FIG. 4:  This Figure shows some data in support of the hypothesis outlined in the previous Figure.  These are tracings from a 27-year-old patient with idiopathic dilated cardiomyopathy and severe OSA.^[1]  The patient is in stage 2 non-rapid eye movement (non-REM) sleep and having an obstructive hypopnea.  There is a reduction in tidal volume (V_T) accompanied by paradoxical motion of the rib cage and the abdomen.

The tracing at the bottom of the Figure shows esophageal pressure, measured with an esophageal balloon catheter.  The upward deflections in this tracing represent negative pressure, so this shows increasingly negative pressure until the end of hypopnea.  Toward the end, the esophageal pressure is reaching –80 cmH₂O or –50 mmHg. 

This is important because that negative intrathoracic pressure (esophageal pressure) is increasing left ventricular afterload, ie, increasing the difference between intracardiac pressure during systole and intrathoracic pressure. 

So for example, if the intracardiac pressure is +150 mmHg, subtracting the intrathoracic pressure of –50 mmHg results in +150 mmHg “minus a minus” –50 mmHg, ie, a sum transmural pressure of +200 mmHg, which is loading the heart by adding 50 mmHg to the left ventricle’s intracardiac pressure of +150 mmHg.  In addition, blood pressure usually increases during these events. 

Finally, the oxygen saturation (SaO₂ in Figure) is falling.  At this point the patient wakes up, starts to breathe again, and the esophageal pressure returns to baseline.  In other words, the negative intrathoracic pressure is a unique noxious stimulus in OSA that is not seen in any other disease.