hypertension. Acute myocardial infraction is damage to the myocard that occurs due to lack oxygen. When acute myocardial infarction occurs, there will be disruption of blood flow in the form of stasis which allows emboli and decreased Cardiac Output which will cause a decrease in Cerebral Blood Flow. There will be a state of ischemia and hypoxia so that the hemostatic mechanism is disturbed which will trigger brain edema. Objective. This research was conducted to see the effect of giving ramipril to histopathological of the brain of wistar rat with brain edema. Methods. This research is an experimental study. We used 32 animals which were divided into 4 groups (K-, K +, P1, and P2). P1 was given 3 mg/kgBW ramipril for 7 consecutive days. P2 was given 4 mg/kgBW ramipril for 7 consecutive days. On days 8 and 9, P1, P2, and K+ induced isoproterenol 85 mg/kgBW for 2 consecutive days to induce brain edema through the mechanism of acute myocardial infarction. Data analysis was performed using One Way Anova test and Post Hoc Bonferroni test. Results. The mean area of ​​brain edema in the K-, K +, P1, and P2 groups respectively were 20.76%, 34.69%, 22.70%, and 21.90%. Conclusion. There was a significant effect of giving ramipril to histopathological of the brain of wistar rat with brain edema

Severely hypothermic patients, especially suffering cardiac arrest, require highly specialized treatment. The most common problems affecting the recognition and treatment seem to be awareness, logistics, and proper planning. In severe hypothermia, pathophysiologic changes occur in the cardiovascular system leading to dysrhythmias, decreased cardiac output, decreased central nervous system electrical activity, cold diuresis, and noncardiogenic pulmonary edema. Cardiac arrest, multiple organ dysfunction, and refractory vasoplegia are indicative of profound hypothermia. The aim of these narrative reviews is to describe the peculiar pathophysiology of patients suffering cardiac arrest from accidental hypothermia. We describe the good chances of neurologic recovery in certain circumstances, even in patients presenting with unwitnessed cardiac arrest, asystole, and the absence of bystander cardiopulmonary resuscitation. Guidance on patient selection, prognostication, and treatment, including extracorporeal life support, is given.

Background Ketamine has cardiac excitatory side-effects. Currently, data on the effects of ketamine and metabolite concentrations on cardiac output are scarce. We therefore developed a pharmacodynamic model derived from data from a randomised clinical trial. The current study is part of a larger clinical study evaluating the potential mitigating effect of sodium nitroprusside on the psychedelic effects of ketamine. Methods Twenty healthy male subjects received escalating esketamine and racemic ketamine doses in combination with either placebo or sodium nitroprusside on four visits: (i) esketamine and placebo, (ii) esketamine and sodium nitroprusside, (iii) racemic ketamine and placebo, and (iv) racemic ketamine and sodium nitroprusside. During each visit, arterial blood samples were obtained and cardiac output was measured. Nonlinear mixed-effect modelling was used to analyse the cardiac output time-series data. Ketamine metabolites were added to the model in a sequential manner to evaluate the effects of metabolites. Results A model including an S-ketamine and S-norketamine effect best described the data. Ketamine increased cardiac output, whereas modelling revealed that S-norketamine decreased cardiac output. No significant effects were detected for R-ketamine, metabolites other than S-norketamine, or sodium nitroprusside on cardiac output. Conclusions S-Ketamine, but not R-ketamine, increased cardiac output in a dose-dependent manner. In contrast to S-ketamine, its metabolite S-norketamine reduced cardiac excitation in a dose-dependent manner. Clinical trial registration Dutch Cochrane Center 5359.

Some patients are more likely to have drug-induced diseases due to a number of risk factors, such as older age. The aim of the study was to analyse the effect of older age on pharmacokinetics and pharmacodynamics of medicines and the risk of developing drug-induced diseases. The analysis of scientific literature demonstrated that changes in the functions of body organs and systems caused by natural aging processes may potentially affect pharmacokinetics and pharmacodynamics of medicines and increase the risk of adverse drug reactions. For instance, older people have a decreased cardiac output both at rest and during exercise, weight loss, loss of elasticity of elastic vessels, a reduced number of functioning nephrons, poorer renal filtration capacity, decreased liver volume, a reduced number of functioning hepatocytes, decreased hepatic blood flow. These changes directly affect absorption, metabolism, distribution, and excretion of medicines, which in turn can affect their safety profiles. Consideration of age-related changes in the functions of body organs and systems, regular monitoring of the efficacy and safety of the prescribed medicine, changing the dosage regimen, and revision of the treatment sheet by healthcare professionals will help optimize pharmacotherapy and reduce the risk of adverse reactions and drug-induced diseases in older patients.

IntroductionEarly hemorrhage is often missed by traditional vital signs because of physiological reserve, especially in the young and healthy. We have developed a novel, wearable, wireless Doppler ultrasound patch that tracks real-time blood velocity in the common carotid artery.Materials and MethodsWe studied eight healthy volunteers who decreased their cardiac output using a standardized Valsalva maneuver. In all eight, we simultaneously monitored the velocity time integral (VTI) of the common carotid artery (using the ultrasound patch) as well as the descending aorta (using a traditional pulsed wave duplex imaging system); the descending aortic VTI was used as a surrogate for left ventricular stroke volume (SV). Additionally, in a subset of four, we simultaneously measured SV using a noninvasive pulse contour analysis device.ResultsFrom baseline to peak effect of Valsalva, there was a statistically significant fall in descending aortic and common carotid VTI of 37% (P = 0.0005) and 23% (P ConclusionIn summary, a novel index from a wireless Doppler ultrasound patch may be more sensitive and specific for detecting decreased cardiac output than standard vital signs in healthy volunteers.

BackgroundPrimary cardiac neoplasms are extremely rare, with an autopsy incidence of 0.0001–0.003%. Primary cardiac sarcoma is usually derived from the right atrium and it manifests as chest pain, arrhythmia, hemoptysis, dyspnea, and fatigue. The most common target organ for metastasis of primary angiosarcoma is the lungs, but the radiological-pathological correlation has been rarely reported.Case presentationA 38-year-old healthy Japanese man was admitted to our hospital with persistent hemoptysis, exaggerated dyspnea, and two episodes of loss of consciousness in the past 3 months. Non-enhanced thoracic computed tomography (CT) revealed multiple scattered nodules with halo signs. Contrast-enhanced thoracic CT revealed a filling defect in the right atrium, which corresponded to the inhomogeneously enhancing tumor in the right atrium on enhanced electrocardiogram-gated cardiac CT. On day 2, acute respiratory failure occurred, and the patient was placed on mechanical ventilation. The patient was diagnosed with primary cardiac angiosarcoma based on the urgent transcatheter biopsied specimen of the right atrium mass and was treated with intravenous administration of doxorubicin. However, his respiratory status rapidly deteriorated, and he died on day 20. Postmortem biopsy showed that the multiple lung nodules with the halo signs corresponded to the intratumoral hemorrhagic necrosis and peripheral parenchymal hemorrhage in their background, suggesting the fragility of the lung tissue where the tumor had invaded, which caused hemoptysis. Furthermore, two episodes of loss of consciousness occurred probably due to a decreased cardiac output because of a massive tumor occupying the right atrium, recognized as an inhomogeneous centripetal enhancement on enhanced electrocardiogram-gated cardiac CT.ConclusionsThis case clearly demonstrated that primary cardiac angiosarcoma could expand in the right atrial cavity, which led to a decreased cardiac output resulting in repeated syncope, together with the fragility of lung tissue by tumor invasion, thereby generating a halo sign on thoracic CT.

