Cardiovascular system Flashcards
what are the two main functions of the cardiovascular system?
transport and exchange
-delivers supplies to cells far removed from the site of uptake or manufacture
which 5 supplies are transported through the cardiovascular system?
1) oxygen (RBC’s pick up oxygen and give it to every cell in the body (almost)
2) water and nutrients (from digestive system - ex: glucose, fatty acids, etc = energy going to all cells picked up and carried by the blood)
3) hormones (chemical signals released from parts of the body - ex: hypothalamus - transported by cardiovascular system)
4) antibodies/ platelets/ leukocytes (antibodies play a key role in immune system (same with leukocytes) - platelets are fragments of cells which have a key role in blood clotting)
5) heat (transported - ex: when fingers and toes get cold - from core body heat to skin (helps us stay warm and cool off)
which 3 ‘wastes’ are transported through the cardiovascular system from the cells for elimination elsewhere?
1) carbon dioxide (CO2) - one of the major waste products through lungs and kidneys
2) urea, creatinine, bilirubin (urea break down of amino acids combined with CO2 - our bodies also harness this to create concentrated urine)
- creatinine - important in muscles - used for immediate energy secreted by kidneys
- bilirubin - cause of jaunice (malfunctioning liver = yellow skin) - secreted with bile
3) heat (excessive exercise)
what are the 3 primary components of the cardiovascular system?
1) blood
2) heart
3) vasculature
3 primary components of the cardiovascular system: blood
- medium for bulk transport of materials
- bulk transport is not diffusion, it’s like a river or the wind - everything is transported together
- blood does move down a gradient (pressure gradient)
2 primary components of the cardiovascular system: heart
- pressure gradient generator (pump)
- highest blood pressure is in your heart as well as lowest blood pressure
- dual pump: right side pump and left side pump
- has many endocrine functions - senses local environment, releases and responds to endocrine cues
3 primary components of the cardiovascular system: vasculature
closed, dual circuit for one way flow of blood (closed because tubes are continuous (there are exceptions - ex: leaky capillaries)
a) pulmonary circuit (low pressure, low resistance)
- blood is under higher pressure than atmosphere which is why we bleed out when cut, in lungs, not a lot of resistance to blood flow - “friction” - friction of blood against blood vessel walls
- smaller amount of pressure is needed
- minimum pressure = 25 mm (25 over 80)
b) systemic circuit (high pressure, high resistance)
- maximum pressure of 120 mm (120 over 80)
- this is five times greater than pulmonary circuit
- even though it’s the same amount of blood that goes through both*****
what are the components of blood?
1) plasma
2) erythrocytes
3) leukocytes
4) platelets
complex suspension of water, solutes, and formed elements
- mostly red blood cells, floating in plasma
- formed elements are mostly cells, but can be just fragments of cells
what makes up the bulk of the blood?
plasma
main components of blood: what is in our plasma?
composed of water (90%) and a variety of dissolved:
1) proteins (ex: albumins (most common (about 60%) - carrier protein), globulins (carrier protein), fibrinogens (key role in hemostasis (blood clotting), hormones)
2) electrolytes (ex: Na+, Cl-, K+, HCO3-)
3) nutrients (ex: glucose, amino acids, lipids, vitamins)
4) gases (ex: N2 (most dominant), O2 (only about 1%), CO2)
5) metabolic waste products (ex: urea, creatinine)
what is serum?
plasma from which fibrinogen and other clotting proteins have been removed
which is the most numerous of our blood cells?
erythrocytes (RBC’s)
-over 99%
how many RBC’s do we have per ml of blood?
5 billion (approx.)
how fast do RBCs reproduce?
5 trillion blood cells, 2 to 3 million blood cells per second are made
-15 million also die in that same time frame
why are RBCs flat cells?
to increase surface area which facilitates diffusion of oxygen (indirect transport of CO2)
all blood cells lack organelles (nucleus, mitochondria, etc) therefore, cannot do oxidative phosphorylation. This categorizes them as anaerobic cells since they do not use the oxygen they carry.
true or false?
false, this is ONLY true in mammals
what are RBCs main function?
to transport O2 directly and CO2 indirectly
How long do RBCs live?
short lived, approx 120 days - rapidly produced in the bone marrow
-they are short lived because they do not fix themselves, can be engulfed by macrophages
definition of hematocrit
the percentage of blood volume that is erythrocytes (fig 16-3)
-approx. 42 % (women) and 47% (men)
(because of body size, menstruation)
kidney cells release ______ in response to low blood O2 saturation, stimulating the production of _______
erythropoietin, RBCs
______ sense blood oxygen saturation, therefore, when red blood cells are under-saturated in this area, this stimulates RBC production
kidneys
if you lose a lot of blood, you’re said to be _____ - unless this is chronic, it corrects itself
anemic
if you produce too many RBCs, you’re said to be _______-this is beneficial at rest, more blood cells to carry oxygen, but can be a problem when it is too elevated and you’re exercising too much (heart attack) - optimal levels are key
polycythemic
leukocytes (WBCs)
- play a key role in the body’s immune response
- primarily act outside of the bloodstream (exit capillaries)
- “mobile units of the body’s protective system”
what are the 5 types of WBCs?
“never let monkeys eat bananas”
1) neutrophils
2) lymphocytes
3) monocytes
4) eosinophils
5) basophils
cellular elements produced from the fragmentation of large bone marrow cells called megakaryocytes
platelets
what is the primary function of platelets?
hemostasis (blood clotting)
-binding to exposed collagen at wound site activates platelets, causing platelet aggregation and release of serotonin (and other chemical agents) in the brain, constricting blood vessels and preventing blood loss
what is the path of blood flow in the heart?
- Left atrium
- left ventricle
- aorta
- other arteries (towards heart or brain)
- everywhere else in body
- branch into arterioles, then capillary beds
- venules
- gas exchange via diffusion is microcirculation (this is where most exchange between blood and tissue occurs)
- venules drain into veins (inferior vena cava)
- superior vena cava
- right atrium (gets deoxygenated blood) - mostly, this has well over 50% of oxygen (unless you’re exercising intensely)
- even at 75% saturation - hemoglobin is a pigment - depending on its oxygenated state, it’s reflection of color differs (darker red)
- this blood leaves through pulmonary arteries
- gets picked up by hemoglobin, fully oxygenated blood (about 98-99%)
the pulmonary system starts at the ____ and ends at the ____
right ventricle, left atrium
the systemic system starts at the ____ and ends at the ____
left ventricle, right atrium
veins carry blood _____ the heart whereas arteries carry blood ____ the heart
towards, away from
arteries always carry oxygenated blood
true or false?
false
which vein/artery carries the blood which is richessed in oxygen?
pulmonary veins
what is microcirculation
the circulation of the blood in the smallest blood vessels, present within organ tissues. The microcirculation is composed of terminal arterioles, capillaries, and venules
what are the 3 layers of the heart?
