Physiology of CVS Flashcards
(145 cards)
1
Q
pumps are in ____
meaning output to all organs is ____
A
series
equal
2
Q
most vascular beds are in ____
meaning:
A
parallel
all tissues get oxygenated blood
and
allows regional redirection
3
Q
exception to parallel vascular beds
A
liver and gut circulation- in series
4
Q
pressure difference =
A
mean arterial pressure
- central venous pressure
5
Q
what controls the resistance and flow in each vascular bed
A
arterioles
6
Q
what controls capacitance and fractional distribution of blood
A
veins and venules
7
Q
1/2 the diameter will reduce blood flow by
A
16 fold
radius to the power of 4
8
Q
aorta is a ___ artery
structure + function
A
elastic
wide lumen and elastic wall- dampens pressure variations
9
Q
other arteries are ___
structure + function
A
muscular
wide non elastic lumen
low resistance conduit
10
Q
resistance vessels are ___
structure + function
A
arterioles
narrow lumen, thick wall to control resistance and flow
11
Q
exchange vessels are ___
structure + function
A
capillaries
narrow lumen THIN wall- for passage
12
Q
capacitance vessels are ___ ___
structure + function
A
venules and veins
wide lumen and distensible wall
low resistance conduit and reservoir
allows distribution of blood between veins and rest of circulation
13
Q
where are mitral valves (left AV valve)
A
between left atrium and left ventricle
14
Q
where are tricuspid valves (right AV valve)
A
between right atrium and right ventricle
15
Q
all valves are
A
passive
16
Q
purpose of chordae tendinae
A
stops valves inverting
17
Q
purpose of papillary muscle
A
lets tendons move so it doesn’t stop valves
18
Q
pulmonary and aortic valves are also known as
A
semilunar
19
Q
cardiac muscles vs skeletal muscles with tetanus
A
skeletal muscles can hold contractions- exhibit tetanus
cardiac muscles can’t hold contractions- no tetanus
20
Q
cardiac muscles forms a functional syncytium, what does that mean?
A
cells work together to make 1 big muscle
electrically connected by: gap junctions
physically connected by: desmosomes
which form intercalated discs
21
Q
why can’t cardiac muscles have tetanus contractions
A
long refractory period
long action potential
22
Q
ionic basis of non pacemaker action potentials in cardiac cells
A
resting membrane- leaky K+ so -90mV
initial depolarisation- increase in NA+
plateau (unique to cardiac)- increase in Ca2+ L type and decrease in K+
repolorisation- decrease in Ca2+ and increase in K+
23
Q
ionic basis of pacemaker action potentials in cardiac cells
A
they have a prepotential:
decrease in K+, increase in Ca2+ T type and Na+
action potential is by increase in Ca2+ L type
24
Q
purpose of SA node
A
fastest/main pacemaker
25
purpose of annulus fibrosus
non conducting- blocks signals
26
purpose of AV node
delay box- so ventricles don't constrict before atria
27
purpose of bundle of His and purkinje fibres
rapid conduction system- ensures all parts of the ventricle conducts at the same time
28
ECG: what is the P wave
atrial depolarisation
29
ECG: what is the QRS wave and how long should it be
ventricular depolarisation
0.08s
30
ECG: what is the T wave
ventricular repolorisation
31
ECG: large square is ___ seconds
0.2
32
ECG: gap between P and QRS should be
0.18s
33
ECG: what is the PR interval and normal time
time from atrial depolorisation to ventricular depolorisation
(from start of P to start of Q)
34
what's the QT interval and how long should it be
time spent while ventricles are depolarised
0.42s at 60bpm (changes with HR)
35
how to measure HR from and ECG
count how many R waves in 30 large squares
| and times by 10
36
bradycardia range
below 60bpm
37
tachycardia range
above 100bpm
38
ECG: what is STEMI
elevation of the S-T segment, indication of something wrong
39
whats worse STEMI or NSTEMI heart attack
NSTEMI is worse
40
peak aortic pressure happens in ______
and value
systole
120
41
pulse pressure
40
42
minimum aortic pressure happens at ____
and value
diastole
80
43
average end diastolic volume
140
44
average end systolic volume
60
45
how to calc stroke volume
EDV-ESV
46
average stroke volume
80
47
how to calculate ejection fraction
and value
SV/EDV
2/3
48
A
C
V
waves on cardiac cycle chart
```
A = contraction of Aorta
C = ventricle contraction and mitral valve bulging into aorta
V = blood flowing from lungs into aorta
```
49
phases of cardiac cycle order
IRS IRS with Contraction first as it starts with a C
```
Isometric contraction
Rapid ejection
Slower ejection
Isometric relaxation
Rapid filling
Slower filling
```
50
what causes first heart sound (lub)
closure of AV mitral and tricuspid valves
| in systole
51
what causes second heart sound (dubb)
closure of semi-lunar (aortic and pulmonary) valves in systole
52
causes of third heart sound
rapid passive filling phase
53
causes of 4th heart sound
active filling phase
54
causes of systolic murmur
stenosis of aortic/pulmonary semilunar valves
or regurgitation or mitral and tricuspid valves
55
causes of diastolic murmur
stenosis of mitral/tricuspid valves
regurgitation through aortic/ pulmonary valves
56
cause of continuous murmur
septal defect
57
how does the sympathetic nervous system effect the heart
releases noradrenalin and adrenalin
