Anda di halaman 1dari 1

B re a t h i n g E x e rc i s e s an d

Inspiratory Muscle
Tr a i n i n g i n H e a r t Fa i l u re
Lawrence P. Cahalin, PhD, PT, CCSa,*,
Ross A. Arena, PhD, PTb

KEYWORDS
 Functional capacity  Respiratory muscle weakness  Rehabilitation  Exercise training

KEY POINTS
 Because of the intimate and linked functional and compensatory relationships it is often difficult to
identify the primary determinant limiting exercise in heart failure (HF).
 Respiratory contributions have been shown to limit exercise in patients with HF due to abnormal-
ities in ventilation, perfusion, or both ventilation and perfusion.
 Breathing exercises and inspiratory muscle training seem to have substantial potential to improve
exercise and functional performance in HF and should be considered as key components of a reha-
bilitation program in this patient population.

INTRODUCTION elevated pulmonary vascular resistance


(PVR).2,8,9,14 Ventilation-perfusion abnormalities in
Respiratory contributions have been shown to limit HF are due to these factors in addition to several
exercise in patients with heart failure (HF). The other potential factors, including ventricular asyn-
manner by which the respiratory system limits exer- chrony, cardiac arrhythmias, and loss of viable
cise is due to abnormalities in ventilation, perfusion, and elastic lung tissue, as in advanced HF. All of
or both ventilation and perfusion.1–16 The key fac- these factors contribute to a ventilation-perfusion
tors limiting ventilation in HF include pulmonary mismatch of varying degrees.1–15 The purpose of
edema, loss of elastic recoil of the lungs, ascites, this article is to demonstrate how breathing
and inspiratory muscle weakness.1–7 Thus, the ab- exercises (BE) and inspiratory muscle training
normalities in ventilation in HF are mostly restrictive (IMT) have the potential to improve many of
in origin, producing a ventilatory response during these abnormalities in ventilation, perfusion, and
exercise in HF that is characterized by: (1) ventilation-perfusion matching. The rationale for
decreased tidal volume, end-tidal carbon dioxide, BE and IMT in HF is provided, followed by an exten-
peak oxygen consumption (VO2), and tidal volume sive review of the literature of BE and IMT in HF. The
to ventilation ratio (VT/VE); and (2) increased respi- role of BE and IMT in HF is expanded to patients
ratory rate, VE, peak dead space ventilation to tidal with pulmonary hypertension (PH) to highlight (1)
volume ratio (VD/VT), ventilation to VO2 ratio (VE/ the manner by which the pulmonary vasculature af-
VO2), and the VE/carbon dioxide consumption fects respiratory performance, and (2) the potential
(VE/VCO2) slope.7–9 The key factors limiting perfu- that both BE and IMT have on improving the pulmo-
sion in HF include poor right ventricular perfor- nary vasculature and pathophysiology of HF.
mance, elevated pulmonary artery pressure, and
heartfailure.theclinics.com

a
Department of Physical Therapy, Leonard M. Miller School of Medicine, University of Miami, Miami, 5915
Ponce de Leon Boulevard, Coral Gables, FL 33146-2435, USA; b Department of Physical Therapy, College of
Applied Health Sciences, University of Illinois at Chicago, 1919 West Taylor Street, Room 459, Chicago, IL
60612, USA
* Corresponding author. Department of Physical Therapy, Leonard M. Miller School of Medicine, University of
Miami, 5915 Ponce de Leon Boulevard, Fifth Floor, Coral Gables, FL 33146-2435.
E-mail address: l.cahalin@miami.edu

Heart Failure Clin 11 (2015) 149–172


http://dx.doi.org/10.1016/j.hfc.2014.09.002
1551-7136/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved.

Anda mungkin juga menyukai