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176 Cards in this Set

  • Front
  • Back
define CHF
heart no longer able to eject venous blood return
low output CHF failure is due to what
decreased contractility
most common causes of L sided failure (6)
1. HTN
2. Mitral valve dz
3. aortic valve dz
4. ischemic heart dz
5. primary myocardial dz
6. myocarditis
most common cause of R sided heart failure?
LV failure
other causes of RSHF
1. lung dz
2. cor pulmonale
3. pulmonic/triscuspid valve dz
4. L --> R shunts (PFO)
conditions causing volume overload
1. valvular regurg
2. abnormal shunts
volume overload causes what kind of hypertrophy
eccentric
pressure overload causes what kind of hypertrophy
concentric
conditions causing pressure overload
1. valvular stenosis
2. HTN
MAJOR cause of death in pts w/ untreated HTN
CHF
difference b/w compensated and decompensated heart failure
compensated: F-S still applies and CO is OK

decompensated: heart is compromised and CO drops. F-S no longer applies
what kind of failure is CHF, backward or forward
backward
why does aldosterone inc. in response to CHF?
b/c CO is decreased in CHF t/f kidney is not being perfused so aldosterone inc's to turn up the RAS to inc. fluid

kidney releases renin. renin turns angiotensinogen to Ang 1. ACE converts Ang1 to Ang2. Ang2 turns up aldosterone.
Most common clinical manifestation of LVF (which is most commonly caused by CHF) is what?
dyspnea
where is BNP secreted from
ventricles
what increases bnp (heart)
increased stretch and inc. volume
how does BNP work? (4)
1. down reg's the RAS
2. dec's sympathetic heart activity
3. increases renal blood flow and
4. Na+ excretion
BNP normal range
<100 PG/mL
BNP can also be found in what other fluid imbalance problem
renal insufficiency
can you use BNP to "rule in" CHF?
NO; BNP is used to r/o CHF in an adjunctive way
what situation is BNP best used?
acute ER setting w/ SOB
List 3 ACS's
1. unstable angina
2. non-STEMI
3. STEMI
List 2 types of Ischemic Heart Dz's (IHD) and describe each
1. Transmural infarct-TI(full wall thickness)
2. Subendocardial infarct-SI(partial wall thickness)
Which is more severe and more common, TI or SI?
TI
Where do TI's usually begin?
least perfused subendocardium
TI's almost all caused by combo of: (4 things)
1. Marked stenosis
2. Thrombosis over the fissure, rupture, or hemorrhage into plaque
3. Plt activation/aggregation and release of thromboxane and other vasoactive products
4. vasospasms from vasoactive products (cocaine)
Name 2 vasoactive substances
1. thromboxane
2. cocaine
Reperfusion injury majorly caused by what 2 things
1. inc. Ca++ inflow
2. free radicals from segs
Is it more common for TI to occure in R ventricle alone or in conjuction w/ LVI? Why?
-RVI more commonly occurs w/ LVI than isolated RVI

-b/c the posterior septum may extend into the posterior R ventricle
vascular distribution of TI's from greatest to least
LAD > RCA > LCA
40-50% > 30-40% > 15-20%
What walls of the heart are infarcted by LCA, LAD, RCA?
LCA --> posterolateral LVFW infarct

