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PHGY210 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

FUNCTIONS of the Cardiovascular system

A
  1. Bring nutrients into the body (e.g. from liver to lungs)
  2. Bringing fuel to cells (e.g. glucose from liver to lungs)
  3. Bringing O2 to cells from lungs
  4. Removal of waste products
  5. Circulation of hormones
  6. Circulation immune cells and antibodies
  7. Regulation of pH
  8. H2O balance
  9. Thermoregulation
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2
Q

What circulation-type in insect circulation?

A

OPEN CIRCULATION with a dorsal vessel

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3
Q

How does fluid move in the insect circulation?

A

Fluid pumps out to the head and loathes all the organs and
seeps back in at a very slow rate to re-enter the
cardiovascular system

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4
Q

What is the pumped fluid in insect circulation?

A

HAEMOLYMPH

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5
Q

What circulation-type in fish/piscine circulation?

A

Blood is always contained in either heart or vessel –> closed circulation

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6
Q

What type of circulation is when blood is always contained in either heart or vessel

A

closed circulation

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7
Q

How many loops in fish/piscine circulation?

A

Single loop circulation

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8
Q

How many chambers in fish/piscine heart?

A

2 chambers

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9
Q

Where does gas exchange occur in fish/piscine?

A

Exchange of gas occurs in gill capillaries

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10
Q

Where does deoxygenated blood come from?

A

the systemic capillaries

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11
Q

How many loops in amphibian/reptile circulation?

A

2

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12
Q

How many chambers in amphibian/reptile circulation?

A

3

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13
Q

What circulation-type in amphibian/reptile circulation?

A

closed

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14
Q

What type of heart do amphibian/reptiles have?

A

Univentricular heart

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15
Q

How can amphibian/reptiles breath

A
  • Can breathe through skin via diffusion
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16
Q

How many loops in avian/mamalian circulation?

A

double-lopped

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17
Q

How many chambers in avian/mamalian circulation?

A

4

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18
Q

What circulation-type in avian/mamalian circulation?

A

closed

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19
Q

How many hearts in avian/mamalian circulation?

A

right and left

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20
Q

What seperates the two hearts

A

Interventricular septum

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21
Q

What circulation is the right heart

A

pulmonary

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22
Q

What circulation is the left heart

A

systemic

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23
Q

Cardiac Muscle Cell/Myocyte length and diameter

A
  • 100μm long, round, 20μm in diameter
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24
Q

Diameter of capillaries

A

~5μm

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25
Q

Max distance between capillary and myocyte

A

~10μm (half of 20μm because of midline)

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26
Q

Ratio on average between capillary and cardiac myocyte

A
  • On average 1 capillary/1 cardiac myocyte
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27
Q

Flow between capillary and myocyte

A

Convective flow to inside

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28
Q

Wall of capillaries

A

~5μm

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29
Q

How does oxygen come into the capillary?

A
  • Oxygen comes in via bulk flow which is internalized
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30
Q

PO2 in alveolus compared to in the RBC in capillary

A

higher

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31
Q

3 Components of the Cardiovascular System

A
  1. Pump = heart 2. Pipes = vessels 3. Fluid = blood
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32
Q

Fick’s law states

A

that flow is directly proportional to:

  • diffusion coefficient,
  • area,
  • concentration difference i.e. gradient

flow is inversely proportional to:
-Thickness of membrane

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33
Q

Flux

A

diameter times the concentration gradient

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34
Q

Blood volume value for the standard man

A

5L

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35
Q

Max oxygen/exercise peaks at what age

A

~25 years of age

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36
Q

blood per kg of body weight

A

~75mL of blood per kg of body weight

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37
Q

Match

  • VENOUS SYSTEM
  • ARTERIAL SYSTEM

> Resistance system
Capacitance system

A

VENOUS SYSTEM –> CAPACITANCE SYSTEM

ARTERIAL SYSTEM –> RESISTANCE SYSTEM

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38
Q

right and left ventricles volumes and pressures

A

Both right and left ventricles are pumping out the same volumes
just with different pressures

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39
Q

the left heart pumps out a flow of blood which

A

splits and divides among all the organs

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40
Q

Where does the flow leave and enter? what side?

A

leaving the left heart

entering the right heart

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41
Q

Lungs connection/flow with the heart

A

lungs are in series with the left heart therefore they have the same flow

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42
Q

organs connection/flow with the heart

A

the organs are in parallel with the heart therefore they have
different flows

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43
Q

Cardiac Output =

A

Venous Return = 5L/min

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44
Q

The flow or flow rate through a vessel depends on 2 factors:

A

Velocity of flow

Cross-sectional area of the lumen

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45
Q

DISTIBUTION VESSELS

A

bring blood from the heart to the organ

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46
Q

The velocity of blood at all points in a cross-section

A

The velocity of blood is not the same at all points in a cross section since the blood close to the walls is
slower and blood close to the middle is faster and therefore, we must take the mean velocity when calculating flow

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47
Q

distribution vessels examples

A 
Aorta and other large vessels are called distribution vessels
function to bring blood from the heart to the organ
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48
Q

vessel that drains the bottom 1⁄2 of the body

A

Lower vena cava

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49
Q

vessel that drains the upper 1⁄2 of the body

A

Superior vena cava

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50
Q

Almost all of resistance to flow lies in the

A

small arteries and arterioles; the anatomical sites that

generate the resistance to flow

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51
Q

What occurs in the capillaries

A

exchange of oxygen and carbon dioxide and sugars (wall = 1 cell thick –> small
diffusion barrier)

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52
Q

Why is the aorta thick?

