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Physiology > cardiac > Flashcards

cardiac Flashcards

1
Q

why do we have the delay in conduction at the Av node

A

This gives the atria time to slow down and eject blood

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2
Q

which is faster? the mechanical or electrical system in the heart

A

Electrical

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3
Q

What’s the electrical conduction pathways in the heart

A

Sa-Av-Bundle of His-Right Bundle branch-L) bundle branch-Purkinje fibres-Ventricular depolarization.

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4
Q

how does the size of muscle affect the pulse firing in heart conduction?

A

The bigger the muscle i.e left ventricle, the bigger the firing.

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5
Q

Veins are bigger than arteries T/F ?

A

T

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6
Q

Greater pressure in the arterial side t/f

A

T

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7
Q

Veins wall are thinner T/F?

A

T

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8
Q

Arterial walls are thicker t/f ?

A

T

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9
Q

Why no valves in the artery?

A

No valves in the artery because blood moves under high pressure

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10
Q

Why do we have valves in the veins

A

Veins flow under low pressure and so they have valve that allows the blood to move in one direction

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11
Q

Longer the vessel the longer it takes to feel pulse wave on blood flow T/ F?

A

T

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12
Q

Stiffer vessels have a faster pressure wave t/f

A

T

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13
Q

What is the dicrotic notch?

A

When the aortic valve closes

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14
Q

Pulse pressure is?

A 
Diff between sys and diastolic pressure.
function of stroke volume and compliance
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15
Q

Do stiffer vessels have a faster or slower pressure?wave?

A

Faster

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16
Q

What happens to the pulse pressure if the vessel is compliant

A

The pulse pressure will be lower

we want compliant blood vessels.

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17
Q

what prevents blood from flowing back into the left ventricle from the Aorta.

A

Aortic valve

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18
Q

What form of energy does it take to move blood through the vessels in the heart

A

The energy used is in form of decrease pressure as blood travel between the Aorta and the system the B/p reduces because energy is used to move the blood

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19
Q

Time difference between 2 sites is shorter when the vessel is stiffer t/f

A

T

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20
Q

Where does most regulation of blood flow take place in the heart circulation?

A

During the big pressure drop between the large arteries and the arterioles.

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21
Q

Ventricles put work into the system after that its the pressure gradient that it unctions off on. t/f?

A

T

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22
Q

In a pipe considering the pressure,if we increase the pressure and keep everything the same, what will happen to flow.?

A

Flow will increase

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23
Q

If the pipe is bigger than the fluid being pushed in it, will there be more flow or less flow.?

A

More flow.

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24
Q

As we move from the artery to the vein,what happens to the vessels

A

The vessels get smaller, but the vessel grows in number that are in parallel…
resistance increases as blood from artery moves to the capillary,but decreases as blood moves from the capillary to the vein back to the heart

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25
Q

Relate flow in the aorta to the total flow in the capillary

A

The total flow in the aorta is equal to the total flow in the numerous capillaries that the blood is going through

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26
Q

As capillaries increase, the velocity of flow reduces,t/f

A

t

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27
Q

The velocity of flow in the capillaries is low because of increase number of parallel capillaries.T/F

A

T

The total cross-sectional area of the capillaries and the velocity is inverse.

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28
Q

Why does the velocity of flow start to increase in the venules as they move along?

A

Because the vain are bigger.

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29
Q

as we move through the cardiac system, What is being held constant?

A

The flow

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30
Q

If we hold pressure constant and increase area, will velocity increase or not.?

A

Velocity will increase

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31
Q

Poiseilles law assumes what kind of flow?

A

Lamina flow

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32
Q

What component is most important in turbulent flow?

A

The mass of the transporting medium

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33
Q

How many percents of blood does the heart get and how much of oxygen is used out of it?

A

4%/ 11%

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34
Q

Why is so much blood sent to the kidney?

A

Kidney cleanse the blood,thats why it gets a lot of blood

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35
Q

FYI

A

AMount of blood ejected from left ventricle should be the same with the one going into the right atrium..meaning a
arterial shud be = to the venous volume

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36
Q

How long does it take blood to go around the body

A

5L/5min= 1min

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37
Q

How do you Calcule the time blood spends in a location

A

Transit time x % of blood in that loaction

64% in vein x 60s=38.4 seconds

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38
Q

Blood moves how fast in the capilaries

A

4secs,but remember the cap is very short,so the flow is slow in there so the nutrients can be absorbed.

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39
Q

Increase activity …variation of blood distribution with this ..like running from the bear

A

Blood flow increase in heart
Blood flow increase in skeletal muscle
Gi blood flow decrease
Kidney Blood flow will decrease

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40
Q

How would the time spent in the capillary change with sending more blood to the capillary during activity

A

A lot more capillaries with be recruited ..and more capillary to be perfused

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41
Q

At rest if CO is increased by factor of 4..Blood moves 4x faster… and no capillaries recruited since no exercise..will Time in capillary will increase or decrease

A

Decrease……..no time to onload oxygen..so there will b a problem…….blood has less than a second in the capillary because of the speed.(High output heart failure)

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42
Q

Smaller blood vessels higher resistance t/f

A

T

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43
Q

Where can we manipulate resistance more?

A

Arteries

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44
Q

The smaller the blood vessels the more we have in parallel T/f?

A

T.

Overall resistance does not really go up since more blood vessels get recruited when they are smaller

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45
Q

Resistance is were in the vessels?

A

Small arteries and the arterioles

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46
Q

Veins have little resistance 7% why?

A

cos its so big

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47
Q

Making vein smaller what happens?

A

Resistance will not really affect much but the
blood volume will increase and more blood goes back to the heart

Change in resistance does not matter with the veins,but blood volume in the vein will be affected…by sending more blood to the heart.

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48
Q

what kind of circulation do we have in the heart per systemic and pulmonary circulation

A

Systemic circulation is high pressure, high resistance

Pulmonary circulation is low pressure, low resistance

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49
Q

In the heart, blood distribution happen as a function of?

A

Blood is distributed between regional circulations as a function of regional resistance

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50
Q

How does blood get distributed in the body?

A

Kidney gets a lot of blood because it needs to filter blood

Skin gets a lot of blood so it can cool off

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51
Q

How does arterial/veinous flow get affected by resistance increase

A

Arterial….increase resistance and decrease flow…

Vein constrict and increase blood flow back to the heart

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52
Q

What is the pericardium made up of

A

Pericardium: double-walled sac that covers the heart

Visceral pericardium…moves in response to fluid filling in
Parietal pericardium…pretty touch does not move..this could cause tampanode.
- Pericardial cavity between two layers

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53
Q

Which heart layer is the muscle layer

A

Myocardium

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54
Q

Where does blood from the heart get dumped into

A

Coronary sinus

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55
Q

What muscles hold the valves shut

A

Papillary muscles

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56
Q

What opens the valve

A

Papillary muscles does not open valve,pressure opens valves…

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57
Q

What does Chordae tendinae do?

A

The are at the valves…open or close.

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58
Q

What vessel takes blood from the heart to the head

A

The common carotid.

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59
Q

Av valves are bigger and the resistance is ?

A

Lower and the pressure gradient is also lower

Chodae tendinae and pap muscles are on the valves because it may pop open easily

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60
Q

Whats the main function of the CV system

A

The main functions of the cardiovascular system are gas transport, nutrient delivery, and waste removal

depends on blood circulation a lot.

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61
Q

FYI

A

Oxy blood flows through systemic circulation]deoxyblood flows through pulmonary circ

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62
Q

Opening and closing of heart valves are due to?

A

passive responses of the valves to pressure gradients

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63
Q

What does the PCWP signify

A

. The measured pulmonary capillary wedge pressure is an approximation of left ventricular end-diastolic pressure.

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64
Q

WHat are the uses of Pulmonary artery catheter

A

Uses include measurement of RA, RV, PA pressures, LA pressure (pulmonary capillary wedge pressure), cardiac output (by indicator dilution or thermal dilution technique

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65
Q

In ultrasound method for measuring CO what factors are considered?

A

The velocity of blood flow x Area.