Systemic absorption of local anesthetics produces effects on the cardiovascular and central nervous systems. At blood concentrations achieved with normal therapeutic doses, changes in cardiac conduction, excitability, refractoriness, contractility, and peripheral vascular resistance are minimal. However, toxic blood concentrations depress cardiac conduction and excitability, which may lead to atrioventricular block and ultimately to cardiac arrest. In addition, with toxic blood concentrations myocardial contractility may be depressed and peripheral vasodilation may occur, leading to decreased cardiac output and arterial blood pressure. Patients aged between 18 to 60 years of either gender, belonging to ASA Grade I and II, for elective lower limb and lower abdominal surgeries under spinal anaesthesia. In this present study, diastolic blood pressure recordings were not statistically significant between the two groups observed at different time intervals.

Cardiac arrhythmias significantly contribute to mortality in Duchenne muscular dystrophy (DMD), a degenerative muscle disease triggered by mutations in the gene encoding for the intracellular protein dystrophin. A major source for the arrhythmias in patients with DMD is impaired ventricular impulse conduction, which predisposes for ventricular asynchrony, decreased cardiac output, and the development of reentrant mechanisms. The reason for ventricular conduction impairments and the associated arrhythmias in the dystrophic heart has remained unidentified. In the present study, we explored the hypothesis that dystrophin-deficient cardiac Purkinje fibers have reduced Na+ currents (INa), which would represent a potential mechanism underlying slowed ventricular conduction in the dystrophic heart. Therefore, by using a Langendorff perfusion system, we isolated Purkinje fibers from the hearts of adult wild-type control and dystrophin-deficient mdx mice. Enhanced green fluorescent protein (eGFP) expression under control of the connexin 40 gene allowed us to discriminate Purkinje fibers from eGFP-negative ventricular working cardiomyocytes after cell isolation. Finally, we recorded INa from wild-type and dystrophic mdx Purkinje fibers for comparison by means of the whole cell patch clamp technique. We found substantially reduced INa densities in mdx compared with wild-type Purkinje fibers, suggesting that dystrophin deficiency diminishes INa. Because Na+ channels in the Purkinje fiber membrane represent key determinants of ventricular conduction velocity, we propose that reduced INa in Purkinje fibers at least partly explains impaired ventricular conduction and the associated arrhythmias in the dystrophic heart.NEW & NOTEWORTHY Dystrophic cardiac Purkinje fibers have abnormally reduced Na+ current densities. This explains impaired ventricular conduction in the dystrophic heart.

Heart failure is a clinical syndrome, resulting in increased intracardiac pressure and/or decreased cardiac output under rest or stress. In acute decompensated heart failure, volume assessment is essential for clinical diagnosis and management. More and more evidence shows the advantages of bioimpedance vector analysis in this issue. Here, we critically present a brief review of bioimpedance vector analysis in the prediction and management of heart failure to give a reference to clinical physicians and guideline makers.

Inotropes are pharmacological agents that are indicated for the treatment of patients presenting with acute heart failure (AHF) with concomitant hypoperfusion due to decreased cardiac output. They are usually administered for a short period during the initial management of AHF until haemodynamic stabilisation and restoration of peripheral perfusion occur. They can be used for longer periods to support patients as a bridge to a more definite treatment, such as transplant of left ventricular assist devices, or as part of a palliative care regimen. The currently available inotropic agents in clinical practice fall into three main categories: beta-agonists, phosphodiesterase III inhibitors and calcium sensitisers. However, due to the well-documented potential for adverse events and their association with increased long-term mortality, physicians should be aware of the indications and dosing strategies suitable for different types of patients. Novel inotropes that use alternative intracellular pathways are under investigation, in an effort to minimise the drawbacks that conventional inotropes exhibit.

Circulation blood volume reduction, vascular tone change and decreased cardiac output are the three major factors constituting the acute hemorrhage syndrome pathogenesis that has originally been referred to as “hemorrhagic shock”. Vascular trend with secondary redistribution of the blood volume and following microcirculatory changes as well as the cellular one with principal metabolic modifications are considered to be the leading ones in the development of shock. After the establishment of the leading role of acute hypovolemia and anemia this phenomenon has been labeled “acute posthemorrhagic anemia syndrome”. The development of polyorganic insufficiency syndrome after acute hemorrhage is to a great extent associated with oxygen transport disturbance due to circulatory hypoxia and to a lesser one — with haemic hypoxia due to circulating red blood cells and hemoglobin deficit. Profound tissue metabolism disorders persist even after central hemodynamics and microcirculatory perfusion restoration thus considerably decreasing the nonspecific immune defense and the ability of tissues to reparation and enhancisng proinflammatory and destructive tendencies.

Background Right (R) or left (L) ventricular outflow tract (VOT) obstruction can be either a dynamic phenomenon or a congenital anatomic lesion, which requires a prompt and optimal timing of treatment to avoid a pathological ventricular remodelling. Objective To develop a simple and reliable numerical tool able to relate the R/L obstruction size with the pressure gradient and the cardiac output. To provide indication of the obstruction severity and be of help in the clinical management of patients and designing the surgical treatment for obstruction mitigation. Methods Blood flow across the obstruction is described according to the classical theory of one-dimensional flow, with the obstruction uniquely characterized by its size. Hemodynamics of complete circulation is simulated according to the lumped parameter approach. The case of a 2 years-old baby is reproduced, with the occlusion placed in either the R/ or the L/VOT. Conditions from wide open to almost complete obstruction are reproduced. Results Both R/LVOT obstruction in the in-silico model resulted in an increased pressure gradient and a decreased cardiac output, proportional to the severity of the VOT obstruction and dependent on the R/L location of the obstruction itself, as it is clinically observed. Conclusion The in-silico model of ventricular obstruction which simulates pressure gradient and/or cardiac output agrees with clinical data, and is a first step towards the creation of a tool that can support the clinical management of patients from diagnosis to surgical treatments.

