Cardiovascular Pathophysiology Flashcards
(135 cards)
1
Q
what are the 2 types of circulation
A
pulmonary and systemic
2
Q
what is the ml/beat at rest
A
75ml/beat
3
Q
pumps in series, output must be equal
vascular beds are in parallel, some in series (gut to liver)
A
ff
4
Q
what is the blood flow at rest? (CO)
A
5L/min
5
Q
what is the CO equation
A
CO = SV x HR
6
Q
what two factors affect blood flow
A
pressure (mean arterial pressure-central venous pressure)
resistance (radius)
7
Q
what is the function of arterioles
A
act as ‘taps’ - resistance vessels
control regional flow of blood
narrow lumen
thick contractile wall
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
9
Q
describe the aorta
A
elastic artery
wide lumen
elastic wall
damp pressure variations
10
Q
describe arteries
A
muscular arteries
wide lumen, thick muscular wall, non-elastic, strong
low resistance conduit
11
Q
what side of the myocardium on the heart is thicker
A
left side of heart
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
13
Q
what opens and closes valves
A
pressure difference
14
Q
what valves are between atrium and ventricle
A
right - tricuspid
left - mitral
15
Q
what stops valves inverting
A
chord tendinae
papillary muscles attaches to bottom of endocardium
16
Q
what makes heart sounds
A
closing of valves
17
Q
What’s the sarcoplasmic reticulum?
A
over muscle fibres, Ca2+ bind to troponin -> actin/myosin interact
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)
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
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
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+
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)
23
Q
where are the pacemakers located
A
sinoatrial node in right atrium
24
Q
whats the tissue that separates the atria and ventricles
A
annulus fibrosis (non-conducting)
25
how does the AP get from atr to ventr
atrioventricular node - conducts slowly
gives time for atria to depolarise and contract first
0.05m/s
26
explain the depolarisation in ventricles
fast 5m/s
bundle of His running down septum
into purkinje fibres
lots of electrical potentials, can summate to create large electrical waves
27
what are the ECG waves
P - atrial depolarisation
QRS complex - ventricle depolarisation
T - ventricle repolarisation
tells conduction and rhythm
28
what is 1st degree block
heart block
AV node slows conduction of AP
delay between P and QRS wave, more than 0.2s
29
whats 2nd degree block
some depolarisations don't get through to V
missed QRS
30
3rd degree block heart block?
Independent P wave and QRS complex
31
whats atrial flutter
each depolarisation much quicker
32
whats atrial fibrillation
individual cells depolarising at Dif times
pacemaker not spreading wave of depolarisation across atria
occasion depolarisation getting through AV node
33
Ventricular fibrillation?
uncoordinated depolarisation + contract of ventricle
defibrillator use to depolarise all cells and let pacemaker set rhythm again
34
which ecg leads look at heart in frontal plane
I, II, III, aVR, aVL, aVF
35
which ecg leads look at heart in horizontal plane
V1-V6 (precordial)
36
where does standard limb lead 1 make a recording from
Left arm w respect to right arm
37
where does standard limb lead 2 make a recording from
right arm wrt to left leg
38
where does standard limb lead 3 make a recording from
left leg wrt to left arm
39
a wave of approaching depolarisation causes an upward causing blip
fff
40
in repolarisation if approaching RI (SLL2) positive blip, why is that
the epicardium has a shorter AP than the endocardium so goes up the way
41
in ecg paper what is 1 large square in time
0.2 secs
42
how do you determine the HR on an ecg
R-R interval, count waves in 30 large boxes (=6secs)
and multiply by 10 for in a minute
43
what is a STEMI
ST elevation myocardial infarction - complete occlusion of arteries
44
what is diastole
Relaxation of the heart
fill chambers w blood
2/3 of cardiac cycle
45
what is systole
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
46
what is systolic pressure
peak pressure of aorta (120mmHg)
47
what is diastolic notch
when aortic valve closes
48
what is diastolic pressure
minimum pressure in aorta (80mmHg)
49
what is pulse pressure
difference between systolic and diastolic pressure
50
what is mean arterial pressure (MAP)
average pressure in the arteries throughout the cardiac cycle
51
what is end diastolic volume (EDV)
peak volume of blood at end of filling phase
52
what is end systolic volume (ESV)
minimum volume of blood at end of ejection phase
53
what is the ejection fraction
SV/EDV
54
What is a phonocardiogram?
