Cardiovascular Function in Cor Pulmonale

Matthay, Richard A.; Berger, Harvey J.

doi:10.1016/s0272-5231(21)00202-1

Cited by 47 publications

(2 citation statements)

References 142 publications

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“…The implication is a potential link between abnormal mechanics of breathing and impaired exercise performance via the circulation rather than a malfunctioning ventilatory pump per se. 32 In this regard, it is well known that changes in respiratory mechanics and intrathoracic pressure surrounding the heart may influence cardiac function, [54][55][56][57][58][59][60] can reduce cardiac output by affecting the return of blood to the heart from the periphery (systemic venous return), or by interfering with the ability of the heart to eject blood into the peripheral circulation [left ventricular (LV) dysfunction]. LV performance can also be influenced by the effect of an increased negative pressure which acts according to two basic mechanisms: increased right ventricular afterload 57 and increase in left ventricular transmural pressure.…”

Section: Vascular Factorsmentioning

confidence: 99%

“…LV performance can also be influenced by the effect of an increased negative pressure which acts according to two basic mechanisms: increased right ventricular afterload 57 and increase in left ventricular transmural pressure. [58][59][60] Aliverti et al 27 and Iandelli et al 28 stressed the role of increase in expiratory chest wall pressure which shifts the blood flow from trunk to extremities in man. Iandelli et al 28 maintain that high expiratory pressures cause severe dyspnea and the possibility of adverse circulatory events, both of which would impair exercise performance.…”

Section: Vascular Factorsmentioning

confidence: 99%

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Pathophysiology of exercise dyspnea in healthy subjects and in patients with chronic obstructive pulmonary disease (COPD)

Grazzini

Stendardi

Gigliotti

et al. 2005

Respiratory Medicine

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In patients with a number of cardio-respiratory disorders, breathlessness is the most common symptom limiting exercise capacity. Increased respiratory effort is frequently the chosen descriptor cluster both in normal subjects and in patients with chronic obstructive pulmonary disease (COPD) during exercise. The body of evidence indicates that dyspnea may be due to a central perception of an overall increase in central respiratory motor output directed preferentially to the rib cage muscles. On the other hand, the disparity between respiratory motor output and mechanical response of the system is also thought to play an important role in the increased perception of exercise in patients. The expiratory muscles also contribute to exercise dyspnea: a decrease in Borg scores is related to a decrease in end-expiratory lung volume and to a decrease in end-expiratory gastric pressure at isowork after lung volume reduction surgery. Changes in respiratory mechanics and intrathoracic pressure surrounding the heart can reduce cardiac output by affecting the return of blood to the heart from the periphery, or by interfering with the ability of the heart to eject blood into the peripheral circulation. Change in arterial blood gas content may affect breathlessness via direct or indirect effects. Old and more recent data have demonstrated that hypercapnia makes an independent contribution to breathlessness. In hypercapnic COPD patients an increase in PaCO2 seems to be the most important stimulus overriding all other inputs for dyspnea. Hypoxia may act indirectly by increasing ventilation (VE), and directly, independent of change in VE. Finally, chemical (metabolic) ventilatory stimuli do not have a specific effect on breathlessness other than via their stimulation of VE. We conclude that exercise provides a stimulus contributing to dyspnea, which can be applied to many diseases.

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Section: Vascular Factorsmentioning

confidence: 99%

Section: Vascular Factorsmentioning

confidence: 99%

Pathophysiology of exercise dyspnea in healthy subjects and in patients with chronic obstructive pulmonary disease (COPD)

Grazzini

Stendardi

Gigliotti

et al. 2005

Respiratory Medicine

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Acute on Chronic Respiratory Failure

Schmidt

Hall²

1989

JAMA

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Patients with acute or chronic respiratory failure exhibit severe pulmonary impairment as a baseline characteristic. Additional minor insults can precipitate cardiopulmonary failure that requires hospital admission and possibly mechanical ventilation. Our approach to these patients emphasizes evaluation of the imbalance between neuromuscular competence and mechanical load on the respiratory system. In this way, reversible factors can be identified and corrected before they progress to inspiratory muscle fatigue and respiratory failure. For cases in which deterioration is inexorable, guidelines for mechanical ventilation are given and approaches to eventual liberation from the ventilator are reviewed.

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