functions of the cardiovascular system
transport: supplies nutrients (food, oxygen, etc) to the body and removes waste (CO2) from body tissues
regulation and homeostasis: hormonal highway and plays important role in temperature regulation
protection: vessels protect against excessive blood loss (clotting); white blood cells serve immune functions
myocardial cells
striated heart muscle cells that contract in a sliding filament mechanism
use actin-myosin filaments in sarcomeres -connected by intercalated discs/gap junctions, therefore cells are electrically connected by flow of charged atoms (ions)
intercalated discs
allow cells to be continuously stimulated
cells are all tightly connected, therefore ions can flow between cells causing depolarization --> muscle cells to contract around the same time
the load is always the same (same amount of blood in your ventricles each time)
myocardium
mass of myocardial cells
functions as a single functional unit: myocardium contracts to its FULL EXTENT each time
when one cell gets a signal to contract, it spreads to all cells through gap junctions
skeletal muscle stimulation vs myocardium
in skeletal we would usually have one neuron stimulate few muscle cells in its motor unit (wouldn't stimulate entire muscle)
the entire heart muscle is stimulated bc all connected to each other through intercalated discs and gap junctions
gap junctions
pores that allow for direct ion flow; cell to cell communication
fluid-filled channels through plasma membrane of adjacent cells that permit conduction of impulses from one cell to the next; connections btwn cytoplasm
dont have to wait for NT- can send action potential straight to adjacent cell via ions
ALLOW HEART MUSCLE CELLS TO CONTRACT AS A UNIT
heart basic structure
arteries that carry blood AWAY from the heart
veins that carry blood TO the heart
2 atria that receive venous blood (blood enters the heart)
2 ventricles that eject blood into arteries (blood leaves the heart); right ventricle pumps deoxygenated blood through the pulmonary artery--> lungs and the left ventricle pumps oxygenated blood through the aorta--> rest of the body
pulmonary circulation
circulation of blood between heart and lungs
deoxygenated blood pumps TO LUNGS via pulmonary ARTERIES
oxygenated blood RETURNS TO HEART via pulmonary VEINS
systemic circulation
circulation between the heart and body tissues
oxygenated blood pumps TO BODY via AORTA
deoxygenated blood RETURNS TO HEART via superior and inferior VENA CAVAE
two atria-ventricular (AV) valves
one-way valves between atria and ventricles
tricuspid valve (between right atria and right ventricle) and mitral/bicuspid valve (between left atria and left ventricle)
make "LUB" sound when close (both close at the same time)
two semi-lunar (SL) valves
one-way valves at the base of major arteries pulmonary valve (between right ventricle and pulmonary artery) and aortic valve (between left ventricle and aorta)
make "DUB" sound when closing
function of valves
allow blood to flow in one direction; prevent back flow and mixing
myocardial septum
separates the left and right ventricles
prevents mixing of oxygenated and deoxygenated blood
what could happen if someone has a hole in their heart?
blood can mix, therefore deoxygenated blood can be transported out of the heart with oxygenated blood to body tissues instead of to the lungs
tissues may not get enough oxygen and must wait until deoxygenated blood circulates all the way back to the heart
flow of blood
deoxygenated blood from body tissues enters the right atrium via the superior and inferior vena cavae
blood flows through the tricuspid (AV) valve into the right ventricle
blood is pumped out of the pulmonary (SL) valve and to the lungs via the pulmonary arteries
blood is oxygenated in the lungs and returns to the heart in the left atria via pulmonary veins
flows through mitral/bicuspid (AV) valve and into the left ventricle
blood is pumped through the aortic (SL) valve out the aorta to body tissues
closing of AV valves
get pulled closed by papillary muscles
get depolarization signal from ventricles and contract--> pulls AV valves shut
make a "LUB" sound when close
systole: when ventricles contract (blood is about to be pushed out of ventricles through contraction so AV valves pulled to shut and SL valves are forced open by pressure)
closing of SL valves
snap shut when "cups" fill with blood
make "DUB" sound when closing
diastole: when ventricles relax
SL snap shut to prevent blood from leaking back into ventricles ( AV valves will be open again to allow blood to fill the ventricles bc no longer contracting)
blood pressure
systolic/diastolic
blood pressure during VENTRICLE CONTRACTION over blood pressure when VENTRICLE RELAXED or dilating
where is blood pressure highest and why?
