Published Jan 27, 2007
Carla25
111 Posts
We are studying CHF, and COPD in gerontology, I am really having a hard time understanding the Pathophysiology behind these diseases and my book is not helpful at all.
Can anyone help
PLEASE!!!!!!!
Little Panda RN, ASN, RN
816 Posts
http://sprojects.mmi.mcgill.ca/mvs/PATHOS/CHF.HTM
http://www.medscape.com/viewarticle/540983
http://www.thevest.com/research/whitepapers/626ABCOPDOverview.pdf
Here are a few sites I googled. The list that will show up when you do a search is extensive. Just keep looking and you will find what you are looking for. Hope this helps.
Daytonite, BSN, RN
1 Article; 14,604 Posts
heart failure. . .heart failure usually proceeds in an orderly fashion from the left side of the heart to the right side. there are actually only two types of heart failure: left and/or right. with both types of heart failure there is some degree of congestion in the lungs although it is more pronounced in left-sided heart failure. there is dyspnea with both. the left ventricle enlarges from increased workload and increased end diastolic volumes. this is also accompanied by the lack of oxygen to the tissue of the left ventricle due to the tissue becoming enlarged and stretched. these enlarged and stretched tissues of the left ventricle are unable function efficiently and allow blood to back up into the pulmonary veins and capillaries which results in engorgement of the pulmonary circulation. [clinical symptoms will be dyspnea on exertion, confusion, dizziness, orthostatic hypotension, decreased peripheral pulses, cyanosis and presence of an s3 gallop.] this also results in sodium and water being forced into interstitial spaces leading to pulmonary edema. [clinical symptoms will be coughing, presence of crackles, tachypnea, elevated pulmonary pressure and increased pco2.] if the patient happens to lie down, fluid from the patient's extremities will move into the systemic circulation and the compromised left ventricle is just unable to deal with this. as a result, fluid pools in the pulmonary circulation which worsens the pulmonary edema. the right ventricle now begins to feel the effect of this stress as it has to pump against increasing pulmonary vascular resistance. the right ventricle compensates over time by enlarging. the result of this enlargement of the tissue of the right ventricle is that electrical conduction times lengthen resulting in a slowing and irregularity of the heart beat. eventually, blood begins pooling in the right ventricle causing pressure and congestion in the vena cava and systemic circulation. [clinical symptoms will be elevated central venous pressures and jugular vein distention.] this backing up of the blood into the systemic circulation (think of this as a traffic jam affecting all the major blood passageways) leads to engorgement of the visceral veins. the engorged hepatic vein, in particular, will produce symptoms of nausea, abdominal pain and abdominal distension as the liver and spleen enlarge due to this engorgement with blood. as the pressure in the capillaries continues to rise, fluid is now being forced into the interstitial spaces of the peripheral circulation leading to pitting edema in the lower extremities and abdomen.
congestive heart failure is a very generic term. when you have a patient with this, you have to read the diagnostic test results carefully to determine just what kind of heart failure (left, right, left and right) is going on.
copd. . .chronic obstructive pulmonary disease is due to emphysema, chronic bronchitis, asthma or a combination of any of these three problems. in the early stages of these conditions the airways become constricted which increases the resistance in the airways. in all these conditions there is inflammation which stimulates the production of mucus which causes further blockage of the air passages and increases resistance. with these chronic inflammatory processes going on the cells of the lungs produce specific proteolytic enzymes as part of the healing process in attempting to clear the inflammation. however, since the inflammation is chronic these enzymes have the opportunity to exert their effects over a long period of time resulting in damage to the alveoli of the lungs by causing the rupture and destruction of alveolar walls. this results in loss of lung elasticity, loss of capillary surface exposure area as well as the loss of fibrous muscle tissue of the internal lung tissue. the result: uncompliant respiratory efforts and slowed inefficient gas exchange in the enlarged alveoli. with advanced disease the airways enlarge with inspiration allowing air to flow to the alveoli. however, with expiration the airways constrict which results in the air being trapped, or ball valving, in the alveoli.
thanks for helping!!!!