High tibia osteotomy and other challenges.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to W H Becker.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A first-pass nuclear angiogram and a multiple-gated acquisition study were obtained in 10 normal physicians and in 10 patients with a 7-to-10 day old transmural myocardial infarction. After the scan the subjects drank 2 oz. of whiskey. After 60 minutes, the multiple-gated acquisition study was repeated. In the normal group the left ventricular ejection fraction was 68% before and 72% after alcohol. The left ventricular end-diastolic volume increased from 89 to 97 ml while the left ventricular end-systolic volume decreased from 29 to 27 ml. The stroke volume rose from 61 to 70 ml/beat (p less than 0.05). The cardiac output increased from 4.0 to 5.0 l/min (p less than 0.05). In the infarction group, the left ventricular ejection fraction was 58% before and 56% after alcohol administration. The left ventricular end-diastolic volume fell from 111 to 96 ml, while the left ventricular end-systolic volume declined from 50 to 44 ml. The stroke volume fell from 61 to 52 ml/beat, while the cardiac output fell from 4.5 to 3.8 l/min. In the left ventricular infarction zones, alcohol produced in 9 of the 10 cardiac patients a decline in the left ventricular regional ejection fraction. In the normal group, alcohol produced no significant changes in the regional ejection fraction. The normal and the postinfarction patients responded differently to alcohol.
The effects of Isuprel administered by means of a mistometer were studied in 8 patients with heart disease. Recordings were made at varied heart rates using atrial pacing. In addition, the functional and effective refractory periods were measured with the use of the extra stimulus technique. Four inhalations of the mistometer were administered to each patient (0.5 mg). The AH interval was 100 +/- 13 msec before and 93 +/- 23 msec 5 minutes after the Isuprel administration (p less than 0.05). Isuprel significantly reduced the AH interval with atrial pacing. The AH interval at an atrial pacing rate of 100/minute was 148 +/- 70 msec before and 131 +/- 51 msec after Isuprel (p less than 0.05). Isuprel had no significant effect on the HV interval. The effective and functional refractory period of the atrioventricular node was not significantly changed after Isuprel. The heart rate and blood pressure showed no significant change after Isuprel. No cardiac arrhythmias were seen. (The systemic absorption of the drug was probably minimal.) Isuprel administered by means of the mistometer can improve conduction through the atrioventricular node. Nevertheless, the potent bronchodilating effects of Isuprel and the absence of tachycardia and cardiac arrhythmias does attest to the safety of this agent.
Therapy with phentolamine can improve the condition of patients with congestive heart failure due to the inotropic effect of this drug as well as its vasodilating action. Therefore, 8 patients with volume-overloaded left ventricles due to aortic insufficiency and mitral insufficiency received 50 mg of phentolamine 4 times a day for 2 weeks. Peak and end systolic wall stress were estimated using a noninvasive echocardiographic technique. The peak systolic wall stress in this group was 133 X 10(3) dynes/sq cm, which is similar to the reported normal value. However, the end systolic wall stress was 89 X 19(3) dynes/sq cm, which is much higher than the reported normal values. After PO administration of phentolamine, the end systolic stress was normalized while the peak systolic stress was reduced below normal. As a result of therapy with phentolamine, the ejection fraction, the percentage of change in the minor axis, and the velocity of circumferential fiber shortening significantly increased. Thus, PO administration of phentolamine can improve left ventricular function in patients with mitral insufficiency and aortic insufficiency.
There is considerable interest in selecting the proper drug to preserve the ischemic myocardium, or twilight zone, in a patient with a recent myocardial infarction. Vasodilator therapy with an infusion of nitroprusside or phentolamine has been shown to improve left ventricular function by reducing both preload and afterload. Sublingual nitroglycerin as well as an infusion of nitroglycerin can also alleviate left ventricular failure in patients with an acute myocardial infarction. Similarly, chronic congestive heart failure patients, irrespective of the etiology, improve hemodynamically after an infusion of phentolamine, nitroprusside or hydralazine. Oral nitrates, phentolamine, and hydralazine have also been demonstrated to produce improvement in chronic heart failure patients. Recently data has become available on the effects of phentolamine, nitroglycerin and nitroprusside on cardiac conduction in man. However there is no information on the electrophysiological properties of hydralazine in man. The present study involving 12 human subjects was undertaken to determine what effect intravenously administered hydralazine has on the human conduction system.
The influence of intravenous phentolamine on hemodynamics, ventilation, and blood gases were studied in 22 patients with cardiac disease. Phentolamine produced a significant increase in the heart rate and cardiac index and a significant decrease in the mean arterial pressure, mean pulmonary artery pressure, left ventricular end diastolic pressure, peripheral vascular resistance, and pulmonary vascular resistance. There was no significant change in the arterial pH, PO2, PCO2, alveolar-arterial PO2, and the dead space-tidal volume ratio. The favorable hemodynamic responses are attributable to the fact that the vasodilator effect of phentolamine is predominately on the arteriolar resistance bed and much less on the venous capacitance bed. In addition, phentolamine has a positive inotropic action which is indirect and dependent on the release of norepinephrine.
His bundle electrograms were recorded in 12 patients before and after the intravenous administration of 5 mEq of potassium. Antegrade and retrograde refractory periods were determined with the extrastimulus technique. The AH interval was 84 +/- 7 msec before and 89 +/- 7 msec after potassium (P < 0.05). The AH interval at an atrial pacing rate of 140/minute was 129 +/- 13 msec before and 143 +/- 16 msec after potassium (P < 0.02). The effective refractory period of the atrium was 264 +/- 9 msec before and 280 +/- 9 msec after potassium (P < 0.001). Thus small amounts of potassium delay conduction at the atrial and AV nodal level.
Explore the source record for details and available documents.
The hemodynamic effects of intravenous morphine were documented by right heart catheterization in six patients with an acute uncomplicated transmural myocardial infarction one to three days after the onset of symptoms. Intracardiac pressures, brachial artery pressure, and cardiac output were determined before and 15 minutes after the termination of the morphine infusion. Five milligrams morphine was given intravenously over a 10-minute period. The brachial artery pressure fell from a mean of 78 to a mean of 73 mm Hg (NS). As a result or morphine administration, the average cardiac index decreased from 2.68 to 2.31 liters/min-m2 (P is less than 0.05), and the stroke index decreased from 27 to 22 ml/beat-m2 (P is less than 0.05). Only small changes were observed in the intracardiac pressures.
The long term prognosis was studied in 50 patients treated for the sick sinus syndrome with pacemaker insertion. The mean age of the patients was 71 years. There were 31 females and 19 males in the series. Nine patients (18%) died during the average follow-up period of 19 months. Dizzy and syncopal episodes were abolished in most patients with pacemaker therapy. However only two of the nine patients in congestive heart failure improved with the pacemaker. Thus the long term prognosis of patients with the sick sinus syndrome is poor despite pacemaker therapy. This is particularly true for the patient in chronic congestive heart failure who does not respond to the pacemaker treatment.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.