Mind map
Cardiovascular System

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Cardiovascular System
Heart
- Generates pressure waves to push blood through blood vessels
- Heart valves ensure one way flow in heart
- When pressure is greater behind valve, it opens
- When pressure is greater in front of valve, it closes
- Surrounded by pericardium which protects it
- Conducting system
- Sequence of excitation:
- 1. Sinoatrial node (pacemaker) generates impulses
- 2. Signal propagates from right to left atrium
- 3. Atria depolarize, fires action potential, calcium comes in and contracts
- 4. Signal reaches atrioventricular node
- 5. Signal goes down and spreads through ventricles, depolarizes, calcium comes in for muscles to contract
- 4. Signal reaches atrioventricular node
- 3. Atria depolarize, fires action potential, calcium comes in and contracts
- 2. Signal propagates from right to left atrium
- AV node delay - period of time signal waits in atrium before travelling to ventricles
- AV node - routes electrical signal so heart contracts from apex (bottom) to base (top); this delay is accomplished by slower conductional signals through nodal cells
- 1. Sinoatrial node (pacemaker) generates impulses
- Sequence of excitation:
- Electrocardiogram - graphic record of heart's electrical activity; signals show changes in voltage
- P wave, PR segment, QRS complex, ST segment, T wave
- Cardiac cycle
- Comprises all events involved with blood flow through heart during one heart beat
- Systole - contraction phase
- End systolic volume - amount of blood left in ventricles at end of systole
- Diastole - relaxation phase
- Longer than systole
- End diastolic volume - volume of blood in ventricles at end of diastole
- EDV determined by venous return
- Stroke volume increases as EDV increases
- How much the myocardium is stretched by the blood coming in
- The larger the stretch, the more forceful the contraction, and the larger the stroke volume
- How much the myocardium is stretched by the blood coming in
- Stroke volume increases as EDV increases
- EDV determined by venous return
- 1. Start at end of diastole
- 2. AV valve is open, and semilunar valve is closed
- 3. Ventricle contracts, pressure rises causing AV valve to shut and SL valves are still closed (isovolumetric contraction)
- 4. Pressure in left ventricle is higher than aorta (ejection phase)
- 5. Pressure in left ventricle lowers below aorta, SL valve shuts (isovolumetric relaxation)
- 6. Pressure in ventricles follows below that of the atria, AV opens (filling)
- 7. Atrial contraction delivers the final blood to the ventricles
- 6. Pressure in ventricles follows below that of the atria, AV opens (filling)
- 5. Pressure in left ventricle lowers below aorta, SL valve shuts (isovolumetric relaxation)
- 4. Pressure in left ventricle is higher than aorta (ejection phase)
- 3. Ventricle contracts, pressure rises causing AV valve to shut and SL valves are still closed (isovolumetric contraction)
- 2. AV valve is open, and semilunar valve is closed
- Stroke volume - amount of blood ejected from ventricles during systole
- SV = EDV - ESV
- Depends on:
- Change sympathetic input to ventricles, which affects contractility of ventricles
- inotropic agent - chemical that affects contractility
- Negative inotropic effects - decrease contractility
- Positive inotropic effects - increase contractility
- Ejection fraction - contractility; EF = SV/EDV
- Increased ejection fraction leads to increased contractility
- inotropic agent - chemical that affects contractility
- Afterload - combined load of EDV and arterial resistance during ventricular contraction
- Preload - amount of myocardial stretch before contraction; this depends on EDV
- Change sympathetic input to ventricles, which affects contractility of ventricles
- Ascultation - listening to heart through chest wall through stethoscope; closing of AV and semilunar valves produces sounds that can be heard through stethoscope
- - Lub (first sound) produced by closing of AV valves
- - Dub (second sound) produced by closing of semilunar valves
- - With every beat the heart pumps about 60% of blood in its chambers or 70 mL
- Innervation of the heart (heart rate)
- Parasympathetic system:
- 1. Vagus nerves
- 2. Acetylcholine connected to muscarinic receptors on atria
- 1. Vagus nerves
- Sympathetic system: (increases heart rate)
- 1. thoracic spinal nerves
- 2. Norepinephrine come from nerves, and epinephrine come from bloodstream
- 3. These bind to beta receptors (adrenergic = bind to adrenaline)
- 2. Norepinephrine come from nerves, and epinephrine come from bloodstream
- 1. thoracic spinal nerves
- To increase heart rate:
- Parasympathetic system:
Blood
- Plasma - blood without cells
- Circulation pathway as drop of blood:
- 1. Starting as deoxygenated blood that arrives in right atrium
- 2. Tricuspid valve (AV valve)
- 3. Right ventricle
- 4. Pulmonary valve (SL valve)
- 5. Pulmonary artery
- 6. Pulmonary capillaries to get oxygenated
- 7. Pulmonary vein
- 8. Left atrium
- 9. Mitral/bicuspid valve (AV valve)
- 10. Left ventricle
- 11. Aortic valve (SL valve)
- 12. Aorta
- 13. Systemic arteries
- 14. Systemic capillaries to get deoxygenated
- 15. Systemic veins
- 16. Superior/inferior cava
- 15. Systemic veins
- 14. Systemic capillaries to get deoxygenated
