Breathing strategy to preserve exercising cardiac function in patients with heart failure

Abstract

SUMMARY The heart and lungs are closely linked as they lie in series, share a common surface area and compete for space within the thoracic cavity. The heart and lungs are exposed to the similar changes in intrathoracic pressure, and reflexes within one organ can influence the other (i.e. vagal influence of lung inflation on heart rate). In patients with heart failure, these cardiopulmonary interactions may be altered due to decreased lung and left ventricular compliance, increased cardiac size, high cardiac filling pressure and altered receptor sensitivity to neural activation. Exercise further affects the cardiopulmonary interactions by stimulating an increase in the depth and frequency of breathing which accentuates the fluctuations in intrathoracic pressure, and by requiring large increases in stroke volume and heart rate in order to respond to the increased metabolic demand. Previous work from our laboratory suggested that patients with heart failure avoid high lung volumes during exercise, often at the expense of unnecessary large positive expiratory intrathoracic pressures resulting in significant wasted effort. Moreover, we also observed that voluntarily increases in lung volume in patients with heart failure induced a mild relative bradycardia, a response not observed in similar aged healthy individuals. Thus, we hypothesized that the rapid shallow low lung volume breathing, in combination with positive expiratory intrathoracic pressure, often adopted by patients with heart failure during exercise is an attempt to preserve, or even enhance, the cardiac response to exercise.

Expiratory Loading Improves Cardiac Output during Exercise in Heart Failure

“…Expiratory loads of 5 and 10 cm H 2 O similarly increased SVI and CI during moderate exercise in relatively asymptomatic patients with stable heart failure, which supports our hypothesis that increased expiratory ITP helps to preserve exercising cardiac function in this population (13). The lack of effect between loads of 5 and 10 cm H 2 O on the cardiac response may be explained by different contributions from the reduction in venous return which may no longer be beneficial at 10 cm H 2 O, and from a decreased LV afterload.…”

“…Despite room to increase tidal volume by encroaching on the inspiratory reserve volume, end-expiratory lung volume remains near residual volume throughout exercise in many patients with heart failure (11). It may be hypothesized that heart failure patients maintain these low end-expiratory lung volumes, possibly resulting in expiratory flow limitation and increased expiratory intrathoracic pressure (ITP), in an attempt to optimize interactions between ITP and stroke volume (SV) which could improve the exercise response in this population (13). …”

Effects of atrioventricular and interventricular delays on gas exchange during exercise in patients with heart failure

“…13, 14, 19, 20 Alterations in cardiopulmonary gas exchange via light or submaximal exercise are clinically used to determine the prognosis or severity of HF and P ET CO 2 , V E /VCO 2 and O 2 pulse have been suggested as specific gas exchange measures to track HF. 6, 7, 11, 21 A lower P ET CO 2 and a higher V E /VCO 2 indicate high dead space ventilation, altered breathing pattern and an increase in V/Q mismatch which is associated with impaired cardiac output.…”

A Multivariable Index for Grading Exercise Gas Exchange Severity in Patients with Pulmonary Arterial Hypertension and Heart Failure

“…Small increases in metabolic demand (e.g., exercise) enhance these cardiopulmonary interactions. Thus it is no surprise that diseases that primarily influence the lungs or the heart significantly impact the other organ system [1, 2]. This can be especially observed in patients with pulmonary arterial hypertension (PAH) where right heart failure evolves and in patients with left heart failure (HF) where significant changes occur in lung mechanics, ventilatory control, and ultimately in respiratory gas exchange.…”