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66
Q

2 types of cardiac cells are ?

A

Contractile and conductile cells

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67
Q

What are contractile cells

A

cardiomyocytes, calcium are in them,they contract..heart ejects blood,
a workforce of the heart
Bulk of atrial and ventricular tissue
Work horses of the heart

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68
Q

what are conductile cells

A

specialized cardiomyocytes
Sole purpose is to generate and propagate electrical activity to spread electrical activity across contractile cells …Not Neurons…..(take away the actin and myosin)
they spread an Ap …they dont contract.

• Sinoatrial Node
• Atrial internodal tracts
• Atrioventricular Node
• Bundle of His (Common Bundle)
• Bundle Branches (Left & Right Branch Bundles)
 Purkinje Fibers
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69
Q

difference btwn cardiac and skeletal muscle is that?

A
  1. both have light and dark band/striated
  2. Cardiac is not attached to a bone/skeletal is
  3. skeletal muscle has a lot of nuclei/runs the entire length,origin to insertion
  4. cardiac muscles has one nucleus(centrally located)/small,or 2 nuclei..maybe centrally located.

5.branched at its ends….this is used for connection with other cells.
cos they are small cells, they are connected to each other..when they contract they try to pull apart..so the connection must be strong..
Lots of tension in the intercalated disc.
Has lots of desmosomes..which will prevent cells from ripping apart when they pull each other.
Has gap junctions btwn cells..
there is a part in the desmosomes that is parallel to the sarcomere….which prevents tension between cells
this part has gap junctions which are weak..
When Na or ca floods a cell right or left.it moves through the gap junction and depolarize neighboring cells…
one cell depolarizes and cause another cell to depolarize

  • mono/bi-nucleated (skeletal muscle cells multinucleated)
  • Reduced SR system but extensive T tubule system??
  • large/numerous mitochondria
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70
Q

how is Ap propagated through the heart

A

By way of Gap junction

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71
Q

Unique Feature of cardiomyocytes:

A

Intercalated Discs 
• Desmosomes – mechanical coupling
• Gap Junctions – electrical coupling

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72
Q

Similarities between skeletal and cardiac muscles

A

Sliding Filaments producing force/shortening
Regulation of contraction by increase in intracellular calcium
Calcium binding to Troponin to move tropomyosin and uncover myosin binding site on actin

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73
Q

Differences between Skeletal and cardiac muscles

A

skeletal
Innervation by Somatic Nervous system
Source of rise in calcium – SR(L type Vgcc or dhp receptor
Removal of calcium – SR…and ECF..pumped into this
Direct control from brain to muscle…brain says contract muscle contract

cardiac
Innervation by Autonomic Nervous System(Uses real neuron..hormones..higher HR…conductile cells??
The brain tells the heart to beat faster or slower ..brain does not tell it to beat…tells it to beat harder or go back to resting state. ..contractility

Source of rise in calcium – from ECF(L type VGcc AND from SR(ryanodine receptor)
Removal of calcium – Ca ATPase pumps (plasma membrane and SR) AND plasma membrane Na/Ca exchanger (3xNa+/1xCa++)
has more exposure to ecf .

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74
Q

Ventricles feel passively or actively?

A

Passively

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75
Q

Early contraction is called

A

Isovolumic contraction.

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76
Q

what direction does the heart contract or squeeze in

A

from the bottom upward

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77
Q

what signal in the heart triggers myocyte contraction

A

Electrical signal

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78
Q

What cells spreads the electrical signal in the heart

A

Conduction System(Conductile cells) of the heart spreads the electrical signal in a highly organized pattern/sequence

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79
Q

What distributes impulse down the ventricular myocardium

A

Purkinje fibres

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80
Q

The normal pacemaker of the heart

A

SA Node:Automaticity:

spontaneous firing at 100b/min

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81
Q

SA Node connected to AV Node by

A

Atrial Internodal Pathway

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82
Q

Sa Node components are

A

specialized conducting cells
~ 50msec
stimulus passed to contractile cells which spread it across both atria
stops at atria – myocardium of atria and ventricles is not connected.
Overdrive suppression– faster firing of SA node suppresses the other cells from acting as pacemakers

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83
Q

AV Node components.

A

smaller cells/slows signal
100msec to move through AV node
Important – allow time for blood flow
AV node normal firing frequency ~ 40/min

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84
Q

What location does the bundle of His enter the interventricular septum

A

Av Bundle, Bundle of His.

The only electrical connection between atria and ventricles

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85
Q

Left and right bundle branches

A

travel toward the apex

left much larger

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86
Q

Purkinje fibre

A 
larger cells
fast conduction system
move upward from apex to base
effect to push blood upward
Purkinje cell normal firing frequency ~ 15- 20/min
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87
Q

Vent Ap phases and explanation

A

4-heart resting.diatole,refilling
0-Na inward flow after threshold is reached and VGSG opens ,rapid upstroke,..depolarization of cell
1-VGCC..ca flows in..responsible for plateau..cardiomyocytes contract..longer the plateaus(btw 1-2)..longer the contraction,stronger the contraction ..cos crossbridges formed and more blood ejected…..its one and done so relaxation can occur..cant keep it so long..so it shud be done emptying..because at this time there is no filling occurring ..because there is emptying
3..Repolarization occurs .potassium leaves the cell,we pump calcium out the cell.
Repolarixzation occurs
4.potassium chanells oppen allow cells to re polarize and and stay re polarize…and then filling can occur.

3-

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88
Q

(SA node Ap )

phases/explain

A

Phase 4 is slow,this is cos Na is not rushing in(slope)..NA leaking in slowly…causing an inward “funny sodium current”.when over threshhold..
T type VG ca channel opens,low amount of
ca come in,getting it to the threshold for L type VG ca to open. Rapid upstroke happens as ca come rushes into cell
3. Repolarization happens when potassium leaves cell after VG potassium chanel opens and ca is pumped out. and start over again

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89
Q

Sa node-Av node-ventricular contraction time ranges

A

0.03…Ap spreads quicly in the atria and -0.16(Bundle branch) …-0.22(Base of the heart)
AV node slows it down

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90
Q

Characteristics of T type voltage gated Ca channel

A

Opens and closes quickly

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91
Q

Explain cardiomyocyte Contractile cell Ap phase 0

A

Threshold (-75 mV)
Depolarization after we get over a treshhold
Quick opening of voltage gated Na+ channel
Na+ influx…then sodium close
T-type VGCC open (not shown) – minor Ca++ influx
Low Threshold for opening….little bit of ca…..gets us over the Vgsc…

Closing of K+ (KI) channels (inward rectifier)….
inward rectifying k chanells open cos the cell is polarized…as cell depolarized…K inward chanels(Ki) close..they cant leave
Voltage gated K+ (Ks & Kr) not open yet…they open slower

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92
Q

Explain cardiomyocyte Contractile cell Ap phase 1

Early repolarization

A

Early repolarization
Na+ channels close
T-type VGCC close (not shown)
K+ efflux thru (to, transient outward) channels
L-type VGCC not fully open yet
Na+ 3/Ca++ 2 reversal(always open)..pumps na and ca based on this depends on
Conc gradient Na
conc gradient ca
Membrane potential
when membrane depolarizes and is high..chanell will reverse above its reversal potential..calcium will come in and sodium will go out
I na/ca…3 sodium out/2 ca in.. this regulates the height of our plateau….
digozin affects the sodium gradient..poisons the na/k pump……..keeps ca in the cell and changes sodium gradient.

