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180 Cards in this Set

  • Front
  • Back
Circulatory System is composed of 3 parts.
What are they and what are their functions?
1. Heart: serves as pump that imparts pressure to blood (Pressure exerted on vessel walls by heart)
2. Blood vessels: passageway for blood to get out to tissues; ultimate site of gas/nutrient exchange at capillary bed
3. Blood: transport medium for dissolved nutrients, O2, CO2, wastes
Why is the heart called a dual pump?
Both atrium and ventricles contract; it imparts the pressure
T/F Blood flows down pressure gradient
True; it flows from high to low pressure
Why is the pressure in the heart important?
Blood flows down pressure gradient from high to low. It drives blood out to tissues where nutrient and gas exchanged occurs
What are the two circulatory systems in the body? (Fig 9.1)
Pulmonary: lungs; all blood in right ventricle pumped to lungs and returns to left heart --> left ventricle --> systemic circulation

Systemic: between left ventricle and rest of body

Fig 9.1
Apex?
Base?
Apex: Tip of heart;
Base: top of heart
T/F Contraction moves from base to apex
False; Contraction moves from apex towards base driving blood out of heart ( like squeezing toothpaste) into circulatory paths
Deoxygenated blood is partially deoxygenated. how?
blood that comes back to right atrium is not completely deoxygenated; it is still carrying 70% of oxygen
--> still plenty of oxygen in blood when return to heart but lower saturation than when it left the left ventricle
Pathway of partially deoxygenated blood from vena cavae
return to vena cava --> right atrium --> right ventricle --> pulmonary trunk --> branches to right/left pulmonary arteries --> lungs --> pulmonary veins --> left atrium --> left ventricle --> aorta --> systemic circulation --> parallel pathways

Fig 9.2
Superior vs Inferior vena cava
Superior vena cava drain the head and upper limbs
Inferior vena cava empty blood from trunks and legs into heart
T/F Any given drop of blood will pass through 1 organ system
True; drop of blood passes through one organ than returns to heart --> parallel pathways
Parallel capillaries pathway vs series capillaries pathway
Series: passes through multiple capillaries before returning to right heart
Parallel: passes through 1 organ system; blood usually flow through one capillary bed then through venous system to right atrium

Rare: blood goes through both parallel and series pathway
Portal System
two capillary beds in series; rare!
Thickness of myometrium right vs left ventricular wall
Not due to volume; due to system that heart pumping against

Right: due to low pressure/resistance, thickness does not need to be great

Left: high pressure/resistance system --> in order to pump same quantity, myometrium must be thicker; stronger muscle to pump same quantity against high pressure/resistance
Right vs left ventricle
Both ventricles pump same quantity of blood with each contractile cycle

Right: Blood goes to pulmonary circulation
Left: Blood goes to systemic circulation
Pressure/resistance Pulmonary circulation Vs Systemic Circularion
Pulmonary: low pressure (doesn't damage structure of lungs) and low resistance (don't impede flow to lungs to get oxygen) system

Systemic: high pressure and high resistance system
Resistance
opposition of flow; impedes flow
Functions of heart valves
ensure unidirectional (open one way) flow of blood

opening and closing is a PASSIVE process
How are heart valves passive?
No contraction or relaxation of muscles for valves to open and close
What causes heart valves to open and close?
The pressure gradient/difference across valves causes opening/closing

Ex: Higher pressure in atria than ventricle then AV opens
What are the four valves? Functions?
Atrioventricular valves (AV)
1. Right AV valve: tricuspid valve (3 flaps)
2. Left AV valve: bicuspid valve aka mitral valve (2 flaps)

Semilunar valves (moon shaped)
3. Aortic valve: left ventricle to aorta
4. Pulmonary valve: right ventricle to pulmonary trunks

Fig 9.4
Pressure in right atrium is greater than pressure in right ventricle --> ?
Right AV valve opens --> blood flows from right atrium to right ventricle
Pressure in right ventricle is greater than pressure in right atrium --> ?
Right AV valve forced close
Pressure of atria vs ventricles
Pressure that can be generated in ventricle is much greater than in atria due to structure (thickness of wall)
How to prevent AV valves from inverting due to high pressure in ventricle?
Chordae tendineae attached to papillary muscles hold cusp/flaps in position and prevent them from inverting
Chordae tendineae
tendinous tissue that connect flats of AV valves to papillary muscles found in ventricle wall
papillary muscles
nipple shaped muscles in the wall of ventricle

don't contract themselves and pull open valves; when ventricle contract, papillary muscle also contract to provide tension on chordae tendineae --> anchor flaps --> flaps cant invert
T/F blood flows only from atrium to ventricle
True
Pressure in ventricle is higher than pressure in pulmonary or aorta --> ?
Semilunar valve open and blood flows out of heart
Pressure in aorta is higher than left ventricle?