left ventricle
must contract to pump blood far throughout the body
systole
ventricle contraction (ventricles contract at the same time)
AV valves shut and SL valves forced open
short time; takes less time to contract and pump blood out than to fill
diastole
relaxation and filling of ventricles
SL valves shut an AV valves open
longer time; takes longer for ventricles to fill
contraction of the atria occurs in the last 0.1 second of ventricular diastole (little extra push/squeeze for ventricle to contract
relaxation of the atria occurs during ventricular diastole
what drives closing of valves
changes in pressure between heart chambers
stages of the cardiac cycle
start in systole
isovolumic contraction
ejection
isovolumic relaxation
rapid filling
atrial contraction
isovolumic contraction
SYSTOLE
contract, but volume stays the same
ventricles begin to contract, causing intraventricular pressure to RISE
AV valves snap SHUT(LUB- and ventricular contraction) --> first sound heard
ventricles are neither filling with blood nor ejecting blood (SL valves not open yet)
both valves are shut, which is causing the pressure to rise
ejection
ventricular pressure is GREATER than aortic pressure, SL valves open and blood is ejected from the ventricles
pressure in the left ventricle and aorta rises to 120 mmHg (being pumped straight into aorta, therefore aortic pressure also rises)
stroke volume: amount of blood ejected by ventricle contraction (about 2/3 of total ventricular volume)
isovolumic relaxation
shift to diastole
ventricular pressure decreases (because relaxing) to below that of arteries, this "back flow" causes SL valves to snap SHUT (DUB- and ventricular relaxation) --> second heart sound; blood starting to fill "cups" of SL valve (from back pressure of ventricle relaxing and expanding)--> SL valves to shut)
pressure in aorta decreases slightly, pressure in left ventricle falls to 0mmHg
both AV and SL valves are closed until...
rapid filling
ventricular pressure falls below pressure of the atria, causing AV valves to open --> rapid filling of the ventricles with blood from the atria
atrial contraction
delivers the final amount of blood into the ventricles immediately before the next phase of isovolumic contraction of the ventricles
why is the myocardium thicker over the left ventricle?
the left ventricle needs to be able to produce a greater contraction to transmit blood farther
summary of pressure changes during the cardiac cycle
ventricles begin contraction, pressure rises, and AV valves close (LUB); isovolumic contraction
pressure builds, SL valves open, and blood is ejected into arteries
pressure in ventricles falls; SL valves close (DUB); isovolumic relaxation
slight inflection in pressure during isovolumic relaxation
pressure in ventricles falls below that of atria and AV valves open --> blood fills ventricles
atria give small squeeze/contraction, sending last of blood to ventricles
automaticity
heart is able to beat on its own; depolarize muscle without need of the nervous system
sinoatrial (SA) node
"pacemaker" of the heart
located in the right atrium
comprised of non-contractile cells (patch of cells) that spontaneously depolarize --> "pacemaker potential" NOT action potential
repolarize and depolarize constantly
atrioventricular (AV) node and purkinje fibers
AV node receives depolarization signal from SA node
act as secondary "pacemakers"- normally suppressed by action potentials from SA node
AV node can depolarize if it doesnt receive a signal from the SA node, however, it is usually slower and less effective
depolarization in purkinje fibers --> ventricle contraction
conduction system of the heart
pacemaker potential originates in the SA node located in the right atria- signal spreads throughout myocardial cells of atrium; electrical depolarization can go through septum--> both atria get depolarization signal--> provide little extra squeeze to push blood into the ventricles
fibrous tissue separates the chambers therefore the potential cant spread directly to the ventricle so the signal is passed through AV node
pacemaker potential continues through bundle of His, down bundle branches until it reaches purkinje fibers
pacemaker potential spreads medial to lateral, causing both ventricles to contract simultaneously
why is there a slight delay of ventricular contraction?
