ライフサイエンスコーパス: precordial

1 et was epicardium, 0.46; body surface, 0.47; precordial, 0.17; and optimal leads, 0.11.

2 y, was epicardium, 0.91; body surface, 0.84; precordial, 0.72; and optimal leads, 0.81.

3 from 4 lead sets: epicardial, body surface, precordial, and a 6-lead optimal set.

4 Precordial blows in sports and daily activities can trig

5 tion from ventricular fibrillation following precordial blows.

6 n of the interval between discontinuation of precordial compression and delivery of the first electri

7 Cardiopulmonary resuscitation, including precordial compression and mechanical ventilation, was s

8 animals were successfully resuscitated with precordial compression and mechanical ventilation.

9 coronary perfusion pressure generated during precordial compression and pupil diameter was documented

10 nd mitral valve closing and opening followed precordial compression and relaxation.

11 herefore serves to minimize interruptions of precordial compression and the myocardial damage caused

12 t combined with epinephrine treatment during precordial compression and then alone in a prolonged car

13 the concept that stroke volumes generated by precordial compression are quantitatively related to the

14 The stroke volume index produced by precordial compression averaged 0.45 mL/kg or approximat

15 of untreated VF, mechanical ventilation and precordial compression began.

16 dy was to measure stroke volumes produced by precordial compression during cardiopulmonary resuscitat

17 Interruptions of precordial compression for rhythm analyses that exceed 1

18 eated ventricular fibrillation and 8 mins of precordial compression in 13 animals, seven of which wer

19 umed for a "hands off" interval during which precordial compression is discontinued to allow for auto

20 lation was not reversed, a 1-min interval of precordial compression preceded a second sequence of up

21 If VF was not reversed, a 1-min interval of precordial compression preceded a second sequence of up

22 We confirmed that precordial compression produces approximately one third

23 Precordial compression together with mechanical ventilat

24 mins of untreated ventricular fibrillation, precordial compression was begun and continued for 6 min

25 e ventricular fibrillation in each instance, precordial compression was begun coincident with mechani

26 Precordial compression was begun together with mechanica

27 One minute after injection of the compound, precordial compression was begun together with mechanica

28 val of between 3 and 5 mins of untreated VF, precordial compression was begun.

29 n was restored in each of 5 animals in which precordial compression was delayed for 3 seconds before

30 on-decompression (Lifestick resuscitator) or precordial compression was initiated.

31 Precordial compression was maintained at 80 per minute t

32 The precordial compression was performed with a pneumaticall

33 Mechanical ventilation and precordial compression were initiated after 8 mins of un

34 ogressive decreases in stroke volumes during precordial compression were predictive of unsuccessful r

35 was monitored and artifacts produced during precordial compression were removed by digital filtering

36 untreated for 3 minutes before the start of precordial compression, mechanical ventilation, and atte

37 untreated for 7 minutes before the start of precordial compression, mechanical ventilation, and atte

38 r 6 mins before attempted resuscitation with precordial compression, mechanical ventilation, and elec

39 P < .01) than that generated by conventional precordial compression.

40 nstraints caused by artifacts resulting from precordial compression.

41 to the right atrium 2 min after the start of precordial compression.

42 rognosticator that would be displayed during precordial compression.

43 variation in the hands-off interval between precordial compressions and shock delivery was observed,

44 particular, the "hands-off" interval between precordial compressions and subsequent defibrillation sh

45 ested whether spectral-phase analysis of the precordial ECG enabled identification of periodic activa

46 by marked ST-segment elevation in the right precordial ECG leads and is associated with a high incid

47 terized by ST-segment elevation in the right precordial ECG leads and is frequently accompanied by an

48 ists of an ST-segment elevation in the right precordial ECG leads, a shorter-than-normal QT interval,

49 Precordial ECGs were recorded from 15 ischemic cardiomyo

50 explored the mechanisms linking clinical and precordial echocardiographic predictors to thromboemboli

51 terized by ST-segment elevation in the right precordial electrocardiographic leads and a high inciden

52 h right ventricular volume overload when the precordial examination is inconclusive.

53 Right bundle-branch block and precordial injury pattern in V1 through V3 is common in

54 otio cordis, or sudden death following blunt precordial injury.

55 anifest a TWI pattern different from that of precordial ischemic TWI, thereby discriminating between

56 QRSp was quantified for each precordial lead as the total number of low-amplitude def

57 annular VAs by lower prevalence of positive precordial lead concordance.

58 haracteristics, including QRS morphology and precordial lead morphology, can help distinguish between

59 p = 0.0004), a more depressed ST-segment in precordial lead V5 (p = 0.0002), and a higher coronary a

60 eversed QTUc prolongation, especially in the precordial leads (quinidine, 590+/-79 to 479+/-35 [+/-SD

61 coved-type ST-segment elevation in the right precordial leads (V1 to V3; type 1 Brugada electrocardio

62 T-wave inversions in right precordial leads are relatively rare in the general popu

63 elevation (type 1 Brugada pattern) in right precordial leads at therapeutic concentrations in 2 pati

64 there was a dominant frequency gradient from precordial leads facing the scar region to the contralat

65 ildren (5.7%) and was localized in the right precordial leads in 131 (4.7%).

