C L Alviar, G Tavazzi
The cardiovascular and pulmonary systems are closely intertwined. The cardiovascular and pulmonary systems are closely intertwined through pressure-dependent interactions that change during the respiratory cycle. These interactions differ substantially between spontaneous breathing and positive-pressure ventilation (PPV). As a result, spontaneous breathing and PPV have distinct effects on right ventricular (RV) and left ventricular (LV) hemodynamics. The taxonomy required to understand these interactions relies on four key pressure domains. The Airway pressure (the pressure within the respiratory tract during breathing). The intrathoracic pressure (the pressure within the pleural cavity surrounding the lungs). The driving pressure which is the distending pressure to the lung to generate tidal volume (calculated as plateau pressure-Pplat- and PEEP). And the transmural pressure which in the context of heart–lung interactions it is primarily defined as the pressure gradient between the intracavitary pressure of the left ventricle or aorta and the surrounding intrathoracic pressure. During the inspiratory phase of spontaneous breathing, contraction of the respiratory muscles (diaphragm and intercostal muscles) expands the thoracic cavity. This leads to a reduction of intrathoracic pressure (and airway pressure-Paw), increasing the pressure gradient from the abdominal venous pool to the right atrium, hence increasing venous return and RV preload. Simultaneously, the negative intrathoracic pressure expands the lung parenchyma promoting pulmonary vascular recruitment and slightly decreasing RV afterload. In contrast the fall of intrathoracic pressure increases LV transmural pressure, increasing the systemic afterload.1 During spontaneous inspiration, the preload to the LV may increase, remain stable or decrease These effects depend on RV and LV size, ventricular interdependence, septal mechanics, and the presence of pericardial disease.2