BS cardiovascular strand Flashcards
(157 cards)
1
Q
what are the 3 layers of a blood vessel from inside to outside
A
intima
media
adventitia
2
Q
what is the layer between the tunica intima and tunica media
A
internal elastic lamina
3
Q
what is the layer between the tunica media and tunica adventitia
A
external elastic lamina
4
Q
which vessel has a major role in resistance to blood flow
A
arterioles
5
Q
what two systems is the venous system organised into?
A
superficial and deep systems
6
Q
why do we get varicose veins?
A
due to leaky superficial veins
7
Q
what is the diff between the tunica intima of veins and arteries
A
- in arteries the endothelium is wavy due to constriction of smooth muscle, but smooth in veins
- elastic membrane present in arteries and not in viens
8
Q
what is the diff between the tunica medias of veins and arteries
A
- thickest layer in arteries, in veins tunica adventitia thicker
- smooth muscle cells and elastic fibres present in arteries, but in veins smooth muscle cells and collagenous fibres
- external elastic membrane preset in arteries and not in veins
9
Q
what is the diff between the tunica adventitia of veins and arteries
A
- in arteries thinner than media, in veins thickest layer
- collagenous and elastic fibers in arteries, collagenous and mouth fibres in veins
10
Q
what is the structure of a continuous epithelium? what is it permeable to? where do we find it
A
endothelial lining with tight junctions
permeable to water and ions
forms BBB barrier
11
Q
what is the structure of a fenestrated epithelium? what is it permeable to? where do we find it
A
- has fenestrations in inner lining- pores and tight junctions
- permeable to larger molecules
- small intestine, kidney filter, endocrine organs
12
Q
what is the structure of a sinusoid epithelium? what is it permeable to? where do we find it
A
- incomplete basement membrane and inner layer with large intercellular gap
- permeable plasma and proteins and even cells
- liver (albumin can get into circulation), spleen, lymph nodes
13
Q
what type of blood flow do we get the fastest blood flow in the centre and slowest blood flow in the periphery
A
laminar flow
14
Q
in what type of blood flow is the speed constantly changing
A
turbulent flow
15
Q
what’s virchows triad
A
thrombosis is caused by:
- endothelial damage (smoking, diabetes)
- hypercoagulability
- abnormal blood flow
16
Q
what’s hydrostatic pressure
A
when blood flow/fluid exerts a pressure on vessels themselves
17
Q
what is blood pressure
A
systemic arterial pressure- pressure of blood in arteries
18
Q
what is pulse pressure? what level should it be at least?
A
difference between systolic and diastolic pressure
should be at lest 25% of systolic pressure- otherwise too low
19
Q
what is MAP? between what range is normal? what happens if levels are too low?
A
- mean arterial pressure - average blood pressure of blood in arteries
- 70-100 is normal
- if levels low (below 60) = hypoxia/ischemia - (eg. death of nerves = pines and needles)
20
Q
how do we calculate MAP
A
= DP + (SP/3)
OR
= DP + 1/3Pulse pressure
21
Q
what is diastolic pressure
A
reflects arterial pressure in diastole
22
Q
what is systolic pressure
A
reflects arterial pressure in systole
23
Q
what 5 factors affect blood flow?
A
- cardiac output
- compliance
- volume of blood
- viscosity of blood
- blood vessel length and diameter
24
Q
how does compliance effect blood flow
A
increases expansion of arteries to accommodate high BP with changing resistance
- if heart wall is stiff, heart will have to work harder
25
what is hypovalemia and hypervalemia and what factors can cause the?
- hypo = low blood volume: bleeding/diarrhoea/ vomiting
| - hyper = high blood volume: retention H20+ sodium/ kidney disease
26
does the viscosity of blood change
not much
only in conditions which affect erythropoiesis (eg. polycthemia and anaemia)
and liver abnormalities due to abnormal albumin
27
how does losing weight reduce the work of the heart
lose lots of blood vessels which reduces overall resistance
28
what factor in poiseulle's law has the biggest effect on blood flow?
radius of blood vessel
r(^4)
changes in diameter has huge effect on resistance
resistance is inversely proportional to radius
29
what are phasic changes in blood flow?
opposite activities of what goes on in the rest of vascular beds
eg. capillary blood flow in left ventricle decreases during systole due to compression of vessel and so increases in diastole (when vessel relaxed)
30
what regulates coronary circulation
auto regulation - local metabolism: no nervous/endocrine control required
31
what do vasodilators and vasoconstrictors have a direct effect on?
precapillary sphincters:
| - vasodilators relax them, vasoconstrictors constrict them
32
what are some vasodilators ?
