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183 Cards in this Set

  • Front
  • Back
endocardium =
innermost layer of the heart

- myocardium = bulky
the epicardium is also called:
the visceral pericaridium
location of heart ~~
costal cartilage 2-6

- the heart cones out posteriorly
what's found in the AV sulci?
vasculature To the heart
diaphragmatic surface of the heart =
the inferior sirface

- base of heart = posterior surface
3 structures of the RA:
1. fossa ovalis (used to be foramen ovale)

2. pectinate muscles (making up most of the wall)

3. right auricle on the outside
3 structures of the RV:
1. trabeculae carne

2. papillary muscles/chordae tendinae

3. *moderator band*
3 structures of the LV:
1. membranous septum

2. muscular part of IV septum

3. trabeculae/pap/chordae
both the pulomnary trunk and the aorta have:
3 cusps

- both called semilunar valves
all 4 of the valves are in:
one plane
the valves are anchored to the heart by:
a fibrous skeleton called the annulus fibrosus
the LV wall is MUCH ____________ than the RV wall
thicker
**in any cross-section of the heart, the posterior surface is:***
the FLAT part
conduction pathway: SA node =>
AV node => Bundle of His => right and left bundle branches => Purkinje
the conduction pathways members are composed of:
modified cardiac muscle
the SA node is found in:
the wall of the RA, at the entrance of the SVC
the AV node is found in:
the interATRIAL septum
the Bundle of His is found in:
the IV septum
the coronary arteries originate at:
the aorta
the right coronary artery travels through the:
right AV sulcus
the right coronary artery becomes the:
posterior descending artery (PDA)
the PDA supplies:

(5)
1. posterior 1/3 of the IV septum

2. SA and AV nodes

3. posterior LV

4. post papillary muscles

5. diaphragmatic surface
the left coronary artery quickly branches into:

(2)
1. the LAD

2. the circumflex branch
the LAD supplies:

(3)
1. anterior 2/3's of IV septum

2. anterior LV

3. apex
histology of myocardium:

(5)
1. sheets running in a direction

2. **striations perpendicular to the sheets**

3. centrally-located nuclei

4. cells branch

5. intercalated disks are obvious
tunica intima =

(3 layers)
1. simple squamous epithelium

2. basement membrane

3. lamina propria (CT)
the 3 layers of the tunica intima are ________________ histologically
indistinguishable
tunica media = muscular layer of variable thickness =
SM and elastic fibers
adventitia =
CT

- think fibroblasts producing pink collagen
**P wave ~~ **

(2)
1. atrial depol

2. beg. of atrial diastole
**QRS ~~ **

(2)
1. ventricular depol

2. beg. of ventricular contraction
* T wave ~~ *
ventricular repol/diastole
** a wave ~~**
atrial contraction
** c wave ~~ **
closing of mitral valve
** v wave ~~ **
LA filling up with blood
prominent a wave ~~

(2)
1. RVH

2. tricuspid stenosis
prominent v wave ~~

(1)
tricuspid regurgitation
S1 = closure of:
AV valves

(mitral and tricuspid)
S1 is heard best at:
the apex
intensity of S1 is a function of:

(3)
1. distance of separation

2. mobility

3. Dp/dt
**S1 is accentuated with:**

(3)
1. short PR interval

2. mild mitral stenosis

3. high CO or HR
**S1 is diminished with:**

(5)
1. long PR

2. AV block

3. mitral regurgitation

4. severe mitral stenosis

5. stiff LV
S2 = closure of:
A3 and P3 valves

- A3 before P3
sometimes, _____________ _____________ of S2 occurs
physiologic splitting
pathologic splitting of S2 occurs with:

(2)
1. RBBB

2. pulm. stenosis
S3 =
tensing of chordae tendinae during *rapid filling of ventricles*
S3 is heard during:
early diastole, following openig of AV valves
S3 is NORMAL in children and YA's, but in adults it indicates:

(2)
volume overload or CHF
S3 is also called:
*ventricular* gallop
S4 occurs:
LATE in diastole
S4 is also called:
*atrial* gallop
S4 occurs with dec. ventricular compliance, so ~~