A

§ The aorta is thick because it needs to withstand a high pressure

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53
Q

Number of each of the vesels, most and least

A

capillaries, then venules, arterioles, veins, arteries, vena cava, aorta

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54
Q

From the vena cava’s blood, where does the blood go?

A

it goes to the right atrium

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55
Q

Arterial tree is created by

A

draining all the blood from a subject and injecting a rubber material a.k.a arterial cast

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56
Q

Vessel place with the most area

A

capillaries

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57
Q

Vessel place with the greates vecloity of blood

A

capillaries

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58
Q

Every cell in the kidney is close to a small vessel why?

A

so diffusion is able to create a large flux

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59
Q

The summed cross-sectional area gets higher from

A

the aorta to the

capillaries

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60
Q

§ The advantages of a branching network

A

Any cell is very close to a capillary
A high total area of the walls and capillaries
A low blood flow velocity in capillaries
A high total cross-sectional area

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61
Q

The practical unit of pressure

A

cm H2O; mmHg

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62
Q

Blood pressure values

A

120/80 mmHg

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63
Q

Central Venous Pressure

A

5-10 cm H2O

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64
Q

Intravenous infusion

A

squeeze bag to increase pressure

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65
Q

The average mean pressure of the aorta

A

100mmHg

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66
Q

Veins mean pressure

A

~ 5mmHg

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67
Q

Resistance vessels

A

arterioles and small arteries

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68
Q

Pressure in systemic circulation

A

120/80 mmHg

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69
Q

Size and pressure of left ventricle vs right

A

The left ventricle is bigger. generates a high pressure to
the systemic circulation and the right ventricle to the pulmonary circulation is a lot smaller and therefore generates a smaller pressure

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70
Q

How long is the aortic value open for? what does this do?

A

Aortic valve opens for ~1/3 of the cardiac cycle which will increase the pressure due to the dumping of stroke volume into the aorta and then the valve will close and stay closed for 2/3 of the cardiac cycle and during that time the blood in the aorta will close and stay closed for 2/3 of the cardiac cycle and during that time the blood in the aorta and the vessels will leak out which decreases the pressure

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71
Q

The waveform of very strong pulse in the arterial system

A

PULSALTILE WAVEFORM

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72
Q

Max pressure vs min pressure on pulse waveform

A

Systolic Pressure = Max

Diastolic Pressure = Min

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73
Q

What happens to oscillations as they reach the veins

A

As you move through the vascular tree, these oscillations get damped out and by the time you get to the veins they are basically gone

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74
Q

Pressure in the venous system

A

almost CONSTANT

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75
Q

SYSTEMIC PRESSURE vs PULMONARY PRESSURE

A

SYSTEMIC PRESSURE > PULMONARY PRESSURE

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76
Q

Hydrostatic Pressure

A

Pressure due to standing water
The pressure exerted by a fluid at equilibrium at a given point within the fluid, due to the force of
gravity

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77
Q

Why does hydrostatic pressure arise

A

Hydrostatic pressure is due to the fact that we are

sitting in a gravitational force field

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78
Q

Mercury Sphygmomanometer

A

Manometer measures pressure in liquid or gas
It is the measure of arterial blood pressure
Mercury is a neurotoxin
As you pump air into a bag the pressure will rise because the pressure at the bottom rises

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79
Q

CVP or RAP is

A

5-10 cmH2O

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80
Q

Perfusion Pressure =

A

inlet pressure (arterial pressure) – outlet pressure (venous pressure)

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81
Q

Normally Perfusion Pressure is

A

Normally the arterial pressure is much bigger than the venous pressure (100 mmHg vs 5 mmHg) so: ∆pressure is ≈ 95 mmHg ≈ arterial pressure

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82
Q

what drives blood flow through the tube

A

Perfusion pressure

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83
Q

Flow =

A

Perfusion pressure/ resistance

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84
Q

Can resistance be directly measured

A

You cannot make direct measurements of resistance

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85
Q

Laminar or Parabolic Flow

A

Blood close to the walls moves the slowest and blood close to the midline moves the fastest
There are infinitely thin layers of blood
sliding over each other therefore, there is friction which produces viscosity and generates heat which results in a loss of pressure
-Viscosity is due to internal friction between layers
-It’s a parabolic velocity profile

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86
Q

Why does pressure drop?

A

§ Pressure drops because of internal friction

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87
Q

Poiseulles Law formula

A

R= 8vL/pi r^4

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88
Q

If you double the radius, how the resistance change

A

get a 16-fold fall in resistance

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89
Q

When is Poiseulles Law valid?

