scholarly journals Level of vital and laboratory values on arrival, and increased risk of 7-day mortality among adult patients in the emergency department: a population-based cohort study

BMJ Open ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. e038516
Author(s):  
Peter Bank Pedersen ◽  
Daniel Pilsgaard Henriksen ◽  
Mikkel Brabrand ◽  
Annmarie Touborg Lassen

ObjectivesThe aim of the study was to provide evidence for, at which vital and laboratory values, increased risk of 7-day mortality in acute adult patients on arrival to an emergency department (ED).DesignA population-based cohort study.SettingED at Odense University Hospital, Denmark.ParticipantsAll patients ≥18 years with a first-time contact within the study period, 1 April 2012 to 31 March 2015.Primary and secondary outcome measuresPrimary outcome was 7-day all-cause mortality.Variables were first recorded vital and laboratory values included in risk stratification scores; respiratory frequency, blood pressure, heart rate, Glasgow Coma Scale, temperature, saturation, creatinine, PaO2, platelet count and bilirubin. The association between values and mortality was described using a restricted cubic spline. A predefined 7-day mortality of 2.5% was chosen as a relevant threshold.ResultsWe included 40 423 patients, 52.5% women, median age 57 (IQR 38–74) years and 7-day mortality 2.8%. Seven-day mortality of 2.5% had thresholds of respiratory frequency <12 and >18/min, systolic blood pressure <112 and >192 mm Hg, heart rate <54 and >102 beats/min, temperature <36.0°C and >39.8°C, saturation <97%, Glasgow Coma Scale score <15, creatinine <41 and >98 µmol/L for PaO2 <9.9 and >12.3 kPa, platelet count <165 and >327×109/L and bilirubin >12 µmol/L.ConclusionVital values on arrival, outside the normal ranges for the measures, are indicative of increased risk of short-term mortality, and most of the value thresholds are included in the lowest urgency level in triage and risk stratification scoring systems.

2019 ◽  
Author(s):  
P. Oras ◽  
H. Häbel ◽  
P. H. Skoglund ◽  
P. Svensson

ABSTRACTObjectivesIn the emergency department (ED), high blood pressure (BP) is commonly observed but mostly used to evaluate patients’ health in the short-term. We aimed to study whether ED-measured BP is associated with incident atherosclerotic cardiovascular disease (ASCVD), myocardial infarction (MI), or stroke in long-term, and to estimate the number needed to screen (NNS) to prevent ASCVD.DesignElectronic Health Records (EHR) and national register-based cohort study. The association between BP and incident ASCVD was studied with Cox-regression.SettingTwo university hospital emergency departments in Sweden.Data sourcesBP data were obtained from EDs EHR, and outcome information was acquired through the Swedish National Patient Register for all participants.ParticipantsAll patients ≥18 years old who visited the EDs between 2010 to 2016, with an obtained BP (n=300,193).Main outcome measuresIncident ASCVD, MI, and stroke during follow-up.ResultsThe subjects were followed for a median of 42 months. 8,999 incident ASCVD events occurred (MI: 4,847, stroke: 6,661). Both diastolic and systolic BP (SBP) was associated with incident ASCVD, MI, and stroke with a progressively increased risk for SBP within hypertension grade 1 (HR 1.15, 95% CI 1.06 to 1.24), 2 (HR 1.35, 95% CI 1.25 to 1.47), and 3 (HR 1.63, 95% CI 1.49 to 1.77). The six-year cumulative incidence of ASCVD was 12% for patients with SBP ≥180 mmHg compared to 2% for normal levels. To prevent one ASCVD event during the median follow-up, NNS was estimated to 151, whereas NNT to 71.ConclusionsBP in the ED is associated with incident ASCVD, MI, and stroke. High BP recordings in EDs should not be disregarded as isolated events, but an opportunity to detect and improve treatment of hypertension. ED-measured BP provides an important and under-used tool with great potential to reduce morbidity and mortality associated with hypertension.


2021 ◽  
Author(s):  
Christian S Hansen ◽  
Marit E Jørgensen ◽  
Marek Malik ◽  
Daniel R Witte ◽  
Eric J Brunner ◽  
...  

<b>Objective</b> <p>Higher resting heart rate (rHR) and lower heart rate variability (HRV) are associated with increased risk of cardiovascular disease (CVD) and all-cause mortality in people with and without diabetes It is unknown whether temporal changes in rHR and HRV may contribute to this risk. We investigated associations between 5-year changes in rHR and HRV and risk of future CVD and death, taking into account participants’ baseline glycemic state. </p> <p><b>Research design and Methods</b></p> <p>In this prospective population-based cohort study we investigated 4,611 CVD-free civil servants (mean age 60, SD=5.9 years, 70% men).<b> </b>rHR and/or 6 indices of HRV were measured. Associations of 5-year change in 5-minute rHR and HRV with fatal- and non-fatal CVD and all-cause mortality or the composite of the two were assessed with adjustments for relevant confounders. Effect modification by glycemic state was tested. </p> <p><b>Results</b></p> <p>At baseline, 63% of participants were normoglycemic, 29% had prediabetes and 8% had diabetes. During a median (IQR) follow-up of 11.9 (11.4;12.3) years, 298 participants (6.5%) experienced a CVD event and 279 (6.1%) died from non-CVD related causes. We found no association between 5-year changes in rHR and HRV and future events. Only baseline rHR was associated with all-cause mortality. A 10 beats per minute higher baseline level showed a 11.4% higher rate of all-cause mortality (95%CI:1.0;22.9%, P=0.032). Glycemic state did not modify associations<b>. </b></p> <p><b>Conclusion</b></p> <p>Changes in rHR and HRV and possibly also baseline values of these measures are not associated with future CVD or mortality in people with or without dysglycemia. </p>


