Survivors Of Prehospital Cardiac Arrest Research Articles

Abstract 300: Long-Term Survival, Quality of Life and Health Care Costs in the Survivors of Pre-Hospital Cardiac Arrest

Background: Understanding the prognosis of out-of-hospital cardiac arrest (OHCA) patients is vital to informing resuscitation and advanced care planning decisions. However, short-term outcomes such as survival to hospital discharge do not account for post-arrest quality of life and medical costs. Objective: To investigate the survival time, long-term health-related quality of life, and health care costs of OHCA survivors. Methods: We conducted a prospective cohort study of all adult OHCA survivors of cardiac origin between 1 August 2016 and 31 December 2017 in a tertiary medical center in Taiwan. Chinese version of EuroQol-5D-5L (EQ-5D-5L) was used for measuring health-related quality of life at 1 month, 6 month and 1 year post-discharge. Survival and health care costs data were collected. Descriptive statistics and Wilcoxon Signed-Ranks Test were used for data analysis. Results: During the study period, 30 of 163 (18.4%) OHCA of presumed cardiac origin survived to hospital discharge. The mean age for the survivors was 59 years. Most survivors were male (83.3%), and received bystander cardiopulmonary resuscitation (73.3%) and defibrillation (86.7%) in the prehospital settings. Of 30 survivors, 23 patients were cerebral performance category score (CPC) of 1 or 2 and 7 were CPC of 3 or 4. The median hospital stay and estimated median survival time for CPC 1-2 and CPC 3-4 were 17 days, 8.8 years and 34 days, 0.4 years, respectively. The mean EQ-5D-5L visual analogue scale score and index score (utility) for 13 CPC 1-2 survivors followed at 6 month post discharge were 75.58 ± 13.31 and 0.856 ± 0.125, respectively, and were significantly higher than the scores (65.38 ± 15.47, 0.689 ± 0.114) at 1 month. The median health care costs of the index admission and 6 month post-discharge for CPC 1-2 survivors were NT$ 655,866 and NT$ 46,550, respectively. Conclusion: The survival time and health related quality of life for OHCA survivors with good neurologic outcome is good and improves over time. It pays to save those lives.

Conduct of emergency research in patients unable to give consent—Experiences and perceptions of patients, their consent providing next of kin, and treating physicians following a prehospital resuscitation trial

ObjectiveAccording to a directive of the European Parliament, informed consent is required to conduct a clinical trial also in emergencies when the patient is unable to provide consent. In these cases surrogate consent can be obtained from the patient's next of kin. There are no reports describing how patients and their next of kin perceive this policy. The perceptions of patients and their spouses involved in an emergency trial conducted under surrogate consent were surveyed. MethodsA survey was sent to survivors of prehospital cardiac arrest, to consent providers regardless of patient outcome, and to physicians who had recruited the patients. Results11 (92%) patients, 17 (68%) consent providers, and all physicians returned the survey. All held a positive attitude towards emergency research and were willing to participate without own consent in a trial approved by an institutional review board (IRB). Opinions among responding groups were similar albeit a significant difference regarding the perceived capability of the consent provider to decide upon patient's enrolment. Spouses felt able to provide consent, but physicians were sceptical of this. Patients and their spouses would have appreciated additional information regarding the index trial after the acute phase. ConclusionsEmergency research was perceived positively by cardiac arrest victims and their spouses previously involved in a resuscitation trial. Possible own participation in an emergency trial without personal consent was considered acceptable. Patients and their spouses would prefer additional research information after enrolment.

Therapeutic hypothermia after cardiac arrest – cerebral perfusion and metabolism during upper and lower threshold normocapnia

