Dyspnea was long considered an expression of pulmonary congestion and desaturation caused by low cardiac output, ie, as a hemodynamic symptom. Although this explanation remains valid for acute heart failure, it has been discarded for chronic heart failure. Thus, there is no correlation during exertion or at rest between dyspnea and the degree of impairment of either left or right ventricular systolic function (ejection fraction) or central hemodynamics (pulmonary pressure). Acute restoration of normal hemodynamics induced by medication or other techniques (surgical valve replacement in severe mitral stenosis) is not accompanied by parallel changes in dyspnea. Dyspnea does not correlate with arterial 02 saturation. For these reasons it is now believed that dyspnea, hyperventilation, and altered respiratory rhythm have other causes, which depend more on the periphery and the nervous system than on central hemodynamics. They also include functional changes in the lungs and respiratory and skeletal muscle.
Ventilation often increases more in patients with heart failure than in healthy subjects at the same workload. Hyperventilation is also often present at equivalent levels of carbon dioxide production. Pulmonary capillary hypertension increases pulmonary rigidity, air resistance, and the mechanical work of breathing. There is an increase in the dead space due to ventilation of the hypoperfused pulmonary apices, and there is also an increase in respiratory rate at equivalent values of minute ventilation. The proportion of ventilated alveoli that do not contribute to gas exchange increases due to the increased alveolar or capillary resistance. Bronchial hyperresponsiveness and diffusion abnormalities may be present, with hyperchemosensitivity to hypoxia.
Respiratory muscle changes
Heart failure is characterized by respiratory muscle weakness (commonly measured by the reduction of the maximum inspiratory and expiratory pressure measured from the mouth) and decreased diaphragmatic endurance (measured as maximal voluntary ventilation and maximum sustainable ventilation). The muscle weakness may reflect the myopathy induced by heart failure. Many pathophysiologic mechanisms are at work, even if some may have opposite effects, eg, muscle deconditioning is a common influence on skeletal muscle but totally absent in respiratory muscle.
Skeletal muscle changes
Heart failure is associated with increased muscle ergo-receptor stimulation, activated by abnormal intracellular metabolism. The increase in ergoreflex activity augments the ventilatory response to exercise (muscle hypothesis), in addition to the sympathetic excitation and vasoconstriction already present.
symptom; diagnosis; dyspnea; etiology; respiratory muscle; skeletal muscle
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