- decrease O2
- increase in CO2
- increase metabolic acids (lactate, NO, K+,H+)
- body temp
33
what are some vasoconstrictors ?
- prostaglandins
- products released by activated platlets
- leukocytes
- endothelins
34
what are the 3 types of circulation we have?
bronchial circulation
pulmonary circulation
cerebral circulation
35
what is the main difference between pulmonary and bronchial circulation ?
lower pressures in pulmonary circulation due to the resistance to flow being less due to less muscular arterioles
36
what are the 3 main components of autoregualtion in the cerebral circulation
- chemical/metabolic response
- myogenic response (vascular smooth muscle response)
- neurogenic response ( communication between brian stem and autonomic centres)
37
name 4 age related changes to blood vessels
- fibrous thickening of intima
- fibrosis scarring of media
- accumulation of ground substance
- fragmentation of elastic lamina
38
describe the process of atherosclerosis
- damage to endothelium (smoking, diabetes, BP, age, increased cholesterol)
- accumulation of oxisdised LDL cholesterol
- blood vessels become less compliant = resistance and pressure increases = more turbulent flow
- smooth muscle cell changes
- ECM accumulation
- inflation of plaque = weakens it
- rupture of plaque = scars artery wall = sclerosis
- formation of thrombus
39
what is the consequence of athersocslosis
coronary heart disease
| MI
40
what is an aneurysm
localised/permanent/ abnormal dilation of blood vessels
41
what are important factors that affect aneurysms
- type
- true/false
- site (eg. can get them in retinas with diabetes)
- aetiology
42
what are the two types of true aneurysms
saccular
| fusiform
43
compare arterial and venous thrombus
- white thrombus in arterial = contains lots of platelets
- red thrombus in veins = lots of RBC
- forms in fast flowing blood in arteries and slow flowing blood in veins
44
what histological changes does hypertension cause?
- fibrinoid changes: type of tissue damage
- hyaline arteriosclerosis - hyaline thickening of arterial walls
- hyperplastic arthroscelrosis - around blood vessels
45
how does diabetes increase the likelihood of injury and decreases heal?
impairs patients ability to sense pain and temp = increases likelihood of injury
= due top damage to small nerves that control blood flow = injuries less likely to heal
46
what are the 3 types of tumours of blood vessels?
- haemangioma
- angiomyolipoma (kidney)
- angiosarcoma (aggressive- old people/ radiography)
47
what is pre-load?
level of stretch a cardiomyocyte is exposed to before ventricular ejection
48
what is pre load also known as?
Left end diastolic volume
49
what is after-load?
pressure against which the heart is contracting when it ejects blood
50
in what condition do we get an increase in after load
hypertension
51
roughly, what does starlings law state?
that generally the energy of contraction of the heart is a function of the length of the muscular fibre
52
what's the process which leads to vasodilation, through a baroreceptor reflex?
- atrerial stretch sensed
- afferent loop ends in nucleas tactus solitarius and rostral ventrolateral medulla
- reduces sympathetic tone
- augments vagal tone
- reduces HR
- reduces SV
= vasodilation
53
in what cases does juxtaglomerular apparatus release renin
- renal perfusion pressure sensed at the glomerulus
- Na+ conc sensed in fluid surrounding distal convoluted tubule
- if either reduced renin released
54
what are the 2 types of myocardial dysfunction?
- diastolic dysfunction
| - systolic dysfunction
55
what is the problem in diastolic dysfunction? what kind of heart failure is this? can it be treated?
LV not able to fill properly
- known as heart failure with preserved ejection fraction (HFPEF)
- no drugs available to treat this
56
what is the problem in systolic dysfunction? what kind of heart failure is this? can it be treated?
heart failure not contracting as effectively- systolic heart failure
- known as heart with reduced ejection fraction (HFREF): ventricles are stretched due to stretch pressure overload
- drugs available to treat this
57
what are the stages which someone with heart failure can develop pulmonary oedema? what are the consequences of this?
- back pressure in LV causes raised pressure in pulmonary circulation
- increase hydrostatic pressure forced fluid outside vascular compartment
- interstitial space in lungs fills with fluid
- causes pulmonary oedema/ pleural effusions
- patient becomes breathless, low O2 sat
(lying flat makes symptoms worse)
58
what happens when we get heart failure in the RV? what are the consequences of this?
