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Background: Observational studies have shown that heart rate (HR), heart rate variability (HRV), P-wave terminal force, P-wave duration, T-wave amplitude and PR interval are associated with risk factors for atrial fibrillation (AF) or bradycardia. Arrhythmias are associated with many causes of hospitalization. However, observational studies are susceptible to confounding factors that have not yet been identified. The objective of this study was to clarify the causal relationships by Mendelian randomization analysis. Methods: We conducted a two-sample and multivariate Mendelian randomization (MVMR) analysis using genome-wide association study (GWAS) data from a European population to assess the total and direct causal effects of HR, three HRV traits, P-wave terminal force, P-wave duration, T-wave top amplitude in five-lead modes, and the PR interval on the risk of AF (N=191,205), bradycardia (N=463,010), and supraventricular tachycardia (SVT) (N=463,010). Results: The results of the univariate MR analysis revealed the following significant causal effects: the higher the genetically predicted PR interval, the lower the risk of AF; the higher the HR and T-wave top amplitude (aVR leads and V3 + V4 + aVL leads), the lower the risk of bradycardia; and the higher HR and the lower PR interval, the higher the risk of SVT. The multivariate MR results indicated that the HRV_ standard deviation of the normal-to-normal (SDNN) interval had an independent causal effect on the risk of AF [odds ratio (OR): 0.515; 95% confidence interval (CI): 0.278–0.954; P=0.03], and the T-wave top amplitude in the aVR leads (OR: 0.998; 95% CI: 0.996–0.999; P<0.001) and the HRV_SDNN (OR: 0.988; 95% CI: 0.976–1.000; P=0.045) had independent causal effects on the risk of bradycardia. Conclusions: The HRV_SDNN had an independent causal effect on AF, while the HRV_SDNN and T-wave top amplitude in the aVR leads had independent causal effects on bradycardia, which suggests that some of the electrocardiog

Swimming and diving are popular recreational activities, representing an effective option in maintaining and improving cardiovascular fitness in healthy people. To date, only little is known about the cardiovascular adaption to submersion in children. This study was conducted to improve an understanding thereof. We used a stepwise apnea protocol with apnea at rest, apnea with facial immersion, and at last apnea during whole body submersion. Continuous measurement of heart rate, oxygen saturation, and peripheral resistance index was done. Physiologic data and analysis of influencing factors on heart rate, oxygen saturation, and peripheral vascular tone response are reported. The current study presents the first data of physiologic diving response in children. Data showed that facial or whole body submersion leads to a major drop in heart rate, and increase of peripheral resistance, while the oxygen saturation seems to be unaffected by static apnea in most children, with apnea times of up to 75 s without change in oxygen saturation.

Objectives: The transradial route is used in most coronary procedures today. Although this method seems to be advantageous in terms of bleeding complications and patient comfort, the small radial artery diameter brings with it complications such as radial artery spasm and occlusion. It has been demonstrated in previous studies that subcutaneous nitrate administration dilates the radial artery. The Glidesheath Slender, which has a thinner outer wall than conventional sheaths, is another method that has been shown to reduce complications by reducing friction on the radial artery wall. Our aim was to compare these two methods in terms of complications. Methods: We retrospectively reviewed patients with complete clinical and radial Doppler ultrasound records who had undergone transradial interventions. We compared procedures using subcutaneous nitrate application plus conventional sheaths with procedures using the Glidesheath Slender sheath in terms of procedural and postprocedural complications. Results: Eighty-seven patients in the subcutaneous nitrate group and 35 patients in the Glidesheath Slender group were included in the study. There were no significant differences between the two groups in terms of procedural and postprocedural complications (p = 0.511 and p = 0.333, respectively). Conclusions: In cases where a thin-walled sheath such as a Glidesheath Slender is not available, subcutaneous nitrate administration seems to be similar, especially in terms of preventing radial artery spasm. © 2024, Republic of China Society of Cardiology. All rights reserved.

Introduction Endurance sport participation has many health benefits including improved cardiovascular fitness and longer life expectancy. It is a paradox that endurance sport participation is also associated with cardiac arrhythmias. The true prevalence and incidence of arrhythmias in endurance athletes is difficult to define due to variable definitions of endurance sport participation and identifying athletes with arrhythmias. There are several proposed mechanisms by which endurance sport may predispose athletes to arrhythmias. Aims The aim of this thesis is to characterise what electrophysiologic changes are normal in endurance athletes, define the risk of arrhythmias attributable to endurance sport participation and investigate the mechanistic causes for an increased burden of arrhythmias. Results To characterise normal electrophysiologic changes in endurance athletes we recruited 223 current and former athletes as well as fifty-two nonathletic control participants. We found that bradycardia and notably ventricular pauses are very common in athletes and rare in non-athletes. We found no significant association of ectopic burden with endurance sport. To investigate the mechanisms by which endurance sport leads to bradycardia in athletes we performed an experimental study in thirty volunteers split equally between nonathletes, endurance athletes and endurance athletes with extreme bradycardia. By administering autonomic blockade, we confirmed that bradycardia in athletes is not due to autonomic influence. Furthermore, this is the first study which has shown high vagal tone does not explain extreme resting bradycardia in athletes. To better define the risk of atrial fibrillation attributable to endurance sport, we performed a case control study which strictly defined past endurance sport participation. We recruited 121 former elite rowers who competed at a national, world championship or Olympic level and compared them to an age, gender and ethnicity matched cohort

Background and objectivesBRAT1 encephalopathy is an ultra-rare autosomal recessive neonatal encephalopathy. We delineate the neonatal electroclinical phenotype at presentation and provide insights for early diagnosis.MethodsThrough a multinational collaborative, we studied a cohort of neonates with encephalopathy associated with biallelic pathogenic variants in BRAT1 for whom detailed clinical, neurophysiologic, and neuroimaging information was available from the onset of symptoms. Neuropathologic changes were also analyzed.ResultsWe included 19 neonates. Most neonates were born at term (16/19) from nonconsanguineous parents. 15/19 (79%) were admitted soon after birth to a neonatal intensive care unit, exhibiting multifocal myoclonus, both spontaneous and exacerbated by stimulation. 7/19 (37%) had arthrogryposis at birth, and all except 1 progressively developed hypertonia in the first week of life. Multifocal myoclonus, which was present in all but 1 infant, was the most prominent manifestation and did not show any EEG correlate in 16/19 (84%). Video-EEG at onset was unremarkable in 14/19 (74%) infants, and 6 (33%) had initially been misdiagnosed with hyperekplexia. Multifocal seizures were observed at a median age of 14 days (range: 1-29). During the first months of life, all infants developed progressive encephalopathy, acquired microcephaly, prolonged bouts of apnea, and bradycardia, leading to cardiac arrest and death at a median age of 3.5 months (range: 20 days to 30 months). Only 7 infants (37%) received a definite diagnosis before death, at a median age of 34 days (range: 25-126), and almost two-thirds (12/19, 63%) were diagnosed 8 days to 12 years postmortem (median: 6.5 years). Neuropathology examination, performed in 3 patients, revealed severely delayed myelination and diffuse astrogliosis, sparing the upper cortical layers.DiscussionBRAT1 encephalopathy is a neonatal-onset, rapidly progressive neurologic disorder. Neonates are often misdiagnosed as hav

