API_Exam 2 Flashcards
what two systems control control contraction and rate
intrinsic
extrinsic
what are causes of alternans
ischemia
myocarditis
digitalis toxicity–purkinje fiber block
what secretes epinephrine and norepinephrine
adrenal medulla
do arterioles need cardiac output to vasoconstrict or vasodilateno
no- operate independently, based on tissue need
how does the bainbridge reflex work
increased volume in atria signals vmc via vagal afferents to increase heart rate/contractility
what beat has alternating amplitudes of qrs currents and why
electrical alternans-
QRS different heights
incomplete intraventricular block
caused by impulses sometimes being blocked and not passing through the purkinje system
caused by ischemia, myocarditis, a dig toxicity
what makes up the instrinsic system
av node
sa node
bundle of his
what can intrinsic system do in the heart
initiate heart beat without any extrinsic impact
why is a heart transplant possible
intrinsic system of the heart- automatic
what still has to occur in the intrinsic system
depolarization and action potential- just doesn’t necessarily need stimulus
what is the order of the intrinsic flow through the heart
sa node-
av node and bundle-
right/left bundle branch-
purkinje fibers
what is the first structure that takes impulse into ventircles
AV bundle
what takes impulse to all parts of the ventricles
left and right purkinje fibers
where does SA node sit
right atrium, top left back portion near where SVC enters
what is the SA node made of
cardiac muscle
what is not found on SA node, internodal pathways, AV node
myofibrils
why is it significant that sa node, internodal pathways, and av node don’t have myofibrils
no contracting abilities
what are the names of the internodal pathways
anterior= most medial
middle= middle pathway
posterior= most lateral
why can internodal pathways conduct action potentials very quickly
no myofibrils
what does internodal pathways spread into and what effect does that have
spreads into muscles
makes conduction instantaneous
what are located between the intercalated disks
gap junctions
what is the significance of gap junctions
lets charge creating action potential to go through easier/quickly
what structure enables whole atrial/ventricle to contract at same time
gap junction
what splits off the anterior internodal and goes to the left atrium
bachmans bundle
what creates contraction of whole left atrium
bachmans bundle
what does bachmans bundle cross through to get to left atria
interatrial septum
why is it significant that bachmans bundle comes off anterior internodal
so left and right atria contract at the same time
what do the internodals come together to form
AV node
what is a distention off the av node
av bundle
what comes off the av bundle
left and right bundle branch
which ventricle is thicker
left
which ventricle has more bundle branches
left
because more muscles
what is the left bundle branch responsible for
depolarization of intraventricular septum
what explains the q wave
depolarization of intraventricular septum by left bundle branch
what direction action potential move through interventricular septum
upwards
what extends off bundle branches
purkinje fibers
what is the flow of action potential through the heart
sa node
internodal pathways
av node
av bundle
left/right bundle branch
purkinje fibers
what is another name for the av bundle
bundle of his
what muscle is the sa node connected to
atrial muscle
why does the sa node act as a pacemaker
low resting membrane potential
-55- -60
higher intrinsic rate 70-80bpm
what is the resting membrane potential of ventricles
-90mv
what it the resting membrane potential of atria
-55
what causes action potential in atria
leaky na channels getting membrane to threshold at -40, then calcium channels open
why is there almost no plateau in atrial contraction
potassium channels open but calcium do not like they do in ventricular ap
why is there no overshoot in atria
not as much influx of sodium and calcium at the same time
what kind of leaky channels does atria have and why is that important
mostly sodium- causes increased rmp at -55
what causes threshold to be met in atria
leaky sodium channels causing mp to hit -40
what happens when mp hits -40 in atria
calcium channels open, action potential
what happens when atrial MP hits 0
potassium channels open
what is the curve at the top of the atrial action potential
Ca channel closing
why doesn’t atria have overshoot in action potential
because Na doesnt overflood
when do leaky sodium channels start having effect during repolarization and what do they prevent
-40mv
hyperpolarization
how does sns primarily increase hr
increases permeability of sodium and calcium channels so action potentials occur quicker
how does pns primarily decrease hr
increases permeability to potassium channels so inside cell is more negative so more calcium/sodium needed to hit threshold, making it harder to get to threshold for action potential
why does there need to be a delay in atria contraction and ventricular contraction and what gives the delay
time for atrium to put blood in ventricle av node, av bundle
what is the delay in the av node, av bundle
av node= 0.09 sec
av bundle= 0.04 sec
sa node delay
0.03
what tissues acts as insulator so charge stays on pathway and doesn’t go back to atrium
atrioventricular fibrous tissue
av node delay
0.09
av bundle delay
0.04
what are the two delay periods that occur and what is total time
1- until you get to atrioventricular fibrous tissue
2-within av bundle
3- 0.12-0.13 seconds
time from the two delay periods that occur and what is the total time
1- until you get to atrioventriculat fibrous tissue
2- within av bundle
3- 0.12-0.13 seconds
time from sa node to start of bundle branch
0.16 seconds
what causes delay through av node-av bundle
less gap junctions- longer for action potential to move
what structure has many gap junctions
purkinje fibers
why does av bundle have one way conduction
atrioventricular fibrous tissue
how long does action potential take to get all the way through the ventricles
0.21
what are the normal rates of discharge
SA- 70-80/min
AV- 40-60/min
Purkinje fibers 15-40/min
why is the SA node the pacemaker
has faster intrinsic rate
what happens in AV block
purkinje fibers pick up pacemaker function
what is the delay in pickup of heartbeat when pacemaker shifts from sa to purkinje in an av block
stokes adams
how long does purkinje take to pick up heartbeat in stokes adams syndrome and what happens during this time
5-20 seconds
syncope
what nerve innervates the SA node and AV node junctional fibers
PNS (vagal)
what neurotransmitter increases potassium permeability and what effect does that have
ach- causes hyperpolarization aka decreased rmp leading to decreased heart rate
what neurotransmitter increased sodium/calcium permeability and what effect does that have
norepinephrine- more action potentials, more sa node discharge, increased conduction, increased heart rate
what is the normal PR interval
0.16 sec
what is the normal QT interval
0.35 sec
what does the p wave represent
atrial depolarization
what does the ECG tell you
electrical conductivity of the heart
what part of EKG represents delay between atrial/ventricle contraction
after p ends and before q
the flat line
what causes spikes on ECG
electrical event caused by action potential
what does qrs represent
ventricular depolarization
what does t wave represent
ventricular repolarization
why is repolarization of atrium hidden
because QRS has greater electrical event so its hidden behind it
when does ventricular contraction happen on ECG
Q to the end of T
what does the p wave immediately precede
atrial contraction
what wave is sometimes not reflected and why
q
discharge from intraventricular septum isnt going straight at probe so its not reflected
what is the magnitude and direction of action potential
vector
what is the axis
the summation of magnitude and direction of action potential
what are the depolarization vs repolarization charges
depolarization= positive charge
repolarization= negative charge
where is the ground lead placed
right leg
what is being read on ECG- electrons impact or direction of electrical charge
direction of electrical charge
what letters on ECG are negative
Q
S
where on ECG is repolarization moving towards a negative pole
T wave
what letter represents large action potential moving toward apex of heart
R wave
what is a R-R interval time
0.83
how do you figure heart beat from R-R interval
60 seconds/0.83= 72
how many chest leads are there
6
which ECG leads are bipolar
1 2 3
which leads are augmented (meaning - and 2+)
aVR
aVL
aVF
what leads give the coronal plane view of the heart?
