1,721,086 research outputs found

    Heart "timing" versus artery "timing". Neurovegetative effects in compensated and decompensated cardiocirculatory failure

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    The hypothesis that the main local goal of the neurovegetative cardiovascular regulation is to set and maintain the cardiac cycle and the time constant of the arterial system within a given reciprocal proportion is discussed in this paper. Drastic changes in this reciprocal proportion can induce cardiocirculatory failure. Three different models of cardiocirculatory failure (congestive, hypovolemic and anaphylactic) have been considered in order to test the hypothesis. It is possible to outline a theory that is, decompensated failure occurs at very high levels of sympathoadrenal activation, when the arterial time constant increases when compared to the cardiac cycle, owing to mechanical properties of the arterial wall

    Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure

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    Deviation of end-expiratory lung volume from the elastic equilibrium volume of the respiratory system is recognized as a cardinal feature in mechanically-ventilated patients with severe chronic obstructive pulmonary disease (COPD) and acute ventilatory failure (AVF). The presence of dynamic hyperinflation implies that alveolar pressure remains positive throughout expiration. At the end of the expiration, this positive pressure is named intrinsic positive end-expiratory pressure (PEEPi). Recent studies have suggested that, in COPD patients with expiratory flow limitation, the application of external PEEP during assisted mechanical ventilation, or the use of continuous positive airway pressure (CPAP) in spontaneously breathing patients, can counterbalance and reduce the inspiratory threshold load imposed by PEEPi, without causing further increase in lung volume and alveolar and intrathoracic pressures until a critical value of PEEP (Pcrit) is reached. Above this critical limit further hyperinflation is observed. A specific and characteristic role of PEEPi in compromising the heart function in COPD patients during AVF may be identified based on: 1) an increase in right ventricular impedance due to lung hyperinflation; 2) an increase in the venous return to the right ventricle and, consequently, a leftward shift of the septum caused by the large negative deflections in intrathoracic pressure due to the inspiratory threshold load; 3) a further increase in venous return to the right ventricle, with the eventual collapse of the vena cava caused by the expiratory recruitment of abdominal muscles; and 4) hypoxia and hypercapnia consequent to acute ventilatory failure, which may further increase right ventricular impedance and venous return to the right ventricle. All these phenomenon are directly correlated to the large negative intrathoracic pressure developed by the respiratory muscles to overcome the inspiratory threshold caused by intrinsic positive end-expiratory pressure (preload effect), and to the increase in lung volume (afterload effect). Application of positive end-expiratory pressure/continuous positive airway pressure in chronic obstructive pulmonary disease patients during acute ventilatory failure may, hence, unload the respiratory muscles as well as the heart

    Aortic pressure and heart rate patterns during the respiratory cycle in different autonomic conditions in conscious dog.

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    The relation between respiratory cycle and aortic pressure and heart rate patterns has been studied in the spontaneously breathing conscious dog in four experimental conditions: presence or absence of both vagal and sympathetic activity, presence of activity of only one autonomic branch. Chronic treatment with guanethidine was used to block adrenergic system, while acute, reversible blockade of activity in the cervical vagus was obtained by cooling the nerve. Vagal block was performed before and after guanethidine. In absence of vagal activity, aortic pressure decreased during inspiration and increased during expiration. This pattern was reversed by vagal activity, while it was enhanced by sympathetic activity. The integrative effects of the two branches are responsible for the classic "pulsus paradoxus". The comparison of the four experimental conditions is compatible with the hypothesis that variations of left ventricular preload play the major role in the regulation of ventricular output during respiratory cycle, while the relation between left ventricular output and aortic pressure is largely dependent on autonomic activity
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