Introduction: Hellp syndrome and hepatic rupture is a rare complication especially in cases of twin pregnancy, we present the case of a ruptured hepatic subcapsular hematoma due to HELLP syndrome complicating a twin pregnancy that required emergency cesarean section and for the management of hypovolemia hepatic packing. Case presentation: Female, 41 years old, twin pregnancy of 35 weeks, came to the emergency room for uterine contractions and absence of fetal movements. Due to severe bradycardia in both fetuses, an emergency cesarean section was performed. When the abdominal cavity was opened, hemoperitoneum was found, and both fetuses were extracted alive. A median, supra and infraumbilical exploratory laparotomy (post cesarean section) was performed and a right lobe hepatic rupture was found. Hepatic packing with 11 gauze compresses, placement of 4 lamellar Penrose drains and temporary abdominal closure, management of hypovolemic shock and preeclampsia was continued in the Intensive Care Unit and the patient was discharged in good condition at 21 days. Conclusion: HELLP syndrome produces serious complications such as hepatic rupture which, if not treated correctly in an early and multidisciplinary manner, can lead to maternal and perinatal mortality., Introdução: a síndrome hellp e a ruptura hepática são complicações raras, especialmente em casos de gravidez gemelar. Neste artigo, apresentamos o caso de um hematoma subcapsular hepático rompido devido à síndrome hellp que complicou uma gravidez gemelar que exigiu uma cesariana de emergência e tamponamento hepático para o manejo da hipovolemia. Apresentação do caso: mulher, 41 anos, gestação gemelar de 35 semanas, recorre ao pronto-socorro por contrações uterinas e ausência de movimentos fetais. Devido à bradicardia grave em ambos os fetos, foi decidida uma cesariana de emergência. Ao abrir a cavidade abdominal o hemoperitônio é localizado, sendo possível extrair ambos os fetos vivos. Foi realizada laparotomia exploradora mediana, supra e infraumbilical (pós-cesariana) sendo constatada ruptura hepática do lobo direito. Foi realizado tamponamento hepático com compressas e fechamento abdominal temporário, e o manejo do choque hipovolêmico e da pré-eclâmpsia foi mantido na Unidade de Terapia Intensiva, onde a paciente recebeu alta em boas condições após 21 dias. Conclusão: a síndrome hellp produz complicações graves como a ruptura hepática que, se não tratada de forma precoce e multidisciplinar, pode levar à mortalidade materna perinatal., Introducción: El síndrome de Hellp y rotura hepática es una complicación poco frecuente especialmente en casos de embarazo gemelar, presentamos el caso de un hematoma subcapsular hepático roto por síndrome de HELLP que complicó un embarazo gemelar que requirió cesárea de emergencia y para el manejo de la hipovolemia el empaquetamiento hepático.Presentación del caso: Femenina, 41 años, gestación gemelar de 35 semanas, acude a emergencia por contracciones uterina y ausencia de movimientos fetales. Ante bradicardia severa de ambos fetos, se decide cesárea de urgencia. Al abrir la cavidad abdominal se encuentra hemoperitoneo, se logra extraer ambos fetos vivos. Se realiza laparotomía media, supra e infraumbilical exploradora (postcesárea) y se halla rotura hepática del lóbulo derecho. Se procede a empaquetamiento hepático con 11 compresas de gasas, colocación de 4 drenes Penrose laminares y cierre temporal abdominal, el manejo del shock hipovolémico y la preeclampsia se continuó en la Unidad de Cuidados Intensivos la paciente se fue de alta en buenas condiciones a los 21 días. Conclusión: El síndrome de HELLP produce complicaciones graves como rotura hepática que si no es tratada correctamente en forma temprana y multidisciplinaria puede llevar a producir mortalidad materno perinatal.

BACKGROUND: Neonates might be exposed to numerous painful procedures due to diagnostic reasons, therapeutic interventions, or surgical procedures. Options for pain management include opioids, non-pharmacological interventions, and other drugs. Morphine, fentanyl, and remifentanil are the opioids most often used in neonates. However, negative impact of opioids on the structure and function of the developing brain has been reported. OBJECTIVES: To evaluate the benefits and harms of opioids in term or preterm neonates exposed to procedural pain, compared to placebo or no drug, non-pharmacological intervention, other analgesics or sedatives, other opioids, or the same opioid administered by a different route. SEARCH METHODS: We used standard, extensive Cochrane search methods. The latest search date was December 2021. SELECTION CRITERIA: We included randomized controlled trials conducted in preterm and term infants of a postmenstrual age (PMA) up to 46 weeks and 0 days exposed to procedural pain where opioids were compared to 1) placebo or no drug; 2) non-pharmacological intervention; 3) other analgesics or sedatives; 4) other opioids; or 5) the same opioid administered by a different route. DATA COLLECTION AND ANALYSIS: We used standard Cochrane methods. Our primary outcomes were pain assessed with validated methods and any harms. We used a fixed-effect model with risk ratio (RR) for dichotomous data and mean difference (MD) for continuous data, and their confidence intervals (CI). We used GRADE to assess the certainty of the evidence for each outcome. MAIN RESULTS: We included 13 independent studies (enrolling 823 newborn infants): seven studies compared opioids to no treatment or placebo (the main comparison in this review), two studies to oral sweet solution or non-pharmacological intervention, and five studies (of which two were part of the same study) to other analgesics and sedatives. All studies were performed in a hospital setting. Opioids compared to placebo o, Sources of support:Internal sources: Institute for Clinical Sciences, Lund University, Lund, Sweden, Sweden.External sources: Vermont Oxford Network, USA. Region Skåne, Skåne University Hospital, Lund University and Region Västra Götaland, Sweden

BACKGROUND: Neonates might be exposed to numerous painful procedures due to diagnostic reasons, therapeutic interventions, or surgical procedures. Options for pain management include opioids, non-pharmacological interventions, and other drugs. Morphine, fentanyl, and remifentanil are the opioids most often used in neonates. However, negative impact of opioids on the structure and function of the developing brain has been reported. OBJECTIVES: To evaluate the benefits and harms of opioids in term or preterm neonates exposed to procedural pain, compared to placebo or no drug, non-pharmacological intervention, other analgesics or sedatives, other opioids, or the same opioid administered by a different route. SEARCH METHODS: We used standard, extensive Cochrane search methods. The latest search date was December 2021. SELECTION CRITERIA: We included randomized controlled trials conducted in preterm and term infants of a postmenstrual age (PMA) up to 46 weeks and 0 days exposed to procedural pain where opioids were compared to 1) placebo or no drug; 2) non-pharmacological intervention; 3) other analgesics or sedatives; 4) other opioids; or 5) the same opioid administered by a different route. DATA COLLECTION AND ANALYSIS: We used standard Cochrane methods. Our primary outcomes were pain assessed with validated methods and any harms. We used a fixed-effect model with risk ratio (RR) for dichotomous data and mean difference (MD) for continuous data, and their confidence intervals (CI). We used GRADE to assess the certainty of the evidence for each outcome. MAIN RESULTS: We included 13 independent studies (enrolling 823 newborn infants): seven studies compared opioids to no treatment or placebo (the main comparison in this review), two studies to oral sweet solution or non-pharmacological intervention, and five studies (of which two were part of the same study) to other analgesics and sedatives. All studies were performed in a hospital setting. Opioids compared to placebo o, Se versionshistorik https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-95889

Purpose: To examine the effect of freediving depth on risk for hypoxic blackout by recording arterial oxygen saturation (SpO2) and heart rate (HR) during deep and shallow dives in the sea. Methods: Fourteen competitive freedivers conducted open-water training dives wearing a water-/pressure proof pulse oximeter continuously recording HR and SpO2. Dives were divided into deep (> 35 m) and shallow (10–25 m) post-hoc and data from one deep and one shallow dive from 10 divers were compared. Results: Mean ± SD depth was 53 ± 14 m for deep and 17 ± 4 m for shallow dives. Respective dive durations (120 ± 18 s and 116 ± 43 s) did not differ. Deep dives resulted in lower minimum SpO2 (58 ± 17%) compared with shallow dives (74 ± 17%; P = 0.029). Overall diving HR was 7 bpm higher in deep dives (P = 0.002) although minimum HR was similar in both types of dives (39 bpm). Three divers desaturated early at depth, of which two exhibited severe hypoxia (SpO2 ≤ 65%) upon resurfacing. Additionally, four divers developed severe hypoxia after dives. Conclusions: Despite similar dive durations, oxygen desaturation was greater during deep dives, confirming increased risk of hypoxic blackout with increased depth. In addition to the rapid drop in alveolar pressure and oxygen uptake during ascent, several other risk factors associated with deep freediving were identified, including higher swimming effort and oxygen consumption, a compromised diving response, an autonomic conflict possibly causing arrhythmias, and compromised oxygen uptake at depth by lung compression possibly leading to atelectasis or pulmonary edema in some individuals. Individuals with elevated risk could likely be identified using wearable technology.

In a healthy heart, contraction/pumping is controlled by an electrical stimulus. This ensures that the heart contracts synchronously. When a problem arises with generating or conducting this electrical stimulus, people are fitted with a pacemaker. Our research shows that - in contrast to current technology - stimulating the ventricular septum is safer and better for the pump function. Stimulation of the ventricular septum can prevent (symptoms of) heart failure. Survival also improves.

Influenza is an acute respiratory illness caused by influenza viruses that occur in outbreaks and epidemics worldwide. Signs and symptoms of upper and/or lower respiratory tract involvement are present, along with indications of systemic illness such as fever, headache, myalgia, and weakness. Influenza is usually a self-limited disease; however, in certain individuals, there can be complications like myocarditis, ARDS, etc. Influenza A virus, subtype H1N1 is known to cause severe illness. We report an unusual case of H1N1 Influenza, in an elderly female presenting with fever and syncope. She was diagnosed case of hypertension and diabetes on treatment. On evaluation, it was found that she had bradycardia, due to myocarditis, which attributed to her symptom of syncope. This kind of presentation of H1N1 Influenza infection is rare, complete examination and high degrees of suspicion are necessary. The rapid progression in lack of active management and treatment can be fatal.

Influenza is an acute respiratory illness caused by influenza viruses that occur in outbreaks and epidemics worldwide. Signs and symptoms of upper and/or lower respiratory tract involvement are present, along with indications of systemic illness such as fever, headache, myalgia, and weakness. Influenza is usually a self-limited disease; however, in certain individuals, there can be complications like myocarditis, ARDS, etc. Influenza A virus, subtype H1N1 is known to cause severe illness. We report an unusual case of H1N1 Influenza, in an elderly female presenting with fever and syncope. She was diagnosed case of hypertension and diabetes on treatment. On evaluation, it was found that she had bradycardia, due to myocarditis, which attributed to her symptom of syncope. This kind of presentation of H1N1 Influenza infection is rare, complete examination and high degrees of suspicion are necessary. The rapid progression in lack of active management and treatment can be fatal.