base to apex, anterior surface
bipolar and augmented leads
what leads look at heart from transverse view (cutting heart in half)
chest leads (precordial leads)
what precordial leads give view of interventricular septum
V1 V2
what precordial leads give anterior view of surface of the heart
V3 V4
what precordial leads give view of left ventricle
V5 V6
where do you put V4
5th intercostal space, mid clavicular line
what does right bundle branch depolarize
right ventricular free wall
what is the direction of magnitude of action potential slightly shifted to the left
left ventricle is thicker which shifts axis to the left
in what direction does action potential go for depolarization of intraventricular septum
left to right
what charge is repolarization
negative
what are the phases of action potential through the heart creating axis
- depolarization of atria- positively charged
- delay phase at av node-av bundle 0.12 seconds
- AV bundle- depolarization of intraventricular septum initiated by left bundle branch going left to right and superior
- depolarization of rest of ventricles (intraventricular septum, left/right ventricular free wall, apex of heart whereaxis is slightly shifted to the left- positive charge)
- depolarization moves up ventricular free walls- axis is moving superiorly towards atrium- positive charge
- all of these yield contraction - repolarization- moving superiorly- negative charge
measuring direction of flow causes
deflection on graph
what are positive/negative direction on ECG
positive= up
negative=down
what does ECG measure
electrical event- each spike is a different event, qrs is only depolarization of ventricle, t wave is only repolarization of ventricle
where is apex of heart pointing toward
left leg
what does lead 1 give view of
across top of heart
explain direction and charge of bipolar leads
1= negative to positive (r to l)
2= negative to positive (r to l downward/diagonal)
3=negative to positive (left side, downward)
how many positive and negative leads do bipolar have
2 neg 1 pos
how many positive and negative leads do augmented have
2 neg 1 positive
what are the negative poles in aVF
top
where are the negative pole in aVR
both left side
where are the negative poles in aVL
one side right, one bottom left
what does the last letter tells you in the augmented leads
where to put the positive lead
L= left arm
R= right arm
F= left foot
what are the angles in augmented leads near the positive pole
30 and 30= 60 total
what view do bipolar and augmented leads give
frontal view
aka coronal view
what lead creates an inverted wave and why
avr-
p wave/qrs/t inverted because positive lead is on right arm
what determines the wave
axis
summation of direction
what are chest leads looking at
transverse section of heart
where do you put V1
4th intercostal space, right side of sternum
where do you put V2
4th intercostal space, left side of sternum
where do you put V4
5th intercostal left midclavicular line
where do you put V3
between V2 and V4
where do you put V5
5th intercostal space, left medial axillary line
where do you put V6
5th intercostal space, left midaxiallary
which leads are in cabreras circle
augmented and bipolar
where does apex of heart point on Cabrera’s circle
59 degrees
which lead points closest to where the apex of the heart points
lead 2, 60 degrees
what is in the center of the Cabreras circle
heart
why is QRS so big
strong summation because of the thickness of the ventricles
what is happening during lag time between S and T
waiting for repolarization
what lead has smaller r wave and why
aVL
depolarization isnt moving directly towards positive pole
what do magnitude of waves depend on
direction of axis flow to charge
what wave do you plot on cabreras circle to determine significance of axis
qrs wave
what is a normal axis deviation
between -30 to 90
what is it called when axis falls between -30 to -90
left axis deviation
what is it called when the axis falles within 90 to 180
right axis deviation
what is it called when axis falls within -180 to -90
extreme axis deviation
what lead do you look at if lead 1 QRS is positive
lead 2
what lead do you look at if lead 1 QRS is negative
aVF
what degrees do you shade if lead 2 has positive QRS
-30 to 150
what degrees do you shade if lead 1 has positive QRS
-90 and 90
what degrees do you shade between if aVF is negative
0 to -180
what is the largest axis and therefore the biggest influence
ventricular depolarization
when looking at ECG why is QRS of primary concern
represents ventricular depolarization which is the largest axis
what is an example of left axis deviation
left ventricular hypertrophy
what deviation occurs when lead 1 is negative and aVF is negative
extreme axis deviation
what deviation occurs when lead 1 QRS is positive and lead 2 is negative
left axis deviation
what deviation occurs when lead 1 QRS is negative and aVF is positive
right axis deviation
what are causes of cardiac arrhythmias
-abnormal rhythmicity of pacemaker shift from sinus node
-blocks at different points in cardiac impulse
-abnormal pathways of transmission in heart
-spontaneous generation of abnormal impulses
what happens when SA node is blocked
no P waves
what does incomplete heart block mean
occasions when it is blocked temporarily
what are the incomplete heart blocks
first degree AVB
second degree AVB
what is normal PR interval
0.16 sec
what is a first degree AVB
PR interval greater than 0.20 seconds
what does PR interval rarely get above
0.45 sec
what has PR interval between 0.25-0.45 sec
2nd degree heart block
what happens in 2nd degree heart block type 1
longer longer drop
lengthened PR interval until QRS is dropped
what happens in second degree type II
multiple p waves with QRS, more skipped, more serious
same long PR interval, and dropped QRS
what is beating faster in 2nd degree AVB
atria faster than ventricles
what is a total block through the AV node or AV bundle
3 degree heart block
complete heart block
what block is the p wave completely dissociated from QRST complex
3rd degree block
in what heart block can stokes adams occur
3rd degree heart block
what causes fainting in stokes adams
ventricles stop contracting for 5-20 seconds because of overdrive suppression, faints because of poor cerebral blood flow until purkinje kicks in
what is provided for stokes adams patients
RV pacemaker
what is happening to SA node in 3rd degree block
firing as normal but impulse cannot get through
SO atria beats independently of ventricles
what block is a incomplete interventricular block
electrical alternans
where does electrical alternans occur
impulse conduction in peripheral portion of ventricles in purkinje system are blocked
what happens in electrical alternans
impulse is sometimes blocked and sometimes not causing some smaller qrs waves -effects sodium-potassium channels
during PACs, what happens to PR interval and P wave
shortened, may be inverted
what happens to impulse in PACs
travels from sa node to av node and then back to sinus node causing another discharge before-atrial-filling
what can cause PACs
toxins
calcifications
ischemia of nodes
what happens to QRS in PVC and why
TALL AND PROLONGED because impulse is conduction through slow muscle tissue instead of purkinje fibers
what happens in the ventricles with PVCs
one depolarizes before the other
what happens to t wave in PVC
inverted
what can cause PVCs
cigarettes
coffee
lack of sleep
what is long qt syndrome caused by and what can it lead to
mutations in Na and potassium channels, torsades
what does torsades de pointe
twisted point
premature depolarization
what can torsades lead to
vfib
what happens to parts of ventricle during vfib
some parts of muscle contract while others are relaxing
no blood flow
what can overwhelm vfib
electrical shock to depolarize ventricle at one time
why can you live with afib
80% of total blood volume from atria to ventricles falls in by gravity
what is the most frequent cause of afib
atrial enlargement due to AV valve dysfunction
why do cardiac arrests occur
hypoxic conditions preventing muscle/conductive fibers from maintaining electrical gradients–DEEP ANESTHESIA
where does blood accumulate in afib and how can you treat it
left atrial appendage
remove appendage or watchman (umbrella)
what heart rate can hypovolemia lead to
tachycardia
what nerve stimulation can cause bradycardia
vagus nerve
what can carotid sinus syndrome cause and why
bradycardia
sensitive baroreceptors
what causes sinus arrythmias
respiration
what is a normal PR interval
0.12-0.20 seconds
in 3rd degree block, why do QRS complexes occur unsynchronized with p waves
av node is trying to take over as pacemaker while sa node is also still firing- both are firing independently of each other
what is ventricular escape and when does it occur
av node is not stimulated by sa node, before av node starts acting as ectopic pacemaker, there is no ventricle contracting because of no signal so syncope occurs and then av node kicks in- stokes adams
what can cause and is associated with electrical alternans
tachycardia
what is a pulse deficit
ventricles cannot fill during PAC/PVC so stroke volume is decreased/absent
what is missing from ecg or occurs after qrs during av node premature contraction
p wave
where does impulse originate during AV node PVC
AV node
what are 3 characteristics of PVC
1- qrs is considerably prolonged (impulse is through slow muscle rather than purkinje)
2- qrs complex is high
