Subject(s)
Blood Proteins/therapeutic use , Ferricyanides/adverse effects , Heart Failure/drug therapy , Hemodynamics/drug effects , Hypotension/chemically induced , Nitroglycerin/adverse effects , Nitroprusside/adverse effects , Plasma Substitutes/therapeutic use , Pulmonary Edema/drug therapy , Aged , Drug Therapy, Combination , Female , Humans , Male , Middle Aged , Nitroglycerin/therapeutic use , Nitroprusside/therapeutic use , Serum Albumin , Serum Albumin, Human , Serum GlobulinsABSTRACT
The risk of aggravated heart failure due to expanded blood volume and augmented left-ventricular filling pressure poses a challenge when transfusion is indicated by severe anemia complicating congestive heart failure. Intravenous (IV) nitroglycerin therapy produces a favorable redistribution of circulating blood volume and may be used to surmount these hemodynamic constraints during transfusion. In four patients with severe anemia and cardiac failure, IV nitroglycerin permitted rapid and large-volume blood transfusion without compromising cardiac function. In two of the four patients, recalcitrant unstable angina abated after the correction of anemia.
Subject(s)
Anemia/complications , Heart Failure/complications , Nitroglycerin/administration & dosage , Aged , Anemia/therapy , Female , Heart Failure/drug therapy , Humans , Injections, Intravenous , Male , Transfusion ReactionABSTRACT
Electrophysiologic studies support significant hypokalemia as a cause of atrial flutter in a patient without manifest heart disease. Atrial flutter, reproducibly initiated and terminated by rapid atrial pacing during hypokalemia, was not inducible after potassium correction. In an individual with existing atrial conduction disease, hypokalemia may generate both non-uniform atrial refractoriness and atrial premature beats, and it may facilitate the development of atrial flutter as a re-entrant arrhythmia.
Subject(s)
Atrial Flutter/etiology , Hypokalemia/complications , Aged , Atrial Flutter/physiopathology , Atrial Flutter/therapy , Electrocardiography , Female , Humans , Hypokalemia/physiopathology , Pacemaker, ArtificialABSTRACT
The cause of pacemaker malfunction in a patient having intermittent pacing failure associated with diminished pacer stimuli was not determined during conventional intraoperative electrical testing. A modest manual pull on the lead, termed the "lead tug" sign, induced an inordinately high lead impedance and established lead fracture as the etiology. The "lead tug" maneuver is proposed as a useful procedure during stimulation studies for the detection of early lead fracture, not apparent from the x-ray film or usual testing protocol.
