Cardiovascular System at rest/exercise(1.1b) Flashcards
4 heart chambers
Right Atrium, Left Atrium, Right Ventricle, Left Ventricle
4 heart Valves
Tricuspid valve, Bicuspid valve, Pulmonary semi-lunar valve, Aortic semi-lunar valve.
4 blood vessels that attach to heart
Vena cava, Pulmonary artery, pulmonary vein, aorta.
4 features of conduction system (NEED TO KNOW)
SA node, AV node, bundles of His, Purkinje fibres.
Conduction system definition
Specialised bundles of tissue that transmit the electrical impulse through the heart causing a coordinated contraction.
SA node
In wall of right atrium.
Sends impulse across both atria to cause Atrial systole.
AV node
In middle wall of heart between atria and ventricles.
Receives impulse from SA node, delays it for a moment to allow for atrial systole to finish and sends it down to bundles of His.
Bundles of His
In middle wall of heart. Transmits impulse to the bottom of the Right and left side of heart.
Purkinje fibres
In walls of ventricles. Causes impulse to penetrate into ventricle walls causing ventricular systole.
The cardiac cycle
All the events associated with the flow of blood through the heart during one complete heartbeat.
1.Atrial diastole
2.Atrial systole
3.Ventricular diastole
4.Ventricular systole
All controlled by conduction system to produce highly coordinated contractions
Systole
Heart working.
The contraction phase when a chamber is pumping blood out
1.Atrial systole- blood pumped into ventricles
2.Ventricular systole- blood pumped into pulmonary artery and aorta
Diastole
Heart relaxing.
When a chamber is receiving blood.
1. Atrial diastole- blood entering the atria via vena cava and pulmonary vein.
2.Ventricular diastole- blood entering ventricles from atria
Atrial Diastole related to Cardiac cycle
- No electrical impulse.
- Atria fill with blood from vena cava and pulmonary vein.
- AV valves closed
- Atrial pressure rises above Ventricular pressure. Blood starts to pass passively into ventricles
Atrial systole related to cardiac cycle
- SA node fires electrical impulse across atria
- Atria contracts
- AV valves forced open
- remaining blood pumped into ventricles
- semi lunar valves closed
Ventricular diastole related to cardiac cycle
- Impulse received by AV node
- Delayed for a moment to allow Atrial systole to complete.
- AV valves close
- AV nodes send impulse Down right and left Bundles of His into Purkinje fibres
Ventricular systole related to cardiac cycle
- Ventricles contract from bottom upwards
- Semi lunar valves forced open
- blood pumped out of ventricles into pulmonary artery and aorta
Heart rate
And average values at rest
Number of times Heart beats per min.
70 Bpm, 50 for endurance athlete
Stroke volume
And average values at rest
Amount of blood ejected from left ventricle per beat (ml)
70 ml, 100 ml for endurance athlete
Cardiac output
Amount of blood ejected from left ventricle per min.
Vascular shunt mechanism
The redistribution of Cardiac output during exercise
Chemoreceptors
Monitor chemical changes in body during exercise and recovery ( carbon dioxide and oxygen )
Increase in carbon dioxide during exercise, increase in oxygen during recovery
Baroreceptors
Monitor blood pressure
Increases during exercise and decreases in recovery
Proprioceptors
Monitor increase in muscle activity during exercise and decrease during recovery
VCC- Vasomotor Control Centre
In Brain, controls vascular shunt mechanism
Sympathetic stimulation
Controls the diameter of arteriole and pre- capillary sphincter
Increasing it- vasoconstriction
Decreasing it- vasodilation
Arteriole
Small artery that Carries oxygenated blood to muscles and organs.
