Cardiac Function

Question 1

What determines strength of heart muscle contraction?

Answer 1

• 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

Question 2

Ionotropic Effect

Answer 2

Sympathetic NS

Inc shortening per unit time

Faster Ca++ saturation of troponin

More efficient cross bridge cycles; take less time

Question 3

Contractility

Answer 3

• 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

Question 4

What 2 factors determine L ventricle filling?

Answer 4

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)

Question 5

Afterload

Answer 5

• 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

Question 6

Law of Laplace for Cardiac Muscle

Answer 6

T = (PR)/ M P=(TM)/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

Question 7

Pressure Volume Curves (what does height and width represent)

Answer 7

X axis is volume so width = SV

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

Question 8

EDPVR

Answer 8

• 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

Question 9

ESPVR

Answer 9

• 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

Question 10

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

Answer 10

• pressure at end of systole = MAP (approx.); pressure when aortic valve closes
• Slope of line connecting top L corners represents contractility (steeper = greater contractility)

Question 11

Stroke Work (SW)

Answer 11

• 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

Question 12

Potential Energy (PE)

Answer 12

• 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

Question 13

PVA

Answer 13

• Pressure-Volume Area (PVA) = total energy needed = SW + PE
• Linear relationship b/n PVA and MVO2 (myocardial O2 consumption)

Question 14

What happens to pressure and volume during tachycardia?

Answer 14

• Dec SV b/c less filing time

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

Question 15

Paradox of Cardiac Function

Answer 15

• 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”