Background: Clonidine is a recommended therapy for the treatment of attention deficit hyperactive disorder in children. As a result of this use in the pediatric population, there is widespread availability of clonidine, and unintentional overdoses occur. Major toxic effects of clonidine include respiratory depression, hypotension, bradycardia, decreased cardiac output, and death. Review of the literature finds that few massive ingestions progressed to respiratory depression and apnea, requiring intubation and ventilatory assistance. Naloxone has been used at high dose(0.8-2mg/kg) to reverse the clonidine toxic effects. Published studies provide no data on dosage response, toxicodynamic response in overdose, or …

If the blood pH levels are not maintained and the body’s acid–base balance remains disturbed for a long time, it may lead to severe acidosis/alkalosis. These conditions may develop into resistance to the action of insulin and infused catecholamines, alteration in oxygen binding to haemoglobin, decreased cardiac output, causing major diseases like heart failure and cancer. So to address this issue, it becomes important to measure pH levels at an early stage. Currently, pH measurement being invasive in nature involves risk of infections, whereas the non-invasive approach offers safety and cost-effectiveness. Hence, we propose a fingertip device prototype similar to a pulse oximeter but which measures the pH levels. For this measurement of pH, the ‘Henderson–Hasselbalch’ equation is used. It requires the concentration of bicarbonate ions and the amount of partial pressure of CO2 for the estimation of buffer pH. The device works on the principle of infrared absorption of CO2 and reflectance properties. Firstly, it calculates the CO2 levels, thereby deriving the bicarbonate levels and then substituting it in the above equation to get the blood pH value. The device, thus, displays the pH values, followed by early recommendations. As we are already measuring the CO2 levels, incorporation of a heart rate sensor additionally will predict cardiovascular as well as respiratory diseases. Further, an alert is sent to the user so that he/she can consult a medical practitioner.

Targeted temperature management, also known as therapeutic hypothermia (TH), is recommended for out-of-hospital cardiac arrest (OHCA). Both internal or external methods of cooling can be applied. Individuals resuscitated from OHCA frequently develop postarrest myocardial dysfunction resulting in decreased cardiac output and left ventricular systolic function. This dysfunction is usually transient and improves with spontaneous recovery over time. Echocardiogram (ECHO) can be a vital tool for the assessment and management of these patients. This manuscript reviewed methods available for TH after OHCA and reviews role of ECHO in the diagnosis and prognosis in this setting.

Introduction: One of the duties of nurses when managing patients with diabetes mellitus is establishing a nursing diagnosis. This study aimed to identify the nursing problems that arise in hospitalized patients with diabetes mellitus. Methods:A descriptive analytical study involving 100 medical records of inpatients with diabetes mellitus from June, July and August 2019 was conducted. The data collection was done through an observation sheet according to the Indonesian Nursing Diagnosis Standards (SDKI). Results: There were 30 types of nursing problems identified with the total number of nursing problems found being 332. The most frequent nursing problems were D.0142 Risiko Infeksi (Risk of Infection) 30.12%, D.0027 Ketidakstabilan Kadar Glukosa Darah (Instability of Blood Glucose Levels) 14.16%, D.0011 Risiko Penurunan Curah Jantung (Risk of Decreased Cardiac Output) 12.65%, D.0017 Risiko Perfusi Serebral Tidak Efektif (Risk of Cerebral Perfusion Not Effective) 8.73%, D.0037 and Risiko Ketidakseimbangan Elektrolit (Risk of Electrolyte Imbalance) 4.52%. Conclussion: This research found there to be 30 variations of nursing problems among the hospitalized patients with diabetes mellitus with the most frequent nursing problems in the physiological category and nutrition and fluid sub-categories.

Blood pressure response to head-up tilt (HUT) in 7 healthy subjects and 9 patients before and after coronary artery bypass grafting (CABG) was measured during supine and 15-min 60° HUT. Stroke volume (SV) and ejection fraction (EF) were assessed by echocardiography. Baseline mean arterial pressure (MAP) and heart rate (HR) in patients before CABG were similar to healthy subjects. MAP in patients decreased by 6 (4–9) mmHg [median (1st–3rd quartiles)] during 7–12 mmHg of HUT with decreased cardiac output (CO = SV × HR) while HR remained unchanged. MAP in healthy subjects remained unchanged during HUT with increased HR. Body weight decreased by 3.5 (2.5–3.7) kg and MAP decreased by 6 (2–13) mmHg during the last 3-min HUT while HR increased after CABG. Decreases in SV and CO during HUT disappeared after CABG. Blood pressure decreased during HUT in patients before and after CABG regardless of HR response.

Giant left atrium is most commonly associated with rheumatic mitral valve disease, causing a series of cardiac and extracardiac complications. Cardiac complications are often reported, such as atrial fibrillation, decreased cardiac output, and atrial thrombus formation. Extracardiac complications are rarely described in the literature. We report an unusual case of a 55-year-old woman who was diagnosed with rheumatic heart disease 20 years earlier. Her chief complaints were episodes of chest tightness and difficulty breathing, which she had for more than 30 years. Echocardiography showed severe mitral stenosis with severe mitral insufficiency. Contrast-enhanced chest CT showed that the left thoracic cavity was occupied by a giant left atrium. The left main bronchus was compressed, and the left lung showed complete consolidation without pulmonary function.

Strangulation of the heart appears to be an exceedingly rare mechanical phenomenon that can develop with epicardial pacing wires in individuals undergoing somatic growth. Over the passage of time, owing to size mismatch between a fixed wire length and dynamically growing heart, the epicardial wire may embed around the heart resulting in the progressive over-pressurizing of involved cardiac structures. Depending on the location of the peak constriction pressures, cardiac strangulation may damagingly affect coronary circulation, heart valves function, or physiologic filling of the heart chambers, with risk of myocardial ischemia, decreased cardiac output, acute cardiac failure, ventricular arrhythmias and death. We report a case of a 29-year-old male with sudden cardiac death owing to cardiac strangulation with epicardial pacing wire that had been retained in place almost 30 years. At autopsy, an enlarged and abnormally contoured heart was found to be strangulated by an epicardial pacing wire; histopathologic examination confirmed hypertrophy of the myocardial fibers, myofiber disarrangement, and replacement-type fibrolipomatosis. In addition, this article consolidates the available literature on cardiac strangulation by an epicardial wire and highlight relevant clinical and medico-legal features for the forensic professionals.

Elderly tend to experience health problems caused by decreased body function due to aging process. The most common health disorder experienced by elderly is the decline of the cardiovascular system. Heart valve thickens and becomes stiff, the heart's ability to pump blood decreases by 1% per year, decreased cardiac output, decreased heart rate to stress response, loss of elasticity of blood vessels, increased blood pressure due to peripheral vascular resistance. This study aims to determine the effect of elderly gymnastics on changes in blood pressure in the elderly in the work area of ​​Rappokalling Health Center. The research design used was pre-experiment with one group pre-test-post test, with the number of samples counted 14 people. Sampling in this research is non probability sampling. Intervention given that elderly gymnastics performed for 3 weeks with a frequency of 3 times a week duration 15-30 minutes. Data were tested with Paired Sample T-test. The results of this study indicate a significant difference in elderly gymnastics treatment to changes in systolic blood pressure (p value 0.02) and diastolic blood pressure (p value 0,000) in elderly hypertension in the work area of ​​Rappokalling Health Center so it can be concluded there is influence of elderly exercise decrease in blood pressure in elderly hypertension and it is expected that elderly gymnastic exercises can routinely be non-pharmacological therapy in the provision of nursing care in elderly patients.

