Pacemaker-twiddler's syndrome: a rare cause of lead displacement and pacemaker malfunction.

Pacemaker-twiddler's syndrome is characterized by spontaneous, subconscious, inadvertent, or deliberate rotation of the pulse generator by the patient resulting in lead dislodgement and pacemaker malfunction. We present a case of pacemaker-twiddler's syndrome that involved an atrioventricular sequential pacemaker. It resulted in failure of atrial lead capture and phrenic nerve stimulation but without loss of ventricular lead capture. A search of the literature revealed only ten previous cases reported; none were in the emergency medicine literature, and none involved an atrioventricular sequential pacemaker.

Digoxin toxicity presenting as altered mental status in a patient with severe chronic obstructive lung disease.

Gastrointestinal and cardiac manifestations are the commonly considered features of digoxin toxicity. This report describes a patient with severe chronic obstructive lung disease whose primary manifestation of digoxin toxicity is acute alteration of mental status. Neurologic dysfunction may be the sole manifestation of digitalis toxicity. The diagnosis of digoxin toxicity should be considered in elderly patients with altered mental status, even when serum levels are within a therapeutic range.

Objectives to direct the training of emergency medicine residents on off-service rotations: pulmonary.

This article outlines the objectives for a resident rotation in pulmonary diseases. It is part of a continuing series on the goals and objectives to direct Emergency Medicine resident training on off-service rotations. Pulmonary disease accounts for a high percentage of presenting complaints and potentially life-threatening disease in the emergency department. Because of the frequency of respiratory disease in Emergency Medicine, many Emergency Medicine residencies offer individual off-service rotations in Pulmonary Medicine. The objectives of this article are viewed as a one-month component of an Internal Medicine Rotation in the first year of training. These objectives are designed to help focus the resident's reading and study during a pulmonary off-service rotation.

A comparison of amrinone and glucagon therapy for cardiovascular depression associated with propranolol toxicity in a canine model.

This study's objective is to evaluate the ability of glucagon and amrinone to reverse propranolol induced cardiovascular depression in a canine model, compared to a control of normal saline. The study design included 18 animals which received intravenous propranolol (10 mg/kg) resulting in significant depression in heart rate, cardiac output, mean arterial pressure, maximal ventricular dP/dt and stroke volume. Each canine was randomly assigned to one of three treatment groups; controls (normal saline only), glucagon (20 micrograms/kg bolus) and amrinone (4 mg/kg bolus). Cardiovascular parameters were monitored at 1, 6, 11, 21 and 31 min after treatment was rendered. Multiple comparison procedures at each time period controlled the overall alpha-level at .05. Compared to control animals, both amrinone and glucagon were effective in reversing propranolol-induced depression of dP/dtmax at 6 and 11 min for glucagon and 11 min for amrinone and cardiac output at 1, 6 and 11 min for glucagon and 1 min for amrinone. Amrinone and glucagon significantly increased stroke volume over control values at 1 min and tended to do so at the remaining time periods. The two days caused a similar degree of arteriolar vasodilation which was significantly greater than that seen in control animals at 1 and 6 min. Beta blocker induced bradycardia did not respond significantly to amrinone while glucagon induced a tachycardia which is unique to canines. It is concluded that in this canine model, amrinone appears to be an effective therapeutic alternative to glucagon for reversing depressed dP/dtmax, cardiac output and stoke volume induced by propranolol toxicity. Unlike glucagon, amrinone appears to lack positive chronotropic activity which may limit its clinical utility in the treatment of beta blocker overdose.

The effects of fructose-1,6-diphosphate on myocardial damage in acute coronary artery occlusion.

Acute myocardial infarction can result from thrombosis of a coronary artery. The purpose of this study was to evaluate the ability of fructose-1,6-diphosphate (FDP; Esafosfina) to reduce myocardial necrosis during acute thrombosis of a coronary artery. A canine model of acute myocardial infarction was used to produce intraluminal thrombosis by placement of a coil of wire in a coronary artery. After developing a coronary thrombosis of the left anterior descending artery, dogs were injected intravenously with 90 mg/kg, 175 mg/kg, or 350 mg/kg of FDP or normal saline (controls). Hemodynamic, biochemical and electrocardiographic parameters were evaluated before, and 30 min and 4 h after occlusion. Four hours after acute coronary occlusion, the animals were sacrificed, and the weights of ischemic and necrotic myocardial tissue were quantified using a histologic-staining method. There were no significant differences between control and treated animals in biochemical or hemodynamic parameters. All animal groups treated with FDP demonstrated significant reductions in the amount of necrotic and ischemic tissue compared to controls (P less than 0.05). However, only the 175 mg/kg group had a significant reduction compared to controls in necrotic tissue weight as a percentage of ischemic myocardium (24 +/- 15% vs. 72 +/- 22%, respectively, P less than 0.01). These data suggest that FDP may have a role in limiting the amount of myocardial damage after an acute coronary artery occlusion.

