Summary:Since 1963 the signal averaging technique has been applied to improve the signal to noise ratio in highly amplified EKG registrations. Based on the experiences from the literature and the authors own laboratory, the applications of the signal averaging technique in clinical cardiology are reviewed: extraction and analysis of the fetal EKG and P-wave variations, His bundle electrograms from the body surface (recovery rate 33-100% of cases), ventricular delayed depolarizations within the ST segment of the surface EKG (recovery rate, 40-90% of cases, depending on patient groups investigated), preatrial activity (sinus nodal potentials) from intracardiac (recovery rate, 80-90% of individuals), or surface EKGs (recovery rate, 60% of patients), analysis of frequency components of surface EKG-QRS complexes in patients with previous myocardial infarctions, and detection of low amplitude diastolic signals from surface phonocardiogram (recovery rate, 80% of cases). At present, advantages and limitations of the signal averaging technique may be appraised as follows: ( 1 ) sinus nodal potentials: S-A conduction times may be more reliable than those obtained by the extra-stimulus technique, since with averaging they are recorded during undisturbed sinus rhythm; direct recordings of changing S-A blocks may be impossible due to the summation process; validation of sinus nodal potentials in man necessary, (2) A-V nodal potentials: demonstration of true A-V nodal rhythm rather than His bundle rhythm; possibly direct identification of abnormal pathways in A-V nodal tachycardias; direct recordings of single A-V nodal blocks impossible due to summation process; (3) surface His bundle potentials: follow-up or screening of patients with A-V nodal and particularly His-Purkinje-system blocks; monitoring of antiarrhythmic drug therapy; atrial overlap in one-third of cases; direct identification of higher degree A-V nodal blocks impossible due to summation process (future developments may overcome this problem); (4) ventricular delayed depolarizations: possible identification of patients at high risk of sudden cardiac death; follow-up of therapeutic measures like antiarrhythmic drug therapy or cardiac surgery (bypass grafting, aneurysmectomy); validation of delayed depolarizations from body surface by direct intracardiac and/or epicardial mapping necessary.
The present study was performed to compare pain‐related oesophageal motility, gastro‐oesophageal reflux and ST‐segment deviations in patients with intermittent chest pain and normal or pathological coronary angiography. Thirty patients (11 males, 19 females; mean age 54.8 years) with normal and 15 patients (12 males, 3 females; mean age 66.7 years) with pathological coronary angiography were investigated by 24‐h oesophageal pressure, pH and ECG recording. Chest pain correlated with motility abnormalities or gastro‐oesophageal reflux occurred in 33% (10/30) of patients with normal coronary arteries and in 26% of patients with pathological coronary angiography. Symptomatic and asymptomatic ST‐segment changes were less frequently observed in patients with normal angiography (4/30) than in patients with pathological coronary angiography (7/14; P = 0.02). Oesophageal dysfunction coincided with ST‐segment deviation in 6.7% (2/30) of patients with normal and 40% (6/15) of patients with pathological coronary angiography (P = 0.02). The conclusions reached were: (1) pain‐correlated abnormal motility or gastro‐oesophageal reflux occurred in patients with normal and pathological coronary angiography at the same frequency; (2) ambulatory motility and pH recording alone does not appear to differentiate between cardiac and non‐cardiac chest pain; (3) simultaneous ECG recording reveals a significant correlation of ST‐segment deviation and gastro‐oesophageal reflux or abnormal motility in patients with coronary artery stenosis.
1 In 46 patients (16 female and 30 male), aged between 18 and 73 years the effect of acute P-adrenoceptor blockade with i.v. pindolol, acebutolol and atenolol has been studied at rest and during ergometric exercise, during routine intracardiac His bundle investigations. 2 At rest the functional parameters of the sinus node were impaired most markedly by atenolol. A-V nodal conduction was more depressed with acebutolol and atenolol than with pindolol. The His-Purkinje system conduction remained unaffected by all three 3-adrenoceptor blocking agents.3 During ergometric exercise the depressant action of P-adrenoceptor blockade on sinus nodal function with lower heart rates and on A-V nodal conduction with slower conduction velocities was equieffective with pindolol, acebutolol and atenolol. His-Purkinje system conduction again remained unchanged with one exception that after administration of pindolol, conduction rate during exercise was faster than before P-adrenoceptor blockade.
