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PHGY 210 > Cardio > Flashcards

Cardio Flashcards

1
Q

cardiovascular system (CVS)

A

organ system to TRANSPORT molecules and other substances rapidly over long distances between cells, tissues and organs

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2
Q

2 heart functions

A
  • push blood through vasculature
  • irrigate other organs and systems
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3
Q

right ventricle function

A

pump blood to lungs to get O2

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4
Q

left ventricle function

A

pump blood to body to deliver O2 to working tissue

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5
Q

what is vasculature designed to do

A

carry out the blood

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6
Q

artery function

A

carry blood away from heart

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7
Q

vein function

A

carry blood back to heart

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8
Q

conductance definition

A

respond to systolic/diastolic pressure

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9
Q

microcirculation

A

exchange between blood and extracellular fluid

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10
Q

erythrocytes

A

red blood cells, carry O2

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11
Q

leukocytes

A

white blood cells, immunity/inflammation

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12
Q

platelets function

A

coagulation

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13
Q

3 things CVS brings to cells

A

nutrients, fuel, oxygen

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14
Q

what does CVS remove

A

waste products (CO2, urea)

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15
Q

2 things that circulate in CVS

A

hormones + antibodies

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16
Q

3 things CVS regulates

A

pH, water balance, temperature

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17
Q

why do simple organisms not have CVS

A

small enough to operate with only diffusion

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18
Q

diffusion definition

A

movement of molecules from high conc area to low conc area

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19
Q

5 factors that affect diffusion

A

distance
temp
density/conc of solvent
molecule mass
barrier characteristics

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20
Q

how does increasing distance affect diffusion

A

decreases diffusion

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21
Q

how does increasing temperature affect diffusion

A

increases diffusion

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22
Q

how does increasing solvent conc affect diffusion

A

increases diffusion

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23
Q

how does increasing molecular mass affect diffusion

A

decreases diffusion

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24
Q

flux of gas equation

A

flux = membrane diffusing capacity x membrane pressure gradient

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25
Q

2 things to increase membrane diffusing capacity

A

area and solubility

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26
Q

2 things to decrease to increase membrane diffusing capacity

A

thickness and size of molecule

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27
Q

why does fibrosis decrease O2 diffusion

A

because thicker membrane

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28
Q

comparative physiology

A

studies and exploits the diversity of functional characteristics of various organisms

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29
Q

what is the circulatory fluid in insects

A

hemolymph

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30
Q

does insect circulation transport O2

A

no because no Hb

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31
Q

is insect circulation open or closed

A

open (from posterior -> anterior)

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32
Q

insect dorsal vessel

A

aorta + thoracic bulbs

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33
Q

what is the insect heart

A

chambers with ostioles

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34
Q

how does circulation occur in insects

A

‘heart’ pumps hemolymph, valves close w each contraction to allow fluid to move in 2 direction

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35
Q

how many chambers do fish have

A

2 (1 atrium, 1 ventricle)

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36
Q

how does circulation occur in fish

A

ventricle pumps blood through artery -> gill capillaries -> systemic capillaries -> atrium

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37
Q

where does blood get oxygenated in fish circulation

A

gill capillaries

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38
Q

how many circulations do amphibs + reptiles have

A

2 (small/pulmonocutaneous, large/systemic)

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39
Q

how many chambers do amphibs + reptiles have

A

3 (2 atria + 1 ventricle)

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40
Q

amphib + reptile small circulation

A

leaves ventricles towards lungs and skin to get oxygenated, high O2 returns to left atrium, then ventricle

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41
Q

amphib + reptile large circulation

A

high O2 blood in ventricle sent to whole body, low O2 blood returns to right atrium, then ventricle

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42
Q

why do high O2 and low O2 blood not mix in amphib and reptile circulation (2)

A

structure and pressure

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43
Q

how many chambers do alligators have

A

2 atria, 2 ventricles

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44
Q

how many aortas do alligators have

A

2

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45
Q

2 alligator circulation pathways

A

LV -> right aorta -> systemic circ
RV -> left aorta -> systemic circ

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46
Q

what valve closes when alligators are underwater and where is it

A

gear-tooth valve (between RV + pulmonary circulation)

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47
Q

what does closing gear-tooth valve do in alligator circulation

A

causes low O2 blood from right heart to enter left aorta -> enters systemic circ -> left heart valve to aorta also closed therefore tissues receive low O2 blood

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48
Q

why are alligators cold-blooded

A

gas exchange less efficient = no temp control

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49
Q

how many chambers for avian and mammalian circulation

A

4 (2 atria + 2 ventricles)

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50
Q

haemodynamics

A

study of circulation and movement of blood in the body, and the forces involved

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51
Q

blood volume

A

5L

(75mL/kg avg)

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52
Q

blood unit

A

450 mL

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53
Q

stroke volume

A

70 mL

(end diastolic (in) volume - end systolic (out) volume)

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54
Q

diastole

A

ventricle opens, blood pours in

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55
Q

systole

A

heart contracts, blood pumps out

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56
Q

capacitance system

A

venous system; compliant and can change accordingly to volume

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57
Q

how much blood is in venous system at any one time

A

61%

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58
Q

resistance system

A

arterial system; ensures enough force for blood flow

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59
Q

how much blood is in arterial system at any one time

A

18%

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60
Q

cardiac output

A

amount of blood heart pumps in 1 min (5L)

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61
Q

cardiac output equation

A

heart rate x stroke volume

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62
Q

venous return

A

blood flow from periphery back to atrium (5L)

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63
Q

is distribution to various organs always the same

A

no, distribution is function-dependent

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64
Q

flow equation

A

flow = V/T AND flow = area x mean velocity (mL/min or L/min)

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65
Q

what is area in flow equation

A

lumen

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66
Q

why do we use mean velocity in flow equation

A

because velocity is not the same at every point in cross-section

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67
Q

why does aorta have large diameter

A

to ensure enough pressure to whole system

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68
Q

large artery function

A

dissipate pressure

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69
Q

why do we have many venules

A

must slow velocity enough for diffusion to occur

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70
Q

2 structures for distribution

A

aorta and large artery

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71
Q

2 structures for resistance

A

small artery and arteriole

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72
Q

structure for exchange

A

capillaries

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73
Q

3 structures for capacitance

A

vena cava, vein, venule

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74
Q

4 advantages of branching capillary network

A
  • cells are close to capillary (reduces distance)
  • high total area of capillary wall
  • low blood flow velocity in capillaries
  • high total CSA
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75
Q

blood pressure definition

A

force exerted by blood on blood vessel wall

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76
Q

systemic blood pressure

A

120/80 mmHg

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77
Q

central venous pressure

A

5-15 cmH2O / 6-12 mmHg

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78
Q

how does pressure in arteries and arterioles compare to pressure in capillaries, venules and veins?