(2)
1. LVH

2. myocardial ischemia
CO =
5L / min
preload = how far back he pulls =
**initial stretch** = **LVEDV**
ideal sarcomere length =
2-2.4 micrometers
***FS relationship:***
inc. preload (up to 2.4 micro) = > inc. SV
the FS Law relates:
preload to function
contractility = elasticity of the band =
how hard the heart contracts at a given preload and afterload

= performance of the heart
contractility is also called:
ionotropy
afterload =
where ejection goes

= R to ejection, in the form of Pressure
ejection fraction is an ___________ of ______ ____________
indication of LV function
the EF is measured by:

(3)
1. ECHO

2. cath

3. nuclear imaging

normally 67%
EF formula =
EDV - ESV / EDV
EKG's measure the:
MEAN direction of flow of all the cells
intervals MUST contain:
waves

- segments ~~ between waves (NO waves in them)
**PR interval:**

(2)
1. from beg. of P wave to beg. of QRS

2. ~~ conduction of AV node
normally, the PR interval should take between:
0.12 and 0.2 seconds
**QT interval:**

(2)
1. beg. of QRS to END of T

2. represents how long the ventricles are electrically active
(there should be no differentiation between an increase in an interval and an increase in:
the width of the wave, for our purposes)
***normal QT interval (time) =
<0.1 sec
>0.12 sec Qt interval =
DEF abnormal
wide QRS ~~

(2)
1. BBB

2. ventricular arrythmias
(ventricles separated from SA rhythm)
limb leads (I, II, and III) measure the:
frontal place
aV stands for:
augmented voltage
precordial/chest leads m. activity in the:
horizontal plane
v1 is found:
in the 3rd IC space, to the right of the sternum
v4 is found:
at the mid-clavicular line, in the 4th IC space
v6 is found:
at the ant. axillary line, 6th IC space
5 sets of **contiguous leads:**
1. I and aVL

2. II, III, and aVF

3. v5, v6

4. v2-v5

5. v1, v2
sinus rhythm = normal rhythm; requires:

(3)
1. P, QRS waves

2. *upright* P in **Lead II**

3. regular
rate: big box =

small box =
0.2 sec

- small = 0.04
QTC (corrected): normal =
<450 ms
QTc of >450 ms ~~
heart isn't repolarizing fast enough
RAE =>

(on EKG)
larger P wave in II, v1
LAE =>
**big P depression* in v1
LVH =>
S wave of v1 or v2 + R wave of v5

> or = to 35 mm
RVH =>
R wave > S wave in v1,

as well as RAD
ichemia =>
T-wave inversions, ST depression
ischemia ~~ angina, which is:
substernal pain that gets worse with exertion and better with rest/nitroglyceride
injury (heart muscle dying in front of you) =>
ST elevation ("tombstones" in v's)
infarct (muscle is dead/has been dead) =>
Q waves look weird on II, III, and aVF
ST segment =
*end* of QRS to *beg* of T
upright P wave in I and II means:
the signal is coming from the SA node
a QRS dsuration of > or = 0.12 always indicates:
BBB

- if upright in v1, then it's RBBB;

if not, it's LBBB
if you have a LBBB,
all criteria for ST elevation, etc are off
atherosclerosis =
progressive accumulation of SM cells, lipids, and CT within intima
athero is a disease of:

(2)
large and medium-sized arteries
athero eventually leads to:
ischemic heart disease,

the leading cause of death in US
spectrum of where ischemia occurs:

(6)
abdominal arteries > coronary arteries > popliteal > descending thoracic aorta > internal carotids > CoW
classic atheroma =

(3)
raised, focal intimal plaque + necrotic lipid core + fibrous cap
cell constituents of atheroma:

(wrt cells, CT, and lipids)
1. SM, macrophages, leukocytes

2. collagen, elastin fibers

3. cholesterol/esters
3 stages of athero, from beginning to intermediate to advanced:
1. fatty streak

2. fibrofatty plaque

3. complicated lesion
fatty streak =
lipid-filled foam cells with T-cells and extracellular lipid in intima
features of fatty streaks:

(2)
1. NOT significantly raised => NO disturbance of flow

2. seen in all children by age 10
fibrofatty plaque =

(2)
necrotic lipid core + fibrous cap

(lipid core includes foam cells and cholesterol)
2 features of fibrofatty plaque:
1. *raised* => disturbance of blood flow

2. media *not* affected
***5 things associated with complicated athero lesions:***
1. patchy or massive calcifications (blue)