1) endocardium
2) myocardium
3) epicardium
myocardium
- cardiac muscle cells joined lengthwise by intercalated disks with many gap junctions that electrically couple them
- formed by a thick layer of contractile cells (99% of total) arranged in circular (atria) and spiral patterns (ventricles)
- a network of non contractile cardiac cells (1%)
- cardiac tissue is directly supplied by O2 and nutrients via the coronary circulation (1st branches off the aorta)
endocardium
- thin inner lining of specialized epithelial tissue
- this is in direct contact with the blood
epicardium
-inner later of a serous membrane that surrounds the heart; secretes pericardial fluid (lubricant) into pericardial cavity
what is the pericardial sac?
- formed by a perietal pericardium which are fused to an outer fibrous pericardium (connective tissue)
- prevents over distension of the heart; anchors the heart to the diaphragm and thoracic wall
the heart has sensory functions and endocrine functions
true or false?
true
which layer of the heart is said to be the “muscle”?
myocardium
the atria contract blood _____whereas the ventricles contract blood _____
downward, upward
which has a larger diameter? contractile cardiac cells or non-contractile cardiac cells?
non-contractile, there are also more gap junctions - this allows electrical signal to travel about 4m per second
what is the name given to the circulatory system of the heart?
coronary circulation
what is the fibrous pericardium made of?
tough tissues with a lot of collagen
which side of the heart is thicker?
-the left side is thicker, this is why people say the heart is on the left side of the chest when really, it’s dead center
what separates the oxygenated from the deoxygenated blood int he heart?
interventricular septum
even though the left side of the heart is bigger, both sides pump the same amount of blood with the same amount of force
true or false?
false, yes both sides pump the same amount of blood per beat, however, the force generated by the left ventricle is much greater than the right ventricle
why is the left side of the heart bigger and pumps blood with more force than the right side?
because the resistance in the systemic system is so much higher, the left ventricle needs to push much harder to get the same amount of blood flow
what is the driving force of the blood in the heart? and consequently, the entire body?
pressure differences created during the heartbeat cycle drive blood flow from atria to ventricles, and from ventricles to arteries
-ALL blood flow follows this pressure gradient
what inhibits the backflow of blood in the heart?
backflow is inhibited by two sets of passive, on-way heart valves:
1) atrioventricular (AV) valves: between atria and ventricles (mitral or bicuspid (left) and tricuspid (right/RST; right side tricuspid) valves)
2) semilunar valves: between ventricles and main arteries (there’s three of these)
- they’re like cups
what is the name of the valve that sits between the atria and the veins?
-there are no valves between the atria and the veins, because of this, there may be a bit of backflow, but it’s very minor
positive pressure ____ valves of the heart opens them
behind
what is the effect of the contraction of the ventricle on the valves in the heart?
-bicuspid valve closes, semilunar valve opens
positive pressure _____ of valves opens them
ahead
each valve in the heart is surrounded by a connective tissue right connected to a central ________ that separates atria from ventricles
fibrous skeleton
what are two other main functions of the valves in the heart other than stopping blood flow?
1) provides origin and insertion sites for cardiac muscle - these are at the same spot and therefore, can only allows the muscle to constrict
2) physically and electrically separates atria from ventricles - without this separation, there could not be a coordinated and strong beat
atria contract from the ______, ventricles contract from the ______
top down, bottom up
what is the definition of a heart beat
the heartbeat is an orderly wave of contraction that sweeps through the myocardium
what coordinates the heartbeat?
coordinated by specialized non-contractile muscle cells (they lack sarcomeres) that generate and conduct action potentials
autorhythmic pacemaker cells
- primarily found int he right atria (there are some in the interventricular septum)
1) sinoatrial (SA) node (approx 75 depol/min) -natural pacemaker of the heart (vein into atrium) - these dictate heart rate during rest and exercise - the fastest depolarizing cell determines the heart rate
2) atrioventricular (AV) node (approx 50 depol/min) - small diameter cells with fewer gap junctions and low AP conducting speed
what is the function of large diameter conducting cells in the heart?
- this is like a backup system in case the autorhythmic pacemaker cells are damaged
- some of these in the ventricles are autorhythmic
- these allow for rapid depolarization through the heart
- firing rate is influenced by the nervous system and the endocrine system
- main job is to act like neurons
internodal and interatrial pathways are examples of which type of heart cell?
large diameter conducting cell
what is the function of the internodal and interatrial pathways?
- carry impulses generated in SA node to the AV node and left atrium, respectively
result: atria contract in unison from top down
the bundle of His is an example of what type of muscle cell?
large diameter conducting cell
what is the purpose of the bundle of His
- it is the sole electrical pathway (an AP pathway) connecting atria to ventricles; splits into two bundle branches
- following a 100 msec delay in the AV node, the electrical signal is quickly transferred through the central fibrous skeleton to the apex of the heart
- this ensures atria empty fully before ventricles begin contraction
-this is also why the ventricles don’t contract from the top down
purkinje fibers are an example of what type of heart cell?
large diameter conducting cell
what is the purpose of the Purkinje fibers?
- extensive network of branches that spread upward towards the valves, transmitting the electrical signal to contractile cells as they go
result: ventricles contract in unison from apex upwards
unlike skeletal muscle cells, the contractile heart cells have very long duration APs (250 msec) due to what?
prolonged opening of Ca++ channels
what prevents tetanus in contractile heart muscle cells?
the absolute refractory period is almost as long as the contractile response (contraction + relaxation)
-this prevents summation and tetanus, and allows adequate time for heart chambers to refill between beats
what is an electrocardiogram (ECG/EKG)?
-not a direct recording, but rather an indirect recording of the sum of the total of all electrical activity occurring in the heart
- electrical activity is detected by pairs of electrodes at 3 points on the skin’s surface (electrical activity leaks and travels through your body)
- indication of the overall spread of electrical current through the heart during cardiac cycle
all contractile cells in the heart are repolarized during which segment of the cardiac cycle?