A

§ Poiseuille’s Law is only valid for Laminar Flow

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90
Q

How do Frictional losses in a viscous fluid affect pressure and heat

A

generate heat which causes

a fall in pressure down the vessel

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91
Q

§ The body controls vessel resistance by:

A

o Perfusion Pressure
o Length of Vessel
o Viscosity of Blood
o Radius of Vessel (vasoconstriction and vasodilation)

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92
Q

Vessel Resistance happens at the level of

A

resistance vessels (small arteries and arteries

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93
Q

what acts on the smooth muscle to make it relax ? why

A

Local metabolites are what act on the smooth muscle to make it relax which causes a decrease in
resistance which increases flow

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94
Q

All arterioles and smooth muscle in the body are innervated by

A

ANS

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95
Q

Restistance vs radius

A

R= 1/r^4

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96
Q

When you put things in series the overall resistance

A

increases, combined resistance is ALWAYS higher than either one of the 2 component’s resistance

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97
Q

When you put things in parallel the overall resistance

A

decreases, combined resistance is ALWAYS lower than either one of the 2 component’s resistance

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98
Q

Compliance

A

how stretchy something is

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99
Q

capacitance vessels

A

Most of the blood is stored in veins and venules which are
capacitance vessels
o Pretty compliant

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100
Q

Compliance in veins

A

the total pressure is low and the volume is higher so the slope is low
which means it has a high compliance

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101
Q

Compliance in arteries

A

the total pressure is

higher than the veins and the total volume is lower, therefore the slope is higher and thus the compliance is lower

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102
Q

Why is the complaince of arteries less than veins?

A

The external diameter of the arteries and the veins are the same but
the lumen is much smaller in arteries because they have a much
thicker vessel wall due to more layers of smooth muscle and
therefore the blood flows through a smaller diameter when passing through

As the fluid increases the pressure increase, once again the veins are much more compliant than the arterie

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103
Q

How many chambers in human heart

A

4

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104
Q

Where is deoxygenated blood in the heart

A

right atrium + ventricle

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105
Q

Where is oxygenated blood in the heart

A

left atrium and ventricle

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106
Q

when the right ventricle contracts what happens

A

the valve opens to go into the pulmonary trunk

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107
Q

Flow in the Right Heart

A 
Superior vena cava
right atrium
right ventricle
pulmonary trunk
bifurcation to the left and right pulmonary arteries
right/left lung
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108
Q

Flow in the Left Heart

A 
2 left + 2 right pulmonary veins bring in blood from the lungs
left atrium
crosses valve
left ventricle
aorta
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109
Q

the right and left atria are separated by

A

The inter-atrial septum

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110
Q

the right and left ventricles are separated by

A

the inter- ventricular septum

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111
Q

Size of ventricular free wall

A

the left ventricular free wall is much bigger than the right ventricular free wall
the thickness of the muscle is much thicker in the left ventricle
o generates 10x greater pressure

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112
Q

valves in heart

A

2 atrioventricular valves, 2 semilunar valves (outlet of the ventricle)

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113
Q

The right atrioventricular valve

A

tricuspid valve

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114
Q

The left atrioventricular valve

A

mitral/bicuspid valve

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115
Q

The right semilunar valve

A

pulmonary valve

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116
Q

The left semilunar valve

A

aortic valve

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117
Q

All 4 of the valves lie in the

A

fibrous ring of the connective tissue

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118
Q

Is the right semilunar valve open or closed? why

A

As the right ventricle contracts the valve is closed but as the pressure builds it pushes the valve open

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119
Q

What is attached to the top of the papillary muscles

?

A

Chordae tendinae

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120
Q

When the ventricles contract, what happens to the pressure and flow?

A

there is a high pressure in the ventricle and a low pressure in the atrium
so the flow goes to the ventricle

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121
Q

When the ventricles contract, what happens to the papillary muscles

A

Papillary muscles contract at the same time as the ventricles, anchored to the end by the free wall

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122
Q

EVERTED

A

When the leaflet of the valve moves out

You want to avoid eversion or prolapse of the valve

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123
Q

endocardium/endothelium

A

The connective tissue that lines the inside of the heart

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124
Q

epicardium

A

The connective tissue that lines the outside of the myocardium

Epicardium (inner), pericardial fluid/space, pericardium (fibrous sac)

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125
Q

If the papillary muscle ruptures, what happens?

A

you get

mitral regurgitation and thus need a mitral valve replacement

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126
Q

What is the electrical/mechanical device in cardio?

A

heart

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127
Q

What causes causes depolarization

and an action potential of the heart muscle cell

A

ACh binds to receptors on the muscle cell

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128
Q

What does the action potential of the heart muscle cell trigger

A

an influx of calcium ions into the cell

which generates the force of contraction

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129
Q

If there is no action potential then there is

A

no mechanical contraction

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130
Q

What makes up 99% of the heart

A

Cardiac muscle cells

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131
Q

Sinus node is made of

A

specialized cardiac cells that drive the beat

of the heart

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132
Q

The heart beats because

A

the cells in the SA (sinoatrial) node are

spontaneously active

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133
Q

Where does the depolartization spead to?