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93
Q

Explain cardiomyocyte Contractile cell Ap phase 2

Phase 2..plateau

A

L-type VGCC open!!(credit for plateau)
Calcium influx
K+ channels (Ks & Kr) partially open, some K+ efflux
Vm near reversal potential of Na/Ca exchanger
Na/ca regulates height of plateau

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94
Q

Explain cardiomyocyte Contractile cell Ap phase 3

Phase 3: Repolarization

A

L-type VGCC close
K+ (Ks & Kr & KI) channels fully open
efflux of K+
Influx of Na+ & efflux of Ca++ via Na/Ca exchanger
cell repolarizes
inward rectifying ki opens…far from nersnt potential..potassium rush out of cell….we roparize a little faster.
Atp/ca pump that pumps calcium back into the SR

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95
Q

Explain cardiomyocyte Contractile cell Ap phase 4

Diastole

A

Phase 4: Diastole
K+ (KI) channels remain open – near Nernst potential
All other channels are closed

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96
Q

Facts about cardiomyocyte contractile cell phase 1-4

A

not shown in the diagram, there is a T-type VGCC open during phase 0 & 1
Ks & Kr are voltage gated and open when cell is depolarized
KI (inward rectifier) is only open when cell is repolarized
Na/Ca exchanger is always open, in phase 4 Ca++ is very slowly removed from cell (Ca++ concentration is too low for effective removal)

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97
Q

Absolute Refractory Periods of Heart Muscle

A

Much longer effective (absolute) refractory period in cardiac muscle compared to nerve/skeletal muscle
limits frequency of action potentials.
one contraction happens and relaxation….
Multiple Ap dose not get sent or generated like the skeletal muscles…because

• built in safety mechanism
 # prevent tetanic contractions
#prevent an ectopic pacemaker from stimulating contraction
#allows time for ventricle to 	fill
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98
Q

what is the role of Role of Calcium in Excitation-Contraction Coupling of the cardiomyocyte

A

Increasae in Ca:
T-tubules present in the cardiomyocyes also .everywhere in the Ttubule is Extracellular.

Calcium enters myocyte via L-Type calcium channels..in skeletal muscle this Chanel is physically connected to the Ryanodine receptor in cardiac muscle it is not.The calcium has to physically bind to the Ryanodine receptor when it comes in
• This calcium binds to ryanodine receptors on SR and stimulates release of calcium from SR.
“Calcium induced ca release”…this is what open the Ryanodine receptor.
More release of ca from the Extracellular space in cardiac muscles than the skeletal muscles..(Ca Chanel blockers) affects the Ltype VGcc in cardiac muscles but not in skeletal and smooth muscles.because of the difference in ca binding to the Ryanodine receptors

Removal of calcium:
Calcium pumped back into SR (SERCA pump)
Calcium extruded to ECF via the Na/Ca exchanger
in cardiac muscles we pump more calcium into the EcF than the SR..
in skeletal muscle almost all goes into the SR because they all came from there.

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99
Q

Explain the Action Potential phases of SA Node:

A 
Phase 4 – pacemaker potential
Na+ channels open – funny current
Voltage gated K+ channels closed
upward drift of membrane potential  
T-type VGCC opens mid-phase
Slow influx of Ca+, slow depolarization...enough to get over sodium threshold

Phase 0 – depolarization
T-type VGCC closes
L-type VGCC opens
Large influx of Ca+, rapid depolarization

Phase 3 – repolarization
L-type VGCC closes
Influx of Ca+ stops
Voltage gated K+ channels open
efflux of K+

NOTE: no phase 1 or 2 for SA node.

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100
Q

Explain Autonomic Regulation of SA node: Dual Regulation

A

Sympathetic Regulation: Beta -1 Receptors/nor-epinephrine :
opening of Na+ and Ca+ ion channels ,influx of Na+ and Ca+ increase steepness of pacemaker potential
More rapid depolarization
Reduced repolarization
start higher.
Effect: shorter time for SA node to reach threshold
INCREASES FIRING RATE OF SA NODE AND THEREFORE HEART RATE: POSITIVE CHRONOTROPIC EFFECT

Parasympathetic Regulation: Muscarinic Receptors/ACh
opening of K+ channels
efflux of K+
Hyperpolarizes cell and decreases steepness of pacemaker potential..we start lower…will be slower
Effect: longer time for SA node to reach threshold
DECREASES FIRING RATE OF SA NODE / HEART RATE: NEGATIVE CHRONOTROPIC EFFECT
Slower depolarization

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101
Q

what is the Q wAVE on the Ekg

A

Signal coming down the purkinje fibre

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102
Q

what are the 2 components must be found in the ekg

A

R and t wave

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103
Q

what is effective refractory period (ERP)

A

is the period during which another action potential cannot be elicited

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104
Q

what is the relative refractory period (RRP)

A

it is more difficult to elicit an action potential than during phase 4

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105
Q

What happens during the Pr interval

A

Time btwn atrial contraction to the ventricular contraction…
time it takes for blood to unload from the Atria to the ventricle….0.12-0.20

or Atrial depolarization + Av nodal delay.

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106
Q

pwave measure

A

0.08-0.10

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107
Q

qrs complex

A

0.06-0.10

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108
Q

Explain standard Limb leads per I,II,III measurement

A

In standard limb leads I, II, and III, voltage differences are recorded between the right arm and left arm, right arm and left leg, and left arm and left leg, respectively, with the first in each pair of electrodes being negative and the second being positive.

For the three augmented leads, the negative electrode is a combination of two limb electrodes, and the third limb electrode is positive

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109
Q

Explain Six precordial leads measurement

A

For the six precordial leads, the three limb electrodes are combined as the negative electrode, and the positive electrodes are placed directly on the chest in specified locations. Analysis of specific types of disease is aided by comparison of tracings made with multiple leads.

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110
Q

what side will have more heart attack

A

left side

because more muscle and harder to perfuse

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111
Q

Occlusion of RCA…

A

Right side of heart and posterior part of Lv.Posterior (Inferior wall)MI

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112
Q

Occlusion of the LCA

A

LAD and LCX:

Massive Anterolateral MI

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113
Q

Occlusion of the LAD

A

Front of Hear anterior part :Anteroseptal MI

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114
Q

Occlusion of the LCX

A

Left side of heart ..Left lateral of heart .

Lateral Wall MI

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115
Q

Which side is the hardest layer to perfuse in the heart

A

Hardest to perfuse the Subendothelial layer of the left ventricle

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116
Q

What happens with obstruction to blood flow

in the heart muscles

A

The end result of obstruction to blood flow is necrosis of the muscle that was dependent on perfusion from the coronary artery obstructed.

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117
Q

what happens to systole in tarcycardia

A

shorter,

feeling time will get shorter..pumping time gets shorter

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118
Q

In Afib

A

No P, we have AV node firing at random times and QRS,Atrial fire at random times.

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119
Q

What does the R-T segment represent.

A

systole

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120
Q

T-R segment

A

Diastole

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121
Q

Atrial tarcy or svt

A

Av nodes fires on its own at a faster pace ..
ventricles working correctly
we get blood flow nornal

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122
Q

Junctional; rythym

A

Av node firing, this is a back up for SA Node…no pwave and slow

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123
Q

Junctional Accelerated rythm

A

same as Junctional rythm but faster…no P wave…The AV node takes over more than its rate of firing

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124
Q

Idioventricular rythm

A

Sa node and AV node not firing…when impulse starts in the ventricle…purkinje fibre fires

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125
Q

Vtach

A 
No pwave
Ventricular pacemaker runs very fast..
no filling
not much blood pump..
ventricle not relaxing
126
Q

PAC

A

Longer diastole…more filling of the heart ..more blood than usual and the more blood pumped..thats the beat noticed as a prenmature beat..Av node fires prematurely

127
Q

PJC

A

came from the ventricle

128
Q

Vfib

A

ventricle quivers..no pumping of blood.
Defib the heart
depolarize the cell.

129
Q

Asystole

A

flatline

130
Q

How do Action potential spread..

A

They do this through conductile cells,they do not contract

131
Q

Whats the benefit of pause in the conduction of the AV Node.