TP segment (near the end)
the flat lines illustrated in the cardiac cycle represent what?
when all fibers are depolarized or repolarized
segment of the cardiac cycle where all cells of the atria are depolarized, respectively
PR segment (after P wave, before QRS complex)
segment of cardiac cycle where all the cells of the ventricles are depolarized, respectively
ST segment (after QRS complex)
in an electrocardiogram (ECG/EKG), the repolarization phase of the atria is masked by what?
the QRS complex
explain the cardiac cycle measured during an EKG
1) P: atrial depolarization - atria contracting (ventricles passively filling)
2) AV nodal delay - atria emptying (topping up ventricles)
3) QRS complex - ventricular depolarization - ventricles contracting - at the same time, we get atrial repolarization
4) all fibers in ventricle contracting (and depolarizing), half way between S and T (muscles are contracted but they start to relax) - ventricles start emptying
5) T: ventricular repolarization - ventricles are emptying (until 1/2 way through T wave) - until the pressure is lower than that of the aorta (pressure decreases in ventricles and increases in aorta)
6) ventricles relaxing (ventricles passively filling) - this is called the TP segment - this is the longest period of the heart cycle (about 2/3 of entire cycle)
during the QRS complex, the first fibers in the ventricle (below AV node) become depolarize during the ____ and the last fibers in the ventricle (base of left ventricle) become depolarized during ____
Q, S
ECG abnormalities cause ______
arythmias
what is a heart block?
damage to the AV node - the relay from the atria to the ventricles
explain the 1st degree heartblock
1st degree: damage decreases rate of AP movement through AV node (increase AV delay) - this results in a longer PR segment - the signal gets “stuck” for longer in the AV node before it gets transmitted
explain 2nd degree heart block
when one of every 3, 4 or 5 atrial AP waves are ‘dropped’
- also called “skipped a heartbeat”
- technically this is not correct because atria still contract, ventricles do not - QRS or T complex are not present, you still get the P wave, so the heart doesn’t technically skip a beat
explain 3rd degree heartblock
complete blockage of the signal from atria to ventricles
- no synchrony between atrial and ventricualr electrical activities
- the ventricles are being driven by slow autorhythmic cells
- when this happens, we have two completely separate pacemakers that are not interacting with each other
- we still get P waves, but we get far fewer Q waves
- therefore, during any type of exercise, you will get an increase in atrial contraction but since this signal is not passed onto the ventricles, there will be no additional blood flow through the body
what is ventricular fibrillation?
when the heart muscle is no longer depolarizing synchronously, making coordinated pumping action impossible
-this can occur due to an infection, heart attack, etc
how do we reverse the effects of ventricular fibrillation?
- defibrillation
- this stops all electrical activity in the heart, in hopes that the SA node will contract first and begin the heart beat normally again
what are the two stages of the cardiac cycle?
systole - period of ventricular contraction
diastole - period of ventricular relaxation
what are the 2 stages of the systole period of the cardiac cycle?
1) isovolumetric contraction
- ventricular tension quickly increases
- AV valve closes, no blood enters or exits the ventricles (volume of ventricles is not changing
2) ventricular ejection
- increasing pressure forces semilunar valves to open
- approx 1/2 of the ventricles blood volume (stroke volume) enters aorta (and pulmonary arteries via the right ventricle)
- once ventricualr pressure declines below aortic pressure, the semilunar valves close (about half way through the T wave)
what are the 3 stages of the diastole period of the cardiac cycle?
1) isovolumetric relaxation
- ventricular tension begins to wane
- ventricular pressure is too high for AV valve to open; no blood enters the ventricles
2) passive ventricular fillin
- blood entering relaxed atria begins to pass into ventricles under its own pressure (AV valve opens)
- ventricular volume increases
** about 80% of all ventricular filling occurs during this phase
3) atrial contraction
- topping up of ventricles (increase in ventricular volume by 20%)
- this stretches the ventricle walls a little bit
when we listen to a heart beat, what are we really hearing?
when our valves close (AV valve), we get the “lub”
the closing of our semilunar valves makes the “dub”
what causes a heart murmur?
when there is a leak between valves
what is blood pressure measured according to?
- by convention, all body pressures are given relative to athmospheric pressure
- so 100mmHg = 100mmHg above atm. pressure (760 mm Hg)
-this is why we bleed “out”
systolic pressure
maximum pressure measured in aorta (approx 120 mmHg)
-midway through ventricualr ejection
diastolic pressure
- minimum pressure measured in aorta (approx 80 mmHg)
- at the end of isovolumetric contraction (measured during systole)
mean arterial pressure
- average aortic pressure during the entire cardiac cycle (approx 93 mmHg)
- driving force pushing blood through the systemic circuit
during cardiac contraction, there is a second increase in pressure (even though there is no blood entering aorta) due to some of the blood going backwards, then rebounding forwards. What is this increase called?
incisura
end diastolic volume (EDV) - def.
- maximum ventricular volume attained during the cardiac cycle
- occurs in systole - phase of isovolumetric contraction
end-systolic volume (ESV) - def.
minimum ventricular volume attained suring blood ejection phase
-measured at the start of diastole
equation for stroke volume
SV = EDV - ESV
stroke volume is influenced by the endocrine and nervous systems
true or false?
true, same as the heart
cardiac output
the rate at which the heart’s ventricles pump blood
Heart rate X stroke volume = cardiac output
-at rest, this is about 5L/min which is about the total blood volume of your body
what happens to cardiac output during exercise? how does it change?
during exercise, CO is increase to about 25L/min by increasing BOTH heart rate and stroke volume (amount of blood per beat)
does training change cardiac output?
yes, training leads to further increases in cardiac output, up to 40L/min instead of 35 by:
1) inducing an increase in heart muscle mass = leads to increased stroke volume
2) resting heart rate drops, but maximal heart rate stays the same (since stroke volume goes up, heart rate must go down) - this leads to a cardiac output that’s about 8 times higher
what are the 2 types of factors that can affect heart rate?
1) neural control
2) hormonal control
heart rate is primarily determined by the frequency of action potential firing by the SA node, which is influenced by which two things?
1) direct input from two competing branches of the autonomic nervous system (ANS) - sympathetic increase, parasympathetic decreases
2) levels of circulating hormones (mostly epinephrine)
*note that these are both outside factors
both divisions of the ANS are active at all times
true or false?
true, however, increases in one usually leads to a decrease in the other
factors affecting heart rate: sympathetic neurons release ____ which binds to ______ receptors, stimulating the _____ second messenger system
norepinephrine, B1 adrenergic, cAMP
how does the release of NE from sympathetic neurons affect our heart rate?
