CVS week 1 Flashcards
1
Q
what are the surfaces of the heart
A
right pulmonary surface
anterior surface
posterior surface
left pulmonary surface
diaphragmatic surface
2
Q
describe the chambers of the heart in relation to the heart surfaces
A
the right atrium is along the right pulmonary surface and posterior surface
the left atrium is along the posterior surface
the right ventricle is along the anterior surface and diaphragmatic surface
the left ventricle is along the anterior surface and diaphragmatic surface
3
Q
describe the chambers of the heart in relation to the cardiac borders
A
the right border forms the right atrium
the left border forms the left ventricle
the inferior border forms the right ventricle
the superior border forms the right and left atria
4
Q
describe the fibrous cardiac skeleton of the heart
A
dense fibrous connective tissue forming the ‘skeleton’ of the heart to allow attachment of the valves and electrical isolation in terms of cardiac conduction
contains the fibrous coronet (aortic and pulmonary valves) and fibrous rings (mitral and tricuspid valves)
5
Q
describe the function of the right atrium
A
receives deoxygenated blood from the body via the IVC and SVC
6
Q
describe the function of the right ventricle
A
receives deoxygenated blood from the right atrium via the right atrioventricular opening, which is then pumped into the pulmonary circulatory system via the pulmonary artery
7
Q
describe the function of the left atrium
A
receives oxygenated blood from the lungs via the 4 pulmonary veins
8
Q
describe the function of the left ventricle
A
receives oxygenated blood from the left atrium via the left atrioventricular opening, which is then pumped into the systemic circulatory system via the aorta
9
Q
describe the function of the atrioventricular (AV) valves
A
the tricuspid valve prevents back flow of blood into the right atrium from the right ventricle
the mitral valve prevents the back flow of blood into the left atrium from the left ventricle
10
Q
how is eversion of the AV valves prevented
A
both AV valves are connected to papillary muscles via cordae tendinae, preventing the valves from collapsing in on themselves
11
Q
describe the function of the semilunar (SL) valves
A
the aortic valve prevents back flow into the left ventricle from the aorta
the pulmonary valve prevents back flow into the right ventricle from the pulmonary trunk
12
Q
why do cardiomyocytes have a high cell to capillary ratio
A
they have a high oxygen demand
13
Q
where are the orifices of the coronary arteries located
A
above the aortic valve
14
Q
the source of the posterior interventricular artery and posterior left ventricular artery determines…
A
whether the coronary circulation has a balanced distribution, left coronary dominance or right coronary dominance
15
Q
describe the left coronary artery
A
ostium in left coronary sinus
runs b/w posterior part of pulmonary trunk and left auricle
gives rise to the LAD and left circumflex
16
Q
describe the left anterior descending (LAD) artery
A
anastomoses w posterior interventricular artery
supplies 2/3 of interventricular septum
supplies adjacent left and right ventricles
gives off lateral branch
17
Q
describe the left circumflex artery
A
runs along the coronary sulcus
gives off left marginal branch (supplies LV)
occasionally posterior left ventricular branch
18
Q
describe the right coronary artery
A
ostium in right coronary sinus
runs along sulcus b/w right side pulmonary trunk and right auricle
gives rise to right marginal branch, AV nodal branch, posterior interventricular branch
19
Q
what does the right marginal branch supply
A
adjacent right ventricle
20
Q
what does the AV nodal branch supply
A
AV node
21
Q
what does the posterior interventricular branch supply
A
1/3 of posterior interventricular septum
adjacent left and right ventricles
22
Q
in a normal balanced distribution of the coronary circulation, what does the LEFT coronary artery supply
A
LV
LA
part of RV
2/3 interventricular septum
AV bundle
SA node (in 40% of ppl)
23
Q
in a normal balanced distribution of the coronary circulation, what does the RIGHT coronary artery supply
A
most of RV
RA
diaphragmatic part of LV
1/3 interventricular septum
AV node (80% of ppl)
SA node (60% of ppl)
24
Q
when is coronary perfusion at its highest
A
during diastole
25
what factors regulate vascular diameter
autoregulation
metabolic factors
endocrine molecules
autonomic innervation
physical factors
endothelial factors
26
what is autoregulation of vascular diameter
maintenance of blood flow in response to different perfusion pressures
27
what are examples of endothelial factors affecting vascular diameter
NO
PGI2
EDHF
ET
28
outline sympathetic innervation of coronary arteries
innervation of conduction system, coronary arteries, cardiomyocytes
pre-ganglionic fibres from lateral horn of spinal cord
