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Medicine Term 2 > Cardiovascular Pathophysiology > Flashcards

Cardiovascular Pathophysiology Flashcards

1
Q

what are the 2 types of circulation

A

pulmonary and systemic

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2
Q

what is the ml/beat at rest

A

75ml/beat

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3
Q

pumps in series, output must be equal

vascular beds are in parallel, some in series (gut to liver)

A

ff

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4
Q

what is the blood flow at rest? (CO)

A

5L/min

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5
Q

what is the CO equation

A

CO = SV x HR

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6
Q

what two factors affect blood flow

A

pressure (mean arterial pressure-central venous pressure)

resistance (radius)

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7
Q

what is the function of arterioles

A

act as ‘taps’ - resistance vessels
control regional flow of blood
narrow lumen
thick contractile wall

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8
Q

what is the function of veins and venules and describe them

A

capacitance vessels

wide lumen, distensible walls (can absorb blood)

low resistance conduit + reservoir (store blood, release when needed)

allow fractional distribution of blood between veins and rest of circulation

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9
Q

describe the aorta

A

elastic artery
wide lumen
elastic wall
damp pressure variations

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10
Q

describe arteries

A

muscular arteries
wide lumen, thick muscular wall, non-elastic, strong
low resistance conduit

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11
Q

what side of the myocardium on the heart is thicker

A

left side of heart

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12
Q

what are the semi lunar valves and where

A

pulmonary - right side to pulmonary arteries

aortic valve - left side between LV and aorta

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13
Q

what opens and closes valves

A

pressure difference

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14
Q

what valves are between atrium and ventricle

A

right - tricuspid

left - mitral

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15
Q

what stops valves inverting

A

chord tendinae

papillary muscles attaches to bottom of endocardium

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16
Q

what makes heart sounds

A

closing of valves

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17
Q

What’s the sarcoplasmic reticulum?

A

over muscle fibres, Ca2+ bind to troponin -> actin/myosin interact

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18
Q

whats the functional syncytium and whats in it

A

allow heart to act as one big muscle

  • gap junctions (electrical connections) - connect individual cardia cells to allow electric current to go through
  • desmosomes (physical connection)

intercalated discs (whole thing)

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19
Q

explain the action potential in the heart cells

A

longer, 200-250ml s

voltage gated Na and Ca channels (doesn’t saturate troponin)

modulate Ca coming in, to regulate strength of contraction

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20
Q

pacemakers explain

A

cells that have unstable resting membrane potentials, spontaneously fire action potential to threshold, make whole heart contract

spread AP’s through gap junctions

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21
Q

explain non-pacemaker cells

A

leaky K+ channels going out cell
cell is -90mV (resting potential)
Na, Ca channels shut
high resting permeability to K+
initial cell depolarises. Na+ flows in from channles
plateu - inc in Ca2+ (long lasting L type) + dec in K+
repolarisation - dec in Ca2+ + inc in K+

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22
Q

explain pacemaker activity

A 
AP - inc in Ca2+ (L-type), slower but stay open longer 
Pacemaker potential (pre-potential) 
- gradual dec in K+
- early inc in Na+
- in in Ca2+ (T-type)
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23
Q

where are the pacemakers located

A

sinoatrial node in right atrium

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24
Q

whats the tissue that separates the atria and ventricles

A

annulus fibrosis (non-conducting)

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25
Q

how does the AP get from atr to ventr

A

atrioventricular node - conducts slowly

gives time for atria to depolarise and contract first

0.05m/s

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26
Q

explain the depolarisation in ventricles

A

fast 5m/s

bundle of His running down septum

into purkinje fibres

lots of electrical potentials, can summate to create large electrical waves

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27
Q

what are the ECG waves

A

P - atrial depolarisation
QRS complex - ventricle depolarisation
T - ventricle repolarisation

tells conduction and rhythm

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28
Q

what is 1st degree block

A

heart block

AV node slows conduction of AP

delay between P and QRS wave, more than 0.2s

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29
Q

whats 2nd degree block

A

some depolarisations don’t get through to V

missed QRS

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30
Q

3rd degree block heart block?