BackgroundDuring cardiac arrest and after successful resuscitation a continuum of ischaemia-reperfusion injury develops. Mild hypothermia exerts protective effects in the postresuscitation phase but also alters CO2 production and solubility, which may lead to deleterious effects if overlooked when adjusting the ventilation of the resuscitated patient. Using a multimodality approach, the effects of different carbaemic states on cerebral perfusion and metabolism were evaluated during therapeutic hypothermia. MethodsEight comatose survivors of prehospital cardiac arrest were cooled to 33°C for 24h and underwent a 60min phase of interventional lower threshold normocapnia according to temperature non-corrected pCO2 (4.2kPa) and higher threshold normocapnia according to corrected pCO2 (6.0kPa) in a random order. Prior to, during and after each phase, cerebral perfusion and metabolites via a microdialysis catheter were measured. ResultsDuring upper-threshold pCO2, an increase in middle cerebral artery mean flow velocity (MFV) and jugular bulb oxygen saturation (jSvO2) were observed with a concomitant decrease in cerebral lactate concentration. Lower threshold normocapnia was associated with a decrease in MFV in most patients. In all patients jSvO2 decreased but no change in cerebral lactate was observed. In seven patients jSvO2 decreased below 55%. These changes were not reflected to intracranial pressure or cerebral oximetry. ConclusionsDuring induced hypothermia, lower threshold normocapnia was associated with decreased cerebral perfusion/oxygenation but not reflected to interstitial metabolites. Upper threshold pCO2 increased cerebral perfusion and reduced cerebral lactate. Vigilance over the ventilatory and CO2 analysis regimen is mandatory during mild hypothermia.

Invited Commentary

Invited Commentary

14. Health Related Quality of Life Among Survivors of Prehospital Cardiac Arrest

Purpose: The purpose of this study was to measure the quality of life of cardiac arrest long-term survivors.Design: Prospective outcome evaluation.Setting: The emergency medical system of a mid-sized city.Type of participants: Prehospital cardiac arrest victims who had a resuscitation attempt from 5/93 through 12/95 and were discharged alive. Patients <18 were excluded.Measurements: Patients were surveyed by mail. Non-responders were telephoned. The questions assessed Glasgow-Pittsburgh overall performance (GPOP) scores before and after the cardiac arrest. Additional items assessed physical, role, affective, and cognitive functioning, and global health status.Main Results: 760 cases were collected. 40 had unknown vital status at hospital discharge. The survival rate to hospital discharge for the 270 patients with cardiac etiology and initial rhythm of ventricular fibrillation was 15%, and it was 6% for the other 450 patients. Of 68 survivors, 23 died before a survey was sent; two had unknown addresses. 21 patients (49%) responded, and four refused to participate. The mean interval from cardiac arrest to survey response was 531 days. Ten reported good post-arrest GPOP scores, 5 had moderate disability, 4 severe disability, and 2 were comatose. Cognitive function was improved in 1, unchanged 6, slightly worse 7, markedly worse 4, and none in 3. Eleven patients reported feeling happy. Global healdi was excellent for 2, very good 8, good 5, fair 2, and poor 3.

Prognosis Among Survivors of Prehospital Cardiac Arrest

Study objective: To describe the prognosis in consecutive patients discharged from hospital after prehospital cardiac arrest. Patients: All patients in the community of Göteborg who were discharged from hospital after out-of-hospital cardiac arrest between 1981 and 1991. Results: Two hundred forty-three patients were discharged from hospital during the observation period, of whom 80% initially experienced ventricular fibrillation. Among patients discharged, 21% died during the first year; after 10 years, 82% had died. Age, sex, previous history of cardiovascular disease, circumstances at the time of cardiac arrest, complications during hospitalization, and discharge medications were assessed as predictors of 1-year mortality. Independent predictors of death during follow-up were history of myocardial infarction ( P<.001), no prescription of β-blockers at discharge ( P<.01), age ( P<.05), and cerebral performance category (CPC) at discharge ( P<.05). Conclusion: Among patients who survived out-of-hospital cardiac arrest, one of five died during the first year and one of five survived 10 years after discharge. Prognosis was associated with a history of myocardial infarction, prescription of β-blockers at discharge, age, and CPC at discharge. [Herlitz J, Ekström L, Wennerblom B, Axelsson Å, Bång A, Holmberg S. Prognosis among survivors of prehospital cardiac arrest. Ann Emerg Med January 1995;25:5863.]

