Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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
|