congestive heart failure occurs when the heart's pumping action is not able to meet the body's metabolic demands either because of increased demands, dysfunction of the heart itself, or both. the heart can compensate for this discrepancy in various ways such as tachycardia, hypertrophy; but with enough time none of these adaptations will suffice. "compensated" refers to such a case of chronic heart failure where increased heart rate or other factors have allowed the heart to maintain adequate CO and perfusion. similarly, "high output" failure refers to congestive heart failure with tachycardia to compensate, which results in peripheral vasodilation and warm extremities.
heart failure affects and is affected by many other systems of the body. generally, the sympathetic nervous system is overactive, causing peripheral vasoconstriction which shunts blood away from extremities. systemic venous congestion will also affect the renal system by way of diminished hepatic metabolism of aldosterone which will lead to increased fluid retention which will unfortunately negatively feed back into creating more pressure for the heart (note that the same heart stressing effect can happen with a patients sudden cessation of diuretics). in the lungs, heart failure cells might appear, which are macrophages full of hemosiderin.
left sided CHF, as we learned in CPD, involves dysfunction of receiving blood from the pulmonary system and thus presents with symptoms of pulmonary congestion such as pulmonary edema. on the other hand, RCHF involves dysfunction of receiving venous blood from the body and thus can present with signs of systemic congestion such as peripheral edema. LCHF is usually caused by infarction/ischemia of the left ventricle, hypertension, or mitral dysfunction whereas RCHF is most commonly caused by LCHF.
cardiomyopathies come in three flavors, dilated (90%), restrictive, and hypertrophic. dilated is when all four chambers are enlarged but not hypertrophic and can be caused by severe alcoholism. hypertrophic is severe hypertrophy of myocardium, especially the ventricular septum, which is generally caused by a genetic defect that causes a mutation in the proteins within sarcomeres. restrictive cardiomyopathy is generally due to hemochromatosis (excess Fe deposition) or amyloidosis (excess amyloid deposition) within the myocardium which renders it dysfunctional.
infectious endocarditis is an infection of the myocardium or heart valves, characterized by formation of "vegetations"- made up of platelets, fibrin, and bacteria. these have a high potential for embolization; septic emboli can manifest as Roth spots in the eye, petechiae on the skin, splinter hemorrhages in the fingernails. the main risk factors for infectious endocarditis include artificial valves, immunocompromise, IV drug abusers, alcoholics, procedures with catheters / grafts. endocarditis can also occur from an inflammatory origin, as in the case of Libman-Sacks endocarditis, which results in the case of SLE.
questions
introduction to CHF...
1. what is congestive heart failure?
2. how does the heart typically respond to heart failure initially?
3. why does frank starling's law not apply in cases of severe heart failure?
4. how many americans does CHF affect per year?
5. what is "compensated" or "decompensated" CHF?
6. describe the sympathetic response in acute CHF which compensates for decreased CO.
7. how can systemic venous congestion lead to fluid retention?
8. what are heart failure cells?
CHF types...
9. what is the difference between primary and secondary CHF?
10. what is a common cause of CHF related to drugs?
11. what are some common underlying conditions that can lead to CHF?
12. what can left sided CHF lead to and why?
13. what is left sided CHF usually caused by?
14. what is the most common cause of right sided CHF?
15. what is cor pulmonale?
16. describe the difference in symptom presentation between RCHF and LCHF.
high and low output failure...
17. what is the difference between high and low output heart failure?
18. what are some causes of high output heart failure?
19. how can Paget's disease cause high output heart failure?
20. what are some causes of low output heart failure?
cardiomyopathies...
21. what are the three types of cardiomyopathies and which is most common?
22. what is dilated cardiomyopathy characterized by? what is the most common cause?
23. what is hypertrophic cardiomyopathy characterized by? what is it caused by?
24. what is restrictive cardiomyopathy characterized by? what are the most common causes?
endocarditis...
25. what are "vegetations" in the context of endocarditis?
