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32 Cards in this Set

  • Front
  • Back
Describe events of systole
Increasing pressure makes AV valves snap shut (= 1st heart sound)

Contraction of ventricle against fixed volume of blood increaes LV pressure until reaches Paortic

Semi-lunar valves open

Ejection of blood into arteries, max pressure = systolic pressure

As LV pressure falls below Paortic, aortic valve snaps shut, then pulmonic valve shuts (closing = 2nd heart sound)
Describe events of diastole
Semi-lunar & AV valves closed, ventricular pressure falls as muscle relaxes @ constant V

LV pressure falls to below atrial pressure and AV valves open

Ventricle refills almost entirely
Atrial contraction provides final portion of ventricular filling

Elastic recoil of arteries smooths out pressure pulse & help maintain pressure (min pressure = diastolic pressure)
components of systemic circulation
left heart and systemic vasculature
components of pulmonary circulation
right heart and pulmonary vasculature
What does "R & L heart are coupled" mean?
output of one = input of the other
What controls the amt of blood flow to each organ?
contraction & dilation of arterioles leading to each organ
dicrotic notch or incisura marks what in the graph?
end of systole/beginning of diastole
Formula for cardiac output
CO = SV x HR

Cardiac output = stroke volume x heart rate
What is the relationship between central venous pressure & right atrial pressure?
they are equal
How is the LV free wall different from RV free wall in terms of pressure?
LV free wall (and IV septum) are thick b/c LV pumps blood into high pressure aorta

RV free wall is thinner, much lower pressure will open the pulm. valve than the aortic valve
What is the order in which the following are activated by electrical impulse:

AV node
SA node
His Purkinje system
atria
ventricles
SA node
atria
AV node
His-Purkinje system
ventricles
Arteriole diameter is regulated by ____ (3 things)
autonomics, circulating vasoactive hormones, local metabolites
3 main components of thin filaments in the sarcomere
g-actin, troponin, tropomyosin
How long are thin filaments?
1.0 um
how long are thick filaments?
1.6 um
component of thick filaments
myosin
what is the function of titin?
connects z-line to actin and actin to myosin
Compare sarcoplasmic reticulum & mitochondria in skeletal vs. cardiac muscles
Cardiac SR has smaller volume than skeletal SR, but cardiac muscle has more mitochondria
Compare junction of SR & sarcolemma in cardiac muscles vs skeletal muscles
Cardiac - cisterna of SR form diads w/ limited SR/T-tubule contact

Skeletal - SR forms triads that envelope T-tubules
Ca-induced-Ca-release is grades by what 2 factors
1) size of the trigger (=amt of Ca influx vi ICa

2) amount of Ca stored in SR
Describe the events in the Ca-induced-Ca-release
A small amt of Ca influx (Ica) via DHP receptors triggers release of large amt Ca from the SR via Ryanodine receptors
What does Ca binding to TnC cause?
causes tropomyosin to unblock the myosin binding site on the thin filament and allow weak binding of actin --> A-M complexes hydrolyze ATP --> generate force
What structures are responsible for Ca efflux out of the cell?
1) Na-Ca exchanger (primary)
2) Sarcolemmal Ca pump
How are the Na-Ca exchanger & Sarcolemmal Ca pump different in terms of capacity & affinity?
Na-Ca exchanger is high capacity, low affinity ( moves lots of Ca but cannot get Ca to low resting level)

Sarcolemmal Ca Pump is low capacity, high affinity (works when Ca is relatively low, pumps out small amt to return to resting level)
2 factors that influence # of cycling cross-bridges
1) # strong actin-myosin complexes (this depends on sarcomere length)

2) fraction of TnC bound to Ca++
Amt of Ca released from SR depends on: (2 things)
1) size of trigger/magnitude of Ica

2) amt Ca in SR
Amt of Ca stored in SR depends on: (3 things)
1) rate of Ca uptake of SR from cytoplasm
2) rate of Ca influx into cell (Ica)
3) rate of Ca extrusion from cell (Na-Ca exchanger, sarcolemma Ca pump)
How do norepinephrine & acetylcholine alter contractility? (increase/decrease)
NE has a + inotropic effect
Ach has a - inotropic effect
how does norepinephrine alter contractility? 2 ways
1) Increases rate of SR Ca uptake by phosphorylation of phospholamban

2) decreases the Ca affinity of troponin, allowing faster release of Ca & its reaccumulation of Ca by the SR
what is rest potentiation?
after a longer than normal interval between beats, the 1st beat will exhibit greater than normal contractile force (reflects kinetics of SR Ca accumulation/cycling)
what is the relationship between resting tension, total tension, active tension?
resting + active = total

resting is determined by preload, total is measured during an isometric contraction, active is determined by subtracting resting from total
what 3 factors shift the force-velocity curve upward & to the right?
1. increased initial length
2. increased contractility
3. increased heart rate