Flashcards in Cardio - Mechanical Performance of the Heart Deck (53):
What is cardiac output?
The amount of blood pumped by each ventricle in one min
What is cardiac output matched to?
The body demand for O2
What is the equation to calculate the Cardiac output (CO)?
CO= heart rate (beats/min) x Stroke volume (ml)
What is the stroke volume?
The amount of blood pumped by each ventricle during one contraction
What is the normal resting value of CO in adults?
-assuming resting heart rate is 70bpm
What is the difference in resting CO values for athletes vs. Couch potatoes?
Nothing, the resting CO will be 5L/min
How does CO increase?
Increases depending on fitness level and exercise
-20 to 40ml
How do you change the CO?
Changing the heart rate or stroke volume
What is the normal and highest heart rate?
70bpm is normal
45-50pbm is low
How do you calculate the max heat rate?
220-age of person
What is the heart rate controlled by?
-includes SNS and PSNS
Which nerves innervate the SA node and ventricular muscle?
PSNS (decreases heart rate) and SNS (increases heart rate) nerves
How do you change the heart rate?
Change the pacemaker potential of the SA nodal cells
-changing the slope of the pacemaker potential
Where are the PSNS nerves mainly distributed?
In the SA node(setting pace) and AV node (slowing AP down for contractions)
-to the ventricular muscles to a minor extent
What does the PSNS release into the SA, AV nodes and ventricular muscles?
-decreases the slope of the pacemaker potential
What effect does the Acetylcholine being released by the PSNS into the SA, AV nodes and ventricular muscles?
When the PSNS is activated it will decrease the hear rate and will cause a small decrease in the force of contraction
What is the pathway of events in order to for the PSNS to decrease the heart rate?
1. Acetylcholine is released and binds to receptors on the cell of the SA node
2. There is an increased permeability of cell membrane to K+ (leak down [gradient])
3. Decrease in Ca++ permeability. Less Ca++ enters
4. More K+ leaving the cell hyper polarizes cells to -70mV
5. Less Ca++ entering SA nodal cells decreases its slope of pacemaker potential
-therefore taking longer to reach an AP
Where are the SNS nerves distributed in the heart?
SA node and AV node
-to a smaller extent ventricular muscle
Which ANS system has a stronger influence on the ventricular muscles?
What does SNS release into the SA, AV nodes and ventricular muscles?
What effect does Norepinephrine have on the SA AV nodes and ventricular muscles?
Will increase the heart rate therefore increasing the force of contraction
-increasing the slope of the pacemaker potential
What is the pathway of events in order to for the SNS to increase the heart rate?
1. Norepinephrine binds to receptors on the SA nodal cells
2. Increased permeability of cells to Na+ and Ca++ in all parts of the heart
3. Increased Na+ and Ca++ permeability increased the slope of the pacemaker potential.
-depolarizing it to threshold quicker
What is the relationship betweenO2 and CO?
When your body demand for O2 is low, the CO will be low
What bpm does the heart need to have in order for the PSNS to be a activated?
Less than 100bpm
Why is the PSNS constantly activated in terms of bpm?
Resting heart rate is 70bpm, PSNS is constantly active to keep the heart rate at 70
-the more the PSNS is activated the slower the heart rate
When does the PSNS stop?
When the bpm is 100 but there is NO activation of the SNS
What does 100bpm equate to naturally in the heart?
100bpm= Hearts own natural intrinsic rate which is set by the SA node
When is the SNS activated?
When bpm is greater than 100
-when there is a high demand for O2
-the more the SNS is activated the higher the heart rate so more O2 is being delivered
When you increase Stroke volume (SV) what do you also increase?
What is the resting SV?
How do you increase SV?
Exercise which is dependent on fitness level
110 to 200ml
What are the 2 major factors that control to SV?
1. Input from the ANS
2. Preload (EDV)
Explain why the PSNS has a small influence on ventricular muscles cells (vagus nerve)?
1. PSNS releases Ach to contractile cells
2. Ach closes Ca++ channels in the contractile cells
3. Less Ca++ flowing into cardiac contractile cells decreases the force of contraction
4. This decreases stroke volume and CO
Explain why the SNS has a stronger influence on ventricular muscle cells (vagus nerve)?
1. SNS releases norepinephrine
2. Norepinephrine opens Ca++ channels in contractile cells
3. More Ca++ flowing into contractile cells
4. This increases the force of contraction, increasing SV and CO
What is EDV?
End diastolic volume= the volume of blood in ventricles at the end of ventricular diastole (just after ventricles contract)
What is ESV?
End Systolic volume= The volume of blood in ventricles at the end of ventricular systole
What will happen if either EDV or ESV changes?
It will change the stroke volume
How much are the ventricles filled during diastole?
Each ventricle will increase to with 160ml of blood
How much blood do the ventricles eject during systole when they are contracting?
70ml into the aorta
What remains in the ventricles after it has contracted?
90ml of blood
What is the equation for SV?
EDV-ESV (at rest)
What happens to ESV when SNS is activated?
SNS will cause the heart to contract more forcefully reducing the end systolic volume to 10-30ml
What happens to EDV when SNS is activated?
SNS increases the flow into the ventricles and can be as high as 200 to 250ml
When combined, when ESV is decreased and EDV is increased what happens?
Starling Law of the heart
-SV can be increased to more than double the resting amount
What is the preload?
The amount of blood before contraction
-load on the cardiac muscle just BEFORE contraction
Where does the "load" come from?
Comes from the blood filling the ventricles which stretches the cardiac muscle
What happens when the ventricles are filled with blood before contraction (High EDV)?
The greater the preload on the heart
All together an increase in EDV causes...?
Increase in preload
Increased stretching of cardiac muscles
Increased contractile force
Increased amount of blood ejected
Increased Stroke volume
What is the Frank-Starling Lae of the heart?
An increase in EDV will always cause an increase in SV
What are the 3 ways in which you can increase EDV?
1. Muscle Pump
2. Respiratory Pump
How does the muscle pump increase EDV?
Veins are between muscles, when muscle contract they squeeze the veins in one direction (due to valves) which is sent to the heart
How does the Respiratory pump increase EDV?
When the chest expands and contracts, inhaling decreases pressure in the chest cavity bringing O2 into the lungs. The difference in pressure on the peripheries of the chest cavity pulls blood back to the heart which can increase venus return to the heart