Cardiovascular system Flashcards
Systematic circulation
Systematic circulation carries oxygenated blood around the body in the arteries and carries deoxygenated blood back to the heart in the veins. (Heart and body)
Pulmonary circulation
Pulmonary circulation includes the lungs. It carries deoxygenated blood from the heart to the lungs to pick up oxygen and then takes oxygenated blood back to the heart so it can be pumped around the systematic circulation. (Heart and lungs)
Arteries
Arteries carry oxygenated blood away from the heart at high pressure towards the muscles and organs
Arterioles
Arterioles carry oxygenated blood from the arteries to capillary beds. Vasoconstrict/ vasodilate to control blood flow.
Arterioles contain a small band of muscle in their wall which can dilate or constrict the arteriole lumen to help control the volume of blood flow.
Veins
Veins carry deoxygenated blood from the muscles and the organs back towards the heart at low pressures
Venules
Venules carry deoxygenated blood from capillary beds to veins for transport back to the heart
Capillaries
Capillaries bring blood slowly into close contact with muscles and organs to assist with gaseous exchange
Vasoconstrict
Narrowing of arteries, arterioles and pre-capillary sphincters
Vasodilate
Widening of arteries, arterioles and pre-capillary sphincters
Venoconstrict
Narrowing of veins and venules
Venodilate
Widening of veins and venules
Pre-capillary sphincters
Smooth muscle segments that regulate blood flow into capillaries. Sphincters direct blood to the tissues that need it most.
Pre-capillary sphincters are ring shaped bands of muscle at the junction between arterioles and capillaries that control blood flow through the capillary bed.
Pre-capillary sphincters open and close to control the entrance to the capillary. Where there is a greater demand for oxygen, more pre-capillary sphincters open to increase gas exchange between blood and tissues.
Cardiac output (Q)
The volume of blood ejected from the left ventricle every minute. (Q= HR * SV)
Cardiac output at rest is approximately 5L/min but it can increase to >20 L/min during intense exercise
Vascular shunt
The redistribution of cardiac output around the body from rest to exercise which increases the percentage of blood flow to the skeletal muscles.
The vasomotor control centre located in the medulla oblongata controls cardiac output distribution and blood pressure. This is done by causing the sympathetic nervous system to vasoconstrict or vasodilate the blood vessels. The VCC processes information from chemoreceptors and baroreceptors to decide whether sympathetic stimulation of the arterioles or pre-capillary sphincters need to be increased or decreased.
Chemoreceptors
In muscles, aortic arch, carotid arteries. Detect chemical changes in the blood (increase in CO2 and lactic acid during exercise) and tell the VCC that exercise has started.
Baroreceptors
In walls of arteries. Detect changes in blood pressure by sensing when artery walls are stretched. Tells the brain the blood pressure has increased or decreased.
Why is the vascular shunt mechanism so important?
- Increased oxygen supply to working muscles to support aerobic energy production
- Removes waste products from the muscles to delay fatigue
- Ensure more blood goes to the skin to regulate body temperature by allowing heat to radiate and evaporate with sweat
- More blood goes to the myocardium (cardiac muscle) which also requires more oxygen during exercise to allow it to beat faster and to increase cardiac output during exercise.
- Blood supply to the brain and heart stays relatively stable because it needs oxygen for energy production to keep working
Vasomotor control of cardiac output in response to exercise
Chemoreceptors detect increasing levels of CO2 and lactic acid. Baroreceptors detect increased stretching of blood vessel walls. The VCC in the medulla oblongata activated the sympathetic nervous system. Sympathetic stimulation of the arterioles and pre-capillary sphincters at the muscle cells decrease - vasodilation. Blood flow to muscles is increased. Sympathetic stimulation of the arterioles and pre-capillary sphincters at the organs increases - vasoconstriction. Blood flow to organs is decreased.
Heart rate
The number of times the heart beats per minute.
