Regulating the SV & HR

Question 1

What is cardiac ischaemia?

Answer 1

A reduction in blood flow to the heart muscle. Usually due to constriction of coronary arteries

Question 2

What does the hearts inotropic state refer to?

Answer 2

The strength of the muscles contraction

Question 3

How does physiological increase of the HR work?

Answer 3

Sympathetic fibres release noradrenaline which works alongiside adrenaline circulating from the adrenal medulla.
Noradrenaline/Adrenaline work on B1-receptors in the sinoatrial node to increase the slope of the pacemaker potential and thus HR

(Also decrease in parasympathetic tone)

Question 4

How does physiological decrease in HR work?

Answer 4

Parasympathetic fibres in the vagus nerve release acetylcholine.
ACh acts on muscarinic receptors in the sinoatrial node.
The Cell hyperpolarises and the slope of the pacemaker potential lengthens causing a decrease in HR

(Also decrease in sympathetic tone)

Question 5

What 4 things affect Stroke Volume?

Answer 5

Preload
Afterload
Neural tone
Pathologys

Question 6

What is preload?

Answer 6

the initial length of the muscle fibres

Question 7

What is starlings law?

Answer 7

Starling’s law dictates that the initial length of the muscle (preload) is proportional to the energy of contraction

Meaning increasing preload will increase energy of contraction and thus SV

Question 8

What determines preload?

Answer 8

The End Diastolic Volume because it stretches the muscle fibres

Question 9

How does EDV relate to SV?

Answer 9

An increased EDV leads to an increased SV
A decreased EDV leads to a decreased SV

Question 10

What determines EDV?

Answer 10

The venous return to that side of the heart

Question 11

How is the stroke volume of each side kept equal?

Answer 11

The stroke volume of the right side is the amount of blood that returns to the left side through the pulmonary veins.
Since: venous return -> EDV -> preload -> SV the venous return to the left should be the same as that of the right.

Question 12

What vessels can affect preload?

Answer 12

The capacitance vessels like venules and veins

Question 13

What is afterload?

Answer 13

The load against which the muscle is trying to contract. In the left side of the heart this is the arterial pressure holding shut the aortic valve

Question 14

What effects aortic pressure? and what does this mean for the SV?

Answer 14

The total peripheral resistance (TPR).
- TPR increase
->Ventricle requires more energy to force open the valve
-> Ventricle has less energy for ejecting blood
-> SV decreases.

Question 15

How does the parasympathetic system affect SV?

Answer 15

Noradrenaline/Adrenaline act on B1-receptors in myocytes.
Contractility increases (inotropic effect)
A Shorter, Stronger contraction occurs
Increased SV

Question 16

Why doesnt the parasympathetic system have much control over the SV?

Answer 16

Probably cos the Vagus nerve only innervates the sinoatrial nerve not the ventricular muscle itself.

Question 17

How does serum calcium affect Stroke Volume?

Answer 17

Hypercalcemia:
Ap fired -> more than normal calcium drawn into the cell -> more troponin is saturated -> More cross bridges acting -> greater strength of contraction
So shifts the EDV vs SV graph up and to the left

Hypocalcemia:
Lower strength of contraction. Opposite of above.
So shifts EDV vs SV graph down and to the right.

Question 18

What effect does cardiac ischaemia have on the SV vs EDV graph?

Answer 18

Shifts it down and to the right (i.e. reduces strength of contraction for any given EDV value)

Question 19

What happens to the heart when theres one sided ischaemia?

Answer 19

One side pumps more than the other
So the damaged side has a greater input then output meaning its EDV slowly increases

Question 20

How does the heart compensate for one sided ischaemia?

Answer 20

As EDV increases stroke volume increases.
Eventually it reaches a stage where stroke volume is back to normal so it stabilizes
This allows people to maintain a normal resting cardiac output despite ischaemia

Question 21

How do we tell if someone with a normal resting CO is ischaemic?

Answer 21

They’ll have reduced ejection fraction and capacity for exercise.

Question 22

What effect do barbiturates have on SV?

Answer 22

They decrease it, shifting the SV vs EDV graph down and to the right.

Question 23

Calculate CO?

Answer 23

CO = HR x SV

Question 24

An increase in HR should increase CO, why does it drop again above ~150bpm?

Answer 24

Increasing HR cuts into the filling time.
Above ~150bpm it starts to reduce the rapid filling phase, this is where it has a significant effect on EDV.
Since EDV -> Preload -> SV, stroke volume falls as EDV falls.

Question 25

What can cause an increase in heart rate that will lead to an increased CO?

Answer 25

An electric pacemaker
Increased Symp. Tone
Decreased Vagal Tone

Question 26

How does contractility of muscle affect CO?

Answer 26

Increasing contractility of muscle shortens systole and increases the CO.

Question 27

What can increase the contractility of muscle?

Answer 27

Increased Symp. Tone

Question 28

How does Venous return affect CO?

Answer 28

Increased Venous Return
-> EDV increases
-> Preload Increases
-> SV increases

(this offsets the reduced filling time caused by an increased HR to some extent and so somewhat maintains SV as HR increases)

Question 29

What causes increased venous return during exercise?

Answer 29

Venoconstriction
Blood pumped out of skeletal muscle by contraction
Blood pumped out of lungs by inhalation

Question 30

How does TPR increase CO during exercise?

Answer 30

During exercise arterioles dilate in skin, muscles & heart.
Therfore TPR decreases
Therefore Afterload decreases
Therefore SV & so CO increases.

Question 31

How much does CO increase during exercise?

Answer 31

4-6 times.