Heart failure patients often complain of tiredness, weakness in the legs, fatigability, and pain in the thighs on walking. As a result, they tend to decrease their activity, thus deconditioning their muscles and further lowering their exercise tolerance. Once fatigue starts to be perceived during daily activities (washing and eating), then malnutrition with increased muscle atrophy and susceptibility to infection tend to follow.
What causes the fatigue?
We now know that there is no correlation between central hemodynamics, in particular left ventricular filling pressures, and the severity of exercise intolerance. Muscle dysfunction is a potential determinant of fatigue. Atrophy is present in about two thirds of patients. The histology reveals an increased percentage of type II and Ha fibers, smaller muscle fibers, decreased vascular conductance, and a decrease in myocyte mitochondrial volumetric and crest densities. Muscle metabolism is also impaired, with increased glycolysis (causing early intramuscular acidosis), altered fatty acid metabolism, and decreased muscle oxidative capacity (causing decreased efficiency). Lactate production is increased, although this does not appear responsible for the fatigue. Ergo-receptors, which are small myelinated and unmyelinated afferents of skeletal muscle, can be stimulated by abnormal levels of potassium and so cause not only the perception of fatigue, but also dyspnea.
The muscle changes are not explained solely by hypoperfusion and physical inactivity. Perfusion is clearly decreased by cardiac dysfunction and depressed local vasodilatation in inactive muscle. Pathological lactate production may also be present, even when muscle flow is still normal. Yet, physical inactivity cannot explain why the same changes arise in respiratory muscle. Other possible causes are malnutrition (reduced calorie intake and negative energy balance) and catabolism (due to sympathetic nervous system activation, insulin resistance, and cytokine activation).
In summary, the causes of muscle fatigue include:
Decreased muscle perfusion (vasoconstriction, decreased capillary density, impaired endothelial vasodilatation).
Histological and biochemical abnormalities (enzyme levels and muscle metabolism).
Atrophy, decreased muscle strength, and decreased muscle resistance.
How do you quantify muscle fatigue?
A complaint of fatigue requires a careful history and a number of investigations to make a differential or additional diagnosis. Thus, pallor suggests anemia (a full blood count will be confirmatory), while other signs might point to hypothyroidism. Hypokalemia needs to be excluded, as does a psychogenic disorder.
Functional performance is readily investigated by determining the tolerability of activities of daily living. As patients tend to limit their activities to avoid symptoms, it becomes informative to ask specific activity questions (eg, going up one or two flights of stairs), including via questionnaire (Table I).
An initial exercise test may be useful if:
The history of dyspnea and fatigue is imprecise.
The patient’s lifestyle is very sedentary.
The patient is not coherent.
The patient denies or plays down his/her symptoms.
The patient’s history conflicts with the family’s account.
The reported symptoms conflict with the clinical assessment.