4 - Frank-starling mechanisms and myocardial contractility

What is the MAIN function of the cardiovascular system? (3)

To transport blood (oxygen, nutrients, waste products, chemical messengers) to and from body tissues

So that the nutrients, wastes, etc can be exchanged between the blood and the tissues

So that one part of the body, can tell the other part of the body what to do!

How does the body deliver the ‘right amount’ of blood to those capillaries?

By maintaining the ‘right’ blood pressure

Cardiac output

The heart needs to pump the ‘right amount’ of blood

Total peripheral resistance

The arterioles need to have the ‘right’ radius

Blood pressure calculation

Blood pressure = CO x TPR

Sometimes we need cardiac output to go up. For example when we exercise, it can go from 5 L/min up to 20-25 L/min! How can this happen? Which of the following will help increase cardiac output when we exercise? (select all that apply)

A. Decrease preload

B. Increase afterload

C. Increase heart rate

D. Increase stroke volume

E. Increase total peripheral resistance

C. Increase heart rate

D. Increase stroke volume

Draw this out

Control of heart rate by the ANS

To increase HR - Decrease PSNS, increase SNS

To decrease HR - Increase PSNS, decrease SNS

What is the inherent rate of the SA node?

100 bpm

If a person’s resting heart rate is 72 bpm, this is because:

A. They have high parasympathetic tone

B. They have high sympathetic tone

A. They have high parasympathetic tone

How does the PSNS lower heart rate? Releases acetylcholine which binds to and activates:

A. Beta 1 receptors on the SA node which decreases phase 0 slope

B. Beta 1 receptors on the SA node which decreases phase 4 slope

C. M receptors on the SA node which decreases phase 0 slope

D. M receptors on the SA node which decreases phase 4 slope

E. N receptors on the AV node

D. M receptors on the SA node which decreases phase 4 slope

EPI and NE activate B1 → increase HR

Depolarization phase controls

Conduction velocity (especially important in AV node)

Pacemaker potential controls

Heart rate (Especially important in the SA node)

What effect will parasympathetic stimulation have on cardiac output?

A. Have no effect on cardiac output

B. Increase cardiac output

C. Decrease cardiac output

C. Decrease cardiac output

CO = HR x SV

The Frank-Starling mechanism (5)

1. Increase venous return →

2. Increase the volume of blood in the ventricle at the end of diastole (end diastolic volume (EDV)) OR increase preload

3. Stretch the chamber wall

4. Stretch the myocytes

5. Myocytes respond by increasing force of contraction

What is preload?

The load or how much the wall of the ventricle is stretched at the end of diastole

The Frank-Starling mechanism result with filaments (2)

• Greater overlap of thin and thick filaments

• Filaments or cross bridge cycling are more sensitive to increases in intracellular Ca++

Frank-Starling Mechanism Ventricular-Function Curve

Because of the Frank-Starling mechanism, in a healthy heart, venous return =

cardiac output

What might happen if the Frank- Starling mechanism doesn’t work? For example, with heart failure? (3)

• ESV and chamber size is larger than normal

• It cannot stretch anymore

• Blood backs up in the veins

Remember, the heart has a right and left pump. When one of the pumps (i.e. ventricles) fail and the Frank-Starling mechanism doesn’t work:

Blood backs up in the veins supplying that side of the heart This increases venous pressure, which ‘pushes’ fluid into the tissue causing edema

Left heart failure will cause:

Pulmonary edema

Edema from left heart failure (2)

1. Left heart failure: Too much blood in left ventricle

2. Blood backs up in the left atria then the pulmonary veins

Edema from right heart failure

1. Right heart failure: Too much blood in right ventricle

2. Blood backs up in the right atria and then the systemic veins

What affects venous return?

How much blood is in your body (blood volume)

A person gets a huge cut and loses a lot of blood. How does that affect cardiac output? (3)

A. Decrease blood volume

A. Decrease venous return

A. Decrease cardiac output

A person quickly stands up and gets dizzy because their blood pressure drops. Normally when you stand up, the veins rapidly constrict to help return blood to the heart. What contributed to his drop in blood pressure? The veins remained dilated a little too long, which reduced venous return and:

A. Increased preload and decreased CO

B. Increased preload and increased CO

C. Reduced preload and decreased CO

D. Reduced preload and increased CO

C. Reduced preload and decreased CO

Inotropy definition

The strength of contraction at ANY GIVEN end diastolic volume (EDV) or preload

Ventricles are essentially not innervated by

the PSNS

Activation of Beta 1 receptors (by a variety of neurotransmitters or drugs – e.g. epinephrine, norepinephrine, dopamine, dobutamine) causes a ____ inotropic effect on the heart

Positive; increased contractility

What type of drugs would have a negative inotropic effect? (Select all that are correct)

A. Beta blockers (block Beta 1 receptors)

B. Calcium channel blockers

C. Potassium channel blockers

D. Sodium channel blockers

A. Beta blockers (block Beta 1 receptors)

B. Calcium channel blockers

What is the difference between the Frank-Starling mechanism and contractility (or inotropy)?

Frank-Starling mechanism - An increase in preload causes the heart to contract more forcefully and squeeze out that ‘extra blood’

Increase in contractility - The heart contracts more forcefully and squeezes out a greater percentage or fraction of blood for a more complete ejection (ejection fraction)

Ejection fraction (EF) definition

the fraction of blood that is ejected from the heart with each heartbeat

Ejection fraction (EF) calculation

EF = Stroke volume / End diastolic volume (EDV)

Normal resting ejection fraction

50% - 75%

Stroke volume calculation

EDV-ESV

Why are both processes (F-S and inotropy) important? (3)

1. Both will cause an increased force of contraction → Increa se volume of ejected blood (stroke volume)

2. Sometimes you need to increase stroke volume just because preload (or end diastolic volume) has increased

3. Sometimes you need to increase stroke volume because of increased ‘oxygen demand by the tissues of the body’ (Contractility)

How does arterial pressure (afterload) affect cardiac output?

A. Afterload has no effect on CO

B. Increase in afterload will increase CO

C. Increase in afterload will decrease CO

C. Increase in afterload will decrease CO

Because pressure in the aorta is working against the output of the heart

Need to contract at a greater force.

Afterload definition

is the ‘load’ against which the ventricles must pump

When does a person most likely have a chronic increase in afterload?

A. Hypertension

B. Hypotension

C. Hypervolemia

D. Hypovolemia

A. Hypertension

An increase in preload (F-S) and an increase in contractility (inotropy) can both increase stroke volume and cardiac output. If everything else is held constant, which will decrease end systolic volume (ESV)?

A. Both will decrease ESV

B. Neither will decrease ESV

C. Increase in preload

D. Increase in contractility

D. Increase in contractility

Which of the following would be most effective in increasing cardiac output in a person who has heart failure?

A. Decreasing contractility

B. Decreasing heart rate

C. Decreasing afterload

D. Decreasing preload

C. Decreasing afterload