What role does cerebral hypoperfusion play in congestive heart failure?

ptimal organ function requires adequate tissue perfusion and thus depends on the distribution of cardiac output, an adequate blood pressure, and a local vasculature responsive to metabolic needs. In heart failure, poor cardiac output causes peripheral maldistribution and impaired organ perfusion, for example to skeletal muscle, where additional factors that include local metabolic changes and impaired reflex mechanisms, especially during physical activity, contribute to exercise intolerance and fatigue.

The techniques of cerebral perfusion study include near-infrared spectroscopy, which is used to continuously record cerebral oxygenated and deoxygenated hemoglobin, and neuroimaging modalities such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) which permit the noninvasive determination of blood flow and metabolic changes in discrete brain regions. With increasing anatomic resolution, changes can be measured in areas as small as the amygdala. Enhanced resolution is of particular importance since specific regions such as the amygdala are likely to be involved in the higher cortical control of cardiovascular autonomic function.

An additional technique is continuous wave transcra-nial Doppler ultrasonography of cerebral blood flow to measure the response to a hypercapnic gas mixture. Changes in the arterial partial pressure of carbon dioxide (pC02) influence the diameter of the brain arterioles and precapillary sphincters: increases in arterial pC02 normally produce an almost immediate increase in cerebral blood flow. Transcranial Doppler monitoring of flow velocity can thus provide semiquantitative information on changes of cerebral perfusion.

Georgiadis et al used transcranial Doppler ultrasound to assess cerebrovascular reactivity in heart failure patients challenged with a hypercapnic gas mixture. Their aim was to determine whether defects in cerebral perfusion account for the cognitive impairment reported in heart failure, in particular in association with vasodilator therapy. Their results suggest not only that cerebrovascular reactivity is impaired in chronic heart failure, but also that declining cerebrovascular reactivity is a corollary of declining cardiac function.

The hypothesis that cerebral perfusion is inadequate in chronic heart failure was based on the demonstration of cognitive impairment in severe heart failure and significant improvement after cardiac transplantation. In patients with adequate cerebrovascular reactivity, dilatation of the brain arterioles, which lowers cerebrovascular resistance, offsets the decrease in cardiac output. However, this limits their potential for further dilatation; it diminishes cerebrovascular reserve, even in partially compensated cardiac failure (New York Heart Association functional class II). Such patients with brain resistance vessels whose capacity for reactive dilatation is partially exhausted may be unable to offset the effects of systemic antihypertensive therapy (diuretics, vasodilators, etc) on cerebral perfusion. This explains why aggressive heart failure therapy may often compound cognitive impairment.

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