[Is morphine still the analgesic of choice in acute myocardial infarction?]. / Sigue siendo la morfina el analgésico de elección en el infarto agudo de miocardio?

Chest pain is the most common symptom of patients who present with ischemic heart disease. Morphine has traditionally been the drug of choice for managing chest pain in acute coronary syndrome (ACS) due to its high analgesic potency, though its physiological effects are poorly understood. Routinely used for managing chest pain, morphine is recommended in the 2002 guidelines of the American College of Cardiology/American Heart Association. This recommendation, however, is not based on a high level of scientific evidence but on expert opinion. Studies have found both for and against the use of morphine in ACS, suggesting that its benefits are perhaps not altogether clear. This review examines the pathophysiological effects of morphine and their cardiac implications, with special attention to a possible negative effect on ACS. We reviewed articles in the MEDLINE database from 1982 to 2006.

¿Sigue siendo la morfina el analgésico de elección en el infarto agudo de miocardio? / Is morphine still the analgesic of choice in acute myocardial infarction?

El dolor torácico es el síntoma más frecuente de presentación en pacientes con cardiopatía isquémica. Tradicionalmente la morfina ha sido el fármaco de elección para el control del dolor torácico en el síndrome coronario agudo (SCA) ya que su potencia analgésica es muy elevada, sin embargo sus efectos fisiológicos no están del todo claros. Su uso como terapéutica para el control del dolor torácico es de rutina, e incluso está incluida como recomendación en las guías de la ACC/AHA (American College of Cardiology/American Heart Association) delaño 2002, aunque esta recomendación no está basada enestudios científicos sólidos, sino en la opinión de expertos de la práctica clínica. La presencia de estudios a favor y en contra del uso de la morfina en el SCA, hacen ver que tal vez su beneficio no esté del todo claro. El objetivo de este trabajo es revisar los efectos fisiopatológicos de la morfina y sus implicaciones a nivel cardiaco, alertando de un posible efecto deletéreo en el SCA. Revisamos artículos desde el año 1982 al 2006 incluidos en la base de datos MEDLINE

Chest pain is the most common symptom of patientswho present with ischemic heart disease. Morphine hastraditionally been the drug of choice for managing chestpain in acute coronary syndrome (ACS) due to its highanalgesic potency, though its physiological effects arepoorly understood. Routinely used for managing chestpain, morphine is recommended in the 2002 guidelinesof the American College of Cardiology/American HeartAssociation. This recommendation, however, is not basedon a high level of scientific evidence but on expertopinion. Studies have found both for and against the useof morphine in ACS, suggesting that its benefits are perhaps not altogether clear. This review examines the pathophysiological effects of morphine and their cardiacimplications, with special attention to a possible negative effect on ACS. We reviewed articles in the MEDLINE database from 1982 to 2006

Effects on intracranial pressure of fentanyl in severe head injured patients.

Despite opioids are routinely used for analgesia in head injured patients, the effects of such drugs on ICP and cerebral hemodynamics remain controversial. Cerebrovascular autoregulation (CAR) could be an important factor in the ICP increases reported after opioid administration. In order to describe the effects on intracranial pressure of fentanyl and correlated such effects with autoregulation status, we studied 30 consecutive severe head injury patients who received fentanyl (2 micrograms/kg) intravenously over one minute. Prior to study, CAR was assessed. Monitoring included MAP, HR, SaO2, ETCO2, SjO2 and ICP. Changes in cerebral blood flow (CBF) were estimated from relative changes in AVDO2. Patients mean GCS was 5.7 +/- 1.7 (mean +/- STD) and mean ICP on admission was 23.8 +/- 16.3 mmHg. Fentanyl caused significant increases in ICP and decreases in MAP and CPP, but CBF remained unchanged when estimated by AVDO2. In patients with preserved CAR (34.5%), opioid-induced ICP increase was greater (but not statistically significant) than in those with impaired CAR (65.5%). We conclude than fentanyl moderately increased ICP and decreased MAP and CPP. Our data suggests that in patients with preserved CAR, potent opioids could cause greater increases of ICP, probably due to activation of the vasodilatadory cascade.

