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Phase 1 flashcards > Cardio > Flashcards

Cardio Flashcards

1
Q

name the layers outside the heart

A

fibrous pericardium, parietal pericardium

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2
Q

name the layers on the heart

A

visceral pericardium, myocardium, endocardium

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3
Q

where does pericardial fluid lie?

A

between the parietal and visceral pericardium

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4
Q

function of the pericardial fluid

A

prevents friction between the visceral and parietal pericardium when the heart contracts

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5
Q

which cells of the heart contract?

A

myocardial cells

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6
Q

what cells are in contact with the blood, inner lining of the heart

A

endocardium

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7
Q

what is the cardiac cycle?

A

the events that occur when blood is being moved in and out of the ventricles

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8
Q

what is systole

A

ventricles are contracting

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9
Q

what is diastole

A

ventricles are relaxing

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10
Q

how long is systole?

A

0.3s

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11
Q

how long is diastole

A

0.5s

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12
Q

cardiac cycle length

A

0.8s

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13
Q

typical resting heart rate, and range of healthy heart rates

A

72bpm, 60-100bpm

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14
Q

what does the cardiac cycle represent

A

one heartbeat

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15
Q

what events occur in systole?

A

ventricular isovolumic contraction and ejection

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16
Q

what is isovolumic contraction?

A

the ventricles contract but the volume of blood in the ventricles does not change
all valves are closed

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17
Q

during ejection, how much of the blood leaves the ventricles?

A

2/3rds

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18
Q

what events happen in diastole?

A

isovolumic relaxation, rapid inflow of blood, diastasis, atrial systole

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19
Q

what causes the rapid of inflow of blood into the ventricles

A

passive movement of blood from atria to ventricles down a pressure gradient
pressure in the atria exceeds ventricles

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20
Q

what is isovolumic relaxation

A

ventricles relax, all valves shut
ventricular pressure falls to below aortic pressure

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21
Q

what is rapid inflow?

A

pressure in the atria exceeds ventricles
AV valves open, blood flows from the atria to the ventricles down a pressure gradient
atria passively fill and blood trickles into ventricles
80% ventricle filling here

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22
Q

what is diastasis

A

Pressure in the ventricles approaches pressure in the atria
pressure gradient means passive filling rate falls

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23
Q

what is atrial systole

A

contraction of atria to fully empty into ventricles

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24
Q

what is the first heart sound and what causes it?

A

lubb, AV valve shuts

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25
Q

what is the second heart sound, and what causes it?

A

dubb, aortic valve shuts

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26
Q

what does a P wave represent?

A

atrial depolarisation

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27
Q

what does the QRS complex represent?

A

ventricular depolarisation and atrial repolarisation

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28
Q

what is the T wave?

A

ventricular repolarisation

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29
Q

what are the two types of blood vessel regulation?

A

intrinsic and extrinsic

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30
Q

what is intrinsic autoregulation?

A

higher volumes of blood mean vessels increase diameter to level out pressure

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31
Q

what is extrinsic autoregulation?

A

myogenic vasoconstriction/ dilation

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32
Q

what is hyperaemia?

A

an increase in blood flow to different tissues in the body

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33
Q

what is active hyperaemia

A

actively increasing perfusion to certain body parts
metabolic response e.g exercise, increase blood flow to calf muscles

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34
Q

what is reactive hyperaemia

A

occluded tissue
after occlusion removed, an increase of blood flow to that area

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35
Q

where are peripheral chemoreceptors found?

A

aortic arch
carotid sinus - dilation at the bifurcation of the common carotid artery, and the beginning of the internal carotid artery

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36
Q

what are the peripheral chemoreceptors sensitive to?

A

an increase in carbon dioxide
a decrease in oxygen
a decrease in pH

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37
Q

what are the responses of the peripheral chemoreceptors?

A

sympathetic response
an increase in blood pressure
impulses to pressor region of medulla

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38
Q

where are arterial baroreceptors located?

A

aortic arch
carotid sinus

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39
Q

what do arterial baroreceptors respond to?

A

increase in blood pressure

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40
Q

mode of action of arterial baroreceptors

A

higher blood pressure causes more distortion of baroreceptor
more distortion of baroreceptor means higher firing rate
more impulses to the depressor centre of the medulla
blood pressure decreases
parasympathetic response

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41
Q

where are cardiopulmonary baroreceptors located?