Pressure in pulmonary is higher than right ventricle?
Aortic valve closes

Pulmonary valve closes
Does semilunar (aortic and pulmonary) valves have chordae tendineae? Why?
No!

because of anatomical moon shape and position of valves that prevent inverting

they seal over greater surface area
What are the three layers of cardiac muscle tissue?
Epicardium: outer most layer, thin external layer

Myocardium: middle layer, bulk of cardiac muscle

Endothelium: inner most layer, thin layer lining heart and blood vessel vascular system
Fig 9.6
Myocardium arrangement significance?
arranged in interlacing bundles that wrap around in spiral shape around heart

important for contraction from apex to base --> squeeze blood up and out pulmonary/aortic valve
Cardiac muscle characteristics
- striated
- mono-nucleated
- branching; branches/ends of cells connect at intercalated disk
what are the junctions at the intercalated disk?
Desmosomes: adhering junctions that anchor/hold cells together; important to hold together because of strain/pressure generated in heart

Gap Junctions: communicating junctions; small openings in connexons allowing small ions through
what ensures coordinated contraction of heart muscles?
Gap junctions --> allows charged ions through (electrical communication) --> rapid spread of AP from cell to cell --> coordinated contraction
__________ are __% of cardiac muscle cells.
Small percentage of muscle cells are _________.
contractile cells are 99% of cardiac muscle cells.
Small percentage of muscle cells are autorhythmic cells
contractile cells
perform mechanical work; sarcomeres shortening to allow pumping

Ventricular or Atrial myocardial cells
autorhythmic cells
aka pacemaker cells; initiate and conduct action potentials

no need for stimulus to cause action potential to be generated --> occurs on own with parasympathetic and sympathetic input to alter rate that is occurring spontaneously
pacemaker cells are
autorhythmic cells that spontaneously depolarize;
they make up specialize electrical conduction pathway in heart
what gives pacemaker cells ability to spontaneously depolarize?
they have host of channels inserted in plasma membrane giving them ability to spontaneously depolarize
What are the pacemaker potential channels?
1. Funny Na+ channels: activated by hyperpolarization at end of AP
2. K+ Channels: cause early decrease in permeabilty --> decrease in K+ flow at end of repolarization
3. T-Type Ca+2 channels: bring membrane to depolarize to threshold
4. L-Type Ca+2 channels: depolarization due to Ca+2 rushing in

Fig 9.7
(pacemaker potential) Why are funny Na+ channels called funny?
They behave differently from other Na+ channels

They are activated by hyperpolarization at end of previous AP = funny current
(pacemaker potential) What are funny Na+ channels? Abbreviation?
They are voltage gated Na+ channels activated by hyperpolarization at end of AP


If
(pacemaker potential) Why don't pacemaker cells have resting membrane potential?
because as soon as it gets to end of AP at hyperpolarization, funny Na+ channels are triggered to open --> spontaneously depolarize
(pacemaker potential) What do the K+ channels do? When?
They cause early decrease in permeability --> decrease in K+ ion flow

At end of repolarization
(pacemaker potential) What are the two Ca+2 channels?
T-type Ca+2 and L-type Ca+2 channels
(pacemaker potential) What are T-type Ca+2 channels?
T for transient: open and closes quickly

important to bringing membrane to depolarize to threshold --> AP generated
(pacemaker potential) What are L-type Ca+2 channels?
L for long lasting: open for longer

responsible for depolarization phase of AP due to Ca+2 rushing in
(pacemaker potential) What is the most negative membrane potential?
-60 mV
(pacemaker potential) What is the threshold?
-40 mV; 20 mV change
Pacemaker activity of cardiac autorhythmic cells
hyperpolarization triggers opening of funny Na+ channels --> increase Na+ permeability (funny current) --> Na+ comes in --> slow depolarization

at same time K+ channels are closing --> decrease K+ permeabilty --> K+ stop flowing out --> only Na+ flowing in --> depolarization

-----> triggers opening of T-type Ca+2 channels --> Ca+2 flows in --> boost depolarization to reach threshold

at same time, depolarization --> funny Na+ channels close

----> at threshold voltage L-type Ca+2 channels open -- T-type Ca+2 closed --> Ca+2 flows in through L-type --> depolarization phase due to Ca+2 flowing in!

