A Marn-Pernat | PubMed Health

PubMed2001

Optimizing timing of ventricular defibrillation.

OBJECTIVE: Our intent was to evolve a prognosticator that would predict the likelihood that an electrical shock would restore a perfusing rhythm. Such a prognosticator was to be based on conventional electrocardiographic signals but without constraints caused by artifacts resulting from precordial compression. The adverse effects of "hands off" intervals for rhythm analyses would therefore be minimized. Such a prognosticator was further intended to reduce the number of electrical shocks and the total energy delivered and thereby minimize postresuscitation myocardial dysfunction. DESIGN: Observational study. SUBJECTS: Medical research laboratory of a university-affiliated research and educational institute. SUBJECTS: Domestic pigs. INTERVENTIONS: Ventricular fibrillation was induced in an established porcine model of cardiac arrest. Recordings of scalar lead 2 over the frequency range of 4-48 Hz were utilized. The area under the curve representing the amplitude and frequency was defined as the amplitude spectrum area (AMSA). MEASUREMENTS AND MAIN RESULTS: A derivation group of 55 animals yielded a threshold value of AMSA that uniformly predicted successful resuscitation. A separate group of 10 animals, a validation group, confirmed that an AMSA value of 21 mV.Hz predicted restoration of perfusing rhythm after 7 of 8 electrical shocks and failure of electrical conversion in 21 of 23 electrical shocks, yielding sensitivity and specificity of about 90%. The negative predictive value of AMSA was 95% and statistically equivalent to that of coronary perfusion pressure, mean amplitude, and median frequency. The positive predictive value that would prompt continuation of cardiopulmonary resuscitation without interruption for an unsuccessful defibrillation attempt was greatly improved with AMSA (78%) as compared with coronary perfusion pressure (42%), mean amplitude (32%), and median frequency (29%). CONCLUSION: AMSA has the potential for guiding more optimal timing of defibrillation without adverse interruption of cardiopulmonary resuscitation or the delivery of unsuccessful high energy electrical shocks that contribute to postresuscitation myocardial injury.

Algorithms↗

PubMed1998

Are insulin metabolism and night-time blood pressure related to left ventricular hypertrophy?

Essential hypertensives in whom blood pressure does not fall during sleep (non-dippers) are thought to be at greater risk of cardiovascular morbidity. Insulin resistance is also suggested to be a risk factor for cardiovascular morbidity. The purpose of the present study was to evaluate the relationship of insulin metabolism to left ventricular hypertrophy in dippers and non-dippers. Thirty male, non-diabetic out-patients with newly diagnosed arterial hypertension were included in the study: 21 dippers (mean age 45+/-13 years; body mass index 28.2+/-4.0 kg/m2) and nine non-dippers (mean age 48+/-10 years, body mass index 28.6+/-3.9 kg/m2). Patients were subdivided into dippers and non-dippers on the basis of 24-h ambulatory blood pressure monitoring. Insulin and glucose responses to an oral glucose load have been evaluated. C-peptide levels were determined. Left ventricular mass was assessed by echocardiography. Non-dippers had significantly higher mean night-time systolic (non-dippers: 148+/-9; dippers: 123+/-16 mmHg; P<0.001), diastolic blood pressure (non-dippers: 90+/-8; dippers: 77+/-8 mmHg; P<0.001) and non-significantly higher left ventricular mass (279+/-92 g) and left ventricular mass index (135+/-46 g/m2). No significant difference was found between C-peptide, insulin, glucose levels and incremental areas between the two groups. Night-time blood pressure, insulin, C-peptide and glucose did not correlate with left ventricular mass in non-dippers. Dippers showed a positive correlation between fasting C-peptide and left ventricular mass (r=0.48, P=0.02) and between glucose and left ventricular mass (r=0.42, P=0.05). Our data indicate that night-time blood pressure and insulin are not related to left ventricular hypertrophy in patients with essential hypertension.

Adult↗