ライフサイエンスコーパス: asystole

1 (ie, pulseless electrical activity [PEA] or asystole).

2 apy) as well as rhythm (primary or secondary asystole).

3 s presenting in ventricular fibrillation and asystole.

4 se four (16% of total) had potentially fatal asystole.

5 ation at low energies and caused less VT and asystole.

6 balloon catheter during a brief ACh-induced asystole.

7 tion than CPR during postcountershock PEA or asystole.

8 tients with severe episodes and demonstrated asystole.

9 ced death, with severe bradycardia preceding asystole.

10 /fibrillation or pulseless electric activity/asystole.

11 om respiratory failure, followed by terminal asystole.

12 rioventricular conduction blocks and cardiac asystole.

13 idence and timing of autoresuscitation after asystole.

14 basis of the initial rhythm as shockable or asystole.

15 s until return of spontaneous circulation or asystole.

16 ion period, including the first 2 mins after asystole.

17 rhythm was pulseless electrical activity or asystole.

18 organ function that time from extubation to asystole.

19 ctor of outcome than time from extubation to asystole.

20 le ventricular fibrillation and nonshockable asystole.

21 ebrafish mutant characterized by ventricular asystole.

22 antidepressant overdose was associated with asystole.

23 ns of (post)ictal cardiac arrhythmias: ictal asystole (103 cases), postictal asystole (13 cases), ict

24 hmias: ictal asystole (103 cases), postictal asystole (13 cases), ictal bradycardia (25 cases), ictal

25 sting was present in 36 patients (86%) (mean asystole, 13.9+/-10.2 seconds).

26 40), pulseless electrical activity (20), and asystole (20), in two sets of ten pigs (ten training, te

27 aracterized by bradycardia, tachycardia, and asystole); 22 (9%) patients experienced 38 nonserious ad

28 The first patient had a cardiac asystole 30 min after receiving sofosbuvir and daclatasv

29 = 0.008, OR 1.78) or atrioventricular block/asystole (30% vs. 19%, p < 0.012, OR 1.57) and to requir

30 cumented rhythm at night was more frequently asystole (39.6% [95% CI, 39.0%-40.2%] vs 33.5% [95% CI,

31 rdia 24%, pulseless electrical activity 16%, asystole 48%, other nonshockable 12%; outcomes: Return o

32 n presentation (41% vs. 30%), women had more asystole (8.8% vs. 7%) and (organized) pulseless electri

33 , pulseless electrical activity (14.6%), and asystole (9.1%).

34 dy tested whether adenosine caused prolonged asystole after transplantation and if it was effective i

35 ular tachycardia/fibrillation in 6 cases and asystole (after approximately 30 minutes of nonresponsiv

36 characterized by 12 minutes of normothermic asystole and a high cardiopulmonary resuscitation rate.

37 ed for demographics, cause of death, time of asystole and cold perfusion.

38 postictal apnoea and bradycardia progress to asystole and death.

39 Because of better survival after asystole and PEA, children had better outcomes than adul

40 children vs 11% [2719/24,987] in adults with asystole and PEA; adjusted OR, 2.73; 95% CI, 2.23-3.32).

41 commonly presents with nonshockable rhythms (asystole and pulseless electric activity).

42 itals, the initial cardiac arrest rhythm was asystole and pulseless electrical activity in 874 childr

43 ents, 9616 (82.2%) had nonshockable rhythms (asystole and pulseless electrical activity) and 2079 (17

44 iac arrests and separately for nonshockable (asystole and pulseless electrical activity) and shockabl

45 to-definitive care of < or =10 mins (primary asystole) and patients found in ventricular fibrillation

46 spection, 56 patients did not proceed due to asystole, and 134 proceeded to donation.

47 r time, proportionate to the period of donor asystole, and was associated with increasing cellular in

48 ed incidence of arrhythmias and intermittent asystoles, as well as compromised performance under stre

49 1 and 3 animals were defibrillated into PEA/asystole at 12 minutes.

50 rd of 2 to 5 mins of demonstrated mechanical asystole before declaring death.

51 t a 2- to 5-min observation after mechanical asystole before the declaration of death.

52 Ictal asystole, bradycardia and AV-conduction block were self-

53 urally mediated syncope (NMS) and documented asystole but syncope still recurred in 25% of them at 2

54 rgans based on time from donor extubation to asystole, but data to support this is incomplete.

55 olus intravenously) 5 mins prior to inducing asystole by bupivacaine overdose.