----> peak of AP ~0 mV --> L-type Ca+2 channels close --> decrease Ca+2 permeability --> stop Ca+2 from flowing in --> K+ channels open --> K+ flows out --> repolarization --> most negative membrane potential --> triggers funny Na+ channels to open -- K+ channel closes ..................
(pacemaker potential) why don't funny Na+ channels cause rapid depolarization?
They are slow activating
(pacemaker potential) why are T-type Ca+2 channels necessary to reach threshold?
there will not be enough depolarization to reach threshold because funny Na+ channels start to close

because they're only activated at hyperpolarization
(pacemaker potential) what triggered T-type Ca+2 channels?
voltage change! It has narrow range of activation. It is activated then quickly deactivated
(pacemaker potential) where is the peak of AP?
It reaches about 0 mV; not as high/ as positive as other AP
What cells exhibit pacemaker potential?
excitable cells part of specialized conduction system in heart
what are the four types of excitable cells?
1. nodal cells: SA and AV nodes
2, bundle of His
3. Purkinje Fibers
4. ventricular myocardial cells

No resting membrane potential due to funny Na+ current

Fig 9.8
How are ventricular myocardial cells different from the other excitable cells?
They dont spontaneously depolarize; they dont exhibit a pacemaker potential
What are the nodal cells?
1. Sinoatrial node (SA node)

2. Atrioventricular node (AV node)
Where are the nodal cells located?
upper right hand side of right atrium
What are functions SA nodes?
drives heart rate because they have fastest spontaneous depolarization at ~100 beats per minute

Signal spread from atrial [myocardial] cells to atrial cell by gap junction -- no connection of gap junctions from atrial to ventricular so it spreads via AV nodes
How fast does SA node cells drive heart rate/depolarize?
they have fastest spontaneous depolarization; override everybody else ~100 beats per minute.
How does signals of nodal cells spread? atrial to atrial? atrial to ventricular?
atrial cells to atrial cells by gap junctions through interatrial pathway

no gap junctions between atrial to ventricular so it spread to ventricle by AV node through internodal pathway (arrives within 30ms)
What is the AV node? Function?
exhibit pacemaker potentials at slower rate ~60 depolarization per minute

spreads depolarization to ventricle through bundle of His

pathway of electrical activity from atria to ventricle (NO GAP JUNCTION BETWEEN THEM)

has nodal delay
How fast does AV node exhibit pacemaker potentials?
slower than SA node ~ 60 depolarization (AP) per minute

SA node overrules AV node
How does the SA node overrule the AV node?
SA node depolarizes faster than AV node so it spreads conduction to AV node, which spreads it on
What happens of SA node stops?
AV node takes over because it does spontaneously depolarize on its own
Pathways of specialized conduction system of the heart (Interatrial and internodal)
SA node -->
a. INTERATRIAL PATHWAY
atrial myocardial cells by gap junctions --> through right atria to left atria --> left and right atria depolarize at same time --> contract at same time
and
b. INTERNODAL PATHWAY
AV node --> bundle of His via right and left bundle branches in interventricular septum --> Purkinje Fibers radiate upward --> synapse with ventricular myocardial cells --> depolarize cells --> spread electrical activity via gap junction to all neighbors through gap junction --> coordinated contraction in ventricle --> contract in apex then up towards base --> squeeze blood up and out
Where is the bundle of His located?
In the interventricular septum
How fast does bundle of His depolarize
~ 40 AP per minute, not enough to keep alive
What are bundle of His?
excitable cells that spontaneously depolarize
What are purkinje fibers?
specialized conductive cells that radiate up from apex of heart back towards base --> myocardial cells

does spontaneous depolarization; slower!

rapid spread ensure unified ventricular contraction
what is the purkinje fibers' rate of autorhythmicty?
they exhibit pacemaker potential ~20 AP per minute
atrial myocardial cells are...
muscle cells in atria
What is nodal delay?
Which excitable cell has nodal delay? how long?
nodal delay is delay of signals/ slow conduction through AV node that lasts ~100 ms

It allows atrial contraction to occur and full ventricle filling before ventricle contraction
How long does it take for conduction to spread from SA node to AV node?
It arrives within 30 ms via internodal pathway
Ventricular/Atrial Myocardial cells
contractile cells that won't contract until they're depolarized