3- inverted t wave
what is another name for long QT syndrome and what causes it
torsades de pointes- premature depolarization- can lead to death
what is it called when ventricle does not repolarize well because of tissue death and causes ST elevation
STEMI
what are inverted T waves indicative of
ischemia, most commonly caused from MI
why do MIs usually impact T wave
tissues will not repolarize as well because of ischemia or necrosis
how much blood is in pulmonary circulation
9%
how much blood is in heart
7%
how much blood is in arteries
13%
how much blood is in arterioles and capillaries
7%
what are major functions of circulatory system
transport nutrients to tissues
transports waste away from tissue
transport hormones tissues
difference between endocrine vs exocrine
endocrine= gets in blood
exocrine=impacts neighboring cell
how much blood does veins, venules, and venous sinuses have
64%
where is body reservoir of blood
veins
what transports blood through high pressure side to get to capillaries
arteries
average heart chamber pressures
ra= 5
rv= 24
la= 8
lv=130
aorta= 120/80
what side of the heart is the high pressure side
left
how do arterioles control blood flow
constrict or dilate
what vascular structure is a major contributor to regulation of BP
arterioles
where is the site of water and solute exchange between vessels and tissues
capillaries
what component of circulation has largest total surface area
capillaries
what part of vasculature has highest velocity
aorta > arterioles > small veins > capillaries
why does pressure decrease in capillaries, venules, veins
because there are so many more of them
large fire hose being connected to 3 smaller= decreased pressure
why is venous pressure so low
veins are distendable
what is blood flow controlled by
tissue needs
exercise=increase tissue needs=increased HR
what is controlled independent of local blood flow or cardiac output control
arterial pressure
what is controlled by local tissue flow
cardiac output
more need=more cardiac output
what 4 ways is arterial pressure controlled by
1- increased force of heart pump
2- contraction of large veins
3. generalized constriction of arterioles
4. long term renin made by kidneys
what do arterioles do when tissue needs more blood flow/less blood flow
dilates- irrespective of co and blood flow
constricts- also irrespective
what do walls of blood vessels create
resistance
because of resistance how does this effect shape of blood flow through vessel
parabolic- arched, blood closest to walls is slower than blood in middle of vessel
what does aortic valve stenosis do and how does it impact flow
increases resistance, decreases flow
what kind of flow is a bruit
turbulent
what can bruit aka turbulent flow cause
damage to intima (inside) vessel, which fills with cholesterol creating plaques creating clots
what organs have the most flow by percent (top 3)
liver
kidney
brain
what is flow through a blood vessel determined by
pressure difference/resistance
what are some causes of turbulent flow
high velocity
sharp turn
rough surfaces
rapid narrowing of blood vessels
what does turbulent flow tend to cause
murmurs or bruits
what does turbulent flow increase
wall stress on vessel
what is measure of blood flow through a vessel for given pressure difference
conductance
larger conductance=smaller resistance
does resistance increase or decrease in capillaries
increase
how does change in hematocrit/viscosity change blood flow
increased viscosity= decreased flow (polycythemia)
decreased viscosity=increased flow (anemia)
what is distendability
ability to stretch
what is compliance
pressure needed to make stretch increased compliance=decreased pressure needed
what is capacitance
volume to cause stretch (capacity)
how many times more distend able are veins than arteries
8x
what kind of muscle is in the artery and where
smooth muscle in media
why can veins not contract as much as artery
smaller, less defined media
why isnt artery as distendable as vein
more defined media
what does artery being less distendable cause
higher pressure
what is vascular capacitance
the total blood that can be stored in given portion of circulation
how much more capacitance do veins have than arteries
24x
veins hold more blood in circulation
what happens to cardiac output when veins contract
increased volume to heart
what is only system that has impact on circulation and heart
SNS
what system only has impact on the heart
PNS
what is tone
constant degree of SNS stimulation in circulation
how do you cause dilation in vessels
inhibit SNS
formula for pulse pressure
systolic-diastolic
why does pressure and therefore speed have to fall in capillaries
to give time for nutrient/co2 exchange
factors that affect pulse pressure
stroke volume
arterial compliance-inverse peripheral resistance
cardiac output
what increases pulse pressure
arteriosclerosis
PDA
aortic regurg
what can decrease pulse pressure
aortic stenosis
how does PDA increase pulse pressure
shoots blood into aorta from pulmonary artery which increases volume increasing systolic
how does aortic regurg increase pulse pressure
aortic valve doesn’t close all the way, blood leaks back into left ventricle
how does aortic stenosis decrease pulse pressure
valve opening is smaller reducing flow of blood
what is pressure in superior sagittal sinus
-10mmhg
what keeps blood from pooling in legs
valves
why do varicose veins occur
+90 pressure is building against valve until it folds in and fluid pools in veins- comes from standing
factors that increase right atrial pressure
increased blood volume
increased venous tone
dilation of arterioles
decreased cardiac function
what are the needs of tissues
delivery of oxygen, glucose, amino acids
removal of carbon dioxide/hydrogen/waste
transport hormones
what 3 factors/systems control blood flow
1- tissue demand
2- neurological system (short term)
3- hormones (long term)
when you have an immediate need for blood flow/pressure adjustment, what responds
neurological system (short term)
what makes long lasting changes in blood pressure in 1-3 days
hormones (renin)
increased number of vessels
size of vessels
what is the growth of new blood vessels
angiogenesis
what causes angiogenesis
increased oxygen demand for sustained period of time
scar, tumor
what is it called when vessels stop growing in retina when premature baby is in o2 chamber, then overgrow once taken out of o2 chamber and cause blindness
retrolental fibroplasia- can cause blindness
what causes angiogenesis
ischemic tissue
rapidly growing tissue (tumors)
tissue with high metabolic rates
what vasoconstrictors control blood flow
norepinephrine and epi
angiotensin II (always vasoconstrict)
vasopressin
Endothelin
what vasodilators control blood flow
bradykinin
serotonin
histamine
prostaglandins
nitric oxide
what does norepi always do
vasoconstrict
what can epi do that norepi cannot
vasodilate
what does the alpha 1 receptor do
vasoconstriction
what does beta 1 receptor do
increase heart rate
beta 2 action
dilates vessels and airway
what does epinephrine do to coronary arteries
vasodilation
targets beta 2 receptors
what is endothelin
inside all vessels and when it gets traumatized causes vasoconstriction
what is a very potent vasoconstrictor
vasopressin
what causes vasodilation to get blood and neutrophils to tissue
bradykinin,
histamine,
prostaglandin
how does nitric oxide affect rbc’s
helps make oxygen more soluble to get out of RBC and into tissue
how does nervous system regulate circulation
redistribute blood flow
increasing pumping activity of heart
rapid control of arterial pressure
regulates via ans
where are baroreceptors found
carotid sinus
aortic arch
right atria
does PNS cause vasodilation
NO
it inhibits the SNS system
what PNS nerve slows down heart rate
vagus nerve
does SNS increase contractility of heart
YES
what structures vasoconstrict and vasodilate
arterioles
why do capillaries not constrict
velocity of blood needs to be low for nutrient exchange
what stimulates the large veins and the heart
SNS
where are SNS vasoconstrictor effects of fibers less potent
cerebral and coronary
where are there more vasoconstrictor fibers
kidney
gut
spleen
skin
what increases with increased venous constriction
cardiac output= increased preload
where is VMC located
medulla(reticular)
lower 1/3 of pons
what is the VMC composed of
vasoconstrictor area
vasodilator area
sensory area
what stimulated vasomotor tone
vasocontrictor area of VMC
continuously transmits signals
what part of VMC causes increased heart rate and contractility
lateral portions
what can cause excitatory/inhibitory effects on VMC
hypothalamus
what part of VMC transmits signals via vagus nerve to heart and what does this signal do
medial
decreases heart rate
what vessel can epi dilate and with what receptor
coronary artery
beta 2
what happens in vasovagal syncope
excitement/stress: stimulates blood vessels to dilate and-vagalcenter-signals-decrease-in-heart-rate= no blood flow to brain= syncope
what is increased/decreased SVR
constriction or dilation of peripheral vessels
how does VMC increase arterial pressure
-constrict arterioles of body to increase svr
-constrict large vessels to increase venous return/cardiac output
-direct increase of co by increasing hr and contractility
what occurs with arterial constriction
venous constriction to keep blood at level cardiac output
nervous system control of arterial pressure