[Comparative study of the efficacy and tolerance of propofol and thiopental in induction and in continuous perfusion with neuroleptanesthesia]. / Estudio comparativo de eficacia y tolerancia de propofol con tiopental en la inducción y en perfusión continua con la neuroleptoanestesia.

We have studied 40 ASA I/II patients aged from 18 to 65 years undergoing otorhinolaryngologic surgery of 40-100 minutes of duration. Patients were randomly assigned to two groups. Anesthesia in group I was induced with thiopental, 4 mg/kg and maintained with N2O at 66% and a variable perfusion of fentanyl. In group II, anesthesia was induced with propofol, 2.5 mg/kg and maintained with a perfusion of 6-12 mg/kg/hour and an initial perfusion of fentanyl, 4 micrograms/kg/hour. Loss of consciousness occurred in 37.49 +/- 9.78 seconds in group I and in 46.25 +/- 12.62 seconds in group II, with no significant differences. Two minutes after induction, propofol group presented a significant decrease in systolic blood pressure of - 12 mm Hg and both groups presented comparable increases in systolic blood pressure and heart rate during intubation. Five minutes later, systolic blood pressure regained normal values. Maintenance in group II was achieved in a proper fashion with a mean propofol consumption of 9.5 +/- 2.6 mg/kg/hour and fentanyl consumption of 4.94 +/- 2.22 micrograms/kg/hour whereas in group II, with N2O at 66%, the amount of fentanyl required was 6.85 +/- 2.95 micrograms/kg/hour, which was significantly higher. Eye opening from the time of interruption of anesthetics was achieved at 6.6 +/- 3.2 minutes in group I and 12.44 +/- 6.34 in group II. Consciousness was regained at 11.25 +/- 3.96 and 16.87 +/- 6.95 minutes, respectively. Pain on injection occurred in 15% with propofol and in 10% with thiopental. No patient presented major complications nor phlebitis after administration of the anesthetic.

[Evaluation of the degree of muscle blockade: a comparative study using electromyography of the muscular relaxation induced by pancuronium, atracurium and vecuronium]. / Evaluación del grado de bloqueo muscular: estudio comparativo mediante electromiografía de la relajación muscular provocada por el pancuronio, atracurio y vecuronio.

To compare the muscle relaxing effect of pancuronium, atracurium and vecuronium, 99 patients operated on under neuroleptanesthesia were divided in three groups depending on whether they had received, during induction, pancuronium 0.1 mg/kg, atracurium 0.5 mg/kg, or vecuronium 0.1 mg/kg. One-fourth of the initial dose was repeated if necessary. The electromyographic study of the muscle relaxing effect was carried out with stimulation of the cubital nerve with courses of supramaximal square wave electric stimuli in 'trains of four'. The time to maximal blockade (TMB), the time of clinical effectiveness (TCE), the total duration time (TDT), the time of duration of the maintenance dose (DM 25) and the recovery index (RI) were measured. TMB was 4.3 +/- 1 min for pancuronium, 3.5 +/- 0.8 min for atracurium, and 3.3 +/- 0.98 min for vecuronium. The differences between pancuronium and the other drugs were statistically significant, but they were not so between the latter two. TCE was 67.9 +/- 13.5 min for pancuronium, significantly longer than with vecuronium and atracurium (28.2 +/- 5.7 and 31.5 +/- 4.7, respectively). TDT was 126.2 +/- 19.9 min for pancuronium, 61.2 +/- 11.5 min for atracurium and 55.5 +/- 16.7 for vecuronium. The mean duration of the repeated dose was 52.7 +/- 8.4 min for pancuronium, 19.9 +/- 5 min for vecuronium and 10.9 +/- 5 min for atracurium. RI, which was similar for atracurium and vecuronium (12.7 +/- 1.7 min and 12.8 +/- 3.3 min), was longer for pancuronium (27.7 +/- 4.3 min).