[Superior vena cava syndrome. Surgery of thrombosis of the right atrium immediately after intravenous fluid therapy is preferable].
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Publications and source records attributed to C Lamm.
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We investigated the effects of halothane, enflurane, and isoflurane on central hemodynamics and left ventricular global and regional function when used to control intraoperative hypertension in 39 patients with coronary artery disease. Left ventricular short-axis, midpapillary images were obtained by transesophageal echocardiography. Using a centerline algorithm, we analyzed left ventricular images for global area ejection fraction (GAEF) and segmental area ejection fraction (SAEF). The SAEF/GAEF ratio was calculated for each of eight segments. Measurements were performed after induction of anesthesia but before skin incision; 1 min after sternotomy; and during administration of the inhaled anesthetic. The increase in arterial blood pressure during sternotomy was due to an increase in vascular resistance accompanied by increases in heart rate and filling pressures while GAEF decreased. No changes in the SAEF/GAEF ratio appeared during sternotomy. The inhaled anesthetics restored arterial blood pressure by a similar decrease in vascular resistance. Isoflurane caused an increase in cardiac index that was not seen with halothane or enflurane (halothane vs isoflurane, P < 0.05). The GAEF was decreased by halothane but unaffected by isoflurane and enflurane (halothane vs enflurane; P < 0.05). Isoflurane induced a decrease in the SAEF/GAEF ratios of two segments corresponding to the inferolateral wall of the left ventricle that was, in one of these segments, significantly more pronounced compared with both halothane and enflurane. Halothane or enflurane did not cause any change in regional wall motion. We conclude that isoflurane is more likely to cause regional wall motion changes than halothane or enflurane in patients with coronary artery disease.
A newly constructed pressure sensor with a diameter of 0.45 mm was evaluated in 15 patients undergoing balloon coronary angioplasty (PTCA). The sensor and an optic fiber were mounted on a 0.018" guide wire, which was used in the balloon catheter. Pressure gradients were recorded before and after PTCA, respectively. The pressure tracings were of satisfactory quality in all cases. The mean systolic and diastolic gradients before PTCA were 32 +/- 20mm Hg and 44 +/- 26mm Hg, respectively. Pressure gradients were also obtained with the balloon placed in the lesion in order to simulate the conventional way of pressure measurement through the balloon catheter. In this setting, the systolic and diastolic gradients were 77 +/- 32mm Hg and 59 +/- 25mm Hg, respectively. Following balloon dilatation, the systolic pressure gradient decreased to 14 +/- 12mm Hg, and the diastolic gradient to 13 +/- 11mm Hg. In conclusion, this new pressure sensor delivers recordings of good quality and may be especially of interest during angioplasty due to its small diameter.
Restenosis after percutaneous transluminal coronary angioplasty (PTCA) cannot currently be prevented. Different medical regimens have been largely unsuccessful. Experimental studies suggest roles for beta-adrenergic blockers and calcium antagonists. Controlled clinical studies have failed to show any decrease in restenosis rate for calcium antagonists. Corresponding studies for beta blockers are lacking. This study evaluates 541 consecutive PTCA procedures, 455 (86%) in patients treated with beta blockers after PTCA (76% metoprolol, 14% atenolol, 4% sotalol, 6% others) and 86 (14%) in patients without beta blockers. Angiographic success was achieved in 483 of 620 lesions (78%), and was not significantly different with or without beta blockers (79 vs 73%, p greater than 0.05). The procedure success rate and the complication rates (myocardial infarction, emergency coronary artery bypass grafting, death) did not differ with or without beta blockers (p greater than 0.05). Follow-up angiograms for 426 of the 483 successfully dilated lesions (88%) revealed that a total of 155 stenoses had recurred (36%). The restenosis rate was not significantly different with (368) or without (58) beta blockers (36 vs 38%, p greater than 0.05). For beta blockers with calcium antagonists (84% nifedipine, 13% diltiazem, 2% verapamil, 1% others), the restenosis rate was 97 of 250 (39%) vs 36 of 118 (31%) (p greater than 0.05). This retrospective study indicates that treatment with beta-adrenergic blockers after PTCA, alone or in combination with calcium antagonists, does not influence either the success rate or the restenosis rate and can be continued if indicated from an antiischemic viewpoint.
The effect of cardiac sympathetic blockade by high thoracic epidural anesthesia (TEA) (T1-T6, bupivacaine) on the luminal diameter of normal and diseased portions of epicardial coronary arteries was determined by quantitative coronary angiography in patients (n = 27) with severe coronary artery disease (CAD). In a separate group of patients (n = 9) with severe CAD, the effects of TEA on coronary arterioles (resistance vessels) were studied, by measuring total and regional myocardial blood flow and metabolism with the retrograde coronary sinus thermodilution technique. At the stenotic segments, TEA induced an increase in luminal diameter from 1.34 +/- 0.11 to 1.56 +/- 0.13 mm (P less than 0.002), but did not change the diameter of the nonstenotic segments (3.07 +/- 0.13 to 2.99 +/- 0.13 mm). In the second group of patients, TEA induced no changes in coronary perfusion pressure, total or regional myocardial blood flow, coronary venous oxygen content, coronary blood flow distribution, regional myocardial oxygen consumption, or lactate extraction or uptake. Two patients had chest pain in the control situation and had regional myocardial lactate production that was attenuated by TEA. We conclude that TEA may increase the diameter of stenotic epicardial coronary artery segments in patients with CAD without causing a dilation of coronary arterioles. These effects may be beneficial when high TEA is used to treat severe ischemic chest pain in patients at rest.