A

Pause in conduction at the AV node allows proper filling of the ventricle

132
Q

PA pressure range

A

15-30/3-12

133
Q

RA PRESSURE RANGE

A

0-8

134
Q

RV pressure range

A

15-28/0-8

135
Q

LA pressure range

A

4-12

136
Q

LV pressure range

A

90-140

end diastolic range..4-12

137
Q

What is the pressure relationship btwn the left ventricle and the aorta

A

Pressure in the lv has to be high or higher than aortic pressure.
Valve opens with change in pressure. And blood flows from the high pressure to the low pressure

138
Q

Whats the relationship between the Av valves and the Semilunar valves

A

Av valves are bigger than the semilunar valves

139
Q

Whats the pressure gradient btwn LA and LV for Mitral vale to open

A

1mmhg pressure gradient;;
this is about have a pressure diff between valves to direct the flow of blood
‘]

140
Q

How does pressure compare between the pulm artery and the pulm vein

A

Blood in the pulm artery has to be higher pressure than the pulm vein and the pressure drop

141
Q

How does pressure compare between the vena cavae and the RA

A

Pressure in the inferior and superior vena cavae has to a little higher than pressure in the RA

142
Q

what happens when pressure in left ventricl gets lower than pressure in the in the LA

A

mitral valve opens …blood flow from LA to LV

143
Q

What happens with the R wave

A

Ventricular depolarization and R wave

144
Q

What happens when LV pressure increases

A

Mitral valves close after pressure in the LV increases higher than LA.Blood rushes backuop to the LA and slams the valve shut

145
Q

When we have all valves closed after the LV increases pressure and Mitral valve closes…Does the volume change?

A

No.

there is no blood leaving the left ventricle since all valves are closed.this is Isovolemic contraction.

146
Q

When pressure in LV greater than Ao pressure.

What happens?

A

Ao valve opens and ejection occurs into the aorta…the Pressure in the Ao increases.The Ao gets bigger so it can absorb blood. Volume of left ventricle gets smaller

147
Q

What happens when pressure in left ventricle gets lower than pressure int the AOrta.

A

Blood trys to rush back into the the LV…Aotic valve slams as seen by the Dicrotic notch

148
Q

Ventricular cardiomyocytes relaxes and repolarize and relaxes,what happens to contraction and pressure

A

relaxation happens. pressure decreaes in the LV

149
Q

Isovolumic relaxation

A

All 4 valves are closed cos LV is relaxing after ejection

150
Q

when does the mitral valve open

A

during diastole

151
Q

when does the MV close

A

During systole

152
Q

Blood continuously flows into the left atrium from where?

A

Pulmonary vein

153
Q

what is the filling pattern of ventricular volume wiggers diagram

A

Rapid passive filling then becomes active

154
Q

whats is the a wave

A

Atrial contraction

155
Q

whats the c wave

A

ventricular contraction

156
Q

what is the v wave

A

Ventricular relaxation(Mitral valve opens

157
Q

What muscles keep the mitral valve intact

A

Chordae tendinae and the papillary muscles

158
Q

what is the first heart sound …

A

S1 and this is the Mitral valve closure(start of isovolumic contraction)

159
Q

What is the second heart sound

A

S2 and this is the aortic valve closure(Start of isovolumic relaxation)

160
Q

what is s3

A

Blood flows rapidly into the ventricle at the start of diastole,blood flow so fast that its hitting the ventricular walls.Happens in young children and also in endurance athletes that have high stroke volume.This volume hitsn the ventricle during passive filling.
in a heart that is not healthy the sound comes from blood filling stiff heart

161
Q

Formular for CO

A

SvxHr

162
Q

s4 heart sound

A

This is heard during atrial contraction.this is pathological.

163
Q

Wiggers diagram peak shows

A

Systolic pressure

164
Q

R wave shows?

A

Ventricular contraction(Calcium comes in quickly and force of contraction gets stronger and more crossbridge formation.)

165
Q

Can both valves open at the same time?

A

No , never

166
Q

What causes the mitral valve to close

A

valve slams shut because of ventricle generates high pressure(Isovolumic contraction)

167
Q

what happens to the pressure in the aorta as blood flows into it

A

Pressure increases

168
Q

During repolarization does contraction happen?

A

No and pressure in the LV decreases.

169
Q

What causes the dicrotic notch

A

Aortic valve closes from blood attempting to go back into the LV from the aorta.

170
Q

When does isovolumic relaxation occur

A

All valves are closed,No blood flow in LV and this is during ventricular relaxation

171
Q

What happens with the blood sitting in the LA

A

Comes from the pV constantly,but sits there during systole waiting for MV to open during diastole for ventricular filling

172
Q

What is the pattern of ventricular volume during filling

A

Rapid passive filling , plateau and then rapid slow filling

173
Q

What location can we see the venous pulse

A

Jugular vein

174
Q

T wave signals

A

Signals relaxation

175
Q

Heart sounds

A

S1: “lubb”
Closure of AV valves

S2: “dubb”
Closure of Semilunar valves

S3: rapid passive filling
Normally not heard in adults
May be present in children + endurance athletes

S4: atrial systole
normally not heard in adults

Murmur:
gurgling sound as blood moves through damaged valves
Bruit:
abnormal sound as blood runs past an obstruction in arteries

176
Q

whats the Benefit of Jugular vein pressure

A

The jugular venous pulse has the same a, v and c waves as the atrial pressure curve.
(no valve separating central venous space from the atrium)

The JVP can be visualized in a reclining patient by observing the filling level of the internal jugular vein

JVP is useful in diagnosis of some forms of heart disease

177
Q

what is stroke volume

A 
Stroke volume (SV) is the volume of blood ejected during systole
SV = LVEDV [left ventricular end diastolic volume] – LVESV [left ventricular end systolic volume]
The ejected blood causes the aorta to distend

this is also the blood ejected with every heart beat

178
Q

What is Aortic compliance and how does it relate to the pressure generated in the LV

A

Compliance is defined to be ΔV / ΔP [change in volume / change in pressure]
The more elastic the aorta is, the greater its compliance
The greater the compliance, the less pressure increase is needed

179
Q

What happens with aortic recoil during diastole

A

During diastole, the aorta recoils

Diastolic recoil helps maintain pressure during diastole

180
Q

What happens with Elasticity and compliance during aging

A

Aging generally results in a decrease in aortic elasticity & compliance
This leads to an increase in pulse pressure
Arteriosclerosis also results in loss of elasticity

Pulse wave velocity increases with decreasing elasticity

181
Q

IS aortic recoil active or passive

A

Passive

182
Q

What happens with PP and Aortic vessel compliance. with young and old people

A

Older stiff vessel…increase PP

Younger elastic vessel …
Decrease pulse pressure

183
Q

What happens with PP with Slower or low HR

A

Results in more time for Aorta to empty and also lower systolic pressure
This results in Increase PP.

184
Q

what happens with pp with arteriosclerosis

A

Higher SBP,Low DBP, higher PP

185
Q

what happens with pp during HTN

A

Higher SBP,Higher DBP

186
Q

What happens With PP during Aortic insufficiency

A

Ventricle fuller than usual due to the blood that is leaking back
..
Inturn ejects more blood than usual on the next cycle hence high SBP,Low DBP and High PP

187
Q

how do we change HR

A

change the slope and change the rate of depolarization

188
Q

What happens to MAP and pp as blood moves through the system

A

These variables will fall as blood moves through the system…AT THE VENOUS SIDE THERE Is no PP from the capillaries

189
Q

Formular/factors that aff for cardiac Output

A

Cardiac Output = Heart rate x Stroke Volume

= HR [ml/beat] X (EDV- ESV) [beats/min]

190
Q

what are the factors that affect your stroke volume

A

Preload (EDV)
more vol in the left ventricle more blood ejected

Contractility:More calcium in cardiac muscle more crossbridges formed and more stronger the contraction,more blood ejjected

Afterload (SBP)..pressure to overcome to eject blood

191
Q

How do we Alter HR via SNS and PSNS innervations

A

Sympathetic Innervation :
 Norepinephrine/epinephrine
Receptors: Adrenergic - beta 1 receptors
Positive chronotropic effect

Parasympathetic Innervation
Acetylcholine
Receptor: Muscarinic Ach - M2 receptor
 Negative chronotropic effect

192
Q

what is EF

A

What amount of blood put in the left ventricle did we actually eject

Ejection fraction = SV/EDV or (EDV – ESV)/EDV
Ejection fraction in a normal heart > 0.5 (> 50%)
Can be measured non-invasively by echocardiography
Example, EDV = 120 ml, ESV = 50  EF = 70/120  58%