Atrial fibrillation is the most common cardiac arrhythmia, affecting approximately 1 out of every 250 people. It is associated with thrombus formation in the left atrium, decreased cardiac output, and deterioration of the myocardium. There are multiple treatments available for paroxysmal atrial fibrillation. This literature review will assess the benefits, risks, and complications associated with radiofrequency ablation and cryoablation, which utilize heat and freezing mechanisms, respectively. The review will also assess the role of echocardiography in determining which treatment, if any, is appropriate for atrial fibrillation.

Pulmonary arterial hypertension (PAH) is a complex pulmonary vascular disease that leads to right ventricular (RV) failure and sudden cardiac death (1). PAH is associated with sympathetic nervous system (SNS) over-stimulation, renin-angiotensin-aldosterone system (RAAS) activation and cardiac arrhythmias. RAAS activation generates vasoactive compounds that result in pulmonary vasoconstriction and vascular remodeling, hallmarks of PAH (2). It is suggested that patients with PAH often have a low cardiac output and that RAAS and SNS over-activation are merely compensatory mechanisms for that decreased cardiac output (3).

Background: assessment of cardiac output is crucial in management of critical ill patients. Various types of tool are available to measure cardiac output. However, most has limitations such as invasive, expensive, and require special skill. Assessment of End-tidal Carbon Dioxide (EtCO2) is expected to be used as an alternative estimation of cardiac output. It is based on the condition that when cardiac output is decreased, it decreased pulmonary blood flow and diffusion of CO2 into the alveolar, thereby increasing alveolar dead space and lowering EtCO2. Objective: to find a correlation between EtCO2 and decreased cardiac output measured by Ultrasonic Cardiac Output Monitor (USCOM) for intubated patients in ICU of Sanglah General Hospital, Denpasar, Bali. Methods: This is a cross-sectional study, the correlation test conducted from June to August 2016 in ICU of Sanglah Hospital. The study involved 75 patients who eligible with a total population sampling technique. Intubated patients admitted to the ICU were evaluated for EtCO2 and USCOM in the first 24 hours by the researchers simultaneously. Shapiro-Francia test was used for normality and Pearson’s correlation tests was used to measure the correlations between variables. Results: The EtCO2 value obtained was positively correlated with cardiac output values (r = 0.373; p 0.001). Conclusion: there is a correlation between EtCO2 and decreased cardiac output measured by USCOM for intubated patients in ICU of Sanglah General Hospital, Denpasar

Purpose Although the underlying mechanisms of reflex syncope remain under debate, there is evidence that it results from decreased cardiac output related to splanchnic blood pooling or a fall in systemic vascular resistance. The aim was to evaluate the response of cerebrovascular and autonomic variables to passive orthostatic challenge in adult patients with different mechanisms leading to reflex syncope. Methods The study included 30 subjects (66% women, mean age 34 ± 14 years) who suffered a hemodynamic collapse during a drug-free head-up tilt test. They were categorized into three groups according to their hemodynamic cardiovascular response during the head-up tilt test: (1) reduced cardiac output (patients, n = 10), (2) reduced systemic vascular resistance (patients, n = 10), and (3) reduced cardiac output and systemic vascular resistance, (reduced cardiac output reduced systemic vascular resistance patients, n = 10). Cardiovascular and cerebrovascular dynamics, as well as autonomic variables, were noninvasively assessed during the head-up tilt test and median values were calculated at baseline and throughout the three phases of the tilt. Results At baseline, the reduced systemic vascular resistance group had lower cardiac output and higher total peripheral resistance index and a sustained increase of heart rate throughout the head-up tilt test in comparison to the other groups. Cerebrovascular dynamics and autonomic variables showed no difference among groups throughout the test. Compared with baseline, these variables had similar percentual change during the orthostatic challenge. Conclusions Although different cardiovascular hemodynamic mechanisms of reflex syncope exist in adult patients, cerebrovascular hypoperfusion and autonomic modulation occur to a similar extent.

With age as an independent risk factor for perioperative morbidity and mortality, it is important for providers to have a working knowledge of age-related changes in pharmacokinetics and pharmacodynamics of the geriatric patient requiring neuroanesthesia. Neuroanesthetic challenges facing the clinician when caring for geriatric patients include polypharmacy, drug interactions, drug-disease interactions, alterations in typical response to perioperative medications, and postoperative cognitive dysfunction. Absorption, distribution, metabolism, and excretion of medications are affected with the aging process and disease states associated with increasing age. Age-related loss in brain mass impairs normal neuronal function in both excitatory and inhibitory neurotransmitter receptors. Geriatric patients are frequently prescribed neuroleptic and antipsychotic medications. Multifactorial changes within the cardiovascular system lead to impaired medication response in the elderly compared to younger individuals. Reduced compliance and elasticity of arteries leads to increased systolic blood pressure, decreased cardiac output, and decreased left ventricular ejection with left ventricular hypertrophy.

Objective. To identify the nursing diagnoses through reports in the medical records of patients monitored in a specialized ischemic heart disease outpatient clinic.Methods. Cross-sectional study with retrospective data collection in the medical records. From the data collected, the nursing diagnoses were proposed by the researchers and submitted for validation by specialist cardiology nurses.Results. A total of 13 nursing diagnoses were evaluated from the medical records of 50 outpatients with the following validation agreements among the specialists: Ineffective health management (100%), Noncompliance (100%), Sedentary lifestyle (100%), Activity intolerance (100%), Decreased cardiac output (88%), Risk of decreased cardiac tissue perfusion (65%), Risk of intolerance to activity (65%), Acute pain (76%), Ineffective health maintenance (65%), Risk-prone health behavior (65%), Risk for decreased cardiac output (65%), Risk for intolerance to activity (65%), Ineffective respiratory pattern (53%), Impaired memory (29%).Conclusion. In this study, the nursing diagnoses validated for stable heart disease patients were linked to adherence to treatment and to the cardiovascular responses of the patients, reinforcing the importance of early intervention. These results allow the multidisciplinary team to individualize the goals and interventions proposed for ischemic heart disease patients.Descriptors: ambulatory care; cross-sectional studies; nursing diagnosis; outpatients; nursing process; myocardial ischemia.How to cite this article: Cardoso PC, Caballero LG, Ruschel KB, Moraes MAP, Silva ERR. Profile of the nursing diagnoses in stable heart disease patients. Invest. Educ. Enferm. 2019; 37(2):e08.ReferencesWorld Health Organization. World Health Statistics 2018: monitoring health for the SDGs, sustainable development goals [Internet]. Geneva: WHO; 2018 [cited: 7 May 2019]. Available from: https://www.who.int/gho/publications/world_health_statistics/2018/en/ Ministério da Saúde. Informações de Saúde (TABNET) - Assistência à Saúde. DATASUS. Departamento de Informatica a Serviço do SUS [Internet]. 2016 [cited: 7 May 2019]. 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Content validation of the dimensions constituting non-adherence to treatment of arterial hypertension. Rev. Esc. Enferm. 2013; 47(5):1076–82. Freitas JS de, Silva AEB de C, Minamisava R, Bezerra ALQ, Sousa MRG de. Quality of nursing care and satisfaction of patients attended at a teaching hospital. Rev. Lat. Am. Enfermagem. 2014; 22(3):454–60. World health Organization. Adherence to long-term therapies: evidence for action [Internet]. Geneve: WHO; 2003 [cited: 7 May 2019]. Available from: https://www.who.int/chp/knowledge/publications/adherence_report/en/