- back pressure in Rv transmits into vena cava
- internal jugular venous pressure rises
- jugular venous pressure raised
- we get ankles/sacrum swell with hepatomegaly and ascites in some cases as gravity and raised orthostatic pressures force fluid from vascular compartment to peripheral tissues
59
what are the 2 differnt types of heart failure which involve scarring of heart tissue
anterolateral infarct
| posteroinferior infarct
60
what is maladaption and what are the consequences this?
when the ejection fraction drops:
- reduced CO
- reduced systolic BP
- reduced arterial stretch
- reduced renal perfusion
61
how does cardiovascular maladaption lead to compensation
- increase in preload lengthens sarcomeres
- raises in end-diastolic pressure in LV
- augments SV
62
Why can cardiovascular maladpation over a long time be bad? what is this called?
- LV stretch exceeds physiological levels so then small rises in LVEDP cause Large drops in sarcomere tension (LV contractility and SV) = reducing CO and impacting ANS and SNS
- decomposition
63
how does the heart undergo adverse remodelling? why does it do this?
Cretes aneurysms
| does this to normalise wall stress as the cavity is enlarged (Laplace's Law)
64
what value is LVEF normal in an ECHO?
>55%
65
what value is LVEF mildly impaired in an ECHO?
45-54%
66
what value is LVEF moderately impaired in an ECHO?
36-44%
67
what value is LVEF severly impaired in an ECHO?
<35%
68
what acute therapy do we administer in heart failure?
O2-optimise alveloar ventilation
- may need to increase pressure in airways to oxygenate blood
- can relax pulmonry vessels to decrease preload and take strain of LV
- morphine helps her breathing and pain
69
how do diuretics help in heart failure
limit absorption of fluid
offloads the ventricles
can maximise LV contractility
(moves us back along starling curve)
70
what are the side effects of direcutics
- renal dysfunction
- reduces Na, K, Mg
- cann induce diabetes
71
what drugs can we sue for symptomatic benefit
diuretics - gets rid of oedema
72
what drugs can we sue for prognostic benefit
ACEi and A2RBs
73
how do ACEi's work?
RASS inactivation:
- block conversion of AgI to AgII
- diminishes release of aldosterone
74
how do A2RB's work?
reeceptor inactivation
| work on AgII
75
how can B-blockers help in chronic failure of the heart
- decrease renin secretion (so reduce CO and HR)
- allows LV more relaxation time = better filling
- blunts RAAS over activation
76
in what conditions must we be cautious in giving B blockers?
asthma
low HR
heart blocks
77
What binds together myocytes?
desmosomes
78
What exists between cells to allow for contraction of cardiac muscle?
gap junctions
79
What structures are found within cardiac muscle fibres? How do these aid function?
- mitochondrion: rich energy source
- myofibrils: composed of actin and myosin which interact to bring about contraction
- sarcoplasmic reticulum: important calcium store
80
What is the importance of calcium ions in cardiac muscle contraction? What are the sources of calcium?
- calcium accommodates the interaction of myosin and actin
| - inside the cell, outside the cell and sarcoplasmic reticulum
81
How is the cytosolic calcium level increased for muscle contraction to occur?
1. Calcium binds to ryanodine receptor on sarcoplasmic reticulum
2. This causes the release of calcium from the SR into cytosol
3. This has the effect of increasing cytosolic calcium
82
How does calcium move into the cells?
Through L-type Calcium Channel receptors
83
Overview of muscle contraction
1. Release of calcium from sarcoplasmic reticulum is stimulated by binding of calcium to ryanodine receptors
2. Calcium binds to topronin inducing a conformational change in the troponin-tropomyosin complex which exposes the binding sites of actin
3. Myosin heads can bind to actin in a process that requires ATP.
4. Myosin heads exert a pulling action on actin which initiates muscle contraction.
84
How much ATP do myocardial cells use per day?
6kg
85
What does the conversion of chemical energy stored in ATP to mechanical energy in myocardial cells result in?
- force generation
| - myofilament shortening
86
What is the hydraulic functioning of the heart?
- force generation leads to ejection of blood
- longitudinal filament shorting leads to horizontal and circumferential thickening
- this reduces LV chamber diameter and causes further ejection
87
What is cardiac functional reserve?
- the difference between normal and maximum cardiac output
| - it is the capacity to augment performance on demand
88
How is cardiac output calculated?
CO=HRxSV
89
How is cardiac reserve calculated?
Cardiac reserve = maximal cardiac output - cardiac output at rest
90
What is heart rate effected by?
- sympathetic innervation
- - speeds up SA node depolarisation
- - more frequent action potentials
- - increase conduction through AV node/bundle
- adrenaline
- - beta-1 agonism
91
How can cardiac output be increased?
- increased stroke volume
| - increased heart rate
92
How can stroke volume be increased?