acting on beta 1 receptors on SA node
increases slope of the pacemaker potential
increasing heart rate
58
how does parasympathetic nervous system effect the heart
vagus releases ACh
acts on muscarinic receptors
hyperpolarises cells aaand decreases slope of pacemaker potential
decreases heart rate
59
starlings law
energy of a contraction is proportional to the initial length of cardiac muscle fibre - preload
60
3 ways to control SV
1. alter preload
2. alter afterload
3. change contractility using neural regulation
61
in vivo preload is affected by
how full the ventricle is - EDV
62
Control of stroke volume through preload: INCREASED venous return effects on stroke volume
increases EDV
| so INCREASES SV
63
Control of stroke volume through preload: DECREASED venous return effects on stroke volume
decreases EDV
| so INCREASES Stroke Volume
64
Control of stroke volume through preload: what does regulation of preload (EDV) ensure
self regulation- SV between L and R ventricles are the same
65
what is afterload
the load the muscle must push against to contract
66
Control of stroke volume through afterload: how does TPR effect stroke volume
```
TPR INCREASES
aortic pressure increases
ventricle needs to work harder to push open aortic valve
less energy is left to eject the blood
SV DECREASES
```
67
Control of stroke volume through neural regulation: sympathetic
sympathetic activation INCREASES CONTRACTILITY- ionotropic effect
gives strong short contraction
INCREASES SV
68
Control of stroke volume through nuera;: parasympathetic
no effect
69
why does parasympathetic NS have no effect on SV
does not innervate ventricular muscle
70
measuring arterial blood pressure
uses korotkoff sounds
first tapping sounds- systolic reading
end of sounds- diastolic reading
71
pressure wave in arteries is affected by
SV
velocity of ejection
elasticity of arteries
TPR
72
order of locations of highest pressure to lowest
```
LV- 120
arteries- 90-95
arterioles- 95- 40
capillaries- 40-20
venules and veins- 20-5
RA
```
73
pressure in arteries
90
74
pressure in arterioles
40
75
pressure in cappiliaries
20
76
pressure in veins
5
77
pressure in pulmonary circulation is
1/5th of systemic
78
velocity is related to
total cross section
fastest is aorta an vena cava
slowest is capillaries
79
things that effect venous return 1: how does gravity effect blood flow
DOES NOT affect driving pressure from arteries to veins
DOES cause venous distension legs- deceases: EDV, preload, SV, CO and MAO
and orthostatic hypotension
DOES cause venous collapse in neck- can estimate central venous pressure
80
things that effect venous return 2: skeletal muscle pump
rhythmic contraction increase venous return and EDV
| prevents loss in preload
81
things that effect venous return 3: respiratory pump
increased resp rate and depth increases venous return and EDV
82
things that effect venous return 4: venomotor control
contraction of smooth muscle surrounding venules and veins
mobolises capacitance and increases EDV and preload
83
things that effect venous return 4: venomotor control
contraction of smooth muscle surrounding venules and veins
mobolises capacitance and increases EDV and preload
84
things that effect venous return 5: systemic filling pressure
pressure created in ventricles and transmitted through CVS
85
why is it important to control venous return
it effects EDV
so it effects proload
which effects pumping ability of the heart
86
2 main parts of a clot
platelet plug
fibrin clot
87
how is fibrin made
fribrinogen is converted to fibrin by thrombin
88
anti clotting mechanisms in endothelium
Stops blood contacting collagen
-no platelet aggregation
Produces prostacyclin and NO
-both inhibit platelet aggregation
Produces tissue factor pathway inhibitor (TFPI)
-stops thrombin production
Expresses thrombomodulin
-binds thrombin & inactivates it
Expresses heparin
also inactivates thrombin
Secretes tissue plasminogen activator (t-PA)
plasminogen converts to plasmin & digests clot
89
continuous capillaries: where are clefted and non clefted found
just clefts: most capillaries inc muscle
non clefts or pores: brain- creates the blood brain barrier and stops K crossing
90
what are fenestrated capillaries
| and where are they found
capillaries with clefts AND pores
needed for specialised fluid exchange- intestine and kidney
91
non polar substances pass using
diffusion across phospholipid membrane
92
polar substances use
clefts and pore to pass through membrane and still use diffusion
93
example of carrier mediated transport
glucose transported in the brain
94
simple way to remember diffusion
more O2 is needed
the more it gets diffused
95
how do starling forces effect water
hydrostatic pressure causes about 20l to leave vessels
while osmotic pressure causes 17l to return
remaining 3l goes to lymphatics which eventually drains to vena cava
96
causes of oedema
lymphatic obstruction from filariasis or surgery
raised CVP in ventricular failure
hypoproteinemia (proteins cause osmotic pressure so nor proteins mean less goes back into blood)
increased capillary permeability in inflammation
97
why is MAP important
main driving force pushing blood through circulation
98
MAP = ? X ?