56 rillation, pulseless electrical activity and asystole (by high-dose intravenous pentobarbitone).

57 Death was declared based on cardiac asystole confirmed by auscultation and transthoracic imp

58 al and ventricular arrhythmias, heart block, asystole, development of pulmonary congestion, acute mit

59 tricular fibrillation without resuscitation, asystole develops.

60 All patients whose initial rhythm was asystole died before 6 months in both groups.

61 ng among patients with recurrent syncope and asystole documented by implantable loop recorder.

62 atients with recurrent vasovagal syncope and asystole documented by implantable loop recorder.

63 yncope, whereas 94% (15/16) of seizures with asystole duration>6 s led to syncope (P=0.02).

64 No seizure with asystole duration</=6 s led to syncope, whereas 94% (15/

65 Duration of asystole during carotid sinus massage was similar in bot

66 defined as any subsequent rhythm other than asystole during continued prehospital resuscitation.

67 as opposed to pulseless electrical activity/asystole (epilepsy, 26%; no epilepsy, 44%; P=0.002), des

68 observed 76 clinical seizures with 26 ictal asystole episodes, 15 of which led to syncope.

69 ET drugs (n = 25); group 4, postcountershock asystole/ET drugs (n = 18); and group 5, primary or seco

70 ystole/i.v. drugs (n = 39); group 3, primary asystole/ET drugs (n = 25); group 4, postcountershock as

71 During ictal asystole events, 4 patients had left temporal seizure on

72 003 to July 2013 for all patients with ictal asystole events.

73 Pre-hospital asystole from trauma has a universally poor outcome.

74 These latter patients had both asystole >/=3 s (mean 7.6+/-2.2 s) and SBP fall to 63+/-

75 test (bradycardia <40 beats/min for 10 s or asystole >3 s).

76 The incidence of clinically significant asystole (>/=12 seconds after adenosine) was quantified.

77 Ictal asystole>6 s is strongly associated with ictal syncope.

78 Ictal asystole had a mean prevalence of 0.318% (95% CI 0.316%

79 5 minutes or until a significant arrhythmia (asystole, heart block, bradycardia, supraventricular or

80 cale scores, time of extubation, and time to asystole, hypotension, pulseless electrical activity, an

81 lowing groups were defined: group 1, primary asystole/i.v. drugs (n = 39); group 2, postcountershock

82 v. drugs (n = 39); group 2, postcountershock asystole/i.v. drugs (n = 39); group 3, primary asystole/

83 73 +/- 16 years), with presenting rhythms of asystole in 61.5% and ventricular tachycardia or ventric

84 There was one arrhythmic death related to asystole in a single ventricle patient.

85 d by refractory hypotension, bradycardia, or asystole in four patients (two of whom died) and by perf

86 from hemorrhage-induced electrocardiographic asystole in large swine.

87 sepsis; and acute myocardial infarction with asystole in the distribution of the stented vessel).

88 Ictal asystole is a rare, serious, and often treatable cause o

89 f SCD because of pulseless electric activity/asystole is growing, the overwhelming majority of resear

90 thesis that a 2-min observation period after asystole is sufficient for the declaration of death in p

91 ously identify four important abnormalities: asystole, left ventricular dysfunction, right ventricula

92 a complications extraordinarily rare, though asystole may occur as part of the oculocardiac reflex.

93 Asystole might underlie many of these deaths, which woul

94 of 285 shocks, with 226 shocks that achieved asystole (n=102), organized rhythm (n=120), or monomorph

95 ents (ventricular tachycardia, n = 44; pause/asystole, n = 36; polymorphic ventricular tachycardia/ve

96 going at hospital arrival, arrest rhythm not asystole, no atropine or NaHCO3, fewer epinephrine doses

97 (n = 18); and group 5, primary or secondary asystole/no drug therapy (n = 15).

98 Asystole occurred in 23 (17 died), pulseless electrical

99 ock-induced ventricular tachycardia (VT) and asystole occurred less often after triphasic shocks.

100 ese had documentation of syncope with >/=3 s asystole or >/=6 s asystole without syncope within 12 +/

101 tricular fibrillation is usually followed by asystole or a nonperfusing rhythm.

102 current-induced ventricular fibrillation or asystole or from respiratory arrest secondary to paralys

103 ountershocks (group 1) and patients found in asystole or PEA (primary asystole or PEA) (group 2) were

104 f patients whose first documented rhythm was asystole or PEA (primary asystole or PEA).

