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year 1 flash cards > BS cardiovascular strand > Flashcards

BS cardiovascular strand Flashcards

1
Q

what are the 3 layers of a blood vessel from inside to outside

A

intima
media
adventitia

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2
Q

what is the layer between the tunica intima and tunica media

A

internal elastic lamina

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3
Q

what is the layer between the tunica media and tunica adventitia

A

external elastic lamina

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4
Q

which vessel has a major role in resistance to blood flow

A

arterioles

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5
Q

what two systems is the venous system organised into?

A

superficial and deep systems

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6
Q

why do we get varicose veins?

A

due to leaky superficial veins

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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
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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
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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

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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

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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
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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
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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

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14
Q

in what type of blood flow is the speed constantly changing

A

turbulent flow

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15
Q

what’s virchows triad

A

thrombosis is caused by:

  • endothelial damage (smoking, diabetes)
  • hypercoagulability
  • abnormal blood flow
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16
Q

what’s hydrostatic pressure

A

when blood flow/fluid exerts a pressure on vessels themselves

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17
Q

what is blood pressure

A

systemic arterial pressure- pressure of blood in arteries

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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

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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)
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20
Q

how do we calculate MAP

A

= DP + (SP/3)
OR
= DP + 1/3Pulse pressure

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21
Q

what is diastolic pressure

A

reflects arterial pressure in diastole

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22
Q

what is systolic pressure

A

reflects arterial pressure in systole

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23
Q

what 5 factors affect blood flow?

A
  • cardiac output
  • compliance
  • volume of blood
  • viscosity of blood
  • blood vessel length and diameter
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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

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25
Q

what is hypovalemia and hypervalemia and what factors can cause the?

A
  • hypo = low blood volume: bleeding/diarrhoea/ vomiting

- hyper = high blood volume: retention H20+ sodium/ kidney disease

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26
Q

does the viscosity of blood change

A

not much
only in conditions which affect erythropoiesis (eg. polycthemia and anaemia)
and liver abnormalities due to abnormal albumin

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27
Q

how does losing weight reduce the work of the heart

A

lose lots of blood vessels which reduces overall resistance

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28
Q

what factor in poiseulle’s law has the biggest effect on blood flow?

A

radius of blood vessel
r(^4)
changes in diameter has huge effect on resistance
resistance is inversely proportional to radius

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29
Q

what are phasic changes in blood flow?

A

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)

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30
Q

what regulates coronary circulation

A

auto regulation - local metabolism: no nervous/endocrine control required

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31
Q

what do vasodilators and vasoconstrictors have a direct effect on?

A

precapillary sphincters:

- vasodilators relax them, vasoconstrictors constrict them

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32
Q

what are some vasodilators ?

A
  • decrease O2
  • increase in CO2
  • increase metabolic acids (lactate, NO, K+,H+)
  • body temp
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33
Q

what are some vasoconstrictors ?

A
  • prostaglandins
  • products released by activated platlets
  • leukocytes
  • endothelins
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34
Q

what are the 3 types of circulation we have?

A

bronchial circulation
pulmonary circulation
cerebral circulation

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35
Q

what is the main difference between pulmonary and bronchial circulation ?

A

lower pressures in pulmonary circulation due to the resistance to flow being less due to less muscular arterioles

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36
Q

what are the 3 main components of autoregualtion in the cerebral circulation

A
  • chemical/metabolic response
  • myogenic response (vascular smooth muscle response)
  • neurogenic response ( communication between brian stem and autonomic centres)
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37
Q

name 4 age related changes to blood vessels

A
  • fibrous thickening of intima
  • fibrosis scarring of media
  • accumulation of ground substance
  • fragmentation of elastic lamina
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38
Q

describe the process of atherosclerosis

A
  • 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
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39
Q

what is the consequence of athersocslosis

A

coronary heart disease

MI

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40
Q

what is an aneurysm

A

localised/permanent/ abnormal dilation of blood vessels

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41
Q

what are important factors that affect aneurysms

A
  • type
  • true/false
  • site (eg. can get them in retinas with diabetes)
  • aetiology
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42
Q

what are the two types of true aneurysms

A

saccular

fusiform

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43
Q

compare arterial and venous thrombus

A
  • 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
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44
Q

what histological changes does hypertension cause?

A
  • fibrinoid changes: type of tissue damage
  • hyaline arteriosclerosis - hyaline thickening of arterial walls
  • hyperplastic arthroscelrosis - around blood vessels
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45
Q

how does diabetes increase the likelihood of injury and decreases heal?

A

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

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46
Q

what are the 3 types of tumours of blood vessels?

