In spontaneous breathing, the contractions of the diaphragm and intercostal muscles reduce ITP, leading to a greater pressure gradient according to the values of atmospheric and airway pressure. The decrease in ITP is transmitted to the intrathoracic organs, resulting in a fall in cardiac P _ex and a rise in P _tm. The increase in P _tm promotes RV diastolic filling. Consequently, RV increases stroke volume via the Frank-Starling mechanism [5]. The subsequent rise in pulmonary flow increases LV pressure load and its end-diastolic volume. Also, LV P _ex falls and P _tm rises during inspiration, increasing LV afterload during the systole. As a result, LV stroke volume and systolic blood pressure fall and LV end-systolic volume rises [5]. Thus, the main consequences of the decrease in ITP during spontaneous breathing are an increase in LV afterload and an increase in RV preload (Table 2.1).

In healthy subjects, spontaneous inspiration is usually associated with a slight fall in systolic blood pressure (<10 mmHg). During spontaneous inspiration, both P _pl and intravascular aortic pressure fall, but the fall in P _pl is relatively greater than the fall in aortic pressure, increasing P _tm and resulting in an increased LV afterload and a reduction in LV stroke volume.

Increased respiratory efforts with a greater variation of P _pl and P _tm, as in asthma and pulmonary edema, or increased sensitivity to changes in P _tm in the heart, as in hypovolemia and congestive cardiac failure, leads to a decrease in systolic blood pressure during inspiration more than 10 mmHg, creating pulsus paradoxus [3].

The effect of spontaneous breathing on pulmonary blood vessels is generally irrelevant and hardly ever causes a significant drop in systolic pressure. In addition, changes in lung volumes during spontaneous ventilation rarely determine an increase in PVR.

Neurohumoral processes probably play a primary role in the long-term effects of ventilation on the cardiovascular system. However, most of the immediate effects of ventilation on the heart are secondary to changes in autonomic tone. The lungs are richly enervated with somatic and autonomic fibers that mediate different homeostatic processes and instantaneously alter the cardiovascular function. The most common of these are the vagally mediated heart rate changes during ventilation [7]. Inflation of the lung to normal tidal volumes (<10 ml/kg) induces vagal-tone withdrawal, accelerating heart rate. This phenomenon is known as respiratory sinus arrhythmia and can be used to document normal autonomic control, especially in patients with diabetes who are at risk for peripheral neuropathy [7]. Inflation to larger tidal volumes (>15 ml/kg) decreases heart rate by a combination of both increased vagal tone and sympathetic withdrawal. Sympathetic withdrawal also determines arterial vasodilation. This inflation/vasodilation response can reduce LV contractility in healthy subjects and, as reported below, in ventilator-dependent patients with the initiation of high-frequency ventilation or hyperinflation [7].

Mechanical ventilation, applying a positive pressure on inspiration and increasing ITP, produces physiological effects that are directly opposite from normal spontaneous ventilation. The positive ITP is transmitted to the alveoli and the interstitial tissues. Intrapulmonary and interstitial pressures remain positive in inspiration and return toward atmospheric pressure on expiration. If a PEEP is added, ITP remains positive even in expiration. As in spontaneous breathing, MV is associated with an inspiratory fall in aortic flow and systolic blood pressure, but the mechanism is considerably different [8].

In the 1940, Cournand et al. [9] studied the physiological effects of a PPV on cardiac function, demonstrating a variable reduction in CO in healthy subjects receiving PPV. Cournand showed that RV filling was inversely related to ITP, and as this became more positive the RV preload fell, producing an evident fall in CO.

PPV determines a simultaneous rise in ITP and in lung volumes. The increase in lung volume plays a significant role in the hemodynamic changes during NIV: tidal volumes are often higher than those in spontaneous breathing.

The interactions with cardiopulmonary function during NIV are complex and may depend on baseline cardiopulmonary function and, in a certain way, differences in the mode of ventilation.

The main hemodynamic effects of PPV include a decrease in venous return of RV and LV, an increase in VI, an increase in PVR, an increase in central venous pressure, and a decrease in LV afterload (Table 2.1).

The positive ITP decreases venous return and alters RV and LV ejection. Increased lung volume enlarges RV size by raising PVR, causing intraventricular cardiac septum shift and decreasing LV filling. In addition, augmented ITP reduces LV afterload, increasing ejection of blood from LV. These effects are proportional to the amount of positive pressure, inspiratory volume, and value of PEEP [4].

The decrease in preload and blood pressure essentially depends on the volume status of the patient and is more pronounced in conditions of reduced venous return (hypovolemia and vasodilation). This is primarily due to the influence of ITP on venous return of RV, leading to a fall in left heart output. Considering ventilation modalities, the decrease in preload and blood pressure can be greater with controlled modes of MV with high tidal volume and high airway pressure. Thus, the application of assisted MV modalities (CPAP, BiPAP, PSV), maintaining a spontaneous inspiratory effort, is favored in these cases [10].

Conversely, patients with fluid overload and congestive heart failure considerably benefit from PEEP or PPV and may radically improve after its application. Because ITP is higher during NIV, volume infusion stabilizes the relationship between venous return and CO.

The intrathoracic cardiovascular system is often described as two sections (RV and LV) connected in series. Therefore, it is clinically more practical to consider the effects of NIV on right and left heart (Table 2.1).