cardiac output and control of heart rate

Question 1

what is stroke volume

Answer 1

volume of blood ejected per contraction
SV = End Diastolic Volume – End Systolic Volume

normal 70ml

Question 2

what is the cardiac output

Answer 2

volume of blood pumped by each ventricle per minute

it is the product of heart rate and stroke volume

Question 3

what can the strength of cardiac muscle contraction and SV be graded by

Answer 3

1. Varying the initial length of the cardiac muscle fibres,
   which in turn depends upon EDV (intrinsic control)
2. Varying the extent of sympathetic stimulation (extrinsic
   control)

Question 4

what is a normal cardiac output at rest

Answer 4

4900 ml/min

Question 5

regulation of stroke volume

Answer 5

1. Varying the initial length of the cardiac muscle fibres,
   which in turn depends upon end diastolic volume (intrinsic control)
2. Varying the extent of sympathetic stimulation (extrinsic
   control)

Question 6

increase in sv is a result of increase in cardiac output

Question 7

what does intrinsic control of stroke volume depend on

Answer 7

the direct correlation between End Diastolic Volume and Stroke Volume

Question 8

what happens in terms of stroke volume when you increase the end diastolic volume and why

Answer 8

it will subsequently increase, due to the volume of blood going into ventricle during diastole, then, blood flows back into heart and on contraction it moves into ventricle, causing ventricle muscle to stretch as large amount of blood is inside

Question 9

what occurs when there is an increase in cardiac muscle fibre length, moving closer to optimal length

Answer 9

increases the contractual tension of heart on the following systole within physiological limits, increasing stroke volume and increasing EDV

Question 10

what causes cardiac muscle fibres to vary in length before contraction

Answer 10

degree of diastolic filling

Question 11

can you describe the frank starling law of the heart

Answer 11

when cardiac muscle fibres increase in length, there is an increase in edv, and greater force on subsequent cardiac contraction thus greater stroke volume - this relationship between edv and sv is the frank starling law

Question 12

what is the frank stirling law dependant on

Answer 12

the physical and biochemical properties of cardiac muscle fibres

Question 13

what are the 2 advantages of the intrinsic relationship matching stroke volume with venous return

Answer 13

• equalising output between left and right sides of the heart so blood is evenly distributed between pulmonary and systematic circulation
• when large CO is required e.g. exercise, venous return is increased through action of sympathetic NS resulting in increase in EDV autonomically increasing SV, this combined with increase in HR increase CO so more blood can be delivered to skeletal muscles

Question 14

what is meant by preload

Answer 14

the extent of filling, because it is the workload imposed on heart before contraction begins

Question 15

what extrinsic controls is stroke volume also subject too

Answer 15

• sympathetic stimulation
• adrenaline

both enhance heart contractility (strength of contraction at an given EDV)

Question 16

describe the result of increased contractility of heart as a result of extrinsic control of stroke volume

Answer 16

it is due to increased Ca2+ entry triggered by noradrenaline/adrenaline

increase in inward Ca2+ fluxduring plateau phase enhances release of Ca2+ from intracellular calcium store

as Ca2+ is required for excitation contraction coupling in cardiac muscle cells, increasing rate of relaxation of cardiac muscle cells by stimulating Ca2+ pumps, take up Ca2+ from cytoplasm more rapidly, shortening systole

Question 17

what is meant by inotropic actions

Answer 17

actions on contractility mediated by increase in sympathetic activity or adrenaline

Question 18

What is afterload, and how does it affect the heart?

Answer 18

the arterial blood pressure that ventricles must overcome to open the semilunar valves during contraction because It represents the workload on the heart after contraction begins.

Question 19

how could the heart compensate for increased afterload

Answer 19

by enlarging
but a diseased or weakened heart may not fully compensate, potentially leading to heart failure.

Question 20

how is the strength of the cardiac muscle contraction and according SV graded by

Answer 20

1. Varying the initial length of the cardiac muscle fibres,
   which in turn depends upon EDV (intrinsic control)
2. Varying the extent of sympathetic stimulation (extrinsic
   control

Question 21

What sets the heart’s rate, and does it need nervous stimulation to contract?

Answer 21

set by the depolarization rate of the sinoatrial (SA) node.

doesn’t require nervous stimulation to initiate contraction but it is influenced by the autonomic nervous system.

Question 22

How do the sympathetic and parasympathetic nervous systems affect heart rate?

Answer 22

Sympathetic nerves increase heart rate (tachycardia).

Parasympathetic nerves decrease heart rate (bradycardia).

Question 23

How do the autonomic nervous system divisions affect heart rate?

Answer 23

Both the sympathetic and parasympathetic systems change the slope of the pacemaker potential in the SA node, leading to changes in heart rate, known as the chronotropic effect.

Question 24

what does the parasypathetic nervous system release

Answer 24

in this case the vagus nerve releases acetylcholine to muscarinic receptors

Question 25

what does the sympathetic nervous system release

Answer 25

noradrenaline to adrenergic receptors

Question 26

what is the effect of the parasympathetic stimulation of the SA node

Answer 26

it decreases the heart rate through 2 effects on pace maker cells

1) Hyperpolarisation of the SA node membrane potential
(takes longer to reach threshold)
 2) Decreases the rate of spontaneous depolarisation as ACh increases K+ permeability by slowing the closure of K+
channels

Question 27

what are some effect of parasympathetic on heart activity

Answer 27

• decreases AV node excitability which delays transmission of impulse to ventricles
• shortens plateau phase of action potential in atrial cells, weakening atrial contractions
• little effect on ventricular contractions

Question 28

what are the overall effects of parasympathetic on heart activity

Answer 28

-Heart rate decreases.
-The time between atrial and ventricular contraction increases.
-Atrial contractions become weaker.

Question 29

what is the effect of sympathetic stimulation on SA node

Answer 29

speeds up heart rate through its effects on pacemaker tissue - tachycardia

speeds up depolarisation so threshold is reached more rapidly

Question 30

what are the effects of the sympathetic stimulation on heart activity

Answer 30

sympathetic stimulation of AV node, reduces AV nodal delay by increasing conduction velocity

speeds up spread of AP throughout specialised conduction pathway

increase contractile strength of the atrial of atrial and ventricular contractile cells (heart beats more forcefully and squeezes out more blood)

• Speeds up relaxation

Question 31

what factors influence heart rate

Answer 31

regulation - Autonomic innervation

Adrenaline (epinephrine) by being released into blood in response to sympathetic stimulation

Both adrenaline and noradrenaline increase heart rate (chronotropic effect) and strengthen heart contractions (inotropic effect).

Adrenaline works similarly to noradrenaline, reinforcing the sympathetic nervous system’s effect on the heart.