Edgar Bautista

Epinephrine fails to hasten hemodynamic recovery in fully developed canine anaphylactic shock.

Background: Epinephrine (Epi) is the treatment of choice for reversing cardiovascular collapse in anaphylactic shock (AS). However, there are few data supporting its use in this condition, and most treatment guidelines have been anecdotally derived. In the present study, the time course of hemodynamic recovery from maximal hypotension was investigated in a canine model of AS in which Epi was administered by the intravenous (IV), subcutaneous (SQ) and intramuscular (IM) routes on different occasions. The findings obtained with Epi treatment were compared to those in a nontreatment study. Methods: Ragweed-sensitized dogs were examined in respective studies approximately 5 weeks apart in which Epi was administered by one of the above routes in a randomized design. Either Epi (0.01 mg/kg) or placebo was administered at maximal hypotension, and hemodynamics were followed for 3 h after shock. The animals were studied while ventilated and anesthetized. Mean arterial pressure (MAP), cardiac output, stroke volume (SV), pulmonary wedge pressure (Pwp) and plasma Epi concentrations were obtained at each measurement interval. Results: In the IV study, Epi produced a transient immediate increase in MAP, SV and Pwp as compared to the nontreatment study (144 vs. 52 mm Hg; 32 vs. 12 ml; 9 vs. 5 mm Hg; p < 0.01), but no differences were observed 15 min after shock. Hemodynamics were not different between Epi and no treatment at any intervals when Epi was given by the SQ and IM routes. AS compared with the placebo study, plasma Epi concentrations were higher in the IV and IM studies, but not in the SQ study. Conclusions: Although higher Epi concentrations were observed in the IM and IV studies, a sustained benefit in hemodynamic recovery was not observed in this anesthetized, ventilated canine model. In AS, when administered during maximum shock after mediators have already been released, a single IM, IV or SQ dose of Epi may have limited utility in the treatment of cardiovascular collapse. Earlier administration of Epi, before maximal hypotension occurs, may produce a more beneficial effect.

Pulmonary Embolism as a Cause of Death in Patients With Heart Disease: An Autopsy Study

STUDY OBJECTIVE To establish the prevalence of pulmonary embolism (PE) in autopsy material at a tertiary cardiac referral center and its importance as a cause of death in patients with heart disease (HD). DESIGN Case series. SETTING National Heart Institute, Mexico City. PATIENTS One thousand thirty-two patients who died at our institution from 1985 to 1994 in whom an autopsy study was performed. MEASUREMENTS AND RESULTS Of the 1,032 autopsies reviewed, 231 cases (24.4%) of PE were found; 100 of these patients had a diagnosis of massive PE. Massive PE (obstruction of either of the main pulmonary arteries or more than two lobar arteries) was found to be the third cause of death in this HD population. By age-group distribution, the global prevalence of massive events was higher in patients < 10 years old. Clinical suspicion (premortem) was raised in only 18% of the cases. CONCLUSIONS PE was a frequent cause of morbidity and mortality in patients with HD who underwent autopsies. The incidence of massive PE was high in children.

Original Research: Pulmonary EmbolismPulmonary Embolism as a Cause of Death in Patients With Heart Disease: An Autopsy Study

STUDY OBJECTIVE To establish the prevalence of pulmonary embolism (PE) in autopsy material at a tertiary cardiac referral center and its importance as a cause of death in patients with heart disease (HD). DESIGN Case series. SETTING National Heart Institute, Mexico City. PATIENTS One thousand thirty-two patients who died at our institution from 1985 to 1994 in whom an autopsy study was performed. MEASUREMENTS AND RESULTS Of the 1,032 autopsies reviewed, 231 cases (24.4%) of PE were found; 100 of these patients had a diagnosis of massive PE. Massive PE (obstruction of either of the main pulmonary arteries or more than two lobar arteries) was found to be the third cause of death in this HD population. By age-group distribution, the global prevalence of massive events was higher in patients < 10 years old. Clinical suspicion (premortem) was raised in only 18% of the cases. CONCLUSIONS PE was a frequent cause of morbidity and mortality in patients with HD who underwent autopsies. The incidence of massive PE was high in children.