A

Independent P wave and QRS complex

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31
Q

whats atrial flutter

A

each depolarisation much quicker

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32
Q

whats atrial fibrillation

A

individual cells depolarising at Dif times

pacemaker not spreading wave of depolarisation across atria

occasion depolarisation getting through AV node

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33
Q

Ventricular fibrillation?

A

uncoordinated depolarisation + contract of ventricle

defibrillator use to depolarise all cells and let pacemaker set rhythm again

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34
Q

which ecg leads look at heart in frontal plane

A

I, II, III, aVR, aVL, aVF

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35
Q

which ecg leads look at heart in horizontal plane

A

V1-V6 (precordial)

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36
Q

where does standard limb lead 1 make a recording from

A

Left arm w respect to right arm

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37
Q

where does standard limb lead 2 make a recording from

A

right arm wrt to left leg

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38
Q

where does standard limb lead 3 make a recording from

A

left leg wrt to left arm

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39
Q

a wave of approaching depolarisation causes an upward causing blip

A

fff

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40
Q

in repolarisation if approaching RI (SLL2) positive blip, why is that

A

the epicardium has a shorter AP than the endocardium so goes up the way

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41
Q

in ecg paper what is 1 large square in time

A

0.2 secs

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42
Q

how do you determine the HR on an ecg

A

R-R interval, count waves in 30 large boxes (=6secs)

and multiply by 10 for in a minute

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43
Q

what is a STEMI

A

ST elevation myocardial infarction - complete occlusion of arteries

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44
Q

what is diastole

A

Relaxation of the heart

fill chambers w blood

2/3 of cardiac cycle

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45
Q

what is systole

A

Contraction of the heart

heart pumps blood out

1/3 of cycle

when mitral and tricuspid valves close and aortic n pulmonary open - blood pumped out

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46
Q

what is systolic pressure

A

peak pressure of aorta (120mmHg)

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47
Q

what is diastolic notch

A

when aortic valve closes

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48
Q

what is diastolic pressure

A

minimum pressure in aorta (80mmHg)

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49
Q

what is pulse pressure

A

difference between systolic and diastolic pressure

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50
Q

what is mean arterial pressure (MAP)

A

average pressure in the arteries throughout the cardiac cycle

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51
Q

what is end diastolic volume (EDV)

A

peak volume of blood at end of filling phase

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52
Q

what is end systolic volume (ESV)

A

minimum volume of blood at end of ejection phase

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53
Q

what is the ejection fraction

A

SV/EDV

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54
Q

What is a phonocardiogram?

A

occurs due to turbulence in blood from closure of AV valves, and closure of semi-lunar valves

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55
Q

what are murmurs and what are they caused by

A

abnormal heart sounds

stenosis - narrowing of valve and cause turbulent blood flow

regurgitation - valve not shut properly

56
Q

what regulates heart rate

A

sympathetic NS - release noradrenaline
act on B1 receptors on SA node
inc slope of pacemaker potential
inc heart rate

parasympathetic - vagus release acetylcholine
act on muscarinic receptors on SA node
hyper polarise cell + dec slope
dec HR

57
Q

what regulates stroke volume

A

preload, contractility, afterload and neural

58
Q

What is stroke volume?

A

volume of blood pumped out by one ventricle with each beat

59
Q

what is the preload for SV

A

how full the ventricle is before contracting, depends on venous return

starlings law - energy of contraction proportional to how stretched the cardiac muscle is bar contracting)

(less blood back, smaller strength of contraction = smaller SV)

60
Q

what is the after load for SV

A

load against which muscle tries to contract blood out

(TPR) how easy for blood to get away through arterioles (constricted/dilated)

(if arterioles constricted -> TPR inc and pressure will be higher at aorta -> ventricle require more pressure to open valve -> less energy to eject blood -> SV dec

