Cardiology Flashcards
what three areas does RCA supply?
-RA -RV -LV (inferior wall)
85% of the time, which artery gives rise to PDA (posterior descending artery)
RCA
what does PDA (posterior descending artery) supply?
-superior interventricular septum -inferior wall
what EKG leads correspond to PDA ischemia?
-ii, iii, AVF (inferior leads) ST-Elevate -reciprocal changes lateral leads (i, AVL, V5/V6); ST depression
LMCA supplies what parts of heart?
-LA -LV (septal, anterior, lateral) walls -most interventricular septum
what parts of left ventricle NOT supplied by Left
-SUPERIOR interventricular septum -inferior wall of LV
SA node supplied 60% by which artery?
RCA
SA node supplied 40% by which artery?
LAD
AV node supplied by which two arteries?
-RCA -circumflex
RCA provides what percent to AV node
85-90%
which artery supplies only 10-15% of AV node?
circumflex
Bundle of His supplied by WHICH two arteries
PDA LAD
blood flow rate to heart is ____ mL/min?
250 mL/min
what is flow to heart per min per 100grams?
80mL/100g/min
what percent of CO does coronary flow take up?
5%
myocardium what percentage extraction of oxygen from blood?
65% (this is maximum extraction)
WHICH EKG LEAD MOST SENSITIVE FOR ISCHEMIA?
lead V - 75% lead II + V - 80%
lateral EKG leads
I, AvL, V5, V6
inferior EKG leads
II, III, AVF
septum leads
V1, V2
anterior leads
V3-V4
AVR lead?
???? supplied by?
what TEE view is most effective for diagnosing ischemia?
transgastric short axis view
which valve is bicuspid USUALLY
mitral
normal Aortic valve area?
2.5-4.5cm^2
chordae tendinae on which valve?
tethers MV to papillary muscles; if rupture muscles, can have acute failure
normal area of MV?
4-6cm^2
sympathetic input to heart from WHAT ganglia of brainstem?
stellate ganglion (to both SA/AV nodes & ventricular mm)
cardioaccelerators at what thoracic level?
T1-4
Vagal input to conduction system of heart from WHICH nucleus in medulla?
nucleus ambiguous
transplanted heart lacks ability to do WHAT things?
-NO BARO-RECEPTOR FUNCTION (norepi has beta and alpha agonist function, increases BP and HR initially, but baroreceptor reflex to decrease HR doesn’t work)
transplanted heart has NO what?
-no Vagal tone -no cardiac accelerators -no baroreceptor reflexes
changes in CARDIAC OUTPUT in transplanted heart happen by WHAT mechanism??
increase in STROKE volume
which sympathomimetic agents work on transplanted heart?
-amines 1) isoproterenol 2) epi 3) dopamine 4) dobutamine
cardiac cells attached together how?
attached by desmosomes
what makes striations in cardiac cells?
from linearly organized sarcomeres
What transmits depolarization in cardiac cells?
T-tubules - transmit depolarization
specialized Calcium reservoir in cardiac cells?
sarcoplasmic reticulum
what cell junction helps heart function as syncytium?
gap junctions
Cardiac MYOCYTE AP maintains plateau phase how?
inward Ca current (against concurrent K efflux); prolongs refractory period to allow mechanical contraction
Phase 0 of Cardiac MYOCYTE Action potential is known as WHAT phase?
-depolarization
Phase 0 of Cardiac MYOCYTE Action potential membrane potential change
-90 to above 0
Phase 0 of Cardiac MYOCYTE Action potential from WHAT ion movement?
-Na entrance thru fast VOLT-gated channels
Phase 1 of Cardiac MYOCYTE Action potential; what happens at BEGINNING?
-Sodium channels close -POTASSIUM CHANNELS [delayed rectifier channels] open to efflux
Phase 2 of Cardiac MYOCYTE Action potential also known as?
plateau phase
Phase 2 of Cardiac MYOCYTE Action potential; PLATEAU phase from WHAT type of channels?
L-type Ca channels