A

The wave of depolarization/activation spreads across the 2 atria but
can’t go further because of the fibrous ring

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134
Q

Where does the AV node travel?

A 
The AV (atrioventricular) node travels down the bundle of His which
branches into the left and right bundle branches
135
Q

Purkinje fibers

A

are cardiac cells and are NOT nerves
2 different action potentials are travelling down and end
up in this branching structure

which are
embedded in the myocardium on the endocardial side of the muscle

136
Q

The activation moves from

A

Purkinje cell to cardiac cell

137
Q

The simultaneous activation of all the cells in the ventricle creates

A

a very

powerful contraction

138
Q

Cardiac cells meet at

A

the intercalated disks and the membranes are

stuck together by gap junctions

139
Q

Gap junctional channels

A

are hemichannels which means that there is half

in each cell

140
Q

as action potential propagation what is the direction of K+ and Na+

A

K+ moves in the same direction as action potential propagation and Na+ moves in the opposite
direction (the local current)

141
Q

What follows the depolarization

wave

A

A Repolarization wave

142
Q

Electrocardiogram

A

Recording of the electrical activity of the heart from the surface of the body

143
Q

ECG

A

extracellular recording

144
Q

This lead is essential as it is the reference lead

A

The right leg lead is essential as it is the reference lead and always needs to be attached to the patient

145
Q

The amplitude of an action potential vs ECG

A

The amplitude of an action potential is ~100mV (intracellular) whereas the amplitude for an ECG is 1mV (extracellular)

146
Q

Action potential vs ECG

A

Action potential- intracellular

ECG - extracellular

147
Q

Where does Atrial excitation start and end

A

Atrial excitation starts at the SA node and ends at the AV node (P-wave)

148
Q

P wave

A

end of Atrial excitation at the AV node

149
Q

How does Ventricular excitation begin

A

after atrial relaxation (Q-wave)

150
Q

How does Ventricular excitation end

A 
completes with the contraction of the
Purkinje fibers (R, S waves)
151
Q

Do you see anything with the activation of the SA node

A

you can see nothing with the activation of the
SA node, only start to see something when the
atrium contracts

152
Q

T-wave

A

Ventricles Relax (T-wave) –> repolarization

153
Q

Leads

A

Electrode itself: e.g. RA lead

Combination of electrodes taken to the voltmeter: e.g. lead 1

154
Q

Bipolar Limb Leads

A

2 leads from the voltmeter are put on the surface of the body
right leg not involved

155
Q

Unipolar chest leads

A

V1-V6 (left to right)

156
Q

Number of unipolar leads

A

12 unipolar leads (maybe 9)

157
Q

ischemia

A

An inverted T-wave

158
Q

Unipolar limb leads

A

aVR, aVL, aVF

159
Q

How do Action potentials spread through the heart

A

Action potentials spread from left to right and from top to bottom through the septum

160
Q

2 steps to ventricular activation

A

Septum

Ventricular walls

161
Q

The duration of action potentials in cardiac muscle vs nerve or skeletal muscle

A

The duration of action potentials in cardiac muscle is longer
than in nerve or skeletal muscle

162
Q

Resting potential in cardiac vs neurons

A

Resting potential more hyperpolarized than in neurons (more

negative)

163
Q

Resting potential cardiac cell

A

-90mV

164
Q

Upstroke of the resting potential

A

local current circuits

activate

165
Q

calcium channels

A

2 CaL (long-lasting)

166
Q

Nernst Potential:

A

quation that relates the reduction
potential of an electrochemical reaction to the standard electrode potential, temperature, and activities of the chemical species undergoing reduction and oxidation

167
Q

Membrane with K+ channels

A

equilibrium potential
-100mV which is why the Nernst potential sits at -
90mV because it’s basically all K+

168
Q

sodium channels at rest

A

Very few sodium channels are open at rest but it rises

and falls very quickly (~ 1ms)

169
Q

At rest compare the following

Pk, P Na P Ca

A

Pk&raquo_space; P Na P Ca

170
Q

What is the upstroke

A

the fast inward Na+ current

171
Q

What is the plateau

A

inward motion of sodium

172
Q

How many potassium channels

A

many

173
Q

Do sinus node cells have a resting potential

A

no,
Sinus node cells are NEVER at rest therefore, they don’t have a resting potential
instead they have a pacemaker potential or a spontaneous diastolic depolarization

174
Q

Slow depolarization is the cause of

A

a spontaneous diastolic depolarization

175
Q

diastole

A

The muscle is relaxing

176
Q

Sinus node vs ventricle action potential

A

The upstroke is much slower because there are no
sodium channels or current
No INa in the sinus node cells, instead they rely on ICaL to
generate the upstroke

