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Flashcards in Cardiac Function Deck (15):

What determines strength of heart muscle contraction?

* Geo arrangement of actin & myosin - better/optimal length w/ stretch by filling w/ blood (inc venous return)

* How long it takes Ca++ to saturate troponin; stretch also inc sensitivity of troponin for Ca++

*Tension proportional to # actin/myosin interactions


Ionotropic Effect

Sympathetic NS

Inc shortening per unit time

Faster Ca++ saturation of troponin

More efficient cross bridge cycles; take less time



* intrinsic property of muscle to generate tension during contraction

Inc by...

*Sympathetic NS- how effective is it at shortening (Ca levels, cross bridging rate, channels, etc)

*adding sarcomeres; after chronic exercise; inc tension of contraction but not RATE


What 2 factors determine L ventricle filling?

1. heart rate (TIME)

2. stiffness of ventricle wall
(stiff b/c presence of titin and connections b/n cells; limits how much it can be stretched when filling w/ blood; worse if MI)



* force against which muscle has to shorten; MAP that must be overcome (MAP= CO*TPR so inc in either will inc after load)

* Inc afterload = dec time available for shortening (b/c takes longer to open aortic valve and pressure drops more quickly in ventricle than aorta after ejection so valve closes faster too)

* Greater BP (hypertension) means aortic valve takes longer to open which dec CO


Law of Laplace for Cardiac Muscle

T = (P*R)/ M P=(T*M)/R **Sphere**

* Greater radius generates LESS pressure (dilated ventricle)

* Thus hypertrophy (inc M - wall thickness) would create greater P for given R; may be offset by inc R due to enhanced venous return


Pressure Volume Curves (what does height and width represent)

X axis is volume so width = SV

Y axis is pressure so height = ventricular pressure during contraction (ESP - EDP)



* curve that shows what happens to pressure as you continue to fill ventricle in diastole

* At > 150 mL the pressure starts to inc rapidly w/ more volume added

* Dec compliance/stiffer chamber will shift curve up so this rapid pressure inc occurs at a lower volume; thus Ventricles overcomes Patria at much lower volume (lower EDV)

* Inc compliance/dilation of ventricles leads to high EDV w/o large pressure; curve shifts down



* curve that shows max pressure that can develop during ventricular systole for a given volume; reflects Frank Starling mechanism

* Greater volume —> greater pressure (more optimal actin/myosin length) up to a point then stretch too much past optimal length (NOT IN REAL LIFE)

*Frank Starling compensation does not work if weak heart (heart failure); if heart is weak then extra stretching from inc venous return does NOT inc contraction tension like normal heart; dec ESPVR


What does top L corner of Pressure-Volume curve represent?

*pressure at end of systole = MAP (approx.); pressure when aortic valve closes

*Slope of line connecting top L corners represents contractility (steeper = greater contractility)


Stroke Work (SW)

* Stroke Work (SW) = work required to generate enough pressure to eject blood in 1 cardiac cycle (external work)
* SW = SV * (MAP-EDP) but EDP negligible so SW = SV * MAP
* So work required inc if greater volume or greater MAP to work against


Potential Energy (PE)

* Potential Energy (PE) = energy required to deform elastic tissue; energy absorbed by ventricle wall to overcome elastic forces (internal energy)
* Inc afterload —> big inc in PE while inc preload —> small inc in PE
* So hypertension greatly inc work done by heart; compensate w/ inc sarcomeres —> hypertrophy —> inc stiffness so less diastolic filling (WORSE)
* Inc contractility has moderate inc PE



* Pressure-Volume Area (PVA) = total energy needed = SW + PE

* Linear relationship b/n PVA and MVO2 (myocardial O2 consumption)


What happens to pressure and volume during tachycardia?

*Dec SV b/c less filing time

*BUT symp NS also inc contractility AND compensate w/ inc venous return


Paradox of Cardiac Function

* Inc CO is good but causes inc in MAP so now greater after load to work against in next cycle

* In next cycle it takes longer to overcome the now greater MAP in aorta so less time ejecting/less stroke volume

* BUT … you can compensate w/ inc in contractility (make slope steeper); this comes at an energy cost (more contractility means more shortening cycles / unit time = ATP ea)

“Working harder to eject same amount of blood”