193
Q

How does Fran-starling law affect the heart

A

we need an Optimal length of stretch produced by filling of the ventricle that will give enough overlap for actin and myosin binding to occur….too little has a low output..
too much will cause a plateau hence no more functional output after this point…we need just enough

194
Q

In a failing heart what is the compensation

A

Increase preload

195
Q

At rest what shud the EF be

A

EF shud be over 50%

196
Q

What determines force of contraction

A

Force of contraction is a function of the number of cross-bridged formed

197
Q

Cross bridge formation can be increased using the following mechanism

A

Frank-Starling Law of the Heart - increasing functional overlap of myosin and actin
Preload – greater filling stretches myocytes

2) Contractility – increasing Ca++ in the cardiomyocytes, via
SNS activation with epinephrine, increases Ca++ influx
The parasympathetic nervous system does NOT affect contractility
Positive inotropes increase contractility, negative inotropes decrease it

198
Q

For maximum increase in contractility as seen in exercise and at rest
u can increasae contractility by using the following

A

1.increase preload and increase cross bridge formation with exercise and hence increase contractility

199
Q

if u are not getting enough blood flow u are

A

cold

200
Q

Enough blood flow is?

A

Warm

201
Q

what does incresing preload do to a failing heart

A

it is bad for a failing heart

202
Q

If we want to Increase Left ventricular diastolic pressure we need to increase what pressure

A

Pulmonary pressure….more pulmonary pressure,more pulmonary edema..
lungs are now wet.

203
Q

If you have Low CO and cold on the Frank sterling curve .How do you get into the warm side.

A

give volume and increase preload and hence SV,then u will be in the warm side.

204
Q

If pt is in HFailure and preload increae continues to move pt from cold to warm …but whats the negative effect in a negative heart

A

pt ‘s HF will worsen and remains in the cold

205
Q

iN the Frank sterling curve the best quadrant is?/

The worst quadrant is?

A

Warm and dry/

Cold and wet. which shows severe heart failure.

206
Q

TReat t cold and wet with what drug

A

Diuretic

207
Q

How do we increase blood pressure in the heart

A

Give Vasodilator

and Give Positive inotrope….this will move from cold and wet to warm and dry.

208
Q

Giving just Inotrope will have pt in what quadrant

A

warm and wet

209
Q

Giving Inotrop and Vasodilator will have pt in what quadrant

A

warm and dry but borderlin close to wet since the cogestion is still there

210
Q

The optimal treatment for heart failure will be?

A

Give p vasolidator,inotrope and diuretic to have them optimally in warm and dry

211
Q

DVI examples are?

A 
D = Diuretic, e.g. furosemide
V = Vasodilator, e.g. amlodipine
I = Inotrope (positive), e.g. digoxin, dobutamine
212
Q

Mechanism of blood flow in a pump

A

Pump turn off pressure same
MCP=7mm every where

pump turned on pressure on inlet side is gonna be
decreased and lower on the outlet side.

heart turned on pressure on the venous side is gonna b lower(2) than that on the arterial side.(120/80)

213
Q

Increase CVP will have increase CO t/f?

A

T

214
Q

What happens to CO and Preload when heart on or off

A

In normal resting function, output is 5 L/min and CVP is ~2 mmHg
When the pump is stopped, pressures equilibrate throughout to a “mean circulatory pressure” (MCP) of ~ 7 mmHg

215
Q

From the vAscular function curve we note that

A

The higher the cardiac output. the lower the venous pressure
Vascular Function Curve: an inverse relationship is observed between CO (the independent variable) and CVP (dependent variable).

216
Q

From the cardiac Function curve, we note that

A

As we increase CVP we will also Increase CO

Cardiac Function Curve: a direct relationship between these variables is observed CVP is the independent variable and CO is the dependent variable (Frank-Starling mechanism)

217
Q

Integration of Cardiac and Vascular Function graph interpretation
slide 17

A

Increase contractility –increase CO(Blood pumped) and Decrease CVP.

Increase Preload(giving Fluids)–Increase CVP and Increase CO.Then CVP will Decrease due to Increase CO but CVP will still be higher than started.

Decrease Arterial size(Inc Resistance)—Decrease CO and CVP will Decrease slightly.

Decrease Resistance will increase CVP and CO, then Decrease CVP due to increase CO

218
Q

Summary of Cardiac Pressure-Volume Loop graph

A

End of systole ..low vol/low pressure at A
…..LV filling Begins and MV opens
Vol of the area of the curve is the work done by the ventricle=FxD( pressure x v2-v1)

219
Q

CArdiac pressure loop with volume variations…..with

Increase preload, increase Afterload and increase in contractility

A

Increase preload has increase in volume ejected..meaning same volume put out as put in.
2.Increase afterload will demand more pressure to pump hence increase pressure.

increase contractility wil increase the force of contraction as more ca be dumped in and stronger force of contraction and more blood pumped out.
So vol will decrease with increase contractility
and vol will increase with decrease in copntractility.

220
Q

With icrease AFterload what happens to cardiac output

A

It falls after a certain level.

With high pressure Aortic valve closes quicker

221
Q

Control of the cardio vascular system

A

Heart rate – chronotropic (HR)
↑ HR  ↑CO, ↑BP

Contractility – inotropic
↑contractility  ↑ejection fraction  ↑CO, ↑BP

Systemic vascular resistance (SVR)
↑SVR  ↓CO, but ↑BP

Central venous pressure (CVP) (aka JVP, venous return)
↑CVP  ↑LVEDV  ↑SV  ↑CO, ↑BP…constriction of veins…increasing blood vol

The sympathetic nervous system tends to increase each of these through epinephrine, norepinephrine, and dopamine.
The parasympathetic nervous system tends to decrease each of these through acetylcholine. PNS has no effect on contractility.

222
Q

What inervates the SA node for Hr Regulation

A

ANS

223
Q

What happens with Filling With fast and slow HR

A

Slow Hr,more time to fill.

Fast HR Less time to fill.
Max Hr is limited by filling time.
With increase HR Co Reduces after a certain point.

224
Q

how is blood pressure monitored with baroreceptors receptors

A

Baroreceptors : respond to changes in stretch

Increased stretch  increased firing of sensory nerves

Decreased stretch decreased firing of sensory nerves

Location: Two sites:

Wall of aortic arch transmit to Sensory nerve: Vagus Nerve

Carotid sinus transmit to Sensory nerve: Glossopharyngeal nerve

this will send info back to the brain about how much pressure we have

225
Q

How do we regulate B/p.what do we manipulate

A

map =CO x SVR

226
Q

During response to an increase in B/p what is the action of the Cardio-inhibitory center

A

Cardiac Decelerator(PSNS) acts on the SA node and hence dercreasing the HR and B/p

227
Q

During response to a decrease in B/p what is the action of the Vasomotor center

A 
Cardiac accelerator(SNS) acts on the SA node and contractility increasing their firing and 
Vasoconstricting the veins and arteri oles increasing the constriction of those vessels,
veins increasing preload and Arterioles increasing afterloadhence b/p increase
228
Q

what should be measure d in HF patients to show how volume overload they are?

A

BNP-in the ventricle

ANP- in the Atrium

229
Q

How does the RAAS regulate blood pressure

A

1) Renal juxtaglomerular cells sense decrease in blood pressure and release renin;
(2) Renin activates angiotensinogen to angiotensin I;
(3) Angiotensin I is converted to angiotensin II via angiotensin-converting enzyme (ACE) in the lung;
(4) Angiotensin II promotes vasoconstriction(increase svr and increases CO) and stimulates aldosterone secretion from the adrenal cortex resulting in
(5) renal sodium and water retention and an increase in blood pressure.

6.Hypothalamus
Minor increase in ADH release: Increase water reabsorption by kidney

Stimuli for renin release:

  1. Decrease in blood pressure (stretch receptors in kidney tubules “renal baroreceptors” )
  2. Sympathetic activation tubules innervated with sympathetic nerves)
  3. Decreased flow of sodium through the kidney tubules

NOTE: vasopressin (ADH) & thyroid hormone also independently increase cardiac output.

