Biomedical subjects
Publications and source records attributed to U Freyschuss.
During the treatment of IRDS with assisted ventilation pneumothorax is a common and dangerous complication where an early diagnosis is important for the successful treatment. In this case report the continuous monitoring of transthoracic electrical impedance has proven to be a sensitive and non-invasive method to detect the development of pneumothorax long before clinical signs are manifest.
In order to study the adjustment of central circulation to postural changes and the mechanism of orthostatic fainting, the pressure in the brachial artery, the pulmonary artery, the right ventricle and heart rate (HR) were recorded in sixteen healthy young men, both supine and after tilting to 45 degrees and 90 degrees head up, before (normovolaemic, NV) as well as after (hypovolaemic, HV) withdrawal and reinfusion of (mostly) 950 g blood (about 15% of blood volume, BV). Two subjects fainted in supine HV, two in 90 degrees NV, four disclosed impending symptoms of fainting, and two fainted in 90 degrees HV. 'Fainters' differed from the others by smaller BV in relation to body height, higher HR in 90 degrees NV and lower arterial mean pressure in HV. In the three fainting situations, right ventricular enddiastolic pressure (PRveD) was markedly lowered to or below 0 mmHg. Arterial diastolic pressure (PaD) was not correlated with PRveD, but the pulse pressure decreased with the fall in PRveD. In 90 degrees HV, PaD fell in the six subjects who fainted or disclosed impending symptoms. Irrespective of the situation, the fainting attack involved a sudden decrease of HR and arterial pressure, concomitantly with a first unchanged then increased PRveD and/or pulmonary artery diastolic pressure. A reflex control of the filling volume/pressure of the heart is assumed to precipitate fainting by counteracting the arterial blood pressure regulation.
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During the years 1965--1974, 125 cases of posterolateral diaphragmatic hernia have been operated at five departments of pediatric surgery in Sweden. The overall operative mortality was 50%. A follow-up investigation included 19 cases, where in 12 cases spirometry and in 11 cases studies of the mobility of the diaphragm were included. Physical examination revealed excellent results in most cases. Lung function studies, however, show a moderate (20--30%) reduction, which is not surprising with regard to lung hypoplasia and impaired movement of the diaphragm on the operated side. In adolescence and younger age, these patients are mostly in excellent condition; but later, when lung function is also reduced by the age factor, their neonatal condition may be of importance.
The effect of tidal volume (VT) and of the intrathoracic pressure (Poes) on the respiratory sinus arrhythmia (RSA) was studied in healthy subjects. They breathed into a spirometer with a VT of 1, 1.5, and 2 1, at a standardized, slow respiratory rate, 6-min-1 (A). Poes was varied by (B) adding a negative inspiratory pressure (NIP) of 5 cm of water and by (C) intermittent positive pressure ventilation (IPPV) at identical VT and respiratory frequency. In separate study (D), intermittent negative pressure ventilation (INPV) was induced by applying negative pressure on the thorax. In A, increasing VT provoked an augmented RSA by a more marked tachycardia as well as bradycardia. On increasing the amplitude of Poes in B, RSA was somewhat more marked due to a lower minimum heart rate. Whem comparing respiratory cycles that had similar Poes but a different VT, the larger VT caused a slight increase in the RSA amplitude due to a more marked deceleration of the heart rate. IPPV almost abolished RSA, whereas INPV did not reduce the arrhythmia. It is concluded that pulmonary stretch reflexes to a minor extent contribute to RSA, whereas the hypothesis of a central nervous origin does not gain support. Cardiovascular reflexes remain the main possible cause of RSA.
The relationship of respiratory sinus arrhythmia (RSA) to the accompanying oscillations of cardiovascular pressure has been studied in five healthy subjects. Tidal volume (VT) of 1.0, 1.5, and 2.0 1 at the breathing rate of 6 c-min-1 were used as reference. With identical VT oesophageal pressure was varied by negative inspiratory pressure (NIP) and intermittent positive-pressure ventilation (IPPV). Compared with control, NIP with 1.01 significantly increased RSA, the oscillations of brachial artery pressures (PBA), and the net filling pressures of the ventricles. IPPV did not significantly change the variations of PBA but reduced RSA and the respiratory variations of the right ventricular end-diastolic net pressure. During control breathing and with NIP the acceleration of heart rate during inspiration was associated with rising PBA and rising net filling pressures of both ventricles. The results indicate that RSA may be elicited by cardiovascular reflexes due to changes in venous filling of the heart rather than by the variations in systemic arterial pressure.
The respiratory effects on heart rate (HR), right ventricular stroke volume (SV RV) and the pulmonary arterial flow (PAF) have been studied beat-by-beat in seven conscious, healthy subjects. Tidal volumes (VT) of 1.0 and 2.0 liters at a breathing rate of 6 c x min-1 were used as controls. With identical VT and respiratory rate intrathoracic was affected by (A) negative inspiratory pressure (NIP) of 5 cm of water and (B) with intermittent positive pressure ventilation (IPPV). In the control experiments all subjects exhibited an inspiratory increase in HR (respiratory sinus arrhythmia) as well as in SV RV. With VT of 1.0 liter, NIP augmented the inspiratory increase in SV RV and the respiratory oscillations of PAF. IPPV decreased SV RV and HR during inspiration. It is concluded that NIP and IPPV affect the SV RV and the right heart blood flow. The similar effects on HR and SV RV suggest a causal relationship which might be explained by heart rate regulating reflexes from the heart.
