Blood Pressure And Hemodynamic Adaptations After A: Fill & Download for Free

Drinking cold water does increase blood pressure and here is an information on that and a reference:The aim of this study was to evaluate baseline and cold stress test values and to determine the changes in blood pressure and heart rate. Thus providing a comprehensive overview of the human physiological responses to acute cold exposure. Measurements of blood pressure by Sphygmomanometer was made in 20 healthy young adults before the test and at 1min, 3min and 5min after immersing the hand up to wrist in cold water maintained at 5°C. The initial 60secs of the test represented vascular reactivity to the cold stimulus, and the hemodynamics at 5mins of hand immersion represented the degree of circulatory adaptation to this stimulus. The statistical analysis was done by paired t-test. Most patients responded to the cold pressor test with statistically significant increase in diastolic blood pressure than systolic blood pressure. There was 12.10% rise in systolic blood pressure and 16.02% rise in diastolic blood pressure with 23.09 % rise in heart rate. Heart rate increased significantly (p < 0.05) after 1min of immersion, and by the end of 5mins it reached pre normal values (p < 0.05). The response to cold immersion can be used to assess vascular disorders and predict hypertension in later life.Blood pressure response to cold water immersion test (PDF Download Available). Available from: https://www.researchgate.net/publication/257919736_Blood_pressure_response_to_cold_water_immersion_test [accessed May 10, 2017].Cold weather also has a higher increase on the BP.Blood pressure generally is higher in the winter and lower in the summer. That's because low temperatures cause your blood vessels to narrow — which increases blood pressure because more pressure is needed to force blood through your narrowed veins and arteries.Reference:http://www.mayoclinic.org/diseases-conditions/high-blood-pressure/expert-answers/blood-pressure/faq-20058250

Whether obesity is framed as a disease or not is not the primary factor in stigmatization of obesity. Diseases can be and are stigmatized.What would stop the stigmatization of obesity is a better informed populace.The myth that [math]calories in - calories out = weight[/math] harms efforts to reduce obesity and creates stigma by creating a false belief system about obesity that leads to character assignations of those who are overweight.You’ve probably heard them all.Just the word fat explodes with pejorative assumptions.LazyDumbLow classIgnorantSlobHave I missed any? I’m sure I have.These are all based on the false belief that someone who gets fat does so because:They’re too lazy to exerciseThey’re too dumb to read labelsThey don’t know enough about nutrition to maintain a healthy weightWhat do you expect from the lower classes?They’re couch potatoes who rarely moveWhat is the truth?There are a great many evidence-based hints and even considerable proof that obesity is much more complex than the simplified [math]calories in - calories out = weight[/math] taught in health classes. It’s no wonder that some people give up when what they were taught in school isn’t effective.What do we know about weight that isn’t tied to [math]calories in - calories out = weight[/math]?Hormones affect how our body processes food.Stress and ObesityChronic stress sends signals (cortisol) that increase appetite and reduce our ability to exert self-control that effects weight gain and the difficulty of losing weight.The same person, while not stressed, will be more able to resist foods that cause weight gain and engage in activities and food choices that support weight loss than they are when they are stressed. Stress adversely effects self-control and increases inner urges to eat.Springer’s scientific journal, Current Obesity Reports, published an article, Stress and Obesity: Are There More Susceptible Individuals?, in 2008 where they reported on this connection:“Increased long-term cortisol levels, as measured in scalp hair, are strongly related to abdominal obesity and to specific mental disorders . . . Stress may play a major role in the development and maintenance of obesity in individuals who have an increased glucocorticoid exposure or sensitivity. These insights may lead to more effective and individualized obesity treatment strategies.”[1]Childhood Stress and ObesityThe Journal of Adolescent Health, published Depression, cortisol reactivity, and obesity in childhood and adolescence in 2009, where it was reported that:“The current findings attest to the significance of psychologic states as potential components in models of childhood obesity, and provide conceptual and empirical support for the inclusion of cortisol reactivity in these models.”Longitudinal Stress Experiences and ObesityAn Elsevier journal, Psychoneuroendocrinology, published Stress-related and basic determinants of hair cortisol in humans: A meta-analysis in 2017 where it was reported that:“Our findings reveal positive associations of HCC with stress-related anthropometric (body mass index, waist-to-hip ratio) and hemodynamic measures (systolic blood pressure).”In other words, higher levels of cortisol (the stress hormone) in the historical record hair provides shows that obesity and stress are related.Sleep Deprivation and ObesityThe scientific journal, Current Opinions in Clinical Nutrition and Metabolic Care published, Sleep and Obesity in 2011 reported on the link between sleep deprivation and obesity.