A

higher

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79
Q

why is pressure higher in arteries and arterioles

A

because resistance is higher

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80
Q

what is the KEY to arteries being resistance vessels

A

structure!
- changing CSA is important for resistance, and arteries are muscular, allowing for efficient contraction

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81
Q
A
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82
Q

how does systemic circ pressure compare to pulmonary circ pressure

A

higher

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83
Q

how do systole pressures compare to diastole pressures and why

A

higher because need more pressure to pump blood to whole body

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84
Q

where are the pressure differences between systole and diastole less significant (2)

A

arterioles and capillaries

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85
Q

where does the pressure difference between systole and diastole disappear (2)

A

venules and veins

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86
Q

perfusion pressure equation

A

inlet pressure - outlet pressure
delta P = Pin - Pout

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87
Q

what is perfusion pressure necessary for

A

good organ feeding

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88
Q

what happens if we have no perfusion pressure

A

no flow

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89
Q

perfusion pressure equation (for an organ)

A

arterial pressure - venous pressure
delta P = Pa - Pv

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90
Q

what is perfusion pressure (delta P) approximately equal to in organs and why

A

arterial pressure (Pa) because it is typically MUCH higher than venous pressure

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91
Q

what is flow proportional to (2)

A

perfusion pressure, and therefore arterial pressure

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92
Q

what type of structure regulates flow and why

A

arteries because they have more resistance

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93
Q

resistance definition

A

force that opposes movement

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94
Q

resistance equation

A

resistance = perfusion pressure / flow

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95
Q

what causes resistance

A

friction between vessel wall and blood

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96
Q

how does resistance change with increase vessel length

A

increases because increased surface

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97
Q

where is resistance greatest and what does this mean for flow

A

near surface, and therefore slowest flow

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98
Q

laminar flow definition

A

entire fluid flows in same direction

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99
Q

viscosity

A

friction between moving particles

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100
Q

what does increased viscosity mean for resistance

A

increased

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101
Q

what does viscosity of blood depend on

A

hematocrit (more red blood cells = more viscosity)

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102
Q

why is viscosity relatively constant

A

because hematocrit varies very little

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103
Q

Poiseuille’s law

A

resistance = 8 x viscosity x (length/radius)

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104
Q

why does CSA determine resistance (using Poiseuille’s law)

A

viscosity = constant
length = constant
only radius (aka CSA) changes

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105
Q

4 controllers of vessel constriction

A
  • local metabolites
  • hormones
  • neurotransmitters
  • endothelial cells
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106
Q

what does increased calcium mean for constriction

A

increases

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107
Q

what does decreased calcium means for constriction

A

decreases

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108
Q

how does vessels in series affect resistance

A

total resistance is sum of both vessels = inefficient

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109
Q

how does vessels in parallel affect resistance

A

lowers it because radius of vessel at the entrance and exit is bigger than the radius of each vessel in parallel

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110
Q

where is most blood found at any one time, and why

A

veins and venules because high compliance

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111
Q

compliance definition

A

ability of blood vessel to stretch

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112
Q

what does compliance depend on

A

vessel volume gradient (delta V) and transmural pressure gradient (delta P)

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113
Q

compliance equation

A

compliance = delta V / delta P

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114
Q

why are veins more compliant

A

little smooth muscle and few elastic fibres

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115
Q

for any given variation in transmural pressure, how does arterial and vein volume change

A

arterial volume = changes very little because stiff therefore low compliance
vein volume - changes a lot because high compliance

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116
Q

how does pressure in peripheral venules compare to pressure in ascending aorta

A

<10% of pressure in ascending aorta

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117
Q

2 mechanisms to maintain blood flow against gravity

A

valves = ensure 1 way flow
skeletal muscle contraction

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118
Q

4 chambers of the heart

A

right atrium + right ventricle (pulmonary)
left atrium + left ventricle (systemic)

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119
Q

superior and inferior vena cava

A

low O2 blood enters the heart

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120
Q

pulmonary trunk

A

branches into 2 pulmonary arteries

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121
Q

right and left pulmonary artery

A

low O2 blood to right and left lungs

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122
Q

left and right pulmonary vein

A

bring high O2 blood to the heart

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123
Q

aorta

A

sends high O2 blood to body

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124
Q

how many organ branches does the aorta have

A

30-40

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125
Q

arteries vs veins (direction and O2 content)

A

arteries. =take blood away from heart, high O2
veins. =bring blood to heart, low O2
** opposite O2 levels in pulmonary vessels **

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126
Q

inter-atrial septum

A

divides left and right atria

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127
Q

inter-ventricular septum

A

divides left and right ventricles (VERY THICK)

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128
Q

left ventricular free wall

A

much thicker for high pressure

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129
Q

right ventricular free wall

A

1/10 as thick as left wall for low pressure system

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130
Q

is the heart fed by aorta and vena cava

A

no

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131
Q

where do coronary arteries branch off

A

just above aortic valve of the aorta

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132
Q

where do coronary veins empty deoxygenated blood

A

right atrium

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133
Q

myocaridal infarction

A

coronary artery block = heart attack

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134
Q

tricuspid valve

A

divides right atrium and right ventricle

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135
Q

pulmonary / pulmonic valve

A

divides right ventricle and pulmonary trunk

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136
Q

bicuspid / mitral valve

A

divides left atrium and left ventricle

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137
Q

aortic valve

A

divides left ventricle and aorta

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138
Q

where is the fibrous ring

A

between atria and ventricles

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139
Q

purpose of fibrous ring

A

electrically isolates atria from ventricles

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140
Q

where are the valves of the heart housed

A

fibrous ring

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141
Q

papillary muscles function

A

contract to prevent valve inversion / prolapse on systole

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142
Q

where do papillary muscles attach

A

cusps of bicuspid and tricuspid valves

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143
Q

chordae tendinae

A

strong fibrous connections between valve leaflets and papillary muscle

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144
Q

pericardium / pericardial sac

A

‘bag’ that surrounds heart and vessels

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145
Q

3 pericardium functions

A
  • prevents overfilling (by not expanding)
  • protects heart physically
  • provides pericardial fluid
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146
Q

