Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 6 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 5 uppsatser.

Thesis (M.E.S.)--The Evergreen State College, 2008. / Title from title screen viewed (4/7/2009). Includes bibliographical references (leaves 114-126).

The grief experienced by the bereaved next of kin after a sudden death can result in both physiological and psychological outcomes. The nurse is often faced with the acute crisis that may arise. The meeting with dying patients is emotionally stressful for the nurse, who may experience a disbelief in their own capacity. The aim of the study was to highlight the nurse’s experiences of meeting with the next of kin after a sudden death. A literature review based on five studies with qualitative design and four with quantitative design. Searches were made in the databases CINAHL Complete, PubMed and Nursing & Allied Health Source. Coping strategies and the concept of health were used as theoretical frameworks. The results consist of five themes. The nurse’s experienced role in the meeting with next of kin which showed that the majority of the nurses experienced the meeting with the bereaved next of kin as their responsibility. Emotional stress of the meeting was for example helplessness, stress, failure and guilt. Fear of the next of kin’s possible reactions meant the nurses fear for the reaction from the next of kin. The experience of education and lack of knowledge were considered as an important foundation in the meeting with the next of kin, and The experience of lack of resources that showed a lack of resources and guidelines. Stress and other external factors may affect nurses’ health negatively; the use of different coping strategies can assist the nurse in affectively handling such stress. The nurse is required to be in good health to adequately meet the next of kin and their needs. Training in and knowledge of the meeting with the next of kin can contribute positively towards the nurse’s well-being. / Närstående som drabbas av en smärtsam förlust till följd av ett plötsligt dödsfall upplever sorg, vilket kan resultera i både fysiologiska och psykologiska besvär. Sjuksköterskan är ofta den som möter närstående i den akuta krisen som kan uppstå. Sjuksköterskan upplever mötet med döende patienter som emotionellt påfrestande och kan uppleva en misstro på sin kapacitet. Syftet var att belysa sjuksköterskans upplevelser av mötet med närstående vid plötsligt dödsfall. En litteraturöversikt baserad på nio vetenskapliga studier, fem av kvalitativ design och fyra av kvantitativ design. Sökningar gjordes i databaserna CINAHL Complete, PubMed och Nursing & Allied Health Source. Copingstrategier och begreppet hälsa användes som teoretisk utgångspunkt. Resultatet består av fem teman. Sjuksköterskans upplevda roll i mötet med närstående där det framkom att sjuksköterskorna upplevde mötet med de plötsligt sörjande närstående som deras ansvarsområde. Emotionella påfrestningar i mötet som exempelvis var hjälplöshet, stress och skuld. Rädslan för närståendes eventuella reaktioner som innebar en rädsla för reaktionen från de närstående. Upplevelsen av bristande utbildning och kunskap som ansågs vara en viktig grund i mötet med närstående och Upplevelsen av bristande resurser som visade på bristande resurser och riktlinjer. Stress och yttre påfrestningar kan påverka sjuksköterskans hälsa negativt och för att hantera detta kan olika copingstrategier användas. För att sjuksköterskan ska kunna möta de närstående på ett adekvat sätt krävs det att hen upplever hälsa. Utbildning och kunskap om mötet med närstående kan bidra positivt till sjuksköterskans välbefinnande och hälsa.

Bakgrund: År 2016 drabbades 7 934 personer i Sverige av plötsligt hjärtstopp där någon slags behandling påbörjats. På grund av ökade kunskaper kring plötsligt hjärtstopp ökar antalet överlevare. Plötsligt hjärtstopp kan upplevas som en traumatisk kris och kan påverka personens liv. Detta medför ett behov av att förbättra kunskapen och förståelsen för hur personer upplever livet efter plötsligt hjärtstopp. Syfte: Att beskriva personers upplevelser av livet efter plötsligt hjärtstopp. Metod: Litteraturöversikt där nio artiklar med kvalitativ ansats analyserats induktivt. Resultat: Tre teman identifierades. Existentiellt kaos med subteman; Varför jag? och Närheten till döden. Tillbaka till tryggheten med subteman; Behov av närhet och Behov av information. Ett nytt liv med subteman; Livet förändras och Livet omprioriteras. Personerna som drabbats av hjärtstopp hade behov av att fylla i minnesluckor, försöka förstå vad som hade hänt samt finna en mening med händelsen. Slutsats: Resultatet visade att personer som genomgått plötsligt hjärtstopp upplevde att det nya livet innebar fysiska, kognitiva och emotionella svårigheter. Att lära sig leva igen innebar omprioriteringar i livet.

