CV Flashcards
atria
ventricle
atria: upper chambers of the heart that receive blood from the blood vessels
ventricle: lower chambers of the heart that pump blood out of the body
pulmonary circuit vs systematic circuit
pulmonary: the portion of circulation that carries blood to and from the lungs
deoxygenated
systematic: portion of the circulation that carries blood to and from most tissues of the body
oxygenated
roles of the circulatory system
primary and secondary
primary: the distribution of dissolved gases and other molecules for nutrition, growth, and repair, while simultaneously removing cellular wastes
secondary: chemical signaling to cells
dissipation of heat
mediation of inflammatory and host defense responses against invading microrganisms
how does blood flow through the cardiovascular system
liquids and gases commonly flow down pressure gradients from regions of high to low pressure
the initial region of high pressure in the CV system is created by contraction of the heart.
as blood flows pressure is lost due to friction
organization of the CV system starting and ending in the aorta
aorta
arteries
arterioles
capillaries
venules
veins
vena cava
posieuilles law
flow, resistance
4 power of the vessel radius divided by 8 x length of the vessel and viscosity of the liquid
resistance opposes flow, higher the resistance the lower the flow
flow is inversely proportional to the length of vessel and viscosity of the liquid
flow is directly proportional to the fourth power of the vessel radius
resistance is inversely proportional to the radius (larger radius = less resistance).
flow vs velocity of flow
flow is the volume of blood that passes a given point in the system per unit time (ml/min or L/min)
velocity of flow, which is the distance a fixed volume of blood travels during a given period of time, or more simply, how fast blood flows past a certain time
Heart valves
atrioventricular valves- allow flow from the atria into the ventricels
1) RA-> RV, Tricuspid valve (3 flaps)
2) LA–> LV mitral valve (bicupsid)
semilunar valves: are one way valves that exist between the ventricle and outflow artery.
both have 3 cup-like leaflets
LV—> aorta: aortic valve
RV—> pulmonary artery: pulmonary valve
dont have connective tendons
electrocardiogram
what is is and why it goes up or down
show the summed electrical activity generated by all the cells of the heart.
if the electrical activity of the heart is moving towards the positive electrode of the lead then an upward deflection is recorded.
electrical activity moving away from the positive electrode is recorded as a downward reflection
moving perpendicular causes no deflection
ECG
waves, segments, intervals
waves: appear as deflections above or below the baseline
segments: are the sections of baseline between two waves
intervals: combo of waves and segments
p wave
p-r segment
qrs complex
t wave
p wave: atrial depolarization
P-R segment: conduction through AV node and AV bundle
QRS complex: ventricular depolarization
T wave: ventricular repolarization
cardiac cycle
2 main phases
what are the 5 phases?
cardiac cycle: one complete contraction and relaxation
two primary phases:
diastole: the time during which cardiac muscles relax
systole: the time during which cardiac muscle contracts
* Atria and ventricle do not contact/relax at the same time
a single cardiac cycle is divided into 5 phases:
1) the heart at rest (atrial and ventricular diastole, late diastole)
2) completion of ventricular filling (atrial systole)
3) early ventricular contraction (isovolumetric ventricular contraction)
4) the heart pumps (ventricular ejection)
5) ventricular relaxation (isovolumetric ventricular relaxation, early diastole)
the 5 phases of cardiac cyle
1) The heart at rest: atrial and ventricular diastole (late diastole)
- The cycle starts with atria relaxed and filling blood from veins.
- The ventricles begin to relax, When the ventricles are relaxed enough and pressure in atria exceeds the ventricles, AV valve opens, and the ventricles passively fill with blood from atria
2) Completion of ventricular filling (atrial systole)
- most blood enters the ventricles passivley but under normal resting conditions that last 20% enters with atrial contract.
EDV
3) early ventricular contraction (isovolumetric contraction)
- the ventricles begin to contract; this builds up pressure in the ventricles and causes the AV valves to snap shut (first head sound “lub”)
when pressure in the ventricle is higher than the atria the blood is going to try to flow backwards
- Both valves are now closed and then ventricles continue to contract, building up pressure.
4) The heart pumps (ventricular ejection)
-as the ventricles contract pressure in ventricles exceeds pressure in the outflow arteries, causes semilunar valves to open and blood to flow out.