LAD --> anterior LVFW infarct near apex and anterior 2/3 of septum

RCA --> Posterior (inferior or diaphragmatic) LVFW infarct and posterior 1/3 of septum
what gross changes occur 0-12 hrs post TI
no change
what gross changes occur 18-24 hrs post TI
pallor
what gross changes occur 24-72 hrs post TI
pallor, hyperemia
gross changes at 3-7 days post TI
hyperemic border, central yellow-brown softening
gross changes 10 days post TI
maximun yellow and soft w/ red-brown margins
gross changes 7 weeks post TI
scarring complete
microscopic changes 0-2 hrs post TI
Subtle: waviness at fiber border, fine cytosol lipid droplets, cellular swelling, band contraction in reperfused areas
mircoscopic changes 4-12 hrs post TI
coagulative necrosis begins, edema, hemorrhage, early PMN infiltration,chromatin margination
microscopic changes 18-24 hrs post TI
coagulative necrosis w/ loss of nuclei and striations, lots of PMN infiltrates
microscopic changes 3-7 days post TI
disintegration of dead fibers w/ macrophage activity, granulation tissue formation
microscopic changes 3 weeks post TI
inc'd collagen, dec'd cellularity
what complication occurs in 4-15% of transmural AMI's (TAMI) b/w days 2-10
rupture of infarct
Do most ruptured TAMI's involve the free wall or interventricular septum
free wall --> 90%
Subendocardial infarcts begin where (layer of heart muscle)
least well perfused myocardium --> subendocardium w/ advanced stenosis
what is a big difference b/w subendocardial and transmural infarcts (layers of heart muscle)
subendocardial --> localized to no more than 1/2 (usually 1/3) of myocardium

transmural --> all layers (endo, myo, epicardium)
do most (80%) of Subendocardial infarcts occur w/ or w/o major trunk thrombosis
w/o
Name 3 things that are notorious for causing hypotensive episode leading to subendocardial infarct
1. shock
2. arrhythmia
3. cardiac surg
which is more likely to dvlp pericarditis, ventricular aneurysm, or rupture SI or TI
TI
___% of Asx AMI's are recognized by EKG or enzymes or both
20%
more than ___% of all IHD deaths are from ventricular arrhythmias
50%
what will rupture of the LVFW lead to
hemopericardium --> cardiac tamponade
What happens to 30% of the TCA's (transluminal coronary angio)
re-stenosis in 2-3 yrs
What happens to CABG vein grafts eventually? Which vein graft is the exception?
-intimal thickening in 5-10 yrs or sooner

-internal mammary
Define IHD
imbalance b/w myocardial need for O2 and supply
almost all O2 deficiency is d/t severe ____ and ____
Aortic stenosis and CAD
4 big causes of IHD
1. inc'd demand
2. dec'd coronary artery perfusion
3. Anemia - dec'd O2 transport
4. sudden loss of BP
4 clinical manifestations of IHD
1. Angina pectoris (AP)
2. MI
3. Chronic ischemic heart dz
4. SCD
T/F: AP is defined as paroxysmal episodes of precordial chest pain/discomfort caused by episodic ischemia which causes an infarction
F--> ...which DOES NOT cause and infarction
define stable AP
provoked by exertion but relieved w/ rest
define variant AP
occurs at rest and relieved by vasodilators (nitroprusside, hydralazine)
variant AP AKA
Prinzmetal's AP
define unstable or crescendo AP
intense, prolonged sometimes worsening pain W/ SUBCLINICAL FINDINGS (mild enzyme/slight EKG changes) and pain responds slowly to vasodilators
all angina can be caused by any combo of what 4 things
1. fixed stenotic lesions
2. vasospasms
3. plt aggregation
4. inc'd myocardial demand
chronic IHD AKA
ischemic cardiomyopathy
chronic IHD is caused by what specifically?
- significant coronary artery stenosis
older pts w/ h/o ____ or previous ____ are good candidates for chronic IHD
- AP (fixed stenotic lesion)