Surgical coronary revascularization in survivors of prehospital cardiac arrest: Its effect on inducible ventricular arrhythmias and long-term survival

In a selected subgroup of 50 survivors of cardiac arrest, the impact of surgical myocardial revascularization on inducible arrhythmias, arrhythmia recurrence and long-term survival was examined. The effects of several clinical, angiographic and electrophysiologic variables on arrhythmia recurrence and survival were also analyzed. All patients had a prehospital cardiac arrest and severe operable coronary artery disease and underwent myocardial revascularization. Preoperative electrophysiologic study was performed in 41 patients; 33 (80%) had inducible ventricular arrhythmias. Of 42 patients studied off antiarrhythmic drugs postoperatively, 19 (45%) had inducible ventricular arrhythmias. Thirty patients with inducible arrhythmias preoperatively underwent postoperative testing off antiarrhythmic drugs; arrhythmia induction was suppressed in 14 (47%). By multivariate analysis, the induction of ventricular fibrillation at the preoperative electrophysiologic study was the only significant predictor of induced ventricular arrhythmia suppression by coronary surgery (p less than 0.001). Inducible ventricular fibrillation was not present postoperatively in any of the 11 patients who manifested this arrhythmia preoperatively. In contrast, inducible ventricular tachycardia persisted in 80% of patients in whom preoperative testing induced this arrhythmia. Patients were followed up for 39 +/- 29 months. There were four arrhythmia recurrences; one was fatal. There were three nonsudden cardiac deaths and three noncardiac deaths. By life-table analysis, 5 year survival, cardiac survival and arrhythmia-free survival rates were 88%, 98%, and 88%, respectively. Depressed left ventricular ejection fraction and advanced age were predictive of death (p = 0.015 and 0.026, respectively) and cardiac death (p = 0.037 and 0.05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Long-term survival after prehospital cardiac arrest: analysis of outcome during an 8 year study.

We analyzed long-term follow-up data accumulated during an 8 year study of survivors of prehospital cardiac arrest. All patients included in this study were primary entrants via community-based rescue systems; patients who were tertiary referrals (survivors of cardiac arrest from other hospitals) were not included in this analysis. In the group of 61 patients entering our study between 1975 and 1980, with a follow-up to 1983, there have been a total of 24 deaths (39%). Sixteen of the 24 deaths were the result of recurrent cardiac arrest; eight were nonsudden cardiac deaths or noncardiac deaths. The mean duration from entry to death in the nonsurvivors was 27.5 +/- 19.7 months, and the time from the index event to last follow-up in the long-term survivors was 59.9 +/- 19.4 months. Life table analysis demonstrated a 10% rate of recurrence of cardiac arrest in the first year, with a 5% per year rate in each of the subsequent 3 years. Left ventricular ejection fractions at entry were not significantly different between survivors (mean = 45.3 +/- 13.6%) and nonsurvivors (mean = 37.6 +/- 12.6%), and the severity of ejection fraction abnormality at entry did not correlate with time to death in the nonsurvivors. However, ejection fraction was significantly lower in patients who died from causes other than recurrent cardiac arrest than in those who died of cardiac arrest (24.5 +/- 9.1% vs 42.7 +/- 9.2%; p less than .002).(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormal quinidine binding in survivors of prehospital cardiac arrest

Quinidine binding was studied in 15 survivors of prehospital cardiac arrest and was compared to 18 normal individuals and 20 patients with coronary artery disease. The unbound quinidine fraction was 6.3 ± 2.8% in the survivors of prehospital cardiac arrest, a value significantly lower than normal individuals (unbound quinidine fraction = 9.9 ± 3.0%, p < 0.005). Furthermore, unbound quinidine fraction correlated with interdose quinidine half-life in the six survivors of prehospital cardiac arrest where this could be measured ( r = 0.79, p < 0.05). The resultant quinidine interdose half-life was significantly prolonged (10 ± 3 hours) when compared to normal (6 ± 2 hours, p < 0.02). The reduction in free drug fraction in cardiac arrest survivors was a nonspecific finding in that free drug fraction was also reduced in the patients with coronary artery disease (unbound quinidine fraction = 7.4 ± 3%) and was independent of the α-1-glycoprotein concentration. Therefore survivors of prehospital cardiac arrest have a mean 40% reduction in free quinidine drug fraction which results in less free drug at any given total drug concentration and may relate to quinidine pharmacokinetics and pharmacodynamics in this patient group.

