Cardiovascular Physiology Flashcards
Hemodynamics
study of blood flow
not the absolute pressure at any point but the different in pressure between two relevant points
F = delta P / R
F = flow
delta P = pressure difference between two fixed points
R = resistance to flow
Blood flows from ____ pressure to ____ pressure
high to low
Hydrostatic pressure
the pressure that the volume of blood within the circulatory system exerts on the walls of the blood vessels
Factors that determine blood flow
viscosity - friction between molecules of the blood (hematocrit - number of RBC in blood)
blood vessel length - long –> more friction
blood vessel diameter - thin –> more friction
R = 8 L n / pi r to the 4
R = resistance to blow flow
L = vessel length
n = blood viscosity
r = inside radius of vessel raised to the 4 (greatest effect)
Functions of the cardiovascular system
- deliver oxygen and nutrients
- remove waste product
- fast chemical signaling to cells by circulating hormones or neurotransmitters
- thermoregulation
- mediation of inflammatory and host defense responses against invading microorganisms
Components of the cardiovascular system
- heart
- blood vessels
- blood
Blood vessels
arteries - carry blood away from heart
arterioles - small branching vessels with high resistance
capillaries - smallest vessel, exchange between cells and blood
venules
veins - carry blood back to heart
Atria
thin walled chambers
low pressure chambers
receive blood returning back to heart
Ventricles
thick walled chambers
responsible for forward propulsion of blood when they contract
left has increased thickness to the right (higher pressure for large lengths it travels)
Apex
lowest superficial surface of heart
Septa
Interatrial septum - separates left and right atria
Interventricular septum - separates left and right ventricle
allows pumps to function as dual pump
Left side of heart pumps ___ blood to ____ circuit
highly oxygenated; systemic
Right side of heart pumps _____ blood to _____ circuit
poorly oxygenated; systemic
Pulmonary circuit
blood enters the lungs poorly oxygenated
oxygen diffuses from lung tissues to blood
blood leaves the lungs highly oxygenated
System circuit
blood enters the body tissues highly oxygenated
oxygen diffuses from the blood to interstitial fluid to tissue cells
blood leaves the body tissues poorly oxygenated
Arteries
carry blood away from heart
most carry highly oxygenated blood except pulmonary trunk and pulmonary arteries
Veins
carry blood to the heart
most carry poorly oxygenated blood except pulmonary venules and pulmonary veins
Functions of the pericadrium
- stabilizes the heart in the thoracic cavity
- provides protection to the heart by physically surrounding it
- reduces friction as the heart beats by secreting the pericardial fluid
- limits overfilling of the heart chambers
3 layers of the pericadrial
fibrous pericardium
parietal pericardium
visceral pericardium
Fibrous pericadrium
out layer
provides protection and stability by attaching to structures in the chest
holds heart in place
limited distensibility which prevents sudden overfilling
Parietal pericardium
part of the serous pericardium
lies underneath the fibrous pericardium and is attached to it
secretes fluid
Visceral pericardium
part of the serous pericardium
innermost layer and is also called epicardium when contact with heart muscle
secretes fluid
Pericardial cavity
separates the parietal and visceral pericardium
holds secreted fluid which decreases friction between pericardial membrane as heart beats
Pericarditis
inflammation of the pericardium caused by virus, bacteria, fungi, trauma, malignancy
leads to fluid accumulation in pericardial cavity
Cardiac tamponade
compression of heart chambers due to excessive accumulation of pericardial fluid
heart’s movement is limited and heart chambers cannot fill with adequate blood
3 layers of the heart wall
epicardium, myocardium, endocardium
Epicardium
also called visceral pericardium
layer immediately outside the heart muscle and covers the surface of the heart
connective tissue attaches to myocardium
protective layer of the heart
Myocardium
muscle wall of heart
underneath the epicardium
contains muscle cells or myocytes that contract and relax as heart beats
contains nerves and blood vessels
Endocardium
innermost layer of the heart wall
lines heart cavities and heart valves
thin layer of endothelium (smooth surface for blood to flow over)
Myocytes
cardiac muscle cells
branched or Y shaped cells
joined longitudinally or end to end to allow for greater connection
striated appearance (actin and myosin)
rich in mitochondria
intercalated disk: 2 different myocytes are closely opposed and very intertwined at attachment
Desmosomes
adhering junctions that hold cells together
mechanically couple one heart cell to another
cadherins, plaques, intermediate filaments
Gap junctions
communication junctions - ion channels
electrically couple one heart cell to another
spread of action potential
connexons
Atrioventricular valves
found between the atria and ventricular on left and right side of heart
left AV - bicuspid valve
right AV - tricuspid valve
Semilunar valves
found between the ventricles and the arteries
tricuspid valve
left - aortic valve
right - pulmonary valve
do not have chordae tendineae or papillary muscles
What are valves made of?