61
Q

how does neural affect SV

A

affects contractility

sympathetic NS - noradrenaline on B1 receptors inc contractility, stronger

62
Q

what affects venous pressure

A
  • gravity (standing up, more pressure in legs, lower in head)
  • skeletal muscle pump
  • respiratory pump
  • venomotor tone (contraction of smooth muscle around veins n venules)
  • systemic filling pressure (pressure difference of ventricles and veins)
63
Q

what are some anticlotting mechanisms in the body

A

produce prostacyclin + nitric oxide (inhibit platelet aggregation)
tissue factor inhibitor (stop thrombin production)
thrombomodulin (inactivate thrombin)
heparin
tissue plasminogen activator (t-PA) (digest clot)

64
Q

What is bulk flow driven by?

A

hydrostatic pressure and osmotic pressure (pushing water back in)

65
Q

what is the equation for MAP

A

MAP = CO x TPR

66
Q

what are the two levels of control on peripheral blood flow

A

local - meet selfish needs of individual tissue

central - ensure total PR (MAP) of whole body stay right

67
Q

How can you measure arterial pressure

A

Auscultation of Korotkoff sounds using
a sphygmomanometer & stethoscope
Oscillatory blood pressure measurement

68
Q

how does Oscillatory blood pressure measurement work

A

turbulent blood flow sets up vibrations (oscillations) in vessel wall
max vibrations at mean arterial pressure

69
Q

what sounds are heard when auscultating bp

A 
silence (above systolic pressure)
tapping (blood pushing through)
thumping
muffled (diastolic pressure)
silence
70
Q

how are elastic arteries (aorta) a pressure resevoir

A

they damp down pressure variations

71
Q

what is the pressure wave affected by

A
  • stroke volume
  • velocity of ejection
  • elasticity of arteries
  • total peripheral resistance
72
Q

pressure falls throughout vascular tree

A

tt

73
Q

what is the pressure drop through arteries

A

95 to 90mmhg

74
Q

what is the pressure drop through arterioles

A

Large drop through arterioles (from ~ 90 to 40 mmHg)

75
Q

what is the the pressure difference from capillaries to veins

A

20 to 5 mmHg

76
Q

what is velocity related to

A

total cross section

77
Q

how does gravity affect mean arterial pressure

A

causes venous distension in legs

dec EDV, dec preload, dec SV, dec CO, decreased MAP

78
Q

how does gravity cause venous collapse

A

further up column, reduced pressure, once past 0mmHg pressure inside vessel lower than pressure out = vein get squashed flat, compressed

79
Q

what are continuous capillaries

A

no clefts or pores e.g brain (blood brain barrier)

clefts only eg muscle

80
Q

what are fenestrated capillaries

A

clefts and pores eg intestine and kidney, specialised for fluid exchange

81
Q

what are discontinuous capillaries

A

clefts and massive pores eg liver

82
Q

how do capillaries exchange with tissue

A
  • diffusion
    non-saturable
    non-polar across memb,
    polar through clefts/pores
  • carrier-mediated transport
    e. g. glucose transporter in the brain
  • bulk flow
83
Q

what is bulk flow

A

Is determined by starlings forces
capillary hydrostatic pressure vs ISF hydrostatic pressure

Plasma osmotic pressure vs ISF osmotic pressure

Hydrostatic pressure pushes fluid out through the leaky capillaries. That builds up an osmotic (oncotic) pressure which draws fluid back in.

84
Q

how much fluid is lost and regained each day

A

20L lost
17L regained into circulation

3L to lymphatic system

85
Q

what is oedema

A

accumulation of excess fluid

lose balance of starlings forces

86
Q

what can oedema be caused by

A

lymphatic obstruction
rasied CVP
hypoproteinemia
increased capillary permeability

87
Q

what is the purpose of the blood brain barrier

A

The blood-brain barrier prevents toxic substances, large molecules, and neurotransmitters released in the blood from entering the brain

88
Q

what is Poiseuille’s law

A

varying radius of resistance vessels is used to control

  • blood flow
  • TPR and regulate MAP
  • redirect blood
89
Q

what is the MAP equation

A

MAP = CO x TPR

90
Q

Reducing resistance of a vascular bed increases flow through that vascular bed

But, reducing total peripheral resistance also reduces mean arterial pressure

A

To keep the blood flow to each vascular bed sufficient, and keep mean arterial pressure in the right range, you have to engage in some resistance juggling.