A
  • haemangioma
  • angiomyolipoma (kidney)
  • angiosarcoma (aggressive- old people/ radiography)
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47
Q

what is pre-load?

A

level of stretch a cardiomyocyte is exposed to before ventricular ejection

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48
Q

what is pre load also known as?

A

Left end diastolic volume

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49
Q

what is after-load?

A

pressure against which the heart is contracting when it ejects blood

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50
Q

in what condition do we get an increase in after load

A

hypertension

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51
Q

roughly, what does starlings law state?

A

that generally the energy of contraction of the heart is a function of the length of the muscular fibre

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52
Q

what’s the process which leads to vasodilation, through a baroreceptor reflex?

A
  • 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
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53
Q

in what cases does juxtaglomerular apparatus release renin

A
  • renal perfusion pressure sensed at the glomerulus
  • Na+ conc sensed in fluid surrounding distal convoluted tubule
  • if either reduced renin released
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54
Q

what are the 2 types of myocardial dysfunction?

A
  • diastolic dysfunction

- systolic dysfunction

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55
Q

what is the problem in diastolic dysfunction? what kind of heart failure is this? can it be treated?

A

LV not able to fill properly

  • known as heart failure with preserved ejection fraction (HFPEF)
  • no drugs available to treat this
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56
Q

what is the problem in systolic dysfunction? what kind of heart failure is this? can it be treated?

A

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
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57
Q

what are the stages which someone with heart failure can develop pulmonary oedema? what are the consequences of this?

A
  • 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)
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58
Q

what happens when we get heart failure in the RV? what are the consequences of this?

A
  • 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
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59
Q

what are the 2 differnt types of heart failure which involve scarring of heart tissue

A

anterolateral infarct

posteroinferior infarct

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60
Q

what is maladaption and what are the consequences this?

A

when the ejection fraction drops:

  • reduced CO
  • reduced systolic BP
  • reduced arterial stretch
  • reduced renal perfusion
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61
Q

how does cardiovascular maladaption lead to compensation

A
  • increase in preload lengthens sarcomeres
  • raises in end-diastolic pressure in LV
  • augments SV
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62
Q

Why can cardiovascular maladpation over a long time be bad? what is this called?

A
  • 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
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63
Q

how does the heart undergo adverse remodelling? why does it do this?

A

Cretes aneurysms

does this to normalise wall stress as the cavity is enlarged (Laplace’s Law)

64
Q

what value is LVEF normal in an ECHO?

A

> 55%

65
Q

what value is LVEF mildly impaired in an ECHO?

A

45-54%

66
Q

what value is LVEF moderately impaired in an ECHO?

A

36-44%

67
Q

what value is LVEF severly impaired in an ECHO?

A

<35%

68
Q

what acute therapy do we administer in heart failure?

A

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
Q

how do diuretics help in heart failure

A

limit absorption of fluid
offloads the ventricles
can maximise LV contractility
(moves us back along starling curve)

70
Q

what are the side effects of direcutics

A
  • renal dysfunction
  • reduces Na, K, Mg
  • cann induce diabetes
71
Q

what drugs can we sue for symptomatic benefit

A

diuretics - gets rid of oedema

72
Q

what drugs can we sue for prognostic benefit

A

ACEi and A2RBs

73
Q

how do ACEi’s work?

A

RASS inactivation:

  • block conversion of AgI to AgII
  • diminishes release of aldosterone
74
Q

how do A2RB’s work?

A

reeceptor inactivation

work on AgII

75
Q

how can B-blockers help in chronic failure of the heart

A
  • decrease renin secretion (so reduce CO and HR)
  • allows LV more relaxation time = better filling
  • blunts RAAS over activation
76
Q

in what conditions must we be cautious in giving B blockers?

A

asthma
low HR
heart blocks

77
Q

What binds together myocytes?

A

desmosomes

78
Q

What exists between cells to allow for contraction of cardiac muscle?

A

gap junctions

79
Q

What structures are found within cardiac muscle fibres? How do these aid function?

A
  • mitochondrion: rich energy source
  • myofibrils: composed of actin and myosin which interact to bring about contraction
  • sarcoplasmic reticulum: important calcium store
80
Q

What is the importance of calcium ions in cardiac muscle contraction? What are the sources of calcium?

A
  • calcium accommodates the interaction of myosin and actin

- inside the cell, outside the cell and sarcoplasmic reticulum

81
Q

How is the cytosolic calcium level increased for muscle contraction to occur?

A
  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
Q

How does calcium move into the cells?