Sudden Infant Death Syndrome (SIDS) is the sudden death of an infant younger than one year of age that remains unexplained after a complete investigation. For these infants, many different reasons have been hypothesized as to the cause of these deaths including: inherent vulnerability and improper hypoxic arousal. Studies done in other laboratories have shown that there seems to be a reduction in the levels of the neurotransmitter serotonin (5-HT) in the neurons of the raphe, extra-raphe, and ventral populations along with projection sites of these neurons. The huge implications of 5-HT in the control of respiration, prompted animal model studies to further investigate a potential connection between 5-HT and SIDS. 5-HT deficient mice were engineered by knocking out the Pet-1 transcription factor so that knockout mice only retained 30-40% of their brainstem 5-HT neurons. By comparing these 5-HT deficient Pet-1 knockout mice to wild-type mice, it was demonstrated that 5-HT deficient mice failed to autoresuscitate themselves after repeated bouts of hypoxia. Intriguingly, these mice only experienced an autoresuscitation deficit during a specific time period during development. To further evaluate the pathological development behind this behavior issue, in the current study we utilized mice that have modified Pet-1-Flpe driver, Egr2-Cre driver, along with a knock-in RC::FPSit allele to observe 5-HT development in the brainstem in a mature adult and across the critical period (postnatal days 8 and 13- P8 and P13). The transgenic mouse model Pet1-Krox20 gives us a way of exploring a specific subset of 5-HT neurons that rise from the developmental rhombomeres r3 and r5. The use of the knock-in RC::FPSit allele allows us to view the axonal projections of these specific 5-HT neurons by utilizing the presynaptic marker synaptophysin-GFP. This model (PKSit) will allow us to target 5-HT neurons that are implicated in respiration. We chose to compare two projection targets of the PKSit 5-HT neuron subtype through the vulnerable period of development and mature adult mouse: the Locus Coeruleus (LC) and the Nucleus Tractus Solitarius (NTS). In this study we tested the amount of colabeling between 5-HT and GFP in the LC and NTS at P8, P13, as well as the mature adult. We hypothesize that the LC undergoes significant serotonergic axon development and increases colocalization with GFP labeled axon projections between the ages of P8 and P13. We sliced mouse brains and ran immunofluorescence before taking confocal images. By utilizing ImageJ software to run colocalization analysis on the images obtained, we were able to quantify the amount of 5-HT labeled axon projections that are colocalized with GFP labeled axon projections. The parameters we used to quantify the amount of colocalization include the Pearson's Coefficient (PC), Mander's Coefficient (M1/M2), Cytofluorograms, Costes' Method, and van Steensel's Cross-Correlation Coefficient (CCF). We found that the LC shows significant changes with age in the colocalization of 5-HT with GFP while the NTS does not exhibit significant changes with age. The significant changes found in the LC 5-HT/GFP expression between the ages of P8 and P13 suggest one possible cause of failure of arousal. At P8, this lack of 5-HT colabeling with GFP projections suggests that there is some development occurring, which prevents the proper function of 5-HT. At P13, there is a significant increase in the colabeling of 5-HT with GFP, which indicates that the Pet1-Krox20 lineage is actively using 5-HT. The colocalization studies demonstrate that as the mouse ages, the amount of 5-HT labeling with GFP-synaptophysin in the NTS stays the same. The lack of overlap even in mature adult mice suggests that the expression of 5-HT in GFP labeled projections is not necessary. This colocalization study shows that there is an effect of age on the development of the serotonergic system in the LC, but no effect of age in the NTS. While this demonstrates that there is a critical period of development in relation to the LC, it is only one aspect of why mice pups failed to respond to repeated bouts of hypoxia.