post-ganglionic fibres from 3 cervical ganglia and sympathetic chain
29
outline parasympathetic innervation of coronary arteries
innervation of conduction system and coronary arteries
pre-ganglionic fibres w cell bodies in vagal nuclei of brainstem and travel w vagus nerve
post-ganglionic fibres from neurons of cardiac plexus
30
what two factors impact blood flow through a vessel
pressure gradient (difference in pressure b/w two ends of a vessel)
vascular resistance (impediment to flow through a vessel)
31
what is Ohm's law
flow = pressure gradient / resistance
32
what are the two types of blood flow typically observed
laminar flow
turbulent flow
33
what is laminar blood flow
blood flows in streamlines with each layer remaining the same distance from the vessel wall
highest velocity in centre of vessel
lowest velocity along vessel wall
34
what is turbulent blood flow
blood flow is disorderly, flowing crosswise in the vessel
increases resistance and energy required to maintain flow
35
when does flow become turbulent
rate of flow too high
blood passes an obstruction or makes sharp turn
blood passes over a rough surface
36
what is reynold's number
tendency for turbulence to occur
37
how is reynold's number calculated
(velocity x diameter x density) / viscosity
38
what are 5 factors affecting vascular resistance
vessel diameter
vessel length
organisation of vascular network
characteristics of blood
extravascular mechanical forces
39
what is vascular conductance
measure of blood flow through a blood vessel for a given pressure gradient
it is proportional to the fourth power of the diameter
it is highly sensitive to variations in vessel diameter
increases in resistance will reduce vascular conductance (vice versa)
40
how is vascular conductance calculated
conductance = 1 / resistance
41
what does poiseuille's equation illustrate and what is the equation
it basically highlights that pressure, vessel radius, blood viscosity, and vessel length are all key factors that influence blood flow
flow = (pi x pressure gradient x fourth power radius) / (8 x viscosity x length)
42
What are 3 features of the coronary circulation
High O2 consumption
High resting O2 extraction
Limited anaerobic capacity
43
Adjustments to supply of O2 to the cardiac muscle is primarily governed by changes in…
Coronary vasomotor tone
44
What is the influence of PO2 in terms of coronary blood flow
Venous PO2 acts as an estimate for myocardial tissue PO2
Hence, a greater O2 demand would potentially decrease coronary venous PO2
A decreased PO2 results in an increase in CBF
45
What are 5 metabolic vasodilatory influences released during periods of high cardiac metabolic demand
PCO2
H+
K+
Adenosine
PO2
46
What is the effect of adrenergic alpha receptors and where are they located
They have a vasoconstrictory effect
Located mostly in larger, upstream epicardial vessels
47
What is the effect of adrenergic beta receptors and where are they located
They have a vasodilatory effect
Located mostly within small, intramuscular vessels
48
What is the effect of endothelial NO on coronary blood flow
NO production is stimulated by endothelial shear stress
It results in a vasodilatory effect
Its effect is greatest under conditions of reduced perfusion pressure e.g ischemia
49
Describe regulation of coronary blood flow under physiological stress
Parallel mechanisms act to increase CBF
This means that no single mechanism is mandatory but they can also work in conjunction to produce larger effects and can also have a compensatory effect when one mechanism is blocked/inhibited
50
What are 2 determinants of coronary blood flow
Coronary perfusion pressure
Coronary vasomotor tone
51
Outline how extravascular influences impact coronary blood flow
Compressive forces generated during LV contraction reduces CBF, more so in the endocardium than the epicardium, resulting in an increased CBF during diastole compared to systole
52
what are the 3 general stages of plaque formation in atherosclerosis
1. initiation of atherosclerosis - inflammation
2. mid stage atherosclerosis - switch from acute to chronic inflammation
3. late stage atherosclerosis - less of an impact of vascular inflammation
53
what are 5 triggers of endothelial injury
physical injury or stress
turbulent blood flow
circulating reactive oxygen species (free radicals)
hyperlipidaemia
chronically elevated blood sugar levels
54
what happens during the initiation stage of atherosclerosis
damage to endothelium which leads to the upregulation of adhesion molecules such as selectins, chemokines, VCAM-1 and ICAM-1
then, LDLs to enter the intimal layer
then, the LDLs are oxidised into ox-LDL
then, due to the selectins, chemokines, integrins and CAMs, monocytes are attracted to the site of endothelial injury
then, the chemokines allow the monocytes to enter the intimal layer too via endothelial transmigration
then, the monocytes differentiate into macrophages