exercise-> vmc-> increase sns/decrease pns-> increased svr/venous return/hr/heart strength= increased arterial pressure
what are baroreceptors important in
short term regulation of arterial pressure
what are baroreceptors sensitive to
stretch
changes in pressure
what nerves do baroreceptors send messages through in carotid artery
hering nerve to glossopharyngeal nerve to vmc
what nerves do baroreceptors utilize to regulate blood pressure in aortic arch
vagus nerve
what are carotid bodies sensitive to
chemicals aka chemoreceptors
do baroreceptors or carotid bodies drive BP
baroreceptors
when is baroreceptor reflex most sensitive
100mmhg
when do carotid baroreceptors respond to change in pressure
60-180 mmhg
pressure increases, so the number of impulses from carotid sinus baroreceptors increases leading to:
inhibition of vasoconstrictor activation of vagal center
how do we maintain consistency in blood pressure
baroreceptors
where are carotid bodies found
carotid bifurcation and aortic arch
what chemicals do chemorecptors sense
lack of O2
CO2 excess
H+ excess
can you see carotid bodies
NO
at what pressure are chemoreceptors stimulated and what does it do when stimulated
below 80mmhg
stimulates VMC
what is the flow of chemoreceptors in carotid bodies
decreased oxygen, increased co2, low ph->chemoreceptors–>vmc–>increase sns= increase bp/resp rate
when is CNS ischemic response activated
cerebral ischemia
what is one of the most powerful activators of sympathetic vasoconstricor
CNS ischemic response
what triggers CNS ischemic response
reduced blood flow causes increased co2 which stimulates vmc to increase art pressure
when is cns ischemic response triggered
60mmhg
greatest at 15-20 mmhg
what happens in the cushing reaction in cns ischemic resonse
csf pressure increases–>collapses brain vessels–>sns reponse–>increased bp/hr to open up vessels in brain
what is activated when venous return increases to right atrium and therefore sa node
baroreceptor response from stretch- increases heart rate to pump blood out
what nerve does the baroreceptors in the right atria transfer signals to brain
vagus afferents (not really on vagus, hitches a ride)
How does atrial natriuretic peptide work?
released by overstretched heart cells in right atria
stimulates kidney to excrete sodium and therefore water
what are the ways right atria contributes to bp regulation
1- baroreceptors- sense stretch
2- anp- stimulates increased na/water excretion
3-decreases renal flow/actvity-increased na/water excretion
4-bainbridge reflex- senses pressure, afferents, vmc, increase hr/contractility
what happens to GFR with vasoconstriction
decreases
what prevents damming of blood in veins, atria, ventricle, and pulmonary circulation
bainbridge reflex
what is the bainbridge reflex
when atrial pressure increases, heart rate increases
what are short and long term regulations of increased atrial pressure
long term= atrial natriuretic peptide
short term=bainbridge reflex
how long do kidneys take to impact pressure control
24-72 hours
when arterial pressure/ecfv increases, how do kidneys react
increased sodium excretion
how much of the body is water
60%
what is difference between natriuresis and diuresis
nat=get rid of na and water
diuresis=get rid of water
do changes in svr affect long term arterial pressure
no- kidneys will respond before then
how does ecfv (extracellular fluid volume) increase affect svr graph
decreases at first to make room, then increases
what is autoregulation in capillary
slows down blood (increase peripheral resistance) to let exchange of nutrients happen even with increased cardiac output
bp vs blood flow
pressure increases with decreased radius= bp, constriction
blood flow= decreases with decreased radius
what controls cardiac output
heart rate
contraction
preload
afterload
what happens to resistance in aortic stenosis
increased resistance, decreased cardiac output, increased blood pressure due to calcium build up
what happens when you try to push same volume of fluid through a smaller hole than normal
increased pressure
what is it called when blood builds up in ventricles because of aortic stenosis
increased afterload
how do you increase/decrease afterload
vasoconstrictors/vasodilations
what makes angiotensinogen and how often
liver
makes it all the time
what produces renin and when
kidney- decrease in bp or ecf (really senses decreased gfr)
increased urine na+
what can angiotensinogen do by itself
nothing
what makes angiotensin 1
angiotensinogen and renin
where is angiotensin converting enzyme produced and when
lungs (alveoli)- produced all the time
where in kidney is renin produced
juxtaglomerular cells
what does angiotensin 1 do by itself
nothing
how is angiotensin II made
angiotensin 1 + ace
what is GFR
pressure required to push blood through kidney
what are the two roles of angiotensin II
1- potent vasoconstrictor by itself
2- stimulates release of aldosterone from adrenal cortex which tells kidney to save sodium and thus water increasing blood volume and bp
what is the only thing more potent than angiotensin II
vasopressin aka adh
where is aldosterone released from and what stimulates its release
adrenal cortex- angiotensin II
what is most common se of ace inhibitor
cough- since it is produced by lungs
what does ace inhibitor do
inhibits binding of ace- so ace is still made and builds up in lungs causing cough
what happens to sodium on ace inhibitors
more excreted through urine since aldosterone isn’t released to stimulate sodium retention
how do arb’s work and what does it not have
angiotensin II receptor blocker- cough side effect
why is using the raas system to control blood pressure preferable
not directly affecting heart so patient can still have good activity levels
what system is important in maintaining normal arterial pressure during changes in na intake
raas
what do renin levels fall to when sodium intake is increased
near 0
when do renin levels increase in relation to Na intake
renin increases when sodium intake decreases
what factors decrease renal excretion and increase bp
1- angiontensin II
2- aldosterone
3- sns activity (vasoconstriction=decreased blood flow)
4-endothelin
what kind of receptors do skeletal muscles have to get more blood flow
beta 2- so vessels dilate to get more blood flow to them
when you exercise, your heart rate increases so you need more blood, where does it come from and how
venous system- vasoconstriction of veins
what factors increase renal excretion and reduce bp
1- atrial natriuretic peptide (excess volume in atria triggers sodium excretion in kidney)
2- nitric oxide
3- dopamine
what drives cardiac output and pressure
tissue demand/metabolic needs
what is prehypertension
120-139/80-89
what is hypertension
greater than 140/90
what is stage 1 hypertension
140-159/90-99
what is stage 2 hypertension
160 or greater/100 or greater
what can increased bp for long periods do to kidneys
decreases filtering ability of kidney
what are ischemic vs hemorrhagic strokes
ischemic= blockage, clot
hemorrhagic- broken vessel, blood leaks out
how many hypertensive patients have primary hypertension and what causes it
90% unknown
how many people with primary hypertension are overweight
2/3
meds for HTN
ace inhibitors
arbs
diuretics
beta blockers
ccb
what anti htn meds do you want to start with
least amount and most natural and then progress to beta blockers and ccb
what determines cardiac output
muscle mass/tissue mass-
peds have increased tissue needs so they have increased hr to increase co
when happens to co as you get older
lose muscle mass= cardiac output needs decrease
does peripheral circulation or heart control cardiac output
peripheral circulation
what is cardiac output proportional to
tissue oxygen use/demand
svr
what does increased right atrial pressure cause in venous system
decreased venous return
when does right atria decrease venous return
when right atrial pressure is higher than veins coming to it
so higher right atrial pressure=lower venous pressure
when volume of blood is increased in right atrium, what happens to cardiac output
increases
what happens to cause cardiac output graph to be hypoeffective
decreased heart ability to pump
stenosis,
valvular disease,
tamponade
what happens to cause cardiac output graph to be hypereffective
1- increase sns/decrease pns
2-hypertrophy (pumps harder, more often)
does hypertrophy of heart have to be pathological
no can be in healthy people that exercise a lot
how does aortic stenosis affect cardiac output
decrease it
what causes normal sinus arrythmias
breathing
what happens to intrapleural pressure during breathing
inhale= increases pressure
exhale=decreases pressure
how does copd affect heart
increased pressure in lungs decreases cardiac output
how does ipp above 0 affect heart
increase pressure on right atria
what is fluid collecting in pericardial sac that increases pressure on heart
tamponade- atria/ventricle cannot fill with blood
how would blowing out on trumpet affect cardiac output
decreased cardiac output because of increased pressure
what is the pressure in the system when heart isn’t pumping or pressure required to fill the system
mean systemic filling pressure
what is normal MSFP
7
when right atrial pressure is low, venous return is high, as right atrial pressure increases due to venous return, venous return decreases. When does venous return stop decreasing
msfp of 7 mmhg
equilibration of venous return and right atrial pressure
when right atrial press increases….