Influenza is an acute respiratory illness caused by influenza viruses that occur in outbreaks and epidemics worldwide. Signs and symptoms of upper and/or lower respiratory tract involvement are present, along with indications of systemic illness such as fever, headache, myalgia, and weakness. Influenza is usually a self-limited disease; however, in certain individuals, there can be complications like myocarditis, ARDS, etc. Influenza A virus, subtype H1N1 is known to cause severe illness. We report an unusual case of H1N1 Influenza, in an elderly female presenting with fever and syncope. She was diagnosed case of hypertension and diabetes on treatment. On evaluation, it was found that she had bradycardia, due to myocarditis, which attributed to her symptom of syncope. This kind of presentation of H1N1 Influenza infection is rare, complete examination and high degrees of suspicion are necessary. The rapid progression in lack of active management and treatment can be fatal.

Influenza is an acute respiratory illness caused by influenza viruses that occur in outbreaks and epidemics worldwide. Signs and symptoms of upper and/or lower respiratory tract involvement are present, along with indications of systemic illness such as fever, headache, myalgia, and weakness. Influenza is usually a self-limited disease; however, in certain individuals, there can be complications like myocarditis, ARDS, etc. Influenza A virus, subtype H1N1 is known to cause severe illness. We report an unusual case of H1N1 Influenza, in an elderly female presenting with fever and syncope. She was diagnosed case of hypertension and diabetes on treatment. On evaluation, it was found that she had bradycardia, due to myocarditis, which attributed to her symptom of syncope. This kind of presentation of H1N1 Influenza infection is rare, complete examination and high degrees of suspicion are necessary. The rapid progression in lack of active management and treatment can be fatal.

The sinoatrial node (SAN), the leading pacemaker region, generates electrical impulses that propagate throughout the heart. SAN dysfunction with bradyarrhythmia is well documented in heart failure (HF). However, the underlying mechanisms are not completely understood. Mitochondria are critical to cellular processes that determine the life or death of the cell. The release of Ca2+ from the ryanodine receptors 2 (RyR2) on the sarcoplasmic reticulum (SR) at mitochondria-SR microdomains serves as the critical communication to match energy production to meet metabolic demands. Therefore, we tested the hypothesis that alterations in the mitochondria-SR connectomics contribute to SAN dysfunction in HF. We took advantage of a mouse model of chronic pressure overload-induced HF by transverse aortic constriction (TAC) and a SAN-specific CRISPR-Cas9-mediated knockdown of mitofusin-2 (Mfn2), the mitochondria-SR tethering GTPase protein. TAC mice exhibited impaired cardiac function with HF, cardiac fibrosis, and profound SAN dysfunction. Ultrastructural imaging using electron microscope (EM) tomography revealed abnormal mitochondrial structure with increased mitochondria-SR distance. The expression of Mfn2 was significantly down-regulated and showed reduced colocalization with RyR2 in HF SAN cells. Indeed, SAN-specific Mfn2 knockdown led to alterations in the mitochondria-SR microdomains and SAN dysfunction. Finally, disruptions in the mitochondria-SR microdomains resulted in abnormal mitochondrial Ca2+ handling, alterations in localized protein kinase A (PKA) activity, and impaired mitochondrial function in HF SAN cells. The current study provides insights into the role of mitochondria-SR microdomains in SAN automaticity and possible therapeutic targets for SAN dysfunction in HF patients.

Influenza is an acute respiratory illness caused by influenza viruses that occur in outbreaks and epidemics worldwide. Signs and symptoms of upper and/or lower respiratory tract involvement are present, along with indications of systemic illness such as fever, headache, myalgia, and weakness. Influenza is usually a self-limited disease; however, in certain individuals, there can be complications like myocarditis, ARDS, etc. Influenza A virus, subtype H1N1 is known to cause severe illness. We report an unusual case of H1N1 Influenza, in an elderly female presenting with fever and syncope. She was diagnosed case of hypertension and diabetes on treatment. On evaluation, it was found that she had bradycardia, due to myocarditis, which attributed to her symptom of syncope. This kind of presentation of H1N1 Influenza infection is rare, complete examination and high degrees of suspicion are necessary. The rapid progression in lack of active management and treatment can be fatal.

Influenza is an acute respiratory illness caused by influenza viruses that occur in outbreaks and epidemics worldwide. Signs and symptoms of upper and/or lower respiratory tract involvement are present, along with indications of systemic illness such as fever, headache, myalgia, and weakness. Influenza is usually a self-limited disease; however, in certain individuals, there can be complications like myocarditis, ARDS, etc. Influenza A virus, subtype H1N1 is known to cause severe illness. We report an unusual case of H1N1 Influenza, in an elderly female presenting with fever and syncope. She was diagnosed case of hypertension and diabetes on treatment. On evaluation, it was found that she had bradycardia, due to myocarditis, which attributed to her symptom of syncope. This kind of presentation of H1N1 Influenza infection is rare, complete examination and high degrees of suspicion are necessary. The rapid progression in lack of active management and treatment can be fatal.

Influenza is an acute respiratory illness caused by influenza viruses that occur in outbreaks and epidemics worldwide. Signs and symptoms of upper and/or lower respiratory tract involvement are present, along with indications of systemic illness such as fever, headache, myalgia, and weakness. Influenza is usually a self-limited disease; however, in certain individuals, there can be complications like myocarditis, ARDS, etc. Influenza A virus, subtype H1N1 is known to cause severe illness. We report an unusual case of H1N1 Influenza, in an elderly female presenting with fever and syncope. She was diagnosed case of hypertension and diabetes on treatment. On evaluation, it was found that she had bradycardia, due to myocarditis, which attributed to her symptom of syncope. This kind of presentation of H1N1 Influenza infection is rare, complete examination and high degrees of suspicion are necessary. The rapid progression in lack of active management and treatment can be fatal.

Background: Currently, 21−30% supplemental oxygen is recommended during resuscitation of preterm neonates. Recent studies have shown that 58% of infants < 32 week gestation age are born with a heart rate (HR) < 100 bpm. Prolonged bradycardia with the inability to achieve a preductal saturation (SpO2) of 80% by 5 min is associated with mortality and morbidity in preterm infants. The optimal oxygen concentration that enables the achievement of a HR ≥ 100 bpm and SpO2 of ≥80% by 5 min in preterm lambs is not known. Methods: Preterm ovine model (125−127 d, gestation equivalent to human neonates < 28 weeks) was instrumented, and asphyxia was induced by umbilical cord occlusion until bradycardia. Ventilation was initiated with 30% (OX30), 60% (OX60), and 100% (OX100) for the first 2 min and titrated proportionately to the difference from the recommended preductal SpO2. Our primary outcome was the incidence of the composite of HR ≥ 100 bpm and SpO2 ≥ 80%, by 5 min. Secondary outcomes were to evaluate the time taken to achieve the primary outcome, gas exchange, pulmonary/systemic hemodynamics, and the oxidative injury. Results: Eighteen lambs (OX30-6, OX60-5. OX100-7) had an average HR < 91 bpm with a pH of <6.92 before resuscitation. Sixty seven percent achieved the primary outcome in OX100, 40% in OX60, and none in OX30. The time taken to achieve the primary outcome was significantly shorter with OX100 (6 ± 2 min) than with OX30 (10 ± 3 min) (* p = 0.04). The preductal SpO2 was highest with OX100, while the peak pulmonary blood flow was lowest with OX30, with no difference in O2 delivery to the brain or oxidative injury by 10 min. Conclusions: The use of 30%, 60%, and 100% supplemental O2 in a bradycardic preterm ovine model did not demonstrate a significant difference in the composite primary outcome. The current recommendation to use 30% oxygen did not achieve a preductal SpO2 of 80% by 5 min in any preterm lambs. Clinical studies to optimize supplemental

OBJECTIVE: Colonoscopy is one of the most frequently performed interventional endoscopic procedures for diagnosis and treatment. During the procedure, the increase in intraabdominal pressure can cause undesirable spikes in intraocular pressure. In the literature, there are no studies on agent combinations that cause the least effect on intraocular pressure and hemodynamic response in colonoscopic procedures, which are performed more frequently in the elderly, the patient group at the greatest risk for glaucoma. This study aimed to compare ketamine-propofol and ketamine-midazolam protocols in terms of their effects on hemodynamic parameters and intraocular pressure. MATERIALS AND METHODS: The research was a randomized clinical controlled double-blind study. The study was conducted on 60 healthy adults who underwent elective colonoscopy. Ketamin-midazolam and ketamine-propofol combinations were used. Hemodynamic parameters, intraocular pressures at five different times, and the satisfaction levels of the endoscopist and the patient were recorded. RESULTS: In both groups, there was a statistically significant difference between the pre-procedure intraocular pressure values and the values at the 1st minute of the procedure and at recovery (p0.05). No statistically significant difference was found between the intraocular pressure values of the study groups at any time point (p>0.05). CONCLUSIONS: Both combinations can be used safely. The combination of ketamine and propofol in subanesthetic doses provides better sedation without disturbing the hemodynamics and is preferable. © 2022 Verduci Editore s.r.l. All rights reserved.