[2]“Recent epidemiological and laboratory evidence confirm previous findings of an association between sleep loss and increased risk of obesity.”The CDC[3] declared sleep deprivation an epidemic public health emergency with 35% of Americans experiencing insufficient sleep.Sleep deprivation is a form of stress that causes all the issues associated with other forms of chronic stress and more. Because sleep is when our bodies and minds repair themselves, inadequate sleep means the person is dealing with the effects of chronic stress without the restorative benefits of sleep.Racism and ObesityAn article published in the Elsevier scientific journal, Journal of the National Medical Association, published Coping With Perceived Racism: A Significant Factor in the Development of Obesity in African American Women? in 2011.[4] This is one of many articles that attempts to identify causes of obesity in black women. Research focuses on this demographic because they have the highest percentage of obesity. Racism is stressful. Stress contributes to obesity. Whether their are other reasons for higher percentages of obesity in this demographic is not yet established, but reducing racism and increasing health promoting coping skills would go a long way toward reducing the prevalence of obesity in every demographic.Another Elsevier scientific journal, Social Science & Medicine, published The weight of racism: Vigilance and racial inequalities in weight related measures in 2018, where they discussed how the stress caused by racism effects weight:[5]“Chronic psychosocial stress may play an important role in obesity inequalities. First, research indicates that consumption of high calorie, high saturated fat foods in response to psychological stress results in the release of certain biochemicals known to reduce feelings of stress (Dallman et al., 2003; Dallman et al., 2005). Moreover, psychosocial stress alters metabolism to result in visceral adipose deposition specifically (Dallman et al., 2005). Second, there are racial inequalities in psychosocial stress and social stressors (Jackson et al., 2010; Schulz et al., 2005; Turner, 2009).”Physiology and ObesityThe physiological effects of stress are too complex for this article. If you would like to explore those relationships at the biological level, Regulation of the Hypothalamic‐Pituitary‐Adrenocortical Stress Response provides a starting point.Clinical Practices Fail Obese PatientsWiley’s scientific journal, Obesity reviews, published an article, A comprehensive diagnostic approach to detect underlying causes of obesity in adults, in 2019, where they elaborated a long list of factors that could cause or contribute to obesity:[6]“Obesity is a worldwide growing problem. When confronted with obesity, many health care providers focus on direct treatment of the consequences of adiposity. We plead for adequate diagnostics first, followed by an individualized treatment. We provide experience‐based and evidence‐based practical recommendations (illustrated by clinical examples), to detect potential underlying diseases and contributing factors. Adult patients consulting a doctor for weight gain or obesity should first be clinically assessed for underlying diseases, such as monogenetic or syndromic obesity, hypothyroidism, (cyclic) Cushing syndrome, polycystic ovarian syndrome (PCOS), hypogonadism, growth hormone deficiency, and hypothalamic obesity. The most important alarm symptoms for genetic obesity are early onset obesity, dysmorphic features/congenital malformations with or without intellectual deficit, behavioral problems, hyperphagia, and/or striking family history. Importantly, also common contributing factors to weight gain should be investigated, including medication (mainly psychiatric drugs, (local) corticosteroids, insulin, and specific β‐adrenergic receptor blockers), sleeping habits and quality, crash diets and yoyo‐effect, smoking cessation, and alcoholism. Other associated conditions include mental factors such as chronic stress or binge‐eating disorder and depression.Identifying and optimizing the underlying diseases, contributing factors, and other associated conditions may not only result in more effective and personalized treatment but could also reduce the social stigma for patients with obesity.”[7]Since that is a bit difficult to read in a direct quote, here’s a list of the factors the scientists encourage physicians to investigate before assuming that obesity is related to overeating or lack of physical activity.[8]Monogenetic or syndromic obesityHypothyroidism(cyclic) Cushing syndromePolycystic ovarian syndrome (PCOS)HypogonadismGrowth hormone deficiencyHypothalamic obesityMedicationCorticosteroidsInsulinSpecific β‐adrenergic receptor blockersSleeping habits and quality (keep in mind that the CDC has declared sleep deprivation an epidemic)Crash dietsYoyo‐effectSmoking cessationAlcoholismChronic stressBinge‐eating disorderDepressionGenetic obesity is related to:Early onset obesityDysmorphic features/congenital malformations with or without intellectual deficitBehavioral problemsHyperphagiaStriking family historyAs long as this list is, one of the newer scientific discoveries about obesity is missing as well as one that has been known for a while. Most of these contributing factors have been known for a long while. The news that obesity is not caused solely, or even primarily, by the dumbed down formula that so many lean on to justify