CO X TPR
99
MAP too low can cause
syncope
100
MAP too high causes
hypertension
101
the 2 levels of control that insure blood flow is sufficient and MAP is sufficient
local/intrinsic mechanisms- for each individual tissue
central/ extrinsic mechanisms- ensure TPR and thus MAP stays in righ balance
102
Local control of blood flow: active metabolic hyperaemia
| trigger
increased metabolic activity
103
Local control of blood flow: active metabolic hyperaemia
| leads to
release of paracrine signal- EDRF or NO
causing arteriolar dilation
washing out metabolites
104
Local control of blood flow: active metabolic hyperaemia
| why does it happen
to ensure blood supply is matched to the metabolic needs of a tissue
105
Local control of blood flow: pressure (flow) autoregulation
| trigger
decrease in perfusion pressure
106
Local control of blood flow: pressure (flow) autoregulation
| leads to
decrease in MAP and therefore decrease in flow
metabolites accumulate
releases paracrine signal
dilating arterioles and returning flow to normal
107
Local control of blood flow: pressure (flow) autoregulation
| why does it happen
ensures that a tissue maintains blood supply despite changes in MAP
108
Local control of blood flow: Reactive hyperaemia
| trigger
occlusion of blood supply
109
Central control of blood flow: hormonal
adrenalin from adrenal medulla
binds to alpha 1
constriction
decrease flow and increase TPR
```
BUT in some tissues- skeletal and cardiac muscle
it also activates beta 2
causing DILATION
increasing flow and decreasing TPR
significant in exercise
```
110
Local control of blood flow: Reactive hyperaemia
| leads to
increase in blood flow
| an extreme version of pressure autoregulation
111
Local control of blood flow: Reactive hyperaemia
| real life example
arm goes red after getting BP taken
112
Local control of blood flow: injury response
| causes activation / release of
c-fibre- pain
substance P
mast cell
histamines
113
Local control of blood flow: injury response
| leads to
arteriolar dilation
so increases blood flow and permeability
114
Local control of blood flow: injury response
| why it happens
aids in delivery of blood born leucocytes to the injured area
115
Central control of blood flow: neural
| sympathetic and parasympathetic actions
sympathetic:
arteriolar constriction
decrease flow and increase TPR
Parasympathetic:
no effect usually
except in genitalia and salivary glands
116
control of blood flow: special area- coronary circulation
blood supply gets interrupted during systole
so shows active hyperaemia- high sensitivity to metabolites
and has a lot of beta 2 receptors
swamping any possible constriction
117
control of blood flow: special area- cerebral circulation
needs to be kept stable whatever
so shows excellent pressure auto regulation
118
control of blood flow: special area- pulmonary circulation
decreases in O2 causes arteriolar constriction- opposite most tissues
ensures blood is directed to a better ventilated part of lungs
119
control of blood flow: special area- renal circulation
shows excellent pressure autoregulation
| as it needs to rely on MAP to filter properly
120
2 SENSORY components of arterial baroreflex
aortic arch baroceptor
carotid sinus baroceptor
121
how doe constriting veins increase BP
increases preload strength and volume
| increasing CO
122
how does constricing arterys increase bp
increasing TPR
123
INTERGRATER component of arterial baroreflex
medullary cardiovascular centre
124
EFFECTOR component of arterial baroreflex: parasympathetic
vagus activation
SA nodes releases acetylcholine
hypopolorising pacemaker cells slowing them
125
EFFECTOR component of arterial baroreflex: sympathetic activation
SA node releases noradrenalin
works on beta 1
pacemaker cells depolarise faster
and increases Ca+ in ventricle
and constricts blood vessels
126
aortic arch nerve supply
vagus nerve
127
other inputs to the medullary cardiovascular centres
cardiopulmonary baroreceptors
blood volume
central chemoreceptors
