2nd half of Cardiac Cycle

Question 1

What is the Frank-Starling Law?

Answer 1

Increased preload (venous return) produces a commensurate increase in stroke volume.

Question 2

True or False? SV increases due to ventricle stretching.

Answer 2

FALSE - SV (stroke volume) increases due to the atrium stretching to accommodate incoming blood.

• When an organ stretches out its wall cannot sustain the internal pressure.
• Contractility is increased to maintain integrity.

Question 3

Why does increasing diastolic filling (preload) increase ventricular strength?

Answer 3

• Force of ventricular contraction depends on muscle fiber length
• during diastolic filling, stretching the ventricle on the ascending portion of the length tension curve increases myocardial contractility (the force of contraction).

Question 4

When is cardiac contraction maximal?

When is cardiac contraction diminished?

Answer 4

• Cardiac contraction is maximum at optimal sarcomere length.
• It diminishes if sarcomere lengthens or shortens.

Question 5

What happens if sarcomere length shortens?

What happens if sarcomere length lengthens?

Answer 5

• If sarcomere length shortens, Ca++ affinity for troponin decreases.
• If sarcomere length increases, contractility force is reduced due to less overlap of actin and myosin.

Question 6

What are the variables of Frank Starling’s law?

Answer 6

The law can be stated with different variables, all related to cardiac performance (Y-axis) and ventricular filling (X-axis).

Y-axis can be- cardiac output, stroke volume or stroke work.

X-axis can be- end diastolic fiber length, end diastolic volume, end diastolic pressure or atrial pressure.

Question 7

What 3 things does preload or EDV depend on?

Answer 7

1- venous filling pressure
2- duration of diastole
3- ventricular compliance

Question 8

True or false? Increased venous pressure (preload) increases stroke volume.

Answer 8

True.

Normal: EDV = 150 mL, venous pressure= 5 mmHg. Increased; EDV = 175 mL, venous pressure= 10 mmHg

Question 9

When does filling cease?

Answer 9

When passive ventricular pressure (due to stretch of CT) equals incoming venous pressure.

Question 10

What does higher EDV lead to?

Answer 10

Increased stroke volume.

Question 11

Give the equation for SV.

Answer 11

SV = EDV - ESV

Question 12

Ventricular hypertrophy _______ compliance and _______ stroke volume.

a) reduces, increases
b) reduces, diminishes
c) increases, increases

Answer 12

b) Ventricular hypertrophy REDUCES compliance and DIMINISHES stroke volume.
* Dr. B loves b’s!

Question 13

Does increased compliance shift the passive pressure curve up or down?

Answer 13

Up.

The equilibrium point of venous and passive ventricular pressure shifts to a lower EDV (110 mL).

Question 14

Define afterload.

Answer 14

Afterload is the systolic pressure needed to overcome the blood pressure within the aorta in order to eject blood.

Includes ISOMETRIC and ISOTONIC contraction during ejection.

Question 15

How is decreased velocity compensated?

Answer 15

By increasing contractility which increases velocity of blood flow during ejection.

Question 16

How does increasing aortic pressure (afterload) effect stroke volume?

How does this effect the pressure volume curve?

Answer 16

Increasing aortic pressure decreases stroke volume.

As aortic pressure rises, equilibrium point of ejection pressure and active isometric tension occurs shifts to a larger ESV.

Question 17

What happens to the passive pressure curve when afterload (aortic pressure) is increased?

Answer 17

The increase in ventricular pressure causes an increase in the ventricular volume.

Because the EDV stays the same, the stroke volume decreases.

Question 18

What is contractility?

Answer 18

The intrinsic ability of myocardial cells to develop force at a given preload and afterload.

Question 19

How is contractility increased?

Answer 19

Any mechanism that increases intracellular levels of Ca++ and its binding to troponin will increase myocardial contractility.

Question 20

What substances increase contractility?

Decrease?

Answer 20

Increase - Catecholamines (sympathetic) and cardiac glycosides.

Decrease - Ach muscarinic (parasympathetic).

Question 21

True or False? A change in contractility involves changes in contraction force and latency of contraction and relaxation.

Answer 21

True.

Increased contractility will result in early onset, increased force and early relaxation (faster and stronger).

Decreased contractility will result in late onset, decreased force and late relaxation (slower and weaker).

Question 22

What substance(s) will increase contractility?

What substance(s) will decrease it?

Answer 22

Increase- NE, EPI (sympathetic)

Decrease- Ach (parasympathetic)

Question 23

How do NE and EPI effect the rate and strength of contraction?

Answer 23

NE and EPI increase contractility

• via beta-1 receptor
• cAMP activates PKA

Results in:
- enhanced Ca++ channel opening (early
contraction)
- increased Ca++ release from SR (stronger
contraction)
- activating phospholambin
- increases SR uptake of Ca++ (early
relaxation)
- reduces Ca++ binding to troponin (early
relaxation)

Question 24

How does increasing contractility effect ESV?

How does this effect troke volume?

How does this effect he active tension curve?

Answer 24

Increased contractility increases ejection, this decreases ESV.

Increased contractility increases stroke volume.

The active tension curve moves up.

Question 25

How does congestive heart failure effect contractility (in late stages)?

Answer 25

CHF leads to decreased contractility.
- weak myocardial contraction causes blood to
back up
- back up of blood over stretches the ventricles
- increases EDV

***In early stages of CHF increased stretching is compensated by increased contractility, temporarily improving heart function.

Question 26

How is CHF compensated?

Answer 26

Increasing preload.

Question 27

What are the effects of cardiac glycosides (e.g. digitalis, digoxin) on cardiac function?

Answer 27

Cardiac glycosides enhance cardiac function by

1) increasing vagal tone
2) increasing contractility

Question 28

How does digitalis result in increased contractility?

Answer 28

• disables Na+/K+ -ATPase pump
• less Na+ out of cell (more Na+ in cell)
• slows Ca++/Na+ exchanger
• Ca++ accumulates within cell
• more Ca++ binds to troponin

= increased contractility!

Question 29

What is the formula for cardiac force?

Answer 29

Force x Distance

Question 30

Compare external and internal work.

Answer 30

External work
= Ventricular Pressure x Stroke Volume
- isotonic ejection of blood
- low O2 requirement

Internal work 
- graphically estimated 
- isometrically builds ventricular pressure (during 
  isovolumic contraction) 
- released as heat 
- increases to overcome aortic pressure 
- high O2 requirement

Question 31

What is aortic stenosis?

Answer 31

Increased aortic pressure requires more internal work and O2 consumption.

Question 32

How do increased aortic pressure and increased contractility effect internal work?

How does this effect Oxygen consumption?

Answer 32

Increased aortic pressure (after load) increases internal work. Increases O2 consumption.

Increased contractility decreases internal work. Decreases O2 consumption.