Background Operations performed with the patient in the prone position can pose a significant challenge to the anesthesiologist. Hypotension is a commonly encountered complication. Intravascular volume depletion and decreased cardiac output secondary to decreased preload are thought to be the most likely cause of hypotension in the prone position. Measurement of inferior vena cava (IVC) diameter via point-of-care ultrasound examination (POC_US) has been used to provide an estimate of intravascular volume status. However, this measurement is most often obtained with the patient in the supine position. Materials and methods In this study, we describe a technique for evaluating IVC diameter via POC_US in the prone position. Right lateral long axis imaging of the IVC was used to assess the intravascular volume status of 10 patients undergoing lumbar spine surgery in the prone position. In addition, we used a non-invasive measure of cardiac output to correlate changes in IVC width with changes in cardiac output. Results Images of the IVC in the prone position were obtainable in all 10 patients. IVC diameter increased in six out of 10 patients on going from supine to prone position. The increase in IVC diameter corresponded to an increase in cardiac output, measured noninvasively in five out of the six patients. Conclusions Our findings indicate that POC_US examination of the IVC is possible in the prone position. Further study of a larger patient population could demonstrate the utility of this technique in assessing intravascular volume status in patients undergoing surgery in the prone position.

The risk of heart failure (HF) is prominently increased in patients with type 2 diabetes mellitus. The objectives of this study were to establish a murine model of diabetic cardiomyopathy induced by feeding a high-sugar/high-fat (HSHF) diet and to evaluate the effect of reconstituted HDLMilano administration on established HF in this model. The HSHF diet was initiated at the age of 12 weeks and continued for 16 weeks. To investigate the effect of reconstituted HDLMilano on HF, eight intraperitoneal administrations of MDCO-216 (100 mg/kg protein concentration) or of an identical volume of control buffer were executed with a 48-h interval starting at the age of 28 weeks. The HSHF diet-induced obesity, hyperinsulinemia, and type 2 diabetes mellitus. Diabetic cardiomyopathy was present in HSHF diet mice as evidenced by cardiac hypertrophy, increased interstitial and perivascular fibrosis, and decreased myocardial capillary density. Pressure-volume loop analysis indicated the presence of both systolic and diastolic dysfunction and of decreased cardiac output in HSHF diet mice. Treatment with MDCO-216 reversed pathological remodelling and cardiac dysfunction and normalized wet lung weight, indicating effective treatment of HF. No effect of control buffer injection was observed. In conclusion, reconstituted HDLMilano reverses HF in type 2 diabetic mice. ispartof: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES vol:20 issue:6 ispartof: location:Switzerland status: published

Advanced diabetes mellitus (DM) may have both insulin resistance and deficiency (double DM) that accelerates diabetic cardiomyopathy (DMCM), a cardiac muscle disorder. Reduced cardiac miR-133a, a cardioprotective miRNA, is associated with DMCM. However, it is unclear whether increasing miR-133a levels in the double DM heart could prevent DMCM. We hypothesized that increasing cardiac levels of miR-133a could prevent DMCM in Akita, a mouse model of double DM. To test the hypothesis, we created Akita/miR-133aTg mice, a new strain of Akita where miR-133a is overexpressed in the heart, by crossbreeding male Akita with female cardiac-specific miR-133a transgenic mice. We validated Akita/miR-133aTg mice by genotyping and phenotyping (miR-133a levels in the heart). To determine whether miR-133a overexpression could prevent cardiac remodeling and cardiomyopathy, we evaluated cardiac fibrosis, hypertrophy, and dysfunction (P-V loop) in 13-15 week male WT, Akita, Akita/miR-133aTg, and miR-133aTg mice. Our results revealed that miR-133a overexpression in the Akita heart prevents DM-induced cardiac fibrosis (reduced collagen deposition), hypertrophy (decreased beta-myosin heavy chain), and impaired contractility (downregulated calcium handling protein sarco-endoplasmic reticulum-ATPase-2a). These results demonstrate that increased levels of miR-133a in the DM heart could prevent cardiac remodeling. Our P-V loop analysis showed a trend of decreased cardiac output, stroke volume, and ± dp/dt in Akita, which were blunted in Akita/miR-133aTg heart. These findings suggest that 13-15 week Akita heart undergoes adverse remodeling toward cardiomyopathy, which is prevented by miR-133a overexpression. In addition, increased cardiac miR-133a in the Akita heart did not change blood glucose levels but decreased lipid accumulation in the heart, suggesting inhibition of metabolic remodeling in the heart. Thus, miR-133a could be a promising therapeutic candidate to prevent DMCM.

Chronic mitral valve disease (CMVD) is the most common cardiovascular disease in dogs, causing decreased cardiac output that results in poor tissue perfusion and tissue damage to kidneys, pancreas, and other organs. The purpose of this study was to evaluate the relationships between heart disease severity and N-terminal pro B-type natriuretic peptide (NT-proBNP) and lipase in dogs with CMVD, as well as to evaluate longitudinal changes in these values. A total of 84 dogs participated in this 2015 to 2017 study. Serum values of NT-proBNP and lipase were analyzed; radiography was used to measure the vertebral heart score and assess various echocardiographic values. NT-proBNP showed a strong positive correlation with increasing stage of heart disease; lipase showed a mild positive correlation with heart disease stage. When the three values (NT-proBNP, lipase and month) were continuously measured at 6-month intervals, all showed a correlation with the increasing length of the disease.