Has a muscle middle layer for vasoconstriction and vasodilation
Pre- capillary sphincter
A small ring shaped muscle at junction between arteriole and capillary
Can vasoconstrict and Vasodilate
Vasodilation
A decrease in sympathetic stimulation causes widening of arteriole and pre capillary sphincter
Vasoconstriction
Increase in sympathetic stimulation causes diameter to narrow of arteriole and pre capillary sphincter
What happens at the muscles during exercise
- VCC decreases sympathetic stimulation of arterioles and pre-capillary sphincters
- this causes vasodilation of arterioles and pre capillary sphincters
- increasing blood flow
Whats happens at the organs during exercise
- VCC increases sympathetic stimulation of arterioles and pre capillary sphincters
- causes vasoconstriction of arterioles and pre capillary sphincters
- decreasing blood flow
What happens at the muscles during recovery
- VCC increases sympathetic stimulation of arterioles and pre capillary sphincters
- causes vasoconstriction of arterioles and pre capillary sphincters
- decreasing blood flow
What happens at the organs during recovery
- VCC decreases sympathetic stimulation at arterioles and pre capillary sphincters
- causes vasodilation of arterioles and pre capillary sphincters
- Increases blood flow
Effects of submaximal exercise on heart rate
5 stages
1) increases (anticipatory rise from adrenalin)
2) fast increase at start of exercise to cope with muscles increased demand for oxygen
3) HR plateaus, supply caught up with demand (steady state)
4) fast decrease at end of exercise due to decrease in Venous Return
5) slower decrease in 2nd stage of recovery until HR returns to pre exercise value
Effects of maximal exercise on Heart rate
Differences to submaximal
- no steady state reached (supply of oxygen never catches up with demand from muscles)
- recovery time takes longer due to exercise being at a higher intensity
Starlings law of the heart
- SV depends on VR (venous return- volume of blood returning to the heart)
-during exercise VR increases.
-this causes the walls of the heart to stretch
-2 types:
Stretch 1- more blood enters atria, walls of atria stretch stimulates SA node causing it to increase fire rate, and so increase HR
Stretch 2- more blood enters ventricles, walls of ventricles stretch, causing more forceful contraction of ventricular walls- increasing SV.
Effect of submaximal exercise on Stroke Volume
- SV volume increases linearly with exercise intensity
- it then plateaus when steady state reached (supply=demand)
- when it hits maximal intensity it decreases
- therefore, SV is at its highest during sub maximal intensity
Why does stroke volume decrease at maximal intensity
- HR increases to highest
- not enough time during ventricular diastole for ventricles to fill completely
- so less blood ejected from ventricles per beat
What happens to SV during recovery
- remains elevated to maintain blood flow so lactic acid and CO2 can be removed from muscles
- it reduces to pre exercise value gradually
- cool downs help maintain SV
Why does Cardiac output increase at submaximal exercise intensity
HR and SV are both increasing
HR x SV = Cardiac output(Q)
Why does Q plateau towards maximal exercise intensity
- HR continues to increase
- SV decreases because of cardiovascular drift
- so, Cardiac output remains constant at maximum value
What happens to Q during recovery
- reduces to pre-exercise value gradually
- HR decreases quickly but SV remains elevated
2 problems with Venous return during exercise
1) blood pressure in the veins that return blood to the heart is 0
2) most of Q is in the legs so has to travel against gravity to get to the heart
5 solutions for Venous return during exercise
1) POCKET VALVES- in larger veins which prevent backflow of blood
2) SKELETAL MUSCLE PUMP- when lower leg muscles contract, they get wider and press against vein walls, squeezing blood to heart
3) SMOOTH MUSCLE- in veins allows some venoconstriction to help move blood up to heart
4) RESPIRATORY PUMP- inspiration causes diaphragm to flatten, decreasing volume & increasing pressure in abdomen to below pressure in thoracic cavity, the pressure differential pulls blood to heart.
5) GRAVITY FROM ABOVE HEART- aids blood from upper body to heart
Intrinsic factors for HR reguation
1) Increased temperature
- this increases speed of nerve transmission
- this stimulates SA node
- causing HR to increase
2) Increased Venous Return
- increases volume of blood to heart
- this causes stretch of atrial and ventricular walls
- Starlings law (HR increases) atrial walls stretch, stimulating SA node, increases fire rate , HR increases
Extrinsic factors ( neural factors ) for HR regulation
- Chemoreceptors - detect increase in CO2
- Baroreceptors - detect increase in blood pressure
- Proprioceptors- detect increase in muscle activity
- These receptors send info to Cardiac control centre in brain
- CCC uses sympathetic stimulation to increase firing rate of SA node- HR increases
Extrinsic factors (hormonal factors)
- Adrenalin released from adrenal glands, stimulates sympathetic nervous system
- this increases fire rate of SA node, so HR increases
- Adrenalin also increases force of contractions- so SV and Q increase as well
Regulation of HR during recovery
-Opposite to during exercise
For example, temperature decreases, decreases speed of nerve transmission, inhibiting SA node, decreasing HR