pericardial fluid

A

lubricant to allow heart to freely contract, generated from serous membrane

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147
Q

epicardium

A

outer layer of heart tissue

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148
Q

what is epicardium made of

A

epithelial cells

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149
Q

myocardium

A

muscle! main layer

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150
Q

endocardium

A

inner layer of heart tissue

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151
Q

what is endocardium made of

A

endothelial cells

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152
Q

what is the main pacemaker

A

SA/sinus node

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153
Q

what 2 other structures can spontaneously beat if SA node fails

A

AV node and His-Purkinje cells

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154
Q

how often does SA node beat

A

1 beat/ second

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155
Q

how does SA node propagate signal through right atrium toward left atrium

A

electrically connected to neighbouring cells

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156
Q

AV node function

A

transmits SA node signal to ventricles via bundle branches

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157
Q

what is the secondary pacemaker

A

AV node

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158
Q

why does the AV node conduct its signal slowly

A

to allow the blood to reach ventricles before they contract

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159
Q

bundle branches function

A

propagate signal along septum

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160
Q

Purkinje fiber structure

A

branched tree structure under endocardium

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161
Q

order of electrical conduction in the heart (7)

A
  • SA node
  • AV node
  • Bundle of His
  • Bundle branches
  • Septum
  • Purkinje fibers
  • Ventricles
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162
Q

why does left bundle branch activate septum but not the right

A

right bundle branch well insulated by connective tissue, left bundle branch not isolated

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163
Q

why do ventricles contract simultaneously

A

to maximize pressure

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164
Q

how does the signal move in the heart

A

endo -> epi

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165
Q

what are gap junctions

A

connection between cells

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166
Q

what do gap junctions contain

A

wavy intercalated disc

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167
Q

voltage of depolarized and resting cell

A

depolarized = +20mV
resting = -90mV

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168
Q

why do positive ions move through gap junction

A

due to electrical gradient between cells

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169
Q

where do Na+ and K+ move in gap junction

A

K+ = from depolarized to resting (inside cell)
Na+ = from resting to depolarized (outside cell)

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170
Q

what does an EKG sense

A

interstitial local circuit currents

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171
Q

local circuit current

A

form basis of depolarization wave front in working myocardium

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172
Q

where are gap junctions concentrated

A

at the ends of myocytes

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173
Q

electrocardiogram (ECG/EKG)

A

recording of the electrical activity of the heart

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174
Q

how is electrocardiogram recorded

A

electrocardiograph (also referred to as ECG/EKG)

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175
Q

4 parts of ECG

A

patient cable
lead-selector switch
voltmeter
ECG

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176
Q

what is the reference lead on ECG

A

right leg - set to 0, always connected

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177
Q

when do extracellular recordings appear on ECG

A

when there is a potential difference

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178
Q

what does 1 cardiac cycle look like on ECG

A

PQRST waves

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179
Q

where do all ECG waves start and end

A

baseline

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180
Q

full cardiac cycle (10)

A
  1. sinus node fires
  2. atrial contraction
  3. AV node activates
  4. His bundle activates
  5. left bundle activates
  6. septum activates
  7. Purkinje fibres activate
  8. ventricles contract
  9. late activation
  10. ventricles repolarize
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181
Q

which steps are invisible on ECG (5)

A

SA node firing
AV node activation
His bundle activation
left bundle activation
Purkinje fiber activation

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182
Q

P wave

A

atrial contraction

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183
Q

why don’t we see the atra relax on ECG

A

because bigger currents mask it

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184
Q

Q wave

A

septum activation (1st negative deflection)

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185
Q

R wave

A

ventricle activation

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186
Q

S wave

A

late activation (not always present)

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187
Q

T wave

A

ventricles repolarize

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188
Q

what is P-R interval a measure of

A

AV transit time

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189
Q

what does long P-R interval mean

A

AV block

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190
Q

what is P-R segment

A

time delay between atrial and ventricular activation

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191
Q

what is S-T segment

A

time between ventricular depolarization and repolarization

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192
Q

what does an S-T segment above 0V indicate

A

some tissue have abnormal APs, typical of infarction

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193
Q

what is Q-T interval proportional to

A

AP duration

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194
Q

what does long QT indicate, and what can it lead to

A

repolarization problem - can lead to arrhythmias

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195
Q

what does a QRS >100ms mean

A

slow excitation

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196
Q

2 possible causes of long QRS interval

A

problems with His-Purkinje (bundle branch block)
slow conduction in cardiac muscle (schemia)

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197
Q

where do positive and negative ions flow in depolarized vs resting cell (inside vs outside cel)

A

inside: + ions from depolarized to resting, - ions from resting to depolarized
outside: + ions from resting to depolarized, - ions from depolarized to resting

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198
Q

how to measure voltage of depolarizing cell

A

positive electrode - negative electrode

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199
Q

2 situations that lead to positive voltage

A

depolarization towards positive electrode
repolarization towards negative electrode

200
Q

2 situations thats lead to negative voltage

A

depolarization towards negative electrode
repolarization towards positive electrode

201
Q

why is T wave positive

A

because depolarization wave moves opposite to repolarization wave due to difference in AP duration from inside to outside the heart

202
Q

bipolar limb lead

A

take 2 measurement, subtract 1 from the other

203
Q

3 bipolar limb lead equations

A

I = Vla - Vra
II = Vll - Vra
III = Vll - Vla

204
Q

why are there 3 bipolar limb leads

A

to form a triangle across the chest that surrounds the heart, sum total of Voltages = 0

205
Q

unipolar lead = ?