their poor treatment of obese individuals, [math]calories in - calories out = weight[/math] is not new news. The knowledge base is continuing to expand but the basics have been known for decades.This childhood cause of obesity was not included in the above list:[9]Prader-Willi Syndrome (PWS)A Dutch scientific journal, NTvG, published an article, Obesitas in de spreekkamer which translates to Obesity in the doctor’s office: First Diagnostics and then Effective Treatment, in 2017 that reported:“In clinical practice, relatively little attention is directed towards identifying underlying causes and contributing factors to weight gain in patients with obesity. However, recognising these "hidden fattening factors" is important as it can lead to more effective treatment strategies. In particular if underlying causes can be solved first, this could help to realise sustainable weight reduction. Besides the well-known lifestyle-related aspects, obesity may be caused or maintained by medication use, endocrine or hypothalamic disorders, monogenetic or syndromic diseases, and mental factors, which may require specific (medical) treatment.”[10]Estrogen and ObesityAn Oxford Academic journal article, Human Reproduction Update, published Ovarian hormones and obesity in 2007 where they began their conclusion with this statement:[11]“We find that estrogens play a leading role in the causes and consequences of female obesity.”Childhood Abuse and ObesityOther studies, such as Associations of child sexual and physical abuse with obesity and depression in middle-aged women, have associated childhood maltreatment as a risk factor for obesity, depression, and eating disorders. For victims of abuse, weight loss may make them feel more vulnerable.[12] The excess weight affords protection against undesired attention, especially sexual advances. Many of these patients regain the weight because they are more comfortable. Until the underlying trauma is healed, they are likely to continue regaining weight following successful weight loss. Treating the trauma should be a priority.In a study of 57,000 women, childhood abuse more than doubled the risk of food addiction.[13] Current estimates are that up to 1 out of 5 children in the United States have a mental health disorder.[14]Let’s pause for a moment. How many people would knowingly choose to kick someone who is down because of horrific experiences they endured as children? Not many people would do so willingly if they were introduced to the scenario in a way that makes it clear that the person was a victim.If we began conversations about weight by talking about the precursors, whether that is the mother’s depression while they were a fetus,[15] childhood abuse, or chronic stress experienced as an adult, few people would treat the word fat as a four-letter word. Few people would kick the proverbial dog while it’s down by stigmatizing obesity, discriminating against individuals who are obese, or subtracting IQ points due to obesity.[16]If a smart person wants to trick someone into believing the smart person is less intelligent than they are, all they have to do is gain weight. — Jeanine JoyGut Microbiota and ObesityThis area of research is very active but human studies have not reached any definitive conclusions, yet.[17] However, animal studies have provided reasons to hope that studying gut microbiota may lead to new treatments for obesity. At least one animal study reported weight loss when a fecal transplant between a lean mouse and an obese mouse was performed.This is an area to watch. It is also something to consider before stigmatizing obesity. We don’t yet know all the factors yet people who are fat are blamed for their obesity. It reminds me of the witch trials that blamed witches for things that the people of the time couldn’t explain because they didn’t know what they didn’t know.Stigma Contributes to the Obesity EpidemicSome people believe that stigmatizing obesity is an effective method of encouraging weight loss. They couldn’t be more wrong.The American Journal of Public Health published an article, Obesity Stigma: Important Considerations for Public Health in 2010, that discussed evidence that stigma worsens the obesity problem.[18]“Stigma and discrimination toward obese persons are pervasive and pose numerous consequences for their psychological and physical health. Despite decades of science documenting weight stigma, its public health implications are widely ignored. Instead, obese persons are blamed for their weight, with common perceptions that weight stigmatization is justifiable and may motivate individuals to adopt healthier behaviors. We examine evidence to address these assumptions and discuss their public health implications. On the basis of current findings, we propose that weight stigma is not a beneficial public health tool for reducing obesity. Rather, stigmatization of obese individuals threatens health, generates health disparities, and interferes with effective obesity intervention efforts. These findings highlight weight stigma as both a social justice issue and a priority for public health.”In other words, those who stigmatize obesity contribute to the problem. They are piling on another form of abuse to people who are often victims of abuse, ill, or chronically stressed. Stigma increases the stress obese individuals experience which makes it more difficult to manage their weight!SummarySociety has been attempting to fight obesity for decades; the epidemic of obesity has