occurs due to turbulence in blood from closure of AV valves, and closure of semi-lunar valves
55
what are murmurs and what are they caused by
abnormal heart sounds
stenosis - narrowing of valve and cause turbulent blood flow
regurgitation - valve not shut properly
56
what regulates heart rate
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
what regulates stroke volume
preload, contractility, afterload and neural
58
What is stroke volume?
volume of blood pumped out by one ventricle with each beat
59
what is the preload for SV
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
what is the after load for SV
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
how does neural affect SV
affects contractility
sympathetic NS - noradrenaline on B1 receptors inc contractility, stronger
62
what affects venous pressure
- 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
what are some anticlotting mechanisms in the body
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
What is bulk flow driven by?
hydrostatic pressure and osmotic pressure (pushing water back in)
65
what is the equation for MAP
MAP = CO x TPR
66
what are the two levels of control on peripheral blood flow
local - meet selfish needs of individual tissue
central - ensure total PR (MAP) of whole body stay right
67
How can you measure arterial pressure
Auscultation of Korotkoff sounds using
a sphygmomanometer & stethoscope
Oscillatory blood pressure measurement
68
how does Oscillatory blood pressure measurement work
turbulent blood flow sets up vibrations (oscillations) in vessel wall
max vibrations at mean arterial pressure
69
what sounds are heard when auscultating bp
```
silence (above systolic pressure)
tapping (blood pushing through)
thumping
muffled (diastolic pressure)
silence
```
70
how are elastic arteries (aorta) a pressure resevoir
they damp down pressure variations
71
what is the pressure wave affected by
- stroke volume
- velocity of ejection
- elasticity of arteries
- total peripheral resistance
72
pressure falls throughout vascular tree
tt
73
what is the pressure drop through arteries
95 to 90mmhg
74
what is the pressure drop through arterioles
Large drop through arterioles (from ~ 90 to 40 mmHg)
75
what is the the pressure difference from capillaries to veins
20 to 5 mmHg
76
what is velocity related to
total cross section
77
how does gravity affect mean arterial pressure
causes venous distension in legs
| dec EDV, dec preload, dec SV, dec CO, decreased MAP
78
how does gravity cause venous collapse
further up column, reduced pressure, once past 0mmHg pressure inside vessel lower than pressure out = vein get squashed flat, compressed
79
what are continuous capillaries
no clefts or pores e.g brain (blood brain barrier)
| clefts only eg muscle
80
what are fenestrated capillaries
clefts and pores eg intestine and kidney, specialised for fluid exchange
81
what are discontinuous capillaries
clefts and massive pores eg liver
82
how do capillaries exchange with tissue
- diffusion
non-saturable
non-polar across memb,
polar through clefts/pores
- carrier-mediated transport
e. g. glucose transporter in the brain
- bulk flow
83
what is bulk flow
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
how much fluid is lost and regained each day
20L lost
17L regained into circulation
3L to lymphatic system
85
what is oedema
accumulation of excess fluid
lose balance of starlings forces
86
what can oedema be caused by
lymphatic obstruction
rasied CVP
hypoproteinemia
increased capillary permeability
87
what is the purpose of the blood brain barrier
The blood-brain barrier prevents toxic substances, large molecules, and neurotransmitters released in the blood from entering the brain
88
what is Poiseuille’s law
varying radius of resistance vessels is used to control
- blood flow
- TPR and regulate MAP
- redirect blood
89
what is the MAP equation
MAP = CO x TPR
90
Reducing resistance of a vascular bed increases flow through that vascular bed
But, reducing total peripheral resistance also reduces mean arterial pressure
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
what does arteriolar radius affect
affects flow through individual vascular beds, and mean arterial pressure
92
why do you have to control the radius of arterioles
to keep blood flow to each vascular bed sufficient and keep MAP in right range
93
how do you control the TPR of arterioles
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
what is active (metabolic) hyperaemia
a local control
- trigger - inc in metabolic activity
- inc local metabolites
- release paracrine signal (EDRF)
- inc flow to wash out metabolites
95
what is pressure (flow) autoregulation
Local (intrinsic) control
trigger = dec perfusion pressure
- dec MAP, dec flow
- paracrine signal cos metabolites conc inc
- arterioles dilate, washes out metabolites
96
what is reactive hyperaemia
Local (intrinsic) control
trigger = occlusion (blocked) of blood supply
- inc in blood flow
- extreme version of pressure autoregulation
97
