[Current aspects of pacemaker therapy].
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Biomedical subjects
Publications and source records attributed to E Volger.
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The effects of parenteral nitroglycerin after acute and continuous infusion were investigated in 12 patients with mitral and (or) aortic valvular disease (stage IV of the New York Heart Association) and severe therapy-resistant pulmonary congestion. Intravenous injection of 1 mg led to immediate and marked decrease of right atrial mean pressure, and pulmonary artery and pulmonary capillary mean pressures, whereas mean arterial blood pressure, stroke volume index, cardiac frequency, and cardiac index remained unchanged. With a dosage of 3-10 mg/h the pressure lowering of the right circulation could be sustained. Pressure lowering of the right circulation abolished pulmonary congestion and led to marked reduction of shortness of breath. The principle of venous pooling can thus not only be used successfully in cases of increased pulmonary capillary pressure due to primary myocardial insufficiency, but also in cases with pulmonary congestion due to decompensated valvular disease.
The flow properties of blood are abnormal in diabetes. The red cell deformability (RCD) is reduced and depends on the metabolic state, the red cell aggregation (RCA) and plasma viscosity are increased independent of the metabolism. 157 diabetics were studied according the following nosological factors: duration of diabetes, type of therapy, ophthalmoscopic status, metabolic state and general health status. Although a deterioration of the flow properties of blood can be observed in long-term diabetics, in patients receiving antidiabetic drugs or insulin and in cases of pronounced retinopathy, these changes can all be attributed to a higher incidence of insufficiently controlled metabolism and the presence of subsequent diseases. There is some evidence that the rheological changes cannot be neglected considering the development and progression of diabetic microangiopathy.
Ten patients in severe cardiac failure were treated with dopamine (4 microgram/kg . min) and dobutamine (7.5 microgram/kg.min). Both drugs brought about a similar increase in stroke volume and cardiac output of about 50% and 60%, respectively, accompanied by a fall in peripheral vascular resistance of about 33%. On dopamine the heart rate increased by 12%, but remained unaltered on dobutamine. There was a significant fall in the preload of both ventricles with dobutamine, while ventricular filling pressure during dopamine infusion was only slightly decreased, unchanged or even increased. The pulmonary (wedge) pressure during dopamine infusion averaged 9 mm Hg higher than during dobutamine (P less than 0.001). There is thus the potential danger with dopamine of aggravating pulmonary congestion. Furthermore, the improvement in cardiac function due to dopamine is at the expense of a higher oxygen demand than with dobutamine. Dobutamine is, therfore, preferable to dopamine in the treatment of advanced myocardial failure.
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24 patients with bradycardiac arrhythmias of various origin were treated with a new depot preparation of orciprenaline. The special galenical preparation guarantees effectiveness ofr 8-10 hours. In 21 patients (87%), therefore, one dragee morning and evening was sufficient to obtain a mean rise in frequency of 57%. The preparation had to be discontinued in 3 cases because of side effects such as increase in ventricular extrasystoles, anginal complaints and critical rise of blood pressure in hypertension. Because of its trouble-free administration in a depot form the preparation not only offers a practical advantage over the short-acting commercial preparations, but also shows a reliable efficacy. It can therefore be given under regular supervision in all forms of bradycardiac arrhythmias with stable ventricular frequency and satisfactory cardiac output.
The rheological behavior of normal and pathological red cell aggregates in viscometric flow (artificial flow in cone plate chamber) is studied by direct microscopy, (rheoscopy) viscometry and photometry. Marked differences between normal and pathological blood are measured in the microrheological properties of red cell aggregates; only discreet differences are measured by blood viscometry (macrorheology). Both in normal and abnormal blood, red cell aggregation is a reversible process in the presence of adequate shear forces; their respective influences on apparent blood viscosity at low rates of shear are complex functions of shear rate, shear time, hematocrit and plasma viscosities. Pathological red cell aggregation (RCA) forms more rapidly and extensively than normal RCA. The pathological aggregates frequently have a tendency to grow at low rates of shear and they are highly shear resistant.
The apparent viscosity of blood strongly increases at low shear in rotational viscometers, this phenomenon is based on the reversible formation of red cell aggregates. The magnitude of this increase strongly depends on the hematocrit value, on plasma viscosity and lastly on the microrheological properties of the aggregates. The independent measurement of the microrheological behavior and the effects on viscosity allows a detailed analysis of the hemodynamic effects of red cell aggregates under defined flow conditions in vivo. The comparative analysis shows that the conventional viscometry strongly underestimates the rheological differences between normal and pathologically intensified aggregation. Based on detailed analysis under defined flow conditions in vitro, the biological significance of viscometric results and the hemodynamic relevance of red cell aggregates are discussed.