Cardiogenic shock is a complex clinical status characterized by a progressive multi-organ dysfunction determined by the failure of the heart to deliver an adequate amount of blood to the tissues. It complicates approximately 5–10% of cases with acute myocardial infarction. Ischemia due to decreased coronary perfusion leads to muscle hypoxia and necrosis which compromises myocardial contractility. This leads to decreased cardiac output and a subsequent drop in the arterial blood pressure. Coronary revascularization should be performed as soon as possible after AMI and shock onset. After the SHOCK trial, we have witnessed the reduction in the incidence of cardiogenic shock due to early revascularization. Although the primary endpoint, all-cause mortality at 30 days, did not differ between the initial medical stabilization and early revascularization group, there was a significant decrease in mortality after 1 and 6 years in patients assigned to early revascularization. In this chapter incidence, pathophysiology, etiology, clinical symptoms, and therapeutic options in cardiogenic shock are discussed. Two clinical cases and a case scenario allow the reader to get through the content.

Heart failure can be challenging to diagnose given the spectrum of associated symptoms and the overlap of those symptoms with other diseases (e.g. renal, pulmonary, hepatic) as well as with aging and frailty. Despite advances in modern medicine, the history and physical exam remain the cornerstone of the diagnosis of heart failure, whether acute or chronic. The patient’s history is highlighted by symptoms of fluid overload (“backward failure”), decreased cardiac output (“forward failure”), or both.

OBJECTIVE To investigate the regional flow distribution in patients with Fontan circulation by using magnetic resonance imaging (MRI). MATERIALS AND METHODS We identified 39 children (18 females and 21 males; mean age, 9.3 years; age range, 3.3-17.0 years) with Fontan circulation in whom flow volumes across the thoracic and abdominal arteries and veins were measured by using MRI. The patients were divided into three groups: fenestrated Fontan circulation group with MRI performed under general anesthesia (GA) (Group 1, 15 patients; average age, 5.9 years), completed Fontan circulation group with MRI performed under GA (Group 2, 6 patients; average age, 8.7 years), and completed Fontan circulation group with MRI performed without GA (Group 3, 18 patients; average age, 12.5 years). The patient data were compared with the reference ranges in healthy controls. RESULTS In comparison with the controls, Group 1 showed normal cardiac output (3.92 ± 0.40 vs. 3.72 ± 0.69 L/min/m², p = 0.30), while Group 3 showed decreased cardiac output (3.24 ± 0.71 vs. 3.96 ± 0.64 L/min/m², p = 0.003). Groups 1 and 3 showed reduced abdominal flow (1.21 ± 0.28 vs. 2.37 ± 0.45 L/min/m², p < 0.001 and 1.89 ± 0.39 vs. 2.64 ± 0.38 L/min/m², p < 0.001, respectively), which was mainly due to the diversion of the cardiac output to the aortopulmonary collaterals in Group 1 and the reduced cardiac output in Group 3. Superior mesenteric and portal venous flows were more severely reduced in Group 3 than in Group 1 (ratios between the flow volumes of the patients and healthy controls was 0.26 and 0.37 in Group 3 and 0.63 and 0.53 in Group 1, respectively). Hepatic arterial flow was decreased in Group 1 (0.11 ± 0.22 vs. 0.34 ± 0.38 L/min/m², p = 0.04) and markedly increased in Group 3 (0.38 ± 0.22 vs. -0.08 ± 0.29 L/min/m², p < 0.0001). Group 2 showed a mixture of the patterns seen in Groups 1 and 3. CONCLUSION Fontan circulation is associated with reduced abdominal flow, which can be attributed to reduced cardiac output and portal venous return in completed Fontan circulation, and diversion of the cardiac output to the aortopulmonary collaterals in fenestrated Fontan circulation.

The Fontan operation was first performed in 1968 and is a palliative procedure for children born with single ventricle forms of congenital heart disease. Today, 70,000 patients worldwide have Fontan circulation today, half of them women, and with an expected 30-year survival of >80%, this population is expected to double in the next 20 years. The Fontan operation surgically redirects systemic venous blood return directly to the pulmonary circulation, bypassing the single ventricle. This abnormal anatomy results in significant challenges for the cardiovascular system and is marked by a sustained, abnormally elevated systemic venous pressure combined with decreased cardiac output. As more women with Fontan circulation reach childbearing age, understanding the unique risks of pregnancy to the mother and fetus and how to best provide clinical care for these women during pregnancy is imperative. However, there are limited clinical data to guide counseling and management in this population. This expert review offers an analysis of the literature about Fontan circulation during pregnancy and describes our center's current multidisciplinary approach to care for these women in the preconception, antepartum, intrapartum, and postpartum periods.

No previous study has investigated the predictive risk factors of the nursing diagnosis of risk for decreased cardiac output after coronary artery bypass grafting (CABG).This study aimed to identify the predictive risk factors of the nursing diagnosis of risk for decreased cardiac output after CABG.This was a prospective cohort study performed at a cardiac university hospital in São Paulo, Brazil and 257 adult patients undergoing CABG were included. Potential risk factors for low cardiac output in the immediate post-operative period were investigated using the patients' medical records. Univariate analysis and logistic regression were used to identify the predictive risk factors of decreased cardiac output. The area under the receiver operating characteristic curve was calculated as a measure of accuracy. The variables that could not be analysed through logistic regression were analysed through Fisher's exact test.One hundred and ninety-five patients had low cardiac output in the immediate post-operative period. The predictive risk factors included age ⩾60 years, decreased left ventricle ejection fraction, not using the radial artery graft, positive fluid balance and post-operative arrhythmia that differed from the pre-operative arrhythmia. This model predicted the outcome with a sensitivity of 62.9%, a specificity of 87.2% and an accuracy of 81.5%. The variables analysed through Fisher's exact test included heart failure, re-exploration and bleeding-related re-exploration.The predictive risk factors for the nursing diagnosis of risk for decreased cardiac output after CABG were found. These results can be used to direct nurses in patient monitoring, staff training and nursing team staffing.

OBJECTIVE To investigate the association of nursing diagnoses (NDs) identified for patients with heart failure (HF) based on their hemodynamic profiles. METHOD Analytical, cross-sectional study conducted in the emergency room of a public hospital in a large cardiology center in Brazil. One hundred medical records of patients with HF whose hemodynamic profile had been established were analyzed. RESULTS The main NDs identified were risk of infection, bathing self-care deficit, risk for decreased cardiac output, risk for falls, and excess fluid volume. There was no statistically significant difference (p > .05) between the different hemodynamic profiles and the ND found. CONCLUSION AND IMPLICATIONS Nurses need to develop skills for improving their diagnostic abilities to ensure implementation of consistent interventions.