A

atria
ventricles
pulmonary artery

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42
Q

what do cardiopulmonary baroreceptors respond to?

A

an increase in blood volume

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43
Q

mode of action of cardiopulmonary baroreceptors

A

an increase in blood volume means an increase in blood pressure
higher blood pressure causes more distortion of baroreceptor
more impulses to depressor centre of medulla
blood pressure decreases
parasympathetic response

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44
Q

what part of the brain is the central control of blood pressure?

A

medulla

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45
Q

what are the two blood pressure centres of the medulla and what response to they elicit?

A

pressor - sympathetic
depressor - parasympathetic

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46
Q

equation for cardiac output

A

CO= SV x HR

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47
Q

equation for blood pressure

A

BP = CO x TPR

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48
Q

what is total peripheral resistance?

A

total resistance of blood vessels to blood flow

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49
Q

equation for pulse pressure

A

systolic - diastolic pressure

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50
Q

equation for MAP (mean arterial pressure)

A

MAP = diastolic pressure + 1/3 pulse pressure

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51
Q

Pouisseile’s Law for blood flow

A

flow = (π x r^4)/ 8 x length x viscosity

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52
Q

equation for blood flow

A

flow = pressure / resistance

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53
Q

equation for blood flow

A

flow = pressure / resistance

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54
Q

what is Frank Starling’s Law

A

the stroke volume of the left ventricle will increase as the left ventricular volume increases
the more the heart chambers fill, the stronger the ventricular contraction, and therefore the greater the stroke volume

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55
Q

explain Frank Starling Law

A

higher EDV (end diastolic volume) = harder contraction
the more ventricles fill, the more myocytes stretched, therefore stroke volume increases and cardiac output increases

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56
Q

what are Starling forces on blood vessels?

A

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

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57
Q

what is oncotic pressure?

A

force keeping blood in the vessel
(albumin)

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58
Q

what is hydrostatic pressure?

A

force squeezing fluid out

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59
Q

mechanisms of controlling blood pressure in the long term

A

RAAS
ADH (vasopressin)
fluid intake

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60
Q

what is the effect of heart failure on cardiac output?

A

decreases

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61
Q

how do we resolve heart failure?

A

usually by increasing stroke volume rather than increasing heart rate as tachycardia is unhealthy
increase ECF volume

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62
Q

how do we regulate circulation in the short term?

A

vasodilators and vasoconstrictors

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63
Q

give some local vasodilators

A

hypoxia
a decrease in pH
an increase in carbon dioxide/ increased acidity
bradykinin
NO
prostacyclin
an increase in K+

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64
Q

give a local vasoconstrictor

A

endothelin 1

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65
Q

when is endothelin 1 released?

A

injured endothelium

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66
Q

give some hormonal/ neurotransmitter vasodilators

A

Ach (acts on muscularinic 2 receptors)
ANP

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67
Q

give some hormonal/ neurotransmitter vasoconstrictors

A

angiotensin II
ADH
NAd

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68
Q

define stroke volume

A

volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction

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69
Q

define cardiac output

A

the volume of blood pumped out of the left ventricle in a minute

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70
Q

define TPR

A

total peripheral SYSTEMIC resistance (not pulmonary)

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71
Q

where is TPR the highest

A

arterioles

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72
Q

define preload

A

amount of myocyte stretch in ventricular filling (a volume)

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73
Q

define afterload

A

resistance myocytes contract against in ventricular systole (a resistance)

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74
Q

define contractility

A

force of contraction of the heart muscle

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75
Q

define compliance

A

how easily the heart fills in diastole

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76
Q

define Frank Starling Law

A

higher EDV = more ventricular filling = harder ventricular contraction

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77
Q

define diastolic distensibility

A

pressure to fill ventricles at diastole to EDV

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78
Q

describe parasympathetic action on the cardiovascular system

A

Ach acts on muscarinic type 2 receptors
negative chronotrophic response (decreased heart rate)
negative ionotrophic response (decreased force of contraction)
fewer Ca2+ enter myocytees
fewer action potentials are triggered
decreases contractility and cardiac output

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79
Q

describe parasympathetic action on the cardiovascular system

A

noradrenaline acts on beta 1 receptors in the heart
positive chonotrophic response (increased heart rate)
positive ionotrophic response (increased force of contraction)
fewer Ca2+ enter myocyte
fewer action potentials are triggered
decreased contractility and cardiac output

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80
Q

describe sympathetic action on the cardiovascular system

A

noradrenaline acts on beta 1 receptors in the heart
positive chonotrophic response (increased heart rate)
positive ionotrophic response (increased force of contraction)
more Ca2+ enter myocyte
more action potentials are triggered
increased contractility and cardiac output

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81
Q

example of an elastic artery

A

aorta

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82
Q

are elastic arteries generally closer or further away from the heart than muscular arteries?

