objective: Describe clinical characteristics of patients (P) admitted to hospital with suspected acute coronary syndrome (ACS), identifying medical treatment and in-hospital mortality.Methods: Evaluated were 860 patients with ACS from January through December, 2003. We evaluated baseline characteristics, ACS mode of presentation, medication during hospital stay, indication for clinical treatment or myocardial revascularization (MR) and in-hospital mortality.Results: Five hundred and three (58.3%) were male, mean age 62.6 years (± 11.9). Seventy-eight (9.1%) were discharged with the diagnosis of acute ST-elevation myocardial infarction (STEMI), 238 (27.7%) with non-ST-elevation myocardial infarction (non-STEMI), 516 (60%) with unstable angina (UA), two (0.2%) with atypical manifestations of ACS and 26 (3%) with noncardiac chest pain. During hospitalization, 87.9% of patients were given a beta-blocker, 95.9% acetylsalicylic acid, 89.9% anti-thrombin therapy, 86.2% intravenous nitroglycerin, 6.4% glycoprotein (GP) IIb/IIIa receptor inhibitor, 35.9% clopidogrel, 77.9% angiotensin-converting enzyme inhibitor, and 70,9% statin drugs. Coronary arteriography was performed in 72 patients (92.3%) with STEMI, and in 452 (59.8%) with non-STEMI ACS (p< 0.0001). Myocardial revascularization (MR) surgery was indicated for 12.9% and percutaneous coronary intervention for 26.6%. In-hospital mortality was 4.8%, and no difference was recorded between the proportion of deaths among patients with STEMI and non-STEMI ACS (6.4% versus 4.8%; p = 0.578). Conclusion:In this registry, we provide a description of ACS patient, which allows the evaluation of the demographic characteristics, medical treatment prescribed, and in-hospital mortality. A greater awareness of our reality may help the medical community to adhere more strictly to the procedures set by guidelines.key words: Acute coronary syndrome, registry, chest pain, unstable angina, acute myocardial infarction.

BackgroundThe effect of vasoconstrictors in prolonged cardiopulmonary resuscitation (CPR) has not been fully clarified.ObjectivesTo evaluate adrenaline and vasopressin pressure effect, and observe the return of spontaneous circulation (ROSC).MethodsA prospective, randomized, blinded, and placebo-controlled study. After seven minutes of untreated ventricular fibrillation, pigs received two minutes cycles of CPR. Defibrillation was attempted (4 J/kg) once at 9 minutes, and after every cycle if a shockable rhythm was present, after what CPR was immediately resumed. At 9 minutes and every five minutes intervals, 0.02 mg/kg (n = 12 pigs) adrenaline, or 0.4 U/kg (n = 12) vasopressin, or 0.2 mL/kg (n = 8) 0.9% saline solution was administered. CPR continued for 30 minutes or until the ROSC.ResultsCoronary perfusion pressure increased to about 20 mmHg in the three groups. Following vasoconstrictors doses, pressure level reached 35 mmHg versus 15 mmHg with placebo (p < 0.001). Vasopressin effect remained at 15-20 mmHg after three doses versus zero with adrenaline or placebo. ROSC rate differed (p = 0.031) among adrenaline (10/12), vasopressin (6/12), and placebo (2/8). Time-to-ROSC did not differ (16 minutes), nor the number of doses previously received (one or two). There was no difference between vasoconstrictors, but against placebo, only adrenaline significantly increased the ROSC rate (p = 0.019).ConclusionThe vasoconstrictors initial pressure effect was equivalent and vasopressin maintained a late effect at prolonged resuscitation. Nevertheless, when compared with placebo, only adrenaline significantly increased the ROSC rate.

Resumo Fundamentos Para ventilação prática e protetora durante a ressuscitação cardiopulmonar (RCP), desenvolveu-se um ventilador mecânico (VLP2000E) de 150 gramas que limita o pico de pressão inspiratória (PPI) durante ventilação e compressões torácicas simultâneas. Objetivos Avaliar a viabilidade da ventilação com VLP2000E durante RCP e comparar os parâmetros monitorados versus ventilação com bolsa-válvula. Métodos Estudo experimental randomizado com 10 porcos intubados por grupo. Após sete minutos de fibrilação ventricular, iniciaram-se ciclos de RCP de 2 minutos. Todos os animais foram ventilados com VLP2000E após o retorno da circulação espontânea (RCE). Resultados Os grupos bolsa-válvula e VLP2000E apresentaram taxa de RCE (60% vs. 50%, respectivamente) e saturação arterial de oxigênio similares na maioria dos ciclos de RCP, volume corrente basal diferente [0,764 (0,068) vs. 0,591 (0,123) L, p = 0,0309, respectivamente] e, em 14 ciclos, diferentes PPI [52 (9) vs. 39 (5) cm H 2 O, respectivamente], volume corrente [0,635 (0,172) vs. 0,306 (0,129) L], ETCO 2 [14 (8) vs. 27 (9) mm Hg], e pico de fluxo inspiratório [0,878 (0,234) vs. 0,533 (0,105) L/s], todos p < 0,0001. A complacência pulmonar dinâmica (≥ 0,025 L/cm H 2 O) diminuiu após o RCE no grupo bolsa-válvula, mas se manteve no grupo VLP2000E [ 0,019 (0,006) vs. 0,024 (0,008) L/cm H 2 O, p = 0,0003]. Conclusões Ventilação com VLP2000E durante RCP é viável e equivalente a ventilação com bolsa-válvula quanto à taxa de RCE e saturação arterial de oxigênio. Esse ventilador produz melhores parâmetros respiratórios, com pressão das vias aéreas e volume corrente menores. Ventilação com VLP2000E também previne a redução significante da complacência pulmonar dinâmica observada após ventilação com bolsa-válvula. Seria interessante realizar mais estudos pré-clínicos para confirmar esses resultados.

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