-NE binds to B1 receptors, stimulating the cAMP second messenger response which causes a decrease in the flux of K+ out of, and an increase in Na+ and Ca++ flux into pacemaker cells, causing the SA node to reach its AP threshold faster
chronotropy
the rate of contraction
_____impulses cause positive chronotropy, whereas ____ impulses cause negative chronotropy
sympathetic, parasympathetic
sympathetic impulses can decrease the rate of systole
true or false?
true, sympathetic impulses to conducting cells increase the speed of AP conduction (including through AV node), decreasing the duration of systole
ACh release by parasympathetic neurons of the vagus nerve binds to muscarinic receptors on cells of:
1) the SA node: curbs inward movement of Na+ and Ca++ and increases K+ permeability which slows the rate of spontaneous depolarization
2) the AV node: decreases the speed of AP movement through AV node and other conducting cells of the heart which increases the duration of systole (causes the PR segment to increase)
do people who have had a heart transplant have higher or lower heart rates? why?
they have higher heart rates
-because of the transplant, the heart is no longer getting nervous input, therefore the parasympathetic nervous system is no longer “putting the breaks on” the heart rate at rest like it normally does
give an example of hormonal control that affect heart rate
-epinephrine secretion by the adrenal medulla in response to increased sympathetic activity reinforces the effect of the sympathetic neural input to the heart (a little bit of NE too)
inotropy - def.
strength of stroke volume
any factor that increases the force of ventricular contraction will increase stroke, thus result in positive inotropy
true or false?
true
most neural control affecting stroke volume is due to parasympathetic neuron APs
true or false?
false, very few vagal nerves project to the ventricles, so most of the influence here is exerted by the sympathetic neurons
factors affecting stroke volume (neural control): how does the increases B1 receptor mediated cAMP second messenger system activation affect stroke volume?
1) increases flow of Ca++ into contractile cells following AP - NE binds to receptors and causes Ca++ channels to open - Ca++ induced Ca++ release
2) increases the release of Ca++ by sarcoplasmic reticulum (SR) (Ca++ can bind more tropomyosin - more cross bridges)
3) increases the speed of actin/myosin cross bridge cycling (muscle is shortening faster and stronger)
** 1 to 3 increase ventricular contractility - the strength of contraction at any given diastolic volume
4) increases rate of SR Ca++ uptake, increase the speed of muscle relaxation - if you pump back in faster, you can pump back out faster
what is the significance of increasing the force of ventricular contraction on stroke volume?
-this ejects a larger fraction of EDV - larger stroke volume increases contraction and relaxation speeds, shorter systole, more time for diastole (heart filling) which is important during exercise
when we have an increase in contraction/relaxation speed (during exercise for example), this decreases the duration of systole. Why is this crucial?
- each cardiac cycle takes about 0.8 seconds at rest, but only 0.3 seconds at 200 beats per minute (0.27 sec systole, 0.53 sec diastole to be exact)
- thus, shortening systole ensures sufficient time for the heart to refill during intense exercise
- if systole did not decrease, it would take up most of the cardiac cycle and the heart would hardly have any time to fill - no oxygen getting anywhere in the body -limiting your maximal heart rate value
sympathetic impulses increase the force of _____ contraction, cause vaso _______ in the peripheral veins (increasing venous return to the heart). Thus, blood enters the ____ faster, further increasing EDV (leading to higher cardiac output)
atria, constriction, ventricles
how does hormonal control affect stroke volume?
epinephrine released from the adrenal glands affects intracellular cAMP levels within contractile cells in much the same manner as norepinephrine
-increasing Ca++, muscle contraction force, etc.
if heart transplant patients no longer have nervous input going to the heart, how does their rate of contraction go up or down?
- hormonal control
- release of epinephrine and norepinephrine by the adrenal medulla is what will increase cAMP levels in contractile cells and cause an increase in muscle contraction and force
what is the influence of EDV on stroke volume?
the force of ventricular contraction also varies in response to how much the ventricular myocardium is stretched upon filing
- ‘length tension relationship’ - the maximal # of active cross bridges are formed between actin/myosin filaments at 2.2 micrometers
- cardiac muscle fibers are well below this optimal length at rest which is why an increased EDV would benefit this
what is the Frank Starling law of the heart?
‘the heart automatically adjusts its output to match the inflow’
Hence, increase EDV = increase force of contraction = increased stroke volume (and CO); decreased EDV causes decreased force of contraction = decreased stroke volume (and CO)
how does MAP have an effect on stroke volume?
stroke volume depends on the arterial pressure against which it is pushing, the semilunar valves will ONLY open once ventricular pressure becomes greater than aortic pressure, thus, an increase in MAP will result in more force being needed to eject the same volume of blood
hypertension
the stiffening of the arteries
-heart has to work harder every beat - it gets stronger which is not a problem until it starts to damage the endocardium and causes the sarcomeres to rearrange, and their efficiency goes down
stenosis
the narrowing of semilunar valves - these get stiffer and contricted
-leads to increase in blood pressure
coarctation
narrowing of the aorta
-leads to increase in blood pressure
increase afterload (MAP) only becomes a problem in disease states
true or false?
true
increased sympathetic stimulation (NE, E) ______ EDV and SV, whereas increased afterload (i.e. hypertension) or decreased sympathetic stimulation _____ EDV and SV
increases, decreases
which two things have major effects on blood flow?
pressure differences and resistance
hemodynamics - def
blood flow regulation
which vessel has a pulse pressure?
a) arteries
b) veins
c) venules
d) capillaries
e) arterioles
f) a and e
g) none of the above
h) all of the above
f) a and e
note that arterioles have a pulse pressure at the beginning but there is no pulse pressure at all when reaching the capillaries
-note that there is also a tiny pulse pressure in veins due to breathing
vascular resistance is governed by which 3 things?