91
Q

what does arteriolar radius affect

A

affects flow through individual vascular beds, and mean arterial pressure

92
Q

why do you have to control the radius of arterioles

A

to keep blood flow to each vascular bed sufficient and keep MAP in right range

93
Q

how do you control the TPR of arterioles

A

2 levels of control over smooth muscle around arterioles

  • Local (intrinsic) mechanisms - concerned with meeting the selfish needs of each individual tissue
  • Central (extrinsic) mechanisms – concerned with ensuring that the total peripheral resistance (and therefore MAP) of the whole body stays right
94
Q

what is active (metabolic) hyperaemia

A

a local control

  • trigger - inc in metabolic activity
  • inc local metabolites
  • release paracrine signal (EDRF)
  • inc flow to wash out metabolites
95
Q

what is pressure (flow) autoregulation

A

Local (intrinsic) control

trigger = dec perfusion pressure

  • dec MAP, dec flow
  • paracrine signal cos metabolites conc inc
  • arterioles dilate, washes out metabolites
96
Q

what is reactive hyperaemia

A

Local (intrinsic) control

trigger = occlusion (blocked) of blood supply

  • inc in blood flow
  • extreme version of pressure autoregulation
97
Q

what central controls are there for TPR

A

sympathetic
parasympathetic
hormonal

98
Q

what effect does sympathetic nerves have on TPR

A 
release noradrenaline
binds to a1-receptors
causes arteriolar constriction
therefore dec flow through that tissue 
inc TPR
99
Q

what effect do parasympathetic nerves have on TPR

A

usually no effect

genitalia and salivary glands are the exception

100
Q

how does adrenaline (hormonal) affect TPR

A

released from adrenal medulla
binds to a1-receptors
causes arteriolar constriction
therefore dec flow through that tissue, inc TPR

in some tissues - B2-receptor
arteriolar dilation
inc flow = dec TPR

101
Q

explain the coronary circulation

A

blood supply interrupted by systole
active hyperaemia - arteriolar dilation (inc in local metabolism)
B2-receptors

102
Q

explain cerebral circulation

A

needs to be stable

has pressure autoregulation (if decrease in perfusion pressure)

103
Q

explain pulmonary circulation

A

dec O2 causes arteriolar constriction

ensure blood is directed to the best ventilated parts of the lung

104
Q

explain renal circulation

A

main function is filtration which depends on pressure
changes in MAP would have big effects on blood volume
pressure autoregulation

105
Q

what is late diastole

A

both chambers relaxed, start filling w blood

106
Q

what is atrial systole

A

atrial contraction, slight delay, blood into ventricles

107
Q

what is isovolumic ventricular contraction

A

pushes AV valves closed

108
Q

what is ventricular ejection

A

ventric pressure rises, exceeds pressure in arteries

semilunar valves open, blood ejected

109
Q

isovolumic ventricular relaxation

A

pressure falls, semilunar valves close

110
Q

why does MAP need to be regulated

A

MAP is the driving force pushing blood through the circulation
cant be too low - fainting
too high - hypertension

111
Q

what are arterial baroreflex

and what 2 types are there

A

sensors that detect changes in bp
aortic arch - vagus nerve to brain
carotid sinus - glossopharyngeal nerve

stretch receptors, will signal by increase in firing APs

112
Q

what does a high firing rate of APs from arterial baroreflex receptors mean

A

high firing rate = high pressure

113
Q

what nerve goes up to the brain from the aortic arch baroreflex and where in the brain?

A

vagus nerve, medullary cardiovascular centres

114
Q

what nerve goes up to the brain from the carotid sinus baroreflex and where in the brain?