pCO2 pO2
chemoreceptors in muscle
metabilite conc
joint receptors
join movement
higher centres
hypothalamus and cerebral cortex
128
how does Valsalva manoeuvre effect heart
increases thoracic pressure in aorta
reduces venous filling pressure
decreasing VR EDV SV CO and MAP
reduced MAP is detected by baroreceptors initiating a reflex in CO and TPR
BASICALLY it stops venous return reducing preload and CO
129
how does Valsalva manoeuvre effect heart
increases thoracic pressure in aorta
reduces venous filling pressure
decreasing VR EDV SV CO and MAP
reduced MAP is detected by baroreceptors initiating a reflex in CO and TPR
BASICALLY it stops venous return reducing preload and CO
130
how do changes in posture effect the CVS
standing causes blood to pool in legs
reducing: EDV, preload, SV, CO and MAP
131
how does the body correct the cvs after standing
baroreceptors detect loss in MAP
The information is sent to, and integrated in, the medullary cardiovascular centres.
and will cause
A parasympathetic - dis-inhibition of HR causing an increase in CO
And sympathetic:
increase in HR causing an increase in CO
increase in contractility causing an increase in SV and CO
venoconstriction causing an increase in preload, stroke volume and CO
arteriolar constriction causing an increase in TPR
132
main organ that controls long term BP
kidneys- controlling plasma volume an therefore MAP
133
how does the kidney control plasma volume
by controlling how much water is passed out or reabsorbed:
using Na+ transport to change osmotic gradient
it can make the collecting duct very permeable to water, increasing reabsorption, little urine and higher plasma volume- therefore increasing BP
or make the collecting duct less permeable, decreasing absorption increasing urine and reducing plasma volume- therefore reducing BP
134
what hormones regulate kidney absorption
RAAS system
ADH and vasopressin
atrial natriuretic peptide and brain natriuretic peptide
135
RAAS system: where is renin produced?
juxtaglomerular (granule cells) in the kidney
136
RAAS system: what triggers renin production
Activation of sympathetic nerves to the juxtaglomerular apparatus
Decreased distension of afferent arterioles (the “renal baroreflex”)
Decreased delivery of Na+/Cl- through the tubule
ALL ARE SIGNS OF LOW MAP
137
what does renin do
Converts inactive angiotensinogen to angiotensin I
Which is in turn converted by angiotensin converting enzyme to angiotensin II
138
what does angiotensin II do
Stimulates release of aldosterone from the adrenal cortex
- Increases Na+ reabsorption in the loop of Henle
- Therefore reduces diuresis and increases plasma volume
Increases release of ADH from the pituitary
- Increases water permeability of the collecting duct
- Therefore reduces diuresis and increases plasma volume
- And increases sense of thirst
and vasoconstricts- increasing TPR
ALL INCREASE MAP
139
what part of the pituitary releases ADH
poosterior
140
what trigger release of ADH
signs of low plasma volume of MAP:
A decrease in blood volume (as sensed by cardiopulmonary baroreceptors and relayed via medullary cardiovascular centres)
An increase in osmolarity of interstitial fluid (as sensed by osmoreceptors in the hypothalamus)
Circulating angiotensin II (triggered by the renin-angiotensin-aldosterone system)
141
what does ADH do
Increases the permeability of the collecting duct to H2O, therefore REDUCES diuresis and increases plasma volume
Causes vasoconstriction (hence its alternative name, vasopressin), therefore INCREASING MAP
142
where are Atrial natriuretic peptide and brain natriuretic peptide (ANP BNP) produced
myocardial cells in the atria & (despite the name)
and the ventricles
143
what triggers ANP and BNP
increased distension of atria and ventricles- sign of increased MAP
144
what does ANP and BNP do
increase excretion of Na+
inhibit secretion of renin
act on medullary CV centres to decrease MAP
145
all systems in long term control of blood pressure a
negative feedback loops