fibrous collagen tissue covered by endothelium
What are valve rings made of?
cartilage
Function of valves
unidirectional flow of blood through the heart
open and close passively to differenced in pressure
do not require energy or muscles
Chordae tendineae
edges of AV valve leaflets
tough thin fibrous cords
attach to papillary muscles
Papillary muscles
cone shaped muscles that protrude from inner surface of ventricular walls
when they contract, they pull chordae tendineae taut
Cardiac skeleton
dense connective tissues
includes the heart valve rings and tissue between them
physically separates atria from ventricles
electrically inactive
Coronary circulation
supplies blood to and provides drainage from the tissue cells of the heart
Coronary arteries - arteries supplying the heart
- aorta sinus
Cardiac veins - collect poorly oxygenated blood and empty into coronary sinus
Coronary sinus
collection of veins joined together to form large vessel that collects blood from the myocardium of the heart and empties into the right atrim
Systole
the time during the left and right ventricles contract and eject blood into respective artery
blow flow almost ceases
Disatole
the time when the ventricles are not contracting; relaxed
blow flow peaks
Coronary artery disease / atherosclerosis
condition where arteries harden and narrow because of excessive accumulation of plaque in vessel wall
plaque is made of up fat, cholesterol and calcium
Angina
when plaque restricts blood flow to the heart muscle and results in chest pain
Myocardial infarction
heart attack
when plaque completely blocks arterial blood flow, heart muscle dies due to loss of blood supply
Cardiac syncytium
mechanically, chemically, electrically connect myocytes to one another
entire heart resembles single enormous muscle cell
all or nothing excitation
2 syncytia: left and right atria, left and right ventricles
Autorhythmicity/automaticity
the heart contracts or beats rhythmically as a result of action potentials it generates itself
action potentials are generated without nervous or hormonal stimulation
Contractile cells
- perform the mechanical work of pumping and contracting the propel blood forward
- 99% of myocytes
- do not initiate action potentials but contract when stimulated by adjacent cell
Conducting cells
- autorhythmic cells which initiate and conduct action potentials
- without nervous or hormonal stimulus
- 1% of myocytes
Conduction system
SAN generates action potential –> internodal pathways –> contractile cells of left and right atria leading to contraction at same time –> stimulus passed to AVN –> passed to Bundle of His –> leads to contraction of left and right ventricles at the same time
Sinoatrial (SA) node
- generate action potentials the fastest; 60-100/min
- stimulus is passed to other regions
- cardiac pacemaker: initiates action potentials that set the heart rate
Atrioventricular (AV) node
- receives stimulus by SAN through internodal pathways
- AV nodal delay: 100 msec to pass through AVN and Bundle of His
- ensures atria depolarize and contract before ventricles do
Bundle of His
- only electrical connection between atria and ventricle
- transmits signal from AVN
Left and right bundle branches
travel along to intraventricular septum and apex
Purkinje fibers
- large number, diffuse distribution, fast conduction velocity
Wolff-Parkinson-White syndrome
- born with abnormal extra connection called an accessory pathway
- connects directly between atria and ventricle
- allows electrical signals to bypass the AVN and move to ventricles faster than usual
- leads to abnormally fast heart beat (tachycardia)
Fast action potentials
- found in contractile myocytes in the atrial myocardium, ventricular myocardium, bundle of His, bundle branches, and Purkinje fibers
- rapid rate of depolarization where threshold potential is reached quickly
Slow action potentials
- found in conducting myocytes in the sinoatrial node and atrioventricular node
- slow rate of depolarization where threshold potential is reached slowly
- Ca2+ currents are responsible for depolarization not Na+
Ion permeability
K+ in > K+ out
Ca2+ out > Ca2+ in
Na+ out > Na+ in
Slow action potential ion channels
- progressive reduction in K+ permeability
- F-type channels - Na+ moves into cell
- T-type channels - Ca2+ briefly enters cell
- L-type channels - Ca2+ enters cell slowly and for long period
- opening of voltage-gated K + channels, K+ leaves cell
Fast action potential ion channels
- stable resting phase: leak of K+ through K+ channels
- depolarization: opening of fast Na+ channels into cell
- notch: due to transient opening of K+ channels