increased, not decreased, for the duration of the battle. This is an indicator that the war is being waged on the wrong battlefront.Psychosocial stress, whether it is the result of childhood abuse, discrimination, racism, poverty, sleep deprivation, or stigma about obesity, mental health, or a combination of these factors is a significant contributing factor to obesity.We’ve also been fighting against racism, poverty, and childhood abuse for decades with little success except on the racism front.It seems that the advances have primarily benefited minorities who manage to escape poverty. Those who remain in poverty experience far more racism than those who are in middle or upper socioeconomic classes. Or, perhaps I am confusing economic stigma with racism. I haven’t seen research that has been able to separate these two factors. Regardless, the stress caused by racism still effects a large number of Americans.Additionally, with up to 1 out of 5 children experiencing mental health issues, we certainly have not resolved childhood abuse and trauma issues. There is a disproportionate effect on children living in poverty because their environments tend to include more trauma, whether it is violence in the streets or in the home, children living in poverty are exposed to more adverse childhood experiences than those living in higher socioeconomic circumstances. That is not to say that children in better socioeconomic situations are immune from trauma and abuse as they aren’t, which is why all children should be screened for mental health needs.A New (Better) Approach to the Obesity EpidemicThere is one approach to obesity that has not yet had a great deal of support from clinicians or public health officials despite a significant and growing body of evidence demonstrating its efficacy.Psychosocial stress is handled in different ways by different people.[19] One person experiencing a specific situation may not feel stressed while a similarly situated person may feel overwhelming stress from the same situation. After decades evaluating the reasons one person feels low stress and another feels high stress in similar situations, it is clear that our habits of thought and underlying beliefs about ourselves and the world determine how much stress we feel in any given situation.When similarly situated person is used, it means that someone with the same economic and social resources, age, race, and education are being compared — not someone with money vs someone without money or someone who is married with someone who is single. It is not the situation, but the way the situation is perceived that determines how much stress is experienced by a specific individual.Coping methods for dealing with stress vary from dysfunctional and maladaptive methods that make the situation worse. These methods include drug and alcohol abuse, self-criticism, avoidance, eating, and a host of other common strategies. The difference between dysfunctional and maladaptive methods is how long it takes for the method to make things worse.Then there are palliative methods which are the most commonly recommended methods of stress management. When someone goes into palliative care, they are given comfort care but no attempts to cure them are made. When it comes to psychological stress reduction, palliative has the same definition. It soothes but does not cure the cause of the stressors.Adaptive coping goes a step further, building skills that make the person better prepared for the stressors encountered. While this method is better than dysfunctional, maladaptive, and palliative care, unless the skills learned increase the skill the person develops to deal with all types of stress they are generally effective on a situational basis. For example, learning how to make a household budget can alleviate financial stress from poor money management but does nothing for the stress of job insecurity or discrimination experienced at work or when job hunting.Advanced coping skills are a level up because they train the mind to use psychological flexibility to change the level of stress experienced without first requiring the situation to change. This opens up resources the individual can then use to change their situation.The final level, Transformational Coping Skills, is the result of continuously applying Advanced Coping Skills. Transformational Coping Skills are in place when the mind automatically perceives situations in ways that are less stressful. Individuals who reach this level are resilient and naturally adjust to life’s challenges without suffering adverse consequences experienced by those whose stress management skills are less developed.Benefits of Increased Healthy Coping SkillsWe cannot stop stressors with the wave of a magic wand but we can change the impact those stressors have on health and the quality of life individuals experience by teaching healthy, evidence-based coping skills.Exploring the research related to this topic reveals that many of the social problems that contribute to disparate health outcomes are driven by dysfunctional and maladaptive coping skills.Whether it is childhood outcomes, workplace engagement or burnout concerns, or mental health, developing healthy habits of thought improves outcomes.An interesting thing happens when someone is no longer detrimentally effected by a stressor, such as stigma. It stops effecting their outcome, yes, but beyond that, those who take pleasure in kicking someone when they are down don’t get the pleasure