5) ventricular relaxation
- the ventricles then begin to relax, pressure in the outflow arteries begin to exceed the ventricles causing blood to attempt ot flow backwards into the ventricles causing the semi lunar valves to snap shut ( dub sound)
pressure volume loop of cardiac cycle
Left side of heart
EDV= end diastolic volume
ESV= end systolic volume
A-A is late dystole. pressure in the ventricle is lower than atria, and the AV valve opens, causing blood to fill in the ventricle (passive because pressure isnt changing).
A-B atrial systole, the last bit of blood is added to ventricle as the atria contract.
B-C isovolumetric (iso cause volume stays the same) ventricular contraction, no change in volume just pressure ventricle contracts causing AV valve to close
C-D: ventricular ejection, decreasine in volume because ventricle pressure exceeds aorta causing aortic valve to open causing ejection of blood.
D-A isovolumetric relaxation
no change in volume just pressure until you reach Point A wher the ventricle has relaxed enough where atria pressure starts to exceed ventricle start over
the wigger diagram
D: late dystole, ventricle relaxes pressure atria begins to exceed the ventricle,, AV valve opens and you get the passive filling of the ventricle
atria then contracts (atria systole) increasing the volume and pressure slightly (20%)
C: ventricle begins to contract, increasing pressure within the ventricle causing the Av valves to snap shut,
E represents EDV
Ventricle continues to contract until it exceeds pressure in aorta which is point A
Aortic valves open and get ejection of blood point E-F
ventricle continues to relax until it lower tahn the atrium and passive filling of the ventricle occurs once again
cardiac volumes EDV, ESV, stroke volume
ejection fraction
end diastolic volume- the maximal volume in the ventricle, after ventricular filling, 70kg man at rest 135ml
End systolic volume- the minimal amount of blood in the ventricles, blood left after ventricular contraction, 65ml
stroke volume: amount of blood during a single ventricular contraction, 70ml
SV= EDV- ESV
= 135- 65
=70ml
ejection fraction = the percentage of EV that is ejected from the heart (SV)
EF= SV/EDV= 70/135=52%
cardiac output
total blood flow (cardiac output)= stroke volume x heart rate
flow of blood delivered from one ventricle in a given time period (usually 1 minute) is the cardiac output
heart rate= beats per minute
stroke volume is the output from a single heartbeat, from either left or right vcentricle
two factors determine the amount of force generated by cardiac muscle
stroke volume is related to the force generated by cardiac muscle.
two factors:
1) the contractility of the heart
- the intrinsic ability of cardiac muscle fibres to contract at any given fibre length and is a function of Ca entering and interacting with the contractile filaments
2) the length of the muscle fibers at the beginning of the contraction
this detrmined by the amount of bloodf in the ventricle at the beginning of the contraction
sympathetic modulation of contraction
has a positive inotropic effect on stroke volume
1) Phosphorylation of Ca channels increase calcium conducatnace during action potentials
2) Phosphorylation of ryanodine receptors enhances sensitivity to Ca, inc release of ca from the SR
3) increase rate of myosin ATPase
4) Phosphorylation of SERCA increases the speed of Ca re-uptake which increases Ca storage
increasing sarcomere length increases force of contraction (stroke volume)
raising sarcomere length increases the Ca sensitivity of the myofilaments.
a stretched sacromere has a decreased diameter, which may reduce the distance that Ca needs to diffuse, increasing probability of cross-bridge cycling.
raising sacromere length puts additional tension on stretch-activated Ca channels, increasing Ca entry from extracellular space and increasing Ca-induced Ca release.
pre load affect on stroke volume
stroke volume depends on the initial stretch of the ventricular walls (from ventricular filling)
the degree of myocardial stretch prior to contraction is known as the preload on the heart
according to Frank-Starling law, stroke volume increases with increasing EDV
venous return how does it affect stroke volume
EDV is normally determined by venous return
increasing venous return increases venous pressure resulting in increased atrial filling leading to incread ventricle villing
*inc stroke volume
factors affecting venous return
skeletal muscle pump: skeletal muscle activity compresses veins in the extremities, pushing blood back to heart
increased muscle activity of the extremities can increase venous return.
respiratory pump: during inspiration, the chest expands and diaphragm moves down creating a subatmospheric pressure in thoraic cavity, this draws blood into the vena cava that exist within this cavity.
also abdomen is compressed, forcing blood back to the heart.
synthetic constriciton of veins: decreases their volume squeezing blood back towards the heart
stroke volume and after load
afterload is the end load/resistance against which the heart contracts to eject blood.
