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.

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.

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).

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).

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).

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.

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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