To define the differential effect of site-specific ventricular counterpacing efficacy during cardiac resynchronization therapy (CRT) to identify the most informative imaging views to quantify it. Cross-sectional and long-axis views commonly are used to assess left ventricular (LV) contractility.The effects of LV apical (LVa) and free-wall (LVfw) pacing during CRT on long- and short-axis contraction, cardiac output, and stroke work were assessed in an open-chested acute canine model to determine whether LVa and LVfw would induce earlier apical than basilar LV radial contraction and earlier free-wall than septal contraction, respectively. Apical (CRTa) and free-wall (CRTfw) using right ventricular (RV) pacing-induced dyssynchrony also were examined.University large animal research laboratory.Ten acutely anesthetized and instrumented open-chested purpose-bred dogs.RV pacing served as the model of cardiac dyssynchrony. Selective LVfw and LVa pacing alone or with RV (CRTfw and CRTa, respectively) were studied relative to right atrial pacing (RA) as the control.Two pairs of 3 ultrasonic crystals were place along the LV longitudinal axis-apex and mid-to-base pairs along septal and free wall lines. Conductance catheter-defined longitudinal LV segmental volumes and pressure-volume data were collected. RV decreased cardiac output and stroke work compared with RA (2.0±0.3 v 1.4±0.1 L/min; 137±22 v 60±14 mJ; p0.05, respectively). LVfw but not LVa decreased stroke work (130±35 mJ), and CRTa but not CRTfw improved both (2.1±0.2 L/min; 113±13 mJ; p0.01 v RV pacing). No difference in time to minimal length free wall-to-septal crystal was seen with pacing. Both LVa and CRTa displayed increased apical-to-basilar shortening delay compared with RA, RV, and LVfw (42±47, 9±105, and 1±46 msec, respectively; p0.05). No matching regional LV volume changes were seen during LVa.LV functional analysis from only a cross-sectional plane may be insufficient to characterize improved LV contraction synchrony during multisite CRT.

OBJECTIVE To determine the clinical and construct validity of the nursing diagnosis “decreased cardiac output” (DCO) in patients with chronic heart failure. METHODS Cross-sectional study. RESULTS A total of 200 people were studied. The defining characteristics with the highest prevalence were as follows: arrhythmia (62.5%) and fatigue (61.5%). Adjustment measures such as infit and outfit were maintained between 0.50 and 1.56 and the total variance explained by the measures was 29.3%. CONCLUSIONS This study determined the clinical validity of the nursing diagnosis DCO. Regarding construct validity, adjustment of the defining characteristics to the Rasch model was observed. IMPLICATIONS FOR NURSING PRACTICE This study improves the evidence-based practice of nursing and strengthened the role of the nurse who leads care to this population. OBJETIVO Determinar la validez clinica y de constructo del diagnostico de enfermeria “Disminucion del Gasto Cardiaco” en pacientes con falla cardiaca cronica. METODOS Estudio de corte transversal. RESULTADOS Un total de 200 pacientes fueron estudiados. Las caracteristicas definitorias con las mayores prevalencias fueron: arritmia (62.5%) y fatiga (61.5%). Medidas de ajuste como el infit y outfit se mantuvieron entre 0.50 y 1.56. El total de la varianza explicada por las medidas fue de 29.3%. CONCLUSIONES Este estudio determino la validez clinica del diagnostico de enfermeria “Disminucion del Gasto Cardiaco”. En cuanto a la validez de constructo, se observo que 19 de las 21 caracteristicas definitorias se ajustaron al modelo Rasch. IMPLICACIONES PARA LA PRACTICA DE ENFERMERIA Este estudio mejora la practica basada en la evidencia de enfermeria y fortalece el rol de las enfermeras que lideran el cuidado en esta poblacion.

Hemorrhagic pericardial effusion with associated cardiac tamponade as a de novo sign of malignancy is seen in about 2% of patients.1 Consequently, cardiac tamponade is an oncologic emergency and considered a unique presentation of a malignancy.2 Cancer emergency is defined as an acute condition that is caused directly by the cancer itself or its treatment and requires intervention to avoid death or significant morbidity.3 The mechanism by which cardiac tamponade is classified as a life-threatening emergency stems from its impairment of right ventricular filling, resulting in ventricular diastolic collapse and decreased cardiac output, which can ultimately lead to death.4 We describe the case of a previously healthy woman in her late 40s who was a nonsmoker with no previous risk factors and who presented with a large pericardial effusion and bilateral pulmonary emboli. She was diagnosed with metastatic epidermal growth factor receptor-positive (EGFR-positive) adenocarcinoma of the lung. This case highlights an oncologic emergency as a de novo presentation of malignancy.

Septic shock presents a high risk of morbidity and mortality. Through therapeutic strategies, such as fluid administration and vasoactive agents, clinicians intend to rapidly restore tissue perfusion. Nonetheless, these interventions have narrow therapeutic margins. Adequate perfusion monitoring is paramount to avoid progressive hypoperfusion or detrimental over-resuscitation. During early stages of septic shock, macrohemodynamic derangements, such as hypovolemia and decreased cardiac output (CO) tend to predominate. However, during late septic shock, endothelial and coagulation dysfunction induce severe alterations of the microcirculation, making it more difficult to achieve tissue reperfusion. Multiple perfusion variables have been described in the literature, from bedside clinical examination to complex laboratory tests. Moreover, all of them present inherent flaws and limitations. After the ANDROMEDA-SHOCK trial, there is evidence that capillary refill time (CRT) is an interesting resuscitation target, due to its rapid kinetics and correlation with deep hypoperfusion markers. New concepts such as hemodynamic coherence and flow responsiveness may be used at the bedside to select the best treatment strategies at any time-point. A multimodal perfusion monitoring and an integrated analysis with macrohemodynamic parameters is mandatory to optimize the resuscitation of septic shock patients.

Supraventricular tachycardia (SVT) commonly presents with palpitations, dyspnea or angina. Syncope is an uncommon manifestation of SVT occurring when the rate impairs ventricular filling, leading to decreased cardiac output. This is thought to happen only in the elderly or during ventricular rates

Purpose: In spite of extensive studies, the mechanism of cardiopulmonary resuscitation (CPR) has not been properly understood and a proper comprehension of the role of regulatory mechanisms of the cardiovascular system during CPR is unavailable. Using computational methods, we try to study the influence of sympathetic activation on the cardiac output and mean arterial pressure (MAP) during CPR at different compression pressures and rates. Methods: A computer model was used to investigate the effect of sympathetic activation during CPR. The model has a detailed representation of the cardiopulmonary resuscitation system and sympathetic control. Sympathetic activation during CPR was achieved through vital cardiac parameters such as contractility and peripheral resistance. We compared the cardiac output and MAP during CPR in four scenarios, namely with; (1) sympathetic activation of heart alone, (2) sympathetic activation of the peripheral arteries alone, (3) sympathetic activation of both heart and peripheral arteries, and (4) no sympathetic activation; for different compression pressures and rates. Results: The results show that the cardiac output and MAP increases with increasing compression pressures and rates during CPR with sympathetic activation of peripheral arteries. The sympathetic activation of peripheral arteries during CPR at the AHA and ERC recommended chest compression pressures and rates resulted in an increased MAP, an augmented aortic diastolic pressure and a decreased cardiac output. The results also show that cardiac output and MAP pressure increases with increasing compression rate during CPR with sympathetic activation of heart. There is a slight increase in the MAP but no substantial improvement in cardiac output during CPR with sympathetic activation of heart at the AHA and ERC recommended pressures and rates. Conclusions: It is observed from the study that sympathetic activation of heart during CPR may not be beneficial at the AHA and ERC recommended chest compression rates as it gives very little improvement in cardiac output and MAP. However, performing CPR at higher compression rate may improve the chances of resuscitation when drugs are used to induce sympathetic activity in the heart. The augmented aortic diastolic pressure during CPR with sympathetic activation of peripheral arteries at the AHA and ERC recommended compression pressure and rates can improve the myocardial perfusion, but the reduced cardiac output is a cause of concern.