Objective: It was aimed to evaluate the effect of intravenous (IV) granisetron used for nausea and vomiting prophylaxis on hypotension and bradycardia caused by spinal anesthesia. Methods: 120 ASA 1-2 patients undergoing elective surgery under spinal anesthesia were randomly divided into Group G (Ganisetron; n=60) and Group P (Placebo; n=60) groups. Five minutes before spinal anesthesia, Group G received 1 mg intravenous granisetron diluted in 10 mL of isotonic sodium chloride solution and Group P received 10 mL of isotonic sodium chloride solution. Spinal anesthesia with hyperbaric bupivacaine 0.5%, 15 mg at the level of L4-5 was applied for both groups. Hemodynamic data, sensory and motor block parameters were recorded before and after spinal anaesthesia every 5 minutes during 20 minutes of surgery. Results: There was no difference in the demographic data of both groups. Although hemodynamic data showed a decrease in both groups according to initial values, blood pressure measurements in group G were significantly higher than the first measure values. There was no significant difference in heart rate values between the groups. Conclusion: Intravenous granisetron reduces hypotension after spinal anesthesia, but it has no significant effect on heart rate. © Copyright Anesthesiology and Reanimation Specialists’ Society. This journal published by Logos Medical Publishing. Licenced by Creative Commons Attribution 4.0 International (CC)

OBJECTIVE: Colonoscopy is one of the most frequently performed interventional endoscopic procedures for diagnosis and treatment. During the procedure, the increase in intraabdominal pressure can cause undesirable spikes in intraocular pressure. In the literature, there are no studies on agent combinations that cause the least effect on intraocular pressure and hemodynamic response in colonoscopic procedures, which are performed more frequently in the elderly, the patient group at the greatest risk for glaucoma. This study aimed to compare ketamine-propofol and ketamine-midazolam protocols in terms of their effects on hemodynamic parameters and intraocular pressure. MATERIALS AND METHODS: The research was a randomized clinical controlled double-blind study. The study was conducted on 60 healthy adults who underwent elective colonoscopy. Ketamin-midazolam and ketamine-propofol combinations were used. Hemodynamic parameters, intraocular pressures at five different times, and the satisfaction levels of the endoscopist and the patient were recorded. RESULTS: In both groups, there was a statistically significant difference between the pre-procedure intraocular pressure values and the values at the 1st minute of the procedure and at recovery (p0.05). No statistically significant difference was found between the intraocular pressure values of the study groups at any time point (p>0.05). CONCLUSIONS: Both combinations can be used safely. The combination of ketamine and propofol in subanesthetic doses provides better sedation without disturbing the hemodynamics and is preferable. © 2022 Verduci Editore s.r.l. All rights reserved.

Objective: It was aimed to evaluate the effect of intravenous (IV) granisetron used for nausea and vomiting prophylaxis on hypotension and bradycardia caused by spinal anesthesia. Methods: 120 ASA 1-2 patients undergoing elective surgery under spinal anesthesia were randomly divided into Group G (Ganisetron; n=60) and Group P (Placebo; n=60) groups. Five minutes before spinal anesthesia, Group G received 1 mg intravenous granisetron diluted in 10 mL of isotonic sodium chloride solution and Group P received 10 mL of isotonic sodium chloride solution. Spinal anesthesia with hyperbaric bupivacaine 0.5%, 15 mg at the level of L4-5 was applied for both groups. Hemodynamic data, sensory and motor block parameters were recorded before and after spinal anaesthesia every 5 minutes during 20 minutes of surgery. Results: There was no difference in the demographic data of both groups. Although hemodynamic data showed a decrease in both groups according to initial values, blood pressure measurements in group G were significantly higher than the first measure values. There was no significant difference in heart rate values between the groups. Conclusion: Intravenous granisetron reduces hypotension after spinal anesthesia, but it has no significant effect on heart rate. © Copyright Anesthesiology and Reanimation Specialists’ Society. This journal published by Logos Medical Publishing. Licenced by Creative Commons Attribution 4.0 International (CC)

Severe hypertension has numerous etiologies. When accompanied by bradycardia, the spectrum of differential diagnoses is greatly narrowed and is commonly seen in patients with increased intracranial pressure. However, other etiologies such as bradycardia-induced hypertension are rarely mentioned. Here we report the case of a 73-year-old woman presenting with symptoms of heart failure, severe hypertension, and bradycardia with a 2:1 atrioventricular block. Echocardiography demonstrated increased left ventricular filling secondary to bradycardia and prolonged diastole, leading to greater ventricular stretch, increased contractile force and greater stroke volume (Frank-Starling mechanism), which subsequently caused elevated systolic blood pressure (BP), low diastolic BP and a wide pulse pressure. Treating the bradycardia by pacing led to an immediate and substantial BP reduction, although complete BP normalization had a slower time course and was probably due to the concomitant effect of the antihypertensive treatment initiation. This pathophysiological mechanism has received little attention in the literature. Further, stimulation of sympathetic afferents located in the heart by distension of the cardiac walls as well as the role of vagally innervated cardiopulmonary receptors due to the increased pressure in the heart and the pulmonary artery should also be kept in mind as alternative hypotheses.

Objective Rare cases of genetically inherited atrioventricular block (AVB) have been reported; however, the heredity of AVB remains unknown. We aimed to assess the heredity of AVB. Design, setting and participants Using data from the Danish Civil Registration Registry, we established a nationwide cohort of individuals with parental links. Data were merged with information from the Danish Pacemaker and Implantable Cardioverter Defibrillator Registry, containing information on all pacemaker implantations performed in Denmark during the study period, to identify patients who received a first-time pacemaker because of AVB. Results A total of 4 648 204 individuals had parental links and a total of 26 880 consecutive patients received a first-time pacemaker due to AVB. Overall, the adjusted rate ratio (RR) of pacemaker implantation due to AVB was 2.1 (95% CI 1.8 to 2.5) if a father, mother or sibling had AVB compared with the risk in the general population. The adjusted RR was 2.2 (1.7-2.9) for offspring of mothers with AVB, 1.9 (1.5-2.4) for offspring of fathers with AVB and 3.5 (2.3-5.4) for siblings to a patient with AVB. The risk increased inversely proportionally with the age of the index case at the time of pacemaker implantation. The corresponding adjusted RRs were 15.8 (4.8-52.3) and 10.0 (3.3-30.4) if a mother or father, respectively, had a pacemaker implantation before 50 years. Conclusion and relevance First-degree relatives to a patient with AVB carry an increased risk of AVB with the risk being strongly inversely associated with the age of the index case at pacemaker implantation. These findings indicate a genetic component in the development of AVB in families with an early-onset disease.

Objective Rare cases of genetically inherited atrioventricular block (AVB) have been reported; however, the heredity of AVB remains unknown. We aimed to assess the heredity of AVB. Design, setting and participants Using data from the Danish Civil Registration Registry, we established a nationwide cohort of individuals with parental links. Data were merged with information from the Danish Pacemaker and Implantable Cardioverter Defibrillator Registry, containing information on all pacemaker implantations performed in Denmark during the study period, to identify patients who received a first-time pacemaker because of AVB. Results A total of 4 648 204 individuals had parental links and a total of 26 880 consecutive patients received a first-time pacemaker due to AVB. Overall, the adjusted rate ratio (RR) of pacemaker implantation due to AVB was 2.1 (95% CI 1.8 to 2.5) if a father, mother or sibling had AVB compared with the risk in the general population. The adjusted RR was 2.2 (1.7-2.9) for offspring of mothers with AVB, 1.9 (1.5-2.4) for offspring of fathers with AVB and 3.5 (2.3-5.4) for siblings to a patient with AVB. The risk increased inversely proportionally with the age of the index case at the time of pacemaker implantation. The corresponding adjusted RRs were 15.8 (4.8-52.3) and 10.0 (3.3-30.4) if a mother or father, respectively, had a pacemaker implantation before 50 years. Conclusion and relevance First-degree relatives to a patient with AVB carry an increased risk of AVB with the risk being strongly inversely associated with the age of the index case at pacemaker implantation. These findings indicate a genetic component in the development of AVB in families with an early-onset disease.