A

glossopharyngeal nerve, medullary cardiovascular centres

115
Q

what effect will parasympathetic nerves have on the heart from the medullary cardiovascular centres

A

release acetylcholine
act on muscarinic receptors
hyperpolarized pacemaker cells will make them depolarise slower.
Reach threshold later and slow down your heart rate

116
Q

what will sympathetic nerves do to the heart from the medullary cardiovascular centres

A

release noradrenaline
B1-receptors in pacemakers
depolarise faster, inc HR

adrenal medulla

also innervate ventricle muscles
inc Ca released in cells
more cross bridges a greater excitation contraction coupling
increase the strength volume

venoconstriction (squeeze blood back to heart, inc preload, inc CO) + arteriolarconstriction (inc TPR, inc MAP)

117
Q

what are other inputs to the medullary cardiovascular centres

A
  • cardiopulmonary baroreceptors, sensing central blood volume
  • Central chemoreceptors, sensing arterial pCO2
  • Chemoreceptors in muscle, sensing metabolite concentrations
  • Joint receptors
  • Higher centres, hypothalamus and cerebral cortex
118
Q

what is the Valsalva manoeuvre

A

forced expiration against a closed glottis

119
Q

what effect does the vasalva manoeuvre have on the cvs

A

Increased thoracic pressure is transmitted through to aorta

Increased thoracic pressure reduces the filling pressure from the veins, which therefore dec VR, dec EDV, dec SV, dec CO, dec MAP

detected by baroreceptors which initiate a reflex increase in CO and TPR

the decrease in thoracic pressure is transmitted through to the aorta

VR is restored so SV 

120
Q

kidneys regulate plasma volume
controlling plasma volume is used to regulate MAP
- long term control of BP

A

gg ff

121
Q

what determines how big the osmotic gradient will be in the kidneys

A

Na+ transport

122
Q

kidney collecting ducts have control of permeability of ducts to water

A

hh

123
Q

what happens if the collecting duct is very permeable to water

A

collecting duct very permeable to water will result in lots of water reabsorption, little urine, and conserve plasma volume

124
Q

what happens if the collecting duct is very impermeable to water

A

result in little reabsorption (back into circulation), lots of urine (= diuresis), and a reduction in plasma volume, goes out body

125
Q

what hormone systems regulate the process of water reabsorption

A 
Renin-angiotensin-aldosterone system
Antidiuretic factor (ADH, vasopressin)
Atrial natriuretic peptide (factor) & brain natriuretic peptide (factor)
126
Q

Where is renin produced?

A

From the juxtaglomerular (= granule cells) of the kidney

127
Q

What triggers renin production?

A
  • Activation of sympathetic nerves due to reduced MAP
  • Decreased distension of afferent arterioles
  • Macula densa, decreased delivery of Na+/Cl- through the tubule

all signal reduced MAP

128
Q

What does renin do?

A

Converts inactive angiotensinogen to angiotensin I

Which is in turn converted by angiotensin converting enzyme to angiotensin II

129
Q

what does angiotensin II do?

A
  • Stimulates release of aldosterone from the adrenal cortex, inc plasma vol = inc MAP
  • Increases release of ADH from the pituitary, inc water permeability, inc plasma vol
  • vasoconstrictor, inc TPR
130
Q

Where is antidiuretic hormone (ADH) produced

A

Synthesised in the hypothalamus

Released from the posterior pituitary

131
Q

What triggers ADH release?

A
  • A decrease in blood volume (sensed by cardiopulmonary baroreceptors)
  • An increase in osmolarity of interstitial fluid
  • Circulating angiotensin II
132
Q

What does ADH do

A
  • Increases the permeability of the collecting duct to H2O, therefore reduces diuresis and increases plasma volume
  • Causes vasoconstriction, inc MAP
133
Q

where are atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) produced

A

myocardial cells in the atria & the ventricles respectively

134
Q

What triggers ANP & BNP release?

A

Increased distension of the atria & ventricles (sign of increased MAP)

135
Q

What do ANP & BNP do?

A

Increase excretion of Na+ (natriuresis)
Inhibit the release of renin
Act on medullary CV centres to reduce MAP

Medicine Term 2 (5 decks)

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