1) vessel length - the longer the vessel, the higher the resistance (this does not affect us during exercise since the length does not change)
2) internal vessel radius - smaller radius = higher pressure
3) blood viscosity - friction between molecules of a flowing fluid (proportional to blood hematocrit)
- the thicker the blood, the higher the resistance (at body temperature, blood is about 2.5 times thicker than water)
- if hematocrit is too high, it can be very dangerous
out of the 3 factors that affect resistance to blood flow (vessel length, vessel radius, blood viscosity) which one has the highest effect on resistance?
the only one that changes is vessel radius
-a small change in radius leads to a BIG change in resistance
what effect does doubling the radius of a vessel have on its resistance?
resistance can be calculated with this equation
R = 1/r(4)
so when you double the radius of a vessel, you increase the resistance by 2(4) which = 16 times less resistance
-so flow increases by 16 times with just a 1mm difference in radius
what is Poiseille’s Law?
blood flow to individual organs/tissues is predominantly controlled by adjusting the radius of vessels leading to them
what are the 5 layers of a basic artery vessel, starting from inner most to outer shell
1) tunica intima (interna)
2) elastica interna
3) tunica media
4) elastica externa
5) tunica externa
tunica intima (interna)
- single layer of endothelual cells continuous with endocardium
- secretes substances that regulate blood flow
- plays a key role in the growth of new blood vessels, responds to signals, key role in transport of substances
elastica interna
composed of stretchable elastin fibers - allows arteries to stretch when blood gets pumped into them, for example when the heart beats, arteries have to stretch
tunica media
layer of smooth muscle encircling the vessel
- allows for contraction and relaxation of the vessel radius
- **this layer is key for determining blood pressure and regulating blood flow to individual tissues, organs, etc. they have “tone” - constantly in state of contraction, they can relax and change resistance
elastica externa
second layer of elastin
tunica externa
sheath of connective tissue (collagen) surrounding the vessel
the 5 layers of a vessel are typically constant in their thickness as they progress towards the capillaries]
true or false?
false, relative thickness of layers 2 - 5 vary as vessels progress towards the capillaries
-as they progress away from capillaries to veins, we start losing these layers - very important that the amount of muscle changes - amount of blood pressure regulation changes
which vessels are compared to “freeways” that have large radii and little resistance to blood flow?
arteries (aorta and larger arterial branches to be specific)
-these are rapid transit passageways linking the heart to organs
the heart pumps a high, fairly steady MAP at all times
true or false?
true, the only job of the heart is to pump blood out, it is the job of individual vessels to decide whether or not they need this blood
arteries act as a pressure reservoir for what?
it is used as the driving force for blood flow during heart diastole (which lasts at rest about 2/3 of the cardiac cycle)
also to ensure constant blood flow to the capillaries (of which about 10% are open at rest)
the pressure reservoir elicited by arteries is achieved through the high _____ of arterial walls
elasticity
during _____, a greater volume of blood enters the arteries than exits towards the arterioles; during_____ passive elastic recoil of the stretched arterial walls pushes excess blood downstream
systole, diastole
blood pressure is blood volume dependent
true or false?
true
what are the major resistance vessels of the body
arterioles
why are the arterioles called the major resistance vessels of the body?
- the resulting decline in pressure establishes the gradient that encourages blood flow from arteries into capillaries
- at the beginning or arterioles, MAP is around 93 mmHg, but at the end it is around 55 mmHg - this massive drop in pressure creates the gradient
arterioles have little ____ and lots of _____ which are richly innervated by which division of the ANS?
elastic tissue, smooth muscle, sympathetic
most arterioles in the body are innervated by the sympathetic nervous system, what are some exceptions?
- brain, penis/clitoris
- you don’t want less blood flow here, you want more
- if it was innervated by the sympathetic nervous system (which released NE and E) muscles would contract and resistance would increase, causing less blood flow
smooth muscle content and degree of innervation increases as they progress from primary to terminal arterioles
true or false?
false, it decreases as it progresses
what are the THREE important functions of arterioles?
1) determine the relative blood flow to individual tissues/organs
2) help regulated MAP (when they work as a team - ex: during exercise - CO increases drastically but MAP stays about the same)
3) eliminate the pulse pressure prior to it reaching the capillaries (important because the capillaries are so small, pulse pressure change would cause them to rupture)
flow rate to each individual organ is a function of its ______ resistance
arterioles’
the radii of arterioles leading to different parts of the body are independent of one another
true or false?
true
blood flow through any part of the system is ALWAYS the same at any given time (ex. arteries, arterioles, capillaries)
true or false?
true
the rate of blood flow to each organ depends upon the degree of ______ leading to that organ
SM contraction
arteriole SM contraction is only one factor that affects the rate of blood flow to an organ, flow entering capillary beds of each organ/tissue are FURTHER controlled by contraction and relaxation of what?
precapillary sphincters - non-innervated bands of smooth muscle at arteriole capillary junctions
the pre-capillary sphincters leading to each organ/tissue respond to what type of signal?
local cues -THESE ARE NOT INNERVATED
-therefore, when capillaries are constricted, most blood can just by pass the tissue and drain straight into venules via conduit vessels called matarterioles
how is arteriolar vasodilation/constriction modulated?
arteriolar smooth muscle has a high degree of spontaneous activity - state of partial contraction, called vascular tone, it is independent of neural and chemical input
-however, this baseline constriction can be altered by external signals that decrease or increase the SM cells’ cytosolic [Ca++]
Mechanisms of blood vessel control: intrinsic (local) autoregulation: myogenic control
the ability of vascular SM within vital organs (ex: brain, heart, kidneys) to self-regulate its tone in response to changes in MAP
what are the 3 intrinsic (local) autoregulation mechanisms of blood vessel control?
1) myogenic control
2) local metabolic control
3) non-metabolic chemical mediators
local metabolic control (blood vessel)
individual tissues can further regulate their own blood supply via the metabolically driven release or paracrine agents to the extracellular fluid surrounding the arterioles that supply them
-these messengers stimulate the endothelium to release vasoactive mediators (ex: nitric oxide which causes less Ca++ release)
what is active hyperemia
increase blood flow to specific tissues in response to an increase in their activity
-this is a response to the fact that active muscles need more ATP, more Ca++, release more Co2 as heat, this is NOT signal from the brain
autoregulation (of blood vessel control) and exercise - rapidly contracting skeletal (and cardiac) muscles leads to:
1) decreased O2 levels (hypoxia)
2) increased CO2, H+, K+ and adenosine levels
-this causes increase NO release at these sites
exercise induces localized _____ by blocking Ca++ entry into smooth muscle cells of arterioles and precapillary sphincters. Why?
vasodilation
- vasodilation of arterioles causes increased flow to tissues
- vasodilation of precapillary sphincters increases the number of open capillaries in a tissue
result: O2 delivery and waste is removed by blood
how are capillaries affected by local signalling?
capillary beds open and close according to the amount of oxygen/CO2 surrounding them, when CO2 goes up, capillary beds open to get more oxygen, they close when sufficient amounts of oxygen are present
THEY ARE NOT INDEPENDENT OF EACH OTHER - they may work together or in opposition
reactive hyperemia
an increase in tissue blood flow following a period of low perfusion (ex: heart attack)
- there is a local arteriolar relaxation in response to diminished stretch
- vasodilation owing to localized hypoxia and metabolic by-product accumulation
-as a result, there is a rapid restoration of local cellular conditions to normal - we get swelling or tissue damage
intrinsic auto-regulation of blood vessel control: what are the 3 non-metabolic chemical mediators?