A

Through L-type Calcium Channel receptors

83
Q

Overview of muscle contraction

A
  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
Q

How much ATP do myocardial cells use per day?

A

6kg

85
Q

What does the conversion of chemical energy stored in ATP to mechanical energy in myocardial cells result in?

A
  • force generation

- myofilament shortening

86
Q

What is the hydraulic functioning of the heart?

A
  • 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
Q

What is cardiac functional reserve?

A
  • the difference between normal and maximum cardiac output

- it is the capacity to augment performance on demand

88
Q

How is cardiac output calculated?

A

CO=HRxSV

89
Q

How is cardiac reserve calculated?

A

Cardiac reserve = maximal cardiac output - cardiac output at rest

90
Q

What is heart rate effected by?

A
  • sympathetic innervation
    • speeds up SA node depolarisation
    • more frequent action potentials
    • increase conduction through AV node/bundle
  • adrenaline
    • beta-1 agonism
91
Q

How can cardiac output be increased?

A
  • increased stroke volume

- increased heart rate

92
Q

How can stroke volume be increased?

A
  • autonomic input (sympathetic)
    • prolonged opening of Ca2+ channels
    • enhances calcium action in excitation/contraction coupling mechanisms
  • preload
93
Q

What affects tension in a sarcomere?

A

Sarcomere length

94
Q

What determines hoe stretched the LV wall is? What does this aid?

A
  • LV end-diastolic volume

- stretching aids contraction

95
Q

How does preload effect cardiac performance?

A

Increased preload increases cardiac performance

96
Q

Why does stretching the LV aid contraction?

A
  • 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
Q

What is the frank stealing curve?

A

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
Q

Explain the relationship behind the Frank-Starling curve

A
  • 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
Q

What causes a left shift of the Frank-Starling curve?

A

exercise, pharmacological stimulation etc

100
Q

What causes a right shift of the frank stealing curve?

A

pharmacological depression, myocardial loss eg heart failure

101
Q

How does sympathetic stimulation affect contraction of the heart?

A
  • noradrenaline and adrenaline stimulate cAMP
  • more calcium can enter the cell
    • this leads to greater cross-bridge linking in sarcomeres
102
Q

Cardiac output is … at all levels of preload

A

augmented

103
Q

How is ejection fraction calculated?

A

stroke volume / end-diastolic volume

104
Q

What are normal levels of ejection fraction?

A
  • physiological = 55-75%
  • exercise = up to 90%
  • falling heart shows reduced EF
105
Q

What happens to myocardium contraction in heart failure?

A

If the myocardium is diseased, it contracts less

  • ischaemia = scarred myocardium
  • viral infection/alcohol = wall thinning
  • increased after load = chronic high output
106
Q

What compensations does the body make for a failing ventricle?

A

SNS overactivates

RAAS kicks in

107
Q

How is heart failure compensated for?

A
  • 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
Q

How is mean systemic arterial pressure calculated?

A

cardiac output x total peripheral resistance

109
Q

What is pre-load measured as?

A

End diastolic volume

110
Q

What is preload increased by?

A
  • 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
Q

What is the Bowditch (Treppe) effect?

A
  • increased heart rate leads to increased force of contraction (or increased cardiac performance)
112
Q

Are the Frank-Starling and Bowditch effect independent of each other?

A

Yes as the length of the muscle is not effected in the Bowditch effect

113
Q

What is the Bainbridge reflex?

A
  • 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
Q

How do the sympathetic and parasympathetic nervous systems differentially affect the heart?

A
  • 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
Q

What does chronotrophy refer to?

A

Heart rate

116
Q

What does dromotrophy refer to?

A

Conduction

117
Q

What does inotrophy refer to?

A

Contraction

118
Q

What does lusitrophy refer to?

A

Relaxation

119
Q

What are the direct cardiac actions of the sympathetic nervous system?

A
  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
Q

What are the systemic effects of the sympathetic nervous system?

A

Activation of Renin-Angiotensin-Aldosterone
Systemic
System (RAAS) 2. Suprarenal stimulation - CATECHOLAMINES

121
Q

What is dobutamine used for?

A
  • acts to stimulate the sympathetic system
  • sympathymynetic
  • aims to increase heart rate and so cardiac performance up to a certain point
122
Q

What are the actions of hormones released in the RAAS?

A 
• Angiotensin II
– Vasoconstriction
– Increased Na+ and H2O retention 
• Aldosterone
– Increased Na+ and H2O retention 
• Vasopressin (Antidiuretic Hormone)
– Promotes H2O retention
123
Q

What actions of the RAAS affect the heart?