Objectives to direct the training of emergency medicine residents on off-service rotations: critical care medicine, Part 2.

This article is the second of two parts outlining the objectives for resident rotations in intensive care units. It is part of a larger continuing series on the goals and objectives to direct the training of emergency medicine residents on off-service rotations. The critical care unit allows the resident an opportunity to provide continuing care for critically ill patients, many of whom enter the health care system through the emergency department. Critical care medicine is a natural continuum of emergency medicine, and provides the resident with the ability to follow the natural progression of seriously ill patients, as well as build confidence and experience in caring for the critically ill and injured. These objectives are designed to help focus the resident's reading and study during the rotation.

Objectives to direct the training of emergency medicine residents on off-service rotations: critical care medicine, Part 1.

This article is the first of two parts outlining the objectives for a resident rotating in the intensive care unit (ICU). It is part of a larger continuing series on the goals and objectives to direct the training of emergency medicine residents on off-service rotations. The critical care unit is a valuable rotation that allows the resident to see and care for critically ill patients, many of whom present initially to the emergency department. Critical care is a logical continuum for the sick and injured patient as he moves from the prehospital and emergency department (ED) settings to the ICU. These objectives are designed to focus the resident's reading and study during a critical care rotation.

Objectives to direct the training of emergency medicine residents on off-service rotations: electrocardiology.

This is a continuing series of objectives to direct resident training in emergency medicine. Electrocardiography may not receive individual attention in many training programs. However, the importance, omnipresence, and medicolegal potential of electrocardiography in the practice of emergency medicine suggests its individual attention. Contents and specific learning objectives are presented to provide guidelines for resident mastery, following the format presented by preceding subjects.

Absence of pulmonary edema during peritonitis and shock in rats.

We evaluated the development of pulmonary edema early in the course of peritonitis and shock in rats. Peritonitis was established by cecal ligation and perforation. In a preliminary experiment, sepsis was induced in five animals and five animals served as sham-operated controls. Lungs harvested for gravimetric analysis at 6 hours revealed no significant difference in wet-dry/dry (W-D/D) ratios. In a second experiment, 15 rats were randomized to three groups: septic animals, septic animals infused with 5% albumin, and sham-operated animals. Thermodilution cardiac output and arterial blood gases were sequentially measured over a 6-hour interval. At 6 hours, the lungs were harvested for gravimetric analysis. Lung W-D/D and arterial oxygenation were not significantly different between the three groups. The W-D/D was 3.46 +/- 0.10 in sham-operated rats, 3.37 +/- 0.12 in septic rats, and 3.88 +/- 0.27 in albumin-infused septic rats. The alveolar-arterial oxygen difference at 6 hours was 10 +/- 2 mm Hg in sham-operated rats, 7 +/- 1 mm Hg in septic rats, and 13 +/- 6 mm Hg in albumin-infused septic rats. These data suggest that overt pulmonary edema and arterial hypoxemia may not occur early in septic shock when fluid infusion is not excessive.

Ruptured thoracic aneurysm presenting as dyspnea and hypotension.

A 65-year-old woman with a two-day history of progressive back pain presented with acute dyspnea, tachypnea, hypotension, and tachycardia. The patient was being treated for chronic obstructive lung disease and long-standing hypertension. She evidenced unilateral diminished breath sounds and wheezing. A portable chest radiograph in the emergency department revealed a large left pleural effusion. A hemothorax was confirmed by thoracentesis, and a 7-cm descending thoracic aortic aneurysm was demonstrated by angiography. The patient underwent successful surgical resection and Dacron graft repair of the aneurysm. This case emphasizes the need for maintaining a high index of suspicion for atypical presentations of ruptured thoracic aneurysms and for using diagnostic thoracentesis in pleural effusions of unknown etiology.

Valvular heart disease: clinical approach to acute decompensation of left-sided lesions.

Acute valvular heart disease is often life-threatening. The diagnosis of acute valvular decompensation is made by attention to the physical assessment and appropriate use of diagnostic techniques. Recent advances in valvular heart disease have centered around noninvasive diagnostics. Doppler echocardiography can accurately diagnose and quantify stenotic and regurgitant lesions; its use with M-mode and two-dimensional echocardiography makes these the noninvasive diagnostic procedures of choice. Acute decompensation is often related to preexisting critical aortic or mitral stenosis, or more commonly, acute severe regurgitation. Although of different etiologies, acute mitral and aortic regurgitation are associated with similar diagnostic and therapeutic modalities. Emergency treatment consists of vasodilator and, possibly, inotropic therapy. However, definitive therapy generally requires surgical intervention.