Module 3.2 - Cardiovascular Physiology Flashcards
1
Q
initiation of heart beat
A
heart has an intrinsic beat (ability to beat on its own)
=> auto-rhythmicity
- can beat outside body
2
Q
coordination of contraction
A
of myocardial cells of atria/ventricles through specialised conducting tissue
3
Q
AP of ventricular contractile fibre
A
- rapid depolarisation as fast as nerve AP due to being Na+ driven
- contraction whenever there is Ca2+ => length of contraction is determined by width of plateau
4
Q
electrocardiogram - Pwave
A
atrial depolarisation
=> atrial contraction
5
Q
electrocardiogram - QRS complex
A
- onset of ventricular depolarisation
- atrial repolarisation (but wave is lost within much bigger QRS complex => shape doesn’t represent)
- spread of activation through ventricles
- shape of wave due to direction of spread
6
Q
electrocardiogram - S-T segment
A
when whole ventricle is depolarised (extended plateau of AP)
=> electrical balance
=> no voltage change
elevation/depression if abnormalities in ventricular wall => chest pain
7
Q
electrocardiogram - Twave
A
- ventricular repolarisation (not as rapid)
=> relaxation / start of diastole
8
Q
electrocardiogram - T-P segment
A
when all cardiac myocytes are at RMP
9
Q
chronotrope
A
something that changes heart beat
- positive chronotrope: increase heart rate
10
Q
inotrope
A
something that changes in contractility/contraction power
- positive => increase, negative => decrease
11
Q
regulation of heart rate
A
(autonomic) nervous system regulation of heart rate originates in the cardiovascular centre of medulla oblongata
12
Q
input to cardiovascular centre
A
from higher brain centres (forebrain) + receptors (proprio, baro, chemo)
13
Q
output to effectors
A
parasympathetic (vagus) / sympathetic nerves to heart+ vasomotor nerves (sympathetic) to blood vessels for vasoconstriction
14
Q
sympathetic / parasympathetic balance at rest
A
SA node is dominated by vagal activity at rest (50-70 bpm)
15
Q
regulation of blood pressure
A
ANS (autonomic nervous system) innervation of heart/baroreceptor complexes that help regulate BP
16
Q
regulation of BP - nerve direction
A
- baroreceptors -> cardiovascular centre in medulla
- cardiovascular centre ->
1) SA/AV node - parasympathetic
2) spinal cord - cardiac accelerator nerves -> spinal cord (thoracic level) -> sympathetic trunk ganglion -> SA/AV node, ventricular myocardium (sympathetic)
17
Q
BP hormones
A
circulating hormones
- adrenalin/noradrenalin
- ion concentrations
etc.
18
Q
proprioceptor input
A
major stimulus that accounts for rapid rise in HR at onset of physical activity
19
Q
hyperthermia
A
increases HR
20
Q
sympathetic nervous system increases
A
- HR
- SV
- spontaneous depolarisation of SA/AV nodes
- contractility of ventricles/atria
21
Q
parasympathetic nervous system decreases
A
- HR
- rate of spontaneous depolarisation of SA/AV nodes
22
Q
dicrotic wave
A
rebound from aortic valve closing
23
Q
can you have negative blood pressure
A
yes
24
Q
cardiac output
A
amount/volume of blood ejected into aorta per minute
25
cardiac output unit
mL/min
L/min
26
average cardiac output
5 L/min
- between 4-7 L/min at rest
- can go up to 5x e.g during exercise
- 40 L/min for athletes
27
cardiac output equation
= HR x SV
28
cardiac reserve
difference between max. cardiac output and cardiac output at rest (rates at which heart pumps blood)
- shows maximum capacity of heart to pump blood
29
normal heart rate
normal = 60-100 bpm
- controlled by SA node (sympathetic/parasympathetic activity)
30
normal stroke volume
50-100 mL per beat
31
stroke volume equation
= end diastolic volume (EDV) - end systolic volume (ESV)
32
EDV
max. volume (most full)
- 120-140 mL
33
ESV
min. volume
- 50-70 mL
34
frank-starling law of heart
in stable system, venous return (diastole) = cardiac output (systole)
- increased return => heart works harder => stretch of myocytes => energy of ventricular contraction => forcefulness of contraction => SV increases
- greater force of contraction can occur if the heart muscle is stretched first
35
factors determining SV
1) preload
2) contractility
3) afterload
36
preload
force that stretches cardiac muscle prior to contraction
- increased diastolic filling => increase EDV => increased SV
37
factors changing diastolic filling
- ∆venous return
- ∆blood volume (more blood in system => more blood to heart)
- ∆filling time (duration of ventricular diastole)
- ∆respiratory pump (inhaling => negative pressure around lungs and heart shares same space => also affected - decreased diastolic filling)
- ∆compliance (MI - myocardial infarction damage - becoming stiffer, can't contract as well due to scarred tissue, attack, disease etc.)