how much TIME between phase 0 and phase 4?
200ms
Phase 3 Cardiac MYOCYTE Action potential; WHAT CHANNELS CLOSE/OPEN?
-CLOSE: Ca -OPEN: K+ delayed rectifier
what helps trigger AP of phase 0 in myocyte?
inward Ca from phase 2/plateau phase
PACEMAKER cells (conducting cells) resting state at what mV?
-60mV
Phase 0 in PACEMAKER cells (conducting cells) is caused by WHAT ion?
Ca
what TYPE of CHANNELS (of ion) causes phase 0 in PACEMAKER cells (conducting cells); WHICH is primary?
-T-type Ca -L-type Ca** **PRIMARY, open after T-type (t-type causes slow gradual upslope of phase 4)
what ion creates automaticity of PACEMAKER cells (conducting cells)
Na
via WHAT CHANNELs does __(ion)__ provide automaticity
-LEAKY (i-funny) -Na channels
what phase(s) does PACEMAKER cells (conducting cells) NOT HAVE?
NO phase 1 NO phase 2
in PACEMAKER cells (conducting cells); what ion/channel provides phase 0 to phase 3 change?
iK (potassium channels)
nodal action potentials spread via WHAT means?
gap junctions in myocytes
when electrical vector of depol in direction of lead, get WHAT?
Positive deflection
P-R interval represents?
AV nodal delay (if any)
normal PR interval?
.12-.20 sec
normal QT?
.36-.44 sec
thick filament?
myosin (head groups that bind ATP)
thin filament
actin (monomers together)
regulatory proteins of myocyte sarcomere?
troponin and tropomyosin?
LONG filament that sits over actin binding sites
(LONG name, LONG filament) tropomyosin
what pulls tropomyosin out of the way? and how?
-troponin -CALCIUM binds it to allow initiation of contractile cycle
when powerstroke, what released?
ADP released
entrance of Calcium into myocytes triggers opening of WHAT other receptors?
RYANODINE receptors
where are Rya receptors?
on surface of sarcoplasmic reticulum
what to the Rya receptors do?
lflood out ca into cytoplasm (Ca-triggered-ca-release)….Ca then binds troponin
in order to STOP contraction cycle, how does cell get rid of Ca from cytoplasm? (2 mechanisms)
**SERCA pump reaccumulates Ca in Sarco retic *Na/Ca exchanger pumps Ca out of cell (3Na in, 1Ca out)
what is phospholamban (PLN)?
tonic inhibitor of SERCA pump; when phosphorylated, SERCA can work
WHAT is lusitropy? HOW is lusitropy related to Phospholamban and SERCA?
LUSITROPY = ability to relax –>phosphorylation of phospholamban allows SERCA to work, which HELPS relaxation more rapidly
which part of brain maintains tight BP control?
-MEDULLA
where does medulla receive input from?
-higher cortical centers -peripheral afferents from chemo and baroreceptors
types of receptors ON the heart? -what neurotrans for each?
Beta1 (NE) Beta2 (NE) ——— M2 (Ach)
chronotropy?
HR
inotropy
force of contraction
dromotropy
velocity of conduction of A.P.
beta receptors are WHAT kind of receptors?
G-protein coupled
G-prot receptor mediation from Sympathetic nerve input changes
aden cyclase–>cAMP–>protein kinases PK’s, increases the funny channels and T-type polarization
how much increase in ventricular filling from Atrial kick?
20-30% increase
usual process of Ventricular filling is done how? based on what pressure?
PASSIVELY; based on pressure decrease from ventricle relaxing goes BELOW atrial pressure
describe what’s happening at each wave part

what happens during “a” part of atrial pressure wave?
a - the end of Atrial contraction

what happens during “c” part of atrial pressure wave?
c - RV Contraction, triCuspid bulge
what happens during “x” part of atrial pressure wave?
x - atrial relaXation

what happens during “v” part of atrial pressure wave?
v - Venous filling

what happens during “y” part of atrial pressure wave?
y - rapid emptYing of the atrium
