Acute Effects of Continuous Positive Airway Pressure on Pulse Pressure in CHF

Today’s reality on non-invasive ventilation (NIV) use has nothing but four key A level indications supported by evidence-based medicine. These, which would be chronic obstructive pulmonary disease (COPD) exacerbation, cardiogenic pulmonary edema, pulmonary infiltrates in immunocompromised patients, and the weaning of already extubated COPD patients, are the so called “the fabulous four”¹. But is this the maximum therapeutic potential of NIV? Probably not. If so, which would be the next one on this selected “fabulous four” group? Maybe it is stable chronic heart failure (CHF). If so, we would be facing a new frontier, yet unexplored, of those chronically stable not respiratory but cardiac patients, opening new applications, none existent up to today.

Quintão et al.² move on into the next step to conquer this new frontier, the NIV application on stable CHF. They do so, analyzing the NIV (Continuous Positive Airway Pressure - CPAP) effects on pulse pressure (PP), as a risk factor with independent negative predictive value for adverse cardiovascular events, followed by left ventricular dysfunction, especially type II, caused by acute myocardial ischemia. They prove not only to affect PP reduction, but also heart rate (HR), mean arterial pressure (MAP), systolic blood pressure (SBP) and respiratory rate (RR).

The results will be explained through the relationship between positive pressure ventilation effects³ on the cardiorespiratory system. In the left heart, pulmonary vein compression followed to translung pressure increases, improving venous return and so the preload. In addition, this translung pressure increase contributes to squeeze the heart chambers and discharge them, this “dUp”⁴ effect increases the stroke volume (SV) and improves left systolic output. The afterload reduction is secondary to the systemic vasodilatation effect as a response to intrathoracic pressure elevation. As a final result, HR, MAP, SAP and PP decrease, protecting myocardial oxygenation and reducing the myocardial infarction risk. In the right heart, translung pressure reduces preload secondary to the vena cava squeeze and elevates afterload³ by the increase in pulmonary vascular resistances. As a result a “dDown”⁴ effect and right SV reduction occur, reducing vascular congestion and lung edema, and once again improving oxygenation and ventilation. Regarding respiratory effects, there will be direct oxygenation by O₂ administration and also the alveolar recruitment effect. As a final result, PaO₂ and mixed venous oxygen (SVO₂) raise, and RR and HR decrease.

In a study by Quintão et al.², hemodynamic monitoring was not continuous, but manually measured (sphygmomanometer); thus, a continuous monitoring might offer more accurate and precise data. Actually additional monitoring with echocardiography will allow to expand data, calculate ejection fraction and SV, which will allow to establish the relationship between PP reduction and ventricular output improvement. The trial lasted 30 minutes, enough to confirm the hypothesis, but a longer time will allow maximum effect assessment to possibly define the best CPAP potential on this matter. Finally, although a CPAP pressure of 6 cm H₂0 is in fact the usual level used in those studies, a bigger pressure of 8 cm H₂0 will probably have a bigger effect, as we usually see in everyday work.