A

V

206
Q

how many unipolar limb leads are there

A

9 (aVR, aVL, aVF & V1-V6)

207
Q

why do we need to look at all 12 leads

A

because not all leads will pick up all the info

208
Q

which 3 leads have special ECGs

A

V2 = no P wave
V3 = no Q wave
aVR = inverted T wave, no R+S wave

209
Q

how can you tell from the membrane potential graphs that the SA node and His-Purkinje cells have a pacemaking current

A

they have no resting potential, only a pacemaking potential that drives them to their threshold until depolarization

210
Q

how does ventricular action potential compare to skeletal muscle action potential

A

longer, and resting potential more hyperpolarized

211
Q

4 stages of ventricular potential

A

resting potential
upstroke
plateau
repolarization

212
Q

what is happening during ventricular resting potential

A

poor Na+ and Ca+ conductance, high K+ conductance

213
Q

what is happening during ventricular upstroke

A

fast inward Na+ current

214
Q

what is happening during ventricular plateau

A

K+ channels start to close, Ca+ channels open for Ca+ influx

215
Q

what is happening during ventricular repolarization

A

K+ channels open, Ca+ channels close

216
Q

why is voltage at rest close to K+ value

A

because Pk much greater than Pca and Pna

217
Q

what generates the upstroke for SA node

A

Ca+ current

218
Q

what generates Purkinje fibres’ upstroke

A

Na+ current (fast upstroke and fast propagation)

219
Q

why does Purkinje signal move faster than SA node signal

A

higher upstroke velocity (faster depolarization)

220
Q

which 2 structures have slow APs

A

SA node and AV node

221
Q

how fast do SA and AV nodes’ APs move

A

0.01-0.05m/sec

222
Q

what is the SA and AV node conduction velocity

A

1-10 V/sec

223
Q

which 5 structures have fast APs

A

ventricular muscle
atrial muscle
His bundle
Purkinje fibres
bundle branches

224
Q

how fast do the ventricular muscle, atrial muscle, His bundle, Purkinje fibres and bundle branches AP move

A

0.5-5 m/sec

225
Q

what is the ventricular muscle, atrial muscle, His bundle, Purkinje fibres and bundle branches conduction velocity

A

100-1000 V/sec

226
Q

how does atrial cell AP compare to ventricular cell AP

A

shorter

227
Q

why does ECG only show atrial and ventricular action

A

because biggest (hides other currents)

228
Q

where and when do local circuit currents occur

A

on cell level, <1ms before wave propagates from A to B

229
Q

why is V=0 when ventricles are excited?

A

positive and negative electrodes see same voltage therefore difference = 0

230
Q

when does Ca2+ flow into cytosol

A

during depolarization plateau

231
Q

where are Ca2+ channels located

A

in T-tubules

232
Q

when Ca2+ flows into cell, where does it bind

A

ryanodine receptors on sarcoplasmic reticulum (SR)

233
Q

what does Ca2+ binding to ryanodine receptors of SR do

A

opens Ca2+ channels intrinsic to these receptors so that Ca2+ flows into cytosol

234
Q

what does increased cytosolic Ca2+ conc do

A

more troponin binding = more contraction

235
Q

function of calcium pump in cell membrane

A

bring Ca2+ back up a gradient into SR for next AP

236
Q

what are calcium sensors in membrane sensitive to

A

voltage

237
Q

why does Ca2+ enter cell with a slight delay (~8ms)

A

because triggered by AP / voltage

238
Q

where can you observe the delay of Ca2+ entering the cell

A

calcium transient graph

239
Q

why does mechanical activity always lag electrical activity

A

because Ca2+ must bind

240
Q

is it possible to have complete dissociation (i.e. no mechanical activity)

A

yes

241
Q

normal sinus rhythm

A

70bpm

242
Q

bradycardia

A

abnormal slow rhythm (<60bpm)

243
Q

tachycardia

A

abnormal fast rhythm (>100bpm)

244
Q

when are bradycardia and tachycardia physiologic / healthy (3)

A
  • trained athletes can have resting HR of 40 bpm
  • during exercise HR can go up to 100bpm
  • respiratory sinus arrhythmia
245
Q

respiratory sinus arrhythmia

A

sinus rate increases as you breathe in and slows as you breathe out (more common when young)

246
Q

pathological sinus tachycardia

A

resting HR > 100 bpm

247
Q

2:1 AV block

A

every 2 atrial contractions has 1 ventricular (every other P has no QRST)

248
Q

how does 2:1 AV block affect HR, CO and BP

A

cuts HR in half
decreased CO
decreased BP

249
Q

where is the system blocked for 2:1 AV block

A

could be anywhere between AV node and bundle branches

250
Q

solution for 2:1 AV block

A

electronic pacemaker

251
Q

complete AV block

A

only P, no QRST

252
Q

why is complete AV block dangerous

A

no ventricular contraction = no perfusion

253
Q

cause of premature ventricular complexes (PVC)

A

ectopic pacemaker

254
Q

ectopic pacemaker

A

excitable group of ventricular cells causes premature heartbeat outside SA node

255
Q

parasystole

A

constantly firing ectopic pacemaker (benign)

256
Q

are PVC common

A

yes, can be benign, just uncomfy

257
Q

ventricular tachycardia

A

parasystole becoming dangerous - leads to fibrillation

258
Q

fibrillation

A

no more synchronous firing, extremely fast + irregular beats; fatal if not treated in minutes

259
Q

automated external defibrillator (AED)

A

treatment for fibrillation; resets all cells in heart to beat at once

260
Q

is atrial fibrillation dangerous

A

no; only quality of life issue

261
Q

what is atrial fibrillation caused by

A

premature atrial contraction (PAC)

262
Q

what can atrial fibrillation lead to

A

irregular ventricle activation

263
Q

how to treat atrial fibrillation

A

pulmonary vein isolation; ensures pulmonary vein waves cannot disturb atria

264
Q

how to map tachycardia

A

sock array (attach electrodes to heart surface)

265
Q

isochronal map

A

shows circus movement around an anatomical obstacle (activation propagates in circle around inexcitable scar)
- treatment = remove scar

266
Q

reentrant ventricular tachycardia

A

dangerously low BP due to inadequate filling

267
Q

what can reentrant ventricular tachycardia transition to

A

ventricular fibrillation

268
Q

who discovered reentry

A

George Mines

269
Q

George Mines experiment explanation

A

found that he could propagate signal in only 1 direction rather than 2 like normal (due to refractory block), but these inactive cells can propagate the single signal later

270
Q

significance of George Mines discovery

A

possible cause of tachycardia (and it was largely true!)