105 Patients found in VF who developed asystole or PEA after countershocks (group 1) and patien

106 ng rhythm has a worse prognosis than primary asystole or PEA and may be related to myocardial electri

107 mented pulseless arrest rhythm was typically asystole or PEA in both children and adults.

108 tcome of prehospital VF victims shocked into asystole or PEA with that of patients whose first docume

109 d patients found in asystole or PEA (primary asystole or PEA) (group 2) were included if the reported

110 cumented rhythm was asystole or PEA (primary asystole or PEA).

111 Cardiac arrests in children are typically asystole or PEA.

112 lation, whereas patients with IHCA caused by asystole or pulseless electric activity were stratified

113 ich are associated with better outcomes than asystole or pulseless electrical activity (PEA).

114 r, countershock is most commonly followed by asystole or pulseless electrical activity (PEA).

115 est and decreased survival after in-hospital asystole or pulseless electrical activity arrest.

116 The proportion of cardiac arrests due to asystole or pulseless electrical activity increased over

117 ients who experienced nonshockable OHCA (ie, asystole or pulseless electrical activity) were assessed

118 In patients whose initial rhythm was asystole or pulseless electrical activity, AEDs were ass

119 rdiac arrest, 79.3% had an initial rhythm of asystole or pulseless electrical activity, and 20.7% had

120 l cooling when the initial cardiac rhythm is asystole or pulseless electrical activity, particularly

121 iac arrest with an initial cardiac rhythm of asystole or pulseless electrical activity, pre-hospital

122 ation from prolonged VF typically results in asystole or pulseless electrical activity.

123 o declined but was offset by more cases with asystole or pulseless electrical activity.

124 tantially worse than those for patients with asystole or pulseless electrical activity.

125 patients after pulseless electrical activity/asystole or resistant ventricular fibrillation who were

126 The new valve shows promise for patients in asystole or shock refractory ventricular fibrillation, w

127 which controlled for gender, age, race, and asystole or ventricular fibrillation/ventricular tachyca

128 The prevalence of ventricular fibrillation, asystole, or organized rhythms at 5, 10, or 20 seconds a

129 ng arrhythmia was VF in 48%, PEA in 25%, and asystole/other in the remainder.

130 .98), ventricular fibrillation (p = .14), or asystole (p = .21).

131 al occurred with the initiating OHCA rhythm (asystole, pulseless electric activity, or VF/VT).

132 up, whereas prompt epinephrine treatment for asystole/pulseless electric activity was associated with

133 Of 28 842 patients with an IHCA caused by asystole/pulseless electric activity, the rate of 1-year

134 erapy after resuscitation from 12 minutes of asystole rapidly and reversibly modulated mitochondrial

135 fibrillation who developed postcountershock asystole (secondary asystole) were included.

136 ized recipients 15, 30, 45, and 90 min after asystole to determine short-term survival patterns, whic

137 The median time from asystole to NRP was 16 min (range 10-23 min).

138 5-minute stand-off period was observed from asystole to skin incision.

139 cy of resuscitation from bupivacaine-induced asystole using lipid emulsion infusion vs. vasopressin,

140 Time from extubation to asystole was 15.9+/-1.9 min and overall warm ischemia ti

141 The prevalence of asystole was 40% (350) in children and 35% (13 024) in a

142 Asystole was achieved with a single dose of bupivacaine

143 However, asystole was an important cause of mortality in sudden c

144 nts with a positive TT even when spontaneous asystole was documented.

145 Mechanical asystole was initially observed in 18 (90%) of 20 cardia

146 ) survived 24 hours after treatment, whereas asystole was observed in 2 patients (0.03%) with 1 resul

147 In 10 patients with ictal asystole, we observed 76 clinical seizures with 26 ictal

148 n times to circulatory arrest and electrical asystole were 8 +/- 1 and 16 +/- 2 minutes, respectively

149 Those presenting with PEA versus VF and asystole were compared with chi(2) tests, ANOVA, and log

150 Times to circulatory arrest and electrical asystole were recorded.

151 veloped postcountershock asystole (secondary asystole) were included.

152 patients (21%) had bradycardia or periods of asystole with subsequent permanent pacemaker insertion.

153 rest whose first documented field rhythm was asystole with time-to-definitive care of < or =10 mins (

154 rolled in the trial (26 shockable rhythm, 10 asystole), with 18 assigned to 34 degrees C and 18 to 32

155 on of syncope with >/=3 s asystole or >/=6 s asystole without syncope within 12 +/- 10 months and met

156 nous bolus of 20 mg/kg bupivacaine to induce asystole (zero time).