- MI
what are 3 normal gross morph wear and tear changes seen in chronic IHD (2 mitral, 1 aortic)
1. thickened mitral leaflets --> from collagen
2. calcifications of mitral annulus
3. senile calcific aortic stenosis
chronic IHD is a Dx of exclusion in elderly with a h/o? (3 things)
1. angina
2. conduction defects
3. infarction
what is the major DDx assoc. w/ chronic IHD?
dilated cardiomyopathy
microscopic morph of chronic IHD (5)
1. diffuse myocardial fiber atrophy w/ dense perinuclear lipofuscin (fine granular yellow-brown pigments) in myocytes
2. perivascular interstitial fibrosis
3. patchy foci of scarring
4. Myocytolysis of cells -- interstitial perimysial (muscle) fibrosis
5. possible previous scarring
how is SCD defined?
sudden death w/in 24 hrs of symptoms
Name some things that can cause SCD (4)
1. PE
2. Heart Dz
3. Ruptured AA
4. CNS d/o
What is the most common cause of SCD?
chronic IHD
chronic IHD can predispose you to what arrhythmia?
V fib
How often is SCD the initial manifestation of IHD?
50%
What is the 2nd most common cause of cardiac death?
HHD (hypertensive heart dz)
2 tests that can discover compensated HHD
1. EKG
2. Echocardiogram
what may be the first 2 signs of HHD
1. A fib
2. CHF
what is a major risk factor that accelerates CAD
HHD
minimum criteria for the Dx of HHD (2)
Aortic Stenosis or Coarctation of the Aorta -->L vent hypertrophy in absence fo other CV path that can induce HHD
AND
hx of HTN
How is LVH defined?
wall thickness of >= 2cm
Dz caused by pulmo HHD resulting from d/o of the lungs or pulmonary vasculature which causes RVH and dilation leading to failure
cor pulmonale (CP)
Acute CP cause causing sudden death? Is the heart grossly normal in this condition?
PE

Yes
chronic CP often follows prolonged pressure overload of _____ and _____

common causes of this
pulmo arteries and arterioles

COPD, TB, pneumoconiosis, sarcoidisis, scleroderma, PF, kyphoscoliosis, Pickwickian syndrome (marked obesity)
T/F: In CP, there is thickening of the muscle below the pulmonary valve which leads to obstruction.
T
Besides the pulmonary valve thickening, what are some other secondary issues (thickening, etc) in CP?
- moderator band
- mild tricuspid regurg and secondary thickening
T/F the LV remains unaffected in CP.
False. It is compressed by the RV
What Dz process is IHD mainly d/t?
coronary atherosclerosis
unstable angina can be d/t ____ of plaque w/ formation of _____ thrombus
- fissuring
- mural
Dx of AMI based on? (3)
1. Symptoms
2. EKG
3. CK-MB and cTn's
Impaired filling of LV w/ LA hypertrophy and dilation --> pulmonary congestion and RV hypertrophy and dilation --> inc'd venous pressure and dec'd periph perfusion ??CHF??describes what type of valvular dz
Mitral stenosis
Is LV hypertrophy found in pure mitral stenosis?
No; however, the rigid mitral valves are often insufficient and may cause regurge --> LA & LV hypertrophy
What is a deadly complication assoc. w/ the enlarged LA in mitral stenosis? (think systemic)
multiple brain infarcts d/t possible mural thrombi
where do the the mural thrombi assoc. w/ brain infarct usually hang out in Mitral Stenosis?
atrial appendage
List some external causes of Mitral Stenosis (3)
1. Ergot alkaloids for migraines
2. Phen-fen
3. Radiation of CA
LA and LV hypertrophy and dilation --> pulmonary congestion-->pulmonary HTN and RV hypertrophy and dilation describe what valvular dz
Mitral Regurg (insufficiency)
How can mitral regurg cause CHF later
LA dilation reduces the load on the LV
List some late complications assoc. w/ mitral regurg (3)
1. thromboemboli
2. supraventricular tachycardia or arrhythmia
3. sudden death
What is most common cause of mitral regurg?
MVP (mitral valve prolapse) AKA "floppy valve"
Age and gender MVP's are usually found
20-40 yo; female
connective tissure d/o assoc. w/ MVP
marfans
chromosome mutation and inheritance of MVP
16p; AD

rarely X-linked recessive
which mitral valve leaflet is most prone to balloon out?
posterior
what 2 things are heard w/ auscultation of MVP?
1. midsystolic click
2. late systolic murmer
Is there an inc'd chance of SCD arrhythmias and infective endocarditis w/ MVP
Yes
aortic stenosis results in ____ hypertrophy and eventual dilation
LV
what kind of overload is aortic stenosis pressure or volume? And what happens to the pulse pressure?
- pressure