Has resting membrane potential
What is the resting membrane potential for contractile cells? Why?
-90 mV which is close to K+ equilibrium potential

It is -90 because of leaky inward rectifier K+ channels --> some K+ move out of cell --> resting membrane potential closer to eq potential of K+
what are the phases of ventricular myocardial (contractile) cell action potential
1. Depolarization: characterized by voltage gated Na+ channels (has acti/inacti gates

2. small repolarization: opening of subclass of K+ channels --> transient outward K+ current (shortlived current)

3. plateau: L-type Ca+2 channels open --> Ca+2 flow in; coupled with decrease in K+ permeability --> plateau phase lasts 250ms

4. Repolarization: opening of voltage gated K+ channel (delated rectifier); coupled with closing of L-type Ca+2 channels --> no more Ca+2 flowing in

Fig 9.10
(contractile potential) How long does the plateau phase last?
250 ms
(contractile potential) what happens during the plateau phase?
Transient K+ channel opens --> slight repolarization battle between --> L-Type Ca+2 channel open to maintain depolarization

L-type Ca+2 --> Ca+2 flowing in and delayed rectifier K+ channel --> K+ flowing out

while L-type Ca+2 start to close and delayed rectifier start to open
(contractile potential) significance of plateau phase?
responsible for longlasting AP in cardiac cell

= long absolute refractory period --> prevent tetany in the heart

AP takes up most of contractile period
step my step phases of action potential in cardiac contractile cells
leaky inward rectifier K+ channel --> K+ constantly leaking out --> resting membrane potential at -90 mV close to K+ eq potential --> rapid opening of Na+ channel activation gate --> Na+ flows in quickly --> DEPOLARIZATION
--> inactivation gate close Na+ channel at peak --> Na+ permeability decreases --> no Na+ flow influx --> Transient K+ channel opens for short time --> K+ flows out --> SMALL REPOLARIZATION
--> L-type Ca+2 channel opens --> Ca+2 flows in --> maintaining depolarization --> PLATEAU
--> slow opening of delayed rectifier K+ channel --> K+ start flowing out --> L-type Ca+2 channels start to close --> balance between K+ out and Ca+2 in --> L-type Ca+2 close -- delayed rectifier K+ fully open --> K+ flows out --> REPOLARIZATION to resting membrane potential
--> leaky K+ channels activated --> no hyperpolarization
(contractile potential) why isnt there a slope to depolarization?
because stimulation/AP arrive from electrically active cells from pacemaker cells --> rapid opening of Voltage gated Na+ channels' activation gate --> Na+ flows in quickly down conc gradient = no slope just steep increase
Electrical activity is coupled to __________
mechanical activity (contraction); depolarization is coupled to release of Ca+2
Why is Ca+2 needed?
It binds to troponin, pushing tropomyosin out of the way --> reveal binding sites on actin for myosin
How is cardiac muscle similar to skeletal muscle regulation?
At rest, troponin and tropomyosin block binding sites on actin for myosin

So Ca+2 is needed
How is cardiac muscle similar to smooth muscle?
Ca+2 induced Ca+2 release
Where does the Ca+2 that bind to troponin/push tropomyosin out of the way come from?
Small amount (10%) of Ca+2 come from ECF
Bulk of it (90%) comes from sarcoplasmic reticulum
Why does sarcoplasmic reticulum release Ca+2
Due to extracellular Ca+2 binding to receptor on the sarcoplasmic reticulum
Cardiac muscle T-tubules
are invagination of plasma membrane
depolarization travels down t-tubule
has modified DHP receptor in membrane - L-type voltage gated Ca+2 channel
DHP receptor in T-tubules
MODIFIED (diff from skeletal muscle); are L-type voltage gated Ca+2 channel
What triggers the release of Ca+2 from sarcoplasmic reticulum?
ECF Ca+2 binds to ryanodine --> comformation change --> open of Ca+2 channels --> SR Ca+2 flows into cytosol
Function of ryanodine recepters?
Receptor in membrane of sarcoplasmic reticulum that Ca+2 binds to --> comformation change --> open Ca+2 channel --> Ca+2 flow out of sarcoplasmic reticulum into cytosol
Explain Ca+2 induced Ca+2 release -- Excitation-contraction coupling in cardiac contractile cells
AP in contractile cell --> travels down T-Tubule --> voltage change trigger opening of (modified DHP receptor) L-type Ca+2 channel --> Ca+2 flow in from ECF --> Ca+2 binds to ryanodine --> comf change --> trigger release of Ca+2 from sarcoplasmic reticulum --> increase in intracellular [Ca+2]--> bind to troponin --> pushes tropomyosin aside --> myosin binds to actin --> cross bridge cycle --> shortening of sarcomere --> CONTRACTION force blood out of heart

