Abstract
Cardiovascular and respiratory systems are anatomically and functionally linked; inspiration produces negative intrathoracic pressures that act on the heart and alter cardiac function. Inspiratory pressures increase with heart failure and can exceed the magnitude of ventricular pressure during diastole. Accordingly, respiratory pressures may be a confounding factor to assessing cardiac function. While the interaction between respiration and the heart is well characterized, the extent to which systolic and diastolic indices are affected by inspiration is unknown. Our objective was to understand how inspiratory pressure affects the hemodynamic assessment of cardiac function. To do this, we developed custom software to assess and separate indices of systolic and diastolic function into inspiratory, early expiratory, and late expiratory phases of respiration. We then compared cardiac parameters during normal breathing and with various respiratory loads. Variations in inspiratory pressure had a small impact on systolic pressure and function. Conversely, diastolic pressure strongly correlated with negative inspiratory pressure. Cardiac pressures were less affected by respiration during expiration; late expiration was the most stable respiratory phase. In conclusion, inspiration is a large confounding influence on diastolic pressure, but minimally affects systolic pressure. Performing cardiac hemodynamic analysis by accounting for respiratory phase yields more accuracy and analytic confidence to the assessment of diastolic function.
Highlights
Cardiovascular and respiratory systems are anatomically and functionally linked; inspiration produces negative intrathoracic pressures that act on the heart and alter cardiac function
We show that end diastolic pressure, and to a lesser extent, systolic pressure is predicted by inspiratory pressure
We provide robust analysis to illustrate the benefit of dividing the respiratory cycle into inspiratory and expiratory phases to assess ventricular systolic and diastolic pressures
Summary
Cardiovascular and respiratory systems are anatomically and functionally linked; inspiration produces negative intrathoracic pressures that act on the heart and alter cardiac function. Many acute stresses and chronic disease states increase the amplitude of intrathoracic pressure swings throughout respiration This can occur as a result of obstruction in the airways (e.g., pulmonary edema, inflammation), diaphragmatic weakness, or elevated end-expiratory p ressures[6,7,12,13]. These changes in intrathoracic pressure change afterload and venous return[14], impacting cardiac hemodynamics without changing the intrinsic function of the myocardium per se. We show a new approach to remove this influence from hemodynamic analyses to provides a more rigorous assessment of diastolic and systolic function
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have