the pacemaker potential/signal has to travel all the way down the fibers
function of an electrocardiogram (ECG/EKG)
-detect changes in voltage current from heart through the skin
change in electrical charge is conducted through the body, which is why can measure from wrist and ankle
measurement for depolarization of heart tissue
P wave
depolarization (and small contraction) across the atria
initiated by the SA node
period before QRS wave
with atrial depolarization complete (potential is back to baseline), the impulse is delayed at the AV node, therefore the ventricles have not received the signal yet
QRS wave
ventricular depolarization Q: ventricle starts to depolarize R: reaches a point where half tissue is depolarized; atria repolarize during this time S: ventricle fully depolarizes (measuring the potential, therefore if the whole tissue is depolarized, its potential is zero)
T wave
repolarization of the ventricles (pumping Ca out of the cytoplasm); begins at apex
back to resting to be able to depolarize again
correlation of ECG with heart sounds
QRS wave is the depolarization of ventricles- stimulates their contraction: rise in intraventricular pressure causes AV valves to close
LUB occurs after the QRS wave as the AV valves close
DUB occurs at the beginning of the T wave as the SL valves close
why do the mechanical changes not happen until after electrical stimulation?
need depolarization to happen before can have muscle contract
have to have ion channels open, voltage changes, release of calcium, etc. --> all takes time, therefore there is a delay between electrical and mechanical
ECG of nonfunctional SA node
absence of P wave
"junctional rhythm"
Av node acting as primary pacemaker
ECG when AV node fails to conduct some impulses
more P waves than QRS waves; missing QRS waves
"second degree heart block"
ECG of ventricular fibrilation
waves all over; no pattern
nervous system control of the heart
can modify heart rate; brain isnt telling your heart to beat but is modifying it based on sensory inputs
autonomic innervation of the SA node= major means of regulation: sympathetic nervous system stimulate heart to beat faster (innervate at SA node, AV node, atria, and ventricles); vagus nerve/parasympathetic nervous system decrease heart rate (innervate only at SA node and AV node)
effects of autonomic nerve activity of the heart
sympathetic nerve effects (fight or flight):
at SA node, increased rate of diastolic depolarization (increased cardiac rate)
at AV node, increased conduction rate
at atrial muscle, increased strength of contraction
at ventricular muscle, increase strength of contraction
parasympathetic nerve effects (rest and digest)
at SA node, decreased rate of diastolic depolarization (decreased cardiac rate)
at AV node, decreased conduction rate
at atrial muscle, no significant effect
at ventricular muscle, no significant effect
arteries
transport blood away from the heart
thick muscle layer
blood being ejected from heart is under high pressure
elastic fibers expand when blood pressure rises and recoils when blood pressure falls
artery--> arteriole--> cappilary
veins
carry blood to the heart
thin muscle layer (can expand very large and store blood-capacitance); larger than artery
contain one way valves to ensure blood returns to heart
blood flowing through at much lower pressure
no elasticity needed bc under low pressure
vein--> venule--> capillary
capillaries
smallest blood vessel; usually one cell layer thick
allow gas exchange between blood and interstitial fluid
endothelium
thin layer of epithelium that lines inside of blood vessels; or only layer for capillaries (one layer makes easy for gas exchange to occur)
venous valves
veins contain valves (similar to SL valves) that prevent the flow of blood away from the heart
veins have large diameter, therefore very low pressure, and need help from skeletal muscles to pump blood back to heart - "skeletal muscle pump" or "venous return"
when not using skeletal muscles much, blood accumulates in the veins--> causing them to bulge
capillary beds
site of exchange of fluid, nutrients, and wastes
blood flow in capillaries is slow; allows time for exchange of substances between the blood and surrounding tissues
all over the body
capillary walls are composed of just one cell layer; simple squamous epithelium (endothelium); allows more rapid exchange of materials to/from tissues