- 13. Systemic arteries
- 12. Aorta
- 11. Aortic valve (SL valve)
- 10. Left ventricle
- 9. Mitral/bicuspid valve (AV valve)
- 8. Left atrium
- 7. Pulmonary vein
- 6. Pulmonary capillaries to get oxygenated
- 5. Pulmonary artery
- 4. Pulmonary valve (SL valve)
- 3. Right ventricle
- 2. Tricuspid valve (AV valve)
- 1. Starting as deoxygenated blood that arrives in right atrium
- Pulse pressure = systolic P - diastolic P
- MAP = diastolic P + 1/3(systolic P - diastolic P)
- Cardiac output - amount of blood moved per unit of time
- CO = HR x SV
- Ventricles are driving force for blood flow
Blood vessels
- capillaries - blood and nutrient exchanges occur here
- Velocity of flow is slow because their total cross sectional area is large
- Nutrient exchange and metabolic end products diffuse across capillary wall
- Blood delivers oxygen and glucose to muscle cells
- Muscle cells then produce carbon dioxide and gives to capillary tube which collects and carries wastes away
- Starts at arteriole, passes through system capillary, and ends at venule
- Blood delivers oxygen and glucose to muscle cells
- Distribution of ECF between blood and interstitial compartments is in state of dynamic equilibrium
- Tube is made up of endothelial cells that lines it and red blood cell (erythrocyte) inside tube along with plasma
- Overall fluid movement in capillaries is determined by net filtration pressure and forces opposing it (starling forces)
- Absence of vascular smooth muscle and elastic tissue reinforcement in capillaries, facilitates exchange
- Capillary hydrostatic pressure = pressure coming from plasma; pushes out
- Interstitial fluid hydrostatic pressure = usually negligible
- Osmotic force due to plasma protein concentration = pushes in; bring water into tube
- Osmotic force due to interstitial fluid protein concentration = pushes in; bring water out of tube and into interstitial tube
- Vein - thin wall but huge lumen (center)
- Have less smooth muscle and are more elastic than arteries
- Contain valves that regulate direction of blood flow
- Open when muscles contract, allowing blood to return to heart
- Close when muscles relax, and blood can't flow backwards
- Because they can stretch and expand, they're called capacitance vessels and blood reservoirs
- Uses pumps because venous pressure itself is not strong enough to push blood back to heart
- Respiratory pump - pressure changes in the central cavity due to the pressure changes due to breathing; this helps to propel blood back to the heart.
- Muscular pump - when muscles contract they squeeze the veins, which results in blood moving forward and being prevented from backflow by veins, moving blood into heart
- Smooth muscle of veins is under SNS control and contract when stimulated
- This increases venous pressure and venous return
- Artery - thick wall but small lumen
- Dicrotic notch and arteries as pressure reservoirs
- Ventricular contraction = contraction of ventricles pushes blood into elastic arteries, causing them to stretch
- Ventricular relaxation = elastic recoil in arteries maintains driving pressure during ventricular diastole
- Dicrotic notch - elastic recoil of aorta
- Dicrotic notch and arteries as pressure reservoirs
- Arteriole - regulates blood pressure
- Arterial pressure is product of cardiac output and peripheral resistance MAP = CO x PR
- most important vessels for regulation of peripheral resistance and thus MAP
- Baroreceptors monitor arterial pressure to ensure adequate perfusion of the brain and heart
- Blood pressure control includes rapid responses from cardio system and slower responses by kidneys
- Baroreceptors sense changes in blood pressure
- Most important of these are localized in aorta and carotic artery
- Baroreceptor neurons project to the medullary center that regulates/monitors blood pressure
- Neurons in that area are constantly active and their activity and their activity is a measure of blood pressure
- This area will then project to the ANS
- Neurons in that area are constantly active and their activity and their activity is a measure of blood pressure
- Baroreceptors sense changes in blood pressure
- Systemic pressures
- - Pressure waves created by ventricular contraction travel into the blood vessels
- - Pressure in arterial side of circulation cycles but pressure waves diminish in amplitude with distance and disappear at capillaries
- capillaries - blood and nutrient exchanges occur here
Cardiac muscle
- Desmosome - prevent cells from tearing apart during contraction
- gap junction - allows for flow of ions between myocytes and autorhythmic cells
- Intercalated disks - border between desmosomes and gap junctions
- 99% of cardiac cells are force making cells (myocytes), which contain striated muscle but can't generate electricity
- Excitation coupling in contractile heart cells
- 1. 1. AP sweeps across cardiac muscle cell membrane
- 2. AP activates DHPRs (L-type calcium channels or LTCCs) - Some calcium from ECF enters cell - Calcium spark
- 3. Intracellular calcium activates RyR in SR membrane - More calcium comes into cytosol from ECF - Calcium induced calcium release
- 4. Calcium signal causes power strokes and contractions identical to skeletal muscle - Calcium binds to troponin - Tropomyosin moves so myosin heads can bind to actin, etc.