then, the macrophages phagocytose the ox-LDL
then, they continue to take up ox-LDL which leads to the formation of foam cells
55
what happens during the mid stage atherosclerosis
macrophages continue to take up LDL in unregulated manner which leads to apoptosis of themselves
then, macrophages secrete pro-inflammatory cytokines (e.g interleukins and chemokines) and sets up a chronic inflammation process
then, smooth muscle cells migrate from the vessel wall into the plaque
then, these SMCs secrete collagen in an effort to form a fibrous cap on the developing plaque to stabilise it
then, neovessels start to invade the plaque
56
what happens during late stage atherosclerosis
the size of the lipid core grows continually
then, the fibrous cap becomes unstable, mainly at their shoulder regions
then, there is increased BP at this site due to increased plaque size, which can trigger the plaque to rupture
then, the contents of the plaque are released into the blood stream which can lead to MI or stroke
then, a thrombus forms, which further occludes the vessel
57
what are selectins
family of 3 C-type lectins expressed exclusively on bone marrow-derived cells and endothelial cells
membrane-bound proteins
58
what are 3 types of selectins
L (leukocyte)
E (endothelial)
P (platelet + endothelial)
59
what is the main role of selectins
mediate monocyte adhesion under flow. ie tether or capture
60
what are 3 key selectin ligands that monocytes can use to bind to the endothelium
PSGL1
ESL1
CD44
61
what are integrins
membrane-bound proteins
must be activated in order to bind their ligands
adherence is weak when activated by selectins
adherence is strong and allows interactions with ICAM and VCAM when activated by chemokines
62
what are 4 examples of integrins
alpha-L-beta-2
VLA-1
alpha-4-beta-1
LFA-1
63
what are CAMs
cell adhesion molecules
transmembrane proteins
64
what is VCAM-1
vascular CAM
induced by inflammatory stimuli
binds to VLA-1 and alpha-4-beta-1 integrins
predominantly expressed on endothelial cells but is also present on SMCs
65
what is ICAM-1
intercellular CAM
induced by inflammation but more constitutively expressed
binds to LFA-1
expressed on endothelial cells and also on leukocytes including neutrophils and monocytes
66
what are chemokines
chemoattractant cytokines
function through 7 transmembrane g-protein-coupled receptors
4 major families
67
what is the fatty streak
early stage atherosclerosis
precursor lesions of complex atheroma as they lack features like fibrosis, thrombosis, calcification
68
is plaque progression linear
no, bursts of growth may occur during life history of plaque prompted by episodes of plaque disruption with thrombosis
69
what can be used to visualise proliferating macrophages in plaque
BrdU
this binds to replicated DNA of macrophages so that proliferating macrophages can be seen in flow cytometry or immunofluorescence
70
what is atherosclerotic plaque neovascularisation
inflammatory process that occurs in late stage plaques
initially driven by hypoxia as plaque becomes larger
vessels deliver inflammatory cells that secrete growth factors that promote further neovascularisation
plaque neovessles are fragile and permeable, which contributes to its instability
71
what 6 things can make plaque unstable or vulnerable
thin fibrous cap
large lipid core
abundant inflammatory cells
punctate or spotty calcification
few SMCs
increased neovascularisation
72
what are 2 types of plaque destabilisation
plaque rupture
superficial erosion
73
what is superficial erosion
lipid poor plaque
proteoglycan rich
high triglycerides
female predominance
endothelial cell apoptosis
74
what are 7 key cell types in atherosclerosis
neutrophils
monocytes
macrophages
smooth muscle cells
platelets
dendritic cells
T cells
75
what is the role of platelet and monocyte interactions in the initiation of atherosclerosis
activated platelets exacerbate atherosclerosis
they release chemokines
increase inflammation
76
what is the role of macrophage and SMCs interaction in initiation of atherosclerosis
they move towards top of plaque, secrete collagen and form a cap
they contribute to plaque expansion by releasing inflammatory chemokines
they anchor monocytes into the plaque
macrophages trigger SMC apoptosis causing further instability
77
describe differentiation of macrophages into dendritic cells that leave the plaque
when exposed to a regressive environment, the macrophages can leave the plaque by increasing their expression of CCR7 which allows them to acquire a macrophage-dendritic dual phenotype so that they can leave via the lymphatic system
78
what are 4 key determinants of blood pressure
intravascular volume
autonomic NS
RAAS
local vascular factors
79
what are the 4 types of adrenergic receptors (adrenoreceptors)
alpha 1
alpha 2
beta 1
beta 2
80
what are the two generic types of hypertension
primary (90-95% of cases)