Fig 9.11
What happens to the Ca+2 after it flows into cytosol and contraction occured (when Ca+2 levels rise)?
Ca+2 pumps in SR to pump Ca+2 back into SR

and in plasma membrane to pump Ca+2 out to ECF
Action potential of contractile cells vs Contractile response
AP duration = 250ms
response duration = 300ms

--> great overlap

PLATEAU PHASE = long absolute refractory period -- inactivation gate of Na+ channel still closed --> can't stimulate another AP --> no summation in heart --> NO TETANY

AP takes up most of contractile period
How is tetany in the heart prevented?
What happens if it occurs?
During long absolute refractory period -- inactivation gate of Na+ channel still closed --> can't stimulate another AP --> no summation in heart --> NO TETANY

tetany = lack of regular contraction --> not filling --> not pumping blood --> no oxygen delivered
What are the two parts of the cardiac cycle?
1. Systole: contraction/emptying of heart

2. Diastole: relaxation/ filling of heart
How long is one cardiac cycle? In each part?
0.8 seconds -- 0.5 in diastole and 0.3 in systole
Phases of systole
1. isovolumetric ventricular contraction: same volume; valves closed; builds tension
2. ventricular ejection: muscle shorten --> valves open --> blood out
Phases of diastole
1. Isovolumetric ventricular relaxation: same volume; all valves closed
2. Ventricular filling: AV valve open, blood flows in.
(cardiac cycle) Left vs right ventricular volume/pressure
qualitatively same to right ventricular because same volume and events
quantatively different because pressure in right is less
(cardiac cycle) What is ECG?
electrocardiogram: spontaneous depolarization of pacemaker cells that lead to electrical activity --> contractile activity

FIg 9.16
(cardiac cycle) What are the three waves of ECG?
1. P-wave: atrial depolarization
2. QRS complex: ventricular depolarization; mask atrial repolarization
3. T-wave: ventricular repolarization

atrial repolarization isn't shown because it is masked by QRS complex
(cardiac cycle)electrical activity
atrial depolarization -->
ventricular depolarization -->
ventricular repolarization -->
atrial depolarization --> atrial contraction
ventricular depolarization --> ventricular contraction
ventricular repolarization --> ventricular relaxation
(cardiac cycle) path of cardiac cycle
starts with electrical activity --> spontaneous depolarization at SA node --> spreads to atrial cells --> lead to atrial depolarization (P Wave) --> ventricle depolarization (QRS complex) --> systole- isovolumetric ventricular contraction --> systole - ventricular ejection --> T-wave --> diastole - isovolumetric ventricular relaxation --> diastole - ventricular filling -->
(cardiac cycle) what happens before P-wave/atrial depolarization?
ventricular filling at end of diastole filled

ventricular vs atrial pressure: atrial pressure is greater than ventricular pressure --> AV valve is open --> filling of ventricle

aortic pressure comes down
(cardiac cycle) what happens during P wave?
atrial depolarization --> atrial contraction --> atrial pressure increase, volume decrease

last 15-20% of ventricular filling
(cardiac cycle) what happens during QRS complex?
ventricular depolarization --> ventricle contraction --> ventricular pressure exceeds atrial pressure --> AV valve close --> LUB --> Systole-isovolumetric ventricular contraction
(cardiac cycle) what leads to ventricular depolarization?
atrial depolarization leads to ventricular depolarization!