because their verbal and behavioral blows no longer have the desired effect.On the flip side, someone who feels good (which is an outcome of healthy habits of thought and coping skills) has no desire to put someone else down. When you feel authentically good, making someone else feel bad would make you feel worse. To preserve their own good feelings, people who feel good don’t deliberately make others feel bad.There are strong arguments in favor of schools and employers teaching these skills. The solutions make financial sense and there are strong public health reasons for pursuing this path. That would move us toward a solution instead of simply renaming the problem.Expanded Information Related to this TopicJeanine Joy's answer to Do you find this as an agreeable possibility that sometimes it's the bad brought up in childhood that manifests as a psychiatric illness later in life? Why or why not?Jeanine Joy's answer to Should you teach kids to thrive in your classroom, as a skill to be taught?Regulating Emotions to Beat Opioid AddictionA broader view of solutions for the physician burnout public health crisis: prevention and recovery. When my husband told me that 10 prominent health system CEO's committed to do 11 things about the healthcare crisis that is physician burnout, I was excited.How Should Your Organization Prioritize Employee Stress and Mental Health?AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY COMPREHENSIVE CLINICAL PRACTICE GUIDELINES FOR MEDICAL CARE... - PubMed - NCBII’m aware that some folks would prefer to hear from an MD. Here’s an MD also saying that obesity isn’t calories in - calories out = weight.Amy Chai's answer to Why did the American medical association decide to label obesity as a chronic disease given that it’s obviously a condition?Amy Chai's answer to Are we normalizing obesity? Is this foresight to an unhealthy future for greater society?Footnotes[1] Stress and Obesity: Are There More Susceptible Individuals?[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3632337/pdf/nihms-459205.pdf (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3632337/pdf/nihms-459205.pdf)[3] CDC Works 24/7[4] Coping With Perceived Racism: A Significant Factor in the Development of Obesity in African American Women?[5] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5617791/pdf/nihms879406.pdf (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5617791/pdf/nihms879406.pdf) [6] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850662/ (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850662/)[7] A comprehensive diagnostic approach to detect underlying causes of obesity in adults[8] A comprehensive diagnostic approach to detect underlying causes of obesity in adults[9] Prader-Willi Syndrome (PWS)[10] [Obesity in the clinic room: diagnostics first, followed by effective treatment].[11] Ovarian hormones and obesity[12] How childhood trauma can affect mental and physical health into adulthood[13] Abuse victimization in childhood or adolescence and risk of food addiction in adult women[14] What Are Childhood Mental Disorders? | CDC[15] Foetal exposure to maternal depression predicts cortisol responses in infants: findings from rural South India.[16] Obesity Discrimination in the Recruitment Process: “You’re Not Hired!”[17] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5933040/pdf/IJE2018-4095789.pdf[18] Obesity Stigma: Important Considerations for Public Health[19] Jeanine Joy's answer to How do people respond to psychological stress?

AbstractWe implanted a continuous-flow total heart replacement device in a 55-year-old man who had severe end-stage heart failure due to amyloidosis and no other options for treatment. The device was composed of 2 modified HeartMate II ventricular assist pumps. After the implantation, our patient recovered normal neurologic function and was able to converse with his family and work on his computer. He died of multisystem organ failure caused by severe amyloidosis 5 weeks after the implantation.During the past 6 years, we have been developing and testing various technological iterations for total heart replacement in our animal laboratory and have achieved survival periods as long as 90 days in calves. We describe the development, preclinical trials, and adaptation for human use of the modified HeartMate II apparatus, as well as its role in our patient's survival.Keywords: Amyloidosis/therapy, biomedical engineering, blood flow velocity, heart, artificial, prosthesis designDuring the past 6 years, we have been developing a continuous-flow device to totally replace the failing heart. The device, composed of 2 continuous-flow ventricular assist devices, has been subjected to extensive in vivo testing, with survival periods as long as 90 days in calves. In March 2011, we first used a similar device to replace the heart of a man who had refractory heart failure due to amyloidosis. The patient had no other treatment options. We describe this device's development, preclinical trials, adaptation for human use, and role in the patient's survival.Case ReportA 55-year-old man was admitted to our institution in February 2011. He had rapidly progressive end-stage heart failure due to amyloidosis, which was confirmed histologically (Fig. 1). Intra-aortic balloon pump counterpulsation and intravenous inotropic therapy were unsuccessful in restoring adequate circulation. The patient had to be intubated because of progressive respiratory distress and was undergoing continuous hemodialysis for anuric renal failure. At that point, we decided to try extracorporeal circulatory assistance with the use of a TandemHeart® (CardiacAssist, Inc.; Pittsburgh, Pa). A transseptal 21F left atrial cannula was placed percutaneously via the right femoral vein, and a 17F cannula was placed via the left femoral artery. Because of severe right ventricular compromise, only 3 L/min of flow was attainable with the device. Despite multiorgan failure, the patient's neurologic function remained intact. An echocardiogram obtained after 2 weeks of TandemHeart support showed a small, akinetic-restricted heart and no evidence of myocardial recovery.An external file that holds a picture, illustration, etc.Object name is 15FF1.jpgFig. 