Nineteen guinea pigs were exposed to impulse noise from gunfire (G3 of the Federal German Army, 156 dB peak SPL), 6+6 shots or 12+6 shots, with a 3-s pulse interval. For simultaneous measurements of pO2, cochlea microphonics (CM) and compound action potentials of the auditory nerve (CAP), we used the thin 0.5 microns microcoaxial needle electrode described by Baumgaertl and Luebbers, which was placed through the roundwindow membrane into the scala tympani to a depth of 1000 microns. After exposure to the first 6 or 12 gunshots, the pO2 increased by about 20% of the original values in 12 guinea pigs (63%). In the following 30 min of recovery time the pO2 decreased, stabilized or showed a further decline. There were only 3 animals with a pO2 loss of 70% of the original values. Most animals showed a decline of 25% at the end of the recovery period. In all animals after 6 additional shots, the pO2 only decreased by another 5% of the original values. Amplitudes of CM and CAP were reduced by about 40% of the original values after 6 or 12 shots and by another 20%-24% (CM) and 5%-15% (CAP) after 6 additional shots. The intra-arterial blood pressure in the common carotid artery remained constant. The results are discussed with respect to the well-known morphological damage, subsequent ion imbalance and hypoxia within the cortilymph after exposure to gunfire. These changes are reflected in the loss of CMs and CAPs.
The purpose of this study was to examine the influence of hyperbaric oxygen on the oxygen tension (pO2) in the normal inner ear. We examined 16 anaesthetised guinea pigs by means of an oxygen-sensitive micro-coaxial needle electrode, using the method described by Baumgaertl and Luebbers. In all animals the pO2 in the perilymph of the scala tympani fell by 34% of the original value during insertion of the sensor into the scala tympani. After we had flooded the hyperbaric chamber with pure oxygen under normobaric conditions the pO2 increased by 244.3% of the original values. Furthermore the pO2 increased by 9.4 times the original values during hyperbaric oxygen at 1.6 bar.
In 14 guinea pigs the pO2 in the perilymph of the scala tympani fell to 50%-80% of the original value during exposure to noise consisting of 4,000 Hz clicks with a repetition rate of 20/s, 100 dB CHL = 120 dB SPL p.e., repeated twice over a period of 24 minutes each time. For the measurements of the pO2 we used the thin 0.5 micron micro-coaxial needle electrode described by Baumgärtl and Luebbers, which was placed through the round-window membrane in the scala tympani to a depth of 600 micron. The simultaneously recorded CAP latency times were prolonged by 0.8 ms at a test loudness of 60 and 80 dB CHL. The amplitudes of the CM had declined by 60%-70% of the original values at a test loudness of 80 dB SPL p.e. The intra-arterial blood pressure in the common carotid artery of all animals remained constant. As the cortilymph spaces communicate with the perilymph of the scala tympani, our measured decline of pO2 in the perilymph could indicate a cortilymph hypoxia. During exposure to noise the oxygen-dependent Na+ and K+ pumps, which maintain the ion balance and function of the organ of Corti, can decompensate due to lack of oxygen. That would lead to a K+ contamination of the cortilymph and to an intracellular Na+ accumulation, which can cause microstructural damage (hair cell-cilia fusion, hair cell, synaptic and dendritic swelling, hair cell contraction and sustained depolarization), which would be reflected in the CMs and CAPs.
Our earlier animal experiments on guinea pigs showed that instrumental perforation of the round window membrane by a 0.2 mm platinum wire leads to an instant loss of the inner ear functions. The membrane defect healed in a few days, the cochlear structures remained intact, and the compound action potential of the auditory nerve and the brain-stem responses could be evoked again with normal latency times within 2 weeks. 1. In the studies reported here we first carried out microperforations with a 1 micron needle electrode, which caused no changes of the hearing potentials (cochlear microphonics, compound action potential of the auditory nerve, brain-stem responses), and no visible defect of the round window membrane and no perilymph outflow. 2. The removal of the round window membrane and the withdrawal of the perilymph led to a loss of the cochlear microphonics and to a considerable increase of the latency times of wave I (Jewett). The hearing potential regained their original values after 2 weeks without closure of the round window niche. The round window membrane had regenerated spontaneously and the scala tympani was again filled with perilymph. After covering the round window niche with a connective tissue graft, the hearing potentials regained their original values after 2 weeks, as they had done without cover of the round window niche. The round window membrane regenerated below the tissue graft and the scala tympani was also filled again with perilymph.(ABSTRACT TRUNCATED AT 250 WORDS)
We studied the ability to predict depressed left ventricular ejection fraction (LVEF) from clinical and exercise test findings prior to surgery in consecutive patients who underwent coronary artery bypass grafting (CABG) from 1988 to 1991 (n = 663). Multivariate analysis showed a history of myocardial infarction, pathological Q-wave in resting ECG, systolic blood pressure at maximal exercise and the degree of mitral regurgitation as significant independent predictors of impaired LVEF. The relative risk (RR) of depressed LVEF was markedly increased for a previous history of myocardial infarction (RR 3.3, p < 0.0001) and a pathological Q-wave in resting ECG (RR 2.4, p < 0.0001). All associations found between depressed LVEF and exercise test results were poor, and of little value for discriminating patients with depressed LVEF. Thus, clinical data appear to be better markers of low LVEF than the information obtained from the exercise test.
Cardiac output was determined with an indicator dilution technique during digital venous angiography of the left ventricle in 11 patients. The contrast medium injected into the right atrium was used as indicator. During and after the injection of contrast medium one blood sample per second was obtained through a catheter placed in the descending aorta. The samples were analyzed for iodine content with x-ray fluorescence analysis and cardiac output determined ad modum Stewart-Hamilton. Thermodilution was used as a reference method. The results indicate that the indicator dilution method with the use of contrast medium might be used for calibration of videodensitometric methods for blood flow measurements.