A
  • increased central venous pressure increases stroke volume

- vasoconstriction increases total peripheral resistance

124
Q

What sympathetic actions cause the effects of RAAS o the heart?

A

release of catecholamine causes release of adrenaline which stimulates RAAS

125
Q

What are the parasympathetic actions on the heart?

A 
• Decreased Heart Rate ( CHRONOTROPY) 
• Decreased AV conduction ( DROMOTROPY) 
• Decreased Atrial Contractility ( INOTROPY) •
 Ventricular contractility
– NO SIGNIFICANT EFFECT • RAAS
– NO SIGNIFICANT EFFECT
126
Q

Where are baroreceptors found? What is their effect on the circulatory system?

A 
• Located: Carotid sinuses, Aortic Arch 
• Decreased arterial pressure
– Decreased firing 
• ↑Baroreceptor firing
– Decreases Sympathetic Tone
– Increases Parasympathetic Tone
127
Q

What is action potential

A

Transient depolarisation of a cell as a result of activity of ion channels

128
Q

What are the two types of cardiac action potential

A

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
Q

What is the hierarchy of pacemakers?

A

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
Q

Where does a pacemaker potential become an action potential?

A

Meets threshold of -40 and ca2+ channels open and funny channels close

131
Q

What does ivabradine do?

A

Inhibits If (funny) channels, slows action potential

132
Q

what are class 1 drugs acting on cardiac action potential?

A

Na+ channel blocker

1c - flecainide, propafenone > 1a - quinidine, procainaminde > 1b - lidocaine, phenytoin

133
Q

what are class 2 drugs acting on cardiac action potential?

A 
beta blockers (K+ rectifier stage)
propanolol/ bisoprolol/ metaprolol
134
Q

what are class 3 drugs acting on cardiac action potential?

A

K+ channel blocker

amiodarone, sotalol

135
Q

what are class 4 drugs acting on cardiac action potential?

A

Ca2+ channel blocker

verapamil, diltiazem

136
Q

where do depolarising currents pass through at intercalated discs?

A

gap junctions

137
Q

why does the AV node delay the electrical conduction?

A

to allow the chambers to fill properly –> much faster down bundle of His then even more in purkinje fibres

138
Q

what results in a positive deflection on ECG?

A

electrical activity towards an electrode (away = negative, ie a dip)

139
Q

what time period does a small box on an ECG represent?

A

0.04 seconds

140
Q

what is the standard ECG strip you use called?

A

rhythm strip

141
Q

what is the PR interval on an ECG?

A

P wave = gradual depolarisation of atria

PR segment = AV nodal delay

142
Q

what is the QRS duration?

A

depolarisation of ventricles
upwards bit = bindle of His
downwards bit = around heart walls

143
Q

what is the ST interval?

A

ST segment = full ventricular depolarisation

ST wave = ventricular repolarisation

144
Q

how would atrial fibrillation appear on an ECG?

A

RR intervals irregularly irregular and discoordinated atrial conductivity (lots of little waves)

145
Q

how would an atrial flutter appear on an ECG?

A

lots of small waves in each RR interval, then regular QRS wave
AVN prevents transmission of all atrial conductions to ventricles

146
Q

how would ventricular fibrillation appear on ECG?

A

complete mess

discoordinated contractions

147
Q

how would ventricular tachycardia appear on an ECG?

A

big tall waves with small gaps

ventricles taking over contractions

148
Q

how would a 1st degree heart block appear on an ECG?

A

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
Q

how would a 2nd degree (Mobitz I) heart block appear on an ECG?

A

progressive lengthening of PR interval, then a missed QRS complex
(like an on and off relationship)

150
Q

how would a 2nd degree (Mobitz II) heart block appear on an ECG?

A

PR interval normal then an absent QRS wave

like an affair

151
Q

how would a 2nd degree (2:1) heart block appear on an ECG?

A

absent QRS waves after alternate P waves

affair

152
Q

how would a 3rd degree heart block appear on an ECG?

A

no relationship between P waves and QRS complexes

divorce

153
Q

what is blood pressure?

A

driving force propelling blood to tissues, balance between organ perfusion and vascular damage

154
Q

what is cardiac output?

A

heart rate x stroke volume

155
Q

what is mean systemic arterial pressure?

A

cardiac output x total peripheral resistance

156
Q

what is total peripheral resistance?

A

R = 8nL/r^4

R = resistance to blood flow
n = viscosity of blood
L = length of vessel
r = radius of vessel
157
Q

how does the autonomic nervous system control blood pressure?

A

baroreceptors located in carotid sinuses and aortic arch

year 1 flash cards (23 decks)

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