271
Q

where on the ECG is the refractory period

A

between QRS and T wave

272
Q

neuron vs myocyte refractory time

A

neuron = few ms
myocyte = 100-300ms

273
Q

what do colliding waves do to each other in signal propagation

A

block (cells are refractory to stimulation)

274
Q

how often do the right and left ventricles beat

A

1/s

275
Q

how does pressure in ventricles compare to pressure in aorta before contraction

A

lower

276
Q

what causes aortic valve to open

A

pressure in ventricles becomes higher than pressure in aorta

277
Q

how does aortic pressure compare to ventricular pressure right after aortic valve opens

A

aortic P tracks ventricular P, then ventricular P drops

278
Q

what happens after ventricular pressure drops

A

aortic valve closes

279
Q

mean arterial pressure equation

A

diastolic pressure + 1/3 pulse pressure

280
Q

why do we only add 1/3 pulse pressure to calculate MAP

A

because pressure wave is wider at the bottom than top

281
Q

for how much of the cycle do ventricles contract to create pressure

A

1/3

282
Q

Windkessel effect

A

distension from compliance of vessels maintains pressure for 2/3 of the cycle where ventricles aren’t contracting

283
Q

what is the old method of measuring BP (direct)

A

vertical tube in an artery (liquid height = BP)

284
Q

does liquid height depend on tube area for BP measurement

A

no

285
Q

palpation

A

measure pressure in cuff to find BP

286
Q

is palpation direct or indirect measure

A

indirect

287
Q

2 components of palpation

A

aneroid sphygmomanometer and aneroid gauge/barometer

288
Q

aneroid sphygmomanometer

A

cuff w bladder, inflating bulb, needle valve and aneroid gauge

289
Q

how does aneroid gauge pressure compare to bladder pressure

A

same

290
Q

what did people use before aneroid sphygmomanometer

A

mercury sphygmomanometer

291
Q

where does palpation measure pulse

A

radial artery

292
Q

palpation method (3 steps)

A
  • fill cuff until no pressure detected
  • release pressure slowly (5mmHg/s)
  • when you feel pulse again = systolic BP
293
Q

why does palpation measure systolic BP

A

the brief period where pulse pressure is higher than cuff pressure allows blood to get through, and this is close to max systolic arterial P

294
Q

auscultation

A

measure Korotkoff sounds to find BP

295
Q

auscultation equipment

A

stethoscope: earpiece, bell, diaphragm

296
Q

what can you hear when there is laminar flow in the arteries and the cuff is deflated (auscultation)

A

nothing

297
Q

auscultation method (3)

A
  1. compress artery
  2. place stethoscope bell on uncompressed artery
  3. flow expansion from compression to no compression leads to turbulence that can be heard
298
Q

between which two points can you hear Korotkoff sounds

A

start at systolic P, end at diastolic P

299
Q

oscillometry

A

machine senses pressure in cuff

300
Q

what is the most common BP measurement method

A

oscillometry

301
Q

oscillometry method (2)

A
  1. heartbeat creates pressure waves in cuff
  2. drop off because cuff loosens therefore don’t sense pressure well
302
Q

nominal BP

A

120/80 mmHg

303
Q

3 reasons BP regulation is important

A
  • adjusts flow according to need e.g. exercise
  • keeps flow in organs constant despite fluctuations in pressure (‘autoregulation’)
  • minimize fluctuations in arterial P (neurohormonal control)
304
Q

total peripheral resistance equation

A

TPR = (MAP - Pa) / CO
TPR = MAP / CO
therefore MAP = HR x SR x TPR

305
Q

mean pulmonary artery pressure and pulmonary vein pressure

A

15 mmHg
5 mmHg

306
Q

why can we not discount vein pressure in pulmonary perfusion pressure like in MAP

A

because error would be 30%

307
Q

pulmonary perfusion pressure

A

10 mmHg

308
Q

how does pulmonary vascular resistance compare to TPR and why do we know this

A

PVR &laquo_space;TPR because flow to lungs is same as system, therefore must have lower resistance

309
Q

4 stages of cardiac cycle

A
  1. isovolumetric ventricular contraction
  2. ventricular ejection
  3. isovolumetric ventricular relaxation
  4. ventricular filling
310
Q

what is the first step is isovolumetric ventricular contraction

A

heart contracts = AV valves close

311
Q

how do pressure and volume of ventricles change during isovolumetric ventricular contraction

A

pressure increases in ventricles, volume stays constant because valves closed

312
Q

what is the state of AV and aortic valves at the end of isovolumetric ventricular contraction

A

AV = closed, aortic and pulm = closed

313
Q

what happens to ventricular pressure at the start of ventricular ejection

A

P increases until ventricular P is higher than pulmonary trunk P and aortic P

314
Q

what does the increase in ventricular P at the start of ventricular ejection do

A

aortic and pulmonary valves open, blood flows out of ventricles

315
Q

what happens to ventricular P during ventricular ejection after valves open

A

ventricular P peaks then falls

316
Q

what is the state of the valves at the end of ventricular ejection

A

AV = closed, aortic and pulm = open

317
Q

what happens at the start of isovolumetric ventricular relaxation

A

ventricular contraction stops, pressure drops

318
Q

what happens as ventricular pressure drops during isovolumetric ventricular relaxation

A

aortic and pulm valves close, Windkessel effect maintains P in aorta and pulmonary trunk

319
Q

what happens to the ventricles during isovolumetric ventricular relaxation, and how does this affect pressure and volume

A

ventricles relax, no change in volume therefore pressure drops to 0

320
Q

what has been happening in the atria during isovolumetric ventricular relaxation

A

they have been filling

321
Q

what is the state of the valves at the end of isovolumetric ventricular relaxation

A

AV = close, aortic + pulm = closed

322
Q

what happens at the start of ventricular filling

A

atrial P > ventricular P -> AV valves open to fill ventricles

323
Q

what happens after AV valves open during ventricular filling

A

SA node fires

324
Q

what happens after SA node fires during ventricular filling

A

atria contract + atrial kick

325
Q

what is the state of the valves at the end of ventricular filling

A

AV = open, aortic and pulm = closed

326
Q

Wiggers diagram

A

shows LV, but parallel events occur in RV with lower pressures

327
Q

how does aortic pressure change on Wickers diagram and why

A

spikes due to ventricular contraction, falls slowly due to Windkessel effect

328
Q

what does the grey space on Wiggers diagram represent

A

ventricular filling

329
Q

what are the blue spaces on Wiggers diagram

A

isovolumetric contraction and isovolumetric relaxation

330
Q

what is the white space on Wiggers diagram

A

ventricular ejection

331
Q

1st heart sound

A

lub = mitral/bicuspid valve closing

332
Q

2nd heart sound

A

dub = aortic valve closing

333
Q

stroke volume equation + values

A

end-diastolic volume (EDV) - end systolic volume (ESV)
120 - 50 = 70mL

334
Q

ejection fraction equation + values

A

stroke volume / end diastolic volume
70 / 120 = 0.6

335
Q

cardiac output equation + values

A

heart rate x stroke volume
70 bpm x 70 mL = 4900mL/min OR 5L/min

336
Q

pulse pressure equation + values

A

max aorta pressure - min aorta pressure OR systolic - diastolic
120 - 80 = 40

337
Q

purpose of pulse pressure

A

doesn’t do anything because it is the difference in pressure at 2 points in time, not a pressure gradient, but it is used as a diagnostic tool because it can change in disease