when afterload is high the ventricle has to work harder to eject blood incresing stroke volume
primarily determined by the combo of the EDV and the pressure in the outflow artery prior to contraction
afterload can be increased in pathological situations (e.g inc arterial blood pressure, decreased aortic compliance)
arteries and arterioles
arteries: walls that are both stiff and springy (pressure reservoir)
thick smooth muscle layer and large amount of elastic and fibrous connective tissue
branch into smaller arterioles that mainly contain vascular smooth muscle,
5 major blood vessels
what do they all contain
arteries, arterioles, capillaries, venules, veins
they all contain inner layer of thin endothelial cells and can be wrapped in a combination of elastic tissue, smooth muscle, or fibrous tissue.
capillaries
smallest vessels in the cardiovascular system, where the majority of exchange between the blood and interstitial space occurs.
single thin endothelial layer surrounded by basal lamina (extracellular matrix)
gases can normally passively diffuse across the endothelial cells
linked by interendothelial junctions that also aid in the transport of small solutes and water
some cells contain fenestrations, membrane-lined conduits running through them to allow the transport
capilleries often surrounded by pericytes (BBB)
types of capillaries
continous capillary: most common, thicker endothelial cells that do not contain fenestrations
only allow passage of water and small ions
fenestrated capillary: thin endotheial cells that have fenestrations.
small molecular passage
discontinuous capillary: lack a basal membrane, have large open fenstrations as weel as gaps between the endothelial cells
methods of transport in capillaries
transcellular transport: diffusion or osmosis across the endothelial cell membrane. gases, small lipid molecules, water (aquaporin channels)
paracellular transport: diffusion through interendothelial junctions, pores, or fenestrations (water, small water-soluble, and small polar molecules)
transcytosis: the combination of endocytosis, vesicular transport, and exocytosis that transports macromolecules across endothelial cells
venules and veins
veins are more numerous and have a lager volume,
thinner walls and less muscle tissue in comparision to arteries
making the venous circulation the volume resvoir of the circulatory system
angiogenesis
the formation of new blood vessels
not really seen in adult unless wound healing, endurance training, inflammation, tumor growth, and in the endometrium during the menstrual cycle.
promoters and inhibitors
angiogenesis is a necessary part of the process in the progression of cancer
blood pressure
ventricular contraction creates the force necessary to propel blood through the CV system
ventricular contraction pushes the blood into elastic arteries, causing them to stretch.
ventricular relaxation: elastic recoil in the arteries maintains driving pressure during ventricular ventricualr diastole
aorta and larger arteries sustain driving pressure during ventricular diasotle
blood pressure when is it the highest and lowest
highest in the aorta and decreases through the circuit
aortic pressure highest during ventricular contraction (systole): Systolic pressure (120 mm Hg) and lowest during ventricular relaxation (diastole) diastolic pressure 80mm Hg
the difference between the systolic and diastolic pressure is known as the pulse pressure.
in the aorta PP= 120-80
= 40 mmhg
mean arterial blood pressure
how it is calculated
is not simply the average of the systolic and diastolic pressures (100 mm hg) because equal amounts of time is not spent in systole and diastole
cardiac cycle 800ms: 250 ms ventricular systole and 550ms ventricular diastole
MAP= diastolic pressure + 1/3 (pulse pressure)
= 80 mm HG + 1/3 (120-80 mm Hg)
= 93 mm Hg
hypotension
hypertension
hypotension represents when the blood pressure falls too low (<90/60)
this can cause the driving force for blood flow to be inadequate to overcome the opposition by gravity.
hypertension: represents when the blood pressure is elevated ( >140/90)
high pressure on the vessel walls can casue them to become weakned or even rupture
if this occurs in the brain it is called a cerebral hemorrhage and can cause stroke
sphygmomanometer
used to measure blood pressure
a) cuff pressure >120 mm Hg
when the cuff is inflated so it stops arterial blood flow, no sound can be heard through a stethoscope placed over the brachial artery
b) cuff pressure b/w 80-120 mm Hg
korotkoff sounds are created by pulsatile blood flow through the compressed artery
C) Cuff pressure <80 mm Hg blood flow is silent when the artery is no longer compressed
mean arterial pressure
what it is
how periperal resitance and cardiac outpit effect it
is the driving force for blood flow
balance between blood flow into the arteries and blood flow out of the arteries
mean arterial pressure = cardiac output x peripheral resistance
if cardiac output increases and peripheral resistance does not change, then blood is pumped into the arteries faster than it is removed from the arteries, inc volume in arteries= inc arteiral blood pressure
changes in blood volume affect blood pressure
small changes in blood volume occur from ingestion of food and liquids
primarily resolved by kidneys
decrease in blood volume requires an integrated response from the kidneys (urination) and the cardiovascular system (decrease cardiac output or vasodilation) and ingestion of fluid
fast response is CV
slow response is kidneys
increased blood volume leads to increased blood pressure
arteriole resistance is the highest because of the drop of pressure
what alters the arteriolar resistance?