The relationship of repiratory sinus arrhythmia (RSA) to the accompanying oscillations of cardiovascular pressures has been studied in five healthy subjects. Tidal volumes (VT) of 1.0, 1.5, and 2.0 1 at a breathing rate of 6 c-min(-1) were used as reference. With identical VT, oesophageal pressure was varied by negative inspiratory pressure (NIP) and intermittent positive-pressure ventilation (IPPV). Compared with control, NIP with 1.01 significantly increased RSA, the oscillations of brachial artery pressures (PBA), and the net filling pressures of the ventricles. IPPV did not significantly change the variations of PBA but reduced RSA and the repiratory variations of the right ventricular end-diastolic net pressure. During control breathing and with NIP the acceleration of heart rate during inspiration was associated with rising PBA and rising net filling pressures of both ventricles. The results indicate that RSA may be elicited by cardiovascular reflexes due to changes in venous filling of the heart rather than by the variations in systemic arterial pressure.
The respiratory effects on heart rate (HR), right ventricular stroke volume (SVRV), and the pulmonary arterial flow (PAF) have been studied beat-by-beat in 7 conscious, healthy subjects. Tidal volumes (VT) of 1.0 and 2.0 liters at a breathing rate of 6 cXmin-1 were used as controls. With identical VT and respiratory rate intrathoracic pressure was affected by (A) negative inspiratory pressure (NIP) of 5 cm of water and (B) with intermittent positive pressure ventilation (IPPV). In the control experiments all subjects exhibited an inspiratory increase in HR (respiratory sinus arrhythmia) as well as in SVRV. With VT of 1.0 liter, NIP augmented the inspiratory increase in SVRV and the respiratory oscillations of PAF. IPPV decreased SVRV and HR during inspiration. It is concluded that NIP and IPPV affect the SVRV and the right heart blood flow. The similar effects on HR and SVRV suggest a relationship which might be explained by heart-rate-regulating reflexes from the heart.
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In eight healthy men 950 g of blood (12.2 17.6% of the blood volume) was withdrawn and reinfused after about half an hour. Respiration and circulation were studied by analyses of expiratory gas, blood gases and data from right heart catheterization. On hemorrhage oxygen uptake and cardiac output decreased by 10 and 28%, repectively; both varied indirectly with the blood loss. The pressures in the right ventricle, pulmonary and systemic arteries fell without relation to the cardiac output. Mean heart rate did not change significantly, but a moderate positive covariation (P less than 0.05) between heart rate and arterial blood pressure was found during bleeding. This result was confirmed by the relative bradycardia noted in the period prior to reinfusion. On refilling of the bood the oxygen uptake and the pulmonary arterial pressures increased above the initial value. The heart rate varied directly with the arterial pressure also during reinfusion. The observations demonstrate a depression of the metabolism and circulation on moderate hemorrhage. Part of these effects is tentatively referred to a lowered set point of the arterial baroreflexes.
Arm and leg work was performed on bicycle ergometers in sitting position by fourteen women and sixteen men. Heart rate, minute volume of ventilation (VE), and oxygen consumption (VO2) were measured. Arm exercise was performed until (muscular) exhaustion, leg exercise up to a heart rate of circa 170 beats/min. At comparable work loads arm exercise evoked higher VO2, VE, and heart rate than leg exercise irrespective of sex. At comparable VO2, the heart rate and VE were higher during arm work in both sexes, VE more so among the men. With the same limbs working, the mechanical efficiency was equal in both sexes. The regression coefficients of heart rate on load or VO2 was higher for the women irrespective of work type. A close correlation was obtained between working capacity at a heart rate of 170 beats/min (W170) during leg and arm exercise and between W170 of leg exercise and W150, similarly calculated during arm work. Thus W170 of leg exercise could be calculated from either a maximal or submaximal arm work.
The effect of tidal volume (VT) and of the intrathoracic pressure (Poes) on the respiratory sinus arrhythmia (RSA) was studied in healthy subjects. They breathed into a spirometer with a VT of 1, 1.5, and 2 1, at a standardized, slow respiratory rate, 6-min-1 (A). Poes was varied by (B) adding a negative inspiratory pressure (NIP) of 5 cm of water and by (C) intermittent positive pressure ventilation (IPPV) at identical VT and respiratory frequency. In a separate study (D), intermittent negative pressure ventilation (INPV) was induced by applying negative pressure on the thorax. In A, increasing VT provoked an augmented RSA by a more marked tachycardia as well as bradycardia. On increasing the amplitude of Poes in B, RSA was somewhat more marked due to a lower minimum heart rate. When comparing respiratory cycles that had similar Poes but a different VT, the larger VT caused a slight increase in the RSA amplitude due to a more marked deceleration of the heart rate. IPPV almost abolished RSA, whereas INPV did not reduce the arrhythmia. It is concluded that pulmonary stretch reflexes to a minor extent contribute to RSA, whereas the hypothesis of a central nervous origin does not gain support. Cardiovascular reflexes remain the main possible cause of RSA.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.