- plateau: Ca2+ entering through L-type channels and slow opening of K+ channels will repolarize cell
- repolarization: opening of K+ channels and closing of Ca2+ channels
ECG/EKG
- a recording of the electrical activity of the heart
- measure of the currents generated in the ECF by the changes occurring in the cardiac cells
- the electrical signal becomes weaker as it travels through the body tissues to skin surface (100 mV –> 1 mV)
- 12 placements for electrodes to get different angles of heart activityP
P wave
- first wave on ECG
- represents depolarization of the atria
- upward deflection in the trace
QRS wave
- second complex on ECG
- represents depolarization of the ventricles
- atria repolarizes but is too small to be recorded on skin surface
T wave
- third wave on ECG
- represents depolarization of the ventricles
- upward deflection in the trace
Partial AV node block
- damaged AV node permits only every other atrial impulse to be transmitted to the ventricles
- every second P wave is not followed by a QRS complex or T wave
Complete AV node block
- electrical depolarizations of the atria are not transmitted to the ventricles
- no synchrony between atrial and ventricular electrical activities
Sarcoplasmic reticulum
special type of smoother ER which stores and pumps Ca2+
Myofibrils
- made up of sarcomeres
- contains actin (thin filaments) and myosin (thick filaments)
T-tubules
invaginations of the sarcolemma, surround myofibrils
transmit action potentials propagating along surface membrane to interior of muscle fiber
Excitation-contraction coupling
- plateau phase - ECF Ca2+ enter cytoplasm of the cardiac muscle cell through L-type Ca2+ channels
- Ca2+ binds to ryanodine receptors on the sarcoplasmic reticulum
- ryanodine allows release of Ca2+ from SR into cytoplasm
- no physical coupling between L-type Ca2+ channel and the ryanodine receptor
Steps involved in ECC contraction
- excitation spreads along sarcolemma by gap junctions and spreads down interior by T-tubules
- during plateau, permeability of Ca2+ increases as L-type calcium channels open
- Ca2+ binds to ryanodine receptors that contains at intrinsic channels that opens to allow Ca2+ to exit the SR into cytoplasm
- cytosolic Ca2+ binds to troponin inducing a conformational change in the complex, binding sites on actin are available, cross-bridge on myosin head
Steps involved in ECC relaxation
- L-type channels close to reduce Ca2+
- SR will no longer be stimulated to release Ca2+ into cytoplasm
- SR contains Ca2+ ATPases to pumps Ca2+ back into SR
- Ca2+ also removed by Na+/Ca2+ exchanger found in the sarcolemma
- reduced binding of Ca2+ to troponin will block sites of interaction allowing for relaxtion
Refractory period
- period during and after an action potential in which membrane cannot be re-excited
- due to long plateau phase, the refractory period lasts almost as long as the contraction
- 250 milliseconds
- prevents tetanus
Cardiac cycle
one heartbeat
one ventricular systole and one ventricular diastole
heart spends more time in diastole
Isovolumetric ventricular contraction
- ventricles contract
- all valves are closed
- blood volume remains constant
- pressure rises
- muscle develops tension
Ventricular ejection phase
- pressure exceeds artery pressure
- opens semilunar valves, AV valve is closed
- ventricular muscle shortens
- eject volume of blood into arteries
Stroke volume
- volume of blood ejected from each ventricle during systole
- left and right eject same volume of blood, but left ventricle has more pressure
- when contracting, ventricles do not eject entire volume
Isovolumetric ventricular relaxation
- all valves are closed
- volume remains constant
- pressure drops
Ventricular filling phase
- AV valve opens
- blood flows from relaxed atria to ventricles passively
- atria blood pressure if greater and opens valve through forward passive gradient
Passive ventricular filling
receives 70% of blood volume
Atrial kick/contraction
completes ventricular filling
End-diastolic volume / EDV
volume of blood in each ventricle at the end of ventricular diastole (mL)
End-systolic volume / ESV
volume of blood in each ventricle at the end of ventricular systole (mL)
Stroke volume equation
SV = EDV - ESV
average adult at rest is 70-75 mL
Pressure-volume curve
Wigger’s diagram
KNOW IT
MEMORIZE IT
Heart sounds
first sound: lub, closure of AV valves at the beginning of isovolumetric ventricular contraction, onset of ventricular systole
second sound: dub, closure of semilunar valves, onset of ventricular diastole
Laminar flow
- makes no sound
- smooth concentric layers of blood moving parallel down length of blood vessel
- highest velocity is at center
- lowest velocity is along the vessel wall