A

closer

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83
Q

what is the difference between elastic and muscular arteries?

A

elastic arteries have more elastic tissue in the tunica media and a large lumen
muscular arteries have more muscle tissue in the TM and a smaller lumen

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84
Q

explain the specialisation of elastic arteries

A

need to withstand great pressures and maintain constant pressure by quick elastic recoil

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85
Q

explain the specialisation of muscular arteries

A

more muscle for vasodilation and vasoconstriction (regulation)

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86
Q

when does an artery become an arteriole?

A

3 or less muscle layers

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87
Q

site of TPR

A

arterioles

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88
Q

what percentage of blood is carried in veins?

A

70%

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89
Q

what blood vessels are responsible for EDV?

A

veins

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90
Q

by which mechanisms is blood returned to the heart in veins?

A

skeletal muscle contraction - exercise
respiratory pump
peristalsis (smooth muscle contraction)

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91
Q

function of capillaries

A

oxygen and nutrient delivery to tissue
carbon dioxide and waste removal from tissue

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92
Q

how is blood flow from arterioles to capillaries regulated?

A

precapillary sphincters

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93
Q

describe continuous capillaries

A

fully intact endothelium

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94
Q

describe fenestrated capillaries

A

endothelial gaps
basement membrane intact

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95
Q

describe discontinuous capillaries

A

large gaps in endothelium
incomplete BM

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96
Q

pressure of the pulmonary circulation

A

25/8

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97
Q

why is the pressure of the pulmonary circulation much lower?

A

prevent oedema

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98
Q

how do pulmonary vessels react to hypoxia?

A

vasoconstriction

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99
Q

pressure of the systemic circulation

A

120/80

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100
Q

how does the systemic circulation react to hypoxia?

A

vasodilation

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101
Q

lifespan of erythrocytes

A

120 days

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102
Q

lifespan of WBC

A

6-10 hours

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103
Q

lifespan of platelets

A

7-10 days

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104
Q

hormone that stimulates erythrocyte production

A

erythropoietin

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105
Q

where is erythropoietin synthesised?

A

kidney

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106
Q

hormone that stimulates WBC production

A

GM-CSF (granulocyte macrophage colony stimulating factor)

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107
Q

hormone that stimulates platelet production

A

thrombopoetin

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108
Q

name of a young RBC

A

reticulocyte

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109
Q

what is the term for blood plasma without clotting factors?

A

serum

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110
Q

constituents of blood

A

plasma and cellular components

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111
Q

what is haematocrit?

A

red blood cells as a proportion of total blood volume

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112
Q

normal value for haematocrit?

A

0.45

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113
Q

precursor to all blood cells

A

haematocytoblast

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114
Q

name for the formation of blood cells

A

haematopoiesis

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115
Q

percentage of blood that is plasma and cellular

A

55% plasma
45% cellular

116
Q

what percentage of the cellular component of blood are erythrocytes?

A

99%

117
Q

stages of formation of platelets from haematocytoblasts

A

common myeloid progenitor - megakaryoblast - megakaryocyte, platelet

118
Q

stages of formation of macrophages from haemocytoblasts

A

common myeloid progenitor - myeloblast - monocyte - macrophage

119
Q

precursor for a RBC

A

proerythroblast

120
Q

precursor for a monocyte

A

monoblast

121
Q

precursor for B and T lymphocytes

A

lymphoblasts

122
Q

stages of formation of basophils, eosinophils and neutrophils from a haematocytoblast

A

haematocytoblast - myeloblast - progranulocyte - basophil/ eosinophil/ neutrophil

123
Q

what type of cell is a haematocytoblast

A

pluripotent stem cell

124
Q

which white blood cells are granulocytes

A

neutrophils, eosinophils, basophils

125
Q

which white blood cells are agranulocytes

A

monocytes, lymphocytes

126
Q

neutrophil function

A

acute inflammatory response

127
Q

appearance of neutrophil on a histological slide

A

multi lobed nucleus
faint granules

128
Q

monocyte function

A

immature cells that become macrophages and APCs

129
Q

appearance of monocyte on a histological slide

A

reniform nucleus (kidney bean shape)