Average population resting HR
- Males: 70bpm
- Females: 72bpm
Trained population
- Males: 50bpm
- Females: 53bpm
Diastole
The cardiac muscle relaxes and heart chambers fill with blood
Systole
The cardiac muscle contracts and blood is ejected from the ventricles to enter pulmonary or systematic circulation
Atrioventricular valves
Tricuspid and bicuspid valves
Semilunar valves
Aortic valve and pulmonary valve
Cardiac cycle
Blood flows into the right and left atria filling them with blood. The atrioventricular valves are shut. Blood pressure in the atria becomes higher than the pressure in the ventricles. This causes the atrioventricular valves to open. Both atria contract and blood flows into the ventricles. The semilunar valves remain shut so that blood does not yet enter the pulmonary artery or aorta. The amount of blood in the ventricle after diastole (cardiac muscle relaxes and heart chambers fill with blood) is called end-diastolic volume. The ventricles contract, which increases blood pressure in the ventricles. This causes the semilunar valves to open. Blood flows into the aorta and pulmonary artery. The semilunar valves shut as the ventricles start relaxing again to prevent blood flowing back into the ventricles. The amount of blood left in the ventricle after systole is called end-systolic volume.
Myogenic
- The cardiac muscle (myocardium) is myogenic
- The heart is myogenic so it can generate it’s own electrical impulse which stimulates the myocardium (cardiac muscle) to contract
Sinoatrial (SA) node
- Acts as the pacemaker of the heart
- Located in the right atrial wall
- How quickly the SA node fires determines heart rate
- Generates the electrical impulse which travels across the muscle cells in the atria
- Causes the atria to contract (atrial systole)
Atrioventricular (AV) node
- Electrical impulses from the SA node travels to the AV node
- AV node delays the impulse for 0.1 seconds to allow the atria to finish contracting and give the ventricles time to fully fill up with blood
- Once the atrioventricular valves (bicuspid and tricuspid) have closed, the electrical impulse moves on.
Bundle of His
- From the AV node the electrical impulse travels down the Bundle of His
- The Bundle of His is a group of conduction cells found in the septum of the heart
- The Bundle of His splits the electrical impulse in two ready to travel separately to either the left or right ventricle
Stroke volume
- The volume of blood ejected from the left ventricle per BEAT
- Average resting value: 70mL
Cardiac output
- The volume of blood ejected from the left ventricle per MINUTE
What impact would a high SV have on HR?
Allows HR to decrease because the same amount of blood can be ejected from the heart each minute using fewer contractions/ beats. The heart is more efficient.
The CCC’S Intrinsic control
- Temperature changes: When the blood gets warmer, its viscosity (thickness) decreases. When the body warms up, the speed of nerve impulse transmission increases.
- Venous return changes: The volume of blood that is returning to the heart through the vena cava will affect how much the ventricles walls are stretched. This affects how forcefully the ventricles contract, which influences stroke volume (Frank-Starling law).
The CCC’S hormonal control
Adrenaline and Noradrenaline:
These hormones are released from the adrenal glands. They increase the force of ventricular contractions (which increases stroke volume). These hormones also speed up the spread of electrical impulses throughout the heart.
The sympathetic nervous system increases heart rate
As exercise begins, energy production in the muscles increases. CO2 and lactic acid in the blood increases, blood temperature increases, the rate of venous return increases and the pH of blood decreases. These changes are detected by receptors that send information to the CCC to say that exercise has begun. The CCC stimulates the sympathetic nervous system to increase heart rate. The sympathetic nervous system increases heart rate by stimulating the release of adrenaline from the adrenal glands. Adrenaline activates the accelerator (cardiac) nerve which increases the firing rate of the sinoatrial node. Adrenaline also increases the strength of ventricular contractions so this increases stroke volume. The sympathetic nervous system stimulates the release of noradrenaline from the adrenal glands. Noradrenaline helps spread electrical impulses throughout the heart to increase HR. Overall the sinoatrial node fires faster to increase cardiac output.
How does long term training affect the heart?
- Long term endurance training causes cardiac hypertrophy (increased strength and size of cardiac muscle/ myocardium)
- A stronger and thicker myocardium produces a more powerful contraction of the heart
- As a result of endurance training, the overall size of the heart may increase
Bradycardia
- Cardiac hypertrophy can lead to bradycardia
- Bradycardia is a resting heart rate of less than 60bpm
Heart response to sub-maxixmal exercise
- Sub-maximal exercise is a low to moderate intensity of exercise within a performer’s aerobic capacity and below their anaerobic threshold. Often aerobic.