1) endothelin-1
2) histamine
3) serotonin
describe endothelin-1’s effect on vessel control (intrinsic autoregulation)
-there are 3 isoforms known (it is 21 amino acids long)
- potent vasoconstrictor released by arteriolar endothelium in response to increased pressure
- opens non-stretch sensitive Ca++ channels and enhances Ca++ release by the SR
when blood vessels get stretched, it is fairly long lived and it opens additional Ca++ channels which reinforces the myogenic response - work hand in hand
describe histamine’s effect on vessel control (intrinsic autoregulation)
- histamine is released by mast cells (similar to basophils)
- potent vasodilator that plays a role in inflammation
- localized release occurs during allergic reaction (quick onset) or in response to injury or infection (2-8 hours onset)
- causes capillaries to get leakier - increased flow to tissues - increase in fluid in interstitial space causing swelling
- putting on a cold compress minimizes actions of histamine
describe serotonin’s effect on vessel control (intrinsic autoregulation)
- practically all blood serotonin is found within platelets (this is about 2% of the body’s serotonin)
- wound activated release induces vasoconstriction
- reduces blood flow to the site of bleeding
- once a clot forms serotonin stops being released (histamine is then released which is what causes the swelling)
ONCE AGAIN, YOUR BRAIN HAS NOTHING TO DO WITH THE SIGNALLING OF THESE CHEMICALS
extrinsic control of arteriolar radius alters _____ and is a very important regulator of MAP
total peripheral resistance (TPR)
MAP = CO X TPR
systemic (extrinsic) regulation of blood vessel caliber can be complimented or opposed by local control mechanisms
true or false?
true
is blood pressure higher in the pulmonary circuit or the systemic circuit?
about 5 times higher in the systemic circuit
-SNS and PNS are regulating CO, and total peripheral resistance - both of these control MAP (which is always about 93 mmHg)
sympathetic neurons mainly release ____ which binds to arteriolar SM ___ receptors causing the blood vessels to do what?
NE, a1 adrenergic, vasoconstriction
why isn’t the brain controlled by extrinsic mechanisms?
brain arterioles (and terminal arterioles) lack the a1-adrenergic receptors (which NE bind to), thus, their caliber is entirely controlled by local mechanisms -there is also a relatively low amount of a1 adrenergic receptors in the skeletal and cardiac muscles - we wouldn't want the vessels in these to contract during exercise limiting blood flow
in places where there are lots of adrenergic a1 receptors (such as vessels), there is a constant discharge which is controlled by what?
the cardiovascular control center (brain stem - medulla)
increased firing rate leads to generalized vasoconstriction (TPR goes up)
decreased firing rate leads to vasodilation (TPR goes down)
sympathetically induced epinephrine release from adrenals can also bind to SM a1-adrenergic receptors, reinforcing vasoconstriction
true or false?
true
epinephrine can weakly bind to a1 receptors which causes vasoconstriction of blood vessels, however, which receptors are epinephrine more likely to bind to? what is the result of this?
arteriolar SM of the heart, liver, and skeletal muscle predominantly possess non innervated B2 receptors that bind epinephrine with much higher affinity
-the resulting dilation at these tissues strengthen local metabolic control mechanisms at work during exercise
-in the heart, this is good because dilation causes more blood flow, dilation in the liver causes release of glucose which fuels muscles
***NOTE: sympathetic nervous system is causing two opposite reactions: constriction and dilation to different areas that need more or less blood
summarize what happens during exercise to the resistance of blood flow
1) sympathetic stimulation releases NE and E
- NE binds to a1 receptors which causes vasoconstriction of nonessential organs (decrease in blood flow) this diverts blood flow to:
- E binds to b2 receptors which cause vasodilation of heart, liver, and skeletal muscle
- this increases local O2 and decreases local CO2 and H+ causing a decrease in blood flow to resting muscles
2) sympathetic stimulation causes an increase in heart rate, stroke volume = increase CO
- local O2 to drop, local CO2 and H+ to increase
- this increases blood flow to exercising muscles (along with the vasodilation of heart, liver, and skeletal muscle which divert their blood flow here)
angiotensin II and its role with vessel control
- decreased renal perfusion pressure causes renin to be secreted by the kidneys, leading to an increase in blood (angiotensin II), an arteriolar vasoconstrictor (which increases TPR)
- angiotensin I is turned into angiotensin II by ASE enzyme
vasopressin and its effect on vessel control
- vasopressin is an antidiuretic hormone (ADH) - it stops us from peeing
- atrial receptors respond to a decrease in blood volume (or MAP) and cause the posterior pituitary to secrete this vasoconstrictor (vasopressin)
atrial natriuretic hormone (ANP) and its effect on vessel control
causes relaxation of vascular smooth muscle; synthesized by specialized atrial cells in response to excess stretch of the heart (increase in blood pressure)
angiotensin II, vasopressin, and atrial natriuretic hormone (ANP) are all closely linked to control of blood volume via their effects on the kidney
true or false?
true
explain the local effects and the systemic effects that would result after a severe hemorrage (loss of blood causes MAP to decrease)
1) local effect (e.g. brain, heart)
a) decreased arteriolar stretch (myogenic response)
b) decreased O2 concentration and increased metabolite [ ] at tissues (metabolic response)
result: dilation of these arterioles; increases brain blood flow but causes MAP to decrease further
2) systemic response
a) increased sympathetic stimulation
- NE - vasoconstriction of SM in non-essential organs
- E - vasodilation of skeletal muscle arterioles; however, this is opposed by dominant local metabolic effects
- TPR increases and MAP increases to counteract blood loss
b) increased plasma [vasopressin], [angiotensin II] - so that you don’t lose more blood volume than you already have
result: SM tone of most arterioles (except brain, heart), increasing MAP towards pre-hemorrage values
smallest, thinnest, and most numerous blood vessels in the body
capillaries
how long would our capillaries be if we put them all together in a line?