Stenotic valve
- heart murmur
- makes a sound
- valve where leaflets do not open completely
- valve leaflets become stiffer due to calcium or scaring
Insufficient valve
- heart murmur
- makes a sound
- valve where leaflets do not close completely
- widening of aorta or scaring
- blood flows backwards through leaky valve
Sympathetic innervation
- thoracic spinal nerves
- atria, ventricle, SA node, AV node
- norepinephrine
Parasympathetic innvervation
- vagus nerve
- atria, SA node, AV, node (no ventricle)
- acetylcholine
Parasympathetic stimulation
- decrease heart rate
- decrease rate of depolarization
- decrease conduction through AVN
- increase AV nodal delay
- decrease contractility
- no effect on ventricle
Sympathetic stimulation
- increase heart rate
- increase rate of depolarization
- increase conduction through AVN
- decrease AV nodal delay
- increase contractility
- effect on ventricle
Cardiac output
- amount of blood pumped by each ventricle in one minute
- CO = HR x SV
HR - heart rate and SV - stroke volume
Tone
sympathetic and parasympathetic systems are active at steady background level
SPS and PSPS are antagonistic for heart rate
How to increase heart rate
- increase activity of SPS
- release of epinephrine from adrenal medulla will stimulate SAN
- increases the slope of the pacemaker potential causing faster depolarization and faster rise to threshold
- F-type channels allow Na+ to enter
- T- type channels allow Ca2+ to enter
*conducting myocytes in the heart are responsible for imitating the heart rate
How to decrease heart rate
- increase activity of PSPS
- inhibit activate of SAN
- decreases the slope of the pacemaker potential causing slowing depolarization and slower rise to threshold
- decreasing F-type channels
- increasing K+ channel permeability so K+ leaves cell, more negative
*conducting myocytes in the heart are responsible for imitating the heart rate
3 factors that affect stroke volume
- end diastolic volume / preload
- contractility of the ventricular myocardium
- the afterload
Stroke volume factors: EDV/preload
- intrinsic
- ventricles will contract more forcefully when they have been stretched prior to contraction
- increased stretch is accomplished by filling ventricles with more blood
- filling ventricles with more blood is done by increasing amount of blood returning to heart through veins
- sympathetic stimulation of venous muscle will also act increase filling (extrinsic)
Frank-Starling mechanism
direct relationship between EDV and stroke volume
intrinsic - independent of neural and hormonal
Preload
the tension or load on the ventricular myocardium before it begins to contract
amount of filing of the ventricles at the end of diastole
Why does an increased EDV lead to increased SV
as ventricles become more filled with blood, the sarcomeres stretch out, putting more load on the sarcomeres, the ventricles will contract more forcefully when they have been stretched out and the SV will increase
Stroke volume factors: contractility
- increased sympathetic stimulation (no parasympathetic stimulation) will increase the strength of contraction of the ventricular myocardium, increasing SV and CO
- stroke volume is greater at any EDV
- increased contractility will lead to more complete ejection of blood increasing ejection fraction (>70%)
- heart contracts and relaxes faster, giving more time for ventricles to fill
- G protein coupled mechanism with L-type Ca2+ channels
Ejection fraction
EJ = SV / EDV
Stroke volume factors: afterload
- the tension against which the ventricle must eject its blood, arterial pressure
- the greater the afterload, the longer the period of isovolumetric contraction, the smaller stroke volume
- afterload is increased by factors that restrict blood flow through the arterial system
Endothelium
smooth single cell layer of endothelial cells that is continuous with the endocardium of the heart and forms a physical lining that blood cells do not stick to
Pulmonary vascular resistance is much _____ than the systemic resistance
lower
Arteries
- walls contain smooth muscle (allow to contract), elastic fibers (passive changes in diameter), connective tissue
- vasoconstriction –> decrease diameter of artery
- vasodilation –> increase diameter of artery
Types of arteries
Elastic - pulmonary truck and aorta, tolerate pressure changes in cardiac cycle
Muscular - arterial system vessels, distribute blood throughout body
Arterioles - smallest, resistance vessel, determines mean arterial pressure (blood pressure)
Arterioles
- walls of arterioles have circular smooth muscle that forms rings around them
- regulated blood flow to organs by regulating amount of blood supplying the organ