Heart failure with preserved ejection fraction (HFpEF) represents a major unmet therapeutic need. This study investigated whether feeding coconut oil (CC diet) for 26 weeks in female C57BL/6N mice induces HFpEF and evaluated the effect of reconstituted high-density lipoprotein (HDL)Milano (MDCO-216) administration on established HFpEF. Eight intraperitoneal injections of MDCO-216 (100 mg/kg protein concentration) or of an equivalent volume of control buffer were executed with a 48-h interval starting at 26 weeks after the initiation of the diet. Feeding the CC diet for 26 weeks induced pathological left ventricular hypertrophy characterized by a 17.1% (p &lt, 0.0001) lower myocardial capillary density and markedly (p &lt, 0.0001) increased interstitial fibrosis compared to standard chow (SC) diet mice. Parameters of systolic and diastolic function were significantly impaired in CC diet mice resulting in a reduced stroke volume, decreased cardiac output, and impaired ventriculo-arterial coupling. However, ejection fraction was preserved. Administration of MDCO-216 in CC diet mice reduced cardiac hypertrophy, increased capillary density (p &lt, 0.01), and reduced interstitial fibrosis (p &lt, 0.01). MDCO-216 treatment completely normalized cardiac function, lowered myocardial acetyl-coenzyme A carboxylase levels, and decreased myocardial transforming growth factor-&beta, 1 in CC diet mice. In conclusion, the CC diet induced HFpEF. Reconstituted HDLMilano reversed pathological remodeling and functional cardiac abnormalities.

Optimal right ventricular (RV) function in pulmonary hypertension (PH) requires structural and functional coupling between the RV cardiomyocyte and its adjacent capillary network. Prior investigations have indicated that RV vascular rarefaction occurs in PH, which could contribute to RV failure by reduced delivery of oxygen or other metabolic substrates. However, it has not been determined if rarefaction results from relative underproliferation in the setting of tissue hypertrophy or from actual loss of vessels. It is also unknown if rarefaction results in inadequate substrate delivery to the RV tissue. In the present study, PH was induced in rats by SU5416-hypoxia-normoxia exposure. The vasculature in the RV free wall was assessed using stereology. Steady-state metabolomics of the RV tissue was performed by mass spectrometry. Complementary studies were performed in hypoxia-exposed mice and rats. Rats with severe PH had evidence of RV failure by decreased cardiac output and systemic hypotension. By stereology, there was significant RV hypertrophy and increased total vascular length in the RV free wall in close proportion, with evidence of vessel proliferation but no evidence of endothelial cell apoptosis. There was a modest increase in the radius of tissue served per vessel, with decreased arterial delivery of metabolic substrates. Metabolomics revealed major metabolic alterations and metabolic reprogramming; however, metabolic substrate delivery was functionally preserved, without evidence of either tissue hypoxia or depletion of key metabolic substrates. Hypoxia-treated rats and mice had similar but milder alterations. There is significant homeostatic vascular adaptation in the right ventricle of rodents with PH.

During physiological stress (e.g., exercise, hypoxia), blood flow is shunted to specific anatomical regions to protect critical organs; yet, splenic blood flow in these circumstances remains to be investigated. Despite being classically viewed as a non-critical organ, recent experimental and epidemiological evidence suggests the spleen plays a significant role in cardiovascular pathophysiology. We hypothesized that splenic blood flow is prioritized in the development of heart failure (i.e., chronic state of reduced cardiac output). Five-week-old male Wistar rats were randomized for either myocardial infarction (MI; n = 58) or sham (n = 56) surgery. At 2, 5, and 9 weeks post-surgery, Doppler ultrasound measurements of the splenic, left renal, left common carotid, and left femoral arteries were performed. Cardiac function was assessed at all time points using echocardiography and at 9 weeks post-surgery using invasive hemodynamic analysis. Splenic and cerebral blood flow was preferentially maintained at 9 weeks post-MI, whereas blood flow to the lower limb and kidney were reduced. Spleen size increased by 5 weeks post-MI and remained elevated. Splenic blood flow was maintained in conditions of decreased cardiac output, when other tissues showed decreased blood flow. The maintenance of blood flow in the face of decreased cardiac output indicates that splenic function is being prioritized during heart failure.

During heart failure, chronically decreased cardiac output can be treated with positive inotropes, but classic inotropes such as β-adrenergic receptor (βAR) agonists that increase cAMP-dependent Ca 2+ mobilization and contractility ultimately enhance patient mortality. Thus, an alternate approach would be to enhance cardiomyocyte contractility without alterations in cAMP and Ca 2+ levels, such as regulation of sarcomeric proteins. Recently, we demonstrated that a small lipidated pepducin designed from the 1 st intracellular loop of β2AR (ICL1-9) enhanced cardiomyocyte contractility in a Ca 2+ -independent, β-arrestin-dependent manner. We also showed that β2AR stimulation in hearts in vivo or neonatal rat ventricular myocytes (NRVM) in vitro activates RhoA in a βarr-dependent manner, therefore we sought to determine whether ICL1-9-dependent cardiomyocyte contractility is mediated downstream of RhoA. Using adult murine cardiomyocytes isolated from wild-type C57Bl/6J mice, we measured basal, ICL1-9- and isoproterenol (ISO, as a positive control)-promoted contractility either alone or in the presence of inhibitors of myosin light chain kinase (ML7), ROCK1 (Y-27632) and MEK (PD181452). Consistent with RhoA activation by ICL1-9, ROCK1 inhibition was able to attenuate ICL1-9-mediated contractility, as was inhibition of MLCK, though inhibition of MEK/ERK signaling had no effect. Through the use of GPCR kinase 5 knockout (GRK5KO) cardiomyocytes, we observed that ICL1-9 was unable to enhance contractility in the absence of GRK5 expression. Further, treatment of isolated cardiomyocytes with ICL1-9 increased phoshphorylation of the myosin light chain regulatory subunit (RLC). Therefore, ICL1-9 acts proximally via β2AR/GRK5/βarr-dependent engagement of RhoA/ROCK1 signaling to distally increase RLC phosphorylation, representing a new signaling paradigm for the enhancement of cardiomyocyte contractility.