Abstract There is substantial evidence on the associations between cold ambient temperature and adverse health effects. Less is known about the role of prolonged episodes of cold weather denoted as cold spells. This study assessed relations between cold spells and adverse health effects globally, and quantified and elaborated the associations between cold spells and sudden cardiac death (SCD) in northern Finland. Based on random-effects models in the meta-analyses of evidence from 9 studies around the world, cold spells were associated with increased mortality rates from all or all non-accidental causes (RR 1.10; 95% CI: 1.04–1.17), cardiovascular diseases (RR 1.11; 95% CI: 1.03–1.19), and respiratory diseases (RR 1.21; 95% CI: 0.97–1.51). Suggestive evidence of other health effects was identified. Investigating 51-years of coordinate-specific weather data at the home coordinates of autopsy-verified cases of SCD, conditional logistic regression in a case-crossover setting produced an estimate for the association between cold spells and the risk of SCD (OR 1.33; 95% CI: 1.00–1.78). A greater number of cold days preceding death increased the risk of SCD approximately 19% per day (OR 1.19; 95% CI: 1.07–1.32). The association between season-specific cold spells and SCD was strongest during autumn and winter, and lowest during spring and summer. The association was stronger for ischemic (OR 1.55; 95% CI: 1.12–2.13) than for non-ischemic SCD (OR 0.68; 95% CI: 0.32–1.45) (Q-statistic 3.85, p 0.05), confirmed by the autopsy finding. Among cases suffering ischemic SCD, the association seemed stronger in those without a prior diagnosis of ischemic heart disease than in those diagnosed during lifetime. The association seemed stronger with severe coronary stenosis (OR 1.60; 95% CI: 1.11–2.30), and weaker with moderate stenosis (OR 0.97; 95% CI: 0.37–2.55). The use of aspirin, β-blockers, and nitrates seemed to decrease the risk of ischemic SCD during cold spells. In conclusion, cold spells increased the risk of ischemic SCD, and patients without appropriate diagnosis and medications for ischemic heart disease seemed most susceptible. The results indicate that coronary stenosis plays a central role in the cold-related pathogenesis of SCD. Timely diagnosis and treatment of ischemic heart disease might reduce weather-related SCDs in a community. / Tiivistelmä Kylmän lämpötilan ja terveyshaittojen välisistä yhteyksistä on vahva tutkimusnäyttö. Vähemmän tiedetään pitkittyneiden kylmäjaksojen ja terveyshaittojen välisistä yhteyksistä. Tutkimuksessa arvioitiin kylmäjaksojen ja terveyshaittojen välisiä yhteyksiä globaalisti, ja määritettiin kylmäjaksojen ja sydänperäisen äkkikuoleman (SÄK) välisiä yhteyksiä Pohjois-Suomessa. Yhdeksän eri puolella maailmaa toteutetun tutkimuksen tulosten meta-analyysissa satunnaisvaikutusten malli osoitti yhteyden kylmäjaksojen ja kaikkien tai luonnollisien syiden (RR 1.10; 95% CI: 1.04–1.17), sydän- ja verisuonisairauksien (RR 1.11; 95% CI: 1.03–1.19), ja hengityselimistön sairauksien (RR 1.21; 95% CI: 0.97–1.51) kuolleisuuden välillä. Viitteellistä näyttöä havaittiin muista terveyshaitoista. Tutkittaessa 51-vuoden koordinaattikohtaista säätä case-crossover-asetelmassa oikeuslääketieteellisesti vahvistettujen SÄK-tapausten kotiosoitteissa, ehdollisen logistisen regression mukaan SÄK:n riski oli yhteydessä kuolemaa edeltävään kylmäjaksoon (OR 1.33; 95% CI: 1.00–1.78). Lisääntyvä kylmien päivien lukumäärä ennen kuolemaa lisäsi riskiä keskimäärin 19% päivää kohden (OR 1.19; 95% CI: 1.07–1.32). Yhteys kausikohtaisten kylmäjaksojen ja SÄK:n välillä oli vahvin syksyllä ja talvella, ja heikoin keväällä ja kesällä. Yhteys oli vahvempi kylmäjaksojen ja iskeemisen SÄK:n (OR 1.55; 95% CI: 1.12–2.13) kuin kylmäjaksojen ja ei-iskeemisen SÄK:n (OR 0.68; 95% CI: 0.32–1.45) välillä (Q-statistic 3.85, p 0.05). Iskeemisen SÄK:n kokeneilla