Noninvasive ventilation (NIV) reduces preload

In this Clinical Guide article, learn how noninvasive ventilation (NIV) benefits your patients by reducing preload.
Last update26th Nov 2020

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’ll begin by discussing how positive pressure through a noninvasive mask will affect venous return and preload, and later we’ll review the effect of NIV on afterload.

What is preload, or end-diastolic pressure?

Preload is defined as the pressure in the right heart at the end of filling. Using more technical terms, preload is the end-diastolic pressure of the right ventricle.

Figure 1. Right ventricular preload is defined as the pressure in the right heart at the end of filling.

Venous return and preload (or end-diastolic pressure) change during the respiratory cycle. When venous return to the heart increases, the preload increases. When venous return to the heart decreases, the preload decreases.

And how the preload changes depends on whether the patient is breathing spontaneously (i.e., with negative-pressure breathing), or breathing with the assistance of a ventilator, which uses positive pressure.

How do venous return and preload change during spontaneous (i.e., negative-pressure) breathing?

First, during inspiration, intrathoracic pressure decreases as the lungs inflate (Fig. 2b). In response to this decrease in pressure, the extrathoracic venous system allows an increased venous return to the right heart (Fig. 2c). Since the change in intrathoracic pressure will increase the volume of blood returning to the heart, the pressure of the right ventricle goes up and preload increases (Fig. 2d).

Figure 2. Changes in venous return and preload due to changes in intrathoracic pressure during a spontaneous breathing cycle, a) end-expiration, b) inspiration and decreased thoracic pressure, c) increased venous return, d) increased end-diastolic pressure (increased preload).

How does NIV (or positive-pressure breathing) affect venous return and preload?

During inspiration on NIV, intrathoracic pressure is positive when the lungs inflate (Fig. 3b). The venous return will decrease due to the higher pressure (Fig. 3c). The decreased venous return decreases preload (Fig. 3d), and this decreased blood volume is transmitted to the left ventricle when the blood flows through the pulmonary circulation to the left atrium and ventricle.

Figure 3. Changes in venous return and preload due to changes in intrathoracic pressure during positive-pressure breathing (with noninvasive ventilation, or NIV), a) end-expiration, b) inspiration, and increased thoracic pressure, c) decreased venous return, d) decreased end-diastolic pressure (decreased preload).

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How are NIV-induced changes in preload and venous return important in the clinic?

The changes in venous return as a result of moving from negative-pressure breathing to positive-pressure breathing can have substantial physiologic implications on patients. Understanding these changes and predicting them in advance can allow for optimal use of NIV.

Hypervolemic patients on NIV

In patients with relative hypervolemia (fluid overload), such as patients with acute cardiogenic pulmonary edema, decreasing venous return and preload may decrease pulmonary blood flow leading to improved pulmonary function.

Hypovolemic patients on NIV

On the contrary, when trialing NIV in patients with status asthmaticus, who may present with relative hypovolemia (low blood volume / inadequate distribution of blood volume) resulting from insensible volume losses due to tachypnea, the positive pressure of NIV may cause further decreases in preload and possible hypotension.

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Recommended reading

  • Kallet, RH and Diaz, JV. 2009. The physiologic effects of noninvasive ventilation. Respir Care. 54: 102–115. PMID: 19111110

About the author

Michael Allison, MD
Chief of Critical Care Medicine at the University of Maryland St. Joseph Medical Center, USA.
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