- 5. Relaxation when calcium pumped back into SR by SERCA and/or cleared into ECF by sodium calcium exchanger
- 4. Calcium signal causes power strokes and contractions identical to skeletal muscle - Calcium binds to troponin - Tropomyosin moves so myosin heads can bind to actin, etc.
- 3. Intracellular calcium activates RyR in SR membrane - More calcium comes into cytosol from ECF - Calcium induced calcium release
- 2. AP activates DHPRs (L-type calcium channels or LTCCs) - Some calcium from ECF enters cell - Calcium spark
- 1. 1. AP sweeps across cardiac muscle cell membrane
- Action potentials of contractile cardiac cells
- Triggered by entry of ions through gap junctions
- 1. Brings muscle fiber to threshold so VG sodium channels open (same as neuron)
- 2. Then VG sodium channels inactivate, and a new VG potassium channel opens briefly
- 3. L-type calcium open, calcium comes in and cause plateau
- 4. Transient potassium channels inactivate
- 5. L-type calcium channels inactivate, new VG potassium channels open, potassium leaves
- 4. Transient potassium channels inactivate
- 3. L-type calcium open, calcium comes in and cause plateau
- 2. Then VG sodium channels inactivate, and a new VG potassium channel opens briefly
- 1. Brings muscle fiber to threshold so VG sodium channels open (same as neuron)
- Triggered by entry of ions through gap junctions
- Excitation coupling in contractile heart cells
- 1% of cells are conducting system, and have no organized sarcomeres
- Pacemaker action potentials
- 1. Calcium enters, causing rapid depolarization
- 2. Small brief calcium plateau; calcium continues to enter but potassium begins to leave
- 3. VG potassium channels activate; potassium leaves and we have rapid repolarization
- 4. Slow spontaneous depolarization brings membrane to threshold on its own
- 3. VG potassium channels activate; potassium leaves and we have rapid repolarization
- 2. Small brief calcium plateau; calcium continues to enter but potassium begins to leave
- No resting potential
- 1. Calcium enters, causing rapid depolarization
- Pacemaker action potentials
- No summation in heart muscles like in skeletal muscles, so long refractory period lasts almost as long as muscle twitch and prevents tetanus
Autonomous nervous system
- Controls contraction and secretion in internal organs
- Divided into:
- - Sympathetic system = fight or flight
- - Parasympathetic system = relaxation/eating
- Enteric system = regulation of the digestive system
- Parasympathetic pathways uses acetylcholine to slow down heartrate
- Sympathetic pathways use acetylcholine and norepinephrine to increase heartrate
- Actions of SNS and PNS are antagonistic (opposing forces)
Hemorrhage
- - Causes blood volume decrease
- - Venous return then decreases -
- EDV decreases
- - Stroke volume decreases
- - Cardiac output decreases
- - MAP decreases lower than normal
- - Baroreceptor activity decreases lower than normal
- - Cardio control center
- - PNS goes down
- - SNS goes up
- - Vasoconstriction goes to arterioles and veins -
- In the veins, venous pressure goes up -
- This brings PR up
- - Heart rate goes up
- - Contractility goes up
- SV goes up
- CO goes up
- SV goes up
- - Contractility goes up
- - Heart rate goes up
- This brings PR up
- In the veins, venous pressure goes up -
- - Vasoconstriction goes to arterioles and veins -
- - SNS goes up
- - PNS goes down
- - Cardio control center
- - Baroreceptor activity decreases lower than normal
- - MAP decreases lower than normal
- - Cardiac output decreases
- - Stroke volume decreases
- EDV decreases
- - Venous return then decreases -
- - Causes blood volume decrease
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- Mind Map on Cardiovascular System, created by Olivia Hart on 17/02/2019.
- Created by
- Olivia Hart
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