CV A&P and Systemic circulation ppt <3 <3 <3 Flashcards
To pass and say FUCK YOU Boyd!!!111
the average heart weighs how much
250- 350 grams
3 main components of the myocardium
RV wall
LV wall
Myocyte
The RV wall is how thick?
0.3-0.5 cm thick
The LV wall is how thick?
1.3-1.5 cm thick
just know that basiclly the LV is over twice as thick
5 components of the myocyte
- cell membrane + T tubules
- Sarcoplasmic reticulum (SR)
- Contractile elements
- Mitochondria
- Nucleus
**** huge volume of mitochondria!!!!!****
The huge volume of mitochondria in the myocyte means what????
aerobic metabolism
what is greater than 90% of the volume of the myocardium
the myocyte
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what is the contractile elemement of the myocyte?
- sacromere (actin and myocin filaments)
A sarcomere (Greek sárx = “flesh”, méros = “part”) is the basic unit of a muscle. Muscles are composed of tubular muscle cells (myocytes or myofibers). Muscle cells are composed of tubular myofibrils. Myofibrils are composed of repeating sections of sarcomeres, which appear under the microscope as dark and light bands. Sarcomeres are composed of long, fibrous proteins that slide past each other when the muscles contract and relax.
Two of the important proteins are myosin, which forms the thick filament, and actin, which forms the thin filament. Myosin has a long, fibrous tail and a globular head, which binds to actin. The myosin head also binds to ATP, which is the source of energy for muscle movement. Myosin can only bind to actin when the binding sites on actin are exposed by calcium ions
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Sacromeres are integrated by what?
- intercalated disk and gap junctions
intercalcated disk are microscopic identifying features of cardiac muscle. Cardiac muscle consists of individual heart muscle cells (cardiomyocytes) connected by intercalated discs to work as a single functional organ or syncitium. By contrast, skeletal muscle consists of multinucleated muscle fibers and exhibit no intercalated discs. Intercalated discs support synchronised contraction of cardiac tissue. They occur at the Z line of the sarcomere and can be visualized easily when observing a longitudinal section of the tissue.
Three types of adhering junctions make up an intercalated disc — fascia adherens, macula adherens and gap junctions.
Fascia adherens are anchoring sites for actin, and connect to the closest sarcomere.
Macula adherens stop separation during contraction by binding intermediate filaments, joining the cells together. Macula adherens junctions are also called desmosomes.
Gap junctions allow action potentials to spread between cardiac cells by permitting the passage of ions between cells, producing depolarization of the heart muscle
What are 3 specialized myocytes?
- SA node
- AV node
- bundle of his
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Which leads shows an inferior MI?
what artery is invloved
II, III, AVF
Right Coronary Artery
Which leads shows a Lateral MI?
what artery is invloved
I, AVL, V5, V6
Left Circ
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Which leads shows an Anterior MI?
what artery is invloved
V3-V4 (I, AVL)
Left Coronary artery
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Which leads shows an Anteroseptal MI?
what artery is invloved
V1-V2
LAD
myocardial circulation occurs mostly during what?
and why
diastole
BC of interruption of blood flow during
systole, due to mechanical compression of vessels by myocardial contraction and the
absence of anastomoses between the left and right coronary arteries
what is the average ml/min of myocardial circulation?
200-250 ml/ml
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Another characteristic of the coronary circulation is that maximal oxygen extraction of ___1__ %
occurs, resulting in a coronary venous oxygen saturation of about __2____%.
- 70%
- 30%
what is the coronary sinus
a collection of veins joined together to form a large vessel that collects blood from the heart muscle (myocardium) and It delivers deoxygenated blood to the right atrium, as do the superior and inferior vena cava.
The coronary sinus is what % of venous return?
75%
(it seems like a lot but thats what his slides say and I cound’t find anythng in the book slide #10)
what veins make up the coronary sinus?
posterior veins
RV=anterior veins
Thebesian veins (shunt)
Layers of the heart
parietal pericardium
epicardium (visceral pericardium)
myocardium
endocardium
Most of the oxygenated
blood reaching the fetal heart is from the ____1____ vein and the __2___ __2___ __2____
- umbilical
- inferior vena cava
what is the fetal blood flow starting with the IVF
oxygenated blood from the IVC goes into the RA then
diverted through the foramen ovale to the LA to the LV then pumped out the aorta to the head
IVC > RA > FO > LA > LV > AO > systemic (head)
What is fetal circulation starting with the SVC
Deoxygenated blood from the superior vena cava enters the RA goes to the RV, then enters the (PA) the pulmonary artery goes through the patent ductus arteriosus (PDA) to the aorta to the feet and umbilical
arteries.