Does Anticoagulation in Eisenmenger Syndrome Impact Long‐term Survival?

OBJECTIVE To determine the impact of anticoagulation on survival in Eisenmenger syndrome. BACKGROUND The use of anticoagulation for primary prevention of adverse events in patients with Eisenmenger syndrome has been proposed but not studied. Strong arguments have been made both for and against anticoagulation based on the known risk of hemoptysis and pulmonary vascular thrombosis. DESIGN AND SETTING Retrospective cohort study at a tertiary referral hospital. PATIENTS AND INTERVENTIONS   One hundred forty-four patients with established Eisenmenger physiology all underwent initial laboratory, echocardiographic, and catheterization evaluation after initial referral. We retrospectively identified patients who were started on anticoagulation (AC) and compared them to patients who did not receive anticoagulation therapy (non-AC). Baseline variables were compared between groups, as well as between survivors and nonsurvivors. Analyses of prognostic factors and survival were done using Cox and Kaplan-Meier methods. OUTCOME MEASURES The primary outcome was death since time of baseline evaluation. RESULTS We identified 48 anticoagulated and 44 non-anticoagulated patients with Eisenmenger physiology (oxygen saturation 82 ± 9%, PaO(2) 48 ± 8 mm Hg, hemoglobin 18.6 ± 4 g/dL). More atrial septal defect patients were in the AC group, but there were no other baseline differences in clinical, functional, or hemodynamic data. After mean follow-up of 7 ± 5.4 years (range 1-31), 11 patients died in the AC and 10 died in the non-AC group. There was no survival difference between groups (log rank test = 1.78; P is not significant). For the entire cohort, mortality was significantly associated with New York Heart Association class 3-4 (hazard ratio = 4.2), evidence of right heart failure (hazard ratio = 13.6), and a mean corpuscular volume <80 fL (hazard ratio = 3.8). Use of anticoagulation did not impact survival. Bleeding complications occurred in seven (16%) of AC patients, including two fatalities. CONCLUSIONS Anticoagulation had no impact on long-term survival in this limited study. These data may be useful in considering future studies addressing this question.

Effect of histamine H3 receptor blockade on venous return and splanchnic hemodynamics in experimental bacteremia

OBJECTIVE In the heart, histamine H3 receptors may function as inhibitory presynaptic receptors that decrease adrenergic neural norepinephrine release in conditions of enhanced sympathetic tone. In a previous study, we found that H3 receptor blockade improved cardiac contractility and systemic hemodynamics in experimental bacteremia in dogs. Because histamine H3 receptors have been found in the splanchnic circulation in other animal models, it was not clear the extent to which H3 receptor blockade may have altered splanchnic hemodynamics, and variables of venous return, that in turn contributed to the overall improvement in systemic hemodynamics observed in the previous experiment. In the present study, we examined splanchnic hemodynamics in the presence of H3 receptor blockade in a canine model of Escherichia coli bacteremia. DESIGN Bacteremia was produced by intravenous infusion of live E. coli administered throughout the experiment. Variables of venous return included mean systemic pressure, resistance to venous return, and mean right atrial pressure. Splanchnic measurements included hepatic and portal pressures and flows. Measurements were obtained before and after H3 receptor blockade with thioperamide maleate. The animals were studied while ventilated and anesthetized. RESULTS H3 receptor blockade caused a decrease in mean right atrial pressure from 5.9 mm Hg pretreatment to 3.5 mm Hg posttreatment (p < .05), although it did not affect mean systemic pressure or resistance to venous return. There were no changes in portal or hepatic flows after H3 receptor blockade. The cardiac function curve after H3 receptor blockade was shifted upward and to the left compared with the pretreatment curve. CONCLUSIONS The results showed that the primary effect of H3 receptor blockade in experimental bacteremia was attributable to an increase in inotropy. There was no evidence to indicate that H3 receptor activation contributed to altered splanchnic hemodynamics in this model.