yhteys vaikutti vahvemmalta tapauksilla joilla ei ollut aiempaa iskeemisen sydänsairauden diagnoosia, kuin tapauksilla jotka oli diagnosoitu elinaikana. Yhteys vaikutti vahvemmalta vaikea-asteisesta sepelvaltimostenoosia sairastavilla (OR 1.60; 95% CI: 1.11–2.30), kuin lievempi-asteisessa stenoosissa (OR 0.97; 95% CI: 0.37–2.55). Aspiriini, β-salpaajat, ja nitraatit vaikuttivat vähentävän iskeemisen SÄK:n riskiä kylmäjakson aikana. Yhteenvetona, kylmäjaksot lisäsivät iskeemisen SÄK:n riskiä, ja potilaat vailla iskeemisen sydänsairauden diagnoosia ja lääkityksiä vaikuttivat olevan alttiimpia kylmäjaksojen haittavaikutuksille. Tulokset viittaavat sepelvaltimostenoosin keskeiseen rooliin kylmään liittyvän SÄK:n patogeneesissä. Varhainen iskeemisen sydänsairauden diagnoosi ja siihen liittyvä sydäntä suojaava lääkitys voisivat vähentää säähän liittyviä SÄK:a.

INTRODUÇÃO. O aumento da densidade de arritmia ventricular e a redução da variabilidade da freqüência cardíaca estão associados com risco de morte súbita e mortalidade total em insuficiência cardíaca. A inibição colinesterásica com brometo de piridostigmina (PIR) aumenta a variabilidade da freqüência de pessoas normais, porém seu efeito em pacientes com insuficiência cardíaca é desconhecido. OBJETIVOS. Testar a hipótese de que a administração a curto prazo de piridostigmina reduz a densidade de arritmia ventricular e aumenta a variabilidade da freqüência cardíaca em pacientes com insuficiência cardíaca. MÉTODOS. Pacientes com insuficiência cardíaca e em ritmo sinusal participaram de um estudo duplo-cego, cruzado, randomizado para placebo e piridostigmina (30mg VO de 8 em 8 horas por 2 dias). Monitorização eletrocardiográfica ambulatorial de 24 horas foi realizada para análise de arritmia e para avaliação dos índices do domínio do tempo da variabilidade da freqüência cardíaca. Pacientes foram separados em 2 grupos, de acordo com a densidade de arritmia ventricular. O grupo Arritmia (n = 11) incluiu pacientes com mais de 10 extrassístoles ventriculares por hora (ESV/h), e o grupo Variabilidade da Freqüêcia Cardíaca (n = 12) incluiu pacientes com um número de ESVs em 24 horas que não excedia 1 % do número total de intervalos RR. RESULTADOS. No grupo Arritmia, PIR resultou em uma redução de 65% no número de extrassístoles ventriculares (Placebo 266 + 56 ESV/h vs. PIR 173 + 49 ESV/h; p = 0,03). No grupo da Variabilidade da Freqüência Cardíaca, a administração de PIR resultou em um aumento do intervalo RR médio (Placebo 733 + 22 ms vs PIR 790 + 33 ms; p = 0,01), e nos índices do domínio do tempo da variabilidade da freqüência cardíaca PNN50 (Placebo 3 + 1,1 % vs PIR 6 + 1,6 %; p = 0,03) e RMSSD (Placebo 21 + 2 vs PIR 27 + 3; p = 0,008). CONCLUSÃO. Em pacientes com insuficiência cardíaca, PIR reduziu a densidade de arritmia ventricular e aumentou a VFC, provavelmente por seu efeito colinomimético. Estudos a longo prazo com PIR em insuficiência cardíaca devem ser realizados. / OBJECTIVE To test the hypothesis that short-term administration of pyridostigmine bromide (PYR) reduces ventricular arrhythmia density and increases heart rate variability in patients with congestive heart failure. BACKGROUND Increased ventricular arrhythmia density and reduced heart rate variability are associated with risk of sudden death and overall mortality in patients with heart failure. Cholinesterase inhibition with pyridostigmine bromide increases heart rate variability in normal subjects, but its effect in patients with heart failure is unknown. METHODS Patients with heart failure and in sinus rhythm participated in a double-blind, cross-over protocol, randomized for placebo and pyridostigmine (30 mg PO TID for 2 days). Twenty-four hour electrocardiographic recordings were performed for arrhythmia analysis and for the measurement of time domain indices of heart rate variability. Patients were separated in 2 