SVC > RA > RV > PA > PDA > AO > systemic (feet)
in the fetal circulation the RV makes up what part of CO
2/3
anatomic closure of the PDA occurs when after birth
2-3 weeks
what are the 2 main classification of valves in the heart
AV
semilunar
WHat are the 2 AV valves
tricuspid
mitral
what are the 2 semilunar valves of the heart
aortic and pulmonic
what is the blood flow through the heart then into circulation? (17 steps, once you leave the heart gets more basic)
- RA
- tricuspid
- RV
- pulmmonic valve
- PA
- lungs
- PV
- LA
- mitral valve
- LV
- Aotic valve
- aorta
- atreries
- aterioles
- capillaries
- venules
- veins
what do arteries do
transport blood under high pressure
what do arterioles do?
contract and dilate to control blood from into the capillaries
(control resistance)
what do capillaries do?
sites for transfer of oxygen and nutrients and recipients of metabolic byproducts
venules
collect blood from capillaries for delivery to veins
what do veins do?
contract or expand to store blood, venos pump mechanism.
what allows veins to return blood to heart
one-way valves and skeletal muscle pumping
what are the 3 layers of arteries and veins from inner to outer
- Tunica intima
- Tunica media
- Tunica adventitia
what layer is smooth muscle fibers mixed with elastic fibers?
tunica media (middle)
what layer is squamous epithelium, connective tissue, and basement membrane
tunica intima
what layer is a thin layer of connective tissue-lengthwise elastic or collagenous fibers?
tunica adventitia
the systemic circulation is accountable for what % of blood volume?
80%
there is low resistance in systemic circulation until arterioles! what are the pressures at the folowing:
Arterioles
Capillaries
Venous end
Arterioles- 85 mmHg
Capillaries- 30 mmHg
Venous end- 10 mmHg
The arterioles account for _____% of the resistance of systemic circulation?
50%
what is pulse pressure
difference of systolic and diasyolic b/p
what does the dicrotic notch indicate?
closure of the aortic valve
the pulse pressure reflects what?
stroke volume and resistance/compliance
the pulse pressure wave form is ______ peripherally in good compliance and goes to almost nothinfg in the capillaries
amplified
4 determinants of tissue flow
- pressure gradien/resistance
- Resistance only calculated
- distensibility
- compliance
Resistance is ___1___ proportional to pressure and __2__ proportional to flow
- Directly
- Inversely
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________ are less musclular, leading to 6-10 x’s more distensible.
(arteries or veins)
Veins
what are the 4 main things for control of tissue blood flow
explian each!!
- Local control-(based on the need for delivery of oxygen or other nutrients)
- Autoregulation-(local mechanism in which a specific tissue is able tomaintain a relatively constant blood flow over a wide range of mean arterial pressures)
- Long-term control-(change in vascularity of tissues with sustained increases in blood pressure, increased metabolism, inadequate oxygen delivery)
- Autonomic nervous system control- (norepinephrine influences resistance to
redistribute tissue blood flow; prominent in the kidneys and skin and
minimal in the cerebral circulation)
what controls systemic b/p?
- Changes in CO and SVR
- Autonomic
- Baroreceptors
- Chemoreceptors
- Atrial reflexes
- CNS
- ischemic reflex
- Hormonal
Baroreptors (control of Systemic b/p)
- located where?
- respond rapidly to what?
- respond with the sympathetic regulation of what center?
- walls of carotids and aortic arch
- b/p changes
- Vasomotor center
Chemoreptors (control of systemic b/p)
- Located where?
- stimulated by what?
- respond with regulation from what center?
- slower responses to b/p and faster action in stimulating what?
- Carotid and aortic bodies
- by decrease O2/ increased CO2/ increased H+
- Vasomotor center
- respirations
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in recap baroreptors do what mainly?
and Chemoreceptors do what mainly?
- respond to B/P Incr/decres
- stimulate respirations
Atrial reflexes (in control of systemic b/p)
- Are mediated by what?
- what do they do when there is more stretch?
- the increased HR is a functino of direct stretch of ____ _____ as well as the bainbridge reflex.
- it releases what atrial granules?
- what does that atrial granule do?