venous return decreases
how does right atria influence cardiac output
amount dumped into right atria from veins determines cardiac output- first portion of co
what happens to msfp when right atria resistance is increased/decreased
decreased/increased- inverse
if sns is decreased what impact does it have on veins
increases venous compliance
what does spinal anesthesia do to sympathetic chain ganglion
suppresses them, so decreases sns response, decreases cardiac output
what is long term blood pressure balancing system
kidneys- raas
what is short term blood pressure balancing system
neurological system
how many ml’s go out of left ventricle per beat
72cc’s- stroke volume
what is stroke volume equation
Esv-edv
normal= 120-50= 70
70/120=58%= ejection fraction
what is volume left in ventricle after contraction and what happens when it is increased
afterload- decreased cardiac output
what does pns do to heart rate
decrease heart rate
what happens to co when right atrial pressure increases
increases- atria is pushing more blood through
when does venous return happen to right atria
diastolic phase
when right atrial pressure decreases, when happens to venous return
increases
i.e. during diastolic phase, right atrial pressure decreases because it pumps out all of it’s blood, so venous fills it
what happens to increase or decrease venous return
increase= venous constriction
decrease= blood loss
what is msfp
pressure required to bring venous return to 0
what are some causes of tachycardia
(1) exercise
(2) increased body temperature
(3) sympathetic stimulation (such as from loss of blood and the reflex stimulation of the heart),
(4) toxic conditions of the heart.
what is bradycardia
means a slow heart rate usually less than 60 beats/min.
Ex: athletes who have a large stroke volume, excessive vagal stimulation (e.g., carotid sinus syndrome)
Impulses through A-V node and A-V bundle (bundle of His) are slowed down or blocked due to
-ischemia of A-V nodal or A-V bundle fibers (can be caused by coronary ischemia).
-compression of A-V bundle (by scarred or calcified tissue).
-A-V nodal or A-V bundle inflammation.
-excessive vagal stimulation.
-excess digitalis.
characteristics of complete heart block
-Total block through the A-V node or A-V bundle
-P waves are completely dissociated from QRS-T complexes.
-Ventricles escape and A-V nodal rhythm ensues.
characterstics of first degree heart block
-Normal P-R interval is 0.16 sec.
-If P-R interval is >0.20 sec, first-degree block is present (but P-R interval seldom increases above 0.35–0.45 sec).
characteristics of 2nd degree heart block
-P-R interval increases to 0.25–0.45 sec.
-Some impulses pass through the A-V node and some do not thus causing “dropped beats.”
–Second-degree Mobitz Type I (Wenckebach)—has increasing P-R interval then a dropped beat.
–Second-degree Mobitz Type II—has fixed long P-R interval then a dropped beat
-Atria beat faster than ventricles.
characteristics of stokes adams syndrome
-Complete A-V block comes and goes.
-Ventricles stop contracting for 5–30 sec because of overdrive suppression meaning they are used to atrial drive.
-Patient faints because of poor cerebral blood flow.
-Then, ventricular escape occurs with A-V nodal or A-V bundle rhythm (15–40 beats/min).
-Pacemakers are needed for these patients.
incomplete intraventricular block (electrical alternans)
-Impulse is sometimes blocked and sometimes not in peripheral portions of Purkinje system resulting in abnormal QRS waves.
-Can be caused by ischemia, myocarditis, and digitalis toxicity
PAC characteristics
-P-R interval is shortened if ectopic foci originating the beat are near the A-V node.
-The impulse travels through the A-V node and back toward the sinus node causing discharge of the sinus node.
-Next sinus discharge will thus be late.
-An early contraction does not allow heart to fill with blood causing a low stroke volume and a weak radial pulse.
PVC characterstics
-QRS is prolonged because impulse is conducted through muscle which has slow conduction.
-QRS voltage is high because one side depolarizes ahead of the other.
-P is absent. QRS is wider and taller. T shows opposing polarity to QRS.
characteristics of atrial paroxysmal tachycardia
-Paroxysmal means a series of rapid heartbeats suddenly start and then suddenly stop.
-Can be stopped with a vagal reflex or drugs
-P wave is inverted if origin is near A-V node.
-Occurs by re-entrant pathways
what can ventricular paroxysmal tachycardia lead to
vfib or vtach
what are causes rentry vfib
-Pathway around the circle is too long (e.g., dilated heart)
-Velocity of conduction is decreased (block, ischemia, high potassium)
-Refractory period is shortened (sympathomimetics, ischemia)
characteristics of vfib defibrillation
1000 volts direct current is applied for a few milliseconds.
All parts of the heart become refractory and remain quiescent for 3–5 seconds until new pacemaker is established.
If used later than one minute after fibrillation, the heart is too weak to defibrillate and may have to be hand-pumped.
how does afib effect the heart efficiency
efficiency is decreased by 20-30%
characteristics of a flutter
-Single large impulse wave travels around atria in one direction
-Atria contracts at 200–350 beats/min.
-A-V node will not pass signal until 0.35 sec elapses after the previous signal.
-Therefore, atria may beat 2 or 3 times as rapidly as the ventricle.
characteristics of cardiac arrest
-Usually occurs due to hypoxic conditions in the heart which prevents muscle and conductive fibers from maintaining their electrolyte gradients
-Unconsciousness after 4–5 seconds
-Fatal after 1–3 minutes if ventricular fibrillation or asystole is not reversed.
-Brain damage if circulatory arrest prolongs over 5 minutes
describe vectorial analysis of ecg
-The current in the heart flows from the area of depolarization to the polarized areas (from − to +).
