Noninvasive ventilation (NIV) decreases afterload
As we mentioned, in addition to the changes to the respiratory system (e.g., improved oxygenation, ventilation, and pulmonary physiology), the positive pressure associated with noninvasive ventilation (NIV) also causes changes in the thoracic cavity that affect cardiovascular physiology.
We began by discussing how positive pressure through a noninvasive ventilation mask affects venous return and preload, and now we’ll turn our focus to the effect of NIV on afterload.
What is afterload?
Afterload is the pressure against which the heart has to pump when ejecting blood during systole.
Pressure changes in the thoracic cavity affect the afterload of the left ventricle just as they cause changes in the preload of the right ventricle. An increase in intrathoracic pressure will increase afterload, and a decrease in intrathoracic pressure will decrease afterload.
Figure 1. Afterload is the pressure against which the heart has to pump when ejecting blood during systole.
Changes in afterload during respiration
During inspiration, the intrathoracic pressure becomes more negative (Fig. 2b). This may be 1–2 mmHg in magnitude. The healthy left ventricle, normally needing to generate a pressure of about 90 mmHg to open the aortic valve (Fig. 2c), will typically easily overcome this negative pressure of 1–2 mmHg (Fig. 2d).
Figure 2. Changes in afterload during breathing, a) before inspiration, b) at the end of inspiration pressure in the intrathoracic cavity is decreased, c) in this lower pressure environment, a greater pressure in the left ventricle is needed to open the aortic valve, d) increased pressure in the left ventricle is sufficient to overcome the change in intrathoracic pressure due to inspiration and blood flows out of the heart.
Changes in afterload during respiration—with a weakened heart
In the case of a patient with a weakened left ventricle with poor compliance, the extra work of the left ventricle may be quite magnified (Fig. 3b). Pulmonary edema may start to develop (Fig. 3c), and, as a result, the patient will take in larger and deeper breaths, which can increase the negative intrathoracic pressure (Fig. 3d). The weakened myocardium must generate greater pressure to overcome both the intrathoracic pressure and the pressure needed to open the aortic valve. If cardiac contractility is not up to the task, further pulmonary edema will develop, and the cycle will continue (Fig. 3e).
Figure 3. Changes in afterload during breathing with a weakened heart, a) increase in pressure in left ventricle needed to overcome the decrease in pressure due to inspiration, b) a weak left ventricle cannot generate the needed pressure, c) pulmonary edema may start to develop, d) a larger inspiration (deeper breath) is taken as a result of fluid buildup, which generates a further decrease in pressure and larger gradient to overcome, e) the weakened left ventricle cannot generate even more pressure so further pulmonary edema develops and the cycle continues.
How does NIV help break the cycle?
With NIV, the positive intrathoracic pressure actually decreases the pressure against which the left ventricle must pump (Fig. 4d). This assists, or offloads, the left ventricle (Fig. 4e). A weak left ventricle with poor contractility may find it easier to pump blood through the body in this situation (Fig. 4f).
Figure 4. Noninvasive ventilation (NIV) can break the cycle of increasing afterload, a) end-expiration, b) decrease in intrathoracic pressure due to inspiration, c) a weak left ventricle cannot generate the needed pressure to overcome the afterload, d) NIV increases the intrathoracic pressure thereby reducing the afterload, e) the weakened ventricle doesn’t have to work as hard to overcome the afterload, f) the blood can flow.
The net result is that the left ventricle when assisted by positive-pressure ventilation, can generate a greater stroke volume for the same preload, due to improved contractility and decreased afterload—in other words, it can improve its compliance.
Figure 5. The left ventricle, when assisted by positive-pressure ventilation, can improve its compliance. Positive-pressure ventilation (e.g., NIV) can move the curve up, allowing a greater stroke volume for the same preload, due to its improved contractility and decreased afterload.
How is afterload important in the clinic?
Take a patient with pulmonary edema due to a weak heart, pumping against a high cardiac afterload. Reducing cardiac afterload will lessen the stress on the heart and help relieve pulmonary edema.
So, knowing how positive-pressure ventilation improves left ventricular function and decreases afterload, we can use NIV to avoid the potential death spiral in patients with pulmonary edema from high afterload or weak hearts. Yet another physiologic win for NIV!
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