atrial depolarize --> reach AV node --> slight nodal delay --> sends to ventricle --> ventricle depolarize
(cardiac cycle) what is the first heart sound and what causes it?
LUB, the closing of the AV valves
(cardiac cycle) what happens during Systole-isovolumetric ventricular contraction?
all valves closed

end-diastolic volume in ventricle

no change in volume because both AV and semilunar valves are closed --> tension built in ventricle --> pressure in ventricle exceeds pressure in aorta --> aortic valve open --> systole: ventricular ejection -->
(cardiac cycle) End-diastolic volume
EDV: most amount of blood in ventricle at that time; volume in ventricle at end of diastole; avg at 130mL
(cardiac cycle) what happens at systole - ventricular ejection?
aortic valve open --> ventricular muscle shortens --> blood pushed up --> pressure of ventricle increase, volume of ventricle decrease --> ventricular ejection --> increase in aortic pressure --> T-wave
(cardiac cycle) What happens during the T-wave?
ventricular repolarization --> ventricular relaxation --> pressure in ventricle decrease --> muscles lengthen -- sarcomere recoil back to regular length --> aortic pressure decrease because less blood forced out --> ventricle pressure less than aortic pressure --> aortic valve closes --> DUB -->end-systolic volume --> enters diastole
(cardiac cycle) what is the 2nd heart sound? What causes it?
DUB caused by closure of semilunar valve
(cardiac cycle) what is end-systolic volume?
volume in ventricle at end of systole; avg 65 mL
what is stroke volume? how is it calculated?
amount of blood pumped out of ventricle with each ejection/beat

Not all blood pumps out during each cycle

EDV - ESV = SV
135 - 65 = 70 mL

stroke volume for each cardiac cycle is 70 mL
(cardiac cycle) what happens during diastole - isovolumetric ventricular relexation?
all valves closed --> ventricular relaxation --> ventricular pressure falls below atrial pressure --> AV valve opens --> ventricular filling
(cardiac cycle) what happens during diastole - ventricular filling?
AV valve opens --> rapid filling due to atria filling during ventricle contraction --> reduced filling -- plateau of blood just coming in --> P-wave --> atrial depolarization --> atrial contraction --> last blimp of 15-20% filling --> QRS complex --> ventricular depolarization --> ventricular contraction --> pressure in ventricle exceeds atria --> AV valve close
(cardiac cycle) signficance rapid vs reduced filling phase of diastole - ventricular filling
when increase heart rate, diastole is going to shorten

can afford to truncate filling phase because most of the filling occurred early in the rapid filling phase
Left ventricular volume vs left ventricular pressure for single cardiac cycle
AV valve open
--> 2nd diastole - ventricular filling: 65 mL to 135 mL but little pressure change --> end diastolic volume
--> systole - isovolumetric ventricular contraction: no change in volume and increase in pressure
--> aortic valve open
--> systole - ventricular ejection --> ventricle relax --> pressure falls off --> end of systole --> enter diastole - isovolumetric ventricular relaxation --> no change in volume but decrease in pressure .......

Fig 9.17
Heart is compliant
measured as change volume over change in pressure; big change in volume but little change in pressure --> great compliance!
What are the two ways of blood flow? Quiet or noisy?
Laminar flow: quiet/silent

Turbulent flow: noisy/murmurs

Fig 9.19
What is laminar flow?
wanted! because it is most efficient for blood to flow through system

blood flowing in concentric cylinders
--> blood flow in blood vessels as concentric cylinders: outer most cylinder up against vessel wall --> cohesive forces between inner surface of vessel and blood --> resistance --> outer most cylinder is slowest/not moving --> inner most cylinder is fastest
Why is laminar flow most efficient?
because it has the least resistance (outer most layer experience most resistance)

it is how blood flows through healthy vessels
What is turbulent flow?
not efficient --> greater resistance

turbulent flow of outer concentric circles --> influences flow of others --> turbulent flow through most of vessels --> blood move forward but not efficient bc of greater resistance
What happens to your artery when your blood pressure is taken?
laminar flow --> Brachial artery is constricted/compressed --> no flow --> slowly release --> turbulent flow --> heard with stethoscope --> stop hearing --> laminar flow --> use sounds to determine systolic and diastolic pressure
What are heart murmurs?
valves don't open and close proper; allow blood to leak through --> turbulent flow
What is cardiac output?
It is the total blood flow/ volume of blood pumped by each ventricle per minute
How to calculate cardiac output (total blood flow)?
CO = HR x SV

ex: 70 b/min x 70 ml/b = 4900 ml/min
what is the average cardiac output for an adult male?
5L/min for each ventricle
Calculate total blood flow (like ohms law)
Pressure difference = Flow x resistance
Can cardiac output change? When? By how much?
yes!

Change in a bad way when we have diseases and a failing heart.

Or GOOD WAY Cardiac output can change when you exercise -- Increase by 7 times
How can cardiac output be altered?
Alter heart rate and stroke volume!