1 Photomicrograph. A section of the left ventricular wall shows eosinophilic deposits of amyloid surrounding individual myocytes, interstitial spaces, and blood vessel walls (H & E, Orig. × 10).Options were limited for this gravely ill patient, partially because of his small physical stature (height, 175.3 cm; weight, 63.2 kg). However, we thought that he might be a candidate for heart and bone marrow transplantation if his other organs could recover enough function.1 Emergent cardiac transplantation was not considered, not only because of the logistical unlikelihood of finding a donor but also because the patient's critical condition would have made post-transplantation survival unlikely.The use of a left or right ventricular assist device was considered for intermediate-term circulatory support. However, the patient's extremely thickened and stiff left ventricular (LV) wall and small, contracted LV cavity were contraindications to LV assist device placement. In such patients, obtaining an unobstructed inlet-cannula position is extremely difficult. In addition, the patient's small body habitus and hepatomegaly greatly limited the space available for an implantable subdiaphragmatic pump, necessitating paracorporeal device placement. The Syn Cardia CardioWest® pneumatically actuated total artificial heart (SynCardia Systems, Inc.; Tucson, Ariz) was also not an option: the patient had a narrow chest cavity, and suturing the device to the stiff amyloid-infiltrated rim of ventricular muscle would have been a technical challenge. For this second reason, advanced cardiac amyloidosis is a contraindication to the use of the SynCardia pump. We finally decided to replace his heart with 2 HeartMate® II axial-flow pumps (Thoratec Corporation; Pleasanton, Calif) that would function as a continuous-flow total heart replacement. To achieve this, we used customized atrial adapters that we had developed for use with the HeartMate II blood pumps during the preceding 6 years of extensive in vitro and in vivo preclinical studies.The Continuous-Flow Total Heart Replacement DeviceThe 2 atrial adapters used in this case were fabricated from knitted polyester Vascutek® Gelseal™ cardiovascular patches (Terumo Cardiovascular Systems Corporation; Ann Arbor, Mich) that were reinforced with 4 layers of 10 × 14-in polypropylene hernia repair mesh (C.R. Bard, Inc.; Murray Hill, NJ). The adapters were impregnated with medical-grade silicone adhesive and subjected to both ethylene-oxide and steam sterilization. Each polyester patch was fashioned into a cone of proper dimension (20° at the apex) by using a single hand-sewn line of 5-0 polypropylene suture. Each polyester cone was then placed over a solid plastic mandrel to hold the conical geometry while the outer layers were reinforced with the polypropylene hernia mesh and medical silicone adhesive. When the adhesive had dried, the cones were removed from the mandrels, and the apex of each cone was excised at a sharp angle. The resulting elliptical opening was then measured, and an elliptical patch of the same dimensions was fashioned from mesh-reinforced polyester. A round hole, 14 mm in diameter, was then cut in each elliptical patch close to one end to accommodate the HeartMate II inflow after removal of the inflow cannulas.Implantation ProcedureAfter extensive discussion with the patient and his family about the procedure, they decided to proceed, and written informed consent was obtained. We implanted the pumps through a median sternotomy, placing a right-angled, wire-reinforced venous cannula in both the superior and inferior venae cavae. The circulation was transferred from the TandemHeart to full cardio-pulmonary bypass, after which circumferential caval tapes were placed and tightened. The heart was excised as if for transplantation, including the removal of all ventricular muscle, all 4 valves, and both atrial appendages. The 2 layers of the atrial septum were carefully teased apart, thereby separating the left and right atria. The fossa ovalis, the only tissue held in common by both atria, was preserved on the left atrial side.2 By separating the atria, we were able to displace the right atrium laterally and the left atrium caudally, which greatly facilitated the anatomic placement of the 2 pumps.The 2 previously constructed cones were tailored by beveling the bases, leaving an opening in each base approximately the same size as the perimeter of each atrial remnant. The bevels were cut so as to direct the apex of each cone inferiorly and to the left, so that the Heart-Mate II inlets would be as far as possible from the transected ends of the aorta and pulmonary artery. The cones were then sutured to the cut edges of the left and right atrial remnants with