Hemodynamics in sleep-induced apnea. Studies during wakefulness and sleep

Twelve patients with predominantly obstructive type sleep apnea underwent cardiac catheterization, hemodynamic monitoring, and arterial blood gas analysis during wakefulness and sleep. Abnormalities during wakefulness included systemic hypertension in four of 12, exercise-induced mild pulmonary hypertension in five of 12, and alveolar hypoventilation in one. During sleep nine patients had cyclic elevations of arterial pressure with each apneic episode, exceeding 200 mm Hg systolic in three of 12. Pulmonary artery pressures increased in 10 of 12, exceeding 60 mm Hg systolic in five. Marked degrees of hypoxemia (arterial P02, less than 50 mm Hg in eight of 12) and moderate hypercapnia with respiratory acidosis were associated with these hemodynamic changes. Cyclic upper airway obstruction during sleep may result in hypercapnia, acidosis, and pronounced hypoxemia, which can lead to hemodynamic abnormalities during sleep. Sustained pulmonary hypertension and possibly systemic hypertension may follow. Tracheostomy is an effective therapy and is recommended to symptomatic patients who have predominantly obstructive apnea but no relievable anatomic cause of upper airway obstruction.     

Quinuclidine chemistry: autocondensation reactions of 3-quinuclidinone

During the synthesis of 3-hydroxy-3-ethinylquinuclidine (I), two additional products were isolated and identified as (E)-3-[2-(3-oxoquinuclidine)]quinuclidylidene (III) and (E)-3-[2-(3-hydroxy-3-ethinylquinuclidine)]quinuclidylidene (V). The base-catalyzed autocondensation of 3-quinuclidinone resulted in the alpha,beta-unsaturated ketone dimer (III) as a single isomer. The geometric configuration was deduced by examination of the NMR spectra of the methyl iodide salt. Compound V was thus the result of attack on the carbonyl carbon of III by the acetylide anion. The isolation and identification of these compounds clarified the reported differences in the physical properties of I and its analogs.     

Factors affecting the uptake of 99mTc-sulfur colloid by the lung and kidney

Occasionally patients injected with 99mTc-sulfur colloid (TSC) for liver--spleen imaging show increased uptake by the lungs or kidneys. In animals, increased lung uptake of TSC can be produced by injecting endotoxin intraperitoneally. Using an intraperitoneal endotoxin model, we studied the effect of heparin on dose-response curves for TSC uptake by the lungs and kidneys. Over a dose range of 1 mug to 10 mg of endotoxin, TSC uptake by the lungs increased progressively; heparin had no effect. In the kidneys, endotoxin in doses from 1 mug to 1 mg resulted in an increased TSC uptake which was less marked than that in the lungs and which was also unaffected by heparin. However, at a dose of 10 mg of endotoxin, a marked increase occurred in TSC uptake by the kidneys, and this could be prevented by heparin. Although the increased TSC uptake by the kidneys at lower doses of endotoxin and by the lungs at all doses is probably not related to intraavascular coagulation, the marked increase in TSC uptake by the kidneys at 10 mg of intraperitoneal endotoxin probably is related to intravascular coagulation, possibly by entrapment in fibrin deposits in the renal capillaries.     

Medial calcinosis of M?nckeberg. A review of the problem and a description of a patient with involvement of peripheral, visceral and coronary arteries

Massive medial calcific deposits (M?nckeberg's calcinosis) are described in the peripheral and visceral arteries, and similar but small-sized deposits in the coronary arteries of a 41 year old woman with diabetes mellitus. Although observed by roentgenogram fairly commonly during life in the muscular arteries of the legs in middle-aged men, medial calcinosis infrequently involves the visceral arteries and has never, to our knowledge, been documented in the coronary arteries. Although it may be associated with intimal atherosclerosis, medial calcinosis, per se, does not obstruct the lumens of the arteries and, therefore, does not lead to symptoms or signs of limb or organ ischemia. The cause of medial calcinosis remains a mystery, but it appears to affect people with diabetes more frequently than those without.     

Cryosurgical ablation of accessory atrioventricular connections: a method for correction of the pre-excitation syndrome

Cryothermia, a new technique for definitive treatment of the pre-excitation syndrome, is described in two patients. The first patient presented with a normal P-R interval with a delta wave and reciprocating tachycardia. Preoperative electrophysiologic study suggested a free-wall atrioventricular connection on the left posterior atrioventricular (A-V) groove. At surgery, epicardial mapping confirmed the site of pre-excitation on the posterior left ventricular (LV) wall. An electrogram arising from the accessory pathway (AP) was recorded at the site of earliest ventricular activation. Interatrial delay combined with an apparently long accessory pathway to the ventricle caused the P-R interval to appear normal. Local pressure abolished pre-excitation. The site of early ventricular activation was cooled to -60 degrees C with a specially designed cryoprobe. All evidence of pre-excitation and arrhythmias disappeared. The second patient presented with a refractory reciprocating tachycardia and was found to have an AP in the septum capable of only retrograde conduction. Retrograde conduction was abolished by applying a temperature of 0 degrees C to the anulus at this site during tachycardia. Conduction over the AP and reciprocating tachycardia returned with rewarming. Ablation of the AP was obtained by applying a temperature of -60 degrees C for 90 seconds on two occasions to the same area. The His bundle was not injured.