338
Q

purpose of aortic pressure

A

it drives flow through systemic circulation

339
Q

frank starling mechanism

A

if you stretch a muscle out, it will contract with greater force

340
Q

normal EDV

A

140 mL

341
Q

what happens when EDV is increased to 210 mL (Frank Starling)

A

ventricular filling increases, muscle is stretched, increase force of contraction therefore SV goes from 70 to 100 mL

342
Q

what context is Frank Starling important for

A

exercise

343
Q

preload definition

A

ventricle wall stretch

344
Q

what is measured as a proxy for preload and why

A

EDV and pressure in right atria are indices of preload; hard to measure directly

345
Q

autoregulation definition

A

some critical organs control their own flow

346
Q

experiment that demonstrates autoregulation

A

attach tubes to coronary arteries so that aorta no longer controls perfusion, then lower coronary perfusion pressure
- coronary flow drops then regulates itself

347
Q

how does coronary flow regulate itself

A

by dilating arterioles to decrease resistance

348
Q

autoregulatory range

A

40 - 160 mmHg
pressures in these ranges lead to minor changes in coronary flow; outside range, effect is lost

349
Q

2 situations that lead to autoregulation

A

decreased perfusion = myogenic autoregulation
increased work = metabolic autoregulation

350
Q

myogenic autoregulation (5 steps)

A
  • drop in local arterial pressure in organ
  • decreased blood flow
  • drop in O2, increased metabolites, less vessel wall stretch in organ
  • arteriolar dilation in organ
  • restoration of blood flow toward normal in organ
351
Q

why does a drop in vessel wall stretch lead to arteriolar dilation

A

less stretch = less calcium = less contraction aka dilation

352
Q

metabolic autoregulation / hyperemia (4 steps)

A
  1. increased metabolic activity of organ
  2. less O2, more metabolites in organ interstitial fluid
  3. arteriolar dilation in organ
  4. more blood flow to organ
353
Q

what kind of feedback systems are autoregulation

A

negative feedback systems

354
Q

3 things sympathetic system modulates

A

HR, SV and TPR

355
Q

1 thing parasympathetic system modulates

A

HR

356
Q

3 ways to increase HR

A
  • increase activity of sympathetic nerves to heart
  • increase plasma epinephrine
  • decrease activity of parasympathetic nerves to heart
357
Q

how do sympathetic and parasympathetic systems modulate HR

A

SA node controls HR, systems modulate the rate (but it still beats on its own)

358
Q

where is parasympathetic preganglionic axon

A

in vagus nerve in brainstem/medulla oblongata

359
Q

what does parasympathetic preganglionic axon go to (and where)

A

ganglion in cardiac fat pads

360
Q

what does parasympathetic preganglionic axon transmit to ganglion (and what receptors does it bind)

A

acetylcholine binds to nicotinic receptors in ganglia, causes ganglion to fire

361
Q

what does parasympathetic postganglionic axon release, what does it bind & where

A

acetylcholine binds to muscarinic receptors in SA

362
Q

how does more parasympathetic neural activity affect HR

A

decreases it

362
Q

drug to block parasympathetic effects (and mechanism)

A

atropine binds and blocks muscarinic receptors therefore increases HR

363
Q

where are sympathetic preganglionic neurons located

A

in spinal cord

364
Q

what do sympathetic preganglionic neurons release onto ganglia

A

acetylcholine

365
Q

where are sympathetic ganglia located

A

next to spinal cord

366
Q

what does sympathetic postganglionic axon release (where does it go and what does it bind to)

A

norepinephrine binds to beta-adrenergic receptors on SA node

367
Q

how does more sympathetic neural activity affect HR

A

more neural activity = higher HR (fight/flight)

368
Q

beta agonists (HR)

A

binds and increases HR

369
Q

beta antagonists (HR)

A

prevents binding therefore decreases HR

370
Q

for SV control, where do the sympathetic ganglia connect

A

ventricular wall

371
Q

what substance binds to ventricular wall (sympathetic)

A

norepinephrine

372
Q

why does norepinephrine increase SV

A

because it increases contractility

373
Q

beta agonist (SV)

A

binds and increases SV

374
Q

beta antagonist (SV)

A

prevents binding therefore decreases SV

375
Q

why does increasing contractility increase SV

A

higher max force, higher force increase rate, decreased duration of contraction (shorter refractory period therefore more APs)

376
Q

how does increasing contractility affect SV curve

A

shift SV curve upwards

377
Q

is increasing contractility the same as Frank Starling mechanism (2)

A

no
- same EDV but higher SV
- Frank Starling moves along same SV curve

378
Q

tone

A

state of contraction of smooth muscle in the walls of the vessel

379
Q

how does sympathetic system control vessel tone

A

norepinephrine binds to alpha-adrenergic receptors in blood vessels

380
Q

how does increased norepinephrine affect vessel tone

A

more NE = higher TPR, higher MAP therefore more constriction / tone

381
Q

can sympathetic system control capillary tone

A

no because no smooth muscle

382
Q

how do sympathetic neurons act, and what does this mean for blood flow

A

discrete and organ-specific manner therefore blood flow can be regulated independently depending on physiological conditions

383
Q

alpha agonist (TPR and MAP / tone)

A

activate alpha-adrenergic receptors therefore higher TPR and MAP

384
Q

alpha blocker (TPR and MAP / tone)

A

bind. to alpha-adrenergic receptors and prevent activation therefore decrease TPR and MAP

