cardiac output and control of heart rate Flashcards
what is stroke volume
volume of blood ejected per contraction
SV = End Diastolic Volume – End Systolic Volume
normal 70ml
what is the cardiac output
volume of blood pumped by each ventricle per minute
it is the product of heart rate and stroke volume
what can the strength of cardiac muscle contraction and SV be graded by
- Varying the initial length of the cardiac muscle fibres,
which in turn depends upon EDV (intrinsic control) - Varying the extent of sympathetic stimulation (extrinsic
control)
what is a normal cardiac output at rest
4900 ml/min
regulation of stroke volume
- Varying the initial length of the cardiac muscle fibres,
which in turn depends upon end diastolic volume (intrinsic control) - Varying the extent of sympathetic stimulation (extrinsic
control)
increase in sv is a result of increase in cardiac output
what does intrinsic control of stroke volume depend on
the direct correlation between End Diastolic Volume and Stroke Volume
what happens in terms of stroke volume when you increase the end diastolic volume and why
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
what occurs when there is an increase in cardiac muscle fibre length, moving closer to optimal length
increases the contractual tension of heart on the following systole within physiological limits, increasing stroke volume and increasing EDV
what causes cardiac muscle fibres to vary in length before contraction
degree of diastolic filling
can you describe the frank starling law of the heart
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
what is the frank stirling law dependant on
the physical and biochemical properties of cardiac muscle fibres
what are the 2 advantages of the intrinsic relationship matching stroke volume with venous return
- 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
what is meant by preload
the extent of filling, because it is the workload imposed on heart before contraction begins
what extrinsic controls is stroke volume also subject too
- sympathetic stimulation
- adrenaline
both enhance heart contractility (strength of contraction at an given EDV)
describe the result of increased contractility of heart as a result of extrinsic control of stroke volume
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
what is meant by inotropic actions
actions on contractility mediated by increase in sympathetic activity or adrenaline
What is afterload, and how does it affect the heart?
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.
how could the heart compensate for increased afterload
by enlarging
but a diseased or weakened heart may not fully compensate, potentially leading to heart failure.
how is the strength of the cardiac muscle contraction and according SV graded by
- Varying the initial length of the cardiac muscle fibres,
which in turn depends upon EDV (intrinsic control) - Varying the extent of sympathetic stimulation (extrinsic
control
What sets the heart’s rate, and does it need nervous stimulation to contract?
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.
How do the sympathetic and parasympathetic nervous systems affect heart rate?
Sympathetic nerves increase heart rate (tachycardia).
Parasympathetic nerves decrease heart rate (bradycardia).
How do the autonomic nervous system divisions affect heart rate?
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.
what does the parasypathetic nervous system release
in this case the vagus nerve releases acetylcholine to muscarinic receptors
what does the sympathetic nervous system release
noradrenaline to adrenergic receptors
what is the effect of the parasympathetic stimulation of the SA node
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
what are some effect of parasympathetic on heart activity
- 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
what are the overall effects of parasympathetic on heart activity
-Heart rate decreases.
-The time between atrial and ventricular contraction increases.
-Atrial contractions become weaker.
what is the effect of sympathetic stimulation on SA node
speeds up heart rate through its effects on pacemaker tissue - tachycardia
speeds up depolarisation so threshold is reached more rapidly
what are the effects of the sympathetic stimulation on heart activity
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
what factors influence heart rate
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.