2. focal rupture or ulceration of luminal surface

3. hemorrhage

4. **superimposed thrombosis**

5. weakening of media
(lesion =
region that's suffered damage)
rupture or ulceration of complicated lesion =>

(2)
1. exposure of thrombogenic elements

2. embolization
hemorrhage tends to occur in complicated lesions b/c:
bunch of small, new vessels form around/within the plaque
weakening of tunica media comes in the form of:

and leads to:
loss of elastic tissue and thinning

=> anuerysm
IHD ~~ ______ of cardiac deaths
>80%
Ischemic Heart Disease =
**coronary** athero with fibrofatty and/or complicated plaques
***examples of ACUTE plaque changes:***

(2)
1. hemorrhage INTO the atheroma

2. rupture or otherwise exposure of thrombogenic elements
***ACUTE plaque changes =>
acute ischemic episodes,

***like acute MI, unstable angina, sudden death***
bottom line of ischemia: inadequate blood flow =>
inadequate O2 to meet demand of the heart
**most common vessel causing infarct =
LAD

- circumflex = least common
circumflex artery supplies:

(2)
1. lateral LV

2. posterolateral LV
MI occur either:
subendocardially (on the inner surface) or transmurally (along the full thickness of the LV)
features of subendocardial MI:

(4)
1. inner 1/3 to 1/2 of LV

2. multifocal/patchy

3. *circumferential*

4. often the *result* of shock
***3 things that you DON'T see with subendocardial MI:***

(like you do with transmural MI)
1. epicarditis

2. coronary thrombosis

3. aneurysms
4 features of transmural MI:
1. uniform damage

2. follows coronary artery distribution

3. often *causes* shock

4. MAY cause aneurysms
interplaque hemorrhage =
hemorrhage INTO the atheroma
reorganization =>

(2)
1. granulocytes

2. recanalization
4 primary manifestations of IHD:
1. angina

2. sudden death

3. MI

4. chronic IHD
acute MI ~~
*discrete* focus of ischemic necrosis in the heart
2 features of AMI:
1. LV much more commonly inbvolved

2. ischemia of 20-30 min can cause it
***AMI is frequently the result of:***
**acute plaque changes** with coronary artery thrombosis
macroscopic features of infarction:

(6)
1. not much before 12 hours

2. => dark mottling (12-24 hrs)

3. central yellow-tan (3-7 days)

4. max yellow-tan, with red-tan border (7-10 days

5. gray-white scar (2-8 wks)

6. mature scar (>2 mths)
contraction band necrosis is typical in infarcts and is seen at the:
borders of infarcts
acute MI =>

(2)
1. a-nucleated cardiac cells

2. INC neutrophilia
healed MI =>
blue collagen staining
10 complications of MI:
1. arrythmias

2. LV failure/cardiogenic shock

3. extension of infarct

4. free wall rupture

5. septal perforation

6. pap. muscle rupture

7. aneurysm

8. mural thrombosis

9. pericarditis

10. Dressler's syndrome
LV failure/cardiogenic shock ~~ MI's of:
>40% of the LV
free wall rupture is most common in days:
1-4 of infarct, when walls are weakest

- a complication of large infarcts (>20%)
free wall ruptures occur at:
*junction* of infarct and normal muscle
free wall ruptures =>
hemopericardium (blood in the pericardial sac)

=> death from tamponade
papillary muscle rupture =>
mitral insufficiency, regurgitation
aneurysms ~~ increased ___________________, =>
workload

=> hypertrophy
"mural thrombi" =
thombi adherent to the vessel wall => embolisms
pericarditis =
inflammation of the epicardium => chest pain, pericardial friction rub
Dressler's syndrome =
delayed pericarditis
CIHD =
progressive heart failure secondary to ischemic myocardial damage
4 features of CIHD:
1. ischemic cardiomyopathy

2. cardiomegaly

3. coronary atherosclerosis, sts with total occlusion s

4. multifocal healed infarcts
ischemic cardiomyopathy =
LV is enlarged, dilated, and weakened
myocardial ischemia results from:
an IMbalance b/w O2 supply and O2 demand
***atherosclerosis disrupts O2 supply by:***

(2)
1. decreasing coronary artery diameter

2. disrupting endothelium function
3 chief determinants of O2 demand:
1. wall stress