385
Q

what is neural control of adrenal glands also known as

A

global control of vessel tone and HR

386
Q

does neural control of adrenal glands have an associated external ganglion

A

no

387
Q

what system are adrenal glands a part of

A

sympathetic nervous system

388
Q

what does adrenal medulla come from

A

cells of the neural crest

389
Q

what are adrenal glands innervated by

A

preganglionic axon that releases ACh

390
Q

what are the cells in adrenal gland

A

modified ganglion cells that don’t project out

391
Q

what do cells in adrenal gland synthesize and release into the blood

A

catecholamines (NE and epinephrine)

392
Q

what are catecholamines and how do they affect HR, SV, TPR and MAP

A

they are alpha and beta agonists therefore increase HR, SV, TPR and MAP

393
Q

how many blood pressure control systems do we have

A

MANY

394
Q

3 ways BP control systems differ

A
  • time scales
  • strengths/feedback gains
  • pressure ranges
395
Q

baroreceptor vs renal time scale

A

baroreceptor = within seconds (changes HR, TPR, SV)
renal = hours to days

396
Q

baroreceptor vs renal strength/feedback gain

A

baroreceptor = strong
renal = strongest

397
Q

baroreceptor vs CNS ischemic reflex pressure ranges

A

baroreceptor = max at healthy normal BP range (120 mmHg)
CNS ischemic reflex = works when BP dangerously low

398
Q

baroreceptor reflex / baroreflex

A

fast response to BP changes

399
Q

baroreceptors

A

receptors in carotid arteries that sense pressure (sensory arm of baroreceptor reflex)

400
Q

what do baroreceptors signal then activate (motor arm of baroreceptor reflex)

A

signal brainstem, then activate autonomic system

401
Q

where are baroreceptors located

A

aortic arch and carotid sinus

402
Q

4 steps of baroreceptors being mechanosensitive

A

heartbeat - aorta and carotid sinus stretch - channels in baroreceptors open - signals brain

403
Q

what does the average frequency of baroreceptor firing change with

A

MAP (higher MAP = more firing)

404
Q

across all MAP levels, where is the highest baroreceptor firing rate

A

at BP peak

405
Q

how does standing up affect blood flow and BP

A

400 mL flows from trunk to legs, decreases BP = increase sympathetic and decrease parasympathetic

406
Q

how does decreased baroreceptor firing affect HR, SV, TPR, capacitance vessels and venous return

A

increase HR, SV, TPR
constrcit capacitance vessels via alpha receptors
increase venous return

407
Q

what kind of system is baroreceptor reflex

A

negative feedback system (decrease baroreceptor firing = increase sympathetic activation

408
Q

result of cutting 2 nerves from baroreceptors

A

labile hypertension - same mean BP but more fluctuations “buffer reflex”

409
Q

where are peripheral chemoreceptors located

A

close to baroreceptors (carotid and aortic body)

410
Q

what 3 things do peripheral chemoreceptors sense

A

PO2, PCO2 and pH in arterial blood

411
Q

what do peripheral chemoreceptors act on

A

breathing (increase frequency and tidal volume)

412
Q

how to peripheral chemoreceptors affect HR

A

increase HR for faster circ (elminiate CO2 and increase O2)

413
Q

how do kidneys control blood volume (2)

A

urinary loss and RAA system

414
Q

pressure diuresis

A

increased arterial pressure leads to higher excretion of H2O and Na+

415
Q

kidney function (2)

A

maintain levels of ions in plasma and remove waste

416
Q

nephrons function (2)

A

expel H2O and waste, followed by H2O reabsorption

417
Q

what kind of system is kidney control of blood volume

A

negative feedback system (increased MAP leads to more urine, and when excreted it decreases MAP)

418
Q

what is 60% blood volume

A

plasma

419
Q

how does decreasing plasma volume affect BV

A

decreases

420
Q

diuretics

A

class of drugs used to control BP

421
Q

RAA system (name and function)

A

renin angiotensin aldosterone system; senses pressure in kidneys

422
Q

what does the RAA system sense changes in filtration rate as

A

changes in Na+ excretion

423
Q

how does RAA system act on changes in filtration

A

signals specialized cells to release renin

424
Q

what incdirectly senses pressure in the brain

A

osmoreceptors in hypothalamic neurons

425
Q

what do baroreceptors pass signals through

A

vagus nerve

426
Q

what does baroreceptor signaling through vagus nerve lead to

A

ADH release from hypothalamus neurons

427
Q

what is RAA system 1

A

renin

428
Q

renin

A

enzyme released into circulation

429
Q

what leads to increased renin in RAA system 1

A

decreased MAP (low Na+ in filtrate leads to specialized cells seeing low BP)

430
Q

renin function in RAA system 1

A

convert angiotensinogen to angiotensin 1

431
Q

where is angiotensinogen made

A

liver

432
Q

what happens to angiotensin 1 in RAA system 1

A

ACE converts it to angiotensin 2

433
Q

where is ACE (angiotensin converting enzyme) produced

A

lungs; produced by pulmonary endothelium

434
Q

what is angiotensin 2

A

vasocontrictor

435
Q

how does angiotensin 2 affect TPR and MAP, and what is the overall result on RAA system 1

A

increases TPR and MAP
high MAP lowers renin, therefore decreases MAP
NEGATIVE FEEDBACK SYSTEM

436
Q

RAA system 2

A

vasopressin / ADH

437
Q

vasopressin / ADH (antidiuretic hormone)

A

synthesized in hypothalamus, released by pituitary gland into blood

438
Q

how does ADH affect TPR

A

ADH = vasoconstriction = increase TPR

439
Q

where does ADH act (+ 7 steps)

A

kidney
- less renal Na+ and H2O excretion
- higher plasma volume
- higher BV
- higher venous return
- higher EDV
- higher SV
- higher CO

440
Q

how is MAP affected by ADH

A

increased by 2 mechanisms (increasing CO and TPR)

441
Q

what is the overall result of ADH on RAA system 2

A

ADH increases MAP, which lowers ADH and decreases MAP
NEGATIVE FEEDBACK SYSTEM

442
Q

RAA system 3

A

aldosterone

443
Q

what does low MAP lead to in RAA system 3

A

more renin, therefore more angiotensin 2

444
Q

where does angiotensin bind (+ effect) in RAA system 3

A

binds receptors in adrenal gland to release aldosterone

445
Q

where does aldosterone bind in RAA system 3 (+ effect)