2021 ◽  
Author(s):  
Christian S Hansen ◽  
Marit E Jørgensen ◽  
Marek Malik ◽  
Daniel R Witte ◽  
Eric J Brunner ◽  
...  

<b>Objective</b> <p>Higher resting heart rate (rHR) and lower heart rate variability (HRV) are associated with increased risk of cardiovascular disease (CVD) and all-cause mortality in people with and without diabetes It is unknown whether temporal changes in rHR and HRV may contribute to this risk. We investigated associations between 5-year changes in rHR and HRV and risk of future CVD and death, taking into account participants’ baseline glycemic state. </p> <p><b>Research design and Methods</b></p> <p>In this prospective population-based cohort study we investigated 4,611 CVD-free civil servants (mean age 60, SD=5.9 years, 70% men).<b> </b>rHR and/or 6 indices of HRV were measured. Associations of 5-year change in 5-minute rHR and HRV with fatal- and non-fatal CVD and all-cause mortality or the composite of the two were assessed with adjustments for relevant confounders. Effect modification by glycemic state was tested. </p> <p><b>Results</b></p> <p>At baseline, 63% of participants were normoglycemic, 29% had prediabetes and 8% had diabetes. During a median (IQR) follow-up of 11.9 (11.4;12.3) years, 298 participants (6.5%) experienced a CVD event and 279 (6.1%) died from non-CVD related causes. We found no association between 5-year changes in rHR and HRV and future events. Only baseline rHR was associated with all-cause mortality. A 10 beats per minute higher baseline level showed a 11.4% higher rate of all-cause mortality (95%CI:1.0;22.9%, P=0.032). Glycemic state did not modify associations<b>. </b></p> <p><b>Conclusion</b></p> <p>Changes in rHR and HRV and possibly also baseline values of these measures are not associated with future CVD or mortality in people with or without dysglycemia. </p>


BMJ Open ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. e043657
Author(s):  
Hua Chen ◽  
Tomas Hemmingsson ◽  
Imre Janszky ◽  
Mikael Rostila ◽  
Yvonne Forsell ◽  
...  

ObjectiveCompelling evidence suggests that childhood adversities are associated with an increased risk of hypertension in middle age and old age. The link between childhood adversities and blood pressure in youth is less clear. In this cohort study, we examined the association between death of a parent during childhood and blood pressure in early adulthood in men.SettingSweden.ParticipantsWe studied 48 624 men born in 1949–1951 who participated in the compulsory military conscription in 1969/1970 in Sweden. Information on death of a parent during childhood was obtained from population-based registers. Information on covariates was obtained from the questionnaire and the clinical examination completed at conscription and from population-based registers.Outcome measuresBlood pressure was measured at conscription according to standard procedures.ResultsThe multivariable least square means of systolic and diastolic blood pressure did not differ between bereaved (128.25 (127.04–129.46) and 73.86 (72.89–74.84) mm Hg) and non-bereaved study participants (128.02 (126.86–129.18) and 73.99 (73.06–74.93) mm Hg). Results were similar when considering the cause of the parent’s death, the gender of the deceased parent or the child’s age at loss. Loss of a parent in childhood tended to be associated with an increased hypertension risk (OR and 95% CI: 1.10 (1 to 1.20)); the association was present only in case of natural deaths.ConclusionWe found no strong support for the hypothesis that stress following the loss of a parent during childhood is associated with blood pressure or hypertension in youth in men.


1985 ◽  
Vol 53 (01) ◽  
pp. 070-074 ◽  
Author(s):  
G Mallarkey ◽  
G M Smith

SummaryThe mechanism of collagen-induced sudden death in rabbits was studied by measuring blood pressure (BP), heart rate, ECG, the continuous platelet count and the plasma levels of thromboxane B2 (TxB2) and 6-keto prostaglandin Fia (6-keto PGF1α). Death was preceded by myocardial ischaemia and a sharp fall in BP which occurred before any fall in platelet count was observed. The calcium entry blockers (CEBs), verapamil, nifedipine and PY 108-068 protected the rabbits from sudden death without any significant effect on the decrease in the platelet count or increase in plasma TxB2 levels. 6-keto PGF1α could not be detected in any plasma samples. Indomethacin and tri-sodium citrate also protected the rabbits but significantly reduced the fall in platelet count and plasma TxB2. In vitro studies on isolated aortae indicated that verapamil non-specifically inhibited vasoconstriction induced by KC1, adrenaline and U46619 (a thromboxane agonist). It is concluded that CEBs physiologically antagonize the vasoconstricting actions of platelet-derived substances and that it is coronary vasoconstriction that is primarily the cause of death.


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