lymphatic system
comprised of lymph, lymphatic vessels, and lymphoid organs
follows circulatory system; lymph vessels are located around blood vessels
important in transport of immune cells and regulation of fluid balance
takes up excess tissue fluid and returns it to the blood
cardiac output
volume of blood pumped per minute by each ventricle
cardiac output= cardiac rate x stroke volume
sympathetic nerves increase cardiac rate--> increase cardiac output
parasympathetic nerves try to depress/slow down cardiac rate
end diastolic volume (EDV): volume of blood in ventricle right before it contracts (relaxed; should be full); effects stroke volume
frank starling: extra lil volume of blood from small atrial squeeze--> ventricle gets bigger and causes overlap to decrease
stretch: when the ventricle is full, the myocardium stretches. the greater the stretch, the more forceful the contraction (greater stretch--> increase contraction strength--> increase stroke volume--> increase cardiac output)
total peripheral resistance and mean arterial pressure affect stroke volume
normal cardiac output of person at rest
resting heart rate= 75 beats/min stroke volume (volume being pushed out) = 70ml/beat
cardiac output during exercise
deeper breathing: expand chest cavity, which pulls on lungs and heart, pulling more blood into the heart--> improved venous return
skeletal muscle activity --> skeletal muscle pump increases venous return
improved venous return increases stroke volume
increase in sympathoadrenal system (pretty much fight or flight) increases venous return, cardiac rate, and stroke volume --> increased cardiac output
increase cardiac output to increase blood flow to skeletal muscles
sympathetic vasoconstriction in viscera: vessels constrict/get smaller so less blood is sent to other organs and more is sent to skeletal muscles
metabolic vasodilation in muscles: blood vessels dilate, allowing blood to flow more efficiently and with less resistance: increase stroke volume
pressure and blood flow
blood flows from a region of higher pressure (arteries) to a region of lower pressure (veins); pressure gradient pushing blood forward
the rate of blood flow is proportional to the difference in pressure
pressure differences in systemic circulation
left ventricle: high pressure
large arteries (aorta): still pretty high pressure
small arteries and arterioles: "resistance vessels"- still seeing higher pressures
capillaries: "exchange vessels"- still some pressure bc need to be abel to force stuff out
venules and large veins: "capacitance vessels"- very low or no pressure; store lots of blood
physical laws of describing blood flow
the rate of blood is inversely proportional to the frictional resistance to blood flow within the vessels: blood flow= (pressure difference/resistance); higher/greater the RESISTANCE, the LOWER the blood flow and the higher/greater the PRESSURE, the GREATER the flow
resistance = (length of vessel x viscosity)/radius of the blood vessel ^4; larger radius will decrease resistance and increase flow
double the radius: resistance is 1/16R and blood flow is 16F
half the radius: resistance is 16R and blood flow is 1/16 F
venous return
veins have high compliance/capacity: stretch more at a given pressure than arteries bc have thinner walls
capacitance vessels : 2/3 of total blood volume is in veins
hold more blood than arteries, but maintain lower pressure
body water distribution
osmotic forces control the mvmt of water between interstitial spaces and the capillaries, affecting blood volume
urine formation and water intake play role in blood volume
fluid is always circulating in a state of dynamic equilibrium
tissue capillary fluid exchange
net filtration pressure= the hydrostatic pressure of the blood in the capillaries minus the hydrostatic pressure of the fluid outside the capillaries
arterial end: higher pressure, therefore fluid is forced out (filtration)
venous end: fluid in tissue at higher pressure and inside capillary is lower pressure, therefore fluid moves in (reabsorption)
edema
excessive accumulation of interstitial fluids
water going out of capillaries/circulatory system and not going back in, therefore filling interstitial space
may be a result of: high arterial blood pressure, venous obstruction, leakage of plasma proteins into interstitial space, decreased plasma protein concentration