Heart Failure

On a physiological basis, heart failure is the state in which cardiac output is not commensurate to the increasing oxygen and substrate demands of the working muscles with an incrementally increasing workload. Although there are a multitude of pathophysiologic mechanisms (e.g. ischemic heart disease, hypertension, valvular disease, idiopathic origins, etc.), heart failure can be broadly classified into two general categories:

    1. Systolic dysfunction
    2. Diastolic dysfunction
    3. Valve Disease

Oxygen uptake is tightly coupled to cardiac output via the relationship defined by the Fick’s equation:

Oxygen uptake (VO2) = cardiac output (CO) x difference in arterial-venous O2 content

    Common CPET characteristics in patients with heart failure are:1

    1. Low peak VO2.
    2. Low anaerobic threshold (AT).
    3. Low peak O2-pulse (i.e. low peak stroke volume)
    4. Low ∆VO2/∆WR slope (<8.5 ml/kg/min)

The anaerobic threshold is an effort independent measure of peak cardiac output in a cardiovascular limited patient. The peak VO2, AT and peak O2-pulse are an effective method to monitor progression of heart failure in a disease management program. The combination of diminished cardiac output, pulmonary venous congestion (both contributing to ventilation/perfusion mismatch), and abnormally heightened chemo/ergo reflex sensitivity may occur in patients with moderate to severe left ventricular dysfunction leading to an abnormally elevated VE/VCO2 slope2,3.  Furthermore, the body of research in this area convincingly demonstrates the VE/VCO2 slope is the strongest prognostic marker obtained from CPET in patients with heart failure while peak VO2 appears to provide complimentary predictive value2.   Expressing peak VO2 as a percent-predicted value, using the equations proposed by Wasserman, has been shown to improve prognostic resolution4

The severity of heart failure is best categorized by the VE/VCO2 slope and peak VO22,  although the value of the latter variable is dependent on near maximal to maximal subject effort. Other variable, such as PETCO22, have also been found to reflect heart failure severity5,6.

Since exercise amplifies an underlying cardiac disease process, it is possible to identify a decreased cardiac output state in the early to middle stages of heart failure with CPET, even before patients demonstrate clinical signs of heart failure. Patients with moderate heart failure tend to have generalized fatigue, poor energy levels with exercise intolerance without abnormalities in BNP or echocardiogrphic evidence of systolic dysfunction. Patients with heart failure pattern on CPET with anatomically normal hearts on echocardiogram represent an earlier stage heart failure consistent with Diastolic Dysfunction. These patients have poor cardiovascular reserve and are at increased risk for presenting to the emergency room with acute heart failure when a precipitating event(s) taxes the patients cardiac output status. Initial evidence indicates the CPET may likewise provide prognostic value in patients with diastolic dysfunction with the VE/VCO2 again demonstrating the highest prognostic insight. Whether the mechanism of heart failure is systolic or diastolic dysfunction, the net effect of impaired stroke volume response during exercise is common to both7.   Because the various cardiac disease states compromise stroke volume with exertion, the aim of our therapies should be to improve cardiac output to optimize functional capacity7.   In fact, numerous interventional investigations have demonstrated a favorable change in CPET variables, indicating this assessment can be used to accurately gauge therapeutic efficacy2.

1. Wasserman K, Hansen JE, Sue DY, Stringer WW, Whipp BJ. Priniciples of Exercise Testing and Interpretation, 4th edition, Lippincott Williams and Wilkins, Philadelphia, 2005.

2. Arena R, Myers J, Guazzi M. The clinical and research applications of aerobic capacity and ventilatory efficiency in heart failure: an evidence-based review. Heart Fail Rev 2008;13:245-69.

3. Arena R, Myers J, Abella J, et al. Development of a ventilatory classification system in patients with heart failure. Circulation 2007;115:2410-7.

4. Arena R, Myers J, Abella J, et al. Determining the preferred percent-predicted equation for peak oxygen consumption in patients with heart failure. Circ Heart Fail 2009; 2:113-20.

5. Matsumoto A, Itoh H, Eto Y, et al. End-tidal CO2 pressure decreases during exercise in cardiac patients: association with severity of heart failure and cardiac output reserve. J Am Coll Cardiol 2000;36:242-9.

6. Tanabe Y, Hosaka Y, Ito M, Ito E, Suzuki K. Significance of end-tidal P(CO(2)) response to exercise and its relation to functional capacity in patients with chronic heart failure. Chest 2001;119:811-7.

7. Kitzman DW and John JM. Exercise Intolerance in Diastolic Heart Failure. Diastology, Saunders, Phladelphia 2008; pages 203-214.

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