what central controls are there for TPR
sympathetic
parasympathetic
hormonal
98
what effect does sympathetic nerves have on TPR
```
release noradrenaline
binds to a1-receptors
causes arteriolar constriction
therefore dec flow through that tissue
inc TPR
```
99
what effect do parasympathetic nerves have on TPR
usually no effect
| genitalia and salivary glands are the exception
100
how does adrenaline (hormonal) affect TPR
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
explain the coronary circulation
blood supply interrupted by systole
active hyperaemia - arteriolar dilation (inc in local metabolism)
B2-receptors
102
explain cerebral circulation
needs to be stable
| has pressure autoregulation (if decrease in perfusion pressure)
103
explain pulmonary circulation
dec O2 causes arteriolar constriction
| ensure blood is directed to the best ventilated parts of the lung
104
explain renal circulation
main function is filtration which depends on pressure
changes in MAP would have big effects on blood volume
pressure autoregulation
105
what is late diastole
both chambers relaxed, start filling w blood
106
what is atrial systole
atrial contraction, slight delay, blood into ventricles
107
what is isovolumic ventricular contraction
pushes AV valves closed
108
what is ventricular ejection
ventric pressure rises, exceeds pressure in arteries
| semilunar valves open, blood ejected
109
isovolumic ventricular relaxation
pressure falls, semilunar valves close
110
why does MAP need to be regulated
MAP is the driving force pushing blood through the circulation
cant be too low - fainting
too high - hypertension
111
what are arterial baroreflex
| and what 2 types are there
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
what does a high firing rate of APs from arterial baroreflex receptors mean
high firing rate = high pressure
113
what nerve goes up to the brain from the aortic arch baroreflex and where in the brain?
vagus nerve, medullary cardiovascular centres
114
what nerve goes up to the brain from the carotid sinus baroreflex and where in the brain?
glossopharyngeal nerve, medullary cardiovascular centres
115
what effect will parasympathetic nerves have on the heart from the medullary cardiovascular centres
release acetylcholine
act on muscarinic receptors
hyperpolarized pacemaker cells will make them depolarise slower.
Reach threshold later and slow down your heart rate
116
what will sympathetic nerves do to the heart from the medullary cardiovascular centres
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
what are other inputs to the medullary cardiovascular centres
- 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
what is the Valsalva manoeuvre
forced expiration against a closed glottis
119
what effect does the vasalva manoeuvre have on the cvs
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
kidneys regulate plasma volume
controlling plasma volume is used to regulate MAP
- long term control of BP
gg ff
121
what determines how big the osmotic gradient will be in the kidneys
Na+ transport
122
kidney collecting ducts have control of permeability of ducts to water
hh
123
what happens if the collecting duct is very permeable to water
collecting duct very permeable to water will result in lots of water reabsorption, little urine, and conserve plasma volume
124
what happens if the collecting duct is very impermeable to water
result in little reabsorption (back into circulation), lots of urine (= diuresis), and a reduction in plasma volume, goes out body
125
what hormone systems regulate the process of water reabsorption
```
Renin-angiotensin-aldosterone system
Antidiuretic factor (ADH, vasopressin)
Atrial natriuretic peptide (factor) & brain natriuretic peptide (factor)
```
126
Where is renin produced?
From the juxtaglomerular (= granule cells) of the kidney
127
What triggers renin production?
- 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
What does renin do?
Converts inactive angiotensinogen to angiotensin I
| Which is in turn converted by angiotensin converting enzyme to angiotensin II
129
what does angiotensin II do?
- 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
Where is antidiuretic hormone (ADH) produced
Synthesised in the hypothalamus
| Released from the posterior pituitary
131
What triggers ADH release?
- A decrease in blood volume (sensed by cardiopulmonary baroreceptors)
- An increase in osmolarity of interstitial fluid
- Circulating angiotensin II
132
What does ADH do
- Increases the permeability of the collecting duct to H2O, therefore reduces diuresis and increases plasma volume
- Causes vasoconstriction, inc MAP
133
where are atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) produced
myocardial cells in the atria & the ventricles respectively
134
What triggers ANP & BNP release?
Increased distension of the atria & ventricles (sign of increased MAP)
135
What do ANP & BNP do?
Increase excretion of Na+ (natriuresis)
Inhibit the release of renin
Act on medullary CV centres to reduce MAP