Sodium and potassium excretion, GFR (inulin clearance), ECF (inulin space) and TRBF (electromagnetic flowmeter) were determined in trained dogs 3 hrs after feeding either sodium poor (0.5 mEq/kg) or sodium rich (14 mEq/kg) meals.Low and high ECF's were induced by 1--4 months of low and high salt feeding, respectively. The animals could be divided into two groups according to prior dietary history.1.3 hrs after sodium rich meals animals with low ECF showed a delayed Na excretion (15°/0 of Na load) whereas animals with high ECF excreted Na at high rates (30°/0 of Na load) in the postprandial phase. The latter group received a low sodium diet a few days before the experimental period. This low sodium period was needed in order to make the two groups comparable.2. The postprandial potassium excretion was augmented in both groups, independently of the size of the ECF prior to the experiment.3. The postprandial ECF increased independently of dietary history or salt content of meals. However, the extent of increase was less after the salt poor meal (+ 12.7°/0) than after the salt rich meal (+ 25.5°/0). 4. GFR also increased postprandially. The maximum, observed on the first day of the salt rich period, amounted to 165°/0 of the preprandial value. It returned progressively during the salt rich period to the value seen in dogs with salt poor diet (131°/0). The return was accompanied by increased sodium excretion. Hence, no direct correlation between GX~R and sodium excretion was found in these experiments.5. TRBF increased postprandially up to 160°/0 of the value of the fasting animal, independently of dietary history and salt content of meals.6. Calculations of Na distribution revealed 20--144 mEq in the intracellular space in the third postprandial hour. A comparable amount of potassium was lost from this space. If a similar shift in renal cells occurs, then content of sodium within renal cells may be a regulatory factor in Na excretion.Wie unsere Untersuchungen an wachen Hunden zeigen [3,28], ist die 24 Std-Bilanz des Natriums selbst bei hoher Koehsalzzufuhr ausgeglichen, wenn der Extracellul/~rraum einen Grenzwert yon 22°/o des KSrpergewichtes erreicht hat. Bei einer t/~glichen Natriumzufuhr, die kleiner ist als der obligate renale und extrarenale Natriumverlust, verkleinert sich das ECF-Volumen im Laufe yon 16 Wochen bis auf 16°/o des KSrpergewich-
24 hour sodium and potassium balances, ECF (inulin space) and GFR (inulin clearance) were determined in trained dogs which had been maintained on high salt or low salt diets. Special attention was directed toward the transition period when animals were switched either from a low salt to a high salt intake, or vice versa.1. When salt depleted dogs were switched to a salt intake of 1.7 or 14 mEq/kg and day, ECF increased to a maximum of 22 =[= 1.7°/0 of body weight. This value was reached within 1--2 days when the higher salt intake was used, and within 8--9 days when the lower amount was added to the food.2. When, in these same dogs, salt feeding was stopped and food with about 0,5 mEq/kg and day (sodium poor diet) was given, the ECF remained unaltered for about 2 weeks. After this period it decreased continously, reaching a new steady state value of 16°/o of body weight within 4 months.3. GFI~, measured at 8 a.m. and before feeding, did not change despite these variations in ECF.4. With high sodium diet (14 mEq/kg and day) a negative potassium balance appeared. This was greatest on the first day. During a 5 day period the potassium loss was 5 times greater than the extracellular potassium store, indicating an intracellular depletion.5. These results may imply an important role for body fluid volumes in the regulation of salt balance.Uber einen Zeitraum yon 3 Jahren besch~ftigen wir uns in langfristigen Versuchen an wachen Hunden mit der Frage, welche Mechanismen an der Einstellung des Natriumgleichgewichtes bei oraler Natriumbelastung betefligt sind. Als wir zu Beginn unserer Versuche an Tieren arbeiteten, deren Vorgeschichte, besonders hinsichthch der Ern~hrung und Salzzufuhr unbekannt war, liel~en sich bald zwei Kollektive voneinander unterscheiden. Die Tiere des einen batten 24 Std nach der yon uns gew~hlten salzreichen Ernahrung (ca. 14 meq Na/kg) das gesamte aufgenommene Natrium ausgeschieden, w~hrend die Tiere des anderen Kollektives mehr oder weniger betri~chtliche Na~riumretentionen zeigten. Doch wiesen auch diese Tiere nach einigen Tagen fortgesetzter Natrium-
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