- stretch
- decrease b/p and increase HR
- SA node
- Atrial natriuretic peptide (ANP)
- decrease preload, decrease afterload, decrease sensitivity to ADH
RAAS system does what in response to
- Low BP
- Increased BP
- retain Na+ (water)
- excrete Na+ (water)
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The normal cardiac action potential results from timedependent changes in the permeability of cardiac muscle cell membranes to __1__, __2__, __3__, __4__ ions during phases __5__ of the action potential
- Na+
- K+
- Ca++
- Cl-
- 0 to 4
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Ion movement for phases of cardiac action potential
Phase ion Movement across cell membrane
Phase ion Movement across cell membrane
0 Na+ IN (if Na+ K+ out)
1 K+ OUT
Cl<sup>-</sup> IN
2 Ca+ IN
K<sup>+</sup> OUT
3 K+OUT
4 Na+ IN
what are the 2 elements that contribute to tension (force) of the heart muscle
- contractile element (active tension)
- Elastic element (resting tension)
what influences tension of the heart?
length of muscle fibers
what is the starlings relationship to heart muscle mechanics and tension
tension (active and resting) vs Length
Velocity is influenced by what?
length and tension
in recap the heart muscle mechanics function off 3 main things __1___, __1__, __1__.
tension is made up of __2__ and __2__ tension.
the length of the muscle fibers influence the __3__. such as in starlings law
and the velocity is influenced by both __4__ and __4__.
- tension, length, velocity
- active and resting
- tension
- length and tension
CO=
HR x SV
SV is affected by what 3 things
- Preload
- After load
- contractility
Law of LaPlace relates what 2 things?
ventricular pressure and wall tension
T= Pr / 2h
tension =
pressure gradient x radius
Laplace law in r/t to the heart
in the LV increased filling > increased wall pressure
6 phases of the cardiac cycle
- isovolumetric ventricular contraction (contracting constant volume)
- Rapid ejection phase
- Reduced ejection phase
- Isovolumetric relaxation
- Rapid filling phase
- slow filling period
the atrial contributation to the cardiac cycle can be __ to ___ % in the failing heart
20-30%
what 4 things determine myocardial function?
- preload
- Afterload
- Contractility
- HR
preload
In normal heart and increased venous return results in an __1__ CO.
In a failing heart the sacromere length is already maximal; so CO increases requires increased __2__ or __2__.
- Increased
- contractility or HR
what is the pressure applied to fill the heart and is represented by the “passive” pressure- volume curve
preload
clinically preload is measured by what?
end diastolic pressure
LVEDP
typical values for LVEDP is what
4-5 mmHg
a sudden increase in filling pressures. (preload) will cause what? 3 main things
- increased LVEDP
- increased heart contraction force ( do to the enhanced thick and thin filament overlap, it contracts to the same ESV- starling law)
- increased SV, CO, PA
what is the pressure in the aorta throughout the ejection phase? it is an estimate if arterial pressure
afterload
a sudden increase in mean arterial pressure (afterload) causes what 3 things to happen
- pressure in the ventricle must rise to a higher level during the isovolumetric contraction phase before the aortic valve will open
- ejected volume goes down
- SV and CO woll decrease
a sustained increase in the mean arterial pressure (afterload) is caused by what?
- the increased ESV plus normal venous return that leads to increased EDV
- the increased EDV makes the heart contract more forcefully (starlings law)
- causing increased SV, CO, PA
altered contractile force is due to the change in the rate or quality of __1__ delivered to the myofilaments, or a change in the affinity or the filaments to __2__.
- Ca++
- Ca++
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a sudden increase in contractility causes what 2 things
- the heart to contract more forcefully from ANY initial length
- the heart to contract more forcefully during EJECTION phase, leading to decreased ESV and increased SV
what are the effects of a sustained increase in contractility?
- reduced ESV plus normal venous return = reduced EDV
- heart contracts less forcefully dur to EDV
- pressure voume curve shifted to left
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explain the cardiac cycle and pressure loops
- ISOVOLUMETRIC RELAXATION (diastole) causes pressure to decreases
- as passive VENTRICULAR FILLING (diastole) occurs, and volume begins to increase
- as ATRIAL KICK finishes and volume is maxed pressure increases during ISOVOLUMETRIC CONTRACTION (systole)
- followed by rapid EJECTION (systole) as pressure continues to increase very slightly and volume decreases greatly
- this leads into REDUCED EJECTION thus lowering pressures and volume and starting cycle over again with ISOVOLUMETRIC RELAXATION
6.
better pic of the cardiac loops
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what occurs during the diastolic phase of the cardiac cycle
- isovolumic relaxation
- filling
- atrial kick
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what occurs during the systole phase of teh cardiac cycle?