66 ary disease, increasing STdep in the lateral precordial leads is associated with increasing LV mass a

67 pattern and ST elevation (STE) in the right precordial leads of the ECG.

68 normalities of repolarization in the lateral precordial leads of the electrocardiogram, as manifested

69 e-branch block and ST elevation in the right precordial leads of the surface ECG.

70 pattern of ST-segment elevation in the right precordial leads should not be seen as a marker of a spe

71 easured ST depression (STdep) in the lateral precordial leads to the presence of left ventricular hyp

72 T-wave inversion in right precordial leads V(1) to V(3) is a relatively common fin

73 T-wave inversions in right precordial leads V(1) to V(3) were present in 54 (0.5%)

74 nts displayed extensive T-wave inversions in precordial leads V1 through V4, with either persistent o

75 T QRS morphologies were measured in limb and precordial leads with electronic calipers.

76 nly present with ST-segment elevation in the precordial leads, chest pain, relatively minor elevation

77 ncy spectral area computed from conventional precordial leads, like coronary perfusion pressure and e

78 a distinct ST-segment elevation in the right precordial leads, the syndrome is associated with a high

79 terized by ST segment elevation in the right precordial leads, V1-V3 (unrelated to ischemia or struct

80 II, III, aVR, and aVF and the mid to lateral precordial leads.

81 elevation and T-wave inversion in the right precordial leads.

82 attern and ST-segment elevation in the right precordial leads.

83 x (the time to the maximum deflection in the precordial leads/QRS duration) was the largest in LV sum

84 A delayed precordial maximum deflection index > or =0.55 identifie

85 Recognition of a prolonged precordial maximum deflection index and early use of tra

86 ar arrhythmia, inverted T-waves in the right precordial or lateral leads, and/or family history of su

87 The value of precordial or transesophageal echocardiography in additi

88 specific for the evaluation of patients with precordial or transthoracic wounds (sensitivity 100%, sp

89 examinations were performed on patients with precordial or transthoracic wounds or blunt abdominal tr

90 However, slowed initial precordial QRS activation, as quantified by a novel metr

91 included the following: syncope; Q waves or precordial QRS amplitudes <1.8 mV; 3 abnormal SAECG para

92 RMVTs with a precordial R wave transition at or before lead V2 are co

93 nts had a QRS configuration during RMVT with precordial R wave transitions at or before lead V2.

94 n resuscitated after receiving three or more precordial shocks were randomly assigned to receive 300

95 likely to initiate VF than impacts at other precordial sites (5 of 55; 9%, p = 0.02).

96 lectrocardiographic criteria, including left precordial ST segment depression, complete atrioventricu

97 erized by ventricular fibrillation and right precordial ST segment elevation on ECG.

98 plete atrioventricular heart block and right precordial ST segment elevation.

99 Precordial T-wave alternans increased from 0.04 +/- 0.02

100 was the only independent predictor for right precordial T-wave inversion (odds ratio, 3.6; 95% confid

101 Postpacing precordial T-wave inversion (TWI), known as cardiac memo

102 The prevalence of right precordial T-wave inversion decreased significantly with

103 ic LV dysfunction had higher odds of lateral precordial T-wave inversions (odds ratio, 18.4; 95% conf

104 nce interval, 1.21-4.01; P=0.01) and lateral precordial T-wave inversions (odds ratio, 9.87; 95% conf

105 Right precordial T-wave inversions did not predict increased m

106 ern that allows discrimination from ischemic precordial T-wave inversions regardless of the coronary

107 ranch block pattern, QRS duration </=175 ms, precordial transition >/=V1, and maximum deflection inde

108 notch in the middle of the QRS in all cases, precordial transition at </=lead V3 in 7 patients, and a

109 bundle branch block, inferior axis and early precordial transition can be ablated in the majority of

110 ace ECG pattern of patients with OTVT with a precordial transition in lead V(3) who underwent success

111 /- 34 ms, p = 0.006), more often exhibited a precordial transition in lead V(6) (3 of 17 [18%] vs. 0

112 A PVC precordial transition occurring later than the sinus rhy

113 bundle branch block, inferior axis and early precordial transition with Rs or R in V2 or V3.

114 from RVOT origin in patients with lead V(3) precordial transition.

115 ischemic group consisted of 47 patients with precordial TWI identified among 228 consecutive patients

116 ositive or isoelectric T(I), and (3) maximal precordial TWI>TWI(III) was 92% sensitive and 100% speci

117 nown as cardiac memory (CM), mimics ischemic precordial TWI, and there are no established ECG criteri

118 ific for CM, discriminating it from ischemic precordial TWI.

119 differences in QRS axis, limb (I, aVr), and precordial (V1, V2, V6) ECG leads.

120 modality for the evaluation of patients with precordial wounds and blunt truncal injuries because it

121 ity of US in the evaluation of patients with precordial wounds and hypotensive patients with blunt to