Ventilation Modes Change Cardiac Output
Take a deep breath. Your diaphragm is contracting downward increasing your intrathoracic volume with a resulting decrease in pressure according to Boyle’s Law. This new pressure is less than that of atmospheric pressure (“negative intrathoracic pressure”), so a gradient is created driving air into your lungs.
Now let’s consider a patient who is intubated and receiving mechanical, positive pressure ventilation (PPV). This form of breathing is different – air is basically being FORCED into the lungs. The diaphragm and other muscles of respiration are allowed to rest in the interim while the ventilator handles the work of breathing.
In either case, respiration causes fluid/pressure shifts which affect cardiac physiology. During normal, spontaneous inspiration, the right ventricle receives a surge of venous blood, and the left ventricle has to work against a greater end load to eject blood to the rest of the body. In more medical jargon, the RV preload and LV afterload increase during spontaneous inspiration. In comparison, inspiration during mechanical PPV will decrease the RV preload and the LV afterload. This decrease in LV afterload can benefit patients who are already struggling with forward flow as in significant mitral regurgitation, cardiogenic pulmonary edema, LV dysfunction, etc.
The clinical significance is apparent when transitioning from one form of ventilation to the other. If I’m going to prepare a patient with severe mitral regurgitation for extubation (going from PPV to normal respiration), I’m imposing a greater afterload on their LV and could tip the patient into heart failure. This is a small but important consideration for at-risk patients emerging from anesthesia! Plan to optimize hemodynamics before extubating.