contributes >60% of total resitance to flow in CV system
is influenced by both local and systemic control mechanisms that alter the vascular smooth muscle changing the radius of vessels and greatly influencing resistance:
1) Local control of anterior resistance matches tissue blood flow to the metabolic needs of the tissue.
-in the heart and skeletal muscle, these local controls often take precedence over reflex control by the CNS
sympathetic reflexes mediated by the CNS maintain mean arterial pressure and govern blood distribution for certain homesotatic needs such as temperature regulation
hormones- particularly those that regulate salt and water exertion by the kindeys, influence blood pressure by acting directly on the arterioles and by altering autonomic reflex control
local control
myogenic autoregulation
some vascular smooth muscle has the ability to regulate its own state of contraction, known as myogenic autoregulation.
an inc in blood pressure causes the vascular smooth muscle in the wall of the arteriole to stretch, which causes the smooth muscle to stretch, leading to vasoconstriction
paracrines alter vascular smooth muscle
local control cell signaling of blood flow is important in allowing individual tissues to regulate their own blood supplies.
they affect blood flow to the tissue they are released from the target tissue.
sympathetic control of vascular smooth muscle
beta and alpha
the main determinant of resistance in the majority of arterioles
primarily sympathetic neurons innervate arterioles and tonically control anterior diameter through activation or deactivation of alpha-1 adrenergic receptors (lead to vasoconstriction).
norepinephrine is released from them when inc of sympathetic
if decreased, then there decrease of nonepinephrine
there is a secondary mechanism involving epinephrine from the adrenal medulla in response to sympathetic activation.
is has a low affininty to alpha receptors and high affinity to beta-2 adrenergic receptors, which lead to vasodilation.
more alpha then beta in muscles and more beta than alpha in Gi tract
tachycardia bradycardia
Tachycardia is sympathetic
bradycardia is parasympathetic
baroreceptor reflex
what it is
the primary reflex pathway for homeostatic control of mean arterial pressure is the baroreceptor reflex
baroreceptors are tonically active (sensory neurons), stretch-sensitive mechanoreceptors that are situated on the aorta and on the carotid artery.
when there is an inc of blood pressure, the baroreceptors sense the stretch in the artery walls and increase their firing rate.
decrease blood pressure decrease firing rate
cardiac vascular control center will cause the appropriate response:
inc in MAP there would be dec in cardiac output and dec peripheral resitance, so dec in sympathetic output (less NE) and inc in parasympathetic
there will
dec in MAP inc in sympatheric output (more NE) and dec in parasympathetic output and inc in peripheral resistance and inc in cardiac output
orthostatic hypotension triggers baroreceptor reflex
Every morning when you stand up out of bed, your baroreceptor reflex is highly engaged
cardiac output falls from 5L/min to 3L/min
within 2 heartbeats, baroreceptors increases CO and peripheral resistance to increase MAP
extended bed rest leads to dec in blood volume, when you finally stand up baroreceptor dont work to return Map due to blood loss
other systems influence cardiovascular function
peripheral chemoreceptors located on aoritc arch and cartid artery
sense alterations in blood-gas concentrartions O and CO2
send info back to the control center which results in autonomic output to return blood gas level to normal
the hypothalamus is capable of altering cardiovascular function in repsonse to emotional stress
some individuals faint in response to sudden emotional distress, sight of blood, acute pain, and needle insertion
results in a large inc of parasympathetic output and reduction in sympathetic output
both these combine to a large fall to MAP
bulk flow
absorption
secretion
bulk flow is the mass movement of fluid as the result of hydrostatic or osmotic pressure gradients.
is bulk flow is resulting in fluid moving in the capillaries, its absorption and osmotic pressure
If bulk flow is resulting in the movement of fluid out of the capillaries, it is filtration and hyrdostatic pressure.