- isovolumic contraction
- ejection
- rapid and reduced ejection
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so now that we learned all of the phases of the cardiac cycle match them up with what is going on in the heart
1st draw a pic then explain it
- during isovolumetric relaxation (diastole)– constant radius (all valves are closed) decreased pressure and tension
- during passive filling AV valves open allowing VENTRICULAR FILLING (diastole) causinga constant pressure with increased radius and tension,
- after ATRIAL KICK all valves are closed
- constant radius increased pressure and tension. during ISOVOLUMETRIC CONTRACTION (systole)
- then Semilunar valvees open during rapid ejection
- and EJECTION (systole) occurs with constant tension decreased radius and increased pressure
- followed by reduced ejection and all valves closed.
-during each phase (or side of the loop) there must be a radius, pressure, and tension.
– the ones ont the right and left have same radius (isovolumetric) (they are not gaining any volume. the left is diastolic loses pressure and tension, the right is the systolic it is gaining pressure and thus tension
- the bottom is straigt filling (diastolic) so a constant pressure. ( no flunctuations) but the radius gets bigger (from more fluids) and thus the tension gets larger.
– the top or ejection is not a constant pressure b/c it has rapid and slowed ejection. but tension is always the same )constant b/c it is one big squeeze. so during ejection we are losing volume so radius decreases, and we are forcing the blood out fast so pressure is increased.
– when all valves are closed the radius is constant (can only fill whats there.
this is bringing it all together!!!!!!!!!!!!!!!!!!!
explain A-B
- filling phase (ventricular filling)
- diastole
- encompasses both passive and atrial kick
- constant pressure
- increased radius
- increased tension
explain B-C
- Isovolumetric contraction
- systole
- radius constant
- tension increased
- pressure increased
Explain C-D
- Ejection phase
- systole
- encompasses both rapid and reduced ejection
- tension constant
- radius decreases
- pressure increases
explain D-A
- Isovolumetric relaxation
- diastole
- radius constant
- pressure decreases
- tension decreases
what occurs in the cardiac pressure volume loop in the filling phase
- AV valves open
- ventricular volume increases to maximum (EDV)
- pressure constant (rises just slightly EDP)
what occurs in the cardiac pressure volume loop during the isovolumetric contraction phase
- mitral valve closes
- ventricular pressure increases without volume change
what occurs in the cardiac pressure volume loop in the ejection phase
- when ventricular preesure exceeds aortic pressure aortic valve opens, and ejection begins (volume decreases)
- initially pressure continues to rise but then falls
what occurs in the cardiac pressure volume loop in the isovolumetric relaxation phase
- aortic valves closes
- volumes in ventricle is ESV
- pressure in the ventricle falls until the AV valve opens (back to step 1)
CO is the product of what?
HR x SV
what is Stroke Volume (SV)
difference between EDV and ESV
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what is ejection fraction?
how is it calculated
- the amount of blood ejected in each beat
- SV divided by EDV
EDV-ESV / EDV = EF
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normal EF is what?
60-65%
an EF of what is indicative of severe Cardiac disease?
<40%
what is 2 ways to control CO
intrinsic control
extrinsic control
which type of control for CO, rapidly compensates for changing conditions an dequalizs R and L outputs
intrinsic
what is an example of intrinsic control of CO
HR
SV (starling law)
Which control of CO changes in contractility (inoropic state)
extrinsic
what are 4 factors that increase O2 consumption?
- Increased afterload or contractility
- dilation of ventricular chamber
- Increased HR
- Increased SV
(basically anything that raises B/P will increase myocardinal O2 requirements)
what determine MAP
the product of CO an dtotal peripheral resistance
CO is propprtional to
the pressure diff b/t aorta and right atrium
CO is inversly proportional to
resistance of circulatory system
automaticity
what sets the pace
the fastest rate
is automaticity of the heart neurally mediated
nope
it is neurally modified though
how does ACh modify rate and automaticity
increases K+ current and slows rate of spontaneous depolarization
how does epinephrine modify rate and automaticity
increases Ca++ current
(CCB have opposite effect)
with ionic NODAL ACTION potentials
What is the unstable “resting” potential?
what are it;s ion currents
and what occurs due to this
~ -60 mV
K+ current present but declining
Increasing Na+ and Ca++ currents
causes SPONTANEOUS DEPOLARIZATION
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with ionic NODAL ACTION potentials
the membrane potential reaches threshhold at ~-40 mV
and what occurs
rapid increase in Ca++ T-type current
fall in IC K+, then willl increase later
Cell reaches 0 to +5 mV
