Despite the decreased survival associated with diabetes with out-of-hospital cardiac arrest and the overall low survival to hospital discharge, we would like to present two cases of OHCA in diabetics who despite prolonged resuscitation efforts had complete neurological recovery likely due to concomitant hypothermia. There is a steady decreasing rate of ROSC with longer durations of CPR so that outcomes are best when <20 minutes compared to prolonged resuscitation efforts (>30-40 minutes). It has been previously recognized that hypothermia prior to cardiac arrest can be neurologically protective even with up to 9 hours of cardiopulmonary resuscitation. Hypothermia has been associated with DKA and although often indicates sepsis with mortality rates of 30-60%, it may indeed be protective if occurring prior to cardiac arrest. The critical factor for neuroprotection may be a slow drop to a temperature <25⁰C prior to OHCA as is achieved in deep hypothermic circulatory arrest for operative procedures of the aortic arch and great vessels. It may be worthwhile continuing aggressive resuscitation efforts even for prolonged periods before attaining ROSC for OHCA in patients found hypothermic from metabolic illnesses as compared to only from environmental exposures (avalanche victims, cold water submersions, etc.) as has been traditionally reported in the medical literature.
Introduction: Intracranial haemorrhage (ICH) is a known, but a rare cause of out of hospital cardiac arrest (OHCA). It results in the development of non-shockable rhythms such as asystole or pulseless electrical activity (PEA).
Case Report: A 77- years old male had an OHCA without any prodrome. An emergency medical services (EMS) team responded to an emergency call and intubated the patient at the site before transporting him to the Acute Care Hospital, New Brunswick, New Jersey, USA. On admission, a non-contrast computed tomography scan of the head revealed a large cerebellar haemorrhage. Non-traumatic ICH is a rare cause of OHCA. Although subarachnoid haemorrhage causing cardiac arrest has been described in the literature, cerebellar haemorrhage leading to cardiac arrest is rare. The mechanism by which ICH patients develop cardiac arrest is likely explained by a massive catecholamine surge leading to cardiac stunning.
Conclusion: A non-shockable rhythm in the setting of a sudden cardiac arrest should raise alarms for a primary non-cardiac ethology, especially a primary cerebrovascular event. The absence of brainstem reflexes increases the likelihood of an intracranial process.
Introduction: In an attempt to identify patients who have successfully survived a resuscitated cardiac arrest (CA), attention is drawn to resistin and S100B protein, two biomarkers that have been studied in relation to CA.
Aim: The study aimed to identify the potential cut-off serum values for resistin and S100B in patients who had CA, compared to healthy volunteers, given that, currently, none of the markers have normal and pathological reference range limits for human assay levels related to this pathology.
Materials and Methods: Forty patients, resuscitated after out-of-hospital CA and forty healthy controls, were included in the study. All patients were followed up for seventy-two hours after CA or until death. Blood samples for biomarkers were collected on admission to the ED (0-time interval) and at 6, 12, 24, 48 and 72 hours following resuscitation. Only one blood sample was collected from the controls. The serum concentrations of biomarkers were measured.
Results: For each time interval, median serum levels of resistin and S100 B were significantly higher in patients with CA compared to healthy controls. The cut-off value for resistin in patients with CA, at the 12-hours versus controls, was > 8.2 ng/ml. The cut-off value for S100B in patients with CA versus controls recorded at 6 hours, was > 11.6 pg/ml.
Conclusion: Serum levels of resistin and S100B are higher among resuscitated CA patients compared to controls.
This review summarizes the most recent developments in providing advanced supportive measures for cardiopulmonary resuscitation, and the results obtained using these new therapies in patients with cardiac arrest caused by acute myocardial infarction (AMI). Also detailed are new approaches such as extracorporeal cardiopulmonary resuscitation (ECPR), intra-arrest percutaneous coronary intervention, or the regional models for systems of care aiming to reduce the critical times from cardiac arrest to initiation of ECPR and coronary revascularization.
Introduction: In patients with out-of-hospital cardiac arrest (OHCA) complicating an ST-segment elevation myocardial infarction (STEMI), the survival depends largely on the restoration of coronary flow in the infarct related artery. The aim of this study was to determine clinical and angiographic predictors of in-hospital mortality in patients with OHCA and STEMI, successfully resuscitated and undergoing primary percutaneous intervention (PCI).
Methods: From January 2013 to July 2015, 78 patients with STEMI presenting OHCA, successfully resuscitated, transferred immediately to the catheterization unit and treated with primary PCI, were analyzed. Clinical, laboratory and angiographic data were compared in 28 non-survivors and 50 survivors.
Results: The clinical baseline characteristics of the study population showed no significant differences between the survivors and non-survivors in respect to age (p=0.06), gender (p=0.8), the presence of hypertension (p=0.4), dyslipidemia (p=0.09) obesity (p=1), smoking status (p=0.2), presence of diabetes (p=0.2), a clinical history of acute myocardial infarction (p=0.7) or stroke (p=0.17). Compared to survivors, the non-survivor group exhibited a significantly higher incidence of cardiogenic shock (50% vs 24%, p=0.02), renal failure (64.3% vs 30.0%, p=0.004) and anaemia (35.7% vs 12.0%, p=0.02). Three-vessel disease was significantly higher in the non-survivor group (42.8% vs. 20.0%, p=0.03), while there was a significantly higher percentage of TIMI 3 flow postPCI in the infarct-related artery in the survivor group (80.% vs. 57.1%, p=0.03). The time from the onset of symptoms to revascularization was significantly higher in patients who died compared to those who survived (387.5 +/- 211.3 minutes vs 300.8 +/- 166.1 minutes, p=0.04), as was the time from the onset of cardiac arrest to revascularization (103.0 +/- 56.34 minutes vs 67.0 +/- 44.4 minutes, p=0.002). Multivariate analysis identified the presence of cardiogenic shock (odds ratio [OR]: 3.17, p=0.02), multivessel disease (OR: 3.0, p=0.03), renal failure (OR: 4.2, p=0.004), anaemia (OR: 4.07, p=0.02), need for mechanical ventilation >48 hours (OR: 8.07, p=0.0002) and a duration of stay in the ICU longer than 5 days (OR: 9.96, p=0.0002) as the most significant independent predictors for mortality in patients with OHCA and STEMI.
Conclusion: In patients surviving an OHCA in the early phase of a myocardial infarction, the presence of cardiogenic shock, renal failure, anaemia or multivessel disease, as well as a longer time from the onset of symptoms or of cardiac arrest to revascularization, are independent predictors of mortality. However, the most powerful predictor of death is the duration of stay in the ICU and the requirement of mechanical ventilation for more than forty-eight hours.
A satisfactory neurologic outcome is the key factor for survival in patients with sudden cardiac death (SCD), however this is highly dependent on the haemodynamic status. Short term cardiopulmonary resuscitation and regained consciousness on the return of spontaneous circulation (ROSC) is indicative of a better prognosis. The evaluation and treatment of SCD triggering factors and of underlying acute and chronic diseases will facilitate prevention and lower the risk of cardiac arrest. Long term CPR and a prolonged unconscious status after ROSC, in the Intensive Care Units or Coronary Care Units, indicates the need for specific treatment and supportive therapy including efforts to prevent hyperthermia. The prognosis of these patients is unpredictable within the first seventy two hours, due to unknown responses to therapeutic management and the lack of specific prognostic factors. Patients in these circumstances require the highest level of intensive care and aetiology driven treatment without any delay, independently of their coma state. Current guidelines sugest the use of multiple procedures in arriving at a diagnosis and prognosis of these critical cases.