- have intrinsic and basal tone, nerves, hormones, local controls (self regulators)
- nitric oxide from noncholinergic neurons vasodilator
- epinephrine from adrenal medulla vasoconstrictor and vasodilator
Local control
mechanisms independent of nerves/hormones by which organs alter its own arteriolar resistance
Active hyperemia
local control which acts to increase blood flow when the metabolic activity of an organ or tissue increases
hyperemia - excess of blood in the vessels supplying an organ
SEE SLIDE FLOW CHART
local chemical changes are the result of changes in metabolic activty and act on smooth muscle to cause vasodilation or vasoconstriction
Flow autoregulation
locally mediated changes in the arteriolar resistance also occur when a tissue or organ experiences a change in its blood supply resulting from a change in blood pressure
no nerve or hormones involves
myogenic response
Myogenic response
direct response of the arteriolar smooth muscle stretch
arteriolar smooth muscle responds to stretch by contracting, this will reduce blood flow to the organ toward normal level
Reactive hyperemia
- form of flow autoregulation
- occurs at constant metabolic
- occurs due to changes in chemical concentrations
- blockage of blood flow, greatly decreases oxygen levels and increases metabolites, arterioles dilates, blood flow greatly increases once blockage removed
Capillaries
- thin walled vessels one endothelial cell thick
- supported by basement membrane
- no smooth muscle or elastic fibers
- function in rapid exchange of material between blood and ICF
- adjacent endothelial cells are joined laterally by tight junctions but leave gaps of unjoined membrane called intercellular clefts
3 types of capillaries
continuous, fenestrated, sinusoidal
Continuous capillaries
- uninterrupted/complete endothelium
- lowest permeability allowing exchange of water, small solutes, and lipid-soluble material only
- found in most tissues
Pericytes
lie external to the endothelium and help stabilize the walls of the blood vessels and regulate blood flow through capillaries
Fenestrated capillaries
- endothelial cells have numerous fenestra/pores
- allow for rapid exchange of water and larger solutes such as small peptides
- found in endocrine organs, choroid plexus, GI tract, kidneys
- lipid insoluble molecules move through intercellular clefts or fenestrae
Sinusoidal capillaries
- large diameter, flattened and irregularly shaped
- called discontinuous capillaries
- very large fenestrae and large gaps
- basement membrane is very thin or absent
- free exchange of water solutes, RBC, cell debris, plasma proteins
- found in liver, bone marrow, spleen
Microcirculation
- arterioles, metarterioles, capillaries, venules, veins
- of one arteriole becomes blocked, blood can enter the capillary bed by another
- precapillary sphincters - ring of smooth muscle which guards the entrance to capillary, no innervation
- metarterioles - small blood vessels with smooth muscle that arise from an arteriole and empty into venule through the capillary network
Capillary exchange
diffusion: nutrients, oxygen, metabolic end products cross
lipid soluble: diffuse across the plasma membrane
water soluble: move through water-filled channel (intercellular cleft, fenestrae, fused vesicle channels)
transcytosis: pick up material by pinocytosis or receptor-mediated endocytosis and discharge on other side by exocytosis
fused vesicle channel: water filled channel
Bulk flow
- movement of protein free plasma across the capillary wall
- function is not the exchange of nutrients but the distribution of the extracellular fluid volume
- driven by hydrostatic pressure and colloid osmotic pressure
Filtration
movement of protein-free plasma by bulk flow from capillary plasma to the interstitial fluid through water-filled channels
Reabsorption
movement of protein-free plasma by bulk flow from the interstitial fluid to the capillary plasma
concentration of solutes in the filtered fluid is the same as in the fluid
Hydrostatic pressure
- force of fluid against a membrane
- capillary hydrostatic pressure: pressure exerted by blood on the inside of the capillary walls and forces protein-free plasma out of capillaries into interstitial fluid
- interstitial fluid hydrostatic pressure: pressure exerted on the outside of capillary walls by interstitial fluid and forces fluid into capillaries, NEGLIGIBLE
Colloid osmotic pressure
- force due to presence of impermeable proteins
- concentration of proteins will not be equal in plasma and interstitial fluid
- proteins draw fluid towards them
- blood colloid osmotic pressure: proteins pull water into the capillaries