26. most common cause of endocarditis is...
27. what are some potential portals of entry for bacteria that might cause endocarditis?
28. what is the difference between acute and sub-acute infectious endocarditis?
29. the most consistent sign of endocarditis is...
30. what is a serious danger of vegetations besides their disruption of blood flow in the heart?
31. septic emboli from endocarditis can manifest in...
32. main risk factors for endocarditis.
most likely organism to cause IE in...
33. patient with native valves...
34. prosthetic valves...
35. IV drug abusers...
36. alcoholics...
37. after a cystoscopy/prostatectomy/catheters...
38. patients with colon cancer...
non-infectious endocarditis...
39. culture negative endocarditis may indicate...
40. what is the endocarditis of SLE called?
41. what is Marantic endocarditis?
answers
1. inability of the heart to pump out enough blood to meet the body's metabolic requirements.
2. increased contractility or increased heart rate.
3. if the myocardium is stretched beyond a certain point as in severe CHF, the optimum length for contractility is surpassed and the ventricles are overstretched; CO begins to decrease again.
4. 2 million.
5. compensated is CHF with adequate CO and decompensated is CHF with inadequate CO.
6. increased catecholamine activity causes peripheral vasoconstriction and shunting of blood away from extremities to internal organs.
7. systemic venous congestion leads to diminished hepatic perfusion which leads to diminished metabolism of aldosterone which leads to fluid retention.
8. hemosiderin laden macrophages in the alveoli.
9. primary is a dysfunction of the heart itself while secondary is a dysfunction of the heart due to the stress placed on it by other systems in the body.
10. cessation of certain heart medications; in particular diuretics, causes a sudden increase in fluid retention and thus stress placed on the heart.
11. conditions that cause myocardial dysfunction: coronary atherosclerosis, arterial hypertension, myocardial ischemia, infarction, inflammatory / degenerative muscle disease.
12. pulmonary congestion because of the increased pressure in the left ventricles (end-diastolic) and atrium.
13. left ventricular infarction / ischemia, hypertension or mitral dysfunction.
14. LCHF.
15. heart failure that results from an underlying lung disorder such as COPD.
16. RCHF presents with symptoms of systemic venous congestion and LCHF presents with symptoms of pulmonary congestion.
17. high output failure characterized by peripheral vasodilation / warm extremities while low output failure characterized by peripheral vasoconstriction / cold extremities.
18. hyperthyroid, stimulants, anemia, Paget's disease.
19. in Paget's, abnormal bone mass is formed with high vascularity, increasing the demand for O2 and thereby increasing the heartrate.
20. infarction, ischemia, endocarditis.
21. dilated restrictive and hypertrophic. dilated 90%.
22. all four chambers enlarged, chronic alcoholism.
23. hypertrophy of chambers (especially ventricular septum), abnormal diastolic filling, intermittent ventricular outflow obstruction. caused by a genetic defect that affects sarcomere function.
24. abnormal tissue that obstructs blood flow. hemochromatosis (excess iron deposition) and amyloidosis are two main causes.
25. infected thrombotic masses on myocardium or valves in infectious endocarditis.
26. bacteria: chlamydia, rickettsiae.
27. dental health, GU tract infection, skin infection, pulmonary infection, any infection in blood, IV drug users.
28. sub-acute is a gradual onset and usually takes place in a heart that already has damage, whereas acute is a sudden infection with a virulent organism with a poor prognosis.
29. fever.
30. their potential for embolization.
31. roth spots in the eye, petechiae, splinter hemorrhages.
32. artificial valves, immunocompromised patients, IV drug abusers, alcoholics, catheters, grafts.
33. strep viridans.
34. staph epidermitis.
35. staph aureus.
36. anaerobes and mouth bacteria.
37. gram- microbes such as ecoli.
38. strep bovis
39. endocarditis with inflammatory origin.
40. Libman-Sacks endocarditis.
41. endocarditis that results from the hypercoagulable state resulting from Trousseau's syndrome.
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