Cardiac Output + Regulation Of Function Flashcards
How much blood does each ventricle pump per minute at rest
5 litres
What is cardiac output
Rate ventricle pumps blood (L/min)
What is heart rate
Number of contractions per minute
What is the equation for cardiac output
Cardiac output = heart rate x stroke volume
CO = HR X SV
What is stroke volume
Volume per contraction
What is extrinsic control
- Regulation of heart by neutral input
- circulating hormones or any other factor from outside the heart (external factors)
What is intrinsic control
Regulation by factors originating in the heart
What system enables to body to switch between resting state and fight or flight
Central nervous system (CNS)
What are the components of the CNS
1) afferent (coming into CNS)
2) efferent (sent out of CNS)
- remember bc E after A in alphabet
What controls muscles and other organs
signals sent through efferent branch of PERIPHERAL NERVOUS SYSTEM (PNS)
What are the 2 branches of the PNS
1) Autonomic
2) somatic (voluntary skeletal muscle control)
What are the 2 division of the autonomic branch of the PNS
1) sympathetic
2) parasympathetic (part of efferal branch)
What is parasympathetic nervous system
- Rest state
- input through autonomic nervous system into different organs (esp the heart)
What is the sympathetic nervous system
Fight or flight response
What is the nerve supply to the parasympathetic nervous system
CRANIOSACRAL
- 4 cranial nerves supply parasympathetic efferent output (III, VII, VIIII, X)
- S2, S3, S4 from sacral levels of spinal cord
- ganglia located in/near target viscera
What do neurones have entering / leaving the ganglia
Entering = pre-ganglionic neurone
Leaving = post ganglionic neurone
What is the structure of neurones in the parasympathetic division
- Pre-ganglionic long
- Synapse with post-ganglionic neurones at ganglia
Which cranial nerve are most major parasympathetic nerves in and what do these supply
VAGUS NERVE (cranial nerve X)
- vagal fibres to heart, lungs, upper GI tract
What is the nerve supply to the sympathetic nervous system
THORACOCOLUMBAR
- nerves originate from thoracic + lumbar levels of spinal cord (T1-L3) = paraspinal ganglia
- nerves come out of spinal cord in thoracic region and reach paraspinal sympathetic trunks
What is the structure of sympathetic neurones
- Pre-ganglionic neurones short
- reach para-spinal ganglia (found either side of spine)
- from here post-ganglionic sympathetic neurones travel to the viscera they supply
How do the divisions of the autonomic nervous system innervate the heart
- para = nerves that innervate heart travel by vagus nerve
- sympa = nerves supply heart from paraspinal ganglia
Where are the nuclei of para neurones
- medulla oblongata
- brainstem
What part of the heart is innervated by para nerves
1) sino-atrial node
2) AV node
What is the neurotransmitter in the parasympathetic division
ACETYLCHOLINE
What part of the heart is innervated by sympathetic nerves
1) SA + AV node
2) ventricular myocardium (innervated by sympathetic neurones directly)
What is the neurotransmitter in the sympathetic division
NORADRENALINE
What influences changes in heart rate
- Different neural inputs to SA + AV nodes Also - age - fitness - emotional state Etc
What is the heart rate of a normal adult
What can heart range range from/to
What regulates this
70-90 BPM
- 30-180BPM
- extrinsic controls
What is the role of pacemaker cells of the SA node (first branch) when sympathetic activity INCREASES
1) increase action potentials
2) increase heart rate
3) increase cardiac output
What is the role of AV node and conduction system (2nd branch) when sympathetic activity INCREASES
1) increase speed of conduction
2) ventricular contraction sooner after atrial contraction
3) decreases duration of systole
Given the action of the pacemaker cells of the SA node and of the AV node and conduction system
How does increased sympathetic activity support an increased heart rate
Decreasing systole
Allows for increased cardiac output so more cardiac contractions
What happens when parasympathetic activity is increased compared to sympathetic
EXACT OPPOSITE of sympathetic
So how does increase in parasympathetic activity support a decreased heart rate
- Duration of systole increases
- so less cardiac output and less blood pumped per minute
How do pacemaker cells of the SA node cause decrease in action potentials in the parasympathetic division
- gradual slow depolarisation from pacemaker cells is prolonged
- so less frequent action potentials
How does cardiac output decrease
- fewer BPM
- but stroke volume is always the same