40-80 thousand km long
how long is the average diameter of a capillary
5 to 10 micrometers (um) in diameter, huge surface area (approc 6000m(2)) for exchange
how much blood to the capillaries contain at rest?
about 5% of the total circulating blood volume
what is the composition of a capillary?
composed of a single layer of endothelial cells encased by a thin glycoprotein/collagen matrix (basement membrane)
capillaries are not permeable to small, lipid-soluble substances because they are too small even for those
true or false?
false, they are permeable to these (O2, CO2, fatty acids, steroid hormones, anaesthetics)
3 things are necessary for efficient exchange. What are they? Which type of blood vessels has all these things?
1) numerous with a high surface area
2) thin so that the diffusion distance is small and faster
3) long time for exchange, blood goes through slowly
capillaries have all these factors
what are the 2 classes of capillaries?
continuous capillaries and fenestrated capillaries
continuous capillaries
cells have small water-filled intracellular channels with narrow intercellular pores between adjacent cells
- exchange sites for small water-soluble substances (H2O, Na+, K+, glucose, amino acids)
- largely impermeable to macromolecules - plasma proteins (ex: albumin) stay in capillary - transcytosis of exchangeable proteins (ATP must be used to transport them)
fenestrated capillaries
loose fitting cells with large intercellular spaces
- kidney, intestines, liver, bone marrow discontinuous capillaries
- these are leaky
- these vessels respond to histamine
movement of material across capillary walls serves two purposed, what are they?
1) exchange of material between blood and cells
2) maintain fluid balance between plasma and interstitial fluid (ISF)
how do capillaries maintain fluid balance between plasma and interstitial fluid (ISF)?
distribution of ECF between plasma and ISF is in a state of dynamic equilibrium due to filtration and absorption of fluid by capillaries
- via bulk flow of protein-free plasma across channels and pores, driven by hydrostatic (water) and colloid (protein) pressure gradients
- starling forces
colloid pressure
protein pressure
what are the Starling Forces?
a) Pc = capillary hydrostatic pressure (HP)
b) Pi = HP of ISF
c) (pi)c = plasma colloid-osmotic pressure
d) (pi)i = colloid-osmotic pressure of ISF
Starling Forces: Pc = capillary hydrostatic pressure (HP)
- HP inside capillary favouring filtration of plasma
- declines as blood moves from arterioles (approx 37 mm Hg) to venule side (approx 17 mm Hg) of capillary
-there is more pressure inside capillaries than outside = pressure gradient
Starling Forces: Pi = HP of ISF
- HP outside capillary favouring absorption of ISF - resisting the outward flow
- approx. 1 mm Hg
Net filtration pressure (Net P) of capillaries
- Pc - Pi at any given point along the capillary
- force favouring plasma filtration along the entire length of the capillary
-there is always an outward force of pressure, this gradient gets smaller but its always there
Starling Forces: (pi)c = plasma colloid-osmotic pressure
- osmotic pressure within capillary due to non-permeating solutes that favours absorption of ISF
- approx. 25 mmHg
-this is NOT osmotic pressure
Starling forces: (pi)i = colloid-osmotic pressure of ISF
- osmotic pressure due to non-permeating solutes within ISF that favours plasma filtration
- approx 0 mmHg
Net osmotic pressure (Net (pi) in capillaries
- (pi)c - (pi)i
- force favouring absorption of ISF along entire length of capillary
-fluid gets pushed out then sucked back in, so what’s the point? this promotes diffusion
how do we calculate net fluid movement at any given point in a capillary
Net fluid movement = Net P - Net (pi)
net absorption of capillaries and net filtration of capillaries are typically equal throughout a day
true or false?
false, the transition point (on diagram) between net filtration and absorption is slightly to the right
-there is an unbalance between them, typically, in one day, net filtration is higher than net reabsorption - capillaries leak about 3L more than they pick up (Net filtration = 20L, net absorption = 17L)
-remember that this is just a general rule, in some areas (kidneys) we only get filtration and vice versa (intestine)
what does the lymphatic system do
excess ISF enters highly porous, blind-ended lymphatic capillaries
-empties into bloodstream via ducts near the jugular veins (aids in picking up any large proteins that leak out - also a gateway for WBCs -key role in immune response)
failure of this system, or disease states affecting one or more of the Starling forces produce edema (accumulation of ISF)
what happens when lymph vessels are obstructed? (2 possibilities)
1) elephatiasis
- affects about 100 million people on the planet
- mosquito borne filaria worm
- fluid leaking out not being able to return - causes extreme swelling
2) removal of lymph nodes
- ex: in the case of cancer
- swelling
what would happen if net reabsorption increased? (lymphatic system and pooling)
heart failure promotes venous pooling, backing up blood into capillaries, increasing Pc
- ex: if the right side of the heart fails, pooling of blood happens before the atrium - systemic system has less venous return - pooling in systemic system
- ex: left side heart failure - fluid build up in lungs
what would happen if net filtration decreased? (lymphatic system)
-liver (decreased plasma protein production) and kidney (increased protein excretion) disease both decrease (pi)c
histamine dilates arterioles (increases Pc) and increases intercellular pore size (increases capilalry permeability for proteins, increasing (pi)i - causing net pi to go down
- this changes the ‘transition point’ between filtration and reabsorption
- leads to edema or leakage
veins (and venules) - def.
thin walled, valved, high compliance vessels
-contain less SM and elastin, but more collagen than arteries
what are the 2 functions of veins?
1) low resistance conduits for blood flow to the heart
2) volume reservoir
why are there valves in veins?
valves prevent back flow because of gravity
why are veins such low resistance?
there is not a large pressure gradient, therefore they have to have low resistance to have the same amount of blood flow (mean driving force for blood flow from peripheral veins to right atrium is only about 10-15 mmHg)
which holds a greater volume of blood? veins or arteries?
veins, even though pressure is much lower
-this reservoir can rapidly be drawn up when required
how much blood is sitting in veins at rest?
about 60% - this blood can be called upon during exercise to promote venous return to the heart
CO is determined by the rate of venous return
true or false?
true
when talking about venous return and CO, why is it a disadvantage to be bipedal?
- gravity pulls blood downwards, so we must be able to return blood to the heart with this low pressure gradient PLUS we have to combat gravitational forces
- below heart level, veins and lymph vessels will tend to fill and be distended - this can cause edema
what is orthostatic hypotension? what are the causes of this?