-The electrical potential generated can be represented by a vector, with the arrowhead pointing in the positive direction.
The length of the vector is proportional to the voltage of the potential.
The generated potential at any instance can be represented by an instantaneous mean vector.
The normal mean QRS vector is about 59 degrees.
draw lead angles
why is axis of lead I zero degrees
because the electrodes lie in the horizontal direction on each of the arms
why is axis lead II +60 degrees
because the right arm connects to the torso in the top right corner, and left leg connects to the torso in the bottom left corner.
what is the axis lead III
120 degrees.
what is the axis of aVR
210 degrees
what is axis of aVL
-30 degrees
what is axis of aVF
90 degrees
where should p wave be positive
Begins at sinus node and spreads toward A-V node.
This should give a + vector in leads I, II, and III.
characteristics of ventricular repolarization
First area to repolarize is near the apex of the heart.
Last areas, in general, to depolarize are the first to repolarize.
Septum and Endocardium: first to depolarize—last to repolarize—longer contraction
Outer surface of ventricles: last to depolarize—first to repolarize
Repolarized areas will have a + charge first; therefore, a + net vector occurs and a positive T wave.
why can you not see atrial t wave
Cannot be seen because of QRS complex.
Atrial depolarization is slower than in ventricles, so first area to depolarize is also the first to repolarize, giving a negative wave in leads I, II, and III.
what can cause left axis deviation
Changes in heart position: left shift caused by expiration, lying down, and excess abdominal fat.
Hypertrophy of left ventricle (left axis shift) caused by hypertension, aortic stenosis, or aortic regurgitation causes slightly prolonged QRS and high voltage.
what can cause right electrical axis deviation
Hypertrophy of right ventricle (right axis shift) is caused by
pulmonary hypertension,
pulmonary valve stenosis, and
interventricular septal defect.
All cause slightly prolonged QRS and high voltage.
characteristics of LBBB
QRS is prolonged (> 0.12 sec).
Lead V1 has a wide negative S wave’.
Lead V6 has a “rabbit ear” pattern.
characteristics of RBBB
QRS is prolonged (> 0.12 sec).
Lead V1 has a positive secondary R wave.
Lead V6 has a slurred terminal S wave.
what can cause increased voltages in bipolar limb leads
Most often caused by increased ventricular muscle mass
(e.g., hypertension, marathon runner, aortic or pulmonary valve stenosis).
characteristics of decreased voltage limb leads
Cardiac muscle abnormalities (old infarcts causing decreased muscle mass, low voltage EKG, and prolonged QRS).
Conditions surrounding heart (fluid in pericardium, pleural effusions, emphysema).
Anterior–posterior rotation of apex of heart.
what is usually the cause if the QRS > 0.12 seconds
usually a conduction block
what is the usual cause of prolonged QRS
caused by delayed conduction of cardiac impulse through ventricles
One cause is cardiac hypertrophy.
One cause is a Purkinje system block.
what can unusual QRS be caused by
local conduction blocks which may cause multiple QRS peaks.
what kind of charge does injured muscle emit
negative charges throughout each heartbeat
describe current of injury
Damaged cardiac muscle remains partially or totally depolarized all the time (goes from injured—negative end—to healthy area)
what are some causes of current of injury
(1) local ischemia,
(2) mechanical trauma,
(3) infection.
what indicated an anterior lesion infarct
If the current of injury in the chest lead is negative, the chest lead is in an area of negative potential which indicates an anterior lesion.
what indicated a posterior lesion infarct
If the current of injury in the chest lead is positive, the chest lead is in an area of positive potential which indicates a posterior lesion.
Bipolar and augmented unipolar leads help to further determine the injured area of the heart.
when would a Q wave develop
A Q wave may develop and represent the “scar” on myocardial muscle after infarction.
The lead/leads that show the Q wave help to identify the location of the scar.
T wave abnormalities of
Ventricular repolarization usually occurs in the opposite direction as depolarization which causes an upright T wave in the three standard leads.
Prolongation of repolarization may change the T wave axis and morphology (flattened, taller, biphasic, inverted).
Examples: Right or left bundle branch blocks, ischemia, digitalis toxicity, changes in K+.
how does SA node act as a pacemaker
Acts as pacemaker because membrane leaks Na+ and membrane potential is −55 to −60mV.
The constant leak of Na+ makes resting potential to gradually rise
when are fast Na channels inactivated
at -55mv
when do slow Na Ca channels open causing an action potential
-40mv
when do Ca channels close and K channels open more
after 100-150msec
helps return membrane potential to -55mv
which internodal pathway carries impulses to left atrium
anterior interatrial band
what is the action of the AV node
Delays cardiac impulse
Delay A-V node—0.09 sec.
Delay A-V bundle—0.04 sec.
what is the transmission time between AV bundles and last of ventricular fibers
0.06 sec (QRS time)
what is the only conducting path between atria and ventricles
AV node and left/right AV bundles
characteristics of purkinje system
Fibers lead from A-V node through A-V bundle into ventricles.
Fast conduction; many gap junctions at intercalated disks
describe cardiac impulse timing
what is ectopic pacemaker
A portion of the heart with a more rapid discharge that surpasses the sinus node
Also occurs when transmission from sinus node through the A-V node is blocked (A-V block).
Sinus node discharge does not get through, and next fastest area of discharge becomes pacemaker of the heart.
New pacemaker is in AV node or penetrating part of AV bundle.
If that region fails, Purkinje fibers take the lead (but at lower rate).
where does PNS nerves innervate
SA node and AV junctional fibers proximal to AV node
what is PNS effects on heart
Acetylcholine decreases SN discharge and excitability of A-V fibers, slowing the heart rate.
Cause hyperpolarization because of increased K+ permeability in response to acetylcholine (increased negativity inside)
This causes decreased transmission of impulses maybe temporarily stopping heart rate.
Ventricular escape occurs.
SNS nerves effect on heart rate
Releases norepinephrine at sympathetic ending
Causes increased sinus node discharge
Increases rate of conduction of impulse
Increases force of contraction in atria and ventricles
how does norepinephrine effect heart
Norepinephrine increases permeability to Na+ and Ca+, causing a more + resting potential, accelerating self-excitation, and excitability of AV fibers.
what is a normal QT interval
0.36 sec
(0.36–0.40, QTc ≤ 0.46) and is the duration of time from the beginning of the Q wave to the end of the T wave
where does ventricular depolarization start
at the ventricular septum and the endocardial surfaces of the heart
describe lead I - and + terminals
The negative terminal of the EKG is connected to the right arm,
the positive terminal is connected to the left arm.
describe lead II - and + terminals
The negative terminal of the EKG is connected to the right arm,
the positive terminal is connected to the left leg.
describe lead III - and + terminals
The negative terminal of the EKG is connected to the left arm,
the positive terminal is connected to the left leg.
what is Einthovens Law
the electrical potential of any limb equals the sum of the other two (+ and − signs of leads must be observed).