2. HR

3. contractility

(all directly proportional)
chronis stable angina is largely treated by reducing:
demand

- unstable angina is treated by increasing supply
b/c O2 carrying capacity is relatively constant, the primary determinant of O2 supply to myocardium =
coronary blood flow
**regulation of blood flow occurs mostly in:**
the smaller "resistance" vessels
coronary blood flow to the heart occurs during:
**diastole**

- increasing HR => inc. syst/diastole ratio => LESS blood flow to heart

thus, decreasing HR => increasing flow to the heart
what is the major determinant of R in blood vessels?
radius

R ~ 1 / r^4
**coronary arteries are capable of sufficient compensatory dilation to prevent ischemia, up to:**
70% occlusion of lumen diameter
2 endothelium factors:
1. N.O.

2. endothelin-1 (vasoconstrictor)
N.O. is the most potent endogenous:
vasoDILATOR
***athero disrupts normal regulation of vascular tone by disrupting the endothelium; 2 ways it does this:***
1. dec. in radius => inc. in R

2. endothelial dysfunction => dec. in vasodilation
formula for wall stress, T:
= P x r / 2 m

where m = thickness
contractility, preload, and afterload are ALL directly proportional to:
O2 demand

inc. Afterload or preload => inc. Pressure => inc. T (wall stress)

while inc. contractility => more ATP req'd => inc. O2 demand
***what do catecholamines do?***

(2)
1. inc. contractility, HR (via B r's)

2. vasoconstrict (via alphas)
***athero and catecholamines: b/c of athero-caused endo dysfunction,***
vasoconstriction due to catecholamines is NOT opposed by endo's counter vasodilation

=> excessive constriction

=> in athero arteries, physical activity/emotional stress can BOTH inc. demand for O2 AND dec. supply

=> ischemia
different severity/duration of ischemia =>
different effects on myocytes

reversible recovery of myocyte function < stunned myocardium < hibernating myocardium < irreversible necrosis/damage
"stunned" =
not functioning as well
angina =
chest pain due to inadequate supply of O2 to the heart muscle
"typical" chest pain features:

(4)

(and relevance)
1. radiation to arm(s)

2. ~exertion

3. described as pressure

4. ~diaphoresis

=> inc. likelihood of AMI
diaphoresis =
sweating
"atypical" chest pain ~~

(3)
sharp, positional, pleuritic
ischemia makes the heart stiffer, thus compromising:
diastole (filling)

and also some pumping (systole)
stress tests ~~
provoking and detecting ischemia
coronary angiographies are reserved for pts with:

(3)
1. angina refractory to drug therapy

2. unstable presentation

3. abnormal non-invasive tests

= gold standard for diagnosis of CAD
3 features of chronic stable angina =
1. exertion/emotion then rest

2. "stable" means the pain is always caused by the same workload

3. result of athero-caused endo dysfunction
***treatment of stable angina:***

(3)
1. reduce demand (B-blockers, nitrates)

2. prevent progression of athero (aspirin, statins)

3. revascularize if refractory
B-blockers do 5 things:
1. dec. contractility

2. dec. HR

3. inc. diastolic time => inc. supply

(4. inhibition of renin)

(5. save lives in CAD, HF)
if stable angina is refractory to medication, use:

(2)
1. PCI

or

2. CABG
PCI = percutaneous coronary intervention; it _______________quality of life, but:
improves;

doesn't improve mortality
CABG =
surgery to treat stable angina

= revascularization of myocardium by bypassing the stenosis of the coronary artery

using LIMA and saphenous vein
LIMA (artery) connects:
the subclavian to the LAD
CABG is preferred to PCI in the following:

(3)
1. >50% stenosis in left coronary artery

2. 2-vessel athero including LAD with low EF or diabetes

3. 3-vessel athero (LAD, circumflex, RCA)
unstable angina =
sudden increase in tempo or severity of angina episodes

- occurs at any time, even at rest
unstable angina is the result of:
rupture or other acute event that causes thrombosis

- ***a supply problem***
treatment of unstable angina =

(3)
1. anti-plat's (e.g. aspirin)

2. anti-thrombotics (e.g. heparin)

(both restore supply)

3. PCI
in unstable angina, PCI CAN:
prolong life
Prinzmetal angina ~~
vasospasms