130
Q

first white blood cells visible in a parasitic infection e.g worms

A

eosinophil

131
Q

eosinophil functions

A

antagonist to an allergic response by producing antihistamines
parasitic infections

132
Q

appearance of an eosinophil on a histological slide

A

pink cytoplasmic granules (think ‘eosinophilic’)

133
Q

name of basophils inside tissue

A

mast cells

134
Q

basophil function

A

produce histamines - allergic response

135
Q

basophil appearance on a histological slide

A

dark blue granules (think b for blue)

136
Q

what receptors do basophils bear?

A

IgE receptors

137
Q

lymphocyte function

A

cell mediated and innate adaptive immune response

138
Q

appearance of lymphocytes on a histological slide

A

very little cytoplasm
large nucleus

139
Q

describe platelet formation

A

megakaryocytic undergoes endomitosis (DNA doubles but cell doesn’t divide)
CSM blebs (ejects platelet functions)

140
Q

appearance of inactive platelets

A

smooth and discoid - circular without any ridges

141
Q

appearance of active platelets

A

increase in surface area, pseudopoid

142
Q

which types of granules do platelets release when they’re activated

A

electron granules
alpha dense granules

143
Q

function of electron dense granules

A

provide energy to produce a platelet plug

144
Q

what do electron dense granules store?

A

ADP
ATP
Ca2+
serotonin

145
Q

what is the function of alpha dense granules?

A

formation of the platelet plug scaffolding

146
Q

what do alpha dense granules contain?

A

PDGF (platelet derived growth factor)
VWF (Von Willebrand factor)
fibrinogen
heparin antagonist PF4

147
Q

name for too many platelets

A

thrombocytosis

148
Q

risks of thrombocytosis

A

increased clot risk

149
Q

name for too few platelets

A

thrombocytopenia

150
Q

risks of thrombocytopenia

A

increased risk of bleeding

151
Q

what triggers platelet formation?

A

endothelial damage

152
Q

what is the first event after the endothelium is damaged?

A

vascular constriction/ spasm

153
Q

which chemical mediators released form healthy endothelium keep vessels open?

A

NO (nitrous oxide) and prostacyclin

154
Q

when the vessel is damaged, which chemical mediator is released?

A

endothelin-1

155
Q

effect of endothelin-1

A

causes vasoconstriction

156
Q

what is the second event after a blood vessel is damaged?

A

primary platelet plug formation

157
Q

what is vWF and what does it do?

A

Von Willebrand factor binds to exposed collagen at the site of injury

158
Q

what receptor does vWF bind too?

A

GP1b (glycoprotein 1b)

159
Q

what is platelet adhesion?

A

platelets bind to vWF on collagen via GPIIa OR IIIb receptors (glycoprotein 2a or 3b)

160
Q

what is platelet activation?

A

change in shape from discoid to pseudopoid
exocytosis of alpha dense and electron dense granules

161
Q

is platelet activation positive or negative feedback and why?

A

positive
activates more platelet activation and aggregation

162
Q

what is the third step after a vessel is damaged?

A

the coagulation cascade

163
Q

what is the coagulation cascade?

A

forming a mesh of fibrin over the primary platelet plug to form a stable secondary platelet plug

164
Q

what are the two initial pathways of the coagulation cascade

A

intrrinsic and extrinsic pathway

165
Q

what triggers the intrinsic pathway of the coagulation cascade?

A

trauma inside the blood vessel
internal damage

166
Q

what triggers the extrinsic pathway of the coagulation cascade?

A

extravascular trauma

167
Q

which pathway is more common?

A

extrinsic

168
Q

what is the order of factor activation in the intrinsic pathway?

A

12, 11, 9, 8 to factor 10 (factor 10 is the start of the common pathway)
remember this as descending order from 12 - 8 missing out 10

169
Q

what is factor 3 and when is it released?

A

tissue factor
released from damaged tissue

170
Q

what is the order of factor activation in the extrinsic pathway?

A

3, 7, 10 (remember this as 3+7=10)

171
Q

what is the order of factor activation in the common pathway?

A

10, 2, 1
factor 5 aids the activation of factor 2 by factor 10
(remember this as 5 x 2 x 1 = 10)

172
Q

what is inactive factor 2 called?

