In response to decreased renal perfusion, intravascular volume rises. Again, several mechanisms contribute. Activation of the renin-angiotensin system is the most important. The dilated, poorly contractile left ventricle becomes less compliant. This means that small increases in volume produce a relatively large increase in pressure. The net result is an increase in preload. Initially, this helps to maintain cardiac output via the Starling mechanism. As with the changes in afterload, more severe rises are counterproductive, and cause pulmonary vascular congestion, and edema.
What happens to heart rate?
It rises. With decreased stroke volume caused by decreased contractility, an increase in heart rate helps preserve cardiac output. The rise in heart rate is due in part to the increased sympathetic tone noted above.
What are the symptoms?
The hallmark of heart failure is exercise intolerance. This is most commonly experienced as dyspnea on exertion, but some patients report easy fatigue. When left heart failure is more severe, patients may complain of orthopnea or paroxysmal nocturnal dyspnea. With this latter symptom, patients are awakened by a severe sensation of shortness of breath, often described as a “smothering” feeling. It is relieved by sitting on the edge of the bed or walking around; some patients get relief from sitting by an open window.
With right heart failure, patients most frequently notice edema of the feet and ankles.
Sometimes, they are aware only of their shoes getting tighter. When edema involves the liver and gut, they notice right upper quadrant discomfort and abdominal fullness.