If Lead I = 0.5 mV
and Lead III = 0.7 mV
Lead II = 0.5 + 0.7 = 1.2 mV.
positive lead flow going toward negative lead=
negative deflection on ECG
negative lead flow going toward positive lead =
positive reading on ECG
a negative pole flow going towards a negative pole =
positive reading on ECG
what leads look at the interventricular septum on ECG
V1 and V2
what leads give you frontal view of the heart
V3 and V4
what leads give you a left side view of the heart
V5 and V6
what are the major functions of the circulatory system
-transporting nutrients to the tissues
-transporting waste products away from the tissues
-transporting hormones
what are the two circulatory systems
pulmonary circulation
systemic circulation
what is the function of arteries
transports blood to tissues under high pressure (100mmHg)
what is the function of arterioles
-control site for blood flow
-major site of resistance in circulation
what is the function of capillaries
major site of water and solute exchange between blood and tissues
what is the function of large veins and venules
returns blood to the heart under low pressure
serves as s reservoir of blood
what is the function of pulmonary circulation
site of oxygen and carbon dioxide exchange
what is the largest component of circulation (vessel wise)
capillaries
what is the purpose of capillaries
allow for reduced pressure and velocity to allow for gas and nutrient exchange
define velocity
blood flow is the speed at which blood flows in the circulation
velocity of blood flow= blood flow/ cross-sectional area
what happens when blood pressure falls
- increase force of heart pumping/ contracting
- contraction of large venous reservoirs (SNS controlled)
- cause generalized constriction of arterioles (SNS)
- LONG TERM (hours to days) Renin produced by kidneys (RAAS)
what is blood flow
the quantity of blood that passes a given point in the circulation in a given period of time
flow through a blood vessel is determined by
- pressure difference between two ends of the vessel
- resistance of the vessel
what can increased velocity cause
turbulence and bruits
what is blood pressure
the force exerted by the blood against any unit area of vessel wall
what is resistance in the blood vessels
it is the impediment to blood flow in a vessel
what is conductance
a measure of the blood flow through a vessel for a given pressure difference
mL/min per mmHg
equation for conductance
conductance=1/ resistance
what is conductance sensitive to
very sensitive to change in diameter of vessel
what three factors effect flow
viscosity
diameter
length
what is vascular distensibility
the fractional increase in volume for each mmHg rise in pressure
what is vascular capacitance
the total quantity of blood that can be stored in a given portion of the circulation for each mmHG
think capacitance more like compliance
what happens when veins are constricted
large quantities of blood are transferred to the heart and increases the cardiac output
what factors contribute to mean pressure
cardiac output
peripheral resistance
what factors contribute to pulse pressure
Stroke volume—increases in
stroke volume increases pulse pressure, conversely decreases in stroke volume decreases pulse pressure.
Arterial compliance—decreases in compliance
increases pulse pressure, also increases in compliance decreases pulse pressure
how does arteriosclerosis effect pulse
decrease in compliance of arterial tree
leads to increase in pulse
Patent ductus arteriosus effects pulse contours
low diastolic pressure
high systolic pressure
very high pulse pressure
aortic regurgitation effect pulse contour
condition associated with backward flow of blood through the aortic valve.
Low diastolic
high systolic pressure
leads to high pulse pressure
how does aortic stenosis effect pulse contours
condition associated with diameter of aortic valve opening is reduced and flow of blood through the aortic valve is low.
Low systolic pressure leads to low pulse pressure
why is the spleen important in circulation
serves as special reservoir for red blood cells
what serves as reservoirs in the body circulation
spleen
liver
large abdominal veins
venous plexus
what is central venous pressure
pressure in the right atrium
usually 0-8mmHg
how is right arterial pressure regulated
balance between
-the ability of the heart to pump
blood out of the atrium
-the rate of blood flowing into the
atrium from peripheral vein
what factors increase right atrium pressure
– increased blood volume
– increased venous tone
– dilation of arterioles
– decreased cardiac function
what happens when pressure is increased in right atrium
cause blood to back up into the venous system
abd pressure and venous pressure in legs increase
what is in the veins to help keep low venous pressure
valves and muscle pump to maintain low venous pressure
what can faulty venous valves lead to
varicose veins
how do tissues control its own blood flow
it controls it in proportion to its own needs
tissue needs include
- delivery of O2 to tissue
- nutrients ( glucose, amino acids, etc)
- remove CO2 and other metabolites
- transport hormones and other substances to different tissues
what is flow closely related to
metabolic rate of tissues
increases in tissue metabolism leads to
increase in blood flow
decreases in O2 availability to tissues
increases blood flow
what are the determinants of blood flow
pressure difference
resistance
what are vasodilator substances
adenosine
CO2
lactic acid
ADP compounds
histamine
K ions
H ions
nitric oxide
increase in tissue O2 concentration=
decrease in blood flow
how do changes in tissue O2 concentration effect blood flow?
define autoregulation
ability of a tissue to maintain blood flow relatively constant over a wide range of arterial pressures
define metabolic theory
suggests that as arterial pressure is decreased, O2 or nutrient delivery is decreased resulting in release
myogenic theory
proposes that as arterial pressure falls the arterioles have an intrinsic property to dilate in response to decreases in wall tension
Law of Laplace
long term local blood flow regulation occurs by
changing the degree of vascularity of tissues (size and number of vessels)
what is an important stimulus for regulating tissue vascularity
Oxygen
what factors does angiogenesis occur in repsonse to
- ischemic tissue
- rapidly growing tissue
- tissue with high metabolic rates
what small peptides are angiogenic factors
-Vascular endothelial cell growth factors (VEGF)
-fibroblast growth factor (FGF)
-angiogen
Vasoconstrictors
norepinephrine
epinephrine
angiotensin II
vasopressin
endothelin
vasodilators
bradykinin
serotonin
histamine
prostaglandins
nitric oxide
what role does the nervous system have in regulation of the circulation
-redistribution of blood flow
-increasing pumping activity of the heart
-rapid control of arterial pressure
-regulates via the ANS
what is sympathetic nervous system in important control of
circulation
what does PNS regulate
heart function
what do sympathetic nerve fibers innervate all vessels except
capillaries
precapillary sphincters
some metarterioles
what does innervation of small arteries and arterioles allows
sympathetic nerves to increase vascular resistance
what are also sympathetically innervated
large veins
heart
what is the PNS mainly in control of
heart rate via vagal nerve
where is sympathetic vasoconstrictor system less potent
coronary circulation and the brain
arterial pressure=
cardiac output x SVR
arterial pressure can be increased by
-constricting almost all arterioles of the body which increases SVR
-constricting large vessels of the circulation thereby increasing venous return and cardiac output
-directly increasing cardiac output by increasing heart rate and contractility
where is the VMC located
bilaterally in the reticular substance of the medulla and the lower 1/3 of the pons
what is the VMC is composed of
- vasoconstrictor area
-vasodilator area
-sensory area
located behind the pons in the medulla
what are some functions VMC
-transmits signals continuously to sympathetic nerve fibers called sympathetic vasoconstrictor tone
-lateral portion controls heart activity by increasing heart rate and contractility
-medial portion transmits signals via vagus nerve to heart to decrease heart
what is the neurotransmitter for the vasoconstrictor nerves
norepineprhine
what else can have powerful excitatory and inhibitory on VMC
hypothalamus
amygdala
the nervous system via the VMC can increase arterial pressure within seconds by
-constricting almost all arterioles of the body which increases total SVR
-constricting large vessels of the circulation thereby increasing venous return and cardiac output
-directly increasing cardiac output by increasing heart rate and contractility
how are signals from the carotid sinus transmitted
herings nerve to glossopharyngeal nerve to nucleus tractus solitarius of the medulla
how are signals from arch of aorta
through vagus nerve to nucleus tractus solitarius
what are chemoreceptors sensitive to
lack of O2
excess CO2
H ion excess
where are carotid bodies located
near carotid bifurcation
aortic arch
when are chemoreceptors stimulated
when pressure falls below 80 mmhg
what is one of the most powerful activators of the sympathetic vasoconstrictor system
CNS ischemic response
when does CNS ischemic response get activated
below 60mmhg
greatest activation at 15-20 mmHg
activation of low pressure receptors enhances
-Na and water excretion by decreasing rate of ADH
-increasing GFR
-decreasing Na reabsorption
why is the bainbridge reflex important
prevents damming of blood in veins, atria and pulmonary circulation
describe the bainbridge reflex
increase in atrial pressure increases the heart rate
stretch of atria sends signals to VMC via vagal
the increase in arterial pressure causes the kidneys to
lose Na and water which returns extracellular fluid volume to normal (ECFV)
what is pressure diuresis
the effect of pressure to increase water excretion
what is pressure natriuresis
the effect of pressure to increase Na excretion
what are the major determinants of long term arterial pressure control
-renal function curve
-salt and water intake line
what leads to long term changes in arterial pressure
changing renal vascular resistance
how does Na determine extracellular fluid volume (ECFV)
-As Na intake is increased, Na stimulates drinking, increased Na concentration stimulates thirst and ADH secretion.