- pulse pressure narrows
Why does the pulse pressure narrow?
b/c the concentric LV hypertrophy inc's the diastolic pressure
aortic stenosis more common in men or women?
men
is MOST aortic stenosis rheumatic (illness) related in origin?
No
is aortic stenosis MOST often calcific, senile, and degenerative?
Yes
Is the mitral valve usually involved in aortic stenosis?
No
Can congenital malformed valves calcify in the early teens?
Yes
Are bicuspid valves more common in men or women
4:1 Men:Women
Biscupid aortic stenosis inc's risk for (3) things
1. ENDOCARDITIS
2. aortic dilation
3. dissection
What accounts for 8-10% of all congenital outflow obstructions and has a gray white fibroelastic endocardial ridge
subaortic (subvalvular) stenosis
which is it supravalvular or subvalvular aortic stenosis, that is the least common and represents an arterial dysplasia?
supravalvular
couple of other causes of aortic stenosis?
1. type II hyperlipidemia
2. glycogen storage diseases
eccentric LVH and dilation w/ volume overload, a wide pulse pressure w/ failure to maintain diastolic pressure with ability to cause SCD d/t impaired coronary filling complicated by inc'd O2 demand of the extremely dilated LV describes what valvular insufficiency (regurg)?
aortic regurg
Aortic stenosis = wide or narrow pulse pressure

Aortic regurg = wide or narrow pulse pressure
AS = narrow

AR = wide
name given to oval defects in the valve above the lines of closure in mitral/aortic valve that have no funtional significance
fenestrae
define Lambl's excrescences
fibrous bands in the centers of the valve
type of deposits that can be found on the mitral/aortic valve after 30 yo
lipid
is Libman-Sacks a BTE or NBTE?
NBTE
what autoimmune dz is libman-sacks endocarditis assoc. w/?
SLE
"Rheumatoid" endocarditis assoc. w/ what dz
ankylosing spondylysis
define NBTE
non-inflammatory accumulation of plts, fibrin, and collagen
In autopsy ~75% of NBTE were assoc. w/ what type of CA
colon adenocarcinoma
2 immunologic mechanisms (general) in NBTE
1. Ab's to tumors
2. Immune complex deposition
is bacterial endocarditis vegetative or verucca like growths
large vegetative, inflammatory
bug rate(%) of occurance in acute bacterial endocarditis?
Staph 33% > Strep 24% > pseudomonas 14% > Klebsiella 5% and Serratia 5%
G- or G+ bugs common in IV drugies and diabetics
G+ bugs
4 predisposing factors for BE
1. deformed valve (RHD)
2. in adults, transient bacteremia w/ dental surg heart caths, UTIs, abortions, endo procedures, IV durgs, etohism
3. kids, congenital heart dz
4. pre-existing NBTE
2 extracardiac consequences of BE
1. skin petechiae
2. Osler's nodes on fingertips
what are janeway lesions
hemorrhagicpainless immune complex deposits on the palms and soles
what are Osler's nodes
red, raised, tender lesions on pads of fingers and toes
Dx of Be consist of: (6)
1. + blood cultures
2. + serology
3. PCR
4. bugs in the lesions
5. Echocardiogram shows lesions
6. fistulas created from abcesses
what layers of the heart does RHD effect?
Pancarditis
time frame for RHD following infxn
10 days to 6 weeks
what infxn causes RHD?
group A strep (S pyogenes --> B hemolytic)
3 NBTE's
1. Rheumatic valvular endocarditis
2. Libman-Sacks endocarditis
3. "Rheumatiod" endocarditis
what areas can RHD effect besides the heart?
joints, skin, brain
what is order of valvular involvement from greatest to least?
mitral > mitral & aortic > aortic & tricuspid > mitral & tricuspid > all 4
is pulmonic valve involvement w/ RHD common or rare?
rare
What are the Jones Major Criteria for Dx of RF? (5)
1. Carditis
2. Migratory polyarthritis
3. Subcutaneous nodules
4. Cutaneous erythema marginatum
5. Sydenham chorea
What are the Jones Minor Criteria for Dx of RF? (3)
1. Fever
2. Arthralgia
3. inc'd acute phase proteins (CRP, ESR)
What does it take to Dx RF w/ Jones criteria?
2 majors OR 1 major and 2 minors
what 2 things (lab test) indicate recent infxn of ~10 days-6wks?
1. Anti streptolysin O (ASO)
2. DNAse B
What is a MacAllum's patch?
thickened fibrous plaque on posterior LA above posterior leaflet of mitral valve
3 things related to gross examination of RF
1. MacAllum's patch
2. Endocardial pocket on upstream side of an incompetent valve
3. LA mural thrombus w/ mitral stenosis
Microscopic RF changes can be seen earliest at what structure?
valve ring
what are the earliest microscopic changes seen in RF path?
edema --> vascularization of leaflets --> infiltration of lymphs, plasma cells, and PMNs
what are 4 other microscopic changes seen in RF path?
1. Fibrinoid change near surface
2. Anitschkov myocytes AKA Aschof cells
3. Aschoff bodies
4. Verrucae at lines of closure
describe what Aschoff cells, Aschoff bodies, and the veruccae consist of in the microscopic changes of RF.
Aschoff cells --> elongated "caterpillar" nuclei