Survivors of Prehospital Cardiac Arrest

BEFORE the early 1970s, the uniform fatality of prehospital cardiac arrest led research efforts almost exclusively to the fields of pathology and epidemiology. Then, with the development of community-based emergency medical systems (EMSs), clinical investigators developed an interest in the prognosis and management of survivors of prehospital cardiac arrest. The outcome of these efforts is summarized in this article. <h3>Mechanisms of Prehospital Cardiac Arrest</h3> The majority of prehospital cardiac arrests occur by the mechanism of ventricular fibrillation (VF), but other mechanisms, primarily ventricular tachycardia (VT) and various forms of bradyarrhythmias or asystole,¹also may cause sudden and unexpected cardiovascular collapse. Of 352 consecutive events observed between 1975 and 1978, in which (1) the onset of cardiac arrest was witnessed, (2) the EMS personnel were summoned without delay, and (3) arrival on the scene was documented to have occurred within four minutes of summons (Fig 1), the initial rhythm recorded

Electrophysiologic testing in survivors of prehospital cardiac arrest: Therapy and long-term follow-up

Electrophysiologic testing in survivors of prehospital cardiac arrest: Therapy and long-term follow-up

Evaluation of postresuscitation left ventricular global and segmental function by radionuclide ventriculography in sudden coronary death survivors of prehospital cardiac arrest: Correlation to subsequent short-term prognosis

Previous data have shown that patients with significant left ventricular (LV) dysfunction, marked abnormalities in resting hemodynamics, and multiple vessel coronary artery disease (CAD) are at increased risk for sudden cardiac death. However, in-hospital assessment of ventricular function in the early postresuscitation period of out-of-hospital cardiac arrest has not been evaluated and related to short-term outcome. By using bedside radionuclide ventriculography (RNV) we evaluated LV ejection fraction (LVEF) and wall motion in 36 nonconsecutive patients within 24 hours of their episode of out-of-hospital cardiac arrest. There were 24 men and 12 women with mean age of 62.3 years (range 21 to 85 years). Total mortality of the entire group was 38.8% at 4 weeks. Eighteen patients had LVEF < 0.30 and 18 had LVEF > 0.30. Mortality in the low LVEF group was 55.5% at 4 weeks versus 22.2% in patients with LVEF > 0.30 ( p < 0.05). Patients with normal LV wall motion had no short-term mortality (none of seven), while patients having abnormal LV wall motion had a significantly higher short-term mortality (14 of 29) ( p < 0.05). We conclude that out-of-hospital cardiac arrest survivors have a high incidence of severe LV dysfunction in the early postresuscitation period and that a significantly higher early mortality is seen in the group with LVEF < 0.30. In addition, abnormalities of LV wall motion by RNV examination demonstrated poorer prognosis in the first 4 weeks than patients with normal LV wall motion.

Resting peripheral blood lactate elevation in survivors of prehospital cardiac arrest: Correlation with hemodynamic, electrophysiologic and oxyhemoglobin dissociation indexes

Thirteen patients who were survivors of sudden unexpected cardiac arrest in the community were followed up for up to 3 years. All showed an anomalous relation between erythrocyte levels of oxygen dissociation (P 50) and 2,3-diphosphoglyceric acid (2,3-DPG). This could not be explained by hemoglobinopathy, carbon monoxide or methemoglobinemias. Because lactate accumulation in red blood cells may alter oxygen dissociation, whole blood and red blood cell lactate levels were measured. An average of 4.4 measurements per patient were obtained over a mean time of 5.6 months of the post-hospital phase of the follow-up period, which had a total mean duration of 22 months. The patients did not have overt congestive heart failure and were not acidotic (mean venous pH = 7.35). Lactate levels were elevated (mean = 15.1 mg/100 ml ± 0.8 mg/100 [standard error of the mean], compared with normal values of 7.6 mg/100 ml ± 1.4 mg/100 ml; P < 0.01). When lactate was plotted against red blood cell 2,3-diphosphoglycerate, a positive curvilinear relation was found ( r 2 = 0.12, P < 0.05). The production of lactate in chronic ischemia may increase red blood cell 2,3-diphosphoglycerate through glycolysis. The expected effect on oxygen dissociation of this increase in 2,3-diphosphoglycerate is offset by a counterbalancing leftward shift of the oxyhemoglobin dissociation curve by an increase in red blood cell lactic acid. When lactate was compared with left ventricular ejection fraction, there was a significant negative correlation ( r = 0.86, P < 0.01). Serial 24 hour ambulatory electrocardiograms (mean 4 per patient) were analyzed for changes in quantity and severity of ventricular arrhythmia at the time of lactate determinations. Six patients had lactate level variation of more than 30 percent, and five of these six patients had an increase in quantity and severity of ventricular ectopic activity when their lactate levels were in the higher range. We conclude that elevated resting lactate levels correlate with impaired ventricular function, and fluctuations in a given patient may identify changes in clinical and electrophysiologic status.