A

prothrombin

173
Q

what is active factor 2 called?

A

thombrin

174
Q

what is inactive factor 1 called?

A

fibrinogen

175
Q

what is active factor 1 called?

A

fibrin

176
Q

how is the secondary platelet plug broken down (fibrinolysis)?

A

tPa converts plasminogen to plasmin
plasmin converts fibrin to fibrinogen

177
Q

where are most clotting factors produced?

A

liver

178
Q

which clotting factor is not produced in the liver, and where is it produced?

A

factor 8 - vWF

179
Q

which are the vitamin K dependent factors?

A

10, 9, 7, 2 (remember as 1972)

180
Q

what produces different blood groups?

A

antigens on the surface of red blood cells

181
Q

features of ABO antigens

A

carbohydrate antigens
cannot cross the placenta
produced by the spleen

182
Q

what are the blood groups?

A

A+, A-, B+, B-, O+, O-, AB+, AB-

183
Q

can Rhesus positive individuals donate to Rhesus negative individuals?
can Rhesus negative individuals donate to Rhesus positive individuals?

A

no
yes

184
Q

which blood group is the universal acceptor?

A

AB+

185
Q

which blood group is the universal donor?

A

O-

186
Q

what type of antigens are Rhesus antigens?

A

peptide

187
Q

can Rhesus antigens cross the placenta?

A

yes

188
Q

describe haemolytic disease of the fetus and newborn

A

mother is Rhesus D negative (dd) and becomes pregnant with Rhesus D positive baby (Dd)
mother makes anti D antibodies but the first child is unaffected
if the mother becomes pregnant with another RhD positive baby, her body produces antibodies more rapidly
causes anaemia in the child

189
Q

what does myogenic mean?

A

heart contracts without external nervous control
the heart muscle initiates it own contraction

190
Q

what is the heart’s pacemaker?

A

sinoatrial node (SAN)

191
Q

where is the heart’s pacemaker?

A

wall of the right atrium

192
Q

how do impulses travel from the SAN to the left atrium?

A

Bachmann bundles

193
Q

where is the atrioventricular node?

A

Posteroinferior interatrial septum wall, within triangle of atrioventricular node (Koch’s triangle)

194
Q

what is the function of the delay at the AVN?

A

allow ventricles to fill before they contract

195
Q

how long is the delay path the AVN?

A

120ms

196
Q

how is the delay physiologically caused?

A

AVN has fewer gap junctions
- gap junctions allow transmission of ions between cells
- slower rate of impulse
AVN has smaller fibres diameter

197
Q

what is the Bundle of His? (atrioventricular bundle)

A

continuation of the specialised tissue of the AV node
transmits the electrical impulse from the AV node to the Purkinje fibres of the ventricles.

198
Q

describe the path of the bundle of His

A

descends down the membranous part of the interventricular septum before dividing into the left and right bundle branches
Right bundle branch – conducts the impulse to the Purkinje fibres of the right ventricle
Left bundle branch – conducts the impulse to the Purkinje fibres of the left ventricle.

199
Q

where is the fastest conduction?

A

purkinje fibres

200
Q

what is the difference between nodal cells and myogenic cells

A

nodal cells carry out conduction of the electrical impulse
myogenic cells are contractile

201
Q

describe what a syncytium is

A

heart contracts as one unit

202
Q

what are the phases of the ventricular action potential in order?

A

phase 4, phase 0, phase 1, phase 2, phase 3

203
Q

what is the change in potential during phase 4, and which ion is responsible?

A

resting potential
K+

204
Q

what is the change in potential during phase 0, and which ion is responsible?

A

rapid depolarisation
Na+ inflow

205
Q

what is the change in potential during phase 1, and which ions are responsible?

A

partial repolarisation
K+ outflow
inflow of Na stops

206
Q

what is the change in potential during phase 2, and which ions are responsible?

A

plateau
Ca2+ slow inflow

207
Q

what is the change in potential during phase 3, and which ions are responsible?

A

repolarisation
K+ outflow
inflow of Ca2+ stops

208
Q

what is the change in potential during phase 4, and which ions are responsible?