secondary
81
what are 5 causes of secondary hypertension
metabolic syndrome
renal e.g parenchymal or vascular disease or phaeochromocytoma
adrenal e.g cushing's syndrome or hyperaldosteronism
other endocrinopathies e.g thyroid issues, increase PTH
medications and non-prescribed drugs
82
what are 7 complications of hypertension
left ventricular hypertrophy
coronary heart disease
heart failure
stroke
renal failure
peripheral vascular disease
retinopathy
83
describe the prevalence of hypertension in men globally
34% of men have hypertension
51% of men w hypertension are not even diagnosed
out of all the men w diagnosed hypertension, only 18% are both treated and controlled
84
describe the prevalence of hypertension in women globally
32% of women have hypertension
41% of women w hypertension are not even diagnosed
out of all the women w diagnosed hypertension, 23% are both treated and controlled
85
describe the prevalence of hypertension in australia
33.7% of the population has hypertension
36% of men have hypertension
31.4% of women have hypertension
86
what classifies as normal BP
<130 systolic
AND
<85 diastolic
87
what classifies as high-normal BP
130-139 systolic
AND/OR
85-89 diastolic
88
what classifies as grade 1 hypertension
140-159 systolic
AND/OR
90-99 diastolic
89
what classifies as grade 2 hypertension
>= 160 systolic
AND/OR
>= 100 diastolic
90
what are the 3 'types' of severe hypertension
severely elevated BP without symptoms
hypertensive urgency
hypertensive emergency
91
describe severely elevated BP without symptoms
180/110 or higher
no symptoms
no end organ damage
no immediate threat to life
1-2 days timeframe to achieve initial BP reduction
92
describe hypertensive urgency
180/110 or higher
symptoms present
acute end organ damage is not present but moderate nonacute damage may be present
no immediate threat to life
few hours timeframe to achieve initial BP reduction
93
describe hypertensive emergency
usually 220/140 or higher
symptoms present
significant acute end organ damage
immediate threat to life
few minutes timeframe to achieve initial BP reduction
94
what are clinical features of hypertension
for the most part, patients may be asymptomatic
however, very high BP can present w headaches, epistaxis, arrythmia, chest pain, dyspnoea, visual issues, and confusion
in terms of end organ damage, coronary heart disease, stroke, renal impairment and retinopathy may be present
95
what is the difference between primary and secondary hypertension
primary hypertension does not have a definitive cause whereas secondary hypertension has a known cause
96
describe the pathophysiology behind secondary hypertension caused by CKD
reduced renal function leads to sodium and fluid retention, which increases intravascular volume, hence an increased BP
97
describe the pathophysiology behind secondary hypertension caused by RENOVASCULAR HYPERTENSION
stenosis of renal arteries reduces blood flow to kidneys, activating the RAAS
98
describe the pathophysiology behind secondary hypertension caused by HYPERALDOSTERONISM
excess aldosterone causes sodium retention and potassium secretion
99
describe the pathophysiology behind secondary hypertension caused by PHAEOCHROMOCYTOMA
adrenal tumours secrete catecholamines which increases heart rate and vascular resistance
100
describe the pathophysiology behind secondary hypertension caused by CUSHINGS SYNDROME
excess cortisol increases blood volume and vascular sensitivity to catecholamines
101
describe the pathophysiology behind secondary hypertension caused by HYPER/HYPOTHYROIDISM
imbalances in thyroid hormones affect cardiac output and vascular resistance
102
describe the pathophysiology behind secondary hypertension caused by COARCTATION OF THE AORTA
narrowing of the aorta increases resistance to blood flow
103
how can primary hypertension be diagnosed and investigated
BP measurements
history and physical exams
basic tests e.g blood tests, urinalysis, ECG
104
how can secondary hypertension be diagnosed and investigated
renal function tests
imaging
hormonal assays
105
What are 5 different types of chest imaging
CXR
Chest CT
Chest MRI
Ultrasound
Digital subtraction angiography
106
What are 5 types of chest CT
High resolution CT chest (HRCT)
Standard post contrast CT chest
CT aortogram (CTA)
CT pulmonary angiogram (CTPA)
CT coronary angiogram (CTCA)
107
What angle is a standard CXR done at
Posteroanterior
Can also do a lateral view
108
What densities can an X-ray depict
Air
Fat
Fluid/soft tissue
Bone
Metal
109
What are X rays good for
Looking at bones and distinguishing air-filled structures from fluid filled/soft tissue
110
What is a limitation of X-ray
Adjacent tissues of the same density cannot be distinguished from each other meaning it does not distinguish different types of soft tissue e.g heart muscle and blood look the same
111
Describe a PA standard X-ray