230
Q

ANP action for Increased BP

A

Hormonal response to atrial stretch:
- Atrial cardiomyocytes release ANP (atrial natriuretic peptide) in response to stretch

Effects of ANP:

- increased sodium excretion 
- water excretion 
- vascular smooth muscle relaxation
- blocking, ADH, Aldosterone, NE

NOTE: BNP, similar hormone, released from ventricles.

↑ Blood in atria ↑ atrial stretch ↑ANP release↑ sodium and water excretion↓Blood volume

if ANP and BNP are elevated it means something has gone wrong

231
Q

To blow off CO2,what should be a good mix for mechanism of action

A

Inc CO and Inc Resp rate to get off co2 faster.

need to get the co2 to th e lungs…so increase co

232
Q

Chemoreceptor reflexes with increase in Co2

A

Specialized receptors:
Respond to pH levels in the blood
Elevated CO2 = decrease in pH

Receptors found within sensory neurons of the carotid sinus and aortic arch.

Increse resp rate,co2 blown off..

233
Q

Whats happens in standing to lying position in short term blood pressure regulation

A 
in response to changes in arterial pressure detected at the carotid sinus and aortic arch baroreceptors
as venous return increases.
Stroke vol inc
Map inc
Inc firing of baroreceptors
this sets off PSNS which inturn will .
reduce HR and CO
234
Q

Long term blood pressure regulation is all about?

A

using Blood volume to maintain blood pressure..much slower process.

235
Q

AFter sudden change in blood pressure ,what systems respond the quickest

A

Baroreceptors…s
Chemo-receptors…s
CNS ischemic responses…s
Stress Relaxation…..s

takes hours for renal blood volume pressure control to kick in but it provides a great amount of support after it does

236
Q

Long term b/p regulation summary

A

In addition to evoking mechanisms for acute adjustment of blood pressure, changes in blood volume and pressure will also activate renal mechanisms for adjusting blood volume.

Reduced blood volume (and therefore arterial pressure) will stimulate the renin-angiotensin-aldosterone system, with the end result of sodium and water retention. Reduced blood pressure will also activate the sympathetic nervous system, which will stimulate renin secretion and have direct effects on the kidneys.

On the other hand, increased volume will stimulate atrial natriuretic peptide (ANP) release by the heart. ANP has direct renal effects (natriuresis and diuresis) and also inhibits aldosterone release by the adrenal cortex. ADH, antidiuretic hormone; CN, cranial nerve.

237
Q

What location does the changes in b/p go to b4 communication for action to be taken

A

NTS = nucleus tractus solitarius

238
Q

Blood vessel structures are subdivided into ?

A

Tunica intima
Endothelia
Internal elastic lamina

Tunica media
Smooth muscle
Elastic fibers, reticular fibers
External elastic lamina

Tunica adventitia
Collagen I, elastic fibers
Vasa vasorum..blood supply of the blood vessel
outermost layer

239
Q

why is the walls of vein smaller than the walls of artery

A

pressure is higher
in the artery
little resistance in veins,low pressure drop in veins

240
Q

why do we have bigger lumen in the vein?

A

constrict and push out blood for adequate cvp volume

241
Q

Arteries are classified into the following sub classes

A

Elastic artery(Internal elastic layer)

Muscular artery(Internal Muscular Layer)

Arteriole(Smooth muscle cells)

Continuous capillary(Endothelial cells)

242
Q

why do we want arteriaL distension and RECOIL

A

we want the elastic artery to recoil to make it easier for the artery to pump blood out and to maintain diastolic b/p between beats or btwn ejection

243
Q

WE note blood pressure drop at where in the arterial system

A

Arterioles and the capillaries

systemic vascular flow and regulating blood flow.

244
Q

Large elastic artery are passive and elastic…t/f

A

T

245
Q

Muscular artery have smooth muscle they change size according to blood flow demand

A

T

there is blood vesels Vasum vesura….feeding the muscular artery

246
Q

The smaller the vessel the easier to constrict it…t/f

A

T

247
Q

Smooth muscle density decrease as we approach arterioles and capillaries T or false

A

T

248
Q

What helps with movement of nutrients to the Interstitial space from the lumen and viceversa of a capillary

A

Fenestration…allows fast move of materials from one side to the other..
wall must be thin

Transcytosis

249
Q

Capillary must be really thin t/f

A

T

250
Q

3 types of capillaries are

A

these are the vessels between arterioles and venules

Continuous capillaries, the most common type, have tight, occluding junctions sealing the intercellular clefts between all the endothelial cells to produce minimal fluid leakage. All molecules exchanged across the endothelium must cross the cells by diffusion or transcytosis.(Every where in the body)

Fenestrated capillaries also have tight junctions, but perforations (fenestrations) through the endothelial cells allow greater exchange across the endothelium. The basement membrane is continuous in both these capillary types. Fenestrated capillaries are found in organs where molecular exchange with the blood is important, such as endocrine organs, intestinal walls, and choroid plexus.
We want things to move rapidly in and out(Kidney glomerulus,intestinal walls)

Sinusoids, or discontinuous capillaries, usually have a wider diameter than the other types and have discontinuities between the endothelial cells, large fenestrations through the cells, and a partial, discontinuous basement membrane. Sinusoids are found in organs where exchange of macromolecules and cells occurs readily between tissue and blood, such as in bone marrow, liver, and spleen.
Allow rbc to leave and enter capillary on the other side.

251
Q

If we have discontinuos sinusoids…what may happen?

A

End up with edema

252
Q

Capillary sphincter and smooth muscle cells will do what in the capillary?

A

Local blood flow regulators. they can close and open as they want

253
Q

If the capillary needs more blood ,the signal will be sent to the?

A

Interstitial tissue..causing the precapillary sphincter that is close enough to relax…only the tissue that needs blood will get blood and the local precapillary sphincter will open and the blood flow in the capillaries will increase.

254
Q

What will happen to blood pressure as it goes through the capillary

A

B/p will drop.

255
Q

btwn the oncotic capillary pressure and the tissue hydrostaic pressure.The difference in filltration will go to what location

A

This starts out with more fluid out of the capillary than in..Midway fluid gets pulled in more than out.Upon finalization the fluid out is more than in.Hence this diff between out and in..will go to the Lymph and then back into the vascular system

256
Q

Valves in veins mostly in legs,allows blood to flow in which direction

A

In one direction.If the veins fail,this is how we develop varicose veins

257
Q

what is the benefit of valves in the veins

A

Need valve to get fliuid back to heart in this case of low pressure

Venous return is augmented during movement and exercise by contraction of skeletal muscle
Veins outside the central venous system contain one-way valves that provide for uni-directional blood flow back toward the heart

.

258
Q

what are the Effects of Gravity on Venous Pressure

A

In standing position, hydro-static pressures in veins are affected by gravity
Upon standing, CO and arterial pressure fall as blood pools in distending veins in the lower parts of the body. Baroreceptor reflex is important in maintaining pressure and CO
Surface veins above the zero point (right atrium) collapse at a point determined by the actual central venous pressure
Orthostatic hypo-tension can result in vertigo and fainting under some conditions

259
Q

aorta characteristics/ large elastic artery

A

little small muscles ..lots of elastic tissue,distend and recoil

260
Q

Arteries

A

little elastic/more muscles

261
Q

arterioles

A

very small or no elastic in the intima/lots of smooth muscles…constrict smooth muscle ,relax to dilate it

262
Q

veins

A

smooth muscles

263
Q

capillaries

A

only endothelial layer

264
Q

venules

A

only endothelial and Fibrous tissue.

265
Q

whats the Relationship Between Flow, Velocity and Area in the aorta and the capillaries

A

Total cross sectional area of the circulation is lowest in aorta, highest in capillaries
Velocity changes proportionally to the inverse of cross sectional area: Flow = V x A
Velocity in aorta ~30 cm/sec; in capillaries, ~0.1 cm/sec

more capillaries in parallel so we have an increase in cross sectional area

266
Q

Velocity will be slow in an area of capillary that is ?