-Changes in Na intake lead to changes in extracellular fluid volume (ECFV).
-ECFV is determined by the balance of Na intake and output.
how is angiotension I turned to angiotensin II
AI is converted to AII by a converting enzyme located in the endothelial cells in the pulmonary circulation
how is angiotensin I made
Renin acts on angiotensinogen to form angiotensin I
where is renin
Renin is synthesized and stored in modified smooth muscle cells in afferent arterioles of the kidney.
how does renin effect the angiotension system
-Causes vasoconstriction
-Causes Na retention by direct and indirect acts on the kidney
-Causes shift in renal function curve to right
what factors decrease renal excretion and increase blood pressure
-angiotensin II
-aldosterone
-sympathetic nervous activity
-endothelin
what factors increase renal excretion and reduce blood pressure
-atrial natriuretic peptide
-nitric oxide
-dopamine
secondary causes of HTN
Renal artery stenosis
Chronic renal disease
Primary hyperaldosteronism
Sleep apnea
Pheochromocytoma
Preeclampsia
Aortic coarctation
how does renal artery stenosis effect BP
Renal artery disease can cause of narrowing of the vessel lumen (stenosis).
The reduced lumen diameter in renal artery increases reduces the pressure at the afferent arteriole in the kidney.
Reduced renal perfusion stimulate renin release by the kidney. This increases circulating angiotensin II (ANGII) and aldosterone.
These hormones increase blood volume by enhancing renal reabsorption of sodium and water. Increased ANGII also causes systemic vasoconstriction.
The net effect of these renal mechanisms is an increase in systemic vascular resistance and an increase in cardiac output (transient).
how does chronic renal disease effect BP
When this occurs, the kidney cannot excrete normal amounts of sodium which leads to sodium and water retention, increased blood volume. Renal disease may also result in increased release of renin leading to a renin-dependent form of hypertension.
The elevation in arterial pressure secondary to renal disease can be viewed as an attempt by the kidney to increase renal perfusion and restore glomerular filtration.
what are some lifestyle changes to treat HTN
Losing weight if you are overweight or obese.
Quit Smoking
Eating a healthy diet,
Reducing the amount of sodium in your diet to 2,300 milligrams
Getting regular aerobic exercise
Limiting alcohol to two drinks a day for men, one drink a day for women
In addition to lowering blood pressure, these measures enhance the effectiveness of antihypertensive medications.
medical treatment for HTN
There are several types of drugs used to treat hypertension, including: -Agnomens converting enzyme (ACE) inhibitors
-Angiotensin receptor blockers (ARBs)
-Diuretics
-Beta-blockers
-Calcium channel blockers
Diuretics are usually recommended as the first line of therapy for most people who have hypertension.
what are 4 factors that can directly affect CO
the basic level of body metabolism
whether the person is exercising
the person’s age, and
the size of the body
what is cardiac index
cardiac index (CI), which is the cardiac output per square meter of body surface area
frank starling law of the heart
Increased quantities of blood flow into the heart stretches the walls of the heart chambers that causes cardiac muscle to contract with increased force
what has direct effect on rhythmicity of heart
Stretch of the sinus node in the wall of the right atrium has a direct effect on the rhythmicity of the node to increase the heart rate as much as 10–15%.
factors that cause a hypereffective heart
Sympathetic stimulation and parasympathetic inhibition does two things to increase the pumping effectiveness of the heart:
-It greatly increases the heart rate
-It increases the strength of heart contraction .
Some of the factors that can decrease the heart’s ability to pump blood are the following:
Increased arterial pressure against which the heart must pump, such as in severe hypertension
Inhibition of nervous excitation of the heart
Pathological factors that cause abnormal heart rhythm or rate of heartbeat
Coronary artery blockage, causing a “heart attack”
Valvular heart disease
Congenital heart disease
Myocarditis, an inflammation of the heart muscle
Cardiac hypoxia
Decreased cardiac output caused by cardiac factors
Severe coronary blood vessel blockage and consequent myocardial infarction
Severe valvular heart disease
Myocarditis
Cardiac tamponade
Cardiac metabolic derangements
factors that affect venous return
Right atrial pressure,
Degree of filling of the systemic circulation
Resistance to blood flow between the peripheral vessels and the right atrium (resistance to venous return)
What’s average map in aorta
94-96 mmHg
What’s the average map in capillaries
16mmHg
What is the most important endothelial derived relaxing factor
Nitric oxide
A lipophilic gas that is released from endothelial cells in response to a variety of chemical and physical stimuli
What vasoconstrictor stimulates NO
Angiotensin II
What is the big importance of angiotensin II
Acts on many arterioles of the body at the same time to increase SVR
Decreases sodium and water excretion by the kidneys to increase arterial pressure
What is a major function of vasopressin
Greatly increases water transportation from the renal tubules back into the blood to help control body fluid volume
What does increase in Ca ions cause
Vasoconstriction
What does increase in k ions cause
Vasodilation
What does increase in Mg ions cause
Powerful vasodilation
What does increase in H ions cause
Large decreases in pH cause Dilation in arterioles
*slight decrease in H ions concentration can cause arteriolar constriction
How do anions effect blood vessels
Acetate and citrate can cause mild vasodilation
What can increased CO2 cause in blood vessels
Moderate vasodilation in tissues
marked vasodilation in the brain
What 2 ways can angiotensin II act on the kidneys
1 acts directly on the kidneys to cause Na and water retention
2 causes adrenal glands to secrete aldosterone to increase salt and water absorption in kidney tubules
Characteristics of primary HTN caused by excess weight gain and obesity
-cardiac output increased
-sympathetic nerve activity (especially in the kidneys) is increased in overweight patients
-angiotensin II and aldosterone levels are increased twofold to threefold in obese patients
-renal pressure natriuresis mechanism is impaired
What 3 mechanisms show blood pressure responses in seconds
Baroreceptor feedback
CNS ischemia
Chemoreceptor mechanism
What blood pressure mechanisms react after minutes
-rasa vasoconstrictor mechanism
-stress/relaxation of vasculature
-shift of fluid through tissue capillary walls
Cardiac output =
Arterial pressure / svr (total peripheral resistance)
Two types of factors that can make the heart a better pump than normal:
Nervous stimulation
Hypertrophy of the heart muscle
What three principles factors affect venous return to the heart
- Right atrial pressure
- Degree of filling of systemic circulation (mean systemic filling pressure)
- Resistance to blood flow between the peripheral vessels and right atrium
how long does it take to transmit a signal from SA node to AV node
0.03 sec
what is the time from AV bundle to last of ventricular fibers
0.06 sec
how much faster is systole than diastole
1/3 faster
where does repolarization start
apex of the heart
last to depolarize is first to repolarize
how much does HR increase with 1 degree increase in body temp
10 bpm
long QT syndrome can be caused by which electrolyte imbalances
hypomagnesemia
hypokalemia
can lead to torsades