38
venous return
amount of blood returning to heart each min from venous system
39
contractility
performance (forcefulness of contraction) of heart (esp left ventricle) at a given preload/afterload
- aka inotropy
- increased contractility => decreased ESV => increased SV
40
factors changing contractility
- autonomic nervous system (increased sympathetic => increased contractility)
- venous return (increased preload => increased contractility)
- [Ca2+] (all factors affecting contractility act by changing [Ca2+])
- drugs (inotropes) - target contractility not longetivity as it doesn't address underlying conditions
- ion balances
- circulating levels of various hormones
41
afterload
amount of pressure that the heart needs to exert to eject blood during ventricular contraction (what heart works against)
- increased afterload => increased ESV => decreased SV
42
factors affecting afterload
- hypertension - high blood pressure
- valve pathologies
- aortic plaques - constriction in aorta
43
ventricular pressure-volume relationship
A: mitral valve opens
B: mitral valve closes
C: aortic valve opens
D: aortic valve closes
44
ventricular pressure-volume relationship - A-B
ventricular filling
- first: pressure decreased due to suction effects of relaxing muscle
- later: pressure rises passively as volume increases
45
ventricular pressure-volume relationship - B-C
isovolumetric contraction
- pressure increases steeply
- no change in volume as aortic valve closed
46
ventricular pressure-volume relationship - C-D
blood ejection
47
ventricular pressure-volume relationship - D-A
isovolumetric relaxation
48
stroke work
heart's pumping action is achieved by mechanical work of myocardium
= area of pressure-volume curve of ventricular contraction (total external work carried out by ventricles during one cardiac cycle)
49
stroke work equation
work done = ∆pressure x ∆volume
50
blood volume distribution
1) systemic veins and venules (blood reservoirs) - 64%
2) systemic arteries and arterioles - 13%
3) pulmonary veins - 9%
4) heart - 7%
5) systemic capillaries - 7%
51
blood pressure
pressure of circulating blood against vessel walls which can vary throughout cardiac cycle
52
mean arterial pressure (MAP) equation
cardiac output (CO) x total peripheral resistance (TPR)
53
total peripheral resistance
amount of force affecting resistance of blood flow through circulatory system
54
poiseuille's law
describes flow is related to factors such as velocity
55
if CO decreases while MAP constant
TPR increases by sympathetic stimulation of smooth muscles => reduce diameter (vasoconstriction) => increase resistance
56
blood hydrostatic pressure (BHP)
force exerted by blood confined within vessels
- arterial: ~35 mm Hg
- venous: ~16 mm Hg
57
blood colloid osmotic pressure (BCOP)
- aka oncotic pressure
form of osmotic pressure induced by proteins in blood
- ~26 mm Hg
58
decreasing BCOP
deficiency/low plasma protein level
59
hemorrhage
release of blood from broken blood vessel
60
interstitial fluid hydrostatic pressure (IFHP)
mechanical pressure exerted on interstitial fluid by elastic recoil of tissues in any region of body
- ~0 mm Hg
61
interstitial fluid osmotic pressure (IFOP)
osmotic force which is the result of differences in water conc. between plasma and interstitial fluid
- ~1 mm Hg
62
capillary exchange
exchange/movement of material between blood and interstitial tissue/fluid across capillary wall
63
ways of capillary exchange
1) diffusion
2) trancytosis
3) bulk flow/filtration
64
diffusion
solute exchange, down conc grad
65
trancytosis
vesicles (contents wrapped in membrane) of large, lipid-soluble (insoluble in H2O/blood)
e.g insulin
66
bulk flow/filtration
- passive movement of flow + substances
- faster than diffusion alone
- net flow is driven by difference between balance of hydrostatic pressure / osmotic pressure gradients (starling's law of capillaries)
67
net filtration - favours filtration
BHP + IFOP
- arterial: 35 + 1
- venous: 16 + 1
68
net filtration - favours reabsorption
BCOP + IFH
- arterial and venous: 26 + 0
69
pressures
(BHP + IFOP) - (BCOP + IFHP)
- arterial: +10 mm Hg
- venous: -9 mm Hg
70
negative pressure means
favours reabsorption
71
organ without lymph vessels
brain - glymphatic system
72
oedema/edema
accumulation of fluid outside vessels
- common symptom of many conditions
- most obvious in legs due to gravity
73
hypertension =>
arterial BHP increases
- vasoconstriction
- increased arterial tone
74
arterial tone
degree of constriction relative to maximally dilated state
75
kidney disease =>
loss of blood proteins (more in urine) => BCOP decreases => low capillary reabsorption
76
heart failure =>
venous BHP increases
77
long-haul travel =>