Antiarrhythmic drug therapy in survivors of prehospital cardiac arrest: comparison of effects on chronic ventricular arrhythmias and recurrent cardiac arrest.

We studied the long-term effects of membrane-active antiarrhythmic agents on chronic ventricular arrhythmias in patients who have survived prehospital cardiac arrest. Among 16 patients treated with a dose-adjusted, plasma level-monitored antiarrhythmic regimen, eight have survived for longer than 12 months and eight have had recurrent cardiac arrests (RCAs). Monthly Holter monitor tapes (HM) recorded during the 4 months before the eight RCAs were compared with monthly HM tapes matched for time of entry and duration of follow-up in the eight patients who did not have RCAs. Transient or persistent complex ventricular ectopic depolarizations (VEDs) have been recorded on 47 of the 63 monthly HM tapes (75%). The difference between VEDs in the RCA patients (mean 153 VEDs/hr, median 19 VEDs/hr) and VEDs in the patients who have not had RCA (mean 122 VEDs/hr, median 8 VEDs/hr) was not significant (p less than 0.2); nor was there a predictable relationship between therapeutic plasma levels of antiarrhythmic agents and the frequency and complexity of chronic asymptomatic VEDs (therapeutic levels--mean 104 VEDs/hr, median 6 VEDs/hr; subtherapeutic levels--mean 184 VEDs/hr, median 21 VEDs/hr). Differences were not significant (p greater than 0.1). In contrast, all eight RCA patients had unstable plasma levels (21 of 31 determinations subtherapeutic) while six of the eight patients who have not had RCA had consistently therapeutic levels (p less than 0.01). Thus, adequate plasma levels of antiarrhythmic agents may protect against RCA, despite failure to suppress VEDs predictably. The apparent dissociation between predictable suppression of chronic VEDs and protection against RCA suggests that clinical effectiveness of these agents may not be best measured by their effect on chronic VEDs.

Long-term antiarrhythmic therapy in survivors of prehospital cardiac arrest. Initial 18 months' experience

Ambulatory rhythm monitoring and chronic arrhythmia management were studied in 16 patients resuscitated from prehospital cardiac arrest. Asymptomatic complex ventricular arrhythmias (ACVA) occurred in 12 patients (75%) entering long-term follow-up during the first 12 months (average follow-up, 13.25 months). The patients' therapy consisted of a dose-adjusted, membrane-active antiarrhythmic drug regimen monitored by blood levels. While there has been little change in the frequency of ACVAs despite carefully controlled antiarrhythmic management, only one death has occurred during 212 patient-months of postarrest follow-up, a 6% one-year mortality. This compares favorably to our previous experience in survivors of prehospital cardiac arrest not receiving a controlled antiarrhythmic program. Despite the failure to suppress ACVAs, the drug-monitored population is showing a trend toward a decreased frequency of recurrent cardiac arrest. (<i>JAMA</i>238:2621-2624, 1977)

Long-Term Antiarrhythmic Therapy in Survivors of Prehospital Cardiac Arrest

Ambulatory rhythm monitoring and chronic arrhythmia management were studied in 16 patients resuscitated from prehospital cardiac arrest. Asymptomatic complex ventricular arrhythmias (ACVA) occurred in 12 patients (75%) entering long-term follow-up during the first 12 months (average follow-up, 13.25 months). The patients' therapy consisted of a dose-adjusted, membrane-active antiarrhythmic drug regimen monitored by blood levels. While there has been little change in the frequency of ACVAs despite carefully controlled antiarrhythmic management, only one death has occurred during 212 patient-months of postarrest follow-up, a 6% one-year mortality. This compares favorably to our previous experience in survivors of prehospital cardiac arrest not receiving a controlled antiarrhythmic program. Despite the failure to suppress ACVAs, the drug-monitored population is showing a trend toward a decreased frequency of recurrent cardiac arrest.