Aschoff bodies --> aggretates of Aschoff cells w/ multinucleated giant cells AKA granuloma

Verrucae --> plt thrombi on altered valve surface at the lines of closure
Why do Aschoff bodies form?
Antibody (Ab) formation
% of pts w/ RF have what Ab's to what? (4)
1. streptolysins
2. Hyaluronidase
3. streptokinase
4. DNAses
Which GAS subtype causes the xreactivity to cell wall antigens (Ag)
type 5 GAS
What are the 4 distinct tissue targets assoc. w/ the xreactivity of RF?
1. subsarcolemmal cytoplasm of cardiac myofibers
2. smooth muscle of intracardiac vessel walls
3. heart valve fibroblast Ag's
4. CNS neuronal Ag's in subthalamic and caudate nucleus
what do immunofluorescent studies correspond and what is the correlation with the severity?
- IgG, IgA, IgM, complement
- proportional
what % of pts w/ post strep glomerulonephritis is not assoc. w/ any carditis
60%
Will all pts w/ RF have detectable xreactive Ab's?
No
Will you have a higher % chance of having xreactive Ab's with recent strep infxns or RF/RHD
RF--> 55%
RHD--> 58%
recent infxns--> 24%
Mechanism by which immune response to strep Ag's in RF occur?
delayed type hypersensitivity

BTW: in vitro stimulation macrophage inhibitory factor (MIF) or blastogenic response (triggering T cell proliferation w/ defined Ag)
3 related COD's related to RF
1. CHF
2. mural thrombotic emboli
3. BE
term "tree barking" which is dilation and scarring of Aorta is used w/ what infective valvular dz
syphilis
Aortitis occurs in ___% of tertiary syphilis if left untx'd
70-80%
where does T pallidum like to lodge
vasa vasorum
"tree barking" can cause (3)
1. aortic regurg
2. coronary ostial stenosis
3. aneyrysms (not common)
where does coronary ostial stenosis assoc. w/ syphilis occur?
just above aortic valve
What kind of aneurysms are commonly found in cardiovascular syphilis?
None; they are NOT common
valvular causing dz assoc. w/ the HLA B-27 Ag?
Ankylosing spondylitis
Inflammation of the intima of an artery which leads to closure of the lumen
endarteritis obliterans
3 collagen d/o's assoc. w/ MV problems
1. marfans
2. Ehlers-Danlos
3. Stickler syndrome
stenosis of which 2 valves account for 2/3 of all valve dz's?
aortic and mitral
General acronym used to describe sterile vegetations of the valves which can cause embolic complications?
NBTE