- autonomic input (sympathetic)
- - prolonged opening of Ca2+ channels
- - enhances calcium action in excitation/contraction coupling mechanisms
- preload
93
What affects tension in a sarcomere?
Sarcomere length
94
What determines hoe stretched the LV wall is? What does this aid?
- LV end-diastolic volume
| - stretching aids contraction
95
How does preload effect cardiac performance?
Increased preload increases cardiac performance
96
Why does stretching the LV aid contraction?
- as the muscle stretches, the diameter of the myofibrils is reduced
- thick and thin filaments are closer together
- more myosin heads can interact with actin
- more contraction can occur
97
What is the frank stealing curve?
Shows that s end-diastolic volume increases, stroke volume increases up to a certain point where the relationship plateaus
Increasing pre-load leads to increased stroke volume
98
Explain the relationship behind the Frank-Starling curve
- venous return always correlates with CO
- - equilibrates right and left heart output (LV CO = RV preload)
- exercise and other demands
- - increased venous demand allows augmentation of stroke volume
99
What causes a left shift of the Frank-Starling curve?
exercise, pharmacological stimulation etc
100
What causes a right shift of the frank stealing curve?
pharmacological depression, myocardial loss eg heart failure
101
How does sympathetic stimulation affect contraction of the heart?
- noradrenaline and adrenaline stimulate cAMP
- more calcium can enter the cell
- - this leads to greater cross-bridge linking in sarcomeres
102
Cardiac output is ... at all levels of preload
augmented
103
How is ejection fraction calculated?
stroke volume / end-diastolic volume
104
What are normal levels of ejection fraction?
- physiological = 55-75%
- exercise = up to 90%
- falling heart shows reduced EF
105
What happens to myocardium contraction in heart failure?
If the myocardium is diseased, it contracts less
- ischaemia = scarred myocardium
- viral infection/alcohol = wall thinning
- increased after load = chronic high output
106
What compensations does the body make for a failing ventricle?
SNS overactivates
| RAAS kicks in
107
How is heart failure compensated for?
- initially the preload is increased
- this leads to LV stretch exceeding physiological levels and we move to the descending limb of the sarcomere tension curve
108
How is mean systemic arterial pressure calculated?
cardiac output x total peripheral resistance
109
What is pre-load measured as?
End diastolic volume
110
What is preload increased by?
- increased circulating volume which increases central venous pressure
- decreased venous compliance
- increased atrial filling or contraction
- increased ventricular compliance
- decreased heart rate which prolongs diastole
- increased aortic or pulmonary pressure
111
What is the Bowditch (Treppe) effect?
- increased heart rate leads to increased force of contraction (or increased cardiac performance)
112
Are the Frank-Starling and Bowditch effect independent of each other?
Yes as the length of the muscle is not effected in the Bowditch effect
113
What is the Bainbridge reflex?
- increased venous return
- baroreceptors in the atria detect increased stretch
- heart rate is increased via sympathetic stimulation to the SAN
- this is antagonistic to the carotid baroreceptor response
- this is involved in sinus arrhythmia
(essentially, increased venous return leads to increased stretch which leads to increased heart rate)
114
How do the sympathetic and parasympathetic nervous systems differentially affect the heart?
- sympathetic system directly innervates the heart and adrenal system
- parasympathetic system has some direct effect on the heart, but not on the adrenal glands
115
What does chronotrophy refer to?
Heart rate
116
What does dromotrophy refer to?
Conduction
117
What does inotrophy refer to?
Contraction
118
What does lusitrophy refer to?
Relaxation
119
What are the direct cardiac actions of the sympathetic nervous system?
1. Positive CHRONOTROPY - SA Node
2. Positive DROMOTROPY (Conduction) – AV node
3. Positive INOTROPY – (Contraction) Ventricles and
Atria
4. Positive LUSITROPY (Relaxation) – Ventricles and
Atria
120
What are the systemic effects of the sympathetic nervous system?
Activation of Renin-Angiotensin-Aldosterone
Systemic
System (RAAS) 2. Suprarenal stimulation - CATECHOLAMINES
121
What is dobutamine used for?
- acts to stimulate the sympathetic system
- sympathymynetic
- aims to increase heart rate and so cardiac performance up to a certain point
122
What are the actions of hormones released in the RAAS?
```
• Angiotensin II
– Vasoconstriction
– Increased Na+ and H2O retention
• Aldosterone
– Increased Na+ and H2O retention
• Vasopressin (Antidiuretic Hormone)
– Promotes H2O retention
```
123
What actions of the RAAS affect the heart?