177
Q

Rate of Rise of Upstroke in slow vs fast

A

§ Slow: 1-10 V/sec

§ Fast: 100-1000 V/sec

178
Q

Conduction velocity in slow vs fast

A

§ Slow: 0.01-0.05 m/sec

§ Fast: 0.5-5 m/sec

179
Q

Examples of slow action potentials

A

SA node

AV node

180
Q

Examples of fast action potentials

A 
ventricular muscle
atrial muscle
bundle of his
bundle branches 
purkinje fibres
181
Q

The ECG is related to the

A

atrial and ventricular AP

182
Q

On the ECG, Atrial AP occurs at the

A

P wave: depolarization of right and left atrium

183
Q

On the ECG, 1st cell in the ventricle to activate

A

happens at the start of the Q wave

184
Q

Premature Ventricular Contraction (PVC)

A

Pain in chest, angina pectoris which means he has myocardial ischemia (aka not getting enough blood flow to the cardiac muscle)

185
Q

ectopic beat

A

comes from an unusual place that it shouldn’t be in the ventricles and is a direct consequence of the fact that the individual is suffering from significant myocardial ischemia;

186
Q

What does a PVC progress to?

A

to a regular ventricular tachycardia (VT) before progressing to ventricular fibrillation (irregular)

187
Q

Ventricular Tachycardia

time?

A

A tachycardia is when the heart rate is too fast due to the PVC
the time between ventricular complexes is 0.2 seconds

188
Q

Ventricular Tachycardia origin

A

the origin is in the ventricles themselves

- ventricular tachycardia

189
Q

What can PVC and ventricular tachycardia result in

A

not enough blood can enter in a short amount of time so the stroke volume and cardiac output will fall
PVC to ventricular tachycardia to ventricular fibrillation (3rd arrythmia)

190
Q

cardiac output during ventricular fibrillation

A

none

191
Q

During VT what is happening to the action potentials

A

when the AP is whipping around, a part of the wave front will block the actual
productions which will stop propagation, by the time you are in VFib there are multiple AP circulating in the heart that come out of nowhere

192
Q

treatment for VFib

A

defibrillation whereby you inject a pulse of current into the ventricles

193
Q

arterial pulse in VFib

A

As soon as you go into VFib there is no more

arterial pulse

194
Q

AED

A

Automated External Defibrillator (external

because the current is applied from the outside of the body)

195
Q

Mapping of Cardiac Electrical Activity

A

Computer constructs an activation map

Base of ventricle at top (rings go from the apex to the base)

196
Q

Heart attack

A

myocardial infarction, death of muscle in the ventricle

197
Q

circus movement re-entry cure

A

To cure this arrythmia they must remove the scar tissue

198
Q

The transition from VT to VF

A

involves the breakup of a single wave with VT into multiple AP in a
circulating, random, chaotic way

199
Q

RE-ENTRANT VENTRICULAR TACHYCARDIA involves

A

cardiac muscle that is inhomogeneous which means that is doesn’t have exactly the same
refractory period everywhere

200
Q

AFib

A

atrial activation (premature) which triggers AFib (PAC)

201
Q

The origin of most PSE

A

is inside the veins (where the ectopic beat comes from)

202
Q

Excitation-Contraction Coupling

A

Process by which the AP sweeps through the atrial and ventricular muscle

203
Q

As the AP arrives, what happens to the channels?

A

As the AP arrives the Ca channels being to open and calcium
floods into the cell and diffuses through the cytoplasm where it
binds to a receptor

204
Q

What does calcium bind to/

A

to a receptoràRyanodine Receptor aka Ca Channel

205
Q

When calcium binds to the receptor it opens, what happens?

A

The Sacroplasmic Receptors is full of
calcium so if the cannel opens the concentration outside is low
and the calcium leaves to make its way into the cytoplasm

206
Q

the initiation of the whole series of contraction with myosin
and actin

A

Ca bind to troponin complex

207
Q

Calcium channels cluster at the

A

base of the T-tubules

208
Q

As the calcium concentration increases in the cytoplasm there will be

A

more binding of the calcium to

the troponin

209
Q

calcium concentration and contraction time compared to AP

A

Both the calcium concentration and contraction are delayed
with respect to the AP
The calcium current comes in a bit later than the action
potential because it takes time for both the binding and
diffusion

210
Q

Does Activation = contraction

A

No Activation ≠ contraction

211
Q

Electro-mechanical dissociation

A

an example of pulseless

electrical activity

212
Q

Can AP propagate if the heart is dead

A

AP can still propagate through the heart even if dead; this would be an example of when the electrics
are working but the mechanics are not

213
Q

When does systole start

A

Systole starts with the contraction of ventricles

214
Q

for

valves to open/close, what does the pressure in the ventricles have to do?

