Effects of increased venous pressure in CCF

My explanation ( LOTS OF POSTULATIONS, ERRORS WILL BE CORRECTED AFTER PCL IF THERE IS ANY)
Increased venous pressure ( a compensatory response to reduced cardiac output) will directly cause the right atrium pressure to elevate since the preload is high. But as time goes by, the compensatory mechanism will cause the myocardium to hypertrophy and stiffens, compromising the heart’s ability to function normally. High venous pressure will increase the hydrostatic pressure of plasma at the venule ends of the capillaries and thus reducing the reabsorption of the filtered fluid from the interstitium. Accumulation of fluid outside plasma in the ECF will result in peripheral oedema as what Rosalyn is experiencing.

As you all know, venous pressure is governed by two factors – volume of blood in the veins as well as the distensibility of the vein walls controlled by smooth muscle. The built up of pressure in the veins will be indicated by jugular venous pressure. An elevated JVP is the classic sign of venous hypertension (e.g. right-sided heart failure). The paradoxical increase of the JVP with inspiration (instead of the expected decrease) is referred to as the Kussmaul sign, and indicates impaired filling of the right ventricle.

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Expert’s view:
In RV failure, systemic venous pressure increases, causing fluid extravasation and consequent edema, primarily in dependent tissues (feet and ankles of ambulatory patients) and abdominal viscera. The liver is affected most, but stomach and intestine also become congested; fluid accumulation in the peritoneal cavity (ascites) can occur. RV failure commonly causes moderate hepatic dysfunction, with usually modest increases in conjugated and unconjugated bilirubin, PT, and hepatic enzymes (eg, alkaline phosphatase, AST, ALT). The impaired liver breaks down less aldosterone, further contributing to fluid accumulation. Chronic venous congestion in the viscera can cause anorexia, malabsorption and protein-losing enteropathy (characterized by diarrhea and marked hypoalbuminemia), chronic GI blood loss, and rarely ischemic bowel infarction.
Cardiac response: If ventricular function is impaired, a higher preload is required to maintain CO. As a result, the LV is remodeled over time: It becomes less ovoid and more spherical, dilates, and hypertrophies. Initially compensatory, these changes eventually increase diastolic stiffness and wall tension, compromising cardiac performance, especially during physical stress. Increased wall stress raises O2 demand and accelerates apoptosis (programmed cell death) of myocardial cells.
http://www.merck.com/mmpe/sec07/ch074/ch074b.html

10:14pm/14Mar