A

larger

267
Q

Blood will spend more time in veins than in Artery

A

true

268
Q

variables of Poiseuille’s law

A

Q=(π(P1-P2 ) r^4)/8ηL
Flow is a function of pressure gradient, vessel radius, fluid viscosity and tube length, according to Poiseuille’s law, where P is pressure, r is radius, L is length and h is viscosity:

269
Q

if vessel radius changes what happens

A

resistance changes to the 4th power

270
Q

Pressure and radius can be changed every second

A

T

271
Q

Flow going through a pipe equals

A

pressure/resistance

272
Q

Relationship between flow and variables in the poisuilles law

A

Flow is directly proportional to pressure.
16th time the radius.
1/2 time the viscocity and the lenght

273
Q

two cells types we care about in our blood vessels are

A

SMooth muscles(tunica media) and the and endothelial layer(tunica intima)

274
Q

Smooth muscles does what?

A

contract and constrict or relax and dialate

if more calcium..it contracts and constricts…less calcium.. less constriction

275
Q

Endothelial cells will work in what way in the smooth muscles

A

Endothelial cells secrete nitric oxide or prostacycline..which will cause relaxation of smooth muscles through vasodialation…Ento T cell will make Nitric oxide 2/2 to stimulus like sheer stress,Histamine,ach,bradykinin,Atp.
….more flow of blood..more sheer stress..less flow less sheer stress.

relaxation of capillary sphincter will increase blood flow that causes vasodilations..that increases blood flow to whoever that needs it…based on what the local cell needs

276
Q

Myogenic reflex

A

Happens because smooth muscles where stretched….form pressure increase…it clamps down everything ..and nobody gets any more blood accept the place that needs it.

277
Q

Active Functions of Vascular cells:Endothelial Cells

A

Secretory Function
Endothelial-derived vasodilators: nitric oxide (NO) and prostacyclin (PGI2)
Endothelial-derived vasoconstrictors: endothelin
Anti-aggregatory for platelets
Anti-mitogenic for vascular smooth muscle
Also helps blood not to clot

Metabolic
Processing of vasoactive factors: production of angiotensin II and breakdown of bradykinin by angiontensin converting enzyme

Plasticity
Angiogenesis (new vessel growth) in response to injury and ischemia
New blood vessels..normally grow.

278
Q

LAminar vs turbulent flow

A

In laminar flow, lamina nearest the wall is stationary
Next layer slides over the stationary layer
Velocity higher and higher toward center
Little mixing between layers
With turbulence, flow is disorganized with whorls and eddies, mixing occurs between layers
Turbulence may lead to vascular disease

Increase in pressure has much less effect on flow.

279
Q

Reynolds number relationship between lamina and turbulent flow

A

Laminar Flow,
Re < 2000
Fluid moves in streamlines parallel to the axis of the tube

Turbulent Flow, Re > 2000
Elements of the fluid move irregularly in
axial, radial, and circumferential directions.
Vortices frequently develop.
Turbulence reduces the flow associated with a pressure gradient
Regions with turbulence are more prone to vascular disease

Velocity and diameter are independent..
More dense and more faster…more likely to be above Reynolds..
Above 2000….turbulent flow.

280
Q

Wall tension

A

Wall tension (force/unit length tangential to the vessel wall) is the tendency for a longitudinal slit in the vessel to pull apart

T = Pr
where T is wall tension, P is transmural pressure and r is radius
Small vessels in the microcirculation are protected by their small radius

increase in pressure,
increase in diameter hence increase in wall tension or rupture

281
Q

Three Mechanisms of Local Control of Blood Flow

A

gets blood to the tissue that needs it
Metabolic regulation

Autoregulation (myogenic regulation)

Shear stress induced vasodilation

Local mechanisms are aimed at controlling flow in the local vascular bed. Neural and humoral mechanisms are mainly aimed at regulation of blood pressure and volume, but also affect flow in regional circulations in a non-uniform manner)

282
Q

How blood flow happens with metabolic regulation

A

active hyperemia: increased blood flow with increased metabolism…i.f we stop exercising ..we decrease blood flow slowly
we are mostly going to use active.

Reactive hyperemia: increased blood flow reacting to occlusion ..2/2 to a previous deficit in blood flow after occlusion.
Changes in flow reflect effects of metabolic products

283
Q

Factors that affect the cascade of Metabolic regulation of local blood flow.

A

Tissues release metabolic products in proportion to the level of metabolism. Substances released include CO2, H+, K+, adenosine, lactate, prostaglandins, etc
These metabolites produce vasodilation
Thus, increased metabolism results in higher local blood flow
Low O2 also contributes to metabolic vasodilation

More active blood flow,inc in oxygen demand, produce more co2 and ph will fall because of this ,atp ..broken to adp…adp broken to cAmp
Precapillary sphincter relax…increase blood flow will remove metabolite….
Less blood flow..metabolites accumulate..
Too much will wash away too much metabolites…so we need jut enough for the areas that its needed.

284
Q

Myogenic reflex and auto regulation of blood flow

A

Increase in pressure,increase in resistance..no change in flow…
Increase in pressure,flow increase if resistance stays constant…..snap back gives increase in resistance after myogenic reflex has taken place
Myogenic reflex is useful to protect kidney from high blood pressure and to protect the brain from stroking out everytime u get excited….smooth muscles constrict.

If perfusion pressure into a vascular bed such as skeletal muscle (above) is raised artificially, flow initially rises, but returns toward the original level over a short period
This is accomplished by constriction of vascular smooth muscle in response to the higher transmural pressure (stretch)
Thus, local flow can be kept relatively constant in the face of fluctuating pressure through myogenic regulation

If perfusion pressure into a vascular bed such as skeletal muscle (above) is raised artificially, flow initially rises, but returns toward the original level over a short period
This is accomplished by constriction of vascular smooth muscle in response to the higher transmural pressure (stretch)
Thus, local flow can be kept relatively constant in the face of fluctuating pressure through myogenic regulation

285
Q

Shear Stress-Induced, Endothelium-Dependent Vasodilation

A

This shear stress-induced vasodilation requires presence of normal, healthy endothelium
Increased flow is associated with greater shear stress, which causes endothelium to synthesize NO, which then dilates smooth muscle.

Because we have more blood going in Everybody upstream sees more increase in blood flow because of shear stress…N.o will be secreted causing vasolidation….precap sphincter will open causing relaxation…too much blood flow will cause alkalosis because of washing away of chemicals, precap sphincter will close, shear stress will reduce…and then open as needed. Functional endothelial cells needed…

286
Q

Energy sources during aerobic exercises

A

ATp is converted to adp during exercise and phosphocreatine will come together with adp and form atp again.
Creatine goes back and forth into the mitochondria to obtain phosphate and thats how it makes phosphocreatine.

Breakdown glycogen …form lactic acid…anaerobic..produce 2atp

With oxygen …add glucose amino acids and fatty acids, adp can be converted back to atp all day long

Liver and kidney gluconeogenesis producing amino acids

287
Q

Oxygen Consumption During Aerobic Exercise graph

A

U are at rest before running,Metabolism increases after u start running,blood flow lags behind,oxygen deficit in the red area on top is noted,aerobic resp begins in the black line (steady state)and repayment of oxygen debt happens at recovery

288
Q

Cardiovascular parameters at variuos levels of aerobic exercises.the graph

A

The Faster u run faster the Hr

Faster u run stroke volume increases but the higher the heart rate..filling time gets shorter,then stroke vol reduces after a while

As u run faster,the heart beats faster and CO keeps increasing as long as u run aerobically.

Map remains relatively contstant ,slight increase in sbp

Peripheral resistance goes down since we are recruiting more tissues and more capillaries and hence more blood flow

O2 consumption will increase with the speed of running

289
Q

Organ blood flow at rest and during aerobic exercise

A

More blood goes to the skeletal muscle(85% increase) and the heart.
brain the same.
kidney blood is reduce but not by much..skin gets a little bit more blood flow to cool the skin.