venous volume increases as heart tries to hold volume (more filled up) => SV increases
venous BHP increases
78
how does long-haul travel increase BHP
- gravity
- leg swelling => venous compression
=> blood pools in venous sytem
=> BHP increased without changing overall blood volume
79
venous volume increases =>
capillary permeability increases => IFOP increases
80
nervous control effect on TPR
decreased frequency of sympathetic nerve activity => vasodilation in systemic blood vessels => increased radius of vessel lumen => decreased resistance to blood flow => decreased total peripheral resistance
81
effect of blood volume on nerve activity
decreased blood volume
=> decreased EDV => decreased SV
and
=> decreased BP => baroreceptors sense => increase sympathetic activity to heart + decreased parasympathetic / vagal
(reflex neural mechanisms that respond to change in arterial pressure)
82
reason for having parallel structure of circulatory structure
allows same hydrostatic gradient at each organ
83
relationship between bloodflow and total cross-sectional area in different blood vessel types
velocity is inversely proportional to cross-sectional area (of all of that type of blood vessel)
84
to increase blood flow
1) increase cardiac output (increase HR and/or SV)
2) redirect existing cardiac output/blood flow to organs that need it (vasoconstriction)
85
what control direction of bloodflow
precapillary sphincters
86
coping with haemorrhage - challenge to homeostasis
- vasoconstriction
- increase HR (need CO to maintain blood)
- clotting to stop bleeding (+ maintain BP)
- redirection
- increase SV by increasing contractility (not much by venous return as blood is being lost
87
baroreceptors
- respond to 'stretch' in arterial wall
- signals connect up to brain via cranial nerves
88
baroreceptors and tonicity
tonically active
- can respond to increases/decreases in BP (not on/off)
89
baroreceptor location
- carotid sinus
- aortic arch
90
carotid sinuses
sits above bifurcation of carotid artery (into two other arteries) along with carotid body
- one of smallest organs
91
vascular tone - increased electrical signals from neuron =>
norepinephrine release onto receptors increases => vasoconstriction / increased HR => increased BP
92
vascular tone and blood vessel size
effect of hormones in response to electrical signals is esp prominent in small arteries/arterioles due to ratio of muscle
- bigger change is required for bigger arteries to cause change
93
total spinal anesthesia
block transmission across neurons in spinal cord from a specific point (below level of heart) down
94
muscle activity in veins and BP
there is smooth muscle in veins but this has a smaller effect on BP due to low pressure, instead affects venous return
95
what increases BP
increased:
- HR
- TPR
- VR (venous return)
96
possible stimuli of change in BP
- haemorrhage
- drinks (1L of water/energy drink)
- standing up quickly
- temperature (hot day => peripheral vasodilation)
97
resistance and radius
resistance is inversely proportional to radius^4
98
redundant physiology
multiple systems that overlap in different ways to affect same variable
99
slow response to increased blood volume
blood volume homeostasis (decreasing) via compensation by kidneys
- need to solve fundamental issue
100
angiotensin II
vasoconstrictor peptide
- increased as a result of low BP (not affected by cardiac sympathetic activity)
101
glossopharyngeal nerves
from carotid sinus -> cardiovascular centre
102
vascular resistance is
1) size of lumen
- inversely proportional to radius^4
2) viscosity
- directly proportional
3) (total) length of blood vessel
- directly proportional
103
alpha receptors
- skeletal muscle
- smooth muscle (blood vessels - arteries/arterioles)
104
beta receptors
- cardiac muscle (myocardium): ventricular muscles, SA/AV nodes
105
Starling’s Law of the Capillaries
the volume of fluid reabsorbed at the venous end of a capillary is nearly equal to the volume of fluid filtered out at the arterial end
106
vagus nerve
only affects heart rate
- NOT contractility/inotropy or vasomotor
107
right subclavian vein
behind collar bone
108
superior sagittal sinus
runs above longitudinal fissure
109
long haul flights
decreased skeletal muscle action => decreased venous return (preload => SV => CO) => increased venous volume => increased venous BHP => stretched pores => increased capillary permeability (large solutes exit vessel) => IFOP increases => NFP increased => interstitial fluid increased => oedema (lymphatic can drain)
110
lactic acid
- causes vasodilation => decrease in BP
- NOT produced when standing still
111
proprioceptive input
does NOT affect HR
- only sends info about location/orientation of joints etc.