running 2-0 polypropylene sutures and felt strips for reinforcement.The inlets of the 2 HeartMate II pumps were removed from the pump housing by unscrewing the blue anodized collets. The inlets were customized by excising the white silicone-elastic bellows. After the bellows were removed, the 14-mm, silicone-coated polyester grafts were visible. These grafts were transected approximately 3 mm from the curved titanium tube that attached the inlets to the pump housing. The 3-mm rim of the 14-mm graft was then sutured to the 14-mm hole in the elliptical patch with a 5-0 polypropylene suture. The elliptical patches were sutured to the elliptical holes at the apex of each cone, completing the construction of the atrial adaptors. Each adaptor was then pressurized with a dedicated system that allowed the suture lines to be inspected for hemostasis. The curved titanium tubes, now attached to the atrial adaptors, were reattached to the inlet end of the HeartMate II pumps.The outflow grafts of each pump were cut to the appropriate length and were sutured in an end-to-end fashion to the cut ends of the aorta and pulmonary artery with the use of 5-0 polypropylene sutures. The curved titanium tube attached to the outlet of the right pump was rotated to direct the outflow graft toward the pulmonary artery anterior to the aorta. A customized straight titanium outflow adaptor was used on the left pump. Tailored anastomoses were performed to accommodate the size discrepancy between the outflow grafts and the 2 large vessels Hemostasis was ensured, and desiring maneuvers were performed. Full mechanical ventilation was then resumed, and the patient was weaned from cardiopulmonary bypass while the left and right pump flows were progressively increased. All cannulas were removed, and protamine was administered to the patient. After undergoing temporary chest closure, the patient was taken to the intensive care unit in guarded condition but with an excellent hemodynamic status. Several hours later, however, he was taken back to the operating room because of excessive bleeding. A leak in the pulmonary anastomosis was found and repaired. The next day, he underwent definitive chest closure. The pericardial sac was reconstructed with polytetrafluoroethylene to facilitate a possible future heart transplantPostoperative ResultsThe patient's hemodynamic values remained stable for the next 5 weeks with little adjustment of the left or right pump speed. Only his central venous pressure and arterial pressure were continuously monitored during the postoperative period; pulmonary pressure was not monitored, nor was left or right atrial pressure. The central venous pressure was maintained between 5 and 10 cm H2O and the arterial pressure between 70 and 90 mmHg. The calculated flow through the left pump was between 5 and 6 L/min. In the immediate postoperative period, the pump speed was altered as necessary to obtain these values. By the 3rd postoperative day, we were able to keep the 2 pumps at constant speeds: the right pump at 8,390 rpm and the left at 10,590 rpm (Fig. 4).An external file that holds a picture, illustration, etc.Object name is 15FF4.jpgOpen in a separate windowFig. 4 Photographs show automaticity of response of the continuous-flow pumps, with direct correlation of inlet pressure to flow at constant revolutions per minute (rpm). A) The right flow is at 6,400 pm, the left at 10,600 pm. The power generated by the pump is directly correlated to blood flow through the pump. B) The right pump has been increased manually to 8,390 rpm. The concomitant increase in the input power of the pump indicates an increased inflow. In the left pump, there is an immediate response in power from 6.9 to 8 W with no change in the rpm. The intrinsic characteristic of continuous-flow pumps to respond automatically to inlet pressure, analogous to the mammalian heart, would enable left- and right-sided heart flow imbalances to be corrected automatically.Although the patient had been intubated for 18 days before implantation, his blood gas values improved quickly, and he was extubated successfully on the 4th postoperative day. After extubation, he was alert, oriented, and conversant with his family. However, on day 9, he aspirated and had to be reintubated. A therapeutic bronchoscopy was performed, and a lung biopsy revealed extensive amyloidosis. Subsequently, a tracheostomy was performed. However, prolonged respiratory support was not required, and the patient was maintained on a tracheostomy collar thereafter. The preoperative anuria persisted throughout the postoperative course, necessitating continued hemodialysis. His liver function continued to worsen slowly. Laboratory evaluation revealed a normal acid-base balance and no evidence of hemolysis, but the bilirubin level progressively rose, and by the 4th postoperative week, liver failure was impairing the patient's prior alert mental status. At that point (5 weeks after implantation), after extensive discussion with the family, we withdrew care, because of the multisystemic amyloid involvement and the extremely poor prognosis.Autopsy results confirmed the presence of advanced multisystemic amyloidosis (heart, liver, lung, and kidney). The atrial adaptors of the total heart replacement device were lined with a smooth, shiny layer of neointima, and both pumps were free of thrombus.Go to:DiscussionWe implanted a continuous-flow total heart replacement device in a patient who had severe end-stage heart failure and