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L T Iseri

Publications and source records attributed to L T Iseri.

27 records · Page 2Linked to original sources
PubMed1978

Prehospital brady-asystolic cardiac arrest.

Of 133 persons with spontaneous cardiac arrest attended by paramedics within 10 minutes, 100 (75%) had ventricular fibrillation as the initial rhythm and 33 (25%) had extreme bradycardia or asystole. The latter group of arrhythmias was characterized by sinus arrest or severe sinus bradycardia (90%) and complete A-V block (10%). Junctional escape rhythm was also absent or markedly retarded. Despite cardiopulmonary resuscitation and the administration of epinephrine, atropine, isoproterenol, and sodium bicarbonate, recovery of the sinus and junctional tissues was infrequent. Ventricular fibrillation developed in 11 cases (33%). One patient lived 12 days, but all others were dead on arrival or died in the emergency room. Among the 13 coronary causes of death proved at autopsy, 10 (77%) were due to a fresh thrombus and seven (54%) to an occluded proximal right coronary artery, suggesting a causal relation to this type of arrest.

Aged↗
PubMed1977

Prehospital cardiac arrest after arrival of the Paramedic Unit.

Rapid response time by paramedic units made it possible to study 26 cases of "primary" cardiac arrests occurring after arrival of the unit. Ventricular fibrillation developed in 14 cases with prodromal ectopy in only two (14%) and rapidly increasing tachycardia in seven (50%). Countershock was successful in 12 (86%) and six (43%) survived. Bradycardia and asystole following countershock forecasted a fatal outcome. Brady-asystolic arrests (BAA) developed rapidly without much warning in 12 cases and were due to sinus arrest or severe sinus bradycardia in 92% and to atrioventricular block in 8%. BAA was 100% fatal. Coronary artery disease was diagnosed as the cause of BAA in seven (58%). All of the three cases, proven to be due to coronary artery disease at autopsy, had an occlusion of the proximal right coronary artery. In the remaining five (42%) cases, BAA was secondary to ruptured aneurysm (2), acute pancreatitis (1), chronic lung disease (1), and mitral stenosis (1). These observations emphasize a need for a more aggressive approach to prehospital management of brady-asystolic cardiac arrests.

Adult↗
PubMed1976

Surgical treatment of infective valvular endocarditis.

Infective valvular endocarditis, whether occurring on a native or prosthetic heart valve, continues to carry a serious prognosis. Death is usually due to congestive heart failure, arrhythmia, or embolic complications, rather than infection per se. While antimicrobial therapy and medications to control congestive heart failure continue to be the treatment of choice in most cases, early valve replacement is indicated in certain situations. During the past four years, 12 patients underwent valve replacement for infective endocarditis. Six patients underwent elective valve replacement after antibiotic or antifugal therapy. All survived the operation and were improved. Six other patients underwent emergency valve replacement. Two patients died intraoperatively and their operations, in retrospect, were delayed unnecessarily. Four patients survived and are improved. Prosthetic valve replacement during the course of infective valvular endocarditis should be considered based on indications such as congestive heart failure, rhythm disturbances, etc, rather than the status of the infection.

Adolescent↗
PubMed1975

Magnesium deficiency and cardiac disorders.

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.

Alcoholism↗
PubMedDate not supplied

Magnesium-potassium interactions in cardiac arrhythmia. Examples of ionic medicine.

Ionic biology involving Ca2+, Na+, K+ and Mg2+ across the cell membrane and in the development of the action potential is reviewed with reference to cardiac arrhythmia. K+ and Mg2+ deficiency which frequently occur together lead to abnormal ionic transfer of Na+, K+ and Ca2+ with development of automaticity, triggered impulses and reentrant tachycardia. Tachycardia occurring in acute myocardial ischemia, congestive heart failure, hypertensives on diuretics and digitalis toxicity is examined according to the concept of ionic imbalance. A protocol for prevention and treatment of cardiac tachyarrhythmia is proposed with this concept in mind.

Action Potentials↗