Minnesota Impedance Cardiograph.
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Biomedical subjects
Publications and source records attributed to W G Kubicek.
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This paper deals primarily with the timing and source of peak (dZ/dt). In observations on human volunteers and anesthetized dogs, the peak (dZ/dt) occurred during the rapid ejection phase of the ventricles. Evidence is presented that the ascending aorta is the source of peak (dZ/dt).
Impedance cardiography was performed on 13 free-living subjects to determine the mechanism which ties modest sodium restriction to a reduction in blood pressure. During salt restriction intervention, significant decreases in systolic and diastolic blood pressure (6 and 7 mmHg) were observed associated with mild reduction in urinary sodium excretion from 176 to 85 mmol/day. The impedance cardiogram demonstrated a significant decrease in stroke volume (12 ml), which was related to a fall in diastolic pressure (r = 0.59, p less than 0.05). In the further analysis of individual parameters in Kubicek's formula calculating stroke volume, thoracic impedance (Zo/L) showed a significant increase during salt restriction and a change (delta) in ln L/Zo related significantly to delta ln diastolic pressure in linear multiple regression analysis. As thoracic impedance has been reported to reflect intrathoracic fluid content, a decrease in extracellular fluid volume was suggested as a possible mechanism of the fall in blood pressure even with modest sodium restriction.
We have noted that the impedance cardiographic waveform of patients with mitral regurgitation may show typical abnormalities not found in other forms of cardiac disease, either valvular or congenital. In order to investigate this we reviewed the impedance cardiograms of all our patients who had also undergone cardiac catheterisation, and selected two groups both of which were inclusive and complete: (1) 22 patients with the diagnosis of normal heart, and (2) 36 patients with the diagnosis of isolated mitral regurgitation. An index was calculated algebraically from the change of impedance (delta L) tracing by adding together the height of the C wave and the height of the nadir of the X descent and subtracting the height of the V wave, that is delta Z index (in units of ohms) = C + X - V. The mean delta Z index for the normal group was 1.64 and for the mitral regurgitation group 0.96 ohms. Similarly, an index was calculated from the first time derivative of the change of impedance (dZ/dt) tracing, that is dZ/dt index (in units of ohms/s) = C' + X' - V'. The mean dZ/dt index for the normal group was 1.32 and for the mitral regurgitation group 0.48 ohms/s. Though there was some overlap of individual points between the two groups, the mean values for both the delta Z index and the dZ/dt index separated the group with mitral regurgitation from the normal group with a high level of statistical significance. We concluded that mitral regurgitation might be associated with a characteristic abnormality of the impedance cardiographic waveform. In addition, an index can easily be calculated from the tracings which may be useful in identifying patients with mitral regurgitation.
beta-Histine-HCl has been shown to be effective in modifying the size of developing myocardial infarcts. In the present study the hypothesis that beta-histine increases the flow of blood through collateral channels and thus supplies blood to ligated areas of the myocardium was investigated in the dog. The methods used were measurement of retrograde coronary blood flow and angiography after coronary artery ligation. beta-Histine administration for 6 h increased retrograde blood flow 68.2--91.0% over controls. Coronary angiography demonstrated the existence of collateral channels 200--400 micrometer in diameter within the myocardium after ligation and 4 h of beta-histine administration.
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The effectiveness of beta-histine-HCL in modifying the size of developing myocardial infarcts was tested in the surgically ligated dog. Branches of the left coronary artery were ligated and a 6-hour continuous intravenous infusion of 0.24 mg/kg/min of beta-histine was administered from 0 to 120 min after ligation. The effect of this treatment was evaluated histologically in studies on acute ischemia by the use of the hematoxylin-basic fuchsin-picric acid stain for early myocardial ischemia. The treatment was also evaluated grossly in a study on chronic ischemia where the dogs were permitted to survive for 30 days before sacrifice. In these experiments the size of infarcts found in the beta-histine-treated animals was compared with those found in the saline controls. Both studies showed that the control ligations produced a large uniform area of ischemia or infarction that was greatly reduced or prevented by immediate treatment with beta-histine. Also, beta-histine was capable of significantly reducing the size of developing infarcts for up to 120 min after ligation.
This report suggests the use of a simple clinical method of codification of the most significant electrocardiographic changes as a result of the exercise stress test. It uses common abbreviations in the evaluation of the electrocardiographic findings before, during and after exercise. The five major categories to be codified include: (1) the basic electrocardiographic pattern, (2) the heart rate, (3) the pattern of ventricular conduction, (4) the pattern of rhythm and (5) the ST segment deviation. The initial sequence of five symbols indicates the findings in the preexercise electrocardiogram. This is followed by the word "to" with a subscript number. The number in subscript indicates the peak heart rate achieved during the exercise. The sequence of symbols following "to[]" serves to indicate the electrocardiographic changes observed in the postexercise period. The data codified using this system have been found to be concise and easily comparable. The familiarity of the symbols used facilitates its learning and application.
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