-standing up too fast and getting dizzy - this happens because when you stand too quickly, you get less blood flow to your heart because your body has to adjust to the difference in gravitational pull, thus there is less cardiac output and less blood getting to your brain
where is the major site of venous volume change? Why? What can this lead to?
in the smaller veins located outside the thorax due to their elliptical shape (they stretch)
- small increases in pressure cause them to expand a lot
- this leads to edema and eventually to fainting if venous pooling occurs and persists (i.e. decreased VR causes EDV and hence MAP to drop - insufficient blood to the brain)
venous return is influenced by which 4 things?
1) neural input
2) skeletal muscle pump
3) respiratory pump
4) cardiac suction
how is venous return influenced by neural input?
walls of veins contain SM which is innervated by SYMPATHETIC neurons - norepinephrine binds to a1 adrenergic receptors (increased Ca++ levels - constriction of blood vessels)
what is the effect of neural input on venous return to the heart? (its significance)
a) neurally driven vasoconstriction in response to decreased MAP (or exercise) strongly increases venous pressure - blood is brought to the heart faster (hemorrhage or exercise)
b) increased wall tension decreases venous compliance, producing a sustained increase in VR and thud cardiac output (this can work for both short and long term)
venous SM only responds to norepinephrine binding to a1 receptors, causing constriction of the vessels
true or false?
false, venous SM also responds to hormonal and paracrine vasodilators and vasoconstrictors - ex: epinephrine
how does a skeletal muscle pump influence venous return?
large muscle groups compress deep veins in the extremities when they contract (pumps blood upwards because of the valves in the veins)
-these (and all veins) (and larger lymphatic vessels) outside the chest cavity have one-way valves to prevent backflow of blood (any kind of movement promotes lymphatic and venous return to the heart) - ex: shaking your leg while sitting or exercising
how does the respiratory pump influence venous return?
- venous return is dependent upon the pressure gradient between peripheral veins and right atrium
- right atrial (and thoracic vena cava) pressure is affected by changes in thoracic cavity pressure (breathing in and out)
- during inspiration, the chest wall expands and the diaphragm descends, causing a decrease in thoracic pressure and an increase in abdominal pressure
how does breathing affect pressure in different parts of the body?
- distends thoracic veins and compresses abdominal veins
- increases the pressure gradient that promotes blood movement towards the heart
- atrial pressure also decreases, pulling blood into the heart
the larger the inhalation, the larger the effect
how does cardiac suction influence venous return?
- during ventricular systole, the atrial flood moves downward, decreasing atrial pressure and pulling blood towards the heart
- the elastic potential energy stored in the myocardium during contraction is released during diastole (this recoil creates a negative pressure which ‘sucks’ blood into the ventricles)
pressure inside the heart can drop below 0
true or false?
true, larger pressure decreases are linked to how strong heart contraction is ex: exercise - this contraction “rebounds” faster
the magnitude of the suction effect of the heart on venous return is dependent on EDV
true or false?
false, it is dependent on ESV
-as ESV decreases, the pressure gradient for early diastolic filing, and hence ventricular filing rate, increases
extrinsic regulatory mechanisms keep MAP at a constant level by which type of feedback control?
negative feedback
short term regulation of MAP
mechanical stretch receptors (baroreceptors) in the aortic arch and carotid sinuses detect changes in blood (and pulse) pressure
- their discharge rate is directly proportional to MAP
- these baroreceptors project to the cardio vascular control center (medulla)
- medulla makes appropriate CV adjustments by sending output to effectors (heart, blood vessels) via BOTH ANS nerve branches
at any given MAP, if pulse pressure increases, firing rate of baroreceptors also increases
true or false?
true, their firing is directly proportional to MAP
low blood pressure causes an increase in _____ firing, whereas a higher blood pressure causes a decrease in this firing
SA node
LOOK AT SAVED DOCUMENT ON LAPTOP
summary of everything
what is the only way to increase blood volume after having lost a lot of blood?
drinking fluids
following a hemorrhage, _____ brings MAP back towards normal but fluid needs to be consumed in order to replace the blood lsot
immediate baroreceptor firing
in simple terms, how do we control MAP in the long term?
occurs via control of blood volume
-this influences venous pressure, venous return, EDV, SV, and CO
long term MAP control is regulated by hormones that are secreted where? What are these hormones?
by the heart, brain, and kidneys
-atrial natriuretic peptide (ANP), vasopressin, and renin (begins conversion of angiotensin to angiotensin II)
how does ANP (atrial natriuretic peptide) help control MAP over the long term?
a) it increases Na+ and H2O excretion by the kidneys (water follwos salt)
b) inhibits vasopressin secretion (which controls water conservation and increases thirst)
c) inhibits renin recretion (production of angiotensin II; same role as vasopressin)
these all work in opposition of ANP
with all sorts of different mechanisms we have to control MAP, why do people still develop hypertension? (or hypotension)
slow changes in MAP are accompanied by ‘resetting’ of the baroreceptor (receptor adaptation or desensitization) and CV center responses
-blood pressure is still opposed minute to minute, but at a higher or lower level
hypertension - def.
represents a failure of pressure homeostasis
-typically a chronic increase in TPR
primary hypertension
- there is no clear cut cause, but it is associated with obesity, high cholesterol, smoking, and genetics (ex: ‘salt sentitive’ - increases in the concentration of Na+ retention)
- initially it leads to ventricular hypertrophy, however, myocardial contractile function diminishes over time - leads to congestive heart failure and edema
this also increases the risk of atherosclerosis, heart attacks, kidney damage, and stroke (because of stiffening of the arteries)
secondary hypertension
- increase in MAP arising from other conditions
- ex: because of pregnancy
what are some treatments for primary hypertension?
a) exercise, decreases Na+ intake, and weight loss to lower resting MAP
b) Ca++ channel blockers - which promote vasodilation of vascular SM; decreases heart contractility and the rate of SA node firing (TPR go down and CO to go down)
c) diuretics - increase urinary excretion of Na+ and H2O; decreases CO with little effect on TPR
d) B-adrenergic receptor blockers - targets B1 receptors, decrease NE and E stimulation of CO (decreased heart rate and slightly smaller SV)
e) angiotensin-converting enzyme (ACE) inhibitors - blocks production of angiotensin II; decreases TPR (vasodilation, causes heart to not diminish in strength)