Afterload

Fig 9.25
How is heart rate generally altered)
Alter strength and rate of contraction by modification of the autonomic innervation
What is autonomic innervation
autonomic nervous system input including parasympathetic and sympathetic nervous system
Where does PNS innervate the heart?
PNS (via vagus nerve) innervates the SA and AV nodes and the atrium (atrial myocardial cells)
How does PNS and SNS alter heart rate?
Both effect heart by altering activty of the cAMP 2nd messenger pathway

ACh binds muscarinic cholinergic receptor --> activates GPCR with alpha-i subunit --> inhibits cAMP

NE binds beta-1 adrenergic receptor --> activates GPCR --> activates cAMP
Where does SNS innervate the heart?
SNS innervates the SA and AV nodes, and both atrium and ventricles (atrial and ventricular myocardial cells)
Which node has spontaneous depolarization? At what rate?
SA node at 100 depolarizations per minute
resting heart rate due to?
heart rate is altered at rest due to parasympathetic input
What are the receptors for PNS and SNS? What is the target organ?
Receptor: G protein coupled receptors linked to 2nd messengers (cAMP)
target organ: cardiac
T/F heart innervated by PNS
False, heart is innervated by both PNS and SNS
How is cAMP inhibited?
ACh binds muscarinic cholinergic receptor whicha ctivates GPCR with alpha-i subunit --> inhibits cAMP
How is cAMP activated?
NE binds adrenergic receptor which activates GPCR with alpha-s subunit -->activates cAMP
What are the three specific ways to change the heart rate?
What channels are involved?
Role of PNS and SNS for each.
Effect on heart rate.
1. increase/decrease rate of depolarization (from most negative to threshold)
-- funny Na+ channels involved
-- PNS decrease depolarization and heart rate
-- SNS increase depolarization and heart rate
Fig 9.20

2. increase/decrease max diastolic potential
-- leaky K+ channel involved
-- PNS opens more K+ channels --> increase K+ flow --> more negative --> max diastolic decrease ----> hyperpol --> --> more time to threshold --> slow heart ratee
-- SNS doesn't influence

3. Increase/decrease threshold
-- Ca2+ channel involved
-- PNS increase threshold --> increase time --> slower heart rate
-- SNS decrease time --> threshold closer to most negative potential --> less time --> faster heart rate

Table 9.3
Acetyl choline, epinephrine, muscarinicR, B1 adrenergicR, norepinephrine

PNS or SNS?
ACh via muscarinicR = PNS

NE/E via adrenergicR = SNS
Role of PNS on depolarization?
Effect on heart rate.
Funny Na+ current is decreased --> decreases slope to depolarization and increase time it takes to depolarize thus slowing heart rate.
Role of SNS on depolarization?
Effect on heart rate.
SNS opens more funny Na+ in nodal cells --> increase slope to depolarization --> faster depolarization --> greater number of heart beats --> increase heart rate
What is max diastolic potential?
Hyperpolarization of most negative membrane potential.
Role of PNS on max diastolic potential?
opens more K+ channels --> increase K+ flow --> more negative --> max diastolic decrease ----> hyperpol --> --> more time to threshold --> slow heart rate
T/F SNS influences max diastolic potential
False, SNS does not influence max diastolic potential at all, just PNS.
Role of SNS on max diastolic potential.
NONE!
Role of PNS on threshold.
PNS decrease Ca2+ current --> depol less steep --> increase threshold --> longer time --> slower heart rate
Role of SNS on threshold.
SNS increase Ca2+ current nodal cells --> decrease threshold --> threshold closer to most negative potential --> faster time --> increase heart rate.
Where is NE/E released from?
NE released from neurons
E released from adrenal medulla
SNS influence on ventricular myocardial cells. (calcium)
increase Ca+2 current --> more intracellular [Ca+2] --> Ca+2 induced Ca+2 release --> more Ca+2 to bind to troponin and push tropomyosin away --> more actin binding sites for myosin --> more force generated --> increase contractile force = POSITIVE IONOTROPIC EFFECT
PNS influence on ventricular myocardial cells.
NONE!! It only innervates the atrium (atrial myocardial cells)
What is the positive ionotropic effect?
SNS influence on ventricular myocardial cells by increasing Ca+2 current --> more intracellular [Ca+2] --> Ca+2 induced Ca+2 release --> more Ca+2 to bind to troponin and push tropomyosin away --> more actin binding sites for myosin --> more force generated --> increase contractile force
Effect of Sympathetic Stimulation on heart Activity