A

Pressure in the ventricles only goes up a few mmHg for

valves to open/close

215
Q

When the aortic valve closes the ventricular pressure

A

falls
extremely quickly and will dip to be lower than the
pressure in the atrium

216
Q

Does the mitral valve close or open until the next beat

A

stays open

217
Q

At resting heart rate diastole takes how much of the cardiac cycle

A

~2/3

218
Q

If the pressure in the atrium is higher than the ventricles, what happens

A

AV valve opens

219
Q

P-wave

A

atrial activation, extra pump of blood due to the atrial contraction

220
Q

The QRS complex starts after the

A

invasion of the ventricular muscle by the AP of strokes where you get the influx of calcium and a rise in ventricular pressure due to the opening of the aortic wave and the closing of the mitral valve

221
Q

T-wave occurs

A

during the fall of ventricular pressure as the levels of free calcium in the cytoplasm fall for the strength of contraction

222
Q

At the end of the diastolic period, wat is the volume in the ventricle? name?

A

At the end of the diastolic period, you have the maximal

amount of volume in the ventricle and that’s called the END DIASTOLIC VOLUME

223
Q

minimum volume in the ventricle

A

The minimum volume is called the END SYSTOLIC VOLUME

224
Q

First heart sound is known as

A

LUB

225
Q

Second heart sound is known as

A

DUB

226
Q

What makes the LUB sound

A

When the mitral/AV valves simultaneously close you get the 1st sound (LUB)

227
Q

What makes the DUB sound

A

When the aortic/pulmonary valves simultaneously close you get the 2nd sound (DUB)

228
Q

What produces the sounds

A

When the valves snap shut it creates vibrations in the blood/valves which produces the sounds

229
Q

What side of the heart is the wiggers diagram for ?

A

left

230
Q

2 phases in systole

A

isovolumeric ventricular contraction

ventricular ejection

231
Q

2 phases in diastole

A

isovolumeric ventricular relaxation

ventricular filling

232
Q

first sound occurs during what phase

A

isovolumeric ventricular contraction

233
Q

second sound occurs during what phase

A

isovolumeric ventricular relaxation

234
Q

Stroke volume

A

END DIASTOLIC VOLUME - END SYSTOLIC VOLUME

235
Q

Stroke volume amount

A

70

236
Q

END DIASTOLIC VOLUME

A

120

237
Q

END SYSTOLIC VOLUME

A

50

238
Q

EJECTION FRACTION

A

STROKE VOLUME/END DIASTOLIC VOLUME

239
Q

EJECTION FRACTION VALUE

A

70/120 = 0.6 or 60%

240
Q

CARDIAC OUTPUT

A

HR x stroke volume

241
Q

CARDIAC OUTPUT VALUE

A

5 L/min

242
Q

major difference between the left and right heart

A

he pressure is much lower in the right heart

243
Q

the peak pressure in the left heart

A

110mmHg

244
Q

the peak pressure in the right heart

A

25mmHg

245
Q

How does increased End-Diastolic Volume (EDV) affect Stroke Volume (SV)

A

increased End-Diastolic Volume (EDV) produces increased Stroke Volume (SV)

246
Q

the more you fill the ventricles, how does the force of contraction change?

A

the more you fill the ventricles, the larger the force of contraction

247
Q

If the pressure in the right atrium increases and the AV valve is open

A

the ventricle will fill more causing
the EDV to increase and thus the stretch in the walls of the ventricles will increase so the force of contraction and thus the stroke volume will also increase

248
Q

What is the Systemic Arterial Blood Pressure (BP) measuring

A

the pressure on the arterial side of circulation NOT venous side

249
Q

Systolic BP

A

maximum pressure (120 mmHg in standard man)

250
Q

Diastolic BP

A

minimum pressure 80 mmHg in standard man)

251
Q

BP

A

[systolic BP / diastolic BP] (120/80)

252
Q

Mean/Average BP (MAP)

A

≈ diastolic pressure + 1/3 pulse pressure = 100 mmHg

253
Q

Windkessel Effect

A

Air decompresses to push air out of the nozzle

254
Q

What happens as you increase stretch

A

contraction is greater because of frank sterling mechanism

255
Q

Windkessel Effect in the heart

A

• For 2/3 of the cycle the ventricles aren’t contributing to the pressure because they are closed
• The stroke volume dumps blood into the aorta which causes it to stretch out
• The aortic valve then closes so the pressure will be available during the diastolic
period to drive blood out of the systemàduring that period the heart is NOT
pumping
• Results in a waveform where the pressure stays high for a long time
• Converting your cyclic pump (where you go up to 120mmHg for 1/3 of the
cycle and then come back down to 0) into a steady pressure that lasts xthroughout the cardiac cycle
• Flow is constant
• There is electrical resistance, capacitance is compliance

256
Q

How to measure BP

A 
direct
indirect
- palpation
- ausultation
- oscillometry
257
Q

Method of Palpation

A

Feel pulse in the radial artery

Artery gets squeezed–> completely occluded

258
Q

When you feel pulse in palpation what are you getting

A

SYSTOLIC BP

259
Q

Why is there no sound during flow

A

• Flow in this artery is laminar -

260
Q

Why do you begin to hear a noise in palpation

A

You begin to hear a noise because the blood is squeezing through to get blood expansion which creates turbulent flow
• The turbulent flow is what shakes the walls of the arteries and creates noise called Korotkoff sounds or BP sounds
• You hear the sounds all the way down until you hit the diastolic pressure because there the artery is partially occluded

261
Q

Method of Auscultation

A

• Most frequently used
• Automated method
• Pressure transducer in the cuff is what makes the measurements
• Computer looks at the shape of the waveforms to make the measurements
of BP

262
Q

Auscultation sounds

A

Systole starts at the start of the 1st heart soundàthe moment the AV valves
close and ends when the diastole starts which is when the aortic valve closes

263
Q

Why is Blood Pressure Important?