A

K+ outflow

209
Q

describe the action potential in ventricular cells/ myocardial cells

A

action potential exits SAN and spreads to other cells by gap junctions called connexions
cardiac myocytes are depolarised by Na+ ions
activation of myocardium results in
- resting potential -90mV
- depolarisation of cell to reach threshold of -70mV which leads to sodium gated fast channels opening
- rapid influx of Na+, membrane is depolarised to +20mV
- K+ channels open and K+ leaves the cell, membrane potential falls to -15mV
- voltage gated Ca2+ channels open and Ca2+ move in and counter the K channels, resulting in a plateau for 200ms
- entry of Ca2+ results in contraction of myocyte
- Ca2+ channels close and repolarisation occurs

210
Q

why is there no hyper polarisation with excitation contraction coupling in contractile cells?

A

contractions are auto rhythmic and continuous - needs to be consistent

211
Q

which phases are the absolute refractory period?

A

phase 1 and 2

212
Q

which phases are the relative refractory period?

A

phase 3

213
Q

resting membrane potential of nodal cells

A

-60mV

214
Q

describe nodal cell depolarisation

A
  • action potential is generated
  • at -60mV it leads to the opening of HCN channels (hyperpolarisation gated cyclic nucleoside channels). HCN allows for Na+ ions to move into the cell
  • depolarisation from -60mV to -40mV
  • voltage gated Ca2+ channels open
  • Ca2+ influx results in depolarisation of cell membrane to +20mV
  • results in the opening of K+ channels
  • K+ moves out of the cell and repolarisation occurs
  • hyperpolarisation threshold gets reached and this then reopens HCN and Na+ moves into the cell again
  • this is a cycle and does not need to be activated by a different cell
215
Q

what does a p wave represent?

A

atrial systole (depolarisation)

216
Q

why is the p wave smaller?

A

atria have less muscle

217
Q

what part of the ECG represents the delay at the AVN?

A

PQ interval

218
Q

what does the QRS complex represent?

A

ventricular systole (depolarisation) and atrial repolarisation

219
Q

what does the T wave represent?

A

ventricular repolarisation

220
Q

what does each big square on an ECG represent?

A

0.2s/ 200ms

221
Q

what does each mini square on an ECG represent?

A

0.04s/ 40ms

222
Q

what does the ST segment represent?

A

interval between depolarisation and repolarisation

223
Q

what is ST elevation?

A

ST segment isn’t isoelectric
ventricles repolarise (relax) less
decrease in EDV and CO

224
Q

duration of the P wave?

A

80-100ms

225
Q

duration of the PR interval? (start of p to start of QRS)

A

120-200ms

226
Q

duration of the QRS complex?

A

0.06s-0.1s

227
Q

what heart rate indicates bradycardia?

A

less that 60bpm

228
Q

what heart rate indicates tachycardia?

A

over 100bmp

229
Q

what does the term ‘lead’ mean in a 12 lead ECG? how many physical electrodes are there actually?

A

view of the heart
10

230
Q

which leads are unipolar?

A

aVR, aVL, aVF

231
Q

which leads are bipolar?

A

II, II, III

232
Q

describe the location of the bipolar leads

A

form a triangle between both wrists and left leg

233
Q

describe the location of the unipolar leads

A

bisect the angles of the triangles
combine two electrodes as reference

234
Q

how many unipolar V chest leads are there?

A

6

235
Q

where is lead V1?

A

right of sternum 4th, intercostal space

236
Q

where is lead V2?

A

left of sternum, 4th intercostal space

237
Q

where is lead V4?

A

left midclavicular line, 5th intercostal space

238
Q

where is lead V3?

A

between second and 4th

239
Q

where is lead V5?

A

5th intercostal space, left anterior axillary line

240
Q

where is lead V6?

A

5th intercostal space, left mid axillary line

241
Q

which leads give the septal heart view?

A

V1 and V2

242
Q

which leads give the anterior heart view?

A

V3, V4

243
Q

which leads give the lateral heart view?

A

V5, V6, I, aVL

244
Q

which leads give the inferior heart view?

A

II, III, aVF

245
Q

what does the right coronary artery supply?

A

SAN, AVN, posterior IV septum

246
Q

what does the right marginal artery supply?

A

right ventricle and apex

247
Q

what does the posterior descending artery (posterior interventricular artery) supply?

A

right ventricle, left ventricle, posterior third of IV septum

248
Q

what does the left coronary artery supply?

A

left atrium, left ventricle, IV septum, AV bundles of His

249
Q

what does the left anterior descending supply?

A

anterior third of IV septum, right ventricle, left ventricle

250
Q

what does the left marginal artery supply?