A

binds receptors in kidney
- causes Na+ and H2O retention
- leads to higher CO and increased MAP

446
Q

what is the overall result of aldosterone on RAA system 3

A

aldosterone increases MAP, which decreases aldosterone and decreases MAP
NEGATIVE FEEDBACK SYSTEM

447
Q

4 BP (hypertension) drugs

A

aldosterone receptor antagonists
angiotensin 2 receptor blockers (ARBS)
ACE inhibitors
renin inhibitors

448
Q

aldosterone receptor antagonists

A

prevent aldosterone binding therefore decrease BP

449
Q

angiotensin 2 receptor blockers (ARBS)

A

prevent angiotensin 2 biding in brain, arterioles and adrenal glands therefore decrease BP

450
Q

ACE inhibitors

A

prevent conversion of angiotensin 1 to 2 therefore decrease BP

451
Q

renin inhibitors

A

prevent conversion of angiotensinogen to angiotensin 1 therefore decrease BP

452
Q

baroreflex in action (standing up) (3 steps)

A
  • BP drops to 75/40 for 10 seconds (without baroreflex it would continue to drop)
  • then recovers to approx normal
  • systolic overall drops a little, diastolic overall increases a little to give same mean MAP
453
Q

hydrostatic pressure equation

A

fluid density x gravity x height
P = pgh

454
Q

how do hydrostatic pressure change throughout body

A

increases from thorax to foot because of gravity

455
Q

why does a small change in hydrostatic pressure in venous compartment lead to large volume change (& what is the result of this)

A

high compliance
leads to blood pooling in legs

456
Q

central blood volume

A

blood in thorax, lungs, heart and great vessels

457
Q

how does central blood volume when you stand up

A

goes from 1.2L to 0.9L

458
Q

how does venous pressure change when standing up

A

decreases because less blood, therefore smaller venous return

459
Q

how does SV change when standing up (and by how much)

A

drops by 50% because of low venous return

460
Q

how does CO change when standing up (by how much and why)

A

drops from 6 to 4.5 (not 50%)
- SV drops by 50%, but HR jumps by 50%, therefore CO = 0.75 of original value

461
Q

how does HR change when standing up

A

increases by 50% (from 60 to 90)

462
Q

if CO is 75% of what it was, how is MAP preserved

A

constriction in arterioles leads to increased TPR (baroreflex)

463
Q

2 reasons we faint when standing too long

A
  • blood pooled in leg veins
  • loss of plasma volume
464
Q

what does blood pooling in leg veins mean for the body

A

less central blood volume therefore less venous return

465
Q

how to avoid blood pooling in leg veins

A

flex calf muscles periodically (‘muscle pump’ = reduces need for high HR)

466
Q

how do we lose plasma volume when standing for too long (2)

A
  • water moves to interstitial space through capillaries
  • higher pressure in legs from standing leads to more plasma volume loss
  • leads to lower venous return therefore lower MAP
467
Q

how much plasma volume can we lose by standing for 15 mins

A

750 mL

468
Q

starling forces

A

physical forces that determine movement of fluid between capillaries and tissue fluid

469
Q

2 starling forces

A

hydrostatic pressure and oncotic pressure

470
Q

hydrostatic pressure

A

force exerted by blood inside capillary / interstitial space

471
Q

oncotic pressure

A

osmotic pressure generated by large molecules (especially proteins)

472
Q

how much water do we lose a day and how does this compare to plasma volume

A

lose 4L of water a day, only 3L of plasma

473
Q

how is water returned per day and how

A

4L returned per day via lymphatic system

474
Q

effect of sympathetic venoconstriction

A

lower venous capacitance and higher venous return

475
Q

natriuresis

A

Na+ excretion in the urine by kidnets

476
Q

chronic venous insufficiency

A

orthostatic hypotension at short time scales

477
Q

2D reentry demo summary

A

showed why some PVCs lead to tachycardia and then fibrillation
- spiral generated by interaction of ectopic beat (PVC) w normal wave of excitation = tachycardia
- hard to get by chance, which explains why PVCs are often benign

478
Q

different between ventricular tachycardia and ventricular fibrillation

A

tachycardia = more beats, but overall process. inright order
fibrillation = system out of sync therefore steps not happening in the right order

479
Q

how does HR change with power (exercise) and values

A

increases linearly (from 60 to 180bpm - 3x increase)

480
Q

why does HR increase with power

A

due to increased sympathetic tone and decrease in parasympathetic tone

481
Q

how does SV change with power (exercise) and why

A

increases a little due to increased sympathetic activity, then dips at very high HR because decreased diastolic period = decreased filling time = decreased EDV = decreased SV (frank starling)

482
Q

how does CO change with power (exercise), by how much and why

A

increases linearly by 3x, mostly depends on HR (from 5 to 15)

483
Q

how does MAP change with power (exercise), by how much and why

A

increases by approx 20%
- systolic increases from 120-190, diastolic has approx no change

484
Q

cardiac stress test

A

check to make sure systolic increases to a high level (~200mmHg); measure of the ventricles’ ability to generate force - low value may mean damage e.g. scar tissue

485
Q

how does TPR change with power (exercise) and why

A

drops to 40% of resting value because muscles consume more O2 and generate more waste (metabolic autoregulation)

486
Q

how does O2 consumption change with power (exercise) and why

A

increases by 9x (up to >2000mL/min) because 3x increase in CO and 3x arteriovenous O2 diff

487
Q

how much does blood flow to muscles, skin, heart and other organs change in exercise

A

increases 12x in muscles
increases 5x in skin
increases 3.5x to heart
decreases to other organs to keep MAP constant

488
Q

how does the increase in flow compare in trained vs untrained individuals

A

untrained = 3.5x increase
trained= 7x increase

489
Q

at rest, what determines tone

A

alpha beta receptor activation balance

490
Q

what overrides the alpha beta receptor activation in exercising muscle

A

metablolic control

491
Q

what experiences vasoconstriction in arterioles during exercise from neural control

A

non-exercising muscle

492
Q

does training affect max HR

A

no

493
Q

why does training increase CO

A

increases SV (contractility) due to hypertrophy (each cell gets bigger = resting HR falls)

494
Q

who are arrhythmias more common for

A

trained athletes

PHGY 210 (3 decks)

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