Cardio I Flashcards
1
Q
describe hypertrophy
A
- increase in size of the cardiac myocytes
- induction of genes coding for proteins:
- actin, myosin (fetal isoforms of proteins) → increased sarcomers
- usually not accompanied by increase in vascularization → relative decrease in capillary density → ischemia → fibrosis → reduced diastolic relaxation
- coupled with increased metabolic and O2 need → cardiac decompensation
2
Q
describe concentric hypertrophy
A
- occurs in pressure overload on ventricles
- e.g. HTN, aortic stenosis → new sarcomeres are added in parallel to existing sarcomeres → increased wall thickness and decreased diameter of cavity
3
Q
describe eccentric hypertrophy
A
- occurs in volume overload on ventricles
- e.g. aortic regurgitation → new sarcomeres are added in series with existing sarcomeres → muscle mass increases proportional to chamber dilatation; there can be significant hypertrophy without any increase in thickness of the walls
4
Q
A
5
Q
A
6
Q
describe systolic dysfunction and examples of when it occurs
A
systolic dysfunction = inability to contract properly
- myocyte loss, e.g. MI
- pressure overload, e.g. hypertension
- volume overload, e.g. valvular regurgitation
- decreased contractility e.g. myocarditis, DCM
7
Q
describe diastolic dysfunction
A
diastolic dysfunction = inability of the heart to relax and fill
- massive ventricular hypertrophy
- myocardial fibrosis
- amyloidosis
- constrictive pericarditis
8
Q
describe high output failure vs. low output failure
A
- high output failure:
- occurs due to increased tissue demands e.g. anemia, hyperthyroidism, pregnancy
- symptoms of heart failure occur in spite of well-functioning heart (high cardiac output)
- is a systolic dysfunction
- low output failure:
- heart failure with decreased cardiac output
- majority of cardiac disease causes low output HF
9
Q
describe forward vs. backward heart failure
A
- forward failure:
- decreased output to the systemic circulation
- leads to renal hypoperfusion → activation of renin-angiotensin system → sodium and water retention → edema
- patient would have low BP, fatigue, syncope, shock
- backward failure:
- pulm. congestion → pulm. edema → pulm. HT → RHF → systemic venous congestion → edema, ascites, raised JVP, congested liver
10
Q
describe compensatory mechanisms found in heart failure
A
11
Q
describe how LHF affects the brain, kidney and lungs
A
- brain: hypoxic encephalopathy
- kidney: acute tubular necrosis
- lungs:
- gross:
- heavy & wet lungs, cut surface → exudes a frothy mixture of surfactant-rich fluid and blood
- histo:
- congestion of pulm. alveolar capillaries
- edema fluid in alveolar spaces
- persistent cases → brown induration of lungs
- gross:
12
Q
describe how RHF affects the liver and spleen
A
- liver:
- chronic passive congestion
- nutmeg liver
- spleen:
- enlargement and congestion of spleen
- soft tissue edema