groups, according to their ventricular arrhythmia density. The Arrhythmia Group (n = 11) included patients with more than 10 ventricular premature beats per hour (VPBs/h), and the Heart Rate Variability Group (n = 12) included patients with a number of VPBs in 24 hours not exceeding 1 % of the total number of RR intervals. RESULTS For the Arrhythmia Group, PYR resulted in 65 % reduction of ventricular ectopic activity (Placebo 266 ± 56 VPBs/h vs. PYR 173 ± 49 VPBs/h; P = 0.03). For the Heart Rate Variability Group, PYR administration resulted in an increment of mean RR interval (Placebo 733 ± 22 msec vs PYR 790 ± 33 msec; P = 0.01), and in the time domain indices of heart rate variability RMSSD (Placebo 21± 2 vs PYR 27 ± 3; P = 0.01) and PNN50 (Placebo 3 ± 1 % vs PYR .6 ± 2 %; P = 0.03). CONCLUSION In patients with heart failure, PYR reduced ventricular arrhythmia density and increased HRV, most likely due to its cholinomimetic effect. Long-term trials with PYR in heart failure should be conducted.

Background and aims: The qualitative literature that has examined the topic of sudden and profound transformation has mostly focused on the antecedent and facilitative factors associated with this form of change. However, previous empirical research has noted the great difficulty participants experience when trying to arrive at an explanation for their change. Within this study, I have aimed to explore the lived experience of sudden personal transformation. Having experienced a life altering epiphany myself, I was compelled to investigate how others, who also identified as having experienced a sudden, transformative change, made sense of it. Participants' struggle to find the 'words that work' when retelling and interpreting their transformation experience developed to become one of the central focuses of this thesis. The lived body is conceptualised as an essential source of meaningful understanding, and therefore, is sought to be used as an instrument of data analysis. Method: Six participants took part in unstructured interviews which were transcribed, before applying an interpretative phenomenological analysis. With the aim of facilitating the development of emotionally receptive forms of understanding, an embodied interpretation was applied to each account, via the application of Gendlin's method of focusing. Found poems were also constructed. Findings: Five master themes were identified: 1) Making sense of what it is difficult to make sense of; 2) Who I was, what happened, who I am now; 3) Illuminating purpose; 4) Compelled to act; and 5) Attempting to capture the ineffable quality. Each master theme was identified as having two related sub-themes. The acceptance and appreciation of the experience as one which can never be fully explained played a vital role in the emerging meaning of the experience. Participants appeared to make sense of their transformation through the separation of their lives into the temporal categories of before and after the event. The lives of the participants were changed. New life paths became clear, and purpose was suddenly illuminated. For all the participants in the study, purpose appeared to be intimately linked with the creation of positive connections with others. Conclusions and Implications: Examination of how people experience positive change outside of the therapy room is of use to those seeking to support people who want to change within the realms of psychological therapy. Attendance to the researcher's bodily response to the research data was understood as enabling movement towards a fuller understanding of the phenomenon under examination, as well as facilitating the production of 'words that work'. It is concluded that therapeutic practitioners and other mental health professionals may benefit from understanding the dimensions of transformative change described here, in such qualitatively rich terms.