A

left ventricle

251
Q

what does the circumflex supply?

A

left atrium and left ventricle

252
Q

what is systolic failure?

A

heart doesn’t pump hard enough

253
Q

what is diastolic failiure?

A

heart doesn’t fill to full volume

254
Q

normal EDV

A

110ml

255
Q

consequences of left sided heart failure

A

blood backs up in lungs
pulmonary oedema

256
Q

consequences of right sided heart failure

A

blood backs up in rest of body
peripheral oedema - commonly in legs

257
Q

at what stage of embryonic development does the heart form?

A

3rd week, gastrulation

258
Q

what does the heart form from?

A

primitive heart tube

259
Q

describe the embryological development of the heart from days 20-35

A

pre-19 - cardiogenic region (horseshoe)
two endocardial tubes are created
day 21 - fusion into a primitive heart tube

260
Q

where does the cardiogenic area begin?

A

in the middle of head pole

261
Q

draw and label the primitive heart tube

A

superiorly to inferiorly:
truncus arteriosus
bulbs cordis
primitive ventricle
primitive atrium
sinus venosus

262
Q

describe the process of cardiac looping

A

bulbs cordis moves inferiorly, anteriorly and right
primitive ventricle shifts left
primitive atrium and sinus venosus moves superiorly and posteriorly

263
Q

why is there asymmetry in the heart ?

A

cilia waft molecules from the right to left side

264
Q

what does the bulbus cordis form?

A

right ventricle and outflow tracts

265
Q

what does the truncus arteriosus form?

A

aortic arches and arteries

266
Q

what does the primitive ventricle form?

A

left ventricle

267
Q

what does the primitive atrium form?

A

parts of right and left atrium

268
Q

what does the sinus venosus form?

A

superior vena cava and right atrium

269
Q

describe septation

A

superior and inferior endocardial tissues grow and meet at the central AV canal
superior grows from top down to divide atria (interatrial septum)
inferior grows from bottom up to divide ventricles (interventricular septum)

270
Q

what is the foramen ovale?

A

allows blood to flow from the right atrium to left atrium

271
Q

what happens to the foramen ovale after birth?

A

closed off to form the fossa ovale

272
Q

which part of the IV septum is membranous and muscular?

A

upper part is membranous
lower part is muscular

273
Q

origin of the aortic arches

A

branch off truncus arteriosus

274
Q

what is the ductus arteriosus?

A

connection between the pulmonary artery and aorta

275
Q

what is the ligamentum arteriosus?

A

small ligament attaching the aorta to the pulmonary artery

276
Q

what do the 1st and 2nd aortic arches become?

A

minor head vessels
1st - small part of maxillary
2nd - artery to stapedius

277
Q

what happens to the 3rd aortic arches?

A

portion between the 3rd and 4th arch disappears
become common carotid arteries and proximal internal carotid arteries
distal internal carotids come from extension of dorsal aortae

278
Q

what happens to the right dorsal aorta and right 4th aortic arch?

A

right dorsal aorta loses connections with midline aorta and 6th arch, remaining connected to right 4th arch
acquires branch 7th cervical intersegmental artery, which grows into right upper limb
right subclavian artery is derived from right 4th arch, right dorsal aorta, and right 7th intersegmental artery

279
Q

what happens to the left dorsal aorta and left 4th aortic arch?

A

left dorsal aorta continues into trunk
left cervical intersegmental artery, which grows into left subclavian artery
right subclavian artery is derived from right 4th arch, right dorsal aorta and right 7th intersegmental artery

280
Q

what happens to the 5th aortic arch?

A

there are no 5th arches

281
Q

happens to the 6th aortic arches?

A

right arch may form part of pulmonary trunk
left arch forms ductus arteriosus - communication between pulmonary artery and aorta

282
Q

where do you auscultate the aortic valve?

A

2nd intercostal space, right sternal edge (counterintuitive because the aorta leaves the left ventricle!)

283
Q

where do you auscultate the pulmonary valve?

A

2nd intercostal space, left sternal edge (counterintuitive because the pulmonary artery leaves the right ventricle)

284
Q

where do you auscultate the tricuspid valve?

A

right 5th intercostal space

285
Q

where do you auscultate the bicuspid valve?

A

left 5th intercostal space

286
Q

contents of the anterior mediastinum

A

thymus
lymph nodes
internal thoracic vessels
thyroid tissue

Phase 1 flashcards (27 decks)

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