no other options for treatment. After the implantation, the patient recovered normal neurologic function and was able to communicate with his family and work on his computer. Unfortunately, after 5 weeks of support, he died of progressive hepatic failure caused by severe amyloidosis.The development of a self-contained, robust, and reliable mechanical pump for replacing the failing human heart has heretofore posed a prohibitive technical challenge. To date, completely implantable pulsatile-output, volume-displacement devices have been limited by cyclic fatigue. Moreover, size constraints have made these pumps useful in only the physically largest of patients. Externally actuated devices, such as the pneumatic Syn-Cardia pump, are smaller but remain susceptible to cyclic fatigue and require an external drive unit, which limits their application to patients who are awaiting transplantation. The need remains for a durable, reliable artificial heart with a useful life of 10 years or longer.More than a decade of clinical experience has clearly revealed that rotary blood pumps have benefits over volume-displacement pumps, especially with respect to size and, more important, durability. Little is known, however, about the long-term effects of true pulseless circulation. Many patients who have received axial-flow or centrifugal-flow rotary blood pumps as LV assist devices no longer have a palpable pulse. In nearly every case, however, the arterial pressure still rises and falls with each cardiac contraction in response to inflow pressure sensitivity, which is characteristic of rotary blood pumps. When a rotary blood pump is used to replace the heart rather than to assist it, there is no time variation in the arterial pressure. In this setting, the pump can be said to provide steady-state, pulseless perfusion, in contrast with the perfusion that results when such a pump is used as a ventricular assist device.For 6 years before encountering the above-described patient, we had been working in our large-animal laboratory to develop a fully implantable total heart replacement device and to characterize the mammalian physiologic response to steady-state, pulseless perfusion. To that end, we implanted various prototypes of the device in more than 40 calves. Each prototype consisted of a pair of rotary blood pumps configured so that they could be readily sutured to the atrial remnant after the excision of the entire heart. The iterative experience gained in this research enabled us to develop adaptors that would meet the requirements of total heart replacement. With progressive refinement of our custom cuffs and surgical technique, we were routinely able to implant the device successfully in the bovine model: the animals generally stood upright within the first 12 hours postoperatively and survived for at least 1 or 2 months. The longest survivor was humanely killed at 90 days. The animals were able to exercise on a treadmill and had normal end-organ function and neuro-hormonal responses throughout their postoperative courses. Most important, we were able to demonstrate the automaticity of these pumps to variations in inflow pressure. This important characteristic of continuous-flow pumps enables correction of the natural imbalance of right and left ventricular output due to the bronchial circulation, which has been a barrier to totally implantable pulsatile heat pump replacements.3 When our calves were placed on treadmill exercise, this inflow responsivity also permitted increased blood flow and oxygen consumption without a need to change the speed. This automatic balancing in response to increased inflow pressure was shown repeatedly in our patient (Fig. 4).Although other pumps used in our preclinical experiments might have been technically easier to implant than the HeartMate II as a clinical cardiac replacement device and would have required less complex atrial adaptors, only the HeartMate II was approved for human use at the time of this implantation. Indeed, we had specifically developed HeartMate II adaptors that would be suitable for use if the opportunity arose for clinical implantation.In this clinical experience, we demonstrated the feasibility of total nonpulsatile circulatory replacement after the removal of a patient's diseased heart. Continuous-flow pumps have a number of advantages for use as a total heart, including durability and small size, making them feasible for people of all sizes—even infants and children. Patients have lived more than 8 years thus far with continuous-flow ventricular assist devices, without evidence of pump wear, and we anticipate that these pumps will last for 10 to 15 years. Of note, the automaticity of response that is characteristic of continuous-flow pumps greatly simplifies the application of this technology to total heart replacement. However, this technology does not confine us to total nonplus-tile flow. If future experience shows that some pulsatility is optimal, continuous-flow pumps can be rendered pulsatile. We have previously induced pulsatility in our experimental models4 and continue to conduct research experiments to test the relative role of pulsatility in experimental animals.AcknowledgmentsThe authors acknowledge Pranav Loyalka, MD, for his clinical care of the patient described in this case; and Diana Kirkland and Marianne Mallia, ELS, of the Department of Scientific Publications at the Texas Heart Institute, for their editorial assistance in the preparation of the manuscript.