A

Perfusion pressure is essentially perfusion pressure divided by resistance to flow
• Organs adjust flow according to their need via the change in resistance
• The body is trying to keep arterial pressure (flow) constant, despite fluctuation is P (autoregulation)
• Minimize fluctuations in P-arterial (neuro-hormonal control)

264
Q

Total Peripheral Resistance (Systemic Vascular Resistance)

A

The resistance that the left ventricle has to pump against, combined with the resistance of all the organs on the systemic side of circulation

265
Q

Total Peripheral Resistance (Systemic Vascular Resistance) formula

A

• [MAP- Pressure in Right Atrium ]/flow of aorta (cardiac output)

  • Mean pulmonary artery pressure = 15mmHg
  • Pulmonary vein pressure = 5 mmHg
  • Pulmonary Perfusion Pressure = 10 mmHg
266
Q

The mean arterial BP is determined by 3 things

A

o Heart Rate
o Stroke Volume
o TPR

267
Q

PVR vs TPR

A

• PVR &laquo_space;TPR (~1/10)

268
Q

Autoregulation (Flow) occurs in

A

Brain, heart, kidneys

269
Q

What is Autoregulation (Flow)? why?

A

• Vital organs like the brain, heart, kidney have a lot of order and thus regulation (other organs it doesn’t
matter)
• Brain/heart are aerobic so they need oxygenated blood

270
Q

Steady state effect

A

Flow is being regulated to be more or less independent of the
perfusion pressure
• Perfusion pressure = 0 –> flow = 0

271
Q

2 Mechanisms of Auto-Regulation

A

Local Metabolic Control

Myogenic Mechanism

272
Q

Local Metabolic Control

A

o Primary is change of metabolic activity of the organ, which then changes the blood flow
o The supply of the blood flow matched the requirement of the tissue
o Autoregulation; the stimulus is a change in BP and the reflex is to bring flow back to normal

273
Q

Hyperemia

A

; e.g. seizure

274
Q

Local Metabolic Control muscle cells

A

skeletal muscle, cardiac muscle

275
Q

Myogenic Mechanism muscle cells

A

Arteriolar smooth muscle

276
Q

Myogenic Mechanism

A
  • Origin of the myo-reflex is in the walls of the smooth muscle vessels
  • Both metabolic and myogenic mechanisms are occurring simultaneously
  • An increase in arterial blood pressure simply flips all the arrows
  • This is very important for vital organs
277
Q

Where is the cell body in the autonomic innervation of the sinoatrial node?

A

The cell body of the neuron sits in the brainstem

278
Q

A drug given frequently to INCREASE HEART RATE is

A

ATROPINE

279
Q

What does ATROPINE do

A

Binds to the muscarinic receptor (PNS ANTAGONIST) or blocker

Increases the heart rate which increases the cardiac output which increases the blood pressure

280
Q

Sympathetic neuro transmitter

A

pre ganglion ACH

post ganglion NE

281
Q

Parasympathetic neuro transmitter

A

pre ganglion ACh

post ganglion ACh

282
Q

Parasympathetic receptors

A

pre ganglion nicotinic receptor

post ganglion muscarinic recptor

283
Q

sympathetic receptors

A

pre ganglion nicotinic receptor

post ganglion ß-receptor

284
Q

Binding of NE to ß-receptor affect on heart

A

results in speeding up

of the heart rate

285
Q

ß-antagonists

A

Slow heart rate

286
Q

ß-agonist

A

activates the receptors therefore the heart rate, cardiac output, and MAP increase

287
Q

What happens to the axons that interact with ventricular muscle

A

NE binds to the same ß-adrenergic receptor which goes through a whole cascade of intracellular events to eventually result with an increase in calcium inside the cell so the force of contraction increases which causes the contractility of the muscle to increase

288
Q

Autonomic Control of Heart Rate

A

this increase the activity of the nerves to the heart rate through activation of the ß-adrenergic receptor which also activates the adrenal glands which causes an increase in the concentrations of epinephrine and norepinephrine in the blood that eventually makes its way to the ß-adrenergic receptors on the SA node

289
Q

Baroreceptor Reflex

A

Baroreceptors are never terminals that lie in 2 places in your body:
o Arch of the Aorta
o Carotid Sinus

290
Q

The carotid artery

A

bifurcates into an internal carotid artery that
supplies your brain and an external carotid artery that supplies your jaw, face, scalp
Right where it bifurcates you have a swelling which is a sinus (carotid sinus)
o The nerve terminals are embedded in the carotid sinus and the arch of the aorta
o They send information to the brain to communicate the state of the blood pressure (MAP)

291
Q

As the rate of MAP increases, affect on rate of firing

A

As the rate of MAP increases, the rate of firing also increases and
vice versa

292
Q

• When the BP falls, the reflexes tries to do 4 things:

A

o Increase Heart Rate
o Increase Contractility of Ventricular Muscles
o Effect of Vasoconstriction
o Effect of Baroreceptor

293
Q

If the stroke volume is cut in 1⁄2 then the cardiac output should? why does it not?