- interstitial fluid colloid osmotic pressure: small and insignificant movement of fluid out of capillaries
Net exchange pressure equation
capillary hydrostatic pressure + interstitial fluid colloid osmotic pressure - interstitial fluid hydrostatic pressure - capillary colloid osmotic pressure
Pc + piIF - PIF - pic
sum of outward and inward pressures
Starling forces
Arterial end of capillary
- positive number
- favours filtration of fluid from capillary into interstitial fluid
Venous end of capillary
- negative number
- favours absorption of fluid from interstitial fluid into capillary
the one Staring force that changes is the
capillary hydrostatic pressure
more filtration than absorption
Blood volume in the veins
- 60% - reservoir of blood
- large volume in liver, bone marrow, skin
- high capacitance and distensible
Venous valves
- low pressure system
- composes of two leaflets to prevent the backflow of blood into capillaries
compartmentalize the blood within the veins
Varicose veins
walls of the veins near the valves becomes weakened or stretched and blood pools in veins and vessels
3 mechanisms for venous return
- smooth muscle in veins - innervated by sympathetic neurons
- skeletal muscle pump - compresses veins
- respiratory pump - deep beathing
Relationship between venous return and Frank-Starling law
increased venous return to the heart will increase the EDV
Components of lymphatic system
lymph nodes, lymphatic vessels, lympathetic capillaries
Lymphatic capillaries
- single cell layer of endothelial cells resting on membrane basement
- large water filled channels permeable to all
- round ends
- interstitial fluid enters lymphatic capillaries through bulk flow
Lymphatic system tract
- lymphatic capillaries empty into lymph vessels (have smooth muscle to generate rhythmic contractions)
- lymph vessels contain one-way valves to ensure on directional flow into right atrium
- lymph passes through lymph nodes on the way to vessels which play a role in defense and immune response
Compliance
- ability of a vessel to distend and increase volume with increasing transmural pressure, which is the pressure inside the vessel minus the pressure outside the vessel
- the greater the compliance of a vessel, the more easily it can be stretched
Arterial blood pressure
1/3 blood volume is ejected by ventricle leaves the artery, the rest of the stroke volume remains in the arteries during systole, stretching the walls and increasing arterial pressure
when ventricular contraction ends the stretched arterial walls recoil passively and blood continues to be drives into arterioles during diastole
large arteries (aorta) act as pressure reservoirs
Arterial pressure is recorded as
systolic pressure (peak ventricular ejection) divided by diastolic pressure (just before ventricular ejection)
Pulse pressure equation
= systolic pressure - diastolic pressure
Hypertension and hypotension
hyper - chronically increased arterial blood pressure
hypo - abnormally low arterial blood pressure
Mean arterial pressure (MAP)
pressure driving blood into tissues averaged over the cardiac cycle
pulsatile as the blood leaves the heart (increases and decreases during systole and diastole)
as distance from heart increases, the pulse pressure decreases due to elastic rebound
no pressure oscillations seen in the capillaries
largest drop is due to high resistance of the arterioles
Mean arterial pressure equation/factors
MAP = cardiac output x total peripheral resistance
Total peripheral resistance
- combined resistance to flow of all the systemic blood vessels
- friction between the blood and the walls of the blood vessels
- major site of resistance = arterioles
Short-term regulation of MAP
baroreceptors reflexes modify the autonomic nerves supplying the heart and blood vessels and secretion of hormones
adjusts CO and TPR by ANS
Long-term regulation of MAP
adjusts blood volume
restores normal salt and water balance through urine output and thirst
Arterial baroreceptors
- mechanoreceptors that detect changes in MAP and pulse pressure
- carotid sinus and aortic arch
- afferent neurons travel from baroreceptors to the brainstem and provide input to the cardiovascular control center
- the rate of discharge on the carotid sinus baroreceptors is directly proportional to the MAP
Baroreceptor action potential frequency
- increase in pressure will increase the action potentials generates by baroreceptors
Medullary cardiovascular center
- located in medulla oblongata
- neurons in the center receive input from baroreceptors which determines the frequency of action potentials sent to alter the vagal stimulation (parasympathetic) to heart and sympathetic innervation to heart, arterioles, veins