- increased central venous pressure increases stroke volume
| - vasoconstriction increases total peripheral resistance
124
What sympathetic actions cause the effects of RAAS o the heart?
release of catecholamine causes release of adrenaline which stimulates RAAS
125
What are the parasympathetic actions on the heart?
```
• Decreased Heart Rate ( CHRONOTROPY)
• Decreased AV conduction ( DROMOTROPY)
• Decreased Atrial Contractility ( INOTROPY) •
Ventricular contractility
– NO SIGNIFICANT EFFECT • RAAS
– NO SIGNIFICANT EFFECT
```
126
Where are baroreceptors found? What is their effect on the circulatory system?
```
• Located: Carotid sinuses, Aortic Arch
• Decreased arterial pressure
– Decreased firing
• ↑Baroreceptor firing
– Decreases Sympathetic Tone
– Increases Parasympathetic Tone
```
127
What is action potential
Transient depolarisation of a cell as a result of activity of ion channels
128
What are the two types of cardiac action potential
Pacemaker - intrinsic, spontaneous time dependent depolarisation of a cell membrane that leads to an action potential
Non pacemaker - classic depolarisation and opening of voltage gated ion channels
129
What is the hierarchy of pacemakers?
The primary pacemaker is described as the tissue with highest firing frequency
SAN>AVN>purkinje fibres
SAN is under constant fatal stimulation which suppresses its intrinsic frequency
130
Where does a pacemaker potential become an action potential?
Meets threshold of -40 and ca2+ channels open and funny channels close
131
What does ivabradine do?
Inhibits If (funny) channels, slows action potential
132
what are class 1 drugs acting on cardiac action potential?
Na+ channel blocker
| 1c - flecainide, propafenone > 1a - quinidine, procainaminde > 1b - lidocaine, phenytoin
133
what are class 2 drugs acting on cardiac action potential?
```
beta blockers (K+ rectifier stage)
propanolol/ bisoprolol/ metaprolol
```
134
what are class 3 drugs acting on cardiac action potential?
K+ channel blocker
| amiodarone, sotalol
135
what are class 4 drugs acting on cardiac action potential?
Ca2+ channel blocker
| verapamil, diltiazem
136
where do depolarising currents pass through at intercalated discs?
gap junctions
137
why does the AV node delay the electrical conduction?
to allow the chambers to fill properly --> much faster down bundle of His then even more in purkinje fibres
138
what results in a positive deflection on ECG?
electrical activity towards an electrode (away = negative, ie a dip)
139
what time period does a small box on an ECG represent?
0.04 seconds
140
what is the standard ECG strip you use called?
rhythm strip
141
what is the PR interval on an ECG?
P wave = gradual depolarisation of atria
| PR segment = AV nodal delay
142
what is the QRS duration?
depolarisation of ventricles
upwards bit = bindle of His
downwards bit = around heart walls
143
what is the ST interval?
ST segment = full ventricular depolarisation
| ST wave = ventricular repolarisation
144
how would atrial fibrillation appear on an ECG?
RR intervals irregularly irregular and discoordinated atrial conductivity (lots of little waves)
145
how would an atrial flutter appear on an ECG?
lots of small waves in each RR interval, then regular QRS wave
AVN prevents transmission of all atrial conductions to ventricles
146
how would ventricular fibrillation appear on ECG?
complete mess
| discoordinated contractions
147
how would ventricular tachycardia appear on an ECG?
big tall waves with small gaps
| ventricles taking over contractions
148
how would a 1st degree heart block appear on an ECG?
delay in atria to ventricles, prolonged PR interval
| like an elderly couple, there is still communication just takes longer for message to get through
149
how would a 2nd degree (Mobitz I) heart block appear on an ECG?
progressive lengthening of PR interval, then a missed QRS complex
(like an on and off relationship)
150
how would a 2nd degree (Mobitz II) heart block appear on an ECG?
PR interval normal then an absent QRS wave
| like an affair
151
how would a 2nd degree (2:1) heart block appear on an ECG?
absent QRS waves after alternate P waves
| affair
152
how would a 3rd degree heart block appear on an ECG?
no relationship between P waves and QRS complexes
| divorce
153
what is blood pressure?
driving force propelling blood to tissues, balance between organ perfusion and vascular damage
154
what is cardiac output?
heart rate x stroke volume
155
what is mean systemic arterial pressure?
cardiac output x total peripheral resistance
156
what is total peripheral resistance?
R = 8nL/r^4
```
R = resistance to blood flow
n = viscosity of blood
L = length of vessel
r = radius of vessel
```
157
how does the autonomic nervous system control blood pressure?
baroreceptors located in carotid sinuses and aortic arch
