Abnormalities in the regional circulations accompanying congestive heart failure.
In congestive heart failure, patients appear to have alimited ability to dilate their resistance vessels in skeletal muscle in response to a metabolic stimulus. This is true whether the metabolic stimulus is ischemia, dynamic, or static exercise. The mechanism for this limited arteriolar capacity is at least twofold; an increased sodium content of the vessels as well as an increased tissue pressure which is seen in edematous states. This can be considered a positive compensatory mechanism in that it helps to maintain systemic arterial pressure during exercise when the cardiac output fails to increase normally. If the resistance vessels were to dilate normally, then in the face of a limited cardiac output, exercise syncope would be expected to occur...
D001485:Basement Membrane; D001783:Blood Flow Velocity; D002319:Cardiovascular System / Q000503:physiopathology; D002395:Catecholamines / Q000502:physiology; D004071:Digitalis Glycosides / Q000494:pharmacology; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D009020:Morphine / Q000494:pharmacology; D009132:Muscles / Q000098:blood supply; D009638:Norepinephrine / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects; D005082:Physical Exertion; D012039:Regional Blood Flow / Q000187:drug effects; D012146:Rest; D012867:Skin / Q000098:blood supply; D014666:Vasomotor System / Q000503:physiopathology; D014690:Venous Pressure
D002395:Catecholamines; D004071:Digitalis Glycosides; D009020:Morphine; D009638:Norepinephrine