SA node
AV node
Ventricular conduction pathway
Atrial muscle
Ventricular muscle
Adrenal medulla
Veins
SA node --> Increases depolarization increasing HR
AV node --> conduction propagated faster decreasing AV nodal delay
Ventricular conduction pathway --> increases excitability hastening conduction through bundle of His and Purkinje ;
Atrial and Ventricular muscle --> increase contractitility (positive ionotropic effect) strengthening contraction
Adrenal medulla --> promotes E release, E binds to heart receptor causing increase effects
Veins --> SNS innervate smooth muscles around veins and vessels causing increase contractility through Frank Starling Mech --> promote venous return

Table 9.3
Effect of Parasymphathetic Stimulation on Heart Activity

SA node
AV node
Ventricular conduction pathway
Atrial muscle
Ventricular muscle
Adrenal medulla
Veins
SA node --> decreases depolarization decreasing HR
AV node --> decreases excitability increasing AV nodal delay
Ventricular conduction pathway --> NA
Atrial muscle -->
Ventricular muscle --> NA
Adrenal medulla --> NA
Veins --> NA

Table 9.3
What are the systems that influence stroke volume?
1. intrinsic control --venous return (intrinsic to heart)
2. extrinsic control -- sympathetic activity (comes from outside the heart)

Fig 9.21
What is intrinsic control?
intrinsic to heart - venous return

Frank-Starling Law of the Heart

increase venous return --> increase end-diastolic volume --> increase strength of cardiac contraction --> increase stroke volume
What is extrinsic control?
comes from outside of heart - sympathetic activity influences strength of cardiac contraction (positive ionotropic effect)

NE/E --> increase Ca+2 current --> increase Ca2+ induced Ca2+ release --> generate more force of contraction --> pump greater volume of blood

also increases venous return because SNS innervates smooth muscle around veins --> cause constriction --> force more blood back to heart
Frank -Starling Mechanism
length-tension relationship !

increase venous return --> increase end-diastolic volume --> increase stroke volume

increase blood returning to heart --> increase fill --> increase length of muscle --> increase end-diastolic volume --> stretch out muscle --> putting sarcomeres more in optimal overlap --> more tension --> greater force of contraction --> increase stroke volume

Fig 9.22
Is cardiac muscle at optimal overlap at rest?
No. Resting cardiac muscle is on the rising phase where there's more overlap.
Optimal overlap
generate maximum force

overlap = relationship of sarcomeres.
How to generate more tension? (frank starling mechanism)
Increase length of muscle and decrease overlap
relationship of optimal overlap and Ca+2
increase myofilament Ca+2 sensitivity

Tropomyosin is in more conducive conformation to bind Ca+2 -- tropomyosin pushed out of way by Ca+2

has to do with spiral arrangement of cardiac muscle.

Contributed by Frank Starling Mechanism
heart's length - tension curve
No right hand side just up to peak ; due to anatomical arrangement of cardiac muscle

Normal resting length at up swing of curve
normal EDV = 135 mL; normal SV = 70 mL

increase EDV --> increase SV

Fig 9. 22
sympathetic stimulation increase heart's contractility at any given _______
sympathetic stimulation increase heart's contractility at any given EDV.

INDEPENDENT of EDV.
Frank Starling curve by sympathetic stimulation
sympathetic innovation shifts FS curve up to left --> greater SV at any given EDV
Afterload
What heart is working against!
Heart works against blood pressure in systemic circulation -- must be exceeded for semilunar valves to open

Increase BP --> increase afterload

Influences CO

FIg 9.26
What must be overcome to open semilunar valves?
Must overcome blood pressure; pressure in ventricle must exceed aortic pressure (systemic blood pressure).
Why is it bad to have high blood pressure?
Heart has to work harder with every beat to work against afterload --> leads to hypertrophy of heart --> influence ability to respond to stimuli
Normal vs failing heart

how does body compensate?
Normal: SV at 70 mL
Failing: decreased SV -- does not provide systemic circulation with all that it needs (nutrient, oxygen)

Must increase EDV! and body kicks in with sympathetic innovation (intrinsic and extrinsic) --> allows failing heart to produce SV

Fig 2.6
Hypertrophy
heart failure leads to hypertrophy in left ventricle --> cut into volume inside ventricle --> decrease EDV --> decrease ability to respond to FSM --> must have greater sympathetic to compensate --> die of heart failure