X-ray beam traverses from patient posterior to anterior
Upright in full inspiration
Beam is horizontal
X ray tube is 6 feet away from film
Patient is close to the film which reduces magnification and increases sharpness
112
Describe a lateral film in a standard X ray
Left side of chest against X ray cassette
Also taken at 6 feet
Left hemidiaphragm is not differentiated from the heart anteriorly as they are of same density
Right sided nodule will appear larger than an identical left sided nodule due to increased magnification
113
Describe an anteroposterior film in a standard X-ray
Usually portable film for adult patients too sick to tolerate normal PA view
Children are viewed using AP
May be supine or sitting
Taken at shorter distance from film therefore greater magnification and less sharp images
Cardiomediastinal contour is augmented
Lung markings may appear crowded
114
Describe a lordotic view of standard X-ray
Patient leans slightly back so that clavicles are raised and projected above the lungs
Allows for assessment of apical pathology that may be obscured on a frontal film
115
Describe a lateral decubitus view of a standard X-ray
Patient lays down on their side
Intrapleural fluid layers differentiate
Intrapleural air rises
If air-trapping is present, there is no physiological collapse of the lungs
116
Describe an expiration view of a standard X ray
Less air in lungs so they appear denser and the lung markings are more crowded
Heart is elevated and appears large
Can be used to detect focal air trapping (obstructed lung will appear blacker)
May accentuate a small pneumothorax (the fixed amount of Intrapleural air is relatively larger)
117
Describe a systemic approach in interpreting a CXR
Go inside out:
Heart
Mediastinum
Hilar
Lungs
Pleural reflections
Upper abdomen
Bones
Soft tissues
118
Describe computed tomography (CT) scans
2D images in the axial plane but can be reconstructed in multiple 2D planes and in 3D
Greater contrast resolution than CXR
Can be given contrast to improve resolution
Images can be manipulated (windowed) post acquisition to accentuate different tissue densities
119
What are CT scans good for
Ability to locate lesions in 3D space
Allows differentiation between different soft tissues
120
What are two other post processing techniques of CT scans
MPR - multiplanar reconstructions
MIP - maximum intensity projection
121
What are hounsfiled units
Standardised unit, relative to water, reflecting attenuation or density
122
What is the hounsfield unit of air
-1000
123
What is the hounsfield unit of fat
-120 to -90
124
What is the hounsfield unit of water
0
125
What is the hounsfield unit of organs
20 to 60
126
What is the hounsfield unit of bone
2000
127
What is the hounsfield unit of metal
3000
128
What can standard CT chest indicate
Pneumonia
Malignancy
Pleural disease
129
What can HRCT indicate
Parenchymal disease e.g interstitial lung disease
130
What can CTA indicate
Aortic pathology
131
What can CTPA indicate
Pulmonary embolism
132
What can CTCA indicate
Coronary artery disease
133
Describe standard CT chest
Performed post contrast
Triggered at ~20 seconds when the contrast is in the arterial system
Also includes upper abdomen (liver)
134
Describe HRCT
Non contrast
Thin slices obtained
Excellent detail of lung parenchyma
Sometimes additionally performed in expiration (to look for air trapping)
Sometimes additionally performed prone (to differentiate b/w dependent change and true pathology)
135
Describe CTA
More rapid injection of contrast
Maximise enhancement of aorta
Can be ‘gated’ to minimise pulsation artefact (scan is triggered to a particular point in the cardiac cycle using ECG)
Usually mid to end diastolic phase
136
Describe CTPA
Contrast injected at rapid rate
Timed for peak contrast enhancement in the pulmonary arteries
Apices to diaphragm only
137
Describe CTCA
Uses high contrast flow rate
Timed for peak opacification of coronary arteries
Medications sometimes used to lower heart rate, avoid arrhythmia and dilate coronary arteries e.g beta blockers
ECG gated
Post processing - curved reconstructions, MPR, MIP
138
Describe MRI
Limited use cases
Superior soft tissue resolution
Can acquire 4D imaging
139
What can MRI be used for
Cardiac MRI
Chest wall pathology
Mediastinal pathology
140
Describe DSA
Better visualisation of inside of vessels
Limited info about surrounding tissues
Allows angiographic interventions e.g angioplasty and stenting
141
What makes up the mediastinal borders on a frontal CXR
Brachiocephalic vein
SVC
RA
IVC
Left subclavian artery
Aortic knob
Main pulmonary artery
Left atrial appendage
LV
142
Describe the position of the cardiac valves in a lateral X-ray
Imaginary line from carina to cardiac apex:
P and A valves above
T and M valves below
Imaginary horizontal line bisect cardiac silhouette:
A valve upper
M valve lower
T valve anterior
P valve posterior