290
Q

comparison of sv,hr,co,lv size btwn ahtlete and non ahtlete at rest and at max exercise

A

Bigger stroke vol and co,lower hr for athlete at rest.Resting hr lower cos of larger co
Bigger left ventricle.

Max exercise, higher sv and higher co due to the enlarged heart of athlete hr inc but not higher than non athlete..
the only thing higher in the non athlete is the hr in both cases

291
Q

Coronary blood flow effects of systole.

A

The heart only pumps blood while its not pumping blood.
Contracting muscles is hard to perfuse.
Upon ejecting blood the lv muscle is contracting
Ventricular myocytes relax during diastole.

Early diatole is when we get the most perfusion to the LV Systole it gets little blood flow

High enough pressure can perfuse contracting muscle
Right ventricle can be perfused during systole cos of the low pressure it generates
In vtach there is no perfusion,cells die.
Coronary sinus do not have a medial layer.
they dont stretch much

During diastole, flow is greatly enhanced in the left coronary circulation by the actions of vasodilator metabolites that build up during systole. The metabolite adenosine is believed to be particularly important in this enhancement of coronary flow

292
Q

Factors that affect the flow of blood through the coronary arteries

A

The coronary arteries supply arterial blood to the muscular wall of the heart.
The pressure gradient for flow through the arteries is affected by tissue pressure in the wall of the heart during systole, particularly in the left coronary circulation. Thus, while flow through both right and left coronary arteries is related to aortic pressure

293
Q

What factors enhance flow during diastole

A

. During diastole, flow is greatly enhanced in the left coronary circulation by the actions of vasodilator metabolites that build up during systole. The metabolite adenosine is believed to be particularly important in this enhancement of coronary flow.

294
Q

What kind of blood is in the The Thebesian vein

A

deoxyblood and also

the bronchial veins supply the left atrium with Deoxy blood

295
Q

Which area of the heart is the hardest to perfuse

A

Intramyocardial pressure is highest in subendocardium (inner third of myocardium)

Perfusion of LV myocardium, esp. subendocardium, is limited during systole by this intervening pressure

closer the heart is to the left ventricle,the hardest it is to perfuse.

296
Q

Explain the oxygen supply and demand balance in the Heart

A

Demand on the heart is a function of co x SBP
This show how hard the heart is working

Area under the LVP curve during systole is a measure of LV work and oxygen demand

The supply its getting is the blood pressure during diastole
Area under the aortic pressure curve during diastole is a measure of oxygen supply since most flow to LV myocardium occurs during diastole

Wide pp(sbp goes up)
Inc sbp inc demand
Wider pp supply down demand up.

Failing heart higher pp,
harder the heart works and less supply

297
Q

Cerebral circulation

A

Blood supply to brain ~ 15 % of resting cardiac output,
brain is least tolerant organ to ischemia and relies heavily on glucose metabolism …death of cells within minutes of ischemia

Brain receives blood through 4 source arteries:

  • 2 internal carotid arteries (branch off common carotid)
  • 2 vertebral arteries (branch off subclavian)
298
Q

Circle of willis

A

Anterior communicating artery allows blood to get from the left side to the right side(this is btw the 2 anterior cerebral artery)

299
Q

Explain regulation of cerebral blood flow

Autoregulation

A

Brain gets the blood it needs, blood flow to the brain is constant through different blood pressure(MAP)

regulatory range 50-150

Autoregulation helps prevent an in increase in blood flow (and intracranial pressure) when blood pressure increases and helps maintain adequate blood flow when blood pressure decreases.

• Mainly via metabolic (increases in demand or waste) and myogenic mechanisms (increased stretch) will stimulate vasoconstriction or vasodilation as needed

Sympathetic nervous system does not influence cerebral blood flow (debated)

300
Q

Control of CBF by CO2, O2 and Cushing’s Reflex

A

Cerebral circulation dilates in response to PaCO2
Effects of hyperventilation
CBF is unresponsive to PaO2 above 50 mmHg
CNS ischemic reflex (response to cerebral ischemia) and Cushing’s reflex (response to high intracranial pressure) cause intense SNS outflow to maintain CBF

Increase co2 in the brain…increase blood flow in the brain due to vasodilation

Co2 falls blood flow will fall,
blood flow falls co2 goes up to compensate and increase the flow.

Control of respirations is by co2 until oxygen gets really low(hypoxic) then cerebral blood flow shoots up

301
Q

what are the Relative feedback gain of compensatory responses to sudden drop in blood pressure

A

With chemoreceptors When brain sees the oxygen decrease at the brain stem, it increases cardiac output to increase oxygen to the brain, hence people get increase bp to get oxygen to the brain if they have an occlusive stroke.
Increase pressure, distension and small muscle response by contracting. Overtime they start to relax.
If b/p falls ..relaxation will happen and then they will slowly constrict again.

With a drop in blood pressure, there will be fluid shift from the interstitial space into the vascular space.
Fluid shifts into the interstitial space if the blood pressure is high.

302
Q

Pulmonary Circulation characteristics

A

Low P; low R
100% of CO
10% blood volume
Short transit time

Blood coming from the right side of the heart goes to the lungs
Oxygenated blood.
Its low pressure and low resistance in the right side
100% of cardiac output is going to the lungs
1% of co in the LV goes to the aorta
More blood goes out of the LV than RV

303
Q

compare Pressures in systemic vs pulmonary circuits

A

Much lower pressure in the right side of the heart compared to the left.

304
Q

Explain Normal and abnormal split heart sounds and the Reason behind it.

A

Normal: Inhale /blood in/lower thoracic pressure/Later pulmonic valve closure
Exhale /blood out/Higher thoracic Pressure/Early pulmonic valve closure
Abnormal:
When it has a noticeable split on exhalation then there is a problem and not split during insp…
pulmonic is always delayed by inspiration
If its splits during insp but not exp..the pulm valve is closing before the aorta which means the right side of heart is not getting enough pressure.

305
Q

What allows for more recruitment in the lungs

slide 27

A

If pressure is increased in the lungs the resistance will go down
And the flow will go up a lot(inc in pulm blood flow) allows for more recruitment.
Decrease lung resistance by inc pressure

Recruitment and Distention of Vessels Accounts for Reduction in PVR with Elevation of Pulmonary Artery Pressure

Increase arterial or venous pressure decrease pulmonary resistance.

Ppv will cause alveoli to expand and cap compresses..pvr goes up with inc positive pressure.

306
Q

What are the Effects of Breathing in a low PO2 Atmosphere.

A

pulmonary blood flow goes down at low PO2 if PAP is held constant, due to higher PVR

In “real life”, PVR and PAP rise in low PO2 atmosphere, while CO is increased to compensate for low O2

Long term compensation through polycythemia

High altitude induced pulmonary edema is a pathologic response to low PO2 atmosphere

We don’t send blood to the part of lung that does not get oxygen that means its not ventilated ..so don’t send blood there because it wont get oxygen..

307
Q

Fetal circulation blood flow

A

Umbilical vein…oxygenated blood blood…..goes to the liver via the doctus venosus…Inferior vena cava…right atrium…left artrium…through foramen ovale…rv..pa..doctus arteriosus into the aorta…

308
Q

Hpw does fetal blood communicate with the placenta?

A

Via the umbilical artery

309
Q

How does the foramen ovale close after birth

A

Right side pressure drops
Pressure on left side goes up
The foramen ovalae closes.

310
Q

Balance of Blood oxygenation in the fetal heart

A

Least oxyblood shud stay on the right side,
Left artrium has more oxygenated blood, than the blood comin from the pulmonary artery…lv more oxyblood than the rv
aorta blood should be more oxy that the blood coming out of the PA
Right common carotid artery gets most oxygenated blood.
Therefore brain gets most oxygenated blood.

311
Q

Where does the oxygenation of fetal blood take place

A

In the placenta

312
Q

What may cause the foramen ovale to repoen

A

Foramen overlae closes as soon as birth and pressure changes.
Pressure on right side of heart increases and this causes this to open again.
Clots form and go through the foramen ovale into the systemic circulation that cant handle clots

Physiology (11 decks)

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