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The anomaly of the viscosity of human blood is more pronounced in diabetics. This is caused by an increase in plasma viscosity, a more pronounced red-cell aggregation, and a reduction of individual cell deformability. The changes in viscosity and in red-cell aggregation both are the consequence of abnormal plasma proteins, the incidence of which is largely independent of the onset and duration of disease, and actual metabolic state. The presence of complicating infectious diseases further aggravates the pathologic red-cell aggregation. The decreased red-cell deformability is largely independent on onset, duration, and complications but depends critically in the incident metabolic control of the diabetics. The possible role of hemorrheologic factors in the development of microangiopathy is discussed.
74 patients (hypocalcemia: 41 patients, hypercalcemia 13 patients, 20 patients as control) without heart disease were examined. A prolongation of the relative QT-interval was found in 90% and a flat or inverted T-wave in 25% of the patients with hypocalcemia. In 77% of the patients with hypercalcemia the QT-interval was shortened. A good, clinically useful correlation between the QT-interval and the serumcalcium-concentration could be established in patients with hypo- and hyper-calcemia.
163 patients (95 hypokalemic, 48 hyperkalemic, 20 healthy) were examined. Electrocardiographic patterns of hypokalemia were evident in 46 p.c. of all patients with serum potassium less than 3,5 mval/l. Patients without cardiac disease showed signs of hypokalemia in the ECG in 68 p.c., those cases with extremly low serum potassium (less than 2,5 mval/l) in 81 p.c. In patients without cardiac disease a good correlation could be observed between ST depression and T wave inversion on one side and serum potassium level below 3,5 mval/l on the other side. The T/U ratio was found to be below unity in only 9 p.c. in mild hypokalemia, but in 82 p.c. in severe hypokalemia. ECG pattern of hyperkalemia could be found in 29 p.c. of all patients with serum potassium levels greater than 5,1 mval/l. These signs were evident in patients without cardiac disease in 29 p.c. in mild hyperkalemia, but in 75 p.c. in severe hyperkalemia. Patients suffering from cardiac disease, however showed the correspondive ECG changes of hyperkalemia only in 5 p.c. There is a good correlation between the P, and T-wave-amplitude and the serum potassium level greater than 5,1 mval/l. According to our findings it can be stated, that the ECG changes in patients with cardiac disease tend to hide the correspondive changes of potassium disorder.
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The formation of primary (rouleaux) and secondary (rouleaux networks) RCA was studied by microcinematography (12 frames/sec) and photometry in a counterrotating "rheoscope" chamber. The blood was first subjected to rapid viscometric flow (460 sec-1, all RBC dispersed and aligned in flow) and then brought abruptly to full stop. In normal human blood, primary and secondary RCA occurred simultaneously, and were completed within 8 to 10 sec after stop. Blood from pregnant women at term, known for its pronounced red cell aggregation, shows a dissociation between the formation of short primary rouleaux (initiated even before full stop and completed 1-2 see thereafter) and secondary RCA completed 3-5 see after stop. RCA increases the light transmission of blood (measured by an increase in photovoltage V), the process and its first derivative (dV/dt equals I) can be recorded. After flow stop, there is an exponential decay of I(I equals t-I-o with e-lambda-t). The half time of this decay is recorded and correlated to the kinetics of red cell aggregate formation In human blood the half time of this process varies between 1.0 and 6.0 sec. In suspensions of human RBC in artificial plasmas, t-1/2 decreases with increasing concentration of fibrinogen and/or Dextran 250000, the second component appearing at concentrations above 500 mg-%. The method lend sitself for the quantification of RCA in small blood samples (20 mul).
Employing both microscopic and photometric methods the rheology of pathological red cell aggregation was studied in model experiments. Suspensions of washed human red blood cells in dextran solutions containing rising concentrations of dextrans (M.W. 40000, 70000, 110000, 250000, 500000) were used. At low concentrations (less than 500 mg-%) of high molecular weight dextrans (greater than 70000) red cell suspensions formed aggregates similar to the ones found in normal human blood. At higher concentrations, the aggregates were similar to those observed in pathological human blood. The aggregates were studied under the condition of stasis, slow flow and at shear rate of their hydrodynamic dispersion. Besides, the flow behavior of the dispersed cells at high shear rates was studied. We found: 1. In all samples the rate of spontaneous aggregate re-formation in stasis (following hydrodynamic desaggregation) rose with rising dextran concentration up to 5.0 g-%. 2. The shear resistance of the aggregates, as measured by the shear stress necessary to keep them dispersed, rose up to concentrations of 2.5g-%, but fell at higher concentrations. 3. Only with dextran of a molecular weight above 110000 coarse agglomerates could be produced at high concentrations. Loose elastic meshes were rapidly produced at high concentrations of Dx 70. 4. When subjected to steady state low shear (m sec-1) only the agglomerates, but not the meshes rapidly grew in size. Most of the aggregation kinetics recorded by photometry and microscopy evaded detection by viscometry.