capillary filtration and absorption
osmotic pressure steady in the capillary and exceeds the interstial space osmotic pressure
hydrostatic pressure decreases as blood travels through the capillaries due to the resistance encountered and exceeds interstitial hydrostatic pressure.
at the arterial end, hydrostatic pressure exceeds osmotic pressure, causing filtration
at the venous end, osmotic pressure exceeds hydrostatic pressure and there is absorption.
overall there is net filtration resulting in loss of 3L of fluid per day
lymphatics
what it is
lymphatic vessels assist the CV system with returning fluid and proteins lost through the capillaries.
single endothelial cell layer
contain large interendothelial junctions
lymphatics how it works
hydrostatic pressur e
the initial lymphatic segment has the interstitial hydrostatic pressure higher than inside the lymphatic, causing the microvalves to open and fluid to flow in
as it fills up with fluid the lymphatic hydrostatic pressure exceeds interstitial, the microvalves close and secondary valves open
collecting lymphatics contain smooth muscle that actively contract to propel fluid
cardiovascular disease
disorders of the heart and blood vessels, such as heart attacks and strokes, play a role in over 1/3 of the deaths in U.S
risk factors for CV disease include:
uncontrolled risk factors: age, sex, family history of early CVD, genetics
controlled risk factors: cigarette smoking, obesity, sedentary lifestyle
combo of both: diabetes, hyperlipdemia
plasma proteins AGFT
albumins: liver, function: contributes to colloid osmotic pressure of plasma, carries for various substances
globulins: liver and lymphoid tissue, function: clotting factors, enzymes, antibodies, carriers for various substances
fibrinogen: liver, function: forms fibrin threads essential to blood clotting
transferrin: liver and other tissues function: iron transport
blood
connective tissue with cellular elements suspended in the extensive fluid matrix
7-8% total body mass
70ml/kg female 80 for male
hematopoiesis
what it is
production of blood cells
75%white blood cells
25% red blood cells (long life span0
cytokines
what are they?
what do they do
they are released from one cell and affect the growth/activity of another cell
they guide in hematopoiesis.
erythropoiesis: RBC production
leukopoiesis: production of WBC
thrombopoiesis: platelelt production
RBC
what are they
what are their main functions
most abundant
life span is about 4 months
non nucleated
functions
1) carrying O2 from the lungs to the tissues
2)carrying CO2 from the tissues to the lungs
3) buffering of acid and bses
hemoglobin
what is it?
what is their structure
role of iron in it
it is a 02 transport protein
structure is 4 protein chains, centered around a heme group, most common is 2 alpha and 2 beta
each heme group consists of a porphyrin ring with a iron atom in the center
70% of iron in the body found in the heme group
WBC (leukocytes)
what do they do?
what are the 2 main types and their substypes
defend against infection
2 major groups
1) Granulocytes: contain cytoplasmic granules, lifespan <12 hours
neutrophil: most abundant, contain granules with enzymes capable of digesting foreign material (phagocytosis)
eosinophil: granules contain major basic protein, which is toxic to parasites, important in response to virus
basophil: least common, contain histamine, helps in allergic reaction
2) non-granule contiang lymphocytes and monocytes
lymphocytes: two types T-lympocytes and B lymphocytes
T cells: 70-80% of all lymphocytes and responsible for cell mediated immunity does not involved with antibodies.
B cells: responsible for humoral immunity, make antibodies to antigens
monocytes: spend life in peripheral tissues developing into macrophages, which serve two purposes
1) phagocytosis of pathogens or cellular debris
2) Present antigens to lymphocytes.
platelets
what is it?
hemostasis
nucleus-free fragments,
A single megakaryocyte can produce thousands of platelets. 10 day life span
contain 2 special types of granules
dense core granules
alpha granules
essential for hemostasis, the process which keeps blood within a damaged vessel
hemostasis steps
the prevention of bleeding
1) Vasoconstriction: contributes to hemostasis by closing the vessel and preventing blood flow to the damaged region.
can be triggered by direct injury to smooth muscle
brings down the pressure within the vessel so a secure mechanical seal can be applied in the form of a clot
2) platelet plug formation:
inactivated platelets do not adhere to themselves or to the intact endothelial cells that line the vessel.
platelets contain cell surface receptors (integrins)
a breach of the endothelium exposes integrins to collagen, fibronectin, and laminin, which are all part of the subendothelial layer, causing platelets to bind
The binding of integrins causes platelets to release the contents of their granules