- There’s an initial anticipatory rise in heart rate before exercise begins.
- Rapid increase in heart rate at the start of exercise to increase blood flow and oxygen delivery.
- Heart rate can plateau if we get to a comfortable, steady state exercise intensity.
- The plateau represents demand for oxygen meeting supply
- Rapid decrease in heart rate in recovery, then a more gradual decrease to resting level.
Heart response to maximal exercise
- Maximal exercise is a high intensity of exercise above a performer’s aerobic capacity. It will cause fatigue very quickly and lead to exhaustion. Often anaerobic.
- Heart rate does not plateau as exercise intensity continues to increase
- The demand for oxygen and need to remove waste products (C02, lactic acid) keeps growing
- The cardiovascular system has to keep working harder and harder to keep up with demand
Why does the anticipatory rise occur?
- The body knows it is about to exercise, so the brain sends signals to the heart via the sympathetic nervous system
- The SNS stimulates the release of adrenaline and noradrenaline to increase heart rate before exercise begins
- The anticipatory rise in heart rate also activates the vascular shunt mechanism to redirect more blood flow to the skeletal muscles and away from other organs
- The anticipatory rise is beneficial because it helps you to adapt to the upcoming exercise quicker and more efficiently
Stroke volume: Response to exercise
- Stroke volume increases in line with exercise intensity
- Stroke volume can increase during exercise because the volume of blood returning to the heart increases (increased venous return).
- The stroke volume will only increase up to 40-60% of maximum exercise intensity (sub-maximal intensity).
- It will reach a plateau and not increase any further because as we get towards a maximal intensity, heart rate speeds up so much that it doesn’t allow enough time for the ventricles to completely fill up with blood during diastole (relaxation/ filling phase of the cardiac cycle).
Cardiovascular drift
The progressive decline in stroke volume, coupled with an upward drift of heart rate over time, in order to maintain a steady cardiac output (Q.)
Venous return
The volume of blood returning to the right atria through the veins
End diastolic volume
The volume of blood in the ventricles at the end of diastole (relaxation/ filling phase) and before ventricular systole (when the ventricles contract.)
Why is it important that blood gets back to the heart quickly and efficiently during exercise?
- During exercise the blood pressure in the veins is not high enough to return blood to the heart at the required rate.
- When venous return is inadequate, the ventricles receive less blood, resulting in a low end diastolic volume.
- When EDV is low, the ventricles fail to stretch. They need to stretch before they forcefully contract (ventricular systole) and eject the greater volume of blood that the exercising body needs.
- This results in low stroke volume, low cardiac output and low blood pressure.
- If there is no increase in venous return during exercise, the oxygen demands of the muscles during exercise will not be met, and waste products will not be cleared away fast enough.
- This speeds up the onset of fatigue and reduces performance
Poor venous return
- Ventricles receive less blood
- Low end diastolic volume (EDV)
- Ventricles do not stretch
- Ventricles do not contract as forcefully as they could
- Lower cardiac output, reduced blood pressure, reduced rate of blood flow
- Heart doesn’t pump enough oxygenated blood to meet oxygen demands of the body
- Reduced performance through faster onset fatigue
Starling’s Law
If venous return increase, end diastolic volume increases too. This means that the ventricles of walls experience greater stretch and will contract/ recoil with more force. This ejects more blood from the heart per beat which increases stroke volume.
- If venous return increases, there will be more blood returning to the heart to fill the ventricles during diastole (heart relaxation.)
- More blood in the ventricles during diastole increases end diastolic volume and stretches the myocardium. This is the ‘pre-load stage.’
- The stretched myocardium has to recoil. The more it is stretched, the more forceful the recoil will be.
- Therefore a greater end diastolic volume increases stroke volume, because a more forceful ventricular contraction (ventricular systole) can occur, forcing a greater volume of blood out of the heart each beat.
- Increased stroke volume contributes to higher cardiac output during exercise due to this formula Q = HR * SV
- A low heart rate maximises this effect, which may explain why trained athletes have a higher exercising SV than untrained people.