A

also be cut in half but it only goes to 3⁄4 the original volume which means that the heart rate increased
-The heart rate increases in the 1st cycle that you stand up due to the action of the baroreceptor reflex

294
Q

orthostasis/static

A

miantenane of an upright stnading posture

295
Q

What would happen if the baroreceptor reflex wasn’t working when going from sitting to standing?

A

Arterial BP would continue to fall

296
Q

baroreceptor reflex

A

negative feedback to one of the body’s homeostatic mechanisms that helps to maintain blood pressure at nearly constant levels.

297
Q

when going from sitting to standing, what happens to arterial blood pressure?

A

no change

298
Q

when going from sitting to standing, what happens to right atrial mean pressure?

A

drops from 6 to 0

299
Q

when going from sitting to standing, what happens to cardiac output?

A

drops by 0.75

300
Q

when going from sitting to standing, what happens to stoke volume?

A

drops by 0.5

301
Q

when going from sitting to standing, what happens to heart rate?

A

increases by 1.5

302
Q

when going from sitting to standing, what happens to forearm blood flow?

A

decreases

303
Q

when going from sitting to standing, what happens to renal blood flow?

A

decreases

304
Q

How does the body maintain arterial blood pressure?

A

contractility
venoconstricture
heart rate
arteriolar constriction

305
Q

when going from standing to calve contractions, what happens to arterial blood pressure?

A

no change (slight increase)

306
Q

when going from standing to calve contractions, what happens to right arterial mean pressure?

A

increases back to resting level

307
Q

when going from standing to calve contractions, what happens to cardiac output?

A

increases back to resting level

308
Q

when going from standing to calve contractions, what happens to stroke volume?

A

increases back to resting level

309
Q

when going from standing to calve contractions, what happens to heart rate?

A

decreases back to resting level

310
Q

when going from standing to calve contractions, what happens to forearm blood flow/renal?

A

increases back to resting level

311
Q

When you stand, what is the hydrostatic pressure as you go lower

A

When you stand, there is a big hydrostatic pressure and the lower down you go the more the pressure
increases

312
Q

Muscle Pump in Orthostasis

A

When you constrict the calf muscles, it increases the pressure in the veins which will push open the one valve while closing another
• This is the muscle pump and the volume of the blood in there is reduced so the pressure will fall
• By simply constricting your leg muscle, you bring the pressure in the veins down to a low level,
otherwise it’s at a very high level

313
Q

Starling forces

A

a pressure that is driving fluid or water out

of vessels

314
Q

Filtration

A

pushing fluid out

315
Q

Absorption

A

pulling fluid in

316
Q

Max Heart Rate =

A

220 – age (years)

317
Q

Max Heart Rate is proportional to

A

Power

318
Q

As you increase the intensity of exercise, you are increasing

A

the activity of the SNS which acts on the
sinus node to increase the heart rate
o You also have inhibition of parasympathetic tone

319
Q

Heart Rate vs Power

A

increases linearly

320
Q

Stroke Volume vs Power

A

increases until very high HR

321
Q

Epinephrine affect on HR and CO

A

• Epinephrine will help to increase HR and CO; they increase during exercise

322
Q

TPR vs Power

A

• Big change in TPR falls to about 40% of what it was

decreases

323
Q

At very high HR, what happens to stroke volume

A

might fall

324
Q

Cardiac output vs power

A

increases 3X

325
Q

Arterial pressure

A

systolic increases slightly
mean flat
diastolic flat

326
Q

oxygen consumption vs power

A

increases 9X

327
Q

arteriovenous oxygen difference

A

oxygen used in ateriovenous exchange increases 3X

328
Q

Blood flows in excercise

A

Heart increases 3.5 x
skeletal muscle increases 12 x
kidneys, abdominal, other, decrease

329
Q

Fick’s Principle:

A

oxygen consumption is the flow x the difference in the content of the blood VO2=COxa–vO2 diff

330
Q

Why does the SNS constrict muscles in the abdomen during exercise?

A

Decrease in flow of the blood to the abdominal organs because the SNS is constricting the muscles, to
keep the TPR up so the BP doesn’t fall

331
Q

What happens to HR, cardiac output, stroke volume if you are a trained athlete?

A

HR decreases at rest
increase your SV
higher cardiac output
By training you make your heart stronger –> hypertrophy

332
Q

Where are norepinepherine and epinephrine made

A

Adrenal medulla

333
Q

NE AND E affect on blood vessel

A

Vasoconstriction and binding to alpha receptors

PHGY210 (6 decks)

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