The heart (p3)

Question 1

What is the Frank Starling Law of the Heart ?

Answer 1

Within defined limits, the heart will pump whatever volume of blood it receives - the same amount of blood is always left behind

FS mechanism ensures that each ventricle pumps the same volume over a period of time - this is because each ventricle is regulated independently and beat to beat

Question 2

What is the preload of the heart?

Answer 2

= Frank Starling Law of the Heart

• the force that stretches the cardiac muscle prior to contraction
• proportional relationship between EDV and stroke volume
• cardiac muscle has optimal length for contraction (resting = shorter than optimal length)

Question 3

What is afterload? What is its influence on SV?

Answer 3

Pressure that ventricles must overcome to force open valves and eject blood from heart (diastolic pressure)

• hypertension reduces ability of ventricles to eject blood → increased ESV and decreased SV = blood pressure is always higher than normal, maybe 135/95 instead of 120/80 and now you need to surpass 95 compared to 80 in a healthy individual

Question 4

What are the effects of chronically elevated BP on cardiac cells? How can this apply to both physical training or a chronic disease?

Answer 4

Heart has to work harder all the time, cardiac muscle cells tend to get worn out and eventually pushes heart towards heart failure or causing heart exhaustion

• someone with a chronic disease, with every single beat, whether relaxed or not their heart will work harder than normal
• In physical training, sometimes you are pushing BP higher but breaks are taken where you heart can relax → training your hearts endurance

Question 5

What are 2 types of extrinsic influences on SV?

Answer 5

1) Sympathetic stimulation = increases strength of contraction as well as rate of contraction and relaxation , with every beart, will push out more blood than usual

2) Drugs (digoxin) = increase heart contractility → helps slow heart rate

Extrinsic → change in strength of contraction due to increased Ca++ influx, not due to greater initial fiber length

• more availability of Ca++ allows more troponin binding, thus more muscle contractions
• factors outside the heart
• changes vigour of contraction w/o changing EDV = change in contractility

Question 6

How do norepinephrine levels affect contractile activity ?

Answer 6

Norephinephrine → increase in Ca++

Increased Ca++ channels opened in cardiac muscle cells → promotes increased contractile activity