Explain the hormonal control of heart rate
- adrenaline acts via the blood stream and is released from adrenal medulla
- increased action potential firing of SA node so increases heart rate (similar to noradrenaline of sympathetic division)
How does adrenaline increase velocity of action potentials
Sympathetic activity is coupled with adrenaline secretion
What else increases force of myocardial contraction thus promote increase in heart rate
1) thyroid hormones
2) glucagon
3) insulin
Why does stroke volume change
- varies between individuals and from moment to moment
What factors affect ventricular contractility (force of ventricular contraction)
1) sympathetic activity increases
2) ventricular contractility increases
3) cardiac output increases
- due to increase is Ca2+ permeability across the membrane
What increases myocardial contractility
adrenaline
What are changes in end diastolic volume controlled by and what does increasing it cause
- intrinsic control
1) increase in EDV
2) increases force of ventricular contraction
3) increases stroke volume and cardiac output
Define starlings law of the heart
‘When the rate at which blood flows into the heart from the veins (venous return) changes, the heart automatically adjusts its output to match the flow’
What is visible on a graph of starlings law of the heart (for normal patient with contrast sympathetic output)
An increase in EDV causes stroke volume to increase
How does an increase in EDV increase the force of contraction in myocardium
- muscle fibres of myocardium stretch
- increases affinity of troponin (contractile proteins expressed in cardiomyocytes) in muscle fibres for calcium
- so increase in number of cross bridges activated in contractile machinery
- in cardiac muscle optimum length of muscle for generating force is greater than the resting length so with increase in EDV muscle fibres are closer to optimum length for contraction
- and are moved into region where they can contract with greater force
So what happens to an (individual cardiomyocyte) cardiac muscle when it’s
A) at rest
B) physically stretched
in buffer suspensions
A) regularly contracting, looks clear
B) increased rate of contraction can see activity is happening inside it
How does an increase in sympathetic activity (increase in contractility) influence starlings law
- shifts curve upwards
- so at any given EDV, SV is higher
- due to increase in ventricular contractility
How does starlings law work to regulate when sympathetic activity is increased
- regulates heart size
- by adjusting SV so CO matches venous return
- blood going in matches blood going out so no backlog
What determines EDV
Pressure of blood inside the heart before contraction
Tension on myocardium
What determines preload
1) Filling time (dependent on heart rate, ie if higher = less filling time)
2) Atrial pressure (dependent on venous return, amount of blood flowing into atria determines its pressure and force of atrial contraction)
What is afterload
- the load/pressure placed on the myocardium by arterial pressure (the arteries) after contraction starts
- when heart ejects blood
- it contracts and pumps blood out
- has to work against arterial pressure (pumping against this)
So how does an increase in arterial pressure influence SV
- DECREASES stroke volume
- heart is working against higher pressure
- so for given amount of force the blood pumped out is slightly less
What determines afterload in the left ventricle
Pressure in the aorta that the heart is pumping against
Describe the factors affecting stroke volume starting with central venous pressure
central venous pressure -> venous return -> atrial pressure -> ventricular end diastolic pressure (pre-load) -> EDV -> SV
Describe the factors affecting stroke volume starting with atrial contraction
Atrial contraction -> atrial pressure -> ventricular end diastolic pressure (pre-load) -> EDV -> SV
Describe the factors affecting stroke volume starting with filling time
Filling time -> ventricular end-diastolic pressure (preload) -> EDV -> SV
Describe the factors affecting stroke volume starting with adrenaline and sympathetic nerves to the heart
adrenaline and sympathetic nerves to the heart -> ventricular contractility -> SV
Describe the factors affecting stroke volume starting with afterload
Afterload -> SV
So in extrinsic control what is the heart regulated by
1) para and sympa neurones
2) hormones
In intrinsic control what is the heart regulated by
1) factors within heart
2) ie influence of EDV on SV -> basis of starlings law
An increase in venous return causes an increase in…
1 - stroke volume
2 - cardiac output