The lifestyle of people has changed over the time. Before the revolution days, people suffered from various diseases and the availability of medicines were not available. Today’s life is busier. Healthcare system has improved a lot but at the same time the number of people getting affected by different sources is still on a rise. The number one cause of death worldwide is due to heart diseases. The death rates due to cardiovascular disease increased. In order to improve the health conditions, there is a continuous development of synthetic and herbal medicines. Recently, rise in the use of herbal medicines have due to its natural origins and less side effects. One of the emerging herbs is Nigella sativa described as the remedy of all diseases. The tropic activity of the extracted volatile oil from Nigella sativa is observed on the isolated frog’s heart. The heart was isolated from the frog and was treated with adrenaline and acetylcholine to study its activity respectively. The isolated heart was also treated with the volatile oil of Nigella sativa seeds which produced dose dependent bradycardia like situation followed by cardiac arrest.

The lifestyle of people has changed over the time. Before the revolution days, people suffered from various diseases and the availability of medicines were not available. Today’s life is busier. Healthcare system has improved a lot but at the same time the number of people getting affected by different sources is still on a rise. The number one cause of death worldwide is due to heart diseases. The death rates due to cardiovascular disease increased. In order to improve the health conditions, there is a continuous development of synthetic and herbal medicines. Recently, rise in the use of herbal medicines have due to its natural origins and less side effects. One of the emerging herbs is Nigella sativa described as the remedy of all diseases. The tropic activity of the extracted volatile oil from Nigella sativa is observed on the isolated frog’s heart. The heart was isolated from the frog and was treated with adrenaline and acetylcholine to study its activity respectively. The isolated heart was also treated with the volatile oil of Nigella sativa seeds which produced dose dependent bradycardia like situation followed by cardiac arrest.

The lifestyle of people has changed over the time. Before the revolution days, people suffered from various diseases and the availability of medicines were not available. Today’s life is busier. Healthcare system has improved a lot but at the same time the number of people getting affected by different sources is still on a rise. The number one cause of death worldwide is due to heart diseases. The death rates due to cardiovascular disease increased. In order to improve the health conditions, there is a continuous development of synthetic and herbal medicines. Recently, rise in the use of herbal medicines have due to its natural origins and less side effects. One of the emerging herbs is Nigella sativa described as the remedy of all diseases. The tropic activity of the extracted volatile oil from Nigella sativa is observed on the isolated frog’s heart. The heart was isolated from the frog and was treated with adrenaline and acetylcholine to study its activity respectively. The isolated heart was also treated with the volatile oil of Nigella sativa seeds which produced dose dependent bradycardia like situation followed by cardiac arrest.

Intrathecal anesthesia is an effective method to provide anesthesia for patients undergoing total knee arthroplasty. Hypotension, bradycardia, and albeit rare asystole can occur following intrathecal anesthesia. These deleterious consequences can lead to poor outcomes for the patient. Effective methods at mitigating the effects of hypotension and bradycardia following intrathecal anesthesia have been studied extensively. Proper examination of the patient and health history can identify risk factors for developing bradycardia or hypotension post neuraxial blockade. Administration of ondansetron or glycopyrrolate prior to intrathecal anesthesia have been shown to be an effective strategy to prevent hemodynamic changes in the patient. Frequently an excessive amount of intrathecal local anesthetic is given to patients for their procedures leading to these adverse hemodynamic changes. Appropriate dosing of intrathecal local anesthetics can decrease the incidence of these changes.

Influenza is an acute respiratory illness caused by influenza viruses that occur in outbreaks and epidemics worldwide. Signs and symptoms of upper and/or lower respiratory tract involvement are present, along with indications of systemic illness such as fever, headache, myalgia, and weakness. Influenza is usually a self-limited disease; however, in certain individuals, there can be complications like myocarditis, ARDS, etc. Influenza A virus, subtype H1N1 is known to cause severe illness. We report an unusual case of H1N1 Influenza, in an elderly female presenting with fever and syncope. She was diagnosed case of hypertension and diabetes on treatment. On evaluation, it was found that she had bradycardia, due to myocarditis, which attributed to her symptom of syncope. This kind of presentation of H1N1 Influenza infection is rare, complete examination and high degrees of suspicion are necessary. The rapid progression in lack of active management and treatment can be fatal.

ObjectivesNeonatal resuscitation guidelines recommend 0.5-1 mL saline flush following 0.01-0.03 mg/kg of epinephrine via low umbilical venous catheter for persistent bradycardia despite effective positive pressure ventilation (PPV) and chest compressions (CC). We evaluated the effects of 1 mL vs 3 mL/kg flush volumes and 0.01 vs 0.03 mg/kg doses on return of spontaneous circulation (ROSC) and epinephrine pharmacokinetics in lambs with cardiac arrest.DesignForty term lambs in cardiac arrest were randomised to receive 0.01 or 0.03 mg/kg epinephrine followed by 1 mL or 3 mL/kg flush after effective PPV and CC. Epinephrine (with 1 mL flush) was repeated every 3 min until ROSC or until 20 min. Haemodynamics, blood gases and plasma epinephrine concentrations were monitored.ResultsTen lambs had ROSC before epinephrine administration and 2 died during instrumentation. Among 28 lambs that received epinephrine, 2/6 in 0.01 mg/kg-1 mL flush, 3/6 in 0.01 mg/kg-3 mL/kg flush, 5/7 in 0.03 mg/kg-1 mL flush and 9/9 in 0.03 mg/kg-3 mL/kg flush achieved ROSC (p=0.02). ROSC was five times faster with 0.03 mg/kg epinephrine compared with 0.01 mg/kg (adjusted HR (95% CI) 5.08 (1.7 to 15.25)) and three times faster with 3 mL/kg flush compared with 1 mL flush (3.5 (1.27 to 9.71)). Plasma epinephrine concentrations were higher with 0.01 mg/kg-3 mL/kg flush (adjusted geometric mean ratio 6.0 (1.4 to 25.7)), 0.03 mg/kg-1 mL flush (11.3 (2.1 to 60.3)) and 0.03 mg/kg-3 mL/kg flush (11.0 (2.2 to 55.3)) compared with 0.01 mg/kg-1 mL flush.Conclusions0.03 mg/kg epinephrine dose with 3 mL/kg flush volume is associated with the highest ROSC rate, increases peak plasma epinephrine concentrations and hastens time to ROSC. Clinical trials evaluating optimal epinephrine dose and flush volume are warranted.

Study Objectives: Preterm infants undergoing intensive care are often placed prone to improve respiratory function. Current clinical guidelines recommend preterm infants are slept supine from 32 weeks' postmenstrual age, regardless of gestational age at birth. However, respiratory function is also related to gestational and chronological ages and is affected by sleep state. We aimed to identify the optimal timing for adopting the supine sleeping position in preterm infants, using a longitudinal design assessing the effects of sleep position and state on cardiorespiratory stability. Method(s): Twenty-three extremely (24-28 weeks' gestation) and 33 very preterm (29-34 weeks' gestation) infants were studied weekly from birth until discharge, in both prone and supine positions, in quiet and active sleep determined by behavioral scoring. Bradycardia (heart rate <=100 bpm), desaturation (oxygen saturation <=80%), and apnea (pause in respiratory rate >=10 s) episodes were analyzed. Result(s): Prone positioning in extremely preterm infants reduced the frequency of bradycardias and desaturations and duration of desaturations. In very preterm infants, prone positioning only reduced the frequency of desaturations. The position-related effects were not related to postmenstrual age. Quiet sleep in both preterm groups was associated with fewer bradycardias and desaturations, and also reduced durations of bradycardia and desaturations in the very preterm group. Conclusion(s): Cardiorespiratory stability is improved by the prone sleep position, predominantly in extremely preterm infants, and the improvements are not dependent on postmenstrual age. In very preterm infants, quiet sleep has a more marked effect than the prone position. This evidence should be considered in individualizing management of preterm infant positioning.Copyright © Sleep Research Society 2019. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved.

IntroductionWhile autoimmune comorbidities are common in alopecia areata, little is known about comorbid cardiovascular disease. The purpose of this study was to evaluate the incidence of bradyarrhythmia in patients with alopecia areata.MethodsRetrospective review of electrocardiograms of 124 patients with [Formula: see text] 50% scalp hair loss (severe alopecia areata) was conducted and compared to National Health and Nutrition Examination Survey (NHANES) data.ResultsThe prevalence of bradycardia in females with alopecia areata was 24.3% (95% CI, 14.5-34.1%) and in those age 40 years or older was 40.8% (95% CI, 22.2-53.5%) compared to 19.5% in the NHANES III population. The prevalence of bradycardia in males with alopecia areata was 36.0% (95% CI, 22.7-49.3%) and in those age 40 years or older was 50.0% (95% CI, 21.7-78.3%) compared to 26.9% in the NHANES III population.ConclusionThe potential association between bradycardia and alopecia areata merits further investigation.

