Regulation of Heart rate and stroke volume Flashcards

1
Q

How does the sympathetic system increase heart rate?

A

sympathetic nerves release noradrenaline
plus circulating adrenaline from adrenal medulla
both act on ß1-receptors on sinoatrial node
increases slope of the pacemaker potential - (by modulating leaky K channels, Type T calcium channels or funny sodium channels)
increases heart rate = tachycardia

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2
Q

How does the parasympathetic system increase the cardiac interval and hyperpolariese the pacemaker cells?

A

vagus releases ACh
acts on muscarinic receptors on sinoatrial node
hyperpolarises cells and decreases slope of pacemaker potential
decreases heart rate = bradycardia

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3
Q

What is starlings law?

A

the energy of contraction is proportional to the initial length of the cardiac muscle fibre

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4
Q

What is preload?

A

How an increase in stretch leads to an increase in contractility, so the stretch of tha heart before contaction. In vivo, preload is affected by the end diastolic volume (how much blood fills up the heart)

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5
Q

How do you increase the pre load in the heart?

A

Increase the amount o blood filling it up! (End diastolic volume)

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6
Q

What is the afterload and what is it affected by?

A

Afterload is the load against which the muscle tries to contract.

Load = TPR = The resistance in the vessles going out from the heart (eg arteries and arteriole backlog in the aorta . Also termed “Total peripheral resistance” - the more resistance, the greater the force needed to overcome the pressure in the aorta for the aortic valve to open, thus meaning there is less force left in the heart for the ejection of blood, leading to a reduced stroke volume.

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7
Q

What is the total perhipheral resistance? Why does it lead to a reduced SV?

A

The resistance in the vessles going out from the heart (eg arteries and arteriole backlog in the aorta . Also termed “Total peripheral resistance” - the more resistance, the greater the force needed to overcome the pressure in the aorta for the aortic valve to open, thus meaning there is less force left in the heart for the ejection of blood, leading to a reduced stroke volume.

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8
Q

What does Ino- mean?

A

Strength - so an inotropic effect is an effect on strength of contraction.

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9
Q

What is a chronotrophic effect?

A

An effect on heart rate

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10
Q

What effect does the parasympathetic on sv?

A

Not really anything, we think because it is mainly the atrial cells that have muscarinic receptors.

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11
Q

Name and explain the 2 factors that affect heart rate

A

The parasympathetic system releases ACh which acts on muscarinic receptors on the pacemaker cells which hyperpolarises them and reduces the slope of the pacemaker potential so that heart rate is slowed (bradycardia).

The sympathetic system releases noradrenaline and adrenaline which act on beta 1 receptors on the pacemaker cells which increases the slope of the pacemaker potential and increases heart rate (tachycardia).

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12
Q

Name and explain the 3 factors that affect stroke volume

A

Preload reflects the length of the muscle before it starts to contract and is determined by the end diastolic volume. In the physiological range, increased end diastolic volume causes an increased strength of contraction and therefore a bigger stroke volume.

Afterload reflects the load the heart is working against once it starts to contract and is determined by the total peripheral resistance. If afterload goes up, the stroke volume goes down.

Contractility is controlled by the sympathetic system which releases noradrenaline and adrenaline that act on beta 1 receptors on the myocardial cells and increases the strength of contraction for any given preload and afterload.

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13
Q

What is CO?

A

SV (stroke volume) x HR (heart rate)

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14
Q

How is CO increased in exercise?

A

Sympathetic system, increase HR and contractility
Parasympathetic system decreases vagal tone and affect on Heart
Veins work to get more blood back to the heart
Arteries dilate so decreased peripheral resistance.

Explained again here:
HR increases via decreased vagal tone & increased sympathetic tone
Contractility increases via increased sympathetic tone alters inotropic state & shortens systole (greater Ca2+ released and taken back up faster, increasing HR and inotropic state (force of contraction))
Venous return increases via venoconstriction & skeletal/respiratory pumps maintains preload
Total peripheral resistance falls due to arteriolar dilation in muscle, skin & heart reduces afterload
CO increase 4-6 times

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15
Q

Pace maker increases HR and only HR, what effect does this have on the Cardiac output?

A

CO = SV x HR

So you would think it would go up, but once hits 140/150bpm cuts into refill time and so less preload and less volume so will reduce and co won’t increase.

In other wprds:
The shortened cardiac interval cuts into the rapid filling phase.
The reduced end diastolic volume reduces preload.
So according to Starling’s law, stroke volume is reduced.

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