Effects of Ventilation on the Circulation
Venous return is equal to Pms-Pra (Mean systemic pressure-right atrial pressure). Mean systemic pressure is the pressure in the veins when there is no flow occurring and is governed by volume status as well as venous capacitance. As right atrial pressure increases towards mean systemic pressure, there is less and less of a gradient for venous flow until the two are equal and flow (cardiac output) ceases.
Figure 1: The venous return and cardiac output curves superimposed
Spontaneous breathing creates negative intrathoracic pressure which tends to decrease Pra, thus leading to increased venous return
Conversely, positive pressure ventilation increases intrathoracic pressure which increases Pra, thus leading to decreased venous return
RV stroke volume declines over positive pressure inspiration due to this decrease in venous return (and hence, reduced RV transmural pressure)
Vascular hypovolemia can exaggerate these affects. Hence, if you have a hypovolemic patient with impaired hemodynamics (ie BMT patient in shock), you might consider volume loading prior to intubation and positive pressure breaths (or having volume readily on hand)
Pulmonary vascular resistance (PVR) is closely related to lung volume. There are two types of vessels: septal (in the wall between two alveoli) and corner (at the corner of several alveoli). As the lung expands towards TLC, one can imagine septal vessels getting compressed, thus raising their resistance. On the other hand, corner vessels would expand, reducing their resistance. The opposite effects occur with decrease in lung volume toward residual volume. Hence, total PVR is determined by the sum of these two resistances and is thus the lowest at FRC
One can also imagine that high PEEP could cause hypoxemia. For example, in the case of a lobar pneumonia, high PEEP could lead to relative overdistension of normal alveoli, compression of septal vessels, and subsequent relative shunting of blood from normally ventilated lung to the area of consolidation, leading to relative intrapulmonary shunt and hypoxemia.
Figure 2: Pulmonary Vascular Resistance as a Function of Lung Volume
Pulmonary vascular resistance is also affected by gravity, due to the tendency for air to distribute to the upper regions of the lung and blood to distribute to the lower regions of the lung. These are known as the West Zones of the lung with Zone 1 demonstrating relative dead space ventilation, Zone 2 adequate V/Q matching, and Zone 3 relative intrapulmonary shunt
Figure 3: The West Zones of the Lung
Pulmonary vascular resistance also is affected by PaO2 (lower PaO2 leads to protective hypoxic pulmonary vasoconstriction) and pH (lower pH leads to increased pulmonary vasoconstiction). Hence, in a patient with pulmonary hypertension, we treat with therapies such as oxygen and relative alkalemia.
Effects on the Left Ventricle
Mechanical ventilation can potentially reduce LV preload via a reduction in RV preload. Overdistension of the lung can also impair RV ejection. This leads to a relative increase in RV size which due to ventricular interdependence, can bow into the LV and thus impair LV complicance, filling, and LV stroke volume. These affects are generally thought to be fairly minimal
Mechanical ventilation decreases LV afterload. It does this by increasing intrathoracic pressure. LV afterload can be thought of as the transmural pressure of the LV (Pressure in - Pressure out). In normal spontaneous respiration, the pressure out, or the intrathoracic pressure, is 0 to negative. In positive pressure ventilation, the "pressure out" becomes positive, thus reducing the transmural pressure. This can be seen in the figure below (3rd diagram). Conversely, exaggerated spontaneous breathing (ie croup) could lead to large negative intrathoracic pressures, thus increasing afterload- this is one explanation for pulsus paradoxus.
(From Bronicki and Anas, PCCM 2016)
Thus, in addition to taking away the metabolic demand of the work of breathing, endotracheal intubation and mechanical ventilation can also reduce the work of the heart by reducing afterload
The dominant effects of mechanical ventilation are decreased RV preload and decreased LV afterload
In general, it is thought that the reduction in venous return and RV preload predominates and would lead to decreased cardiac output with initiation of PPV. This is particularly true for hypovolemic patients who are "preload dependent." Again, as venous return= Pms-Pra, patients with lower Pms are more sensitive to significant increases in Pra due to initiation of PPV
The converse can also be considered. In a patient with congestive heart failure, they likley have a high Pms, making them less sensitive to changes in Pra. In these patients, the reduction in afterload from PPV may be more significant than the potential decrease in venous return and RV preload
As PPV breaths decrease LV afterload, they lead to an increase in systolic and pulse pressure. This variation in pulse pressure (max-min) over the respiratory cycle has been shown to be correlated with "preload dependence," or increase in cardiac output with fluid administration. In adults, a greater than 15% inspiratory rise in pulse pressure identifies patients with preload dependence in PPV
Similarly, large changes in pulse pressure with PPV also predict patients who will have larger decreases in venous return and cardiac output with application of increased PEEP as again, they are more preload dependent.