INTRODUÇÃO. O aumento da densidade de arritmia ventricular e a redução da variabilidade da freqüência cardíaca estão associados com risco de morte súbita e mortalidade total em insuficiência cardíaca. A inibição colinesterásica com brometo de piridostigmina (PIR) aumenta a variabilidade da freqüência de pessoas normais, porém seu efeito em pacientes com insuficiência cardíaca é desconhecido. OBJETIVOS. Testar a hipótese de que a administração a curto prazo de piridostigmina reduz a densidade de arritmia ventricular e aumenta a variabilidade da freqüência cardíaca em pacientes com insuficiência cardíaca. MÉTODOS. Pacientes com insuficiência cardíaca e em ritmo sinusal participaram de um estudo duplo-cego, cruzado, randomizado para placebo e piridostigmina (30mg VO de 8 em 8 horas por 2 dias). Monitorização eletrocardiográfica ambulatorial de 24 horas foi realizada para análise de arritmia e para avaliação dos índices do domínio do tempo da variabilidade da freqüência cardíaca. Pacientes foram separados em 2 grupos, de acordo com a densidade de arritmia ventricular. O grupo Arritmia (n = 11) incluiu pacientes com mais de 10 extrassístoles ventriculares por hora (ESV/h), e o grupo Variabilidade da Freqüêcia Cardíaca (n = 12) incluiu pacientes com um número de ESVs em 24 horas que não excedia 1 % do número total de intervalos RR. RESULTADOS. No grupo Arritmia, PIR resultou em uma redução de 65% no número de extrassístoles ventriculares (Placebo 266 + 56 ESV/h vs. PIR 173 + 49 ESV/h; p = 0,03). No grupo da Variabilidade da Freqüência Cardíaca, a administração de PIR resultou em um aumento do intervalo RR médio (Placebo 733 + 22 ms vs PIR 790 + 33 ms; p = 0,01), e nos índices do domínio do tempo da variabilidade da freqüência cardíaca PNN50 (Placebo 3 + 1,1 % vs PIR 6 + 1,6 %; p = 0,03) e RMSSD (Placebo 21 + 2 vs PIR 27 + 3; p = 0,008). CONCLUSÃO. Em pacientes com insuficiência cardíaca, PIR reduziu a densidade de arritmia ventricular e aumentou a VFC, provavelmente por seu efeito colinomimético. Estudos a longo prazo com PIR em insuficiência cardíaca devem ser realizados. / OBJECTIVE To test the hypothesis that short-term administration of pyridostigmine bromide (PYR) reduces ventricular arrhythmia density and increases heart rate variability in patients with congestive heart failure. BACKGROUND Increased ventricular arrhythmia density and reduced heart rate variability are associated with risk of sudden death and overall mortality in patients with heart failure. Cholinesterase inhibition with pyridostigmine bromide increases heart rate variability in normal subjects, but its effect in patients with heart failure is unknown. METHODS Patients with heart failure and in sinus rhythm participated in a double-blind, cross-over protocol, randomized for placebo and pyridostigmine (30 mg PO TID for 2 days). Twenty-four hour electrocardiographic recordings were performed for arrhythmia analysis and for the measurement of time domain indices of heart rate variability. Patients were separated in 2 groups, according to their ventricular arrhythmia density. The Arrhythmia Group (n = 11) included patients with more than 10 ventricular premature beats per hour (VPBs/h), and the Heart Rate Variability Group (n = 12) included patients with a number of VPBs in 24 hours not exceeding 1 % of the total number of RR intervals. RESULTS For the Arrhythmia Group, PYR resulted in 65 % reduction of ventricular ectopic activity (Placebo 266 ± 56 VPBs/h vs. PYR 173 ± 49 VPBs/h; P = 0.03). For the Heart Rate Variability Group, PYR administration resulted in an increment of mean RR interval (Placebo 733 ± 22 msec vs PYR 790 ± 33 msec; P = 0.01), and in the time domain indices of heart rate variability RMSSD (Placebo 21± 2 vs PYR 27 ± 3; P = 0.01) and PNN50 (Placebo 3 ± 1 % vs PYR .6 ± 2 %; P = 0.03). CONCLUSION In patients with heart failure, PYR reduced ventricular arrhythmia density and increased HRV, most likely due to its cholinomimetic effect. Long-term trials with PYR in heart failure should be conducted.