Study Objectives: Preterm infants undergoing intensive care are often placed prone to improve respiratory function. Current clinical guidelines recommend preterm infants are slept supine from 32 weeks' postmenstrual age, regardless of gestational age at birth. However, respiratory function is also related to gestational and chronological ages and is affected by sleep state. We aimed to identify the optimal timing for adopting the supine sleeping position in preterm infants, using a longitudinal design assessing the effects of sleep position and state on cardiorespiratory stability. Method(s): Twenty-three extremely (24-28 weeks' gestation) and 33 very preterm (29-34 weeks' gestation) infants were studied weekly from birth until discharge, in both prone and supine positions, in quiet and active sleep determined by behavioral scoring. Bradycardia (heart rate <=100 bpm), desaturation (oxygen saturation <=80%), and apnea (pause in respiratory rate >=10 s) episodes were analyzed. Result(s): Prone positioning in extremely preterm infants reduced the frequency of bradycardias and desaturations and duration of desaturations. In very preterm infants, prone positioning only reduced the frequency of desaturations. The position-related effects were not related to postmenstrual age. Quiet sleep in both preterm groups was associated with fewer bradycardias and desaturations, and also reduced durations of bradycardia and desaturations in the very preterm group. Conclusion(s): Cardiorespiratory stability is improved by the prone sleep position, predominantly in extremely preterm infants, and the improvements are not dependent on postmenstrual age. In very preterm infants, quiet sleep has a more marked effect than the prone position. This evidence should be considered in individualizing management of preterm infant positioning.Copyright © Sleep Research Society 2019. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved.

Background: Coronavirus disease 2019 (COVID-19) has led to over 1 million deaths worldwide and has been associated with cardiac complications including cardiac arrhythmias. The incidence and pathophysiology of these manifestations remain elusive. In this worldwide survey of patients hospitalized with COVID-19 who developed cardiac arrhythmias, we describe clinical characteristics associated with various arrhythmias, as well as global differences in modulations of routine electrophysiology practice during the pandemic. Methods: We conducted a retrospective analysis of patients hospitalized with COVID-19 infection worldwide with and without incident cardiac arrhythmias. Patients with documented atrial fibrillation, atrial flutter, supraventricular tachycardia, nonsustained or sustained ventricular tachycardia, ventricular fibrillation, atrioventricular block, or marked sinus bradycardia (heart rate<40 bpm) were classified as having arrhythmia. Deidentified data was provided by each institution and analyzed. Results: Data were collected for 4526 patients across 4 continents and 12 countries, 827 of whom had an arrhythmia. Cardiac comorbidities were common in patients with arrhythmia: 69% had hypertension, 42% diabetes, 30% had heart failure, and 24% had coronary artery disease. Most had no prior history of arrhythmia. Of those who did develop an arrhythmia, the majority (81.8%) developed atrial arrhythmias, 20.7% developed ventricular arrhythmias, and 22.6% had bradyarrhythmia. Regional differences suggested a lower incidence of atrial fibrillation in Asia compared with other continents (34% versus 63%). Most patients in North America and Europe received hydroxychloroquine, although the frequency of hydroxychloroquine therapy was constant across arrhythmia types. Forty-three percent of patients who developed arrhythmia were mechanically ventilated and 51% survived to hospital discharge. Many institutions reported drastic decreases in electrophysiology procedures per

Neonatal encephalopathy is referred to a multiplicity of clinical neurological symptoms that can range from changes in mental status, irritability, hypotonia, abnormal movements, poor diet, decreased primitive reflexes, to seizures and coma. It is a syndrome of central nervous system dysfunction that affects neonates 35 or more weeks of gestation. Although at first it was believed that its etiology was due to hypoxic-ischemic events, and for this reason it was called hypoxic-ischemic encephalopathy, it is already clear that this condition is multicausal. The objective of this research is to review and refer updated literature with which to discuss the symptoms and risk factors of neonatal encephalopathy. For this reason, a bibliographic design study was developed, within the framework of a review methodology. In the results, several interpretations and literal extracts from writers are presented as evidence that explain and characterize the signs and risks of neonatal encephalopathy. In short, the symptoms and signs of neonatal encephalopathy can range from mild to severe, depending on the cause and severity of brain damage, while the associated risk factors will basically correspond to the perinatal and prenatal ones; the latter can also be subdivided into maternal and fetal ones., La encefalopatía neonatal esta referida a una multiplicidad clínica de síntomas neurológicos que pueden ir desde cambios en el estado mental, irritabilidad, hipotonía, movimientos anormales, mala alimentación, disminución de los reflejos primitivos, hasta convulsiones y coma. Es un síndrome de disfunción del sistema nervioso central que perjudica a neonatos 35 o más semanas de gestación. Aunque en principio se creyó que su etiología era por eventos hipóxico-isquémicos, y por ello se denominó encefalopatía hipóxico-isquémica, ya se tiene claro que esta condición es multicausal. El objetivo de esta investigación es revisar y referir literatura actualizada con la cual exponer sobre los síntomas y facto0res de riesgo de la encefalopatía neonatal. Por ello, se desarrolló un estudio de diseño bibliográfico, en el marco de una metodología de revisión. En los resultados se presenta como evidencia, varias interpretaciones y extractos literales de tratadistas que explican y caracterizan los signos y riesgos de la encefalopatía neonatal. En definitiva, los síntomas y signos de la encefalopatía neonatal pueden oscilar de leves a graves, conforme a la causa y severidad del daño cerebral, mientras que los factores de riesgo asociados, básicamente corresponderán a los perinatales y prenatales; pudiendo éstos últimos subdividirse también entre los maternos y fetales.

Neonatal encephalopathy is referred to a multiplicity of clinical neurological symptoms that can range from changes in mental status, irritability, hypotonia, abnormal movements, poor diet, decreased primitive reflexes, to seizures and coma. It is a syndrome of central nervous system dysfunction that affects neonates 35 or more weeks of gestation. Although at first it was believed that its etiology was due to hypoxic-ischemic events, and for this reason it was called hypoxic-ischemic encephalopathy, it is already clear that this condition is multicausal. The objective of this research is to review and refer updated literature with which to discuss the symptoms and risk factors of neonatal encephalopathy. For this reason, a bibliographic design study was developed, within the framework of a review methodology. In the results, several interpretations and literal extracts from writers are presented as evidence that explain and characterize the signs and risks of neonatal encephalopathy. In short, the symptoms and signs of neonatal encephalopathy can range from mild to severe, depending on the cause and severity of brain damage, while the associated risk factors will basically correspond to the perinatal and prenatal ones; the latter can also be subdivided into maternal and fetal ones., La encefalopatía neonatal esta referida a una multiplicidad clínica de síntomas neurológicos que pueden ir desde cambios en el estado mental, irritabilidad, hipotonía, movimientos anormales, mala alimentación, disminución de los reflejos primitivos, hasta convulsiones y coma. Es un síndrome de disfunción del sistema nervioso central que perjudica a neonatos 35 o más semanas de gestación. Aunque en principio se creyó que su etiología era por eventos hipóxico-isquémicos, y por ello se denominó encefalopatía hipóxico-isquémica, ya se tiene claro que esta condición es multicausal. El objetivo de esta investigación es revisar y referir literatura actualizada con la cual exponer sobre los síntomas y facto0res de riesgo de la encefalopatía neonatal. Por ello, se desarrolló un estudio de diseño bibliográfico, en el marco de una metodología de revisión. En los resultados se presenta como evidencia, varias interpretaciones y extractos literales de tratadistas que explican y caracterizan los signos y riesgos de la encefalopatía neonatal. En definitiva, los síntomas y signos de la encefalopatía neonatal pueden oscilar de leves a graves, conforme a la causa y severidad del daño cerebral, mientras que los factores de riesgo asociados, básicamente corresponderán a los perinatales y prenatales; pudiendo éstos últimos subdividirse también entre los maternos y fetales.

Neonatal encephalopathy is referred to a multiplicity of clinical neurological symptoms that can range from changes in mental status, irritability, hypotonia, abnormal movements, poor diet, decreased primitive reflexes, to seizures and coma. It is a syndrome of central nervous system dysfunction that affects neonates 35 or more weeks of gestation. Although at first it was believed that its etiology was due to hypoxic-ischemic events, and for this reason it was called hypoxic-ischemic encephalopathy, it is already clear that this condition is multicausal. The objective of this research is to review and refer updated literature with which to discuss the symptoms and risk factors of neonatal encephalopathy. For this reason, a bibliographic design study was developed, within the framework of a review methodology. In the results, several interpretations and literal extracts from writers are presented as evidence that explain and characterize the signs and risks of neonatal encephalopathy. In short, the symptoms and signs of neonatal encephalopathy can range from mild to severe, depending on the cause and severity of brain damage, while the associated risk factors will basically correspond to the perinatal and prenatal ones; the latter can also be subdivided into maternal and fetal ones., La encefalopatía neonatal esta referida a una multiplicidad clínica de síntomas neurológicos que pueden ir desde cambios en el estado mental, irritabilidad, hipotonía, movimientos anormales, mala alimentación, disminución de los reflejos primitivos, hasta convulsiones y coma. Es un síndrome de disfunción del sistema nervioso central que perjudica a neonatos 35 o más semanas de gestación. Aunque en principio se creyó que su etiología era por eventos hipóxico-isquémicos, y por ello se denominó encefalopatía hipóxico-isquémica, ya se tiene claro que esta condición es multicausal. El objetivo de esta investigación es revisar y referir literatura actualizada con la cual exponer sobre los síntomas y facto0res de riesgo de la encefalopatía neonatal. Por ello, se desarrolló un estudio de diseño bibliográfico, en el marco de una metodología de revisión. En los resultados se presenta como evidencia, varias interpretaciones y extractos literales de tratadistas que explican y caracterizan los signos y riesgos de la encefalopatía neonatal. En definitiva, los síntomas y signos de la encefalopatía neonatal pueden oscilar de leves a graves, conforme a la causa y severidad del daño cerebral, mientras que los factores de riesgo asociados, básicamente corresponderán a los perinatales y prenatales; pudiendo éstos últimos subdividirse también entre los maternos y fetales.

Neonatal encephalopathy is referred to a multiplicity of clinical neurological symptoms that can range from changes in mental status, irritability, hypotonia, abnormal movements, poor diet, decreased primitive reflexes, to seizures and coma. It is a syndrome of central nervous system dysfunction that affects neonates 35 or more weeks of gestation. Although at first it was believed that its etiology was due to hypoxic-ischemic events, and for this reason it was called hypoxic-ischemic encephalopathy, it is already clear that this condition is multicausal. The objective of this research is to review and refer updated literature with which to discuss the symptoms and risk factors of neonatal encephalopathy. For this reason, a bibliographic design study was developed, within the framework of a review methodology. In the results, several interpretations and literal extracts from writers are presented as evidence that explain and characterize the signs and risks of neonatal encephalopathy. In short, the symptoms and signs of neonatal encephalopathy can range from mild to severe, depending on the cause and severity of brain damage, while the associated risk factors will basically correspond to the perinatal and prenatal ones; the latter can also be subdivided into maternal and fetal ones., La encefalopatía neonatal esta referida a una multiplicidad clínica de síntomas neurológicos que pueden ir desde cambios en el estado mental, irritabilidad, hipotonía, movimientos anormales, mala alimentación, disminución de los reflejos primitivos, hasta convulsiones y coma. Es un síndrome de disfunción del sistema nervioso central que perjudica a neonatos 35 o más semanas de gestación. Aunque en principio se creyó que su etiología era por eventos hipóxico-isquémicos, y por ello se denominó encefalopatía hipóxico-isquémica, ya se tiene claro que esta condición es multicausal. El objetivo de esta investigación es revisar y referir literatura actualizada con la cual exponer sobre los síntomas y facto0res de riesgo de la encefalopatía neonatal. Por ello, se desarrolló un estudio de diseño bibliográfico, en el marco de una metodología de revisión. En los resultados se presenta como evidencia, varias interpretaciones y extractos literales de tratadistas que explican y caracterizan los signos y riesgos de la encefalopatía neonatal. En definitiva, los síntomas y signos de la encefalopatía neonatal pueden oscilar de leves a graves, conforme a la causa y severidad del daño cerebral, mientras que los factores de riesgo asociados, básicamente corresponderán a los perinatales y prenatales; pudiendo éstos últimos subdividirse también entre los maternos y fetales.

Neonatal encephalopathy is referred to a multiplicity of clinical neurological symptoms that can range from changes in mental status, irritability, hypotonia, abnormal movements, poor diet, decreased primitive reflexes, to seizures and coma. It is a syndrome of central nervous system dysfunction that affects neonates 35 or more weeks of gestation. Although at first it was believed that its etiology was due to hypoxic-ischemic events, and for this reason it was called hypoxic-ischemic encephalopathy, it is already clear that this condition is multicausal. The objective of this research is to review and refer updated literature with which to discuss the symptoms and risk factors of neonatal encephalopathy. For this reason, a bibliographic design study was developed, within the framework of a review methodology. In the results, several interpretations and literal extracts from writers are presented as evidence that explain and characterize the signs and risks of neonatal encephalopathy. In short, the symptoms and signs of neonatal encephalopathy can range from mild to severe, depending on the cause and severity of brain damage, while the associated risk factors will basically correspond to the perinatal and prenatal ones; the latter can also be subdivided into maternal and fetal ones., La encefalopatía neonatal esta referida a una multiplicidad clínica de síntomas neurológicos que pueden ir desde cambios en el estado mental, irritabilidad, hipotonía, movimientos anormales, mala alimentación, disminución de los reflejos primitivos, hasta convulsiones y coma. Es un síndrome de disfunción del sistema nervioso central que perjudica a neonatos 35 o más semanas de gestación. Aunque en principio se creyó que su etiología era por eventos hipóxico-isquémicos, y por ello se denominó encefalopatía hipóxico-isquémica, ya se tiene claro que esta condición es multicausal. El objetivo de esta investigación es revisar y referir literatura actualizada con la cual exponer sobre los síntomas y facto0res de riesgo de la encefalopatía neonatal. Por ello, se desarrolló un estudio de diseño bibliográfico, en el marco de una metodología de revisión. En los resultados se presenta como evidencia, varias interpretaciones y extractos literales de tratadistas que explican y caracterizan los signos y riesgos de la encefalopatía neonatal. En definitiva, los síntomas y signos de la encefalopatía neonatal pueden oscilar de leves a graves, conforme a la causa y severidad del daño cerebral, mientras que los factores de riesgo asociados, básicamente corresponderán a los perinatales y prenatales; pudiendo éstos últimos subdividirse también entre los maternos y fetales.

Neonatal encephalopathy is referred to a multiplicity of clinical neurological symptoms that can range from changes in mental status, irritability, hypotonia, abnormal movements, poor diet, decreased primitive reflexes, to seizures and coma. It is a syndrome of central nervous system dysfunction that affects neonates 35 or more weeks of gestation. Although at first it was believed that its etiology was due to hypoxic-ischemic events, and for this reason it was called hypoxic-ischemic encephalopathy, it is already clear that this condition is multicausal. The objective of this research is to review and refer updated literature with which to discuss the symptoms and risk factors of neonatal encephalopathy. For this reason, a bibliographic design study was developed, within the framework of a review methodology. In the results, several interpretations and literal extracts from writers are presented as evidence that explain and characterize the signs and risks of neonatal encephalopathy. In short, the symptoms and signs of neonatal encephalopathy can range from mild to severe, depending on the cause and severity of brain damage, while the associated risk factors will basically correspond to the perinatal and prenatal ones; the latter can also be subdivided into maternal and fetal ones., La encefalopatía neonatal esta referida a una multiplicidad clínica de síntomas neurológicos que pueden ir desde cambios en el estado mental, irritabilidad, hipotonía, movimientos anormales, mala alimentación, disminución de los reflejos primitivos, hasta convulsiones y coma. Es un síndrome de disfunción del sistema nervioso central que perjudica a neonatos 35 o más semanas de gestación. Aunque en principio se creyó que su etiología era por eventos hipóxico-isquémicos, y por ello se denominó encefalopatía hipóxico-isquémica, ya se tiene claro que esta condición es multicausal. El objetivo de esta investigación es revisar y referir literatura actualizada con la cual exponer sobre los síntomas y facto0res de riesgo de la encefalopatía neonatal. Por ello, se desarrolló un estudio de diseño bibliográfico, en el marco de una metodología de revisión. En los resultados se presenta como evidencia, varias interpretaciones y extractos literales de tratadistas que explican y caracterizan los signos y riesgos de la encefalopatía neonatal. En definitiva, los síntomas y signos de la encefalopatía neonatal pueden oscilar de leves a graves, conforme a la causa y severidad del daño cerebral, mientras que los factores de riesgo asociados, básicamente corresponderán a los perinatales y prenatales; pudiendo éstos últimos subdividirse también entre los maternos y fetales.

IntroductionWhile autoimmune comorbidities are common in alopecia areata, little is known about comorbid cardiovascular disease. The purpose of this study was to evaluate the incidence of bradyarrhythmia in patients with alopecia areata.MethodsRetrospective review of electrocardiograms of 124 patients with [Formula: see text] 50% scalp hair loss (severe alopecia areata) was conducted and compared to National Health and Nutrition Examination Survey (NHANES) data.ResultsThe prevalence of bradycardia in females with alopecia areata was 24.3% (95% CI, 14.5-34.1%) and in those age 40 years or older was 40.8% (95% CI, 22.2-53.5%) compared to 19.5% in the NHANES III population. The prevalence of bradycardia in males with alopecia areata was 36.0% (95% CI, 22.7-49.3%) and in those age 40 years or older was 50.0% (95% CI, 21.7-78.3%) compared to 26.9% in the NHANES III population.ConclusionThe potential association between bradycardia and alopecia areata merits further investigation.

ObjectivesNeonatal resuscitation guidelines recommend 0.5-1 mL saline flush following 0.01-0.03 mg/kg of epinephrine via low umbilical venous catheter for persistent bradycardia despite effective positive pressure ventilation (PPV) and chest compressions (CC). We evaluated the effects of 1 mL vs 3 mL/kg flush volumes and 0.01 vs 0.03 mg/kg doses on return of spontaneous circulation (ROSC) and epinephrine pharmacokinetics in lambs with cardiac arrest.DesignForty term lambs in cardiac arrest were randomised to receive 0.01 or 0.03 mg/kg epinephrine followed by 1 mL or 3 mL/kg flush after effective PPV and CC. Epinephrine (with 1 mL flush) was repeated every 3 min until ROSC or until 20 min. Haemodynamics, blood gases and plasma epinephrine concentrations were monitored.ResultsTen lambs had ROSC before epinephrine administration and 2 died during instrumentation. Among 28 lambs that received epinephrine, 2/6 in 0.01 mg/kg-1 mL flush, 3/6 in 0.01 mg/kg-3 mL/kg flush, 5/7 in 0.03 mg/kg-1 mL flush and 9/9 in 0.03 mg/kg-3 mL/kg flush achieved ROSC (p=0.02). ROSC was five times faster with 0.03 mg/kg epinephrine compared with 0.01 mg/kg (adjusted HR (95% CI) 5.08 (1.7 to 15.25)) and three times faster with 3 mL/kg flush compared with 1 mL flush (3.5 (1.27 to 9.71)). Plasma epinephrine concentrations were higher with 0.01 mg/kg-3 mL/kg flush (adjusted geometric mean ratio 6.0 (1.4 to 25.7)), 0.03 mg/kg-1 mL flush (11.3 (2.1 to 60.3)) and 0.03 mg/kg-3 mL/kg flush (11.0 (2.2 to 55.3)) compared with 0.01 mg/kg-1 mL flush.Conclusions0.03 mg/kg epinephrine dose with 3 mL/kg flush volume is associated with the highest ROSC rate, increases peak plasma epinephrine concentrations and hastens time to ROSC. Clinical trials evaluating optimal epinephrine dose and flush volume are warranted.

Neonatal encephalopathy is referred to a multiplicity of clinical neurological symptoms that can range from changes in mental status, irritability, hypotonia, abnormal movements, poor diet, decreased primitive reflexes, to seizures and coma. It is a syndrome of central nervous system dysfunction that affects neonates 35 or more weeks of gestation. Although at first it was believed that its etiology was due to hypoxic-ischemic events, and for this reason it was called hypoxic-ischemic encephalopathy, it is already clear that this condition is multicausal. The objective of this research is to review and refer updated literature with which to discuss the symptoms and risk factors of neonatal encephalopathy. For this reason, a bibliographic design study was developed, within the framework of a review methodology. In the results, several interpretations and literal extracts from writers are presented as evidence that explain and characterize the signs and risks of neonatal encephalopathy. In short, the symptoms and signs of neonatal encephalopathy can range from mild to severe, depending on the cause and severity of brain damage, while the associated risk factors will basically correspond to the perinatal and prenatal ones; the latter can also be subdivided into maternal and fetal ones., La encefalopatía neonatal esta referida a una multiplicidad clínica de síntomas neurológicos que pueden ir desde cambios en el estado mental, irritabilidad, hipotonía, movimientos anormales, mala alimentación, disminución de los reflejos primitivos, hasta convulsiones y coma. Es un síndrome de disfunción del sistema nervioso central que perjudica a neonatos 35 o más semanas de gestación. Aunque en principio se creyó que su etiología era por eventos hipóxico-isquémicos, y por ello se denominó encefalopatía hipóxico-isquémica, ya se tiene claro que esta condición es multicausal. El objetivo de esta investigación es revisar y referir literatura actualizada con la cual exponer sobre los síntomas y facto0res de riesgo de la encefalopatía neonatal. Por ello, se desarrolló un estudio de diseño bibliográfico, en el marco de una metodología de revisión. En los resultados se presenta como evidencia, varias interpretaciones y extractos literales de tratadistas que explican y caracterizan los signos y riesgos de la encefalopatía neonatal. En definitiva, los síntomas y signos de la encefalopatía neonatal pueden oscilar de leves a graves, conforme a la causa y severidad del daño cerebral, mientras que los factores de riesgo asociados, básicamente corresponderán a los perinatales y prenatales; pudiendo éstos últimos subdividirse también entre los maternos y fetales.

Neonatal encephalopathy is referred to a multiplicity of clinical neurological symptoms that can range from changes in mental status, irritability, hypotonia, abnormal movements, poor diet, decreased primitive reflexes, to seizures and coma. It is a syndrome of central nervous system dysfunction that affects neonates 35 or more weeks of gestation. Although at first it was believed that its etiology was due to hypoxic-ischemic events, and for this reason it was called hypoxic-ischemic encephalopathy, it is already clear that this condition is multicausal. The objective of this research is to review and refer updated literature with which to discuss the symptoms and risk factors of neonatal encephalopathy. For this reason, a bibliographic design study was developed, within the framework of a review methodology. In the results, several interpretations and literal extracts from writers are presented as evidence that explain and characterize the signs and risks of neonatal encephalopathy. In short, the symptoms and signs of neonatal encephalopathy can range from mild to severe, depending on the cause and severity of brain damage, while the associated risk factors will basically correspond to the perinatal and prenatal ones; the latter can also be subdivided into maternal and fetal ones., La encefalopatía neonatal esta referida a una multiplicidad clínica de síntomas neurológicos que pueden ir desde cambios en el estado mental, irritabilidad, hipotonía, movimientos anormales, mala alimentación, disminución de los reflejos primitivos, hasta convulsiones y coma. Es un síndrome de disfunción del sistema nervioso central que perjudica a neonatos 35 o más semanas de gestación. Aunque en principio se creyó que su etiología era por eventos hipóxico-isquémicos, y por ello se denominó encefalopatía hipóxico-isquémica, ya se tiene claro que esta condición es multicausal. El objetivo de esta investigación es revisar y referir literatura actualizada con la cual exponer sobre los síntomas y facto0res de riesgo de la encefalopatía neonatal. Por ello, se desarrolló un estudio de diseño bibliográfico, en el marco de una metodología de revisión. En los resultados se presenta como evidencia, varias interpretaciones y extractos literales de tratadistas que explican y caracterizan los signos y riesgos de la encefalopatía neonatal. En definitiva, los síntomas y signos de la encefalopatía neonatal pueden oscilar de leves a graves, conforme a la causa y severidad del daño cerebral, mientras que los factores de riesgo asociados, básicamente corresponderán a los perinatales y prenatales; pudiendo éstos últimos subdividirse también entre los maternos y fetales.

Neonatal encephalopathy is referred to a multiplicity of clinical neurological symptoms that can range from changes in mental status, irritability, hypotonia, abnormal movements, poor diet, decreased primitive reflexes, to seizures and coma. It is a syndrome of central nervous system dysfunction that affects neonates 35 or more weeks of gestation. Although at first it was believed that its etiology was due to hypoxic-ischemic events, and for this reason it was called hypoxic-ischemic encephalopathy, it is already clear that this condition is multicausal. The objective of this research is to review and refer updated literature with which to discuss the symptoms and risk factors of neonatal encephalopathy. For this reason, a bibliographic design study was developed, within the framework of a review methodology. In the results, several interpretations and literal extracts from writers are presented as evidence that explain and characterize the signs and risks of neonatal encephalopathy. In short, the symptoms and signs of neonatal encephalopathy can range from mild to severe, depending on the cause and severity of brain damage, while the associated risk factors will basically correspond to the perinatal and prenatal ones; the latter can also be subdivided into maternal and fetal ones., La encefalopatía neonatal esta referida a una multiplicidad clínica de síntomas neurológicos que pueden ir desde cambios en el estado mental, irritabilidad, hipotonía, movimientos anormales, mala alimentación, disminución de los reflejos primitivos, hasta convulsiones y coma. Es un síndrome de disfunción del sistema nervioso central que perjudica a neonatos 35 o más semanas de gestación. Aunque en principio se creyó que su etiología era por eventos hipóxico-isquémicos, y por ello se denominó encefalopatía hipóxico-isquémica, ya se tiene claro que esta condición es multicausal. El objetivo de esta investigación es revisar y referir literatura actualizada con la cual exponer sobre los síntomas y facto0res de riesgo de la encefalopatía neonatal. Por ello, se desarrolló un estudio de diseño bibliográfico, en el marco de una metodología de revisión. En los resultados se presenta como evidencia, varias interpretaciones y extractos literales de tratadistas que explican y caracterizan los signos y riesgos de la encefalopatía neonatal. En definitiva, los síntomas y signos de la encefalopatía neonatal pueden oscilar de leves a graves, conforme a la causa y severidad del daño cerebral, mientras que los factores de riesgo asociados, básicamente